The Most Useful International Business Languages You Should Know

Business is business, and if you have an international company, you must work harder than the average businessman. Since you’ll have to deal with people from other countries, it’s only normal that you’ll have to speak foreign languages to get along with people. Not to mention, speaking multiple languages will give you a better reputation as a person who does business, while your presence abroad will get a boost as well.

The world has many languages, so many that’s it hard to grasp all of them. The average number of languages is said to be 6,500. However, not all of them are used – in reality, there are 2,000 languages that less than 1,000 speakers are using.

Since it’s hard to learn a lot of languages as a single person, it will take a while for you to get used to the business languages. Nowadays, the top languages spoken in business are English, Russian, Spanish, Mandarin Chinese, and Portuguese. Here’s what you should know about them:

The Most Important Languages to Know for Business

  • English

It’s only expected to have English on this list. It’s the international language, and a lot of non-native English or American people speak it. This is why knowing it unlocks one of the obstacles in communication, giving you the opportunity to connect with multiple people.

Apparently, there are more than 1.75 billion people in the world who speak English and can have a conversation in it. So, in business, it’s very likely that you’ll stumble upon it. Even big companies like Airbus or Nokia have chosen it as their official language.

English is the official language of multiple countries including the United Kingdom, Australia, South Africa, and the United States. Knowing it is a big advantage, so if you don’t speak it too well yet, you’d better grab an English grammar manual and start practicing.

  • Russian

Russia is known to be one of the biggest powers of the world, in politics and economics. They’re also known for their potential when it comes to real estate investment, as well as rich culture and reserves of gas. So, Russia being on this list with their language is not too much of a shock. It is spoken in countries outside of Russia too, such as Ukraine, Israel, and the USA. Furthermore, it’s said to be history’s most influential Slavonic language.

If you’ve learned the language, you have a bigger reach in the business world, because workers and entrepreneurs are welcomed by the country if they speak it.

  • Spanish

Spanish is a language that is increasing in influence, and it’s becoming more widely spoken in the USA too. In the USA, there are more than 37 million citizens speaking it, while in the world, 577 million people speak it, and the number continues to grow.

The advantage with Spanish is that it’s not too difficult. In fact, it might be an easy language to learn for English speakers, so you should give it a try if you can.

  • Mandarin Chinese

Did you know that more than 1 billion people speak Mandarin? In any case, you know now. Mandarin is the official language of China, although Chinese has two variations, one being Mandarin, and the other being Cantonese.

China is a big business power and it’s already common knowledge that a lot of products are being imported from China annually. And if you’re an entrepreneur yourself, chances are you’ll clash with Chinese partners or clients at one point in time.

Given they have such an influence, knowing their language will be a big plus. It’s definitely one of the most important business languages, so knowing it won’t be useless.

  • Portuguese

You might be a little surprised to see Portuguese on this list, but even more surprised to know that more than 200 million people speak it. The language is the official one in Brazil, a country that has established as one of the largest economic powers on the planet.

Portuguese is great to learn if your business will have youth as a target. Basically, more than 60% of Portugal’s population consists of young people, respectively people below the 30-year-old mark. So, it would be a good opportunity for you to reach your target market.

Learn Portuguese, and you’ll have better opportunities as an entrepreneur.

Final Thoughts

Languages are a wonderful, interesting thing, all with specific grammar rules and histories. Nowadays, some are more spoken while others are very rare. The most powerful countries, however, have established their languages and thus they’ve become the most important international business languages in the world. Mandarin, Spanish, Portuguese, Russian and English are languages with great potential in business for any worker.

You should learn whichever is more convenient for your situation. Until getting used to working in a different language, maybe you should try Spanish, Mandarin, Portuguese or Russian translation services to help you out.

State of Michigan Nursing Home Administrator Exam

PATIENT TRUST FUNDS

1) Policy:
Must have a policy.
May state that the facility will not handle monies in excess of $5,000.00.
The facility may charge a reasonable fee not to exceed the ACTUAL COST of providing service.

2) Required Printed Information:
This must be given resident upon admission.
A statement that the facility will handle personnal funds if no other person is available.
Periodic statement of accounts (Minimum: Quarterly)

3) Procedure: American Institute of CPA
Quarterly statements including all activity, (A-H) in easily readable form.

Written account of all personal funds held in trust must be sent to the executor, administrator, rep payee or next of kin within 10 DAYS OF THE DEATH OF A PATIENT.

Account must be closed and balance sent to resident within 3 DAYS OF DISCHARGE.

Access to Funds

4) Financial records:
not less than two (2) hours during normal business hours.

5) Petty Cash:
during all normal business hours.

Accounts

6) Funds:
Cannot be CO-MINGLED with any other facility funds (Can with Residents’)

7) Interest Bearing Accounts:
May keep up to $200.00 in a non-interest bearing account of petty cash fund.

Money in excess of $200.00 shall be deposited in an interest bearing account within 15 days of the date the $200.00 minimum is exceeded.

8) Designation For Patient Unable To Handle Own Funds:
Facility notifies the Family Independence Agency, Adult Protective Services in writing when a mentally incompetent patient has no one to act on his behalf.

9) Sale Or Transfer of Ownership
Written receipt from new owner acknowledge receipt of the funds for safeguarding.

10) Surety Bond:
Not LESS than $2,000.00 or 125% of the previous year’s patient trust funds average balance held, whichever is greater.

Michigan State Plan For Long Term Care

11) Department of Community Health (MDCH or DCH)
DCH is responsible for the Medicaid Program under contract to the federal agency named Centers for Medicare and Medicaid Services (CMS).

MDCH also contracts with other departments and agencies to provide specific services.

12) Medical Services Administration (MSA)
This agency, under authority of MDCH writes policy, acts as fiscal intermediary, designs categorical reimbursement programs, audits and authorizes facility-specific reimbursement rates.

13) Bureau of Health Systems: DCH
has this bureau under its department for oversight of the quality of care within nursing homes through the certification process.

The actual certifying agency is CMS. This is accomplished through the surveys and inspections.

14) Department of Community Health, Bureau of Construction Codes, Office of Fire Safety.
DCH contracts with Office of Fire Safety to conduct the Life Safety Code portion of the survey.

15) Michigan Department of Human Services (DHS):
DCH contacts with DHS who determine an individuals Medicaid eligibility and “co-payment” responsibility. DHS utilized the local offices for direct contract with applicants.

16) Bureau of Health Professions: DCH
Has this bureau under its department for oversight and licensing of Nursing Home Administrator (NHA)

17) Michigan Department Community Health
This Department contracts directly with the federal agency CMS and as such is designated responsibility for Title XIX of the Social Security Act.

Currently this program is 56% federally funded and 44% state funded.

18) Medical Service Administration (MSA)
itself handles two primary aspects of the program POLICY AND REIMBURSEMENT.

Medicaid Policy

19) Providers must adhere to
ALL POLICIES TO PARTICIPATE

20) Facility must be licensed
MANDATORY

21) Certification of Facility
VOLUNTARY

22) MDCH uses the
Bureau of Health Systems to perform surveys for this certification.

23) Delivery of Services (Fairness/Non-Discrimination Doctrine)
Services Reimbursed by MSA are listed in the Medicaid manual.

Facilities MUST render covered services to ALL ELIGIBLE recipients in the same scope, quality, and manner as provided to the general public.

24) Compliance:
Facility must render services in accordance with all federal and state statutory and regulatory requirements.

25) Medicaid is Payor of :
LAST RESORT

26) Medicaid Payment is:
PAYMENT IN FULL (critical issue)

For covered services the facility must except the Medicaide reimbursement rate as payment in full for each and every Medicaid recipient.

The facility may not seek additional payment from residents or families for covered services.

27) For NON-COVERED SERVICES
The facility may seek payment from the recipient IF the resident chooses the service AND is informed of the charge PRIOR to receiving the service.

Record Keeping

28) Retention:
Facility services – 6 years
Orders of Contracted Services (Not records) – 6 years

Attending Physician

29) Attending Physicians’ responsibility
Federal and State regulations require the attending physician (MD or DO licensed in Michigan) to provide specific services to recipients.

30) Physician Compliance
It is the facilities responsibility

31) Physician Visits
Every 30 days for first 90 days, then every 60 days thereafter (more frequently if medically necessary)

32) Physicians’ must have
Written Plan of Care, signed

Annual Requirements for Inspection of Care

33) Under State Plan, DCH utilizes its
Bureau of Health Services to complete this during the annual survey.

Process assures that residents are receiving the appropriate care at the APPROPRIATE level of care.

Grounds for Termination of Enrollment or Refusal to Renew

34) Facility actions that:
Threaten the health, safety, or welfare of Medicaid recipients (determined through the survey process)

35) Facility actions that:
Threaten the fiscal integrity of the Medicaid program.

Abuse of Resident Trust Fund

36) Enforcement actions:
Failure to meet the federal conditions of enrollment or participation

Failure to meet the Certification Standards

Termination or suspension of Medicare automatically does the same to Medicaid

37) Patient Pay Amount
recipient must pay to the nursing home each month the amount of income determined to be in excess.

Facility is responsible for collecting

May NOT bill Medicaid for uncollected portion.

38) Co-insurance:
Must be applied to the FIRST DAYS OF STAY.

Remember facility MAY NEVER CHARGE A MEDICAID RECIPIENT MORE than the MEDICAID RATE.

39) Medicaid resident is discharged on the 11th of the month. How much do you charge whom if:

Private Pay Rate: $100.00 per day
Medicaide Rate: $80.00 per day
Patient Payed: $1000.00 per day

Amount due = Medicaid Rate X Days of Stay (80.00 X 10 = 800.)

Facility may charge for day of Admission, but not day of Discharge.
So stay = 10 days.

You must notify the local DSS office of all discharges.

Amount due from (to) resident = Amount Due – Patient Pay Amount for month
(800 – 1000 = -200)
You owe resident $200.00
Bill Medicaid 0.00

39). Under NO circumstances may a facility change the payment status of the resident to private pay and charge the full $100.00.
The DHS determines whether or not the recipient is Medicaid eligible. If the resident had stayed more days, you would have billed Medicaid.

40) Prior authorization for Services is Mandatory for
all recipients BEFORE receiving care.

41) Prior authorization for Routine Services is accomplished
Through the PreAdmissions Screening of PASAAR. Conducted by MDCH by contract to local Community Mental Health (CMH).

Pre-payment review for nursing need.

42) Prior Authorization for Ancillary Services
is Mandatory for all ancillary services (Therapies and Durable medical equipment).

43) Invoice (DSS-1073) is submitted to DCH AFTER
SERVICES RENDERED. You may bill both ROUTINE and ANCILLARY services on the same bill.

44) Therapeutic Leave Days:
Each recipient is entitled to 10 hospital leave days providing:

Hospitalization is unexpected
Return Anticipated within 10 days
Resident returns before day 10

REIMBURSEMENT

45) DCH
is the fiscal intermediary for Medicaid program.

46) Reimbursement Structure:
limits are established by legislature.

47) Cost Reporting:
to determine the facility-specific rates, DCH utilizes the MICHIGAN STATISTICAL and OPERATING COST REORT which must be filed within 90 days of the facility’s fiscal year end.

Relationship Between Medicare and Medicaid

48) Many recipients are eligible for both types of benefits.
If so, then facility MUST first bill Medicare, receive initial payment and then bill Medicaid

49) Medicare Part A:
Routine Services plus Ancillaries

Medicare pays in full for days 1 – 20

On Day 21, you begin to bill co-insurance (Medicaid) for day 21 – 100.

50) A recipient must enroll in Medicare Part A to be eligible for Medicaid.
If a recipient refuses to enroll, he is automatically denied Medicaid.

51) Medicare Part B:
Ancillary Services provided

Outpatient or Medical Services

Therapies (Non Medicare A)

Billable Medical Supplies D.M.E.

Diagnostic Services

Payment: Bill deductible to Medicaid

Workers Compensation

52) Purpose:
Alternative to employer “tort” liability in the legal system.

53) Sole:
Workers Compensation is the sole remedy for workers injured or disabled in the corse of employment.

54) Employees accepting workers compensation
cannot sue the employer

55) Workers Compensation Benefits
are statutory

56) Workers Compensation Rates
are set by rating agency on behalf of insurers

57) Workers Compensation Claims
appeals process is handled by state bureau

58) “Rate Making”
Process used in determining rates to be charged by insurance companies. Rates are set by the bureau

59) “Loss Experience”
Actual Payments and reserves for anticipated payments added together.

60) “Manual (or Book) Rate”
Assume parity with the averages within a given employer group, such as clerical, nursing, maintenance.

61) “Reserves”
Estimates of medical cost and lost time payment (including fringe benefits) that are set aside by the carrier for each anticipated injury AT THE TIME THE CLAIM IS FILED.

62) Michigan is a Total Disability State:
any injury is considered total disability. Either you can work or you can not.

63) Compensable injuries:
any injury arising out of and in the course of employment.

death due to or rising out of the course of employment

any injury received going to or from the workplace on the premises
where work is to be performed and within a reasonable time before and after working hours.

Coverage Liabilities

64) Employers Mandatory Participation:
Every private employer who employs one or more employees 35 hours per week or more for 13 weeks or longer.

65) Compensation Payments:
No loss time compensation shall be paid unless the employee is incapacitated from earning wages for more than one week.

66) Benefits Level:
Maximum weekly benefit is 90% of State average weekly wages as set by the Department of Consumer and Industry Services

67) Statue of Limitations:
Two years from date of injury, or two years from the time that employee knows that injury is work related.

Employers’ Responsibility To Bureau

68) Form 100
“Employers’ Basic Report of Injury” Filed immediately with
The “Bureau of Workers’ Compensation” and copies distributed to
The insurance carrier
The employer and
The employee

69) Form 104
“Petition for Hearing” –

70) Form 107
“Notice of Dispute” aq

Union Process of Recognition and Certification

71) Petition NLRB (National Labor Relations Board
potential union members for interest with signature cards.

show interest must be equal to or greater than 30% of potential bargaining unit interested.

the election (NLRB Conducts; 50% plus 1 of potential bargaining unit members voting wins)

The Nursing Home shall provide a written copy of facility rules and regulations:
to the patient or the patient’s representative upon admission and when the rules and regulations are changed.

The Policy shall be developed by a:
Patient Care Policy Committee

The Patient Care Policy Committee must consist of:
At least 1 Physician, the Director of Nursing, and the Administrator, with such additional memebers as the committee dems appropriate.

Oxygen Administration:
Only personnel who have been trained to administer oxygen shall do so and that Oxygen shall only be administered on the Order of a Physician or as authorized in Emergency Situations.

Infection Control Committee
The Director of Nursing and Representative of Administration, dietary, housekeeping, and maintenace services.

Medical Examination of Patients
1) Except in the case of a Friday Admission, in which case the patient shall be exaimed by a licensed physician within 72 hours.

2) A patient admiitted to a home shall be examained by a licensed physician within 48hours after admission

Medical Examination of Patient currently in the facility:
Shall be seen and, to the extent appropriate, shall be examined by a licensed physician at least once every 60 days, unless justified otherwise and documented by the attending

Standing Orders Must be:
Reproduced in the patients Clinical record and shall be signed by attending physician within 48 hours.

Telephone or Verbal Orders Recorded by the licensed nurse in charge
Shall be countersigned by the physician withhin 48 hours.

The Director of Nursing
Shall be a Registered with specialized training or relevant experience in the area of gerontology and shall be employed FULL TIME BY ONLY 1 NURSING HOME

The Charge Nure
A licensed nurse shall be the charge nurse on each shift or tour of duty and shall be responsible for the immediate direction and supervision of nursing care provided to patients.

In Homes less than 30 beds the Director of Nursing
May serve as Charge Nurse on a shift when present for full shift.

Reporting and enforcement of nurse staff requirements:
A home Shall maintain for a priod of Not Less than 2 years , employee time records, including time cards or their equivalent and payroll record

An Ambulatory Resident/Patient shall have a complete Tub or Shower
under staff supervision at least once a week, unless the physician writes an order to the contrary.

A Bedfast Resident/Patient shall be assisted with bathing or bathed completelt
at least twice a week and shall be partially bath daily and as required due to secretions, excretions, or odoors.

A patient’s Clothing or Bedding shall be changed Promptly
when they become wet or soiled

A patient shall be Weighed and have his or her vital signs tanken and recorded
On Admission and at least Monthly thereaftter or more frequently if ordered by a physician.

Begining Patient Care Planning
An assessment of a patient shall be initiated by licensed nursing personnel within 24 hours of admission and the results of the assessment shall be documented in the patients clinical record.

A Patient Care Confrence
shall be held periodically, but not less than Once Every 90 Days to evaluate a patient’s needs and evaluate care plan

Equipment and Supplies Bed
An individual bed not less than 36 inches wide and 72 inches long, or longer when necessary, with springs in good condition, and a mattress not less than 5 inches thick in good condition, with a nonobsorbent cover.

The home Shall provide a written copy of facility rules and regulations
To the patient or the patients representative upon admission and when the rules and regulations are changed

Diversional Activities
A Home shall provide an on going diversional activities program that stimulates and promotes social interaction, communication, and constructuctive living.

Patient Counsel
shal permit the formation of a patient/resident counsel by interested patients, and at time of admission to home shall inform all of the counsel and the rules if any

When the Dietary or Food service supervisor is other than a registered dietitian
The supevisor shall receive routine consultation and tecnical assisstance from a registered dietitian (R.D) not less than 4 hours every 60 days.

Food and Nutritional Needs of a patient
Shall be met in accordance with the physicians orders in keeping with acceptable standards of practice of most recent recommended daily dietary allowences

Not less than 3 meals or their equivalent
shall be served daily, at regular times, with not more than a 14 – hour span between a substantial evening meal and breakfast.

Menus, postings, filing
as actually served to patients must be kept for preceding 3 montns on file in the home

Food acceptance record
shall be retained in the facility

Self Administration of Medication by a Patient
shall not be permitted, except when special circumstances exist and when supported by a physician’s written order and justification

Diagnostic Services
An arrangement shall be made by the administrator for obtaining promptly and conveniently a clinical laboratoy, x-ray, or other diagnostic services ordered by the physician

A written report of each diagnostic test and service
shall be included in the patients clinical record within 1 week

Clinical Records of DISCHARGED patients
shall be completed within 30 days following discharge.
Clinical records shall be under the supervision of a full time employee of the home

Clinical Records are Retained for a Minimum of
6 years from date of discharge or, in the case of a minor, 3 years after the individual comes of age under state law, which ever is longer.

Accident Records and Incident Reports
shall be prepared for each accident or incident involving a patient, personnel, or visitor and shall include all of the following information.

Employee Records and work Schedules
a daily work schedule shall be prepared in writting and be maintaned to show the number and type of personnel on duty in the home for the previous 3 months

A Time Record for each employee
shall be maintained for not less than 2 years

“Medical Audit”
means the retrospective examination, review, and evaluation of the clinical application of medical knowledge utilized in the diagnosis and treatment of poatients as revealed n the patient’s clinical record and carried out for purpose of education, accountability, and quality control.

“Quality Control”
means the planned and systematic medical management actions which assures the consistent acceptabe quality of health care and services rendered to patients including the use of variousmonitoring techniques.

“Utilization Review”
means retrospective, concurrent, and prospective review of the provision and utilzation of health care services by providers and recipients in terms of cost, effectiveness, efficiiency, and quality

Home Entrance for Physically Hanicapped
IN A NEW CONSTRUCTION, addition, major change, or conversion after AUGUST 22, 1969, at least 1 entrance Shall provide easy access for the Physically handicapped

A minimum od 20 square feet of floor space per patient bed
Shall be provided for dayroom, dining room, recreation, and activity purposes.

A new contruction after August 22, 1969 Shall provide
A sleep, day, dining room, recreation, or activity room with a minimum ceiling height of 8 feet

20 feet of unobstructed vision space outside of any
window in a room requiring windows. One additional foot shall be added to the minimum distance of 20 feet for each 2 foot rise above the first story up to a max of 40 feet of required unobstructed space

A multi bed patient room (not more than 4 beds)
shall have a 3 foot clearance btw beds and not less than 70 square feet of usable floor space per bed

The temerature of HOT WATER at plumbing fixtures used by patients
shall be regulated to provided tempered water NOT LESS than 120 degrees fahrenheit.

A room used for patients shall maintain a regular daytime temperature
of NOT LESS than 72 dehrees fahrenheit

Kitchen and Dietary
A Reliable Thermometer
shall be provided for each refrigerator and freezer

In new construction (August 22, 199) general storage space of
10 square feet shall be provided in the home

In a 100 bed Nursing Home Day Staff
8:1 ration RN?LPN/ CNA

In a 100 bed Nursing Home Evening Staff
12:1 ratio RN/LPN/CNA

In a 100 bed Nursing Home Night Saff
15:1 ration RN/LPN/CNA

Class Outlines and Lesson Plans
shall be retained in the facility for not less than 2 years

MIOSHA
General recording criteria
You must consider an injury or illness to meet the criteria, if it results in
a) DEATH
b) Days away from work
c) Restricted work or transfer to another job
d) Medical treatment beyond first aid
e) LOSS of consciousness

MIOSHA
Retention and Updating
Must save MIOSHA 300 Log during the 5 year storage period

MIOSHA
Hospitilization
Within 8 hours after death of any employee from a work-related incident or the inpatient hospitialization of 3 ormore employees as a result of a work-related incident

MIOSHA incident reporting
You must orally report the fatality/multiple hospitilization by telephone or in person to the Michigan Department of Consumer and Industrial Services, Bureau of Safety and Regulation, State Secondary complex

MIOSHA
If the Building Office is Closed, May I report the incident by leaving a message on MIOSHA’s answering machine, faxing the bureau office, or sending an e-mail?
NO! If you can’t talk to a person at the bureau office you must report the fatality or multiple hospitilization incident using the 800 number

800-858-0397

“Licensed bed capacity”
means the autorized and licensed bed complement of a nursing home

Rule #107 Type Documentation
When the statue or these rules required a document or parts of a document to be printed in 12 point type the distance btw the top

Rule # 111 Governing Body
The governing body of the nursing home shall assume full responsibility for the overall conduct and operation of the home

The Governing Body Shall Appoint a
Licensed Nursing Home Administrator and shall deligate to the administrator the responsibility of operating the facility according to the policy and perceedures they established

Rule #112 Posting Resident Rights
Shall develop, adopt, post in a public place, distribute, and implement a Policy on the rights and responsibilities of patients in accordance with the requirements

All patient complaints shall be investigated with in
15 days of the complaint and home within 30 days following the complaint the home shall provide complintee a written status report or results of investigation

Patient Trust
Policy that home will not handle funds freater than $5,000.00

Patient has the right to have a representative from_____________ to handle his/her funds
Social Security Administration

Disaster Plan
Shall have a written Plan or procedure to be followed in case of fire, explosion, or other emergency

A regular Simulated Drill
shall be held for each shift NOT LESS than 3 times per year

Building Construction
If the building has a common wall with a nonconforming building, the common wall is a fire barrier having at least two hour fire resistance rating

Interior Walls and Partitions in building of Type I or Type II
construction shall be noncombustible or limited-combustible material.

Interior Walls and Partitions in building of Type I or Type II
shall be noncombustible or limited-combustible materials

Interior Finish 2000 EXISTING
Interior finish for corridors and exitways, includeing exposed interior surface of building has flame spread rating of Class A or Class B

Interior Finish 2000 NEW
Must have Flame Spread Rating of Class A or Class B. LOWER PORTION OF CORRIDOR WALLS CAN BE CLASS C

Corridor Walls and Doors 2000 EXISTING
are separated from use areas by walls constructed with at least 1/2 hour fire resistance rating.

Corridor Walls 2000 NEW
NO fire resistance rating is required for corridor walls.

Doors 2000 EXISTING
doors protecting corridor opening in other than required enclosures of verticle openings, exits, or hazardous areas shall be constructed of 1 3/4 inch sold-bond wood

Doors in Sprinkler buildings
are only required to resist smoke.

Exit Components 2000 Exists
such as stairways are enclosed with construction having a fire resistance rating of at least one hour,

Smoke Barriers New 2000
shall be provided to form at least two smoke compartments on every sleeping room floor for more than 30 patients

The smoke compartment
shall not exceed 22,500 square feet and smoke barrier shall not exceed 200 feet

Exit and Exit Access
Not less than Two exits, REMOTE from each other, are provided for each floor or fire section of the building

Exit and Exit access shall be arranged such that no
cooridor, aisle or passageway has a pocket or dead-end exceeding 30 feet

Width of Aisle or Corridors 2000 EXISTING
clear and unobstructed, serving as exits shall be at least 4 feet

Width of Aisles or Corridors 2000 NEW
clear and unobstructed serving as exit access in hospitals and nursing homes shall be at least 8 feet

Illumination of Means and Egress including exit discharge
is arranged so that failor of any single lighting fixture (bulb) will not leave the area in darkness

Emergency Lighting of at least
1 1/2 hour duraton is provided in accordance

Fire Alarm System 2000 Existing
There shall be ANNUNCIATION of the fire alarm system to an approved central station.

Fire Alarm System 2000 NEW
There shall be remote annunciation of the fire alarm system to an approved central station

Automatic Smoke Detection 2000 New
An automatic dectection system is installed in all cooridors with detector spacing not further apart than 30 ft on center, nor more than 15 ft from any wall.

Windor and Door 2000 Existing
Every patient sleeping room shall have an outside window or outside door.

The allowable height shall not exceed 36 inches (91 cm) above the floor.

Soiled linen or trash collection receptacles
shall not exceed 3 gal (121) in capacity

Oxygen storage locations of greater than
3,000 cu ft are enclosed by a one-hour separation.

Generators are inspected
weekly and exercised under LOAD for 30 minutes per month and shall be in accordance

National Fire Protection Association
Private, nonprofit organizaton – NOT A GOVERNMET AGENCY.

Author of Life Safety Code

Nursing Homes are required by OBRA to meet LSC

Proceedure in Event of Fire
1) Removing all residents involved
2) Transmitting alarm
3) Isolating the fire by closing doors
4) Evacuating by plan

Stairs: Clearance
44″; riser height – 7″ max

Smoke Towers
stair enclosure designed to limit penetration of heat and smoke. No more than 1% of the volume of air in stairwell will emanate from fire area

Handrails at bottom of stairs
Must extend parallel to floor for 12″

Windows must have
opening force requirement of no more 5lbs.

Preventive Maintenance
1) Save expense of requirs
2) Save labor
3) Assure safety

Facility Temperature
71F – 81F

Bed Space for each Patient
80 sq ft per resident in multi-bed rooms,
100 sq ft in private room

Obra Requirement for Housekeeping
Services necessary to maintain a sanitary, orderly, and clean interior.

Pharmacology – Ch. 3 – Pharmacokinetics

aka Biodisposition; The effects of biologic systems on drugs. It deals w/ the Absorption, Distribution, & Elimination of Drugs. Loading & Maintenance Doses can be calculated.
What is Pharmacokinetics? What processes are involved? What can be calculated in Pharmacokinetics?

The concentration of a drug AT THE RECEPTOR SITE (in contrast to drug concentrations that are more readily measured like in the blood)
What is Effective Drug Concentration?

Vd = (Amount of Drug in the Body) / (Plasma Drug Concentration) in Volume Units; The higher the Vd, the more the drug has been distributed to the tissues as opposed to free flowing in the plasma
What is the Volume of Distribution (Vd)?

CL = (Rate of Elimination of Drug) / (Plasma Drug Concentration) in Volume per Unit Time
What is Clearance (CL)?

CONSTANT (the ratio of elimination to plasma concentration is the same regardless of plasma concentration)
What is the Clearance of Drugs that are eliminated w/ 1st Order Kinetics?

1) Type of Drug; 2) Condition of Organs of Elimination (Liver, Kidney, etc); Clearance is often Flow-Limited because the clearance of a drug is sometimes very effectively extracted by an organ (the blood is completely cleared of the drug as it passes thru the organ); In these conditions, blood flow thru the eliminating organ is more important
What 2 things is Clearance dependent on? How is Clearance often Flow-Limited?

1) Ethanol; 2) Aspirin; 3) Phenytoin
Majority of Drugs follow 1st Order Kinetics. Which 3 important drugs do NOT follow this?

t1/2 = (.7 x Vd) / (CL); The time required for the amount of drug to fall to 50% of an earlier measurement; derived from Vd & Clearance; CONSTANT for 1st order kinetics
What is Half-Life? What is the Half-Life of drugs following 1st Order Kinetics?

The fraction (or %) of drug concentration/dose that reaches the Systemic Circulation; Unity or 100%
What is Bioavailability? Bioavailability of IV administered drugs?

Incomplete Absorption (expulsion of drug by intestinal transporters by intestine), 1st Pass Metabolism, & Any Distribution into Other Tissues that occurs before the drug enters the systemic circulation
What factors REDUCE Bioavailability of drugs administered other ways besides IV?

It is the Area Under the Plasma Concentration Curve (or AUC); (AUCroute) / (AUCiv); AUC is the graphic area under a plot of Drug Conc. versus Time after a single dose
How is Bioavailability measured on a graph curve? What is AUC?

The elimination of drug that occurs after administration but before it enters the systemic circulation; Ex: during passage thru Gut Wall, Portal Circulation, or Liver for an orally administered drug)
What is the 1st Pass Effect?

The fraction of the drug removed from the perfusing blood during its passage thru the organ; Drugs that have a high hepatic extraction ratio have a large 1st pass effect so the bioavailability of these drugs after oral administration will be low
What is Extraction Ratio?

Oral administration
What route of administration has a large 1st pass effect & therefore low bioavailability?

A plan for drug administration over a period of time. An appropriate regimen results in the achievement of therapeutic levels of the drug in the blood w/o exceeding the minimum toxic concentration;
What is a Dosage Regimen?

Maintenance: To maintain the plasma concentration w/in a specified range over long periods of therapy; Loading Dose: Necessary to achieve the target plasma level Rapidly and the volume of distribution is large; it is used to “Load” the volume of distribution w/ the drug
When are Maintenance Doses given? Loading Doses?

Dosing Rate = (Clearance x Desired Plasma Concentration) / (Bioavailability); Vd is not involved
What is Maintenance Dose? Which parameter is not involved?

Loading Dose = (Vd x Desired Plasma Concentration) / (Bioavailability); Clearance is not involved
What is Loading Dose? Which parameter is not involved?

The safe range b/t the minimum therapeutic concentration (Trough) & the minimum toxic concentration of the drug (Peak)
What is the Therapeutic Window? What are the Trough & Peak concentrations of a drug?

Renal Disease or Reduced Cardiac Output, sometimes Liver Disease; Corrected Dose = (Average Dose) x (Patient’s Creatinine Clearance / 100mL/min)
Which conditions normally reduces the clearance of drugs? What is the formula for the corrected dose needed for patient’s where the elimination of their drugs is altered by disease?

The condition in which the average total amount of drug in the body does NOT change over multiple dosing cycles (ex: The condition in which the rate of drug elimination = The rate of Administration)
What is Steady State?

Target English, Grade 9, Unit 7, Lesson 1

Survival equipment
Survival equipment

Emergency blankets
Emergency blankets

Whistle
Whistle
A thing you blow that makes a sound

Signal flare
Signal flare

first aid kit
first aid kit
A set of tools that you use for a simple medical treatment that is given as soon as possible.

oars
oars
A long, thin, usually wooden pole with a blade at one end, used to row or steer a boat.

survive (v)
stay alive

sea sickeness tablet
sea sickeness tablet

survival manual

priority (n)
of great importance

induce (v)
persuade; bring about

Emergency Care-Chapter 20-Cardiac Emergencies-

4 heart valves
tricuspid, bicuspid (mitrosol), pulmonary, aortic

cardiopulmonary resuscitation
actions taken to revive a person by keeping the person’s heart and lungs working

defibrillation
delivery of an electrical shock to stop the fibrillation of heart muscles and restore a normal heart rhythm

acute coronary syndrome (cardiac compromise)
a blanket term used to represent any symptoms related to lack of oxygen (ischemia) in the heart muscles

ischemia
hypoxia for the heart; will result in tissue damage

the heart fails because of 2 functions
electrical, mechanical or both

cardiac compromise pain radiates
along the arms, down to upper abdomen, or up to the jaw; patients complain of radiation to the left arm more than the right

dyspnea
shortness of breath; labored or difficult breathing

bradycardia
heart rate below 60

tachcardia
heart rate above 100

what drugs can I administer
oxygen, aspirin, nitroglycerin

what do I need to administer those drugs
Online medical direction for aspirin and nitroglycerin

dose of aspirin
81 mg cheweable *4 or 325 mg

dose of nitroglycerin
0.4 mg

acute coronary syndrome: what position
place in position of comfort, typically sitting up. Except, those who are hypotensive (systolic below 90-100) will feel better lying down.

Scan 20-2 on page 476
GREAT for drugs

7 types of cardiac conditions
coronary artery disease, aneurysm, electrical or mechanical malfunctions, angina pectoris, acute myocardial infarction, congestive heart failure

coronary artery disease
diseases that affect the arteries of the heart

CAD: result of
fatty deposits on the inner walls of arteries, plaque, calcium hardened

CAD: thrombus
a clot formed of blood and plaque attached to the inner wall of an artery or vein

CAD: occlusion
blockage, cutting off blood flow

CAD: embolism
blockage of a vessel by a clot or foreign material brought to the site by the blood current, from upstream

aneurysm
the dilation, or ballooning, of a weakened section of the wall of an artery

Aneurysm: if ruptures
tissues beyond the rupture can be damaged because the oxygenated blood they need is escaping and not reaching the tissue. Death from shock can occur very quickly

dysrhythmia
an irregular, absent heart rhythm. Brady or tachycardia, and activity with no pulse.

mechanical malfunctions of the heart
hypoxia causes death of parts of the myocardium. The dead area could be a mechanical portion (valves, muscle strength)

angina pectoris
pain in the chest due to reduced blood supply to the heart and a portion of the heart muscle is hypoxic

angina pectoris: onset then what?
comes on after stress or exertion, goes away within minutes after no more exertion

nitroglycerin
medication that dilates the blood vessels

acute myocardial infarction
the condition in which a portion of the myocardium dies as a result of oxygen starvation; often called a heart attack by laypersons

sudden death
a cardiac arrest that occurs within 2 hours of the onset of symptoms. The patient may have no prior symptoms of coronary artery disease

AMI: treatments
fibrinolytics, balloon angioplasty or balloon catheterization, beta blocker

fibrinolytics
to dissolve the clot that is blocking the coronary artery

angioplasty or catheterization
insert a catheter with a balloon that can be inflated to reopen circulation to the heart

beta blocker
slows the heart and makes it beat less strongly

congestive heart failure
the failure of the heart to pump efficiently, leading to excessive blood or fluids in the lungs, the body, or both

edema
swelling resulting from a buildup of fluid in the tissues

pulmonary edema
accumulation of fluid in the lungs

when alveoli burst from edema you will hear
crackling or bubby lung sounds called rales

pedal edema
accumulation of fluid in the feet or ankles

2010 Buck Module 11 Exam B

Anesthesia code for a biopsy of the clavicle.
00454 Hint: Anesthesia, clavicle

Anesthesia for bilateral vasectomy.
00921 Hint: Anesthesia, vasectomy. Do not use modifier -50 because the ‘bilateral’ procedure is included in this code.

Assign a CPT® anesthesia code for debridement of third-degree burns of right arm, 6% body surface area.
01952 Hint: Anesthesia, burns, debridement, and/or excision

Anesthesia for diagnostic arthroscopic procedure of the knee joint.
01382 Hint: Anesthesia, knee

Anesthesia code for a tympanotomy of the left ear performed on an 11-month-old female. Include the qualifying circumstances code.
00126, 99100
Hint: Anesthesia, tympanotomy. To locate the qualifying circumstances code, see anesthesia, special circumstances, extreme age.

Anesthesia for radical hysterectomy.
00846 Hint: Anesthesia, hysterectomy, radical

Anesthesia for tracheobronchial reconstruction.
00539 Hint: Anesthesia, trachea, reconstruction

Assign a CPT® anesthesia code for repair of cleft palate.
00172 Hint: Anesthesia, cleft palate repair

Assign a CPT® anesthesia code for total hip replacement, open procedure.
01214 Hint: Anesthesia, replacement, hip

Anesthesia for burr holes.
00214 Hint: Anesthesia, burr holes

Dermatology Pathology Slides from Lecture

B. Papule<br />
palpable lesion, <10 mm
B. Papule
palpable lesion, <10 mm
What is the type of lesion?
A. Macule
B. Papule
C. Patch
D. Plaque
E. Ulcer
C. Patch
C. Patch
What is the type of lesion?
A. Macule
B. Papule
C. Patch
D. Plaque
E. Ulcer

D. Plaque
D. Plaque
What is the type of lesion?
A. Macule
B. Papule
C. Patch
D. Plaque
E. Ulcer
E. Ulcer
E. Ulcer
What is the type of lesion?
A. Macule
B. Papule
C. Patch
D. Plaque
E. Ulcer
Scabies
Scabies
axilla distribution, *burrows*
Scabies
Scabies
*burrows*
Scabies
Scabies
*burrows*; finger web involvement
Scabies
Scabies
RIGHT mite itself
MIDDLE poop
LEFT cyst
Nodular Scabies
Nodular Scabies
Nodular Scabies
Nodular Scabies
hundred to thousands of mites
Fire Ant Sting
Fire Ant Sting
pustules
papulovesicles
Head lice
Head lice
nits
Pubic Louse
Pubic Louse
Body/Head Louse
Body/Head Louse
Tick
Tick
Flea
Flea
Flea Bites
Flea Bites
leg involvement
not displaying “breakfast, lunch, and dinner” pattern
Brown Recluse Bite (Note that Black Widow bites do not cause cutaneous lesions.)
Brown Recluse Bite
(Note that Black Widow bites do not cause cutaneous lesions.)
necrotic ulceration
Brown Recluse Bite (Note that Black Widow bites do not cause cutaneous lesions.)
Brown Recluse Bite
(Note that Black Widow bites do not cause cutaneous lesions.)
necrotic ulceration
*Lichen Planus* (*Can progress to squamous cell carcinoma.*)
*Lichen Planus*
(*Can progress to squamous cell carcinoma.*)
purple, polygonal, pruritic papules and plaques
commonly seen on the wrists, genitalia, and buccal mucosa
*Lichen Planus* (*Can progress to squamous cell carcinoma.*)
*Lichen Planus*
(*Can progress to squamous cell carcinoma.*)
purple, polygonal, pruritic papules and plaques
*Wickham’s striae* (reticulated scaling) on the *buccal mucosa*
also seen on the wrists and genitalia
Miliaria Crystalina (Caused by occlusion of eccrine sweat ducts and seen in
Miliaria Crystalina
(Caused by occlusion of eccrine sweat ducts and seen in “hot, humid” weather. Note that miliaria *rubra [monomorphic red papules]* and *profunda [with pustules]* are progressively deeper with more inflammation.)
“dew drops” without inflammation
Keratosis Pilaris
Keratosis Pilaris
keratotic firm flesh-colored to red follicularly based papules
seen on lateral arms, thighs, +/- cheeks
Lichen Nitidus (Histology demonstrates a characteristic *ball and claw* pattern.)
Lichen Nitidus
(Histology demonstrates a characteristic *ball and claw* pattern.)
flat-topped, asymptomatic, shiny papules
seen on arms, dorsal hands, genitalia, and trunk
D. Mouth *Lichen planus
D. Mouth
*Lichen planus “likes” the buccal mucosa, specifically.*
What other body parts does this “like?”
A. Eye
B. Feet
C. Finger
D. Mouth
E. Scalp
Open comedonal (non-inflammatory) (Acne is caused by the gram positive anaerobe **Proprionibacterium acnes**.)
Open comedonal (non-inflammatory)
(Acne is caused by the gram positive anaerobe **Proprionibacterium acnes**.)
Name the acne.
Severe Nodulocystic Acne
Severe Nodulocystic Acne
Name the acne.
(“Are you impressed by it?”)
Acne Rosacea (Findings include facial erythema, telangiectasias, papules, and pustules. *Does not present with comedomes.* Rosacea is exacerbated by sun exposure, ethanol, and
Acne Rosacea
(Findings include facial erythema, telangiectasias, papules, and pustules. *Does not present with comedomes.* Rosacea is exacerbated by sun exposure, ethanol, and “flushing” agents.)
central facial erythema
Rhinophyma (This is a complication of rosacea. Ocular symptoms include blepharitis, conjunctivitis, keratitis.)
Rhinophyma
(This is a complication of rosacea. Ocular symptoms include blepharitis, conjunctivitis, keratitis.)
usually in males with long history of sun exposure and ethanol consumption
Gram Negative Folliculitis (Treat with ampicillin or augmentin.)
Gram Negative Folliculitis
(Treat with ampicillin or augmentin.)
pustules on acne patient
Impetigo (Caused by S. aureus or Streptococcus pyogenes.)
Impetigo
(Caused by S. aureus or Streptococcus pyogenes.)
*honey crusts*
can have vesicles or bullae
Satellite Candida (Associated with obesity and DM.)
Satellite Candida
(Associated with obesity and DM.)
beefy red eroded plaque, intertriginous areas
*satellite pustules and papules*
Satellite Candida (Associated with obesity and DM.)
Satellite Candida
(Associated with obesity and DM.)
beefy red plaque, intertriginous areas
*satellite pustules and papules*
Pustular Psoriasis (Most commonly limited to palms and soles. Treat with MTX or Soriatane.)
Pustular Psoriasis
(Most commonly limited to palms and soles. Treat with MTX or Soriatane.)
*lake of pus* with skin sloughing
A. Comedonal
A. Comedonal
Type of acne?
A. Comedonal
B. Inflammatory
C. Mixed
D. Nodulocystic
E. Rosacea
Morphea (Biopsy shows markedly thickened collagen bundles, with entrapment or compression of sweat glands, adnexal structures, and blood vessels. *Labs results are negative for ANA, anti-centromere, and Scl-70.*)
Morphea
(Biopsy shows markedly thickened collagen bundles, with entrapment or compression of sweat glands, adnexal structures, and blood vessels. *Labs results are negative for ANA, anti-centromere, and Scl-70.*)
white, well demarcated plaque of induration with rim of hyperpigmentation
perhaps some violaceous change
Morphea (Biopsy shows markedly thickened collagen bundles, with entrapment or compression of sweat glands, adnexal structures, and blood vessels. *Labs results are negative for ANA, anti-centromere, and Scl-70.*)
Morphea
(Biopsy shows markedly thickened collagen bundles, with entrapment or compression of sweat glands, adnexal structures, and blood vessels. *Labs results are negative for ANA, anti-centromere, and Scl-70.*)
*coup de sabre*
Progressive Systemic Sclerosis (*Positive for ANA, Scl-70. Treat with physical therapy.* Complications include severe HTN, conduction defects, pericarditis, CHF, renal failure, pulmonary fibrosis; esophageal dysmotility and strictures.)
Progressive Systemic Sclerosis
(*Positive for ANA, Scl-70. Treat with physical therapy.* Complications include severe HTN, conduction defects, pericarditis, CHF, renal failure, pulmonary fibrosis; esophageal dysmotility and strictures.)
shiny, swollen fingers
difficulty opening mouth (beaked facies)
CREST Syndrome: Telangiectasias (Calcinosis of skin, Raynaud's, Esophageal dysmotility, Sclerodactaly, Telangiectasias; *positive for ANA, anti-centromere, negative for Scl-70.*)
CREST Syndrome: Telangiectasias
(Calcinosis of skin, Raynaud’s, Esophageal dysmotility, Sclerodactaly, Telangiectasias; *positive for ANA, anti-centromere, negative for Scl-70.*)
superficial dilated blood vessels
CREST Syndrome: Raynaud's (Calcinosis of skin, Raynaud's, Esophageal dysmotility, Sclerodactaly, Telangiectasias; *positive for ANA, anti-centromere, negative for Scl-70.*)
CREST Syndrome: Raynaud’s
(Calcinosis of skin, Raynaud’s, Esophageal dysmotility, Sclerodactaly, Telangiectasias; *positive for ANA, anti-centromere, negative for Scl-70.*)
sausage digits, swollen, shiny
Lichen Sclerosus (et atrophicus) (Commonly misdiagnosed as child abuse. Treat with high potency topical steroids with or without minocyclin/doxycycline.)
Lichen Sclerosus (et atrophicus)
(Commonly misdiagnosed as child abuse. Treat with high potency topical steroids with or without minocyclin/doxycycline.)
porcelain white; sharply demarcated with purpura; *cigarette paper* skin
usually seen in genital area, but may be generalized
Granuloma Annulare (Commonly diagnosed as *ringworm, which displays annular papules/plaques with scaling.*)
Granuloma Annulare
(Commonly diagnosed as *ringworm, which displays annular papules/plaques with scaling.*)
annular papules/plaques with central clearing
seen on the dorsal hands and feet
Necrobiosis Lipoidica (Called
Necrobiosis Lipoidica
(Called “diabeticorum,” as 2/3 of patients also have abnormal glucose metabolism.)
red-brown to yellow plaques with prominent telangiectasias
commonly seen on the shins
B. Morphea (
B. Morphea
(“coup de sabre*)
What is the diagnosis?
A. Granuloma annulare
B. Morphea
C. Necrobiosis lipoidica
D. Lichen sclerosus
E. Systemic sclerosis
Petechiae (Most prominent in legs; if patient is bedridden, in back and sacrum.)
Petechiae
(Most prominent in legs; if patient is bedridden, in back and sacrum.)
pinpoint to 3mm in size
Actinic (
Actinic (“Solar”) Purpura
(Chronic sun induces blood vessel fragility; loss of “shock absorbers” of the dermis. Skin atrophy and solar elastosis is usually severe.)
ecchymoses; skin atrophy and bleeding
usually seen on dorsolateral arms and dorsal hands
Systemic Amyloidosis (Also shows pinch purpura and macroglossia.)
Systemic Amyloidosis
(Also shows pinch purpura and macroglossia.)
eyelid purpura
DIC
(Uncontrolled clotting causes diffuse thrombus formation, which leads to consumption of platelets and thrombocytopenia. Other findings include prolonged prothrombin time, hypofibrinogenemia, and fibrinogen degradation products.)
petechiae, purpuric stellate (irregular) ecchymosis; central necrosis most characteristic
Leukocytoclastic Cutaneous Vasculitis
(Check for fever and arthritis in order to rule out sepsis. Causes include SLE and RA. Order ANA, viral hepatitis panel [especially for Hepatitis C] and rheumatoid factor to determine cause.)
palpable purpura of the legs
Gonococcemia caused by N. gonorrhoeae (Culture cervical/penile urethra, oropharynx, and rectum; treat with IV ceftriaxone.)
Gonococcemia caused by N. gonorrhoeae
(Culture cervical/penile urethra, oropharynx, and rectum; treat with IV ceftriaxone.)
necrotic, hemorrhagic pustule on extremity
may also present with swollen knee
Tinea (Pityriasis) Versicolor (*Worse in hot/humid environments.*)
Tinea (Pityriasis) Versicolor
(*Worse in hot/humid environments.*)
fairly well demarcated, hypopigmented atrophic plaques with fine scale
usually seen on chest, back, and shoulders
Tinea (Pityriasis) Versicolor (*Worse in hot/humid environments.*)
Tinea (Pityriasis) Versicolor
(*Worse in hot/humid environments.*)
fairly well demarcated, hyperpigmented atrophic plaques with fine scale
usually seen on chest, back, and shoulders
Tinea (Pityriasis) Versicolor (*Worse in hot/humid environments.*)
Tinea (Pityriasis) Versicolor
(*Worse in hot/humid environments.*)
fairly well demarcated, erythematous atrophic plaques with fine scale
usually seen on chest, back, and shoulders
Tinea (Pityriasis) Versicolor (Hyphae and spores can be seen.)
Tinea (Pityriasis) Versicolor
(Hyphae and spores can be seen.)
*chopped spaghetti and meatballs*
KOH stain
Vitiligo (Associated with Grave's disease and autoimmune thyroiditis, pernicious anemia, alopecia areata, and Addison's disease.)
Vitiligo
(Associated with Grave’s disease and autoimmune thyroiditis, pernicious anemia, alopecia areata, and Addison’s disease.)
periorificial, sharply marginated white (depigmented) non-scaly patches
Vitiligo (Associated with Grave's disease and autoimmune thyroiditis, pernicious anemia, alopecia areata, and Addison's disease.)
Vitiligo
(Associated with Grave’s disease and autoimmune thyroiditis, pernicious anemia, alopecia areata, and Addison’s disease.)
periorificial, sharply marginated white (depigmented) non-scaly patches
Repigmentation in Vitiligo (Vitiligo is associated with Grave's disease and autoimmune thyroiditis, pernicious anemia, alopecia areata, and Addison's disease.)
Repigmentation in Vitiligo
(Vitiligo is associated with Grave’s disease and autoimmune thyroiditis, pernicious anemia, alopecia areata, and Addison’s disease.)
process from hair follicle outward
Pityriasis Alba<br />
(Usually first noticed in spring or summer. Repigmentation takes >1 year.)
Pityriasis Alba
(Usually first noticed in spring or summer. Repigmentation takes >1 year.)
hypopigmented poorly demarcated atrophic plaques with fine white scale.
usually affects the cheeks; also commonly involves upper outer arms
Postinflammatory Hypopigmentation (Can be caused by contact dermatitis, autoimmune effects, local trauma; Xrays and frostbite; phenols and sulfhydryl compounds, discoid lupus erythematosus, atopic dermatitis, psoriasis.)
Postinflammatory Hypopigmentation
(Can be caused by contact dermatitis, autoimmune effects, local trauma; Xrays and frostbite; phenols and sulfhydryl compounds, discoid lupus erythematosus, atopic dermatitis, psoriasis.)
rim of hyperpigmentation at edge
scarring in center
Postinflammatory Hypopigmentation (Can be caused by contact dermatitis, autoimmune effects, local trauma; Xrays and frostbite; phenols and sulfhydryl compounds, discoid lupus erythematosus, atopic dermatitis, psoriasis.)
Postinflammatory Hypopigmentation
(Can be caused by contact dermatitis, autoimmune effects, local trauma; Xrays and frostbite; phenols and sulfhydryl compounds, discoid lupus erythematosus, atopic dermatitis, psoriasis.)
subtle, somewhat well-demarcated scaly white patches/macules
Tuberous Sclerosis (Cutaneous findings include *ash leaf macules/patches*: 80-90%, *adenoma sebacum*/facial angiofibromas): 80-90%; periungual fibromas/*Koenen's tumors*: 50% *shagreen patches*: 21-80%; flesh to yellowish-orange plaques (*orange peel/pigskin*) usually in the lumbosacral area. Other findings include calcified brain
Tuberous Sclerosis
(Cutaneous findings include *ash leaf macules/patches*: 80-90%, *adenoma sebacum*/facial angiofibromas): 80-90%; periungual fibromas/*Koenen’s tumors*: 50% *shagreen patches*: 21-80%; flesh to yellowish-orange plaques (*orange peel/pigskin*) usually in the lumbosacral area. Other findings include calcified brain “tubers,” mental retardation, seizure disorders, brain tumors, renal cysts, cardiac rhabdomyomas.)
)
“ash-leaf” macule/patch
Tuberous Sclerosis (Cutaneous findings include *ash leaf macules/patches*: 80-90%, *adenoma sebacum*/facial angiofibromas): 80-90%; periungual fibromas/*Koenen's tumors*: 50% *shagreen patches*: 21-80%; flesh to yellowish-orange plaques (*orange peel/pigskin*) usually in the lumbosacral area. Other findings include calcified brain
Tuberous Sclerosis
(Cutaneous findings include *ash leaf macules/patches*: 80-90%, *adenoma sebacum*/facial angiofibromas): 80-90%; periungual fibromas/*Koenen’s tumors*: 50% *shagreen patches*: 21-80%; flesh to yellowish-orange plaques (*orange peel/pigskin*) usually in the lumbosacral area. Other findings include calcified brain “tubers,” mental retardation, seizure disorders, brain tumors, renal cysts, cardiac rhabdomyomas.)
4+ ash-leaf patches
Tuberous Sclerosis (Cutaneous findings include *ash leaf macules/patches*: 80-90%, *adenoma sebacum*/facial angiofibromas): 80-90%; periungual fibromas/*Koenen's tumors*: 50% *shagreen patches*: 21-80%; flesh to yellowish-orange plaques (*orange peel/pigskin*) usually in the lumbosacral area. Other findings include calcified brain
Tuberous Sclerosis
(Cutaneous findings include *ash leaf macules/patches*: 80-90%, *adenoma sebacum*/facial angiofibromas): 80-90%; periungual fibromas/*Koenen’s tumors*: 50% *shagreen patches*: 21-80%; flesh to yellowish-orange plaques (*orange peel/pigskin*) usually in the lumbosacral area. Other findings include calcified brain “tubers,” mental retardation, seizure disorders, brain tumors, renal cysts, cardiac rhabdomyomas.)
Shagreen patch
“ash-leaf” patch
Tuberous Sclerosis (Cutaneous findings include *ash leaf macules/patches*: 80-90%, *adenoma sebacum*/facial angiofibromas): 80-90%; periungual fibromas/*Koenen's tumors*: 50% *shagreen patches*: 21-80%; flesh to yellowish-orange plaques (*orange peel/pigskin*) usually in the lumbosacral area. Other findings include calcified brain
Tuberous Sclerosis
(Cutaneous findings include *ash leaf macules/patches*: 80-90%, *adenoma sebacum*/facial angiofibromas): 80-90%; periungual fibromas/*Koenen’s tumors*: 50% *shagreen patches*: 21-80%; flesh to yellowish-orange plaques (*orange peel/pigskin*) usually in the lumbosacral area. Other findings include calcified brain “tubers,” mental retardation, seizure disorders, brain tumors, renal cysts, cardiac rhabdomyomas.)
adenoma sebaceum
angiofibromas
dental enamel pits
Tuberous Sclerosis (Cutaneous findings include *ash leaf macules/patches*: 80-90%, *adenoma sebacum*/facial angiofibromas): 80-90%; periungual fibromas/*Koenen's tumors*: 50% *shagreen patches*: 21-80%; flesh to yellowish-orange plaques (*orange peel/pigskin*) usually in the lumbosacral area. Other findings include calcified brain
Tuberous Sclerosis
(Cutaneous findings include *ash leaf macules/patches*: 80-90%, *adenoma sebacum*/facial angiofibromas): 80-90%; periungual fibromas/*Koenen’s tumors*: 50% *shagreen patches*: 21-80%; flesh to yellowish-orange plaques (*orange peel/pigskin*) usually in the lumbosacral area. Other findings include calcified brain “tubers,” mental retardation, seizure disorders, brain tumors, renal cysts, cardiac rhabdomyomas.)
Koenen’s tumors
C. Neisseria infection Gonococcemia is the diagnosis; culture cervical/penile urethra, oropharynx, and rectum; treat with IV ceftriaxone.
C. Neisseria infection
Gonococcemia is the diagnosis; culture cervical/penile urethra, oropharynx, and rectum; treat with IV ceftriaxone.
What is the best diagnosis?
A. ITP
B. Leukocytoclastic vasculitis
C. Neisseria infection
D. Solar purpura
E. TTP
Idiopathic Guttate Hypomelanosis (No good therapy.)
Idiopathic Guttate Hypomelanosis
(No good therapy.)
macules, “sprinkled confetti”
seen on shins of females
Leprosy (Tissue biopsy for Fite stain. Caused by Mycobacterium leprae and spread by armadillos.)
Leprosy
(Tissue biopsy for Fite stain. Caused by Mycobacterium leprae and spread by armadillos.)
hypopigmented, hypestetic macule/patch/plaque
Hypopigmented Mycosis Fungoides (Cutaneous T-Cell Lymphoma.)
Hypopigmented Mycosis Fungoides
(Cutaneous T-Cell Lymphoma.)
hypopigmented areas, bathing trunk distribution
D. Shagreen patch Cutaneous findings in Tuberous Sclerosis include ash leaf macules/patches: 80-90%, adenoma sebacum/facial angiofibromas): 80-90%; periungual fibromas/Koenen's tumors: 50% shagreen patches: 21-80%; flesh to yellowish-orange plaques (orange peel/pigskin) usually in the lumbosacral area.
D. Shagreen patch
Cutaneous findings in Tuberous Sclerosis include ash leaf macules/patches: 80-90%, adenoma sebacum/facial angiofibromas): 80-90%; periungual fibromas/Koenen’s tumors: 50% shagreen patches: 21-80%; flesh to yellowish-orange plaques (orange peel/pigskin) usually in the lumbosacral area.
Which of the following may be found in this patient?
A. Cafe au lait macules
B. Coup de sabre
C. Neurofibromas
D. Shagreen patch
Telogen Effluvium (Pull test: many telogen hairs (small bulb at end of hair), club-shaped hairs. Order CBC, ANA, RPR, thyroid to rule out anemia, hypothyroidism, nutritional, toxic drugs, lupus, syphilis.)
Telogen Effluvium
(Pull test: many telogen hairs (small bulb at end of hair), club-shaped hairs. Order CBC, ANA, RPR, thyroid to rule out anemia, hypothyroidism, nutritional, toxic drugs, lupus, syphilis.)
significant thinning of the parietal region
no inflammation or scarring
Telogen Effluvium (Pull test: many telogen hairs (small bulb at end of hair), club-shaped hairs. Order CBC, ANA, RPR, thyroid to rule out anemia, hypothyroidism, nutritional, toxic drugs, lupus, syphilis.)
Telogen Effluvium
(Pull test: many telogen hairs (small bulb at end of hair), club-shaped hairs. Order CBC, ANA, RPR, thyroid to rule out anemia, hypothyroidism, nutritional, toxic drugs, lupus, syphilis.)
thinning of the vertex scalp
Androgenic Alopecia
(Caused by a testosterone-induced reversion of mature hair to vellus hairs in a specific pattern; physical exam shows nonscarring, frontal, vertex affected terminal hairs replaced by vellus, smooth shiny scalp; will see diffuse thinning of vertex in women.)
no scarring or inflammation
Androgenic Alopecia
(Caused by a testosterone-induced reversion of mature hair to vellus hairs in a specific pattern; physical exam shows nonscarring, frontal, vertex affected terminal hairs replaced by vellus, smooth shiny scalp; will see diffuse thinning of vertex in women.)
no scarring or inflammation
Androgenic Alopecia
(Caused by a testosterone-induced reversion of mature hair to vellus hairs in a specific pattern; physical exam shows nonscarring, frontal, vertex affected terminal hairs replaced by vellus, smooth shiny scalp; will see diffuse thinning of vertex in women.)
vertex loss
Trichotillomania (Caused by self-induced traumatic hair loss by plucking, twisting or rubbing; physical exam shows empty hair follicles in *strange geometric patterns*, traumatized follicles, perifollicular hemorrhage, pigmentary casts, increased number of catagen hairs.)
Trichotillomania
(Caused by self-induced traumatic hair loss by plucking, twisting or rubbing; physical exam shows empty hair follicles in *strange geometric patterns*, traumatized follicles, perifollicular hemorrhage, pigmentary casts, increased number of catagen hairs.)
irregularly-shaped with variable hair length
no scaling or erythema
Trichotillomania (Caused by self-induced traumatic hair loss by plucking, twisting or rubbing; physical exam shows empty hair follicles in *strange geometric patterns*, traumatized follicles, perifollicular hemorrhage, pigmentary casts, increased number of catagen hairs.)
Trichotillomania
(Caused by self-induced traumatic hair loss by plucking, twisting or rubbing; physical exam shows empty hair follicles in *strange geometric patterns*, traumatized follicles, perifollicular hemorrhage, pigmentary casts, increased number of catagen hairs.)
diffuse thinning
“difficult to tell here”
Trichotillomania (Caused by self-induced traumatic hair loss by plucking, twisting or rubbing; physical exam shows empty hair follicles in *strange geometric patterns*, traumatized follicles, perifollicular hemorrhage, pigmentary casts, increased number of catagen hairs.)
Trichotillomania
(Caused by self-induced traumatic hair loss by plucking, twisting or rubbing; physical exam shows empty hair follicles in *strange geometric patterns*, traumatized follicles, perifollicular hemorrhage, pigmentary casts, increased number of catagen hairs.)
bizarre geometric shape
Alopecia Areata (Caused by autoimmune hair loss; physical exam shows *round or oval patches, exclamation point hairs*, no inflammation or scarring and skin biopsy shows *
Alopecia Areata
(Caused by autoimmune hair loss; physical exam shows *round or oval patches, exclamation point hairs*, no inflammation or scarring and skin biopsy shows *”Swarm of Bees”*- lymphocytes surrounding base of hair follicles.)
oval/round patch, exclamation point hairs
Alopecia Areata, Ophiasis type (most common) (Caused by autoimmune hair loss; physical exam shows *round or oval patches, exclamation point hairs*, no inflammation or scarring and skin biopsy shows *
Alopecia Areata, Ophiasis type (most common)
(Caused by autoimmune hair loss; physical exam shows *round or oval patches, exclamation point hairs*, no inflammation or scarring and skin biopsy shows *”Swarm of Bees”*- lymphocytes surrounding base of hair follicles.)
sharply demarcated, oval and smooth patch
Alopecia Areata (Caused by autoimmune hair loss; physical exam shows *round or oval patches, exclamation point hairs*, no inflammation or scarring and skin biopsy shows *
Alopecia Areata
(Caused by autoimmune hair loss; physical exam shows *round or oval patches, exclamation point hairs*, no inflammation or scarring and skin biopsy shows *”Swarm of Bees”*- lymphocytes surrounding base of hair follicles.)
totalis
Nonspecific nail pitting, here associated with Alopecia Areata
Nonspecific nail pitting, here associated with Alopecia Areata
Lupus Erythematosus (Causes chronic/discoid patchy scarring or non-scarring alopecia; broken hairs at frontal hairline, carpet tack scale, dyspigmentation, inflammation. Biopsy shows interface dermatitis- lymphocytic infiltrate and DE junction, liquifactive degeneration of basal cells, follicular plugging.)
Lupus Erythematosus
(Causes chronic/discoid patchy scarring or non-scarring alopecia; broken hairs at frontal hairline, carpet tack scale, dyspigmentation, inflammation. Biopsy shows interface dermatitis- lymphocytic infiltrate and DE junction, liquifactive degeneration of basal cells, follicular plugging.)
erythema
scaling
some scarring, possibly
Lupus Erythematosus (Causes chronic/discoid patchy scarring or non-scarring alopecia; broken hairs at frontal hairline, carpet tack scale, dyspigmentation, inflammation. Biopsy shows interface dermatitis- lymphocytic infiltrate and DE junction, liquifactive degeneration of basal cells, follicular plugging.)
Lupus Erythematosus
(Causes chronic/discoid patchy scarring or non-scarring alopecia; broken hairs at frontal hairline, carpet tack scale, dyspigmentation, inflammation. Biopsy shows interface dermatitis- lymphocytic infiltrate and DE junction, liquifactive degeneration of basal cells, follicular plugging.)
lots of erythema
scaling
Tinea Capitis (Demonstrates scarring alopecia [*if you see scarring on the scalp of a child, think tinea*]; useful labs include Wood's light, KOH exam, culture; griseofulvin is the gold standard of treatment; *topicals do not work.*)
Tinea Capitis
(Demonstrates scarring alopecia [*if you see scarring on the scalp of a child, think tinea*]; useful labs include Wood’s light, KOH exam, culture; griseofulvin is the gold standard of treatment; *topicals do not work.*)
young children
Tinea Capitis (Demonstrates scarring alopecia [*if you see scarring on the scalp of a child, think tinea*]; useful labs include Wood's light, KOH exam, culture; griseofulvin is the gold standard of treatment; *topicals do not work.*)
Tinea Capitis
(Demonstrates scarring alopecia [*if you see scarring on the scalp of a child, think tinea*]; useful labs include Wood’s light, KOH exam, culture; griseofulvin is the gold standard of treatment; *topicals do not work.*)
exclamation point
young child
E. Tinea capitis (Demonstrates scarring alopecia [*if you see scarring on the scalp of a child, think tinea*]; useful labs include Wood's light, KOH exam, culture; griseofulvin is the gold standard of treatment; *topicals do not work.*)
E. Tinea capitis
(Demonstrates scarring alopecia [*if you see scarring on the scalp of a child, think tinea*]; useful labs include Wood’s light, KOH exam, culture; griseofulvin is the gold standard of treatment; *topicals do not work.*)
Diagnosis in this 8 year old?
A. Exzema
B. Discoid Lupus erythematous
C. Psoriasis
D. Seborrheic Dermatitis
E. Tinea capitis
Onychomycosis (Most commonly caused by T. rubrum, T. mentagrophytes; physical exam shows yellow, thickening and dystrophy, subungual debris, superficial white changes.)
Onychomycosis
(Most commonly caused by T. rubrum, T. mentagrophytes; physical exam shows yellow, thickening and dystrophy, subungual debris, superficial white changes.)
“crumbly nails”
debris, yellow changeDIFFERENTIAL psoriasis, trauma, lichen planus

Onychomycosis (Most commonly caused by T. rubrum, T. mentagrophytes; physical exam shows yellow, thickening and dystrophy, subungual debris, superficial white changes.)
Onychomycosis
(Most commonly caused by T. rubrum, T. mentagrophytes; physical exam shows yellow, thickening and dystrophy, subungual debris, superficial white changes.)
hallux involvement
Psoriasis (Caused by increased rate of proliferation of keratinocytes; physical exam shows *nail pitting*, dystrophy, onycholysis, *
Psoriasis
(Caused by increased rate of proliferation of keratinocytes; physical exam shows *nail pitting*, dystrophy, onycholysis, *”oil drop sign”* [yellow color under nail], fingernails affected more than toenails.)
onycholysis
oil drop
Psoriasis (Caused by increased rate of proliferation of keratinocytes; physical exam shows *nail pitting*, dystrophy, onycholysis, *
Psoriasis
(Caused by increased rate of proliferation of keratinocytes; physical exam shows *nail pitting*, dystrophy, onycholysis, *”oil drop sign”* [yellow color under nail], fingernails affected more than toenails.)
pitting
Pustular Psoriasis (Most commonly limited to palms and soles. Treat with MTX or Soriatane.)
Pustular Psoriasis
(Most commonly limited to palms and soles. Treat with MTX or Soriatane.)
nail and skin involvement
pustules, “lakes of pus”
Psoriasis (Caused by increased rate of proliferation of keratinocytes; physical exam shows *nail pitting*, dystrophy, onycholysis, *
Psoriasis
(Caused by increased rate of proliferation of keratinocytes; physical exam shows *nail pitting*, dystrophy, onycholysis, *”oil drop sign”* [yellow color under nail], fingernails affected more than toenails.)
Acute Paronychia
(ACUTE S. aureus infection leading to inflammation and infection of proximal and lateral nail folds; red, swollen, painful; CHRONIC Candida infection leading to inflammation and infection of proximal and lateral nail folds; loss of cuticle, creases in nail plate, scaling)
red, swollen
Acute Paronychia
(ACUTE S. aureus infection leading to inflammation and infection of proximal and lateral nail folds; red, swollen, painful; CHRONIC Candida infection leading to inflammation and infection of proximal and lateral nail folds; loss of cuticle, creases in nail plate, scaling)
swollen
Clubbing<br />
(Bulbous thickening of distal digit, proximal nail fold soft and thickened; hypertrophic osteoarthropathy; Lovibond's angle > 180 degrees)
Clubbing
(Bulbous thickening of distal digit, proximal nail fold soft and thickened; hypertrophic osteoarthropathy; Lovibond’s angle > 180 degrees)
Koilonychia (Caused by iron deficiency anemia, Plummer-Vinson syndrome, Hemachromatosis, CAD, syphilis, polycythemia, acanthosis nigricans, familial forms; physical exam shows spoon nails, thin and concave)
Koilonychia
(Caused by iron deficiency anemia, Plummer-Vinson syndrome, Hemachromatosis, CAD, syphilis, polycythemia, acanthosis nigricans, familial forms; physical exam shows spoon nails, thin and concave)
spoon-shaped
Beau's Lines (Temporary arrest of growth of nail plate leading to ransverse furrows that grow out; Triggered by traumatic/stressful events: childbirth, febrile illness, drug reaction. Note that the nails *grow out at a rate of 1mm/month.*)
Beau’s Lines
(Temporary arrest of growth of nail plate leading to ransverse furrows that grow out; Triggered by traumatic/stressful events: childbirth, febrile illness, drug reaction. Note that the nails *grow out at a rate of 1mm/month.*)
transverse furrows affecting all nails
A. Beau's Lines (Temporary arrest of growth of nail plate leading to ransverse furrows that grow out; Triggered by traumatic/stressful events: childbirth, febrile illness, drug reaction. Note that the nails *grow out at a rate of 1mm/month.*)
A. Beau’s Lines
(Temporary arrest of growth of nail plate leading to ransverse furrows that grow out; Triggered by traumatic/stressful events: childbirth, febrile illness, drug reaction. Note that the nails *grow out at a rate of 1mm/month.*)
What is the diagnosis?
A. Beau’s lines
B. Clubbing
C. Fungus
D. Koilonychia
E. Paronychia
F. Psoriasis
Stasis (Venous Insufficiency) Ulcers (Common in CHF and incompetent leg vein vales; physical exam shows significant, bilateral swelling of medial lower legs, brownish dyspigmentation and petechiae, commonly *Most common etiology of leg ulcers,* check DP/PT pulses to rule out associated arterial disease.)
Stasis (Venous Insufficiency) Ulcers
(Common in CHF and incompetent leg vein vales; physical exam shows significant, bilateral swelling of medial lower legs, brownish dyspigmentation and petechiae, commonly
*Most common etiology of leg ulcers,* check DP/PT pulses to rule out associated arterial disease.)
medial aspect of lower leg
full thickness epidermal loss with petechiae (pinpoint – 3 mm)
Arterial Ulcers (History commonly shows intermittent claudication, rest pain; physical exam demonstrates punched out ulcers on the lateral aspects of the legs (classically); DP/PT pulses absent, cool extremities, local hair loss.)
Arterial Ulcers
(History commonly shows intermittent claudication, rest pain; physical exam demonstrates punched out ulcers on the lateral aspects of the legs (classically); DP/PT pulses absent, cool extremities, local hair loss.)
sharply demarcated, “punched out” ulcer
Pyoderma Grangrenosum (Physical exam shows distinctive ulceration: acute onset of a painful ulcer with an undermined border [Dr. Stetson likes to say
Pyoderma Grangrenosum
(Physical exam shows distinctive ulceration: acute onset of a painful ulcer with an undermined border [Dr. Stetson likes to say “you could stick a probe into it”], which heals with *cribriform scarring*; associated with ulcerative colitis, rheumatoid arthritis, and acute myeloblastic leukemia; *biopsy reveals neutrophils throughout the dermis, but cultures are negative.*)
cribriform scarring
Chancre in Primary Syphilis (Note that the *chancre caused by Treponema pallidum is painless*, whereas the *chancroid caused by Haemophilus ducreyi is painful*.)
Chancre in Primary Syphilis
(Note that the *chancre caused by Treponema pallidum is painless*, whereas the *chancroid caused by Haemophilus ducreyi is painful*.)
Spirochetes (You can test for the syphilitic Treponema pallidum by dark field microscopy.)
Spirochetes
(You can test for the syphilitic Treponema pallidum by dark field microscopy.)
dark field microscopy
Secondary Syphilis HIGHLY STRESSED)

Secondary Syphilis

HIGHLY STRESSED)

*”nickles and dimes” on palm*
Secondary Syphilis
Secondary Syphilis
“moth-eaten” alopecia
Chancroid (This is caused by Haemophilus ducreyi, and should be differentiated from the chancre of primary syphilis, as caused by Treponema pallidum.)
Chancroid
(This is caused by Haemophilus ducreyi, and should be differentiated from the chancre of primary syphilis, as caused by Treponema pallidum.)
“punched out, painful” ulcers
Chancroid (This is caused by Haemophilus ducreyi, and should be differentiated from the chancre of primary syphilis, as caused by Treponema pallidum.)
Chancroid
(This is caused by Haemophilus ducreyi, and should be differentiated from the chancre of primary syphilis, as caused by Treponema pallidum.)
painful, ragged ulcer
“undetermined”NOTE difficult to culture

Haemophilis ducreyi (Causative agent of chancroid.)
Haemophilis ducreyi
(Causative agent of chancroid.)
“school of fish”
gram negative coccobacilli
HSV
HSV
grouped ulcerations on erythematous base
HSV
HSV
grouped vesicles on erythematous base
HSV
HSV
Tzanck smear showing multinucleated keratinocytes, ballooning degeneration
steel-gray nuclei
chromatin margination
Factitial Ulcer
(Causes include a variety of insults: deep excoriations, injections of foreign material, heat/cold. Note that the patient will often deny causing the ulceration and the history will be unreliable. These ulcers appear as bizarre, geometric shaped angulated ulcers. Must be suspected clinically; especially if location is unusual for ulcerations, and there are no other explanation for the ulcer.)
*angulated linear heme-crusted ulcer*
C. Pyoderma gangrenosum Note underlying edge, where
C. Pyoderma gangrenosum
Note underlying edge, where “one could stick a probe.”
What is the best diagnosis?
A. Arterial ulcer
B. Factitial ulcer
C. Pyoderma gangrenosum
D. Stasis ulcer
E. Syphilis
Eczema, Atopic Dermatitis (Most common form is atopic dermatitis; appearance is classically more ill-defined scaly erythematous coalescing papules and plaques; *infantile form favors face*, scalp and extensors; 80% develop allergic rhinitis)
Eczema, Atopic Dermatitis
(Most common form is atopic dermatitis; appearance is classically more ill-defined scaly erythematous coalescing papules and plaques; *infantile form favors face*, scalp and extensors; 80% develop allergic rhinitis)
cheek, arms
Eczema, Atopic Dermatitis (Appearance is classically more ill-defined scaly erythematous coalescing papules and plaques; *childhood form favors flexors; often lichenified*; 40% have persistent disease as adults)
Eczema, Atopic Dermatitis
(Appearance is classically more ill-defined scaly erythematous coalescing papules and plaques; *childhood form favors flexors; often lichenified*; 40% have persistent disease as adults)
plaque, erythematous papules
seborrheic appearance
Eczema (Appearance is classically more ill-defined scaly erythematous coalescing papules and plaques; *childhood form favors flexors; often lichenified*; 40% have persistent disease as adults)
Eczema
(Appearance is classically more ill-defined scaly erythematous coalescing papules and plaques; *childhood form favors flexors; often lichenified*; 40% have persistent disease as adults)
possible lichenification in the cubital fossa
Eczema (Associated with keratosis pilaris, xerosis, icthyosis vulgaris, Dennie-morgan lines, *hyperlinear palms*, pityriasis alba; can become erythrodermic. Often impetiginized [S. aureus, honey crusted] or considered *eczema herpeticum [painful super-infection by HSV]*).
Eczema
(Associated with keratosis pilaris, xerosis, icthyosis vulgaris, Dennie-morgan lines, *hyperlinear palms*, pityriasis alba; can become erythrodermic. Often impetiginized [S. aureus, honey crusted] or considered *eczema herpeticum [painful super-infection by HSV]*).
hyperlinear palms
Hand Dermatitis (Caused by contact irritant or allergy; can also be associated with foot/ feet dermatitis; related to atopic dermatitis)
Hand Dermatitis
(Caused by contact irritant or allergy; can also be associated with foot/ feet dermatitis; related to atopic dermatitis)

thickening

NOTE the papulovesicles on the lateral finger

Hand Dermatitis (Caused by contact irritant or allergy; can also be associated with foot/ feet dermatitis; related to atopic dermatitis)
Hand Dermatitis
(Caused by contact irritant or allergy; can also be associated with foot/ feet dermatitis; related to atopic dermatitis)
Hand Dermatitis (Caused by contact irritant or allergy; can also be associated with foot/ feet dermatitis; related to atopic dermatitis)
Hand Dermatitis
(Caused by contact irritant or allergy; can also be associated with foot/ feet dermatitis; related to atopic dermatitis)
Asteatotic Eczema (Appearance is termed
Asteatotic Eczema
(Appearance is termed “eczema craquele” and “dried river bed;” favors shins, flanks, post axillary line. Associated with aging, xerosis, low humidity, frequent bathing)
“plate-like or fish-like” changes
dry river bed
Nummular Dermatitis
(Appears as pruritic coin-shaped eczematous lesions with a chronic, recurrent course. Associated with contact sensitization and stasis, but not atopy. More common in older patients.)
*coin-shaped*, scaly
Nummular Dermatitis
(Appears as pruritic coin-shaped eczematous lesions with a chronic, recurrent course. Associated with contact sensitization and stasis, but not atopy. More common in older patients.)
Phyto Contact Dermatitis (Poison Ivy here) (Usually eczematous in appearance; caused by irritants in 80% of cases and by allergies in 20% of cases [this includes application of *Neosporin/Polysporin/Triple antibiotics or topical benadryl*])
Phyto Contact Dermatitis (Poison Ivy here)
(Usually eczematous in appearance; caused by irritants in 80% of cases and by allergies in 20% of cases [this includes application of *Neosporin/Polysporin/Triple antibiotics or topical benadryl*])
eye involvement
linear pattern
Acute Contact Dermatitis
(Usually eczematous in appearance; caused by irritants in 80% of cases and by allergies in 20% of cases [this includes application of *Neosporin/Polysporin/Triple antibiotics or topical benadryl*])
eczematous changes with vesicles
Contact Dermatitis, caused by leather (Usually eczematous in appearance; caused by irritants in 80% of cases and by allergies in 20% of cases [this includes application of *Neosporin/Polysporin/Triple antibiotics or topical benadryl*])
Contact Dermatitis, caused by leather
(Usually eczematous in appearance; caused by irritants in 80% of cases and by allergies in 20% of cases [this includes application of *Neosporin/Polysporin/Triple antibiotics or topical benadryl*])
Seborrheic Dermatitis (Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale]; can be severe and refractory in HIV)
Seborrheic Dermatitis
(Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale];
can be severe and refractory in HIV)
scalp involvement
Seborrheic Dermatitis, here as cradle cap in infant (Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale]; can be severe and refractory in HIV)
Seborrheic Dermatitis, here as cradle cap in infant
(Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale];
can be severe and refractory in HIV)
intertrigious area
Seborrheic Dermatitis (Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale]; can be severe and refractory in HIV)
Seborrheic Dermatitis
(Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale];
can be severe and refractory in HIV)
eyebrow scaling
Seborrheic Dermatitis (Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale]; can be severe and refractory in HIV)
Seborrheic Dermatitis
(Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale];
can be severe and refractory in HIV)
scalp and forehead involvement
Seborrheic Dermatitis (Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale]; can be severe and refractory in HIV)
Seborrheic Dermatitis
(Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale];
can be severe and refractory in HIV)
brown, angular, ring shaped
could be fungal
Seborrheic Dermatitis (Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale]; can be severe and refractory in HIV)
Seborrheic Dermatitis
(Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale];
can be severe and refractory in HIV)
impressive scaling and redness over the face
guttate (drop-like)
Seborrheic Dermatitis (Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale]; can be severe and refractory in HIV)
Seborrheic Dermatitis
(Favors scalp, ears, face, central chest, and intertrigious areas; associated with with Malassezia Furfur [pitrysorom ovale];
can be severe and refractory in HIV)
Stasis Dermatitis
(Appears as eczematous dermatitis due to venous insufficiency and dependent edema; often associated with allergic contact dermatitis. Stasis dermatitis is often seen in combination with venous hypertension, varicosities, edema, venous ulceration, hemosiderin deposits, and lipodermatosclerosis, and confers a risk for stasis ulcer and contact sensitization/ dermatitis)
varicosities, venous ulceration
pigmentary changes
Stasis Dermatitis
(Appears as eczematous dermatitis due to venous insufficiency and dependent edema; often associated with allergic contact dermatitis. Stasis dermatitis is often seen in combination with venous hypertension, varicosities, edema, venous ulceration, hemosiderin deposits, and lipodermatosclerosis, and confers a risk for stasis ulcer and contact sensitization/ dermatitis)
petechiae, ulceration, hyperpigmentation
Stasis Dermatitis
(Appears as eczematous dermatitis due to venous insufficiency and dependent edema; often associated with allergic contact dermatitis. Stasis dermatitis is often seen in combination with venous hypertension, varicosities, edema, venous ulceration, hemosiderin deposits, and lipodermatosclerosis, and confers a risk for stasis ulcer and contact sensitization/ dermatitis)
pigmentary changes only, longstanding
Lichen Simplex Chronicus (Secondary finding due to chronic rubbing and scratching; continued by *Itch-scratch-itch cycle*)
Lichen Simplex Chronicus
(Secondary finding due to chronic rubbing and scratching; continued by *Itch-scratch-itch cycle*)
Lichen Simplex Chronicus (Secondary finding due to chronic rubbing and scratching; continued by *Itch-scratch-itch cycle*)
Lichen Simplex Chronicus
(Secondary finding due to chronic rubbing and scratching; continued by *Itch-scratch-itch cycle*)
spikiness; not all at same level
vertical streaking of collagen
*irregular epithelial hyperplasia*NOTE compare to psoriasis histology

Neurodermatitis (Neurodermatitis/Neurodermatology includes delusions of parasitosis, factitional disorders, and endogenous pruritus [kidney, liver, thyroid, anemia, lymphoma, parasites, other])
Neurodermatitis
(Neurodermatitis/Neurodermatology includes delusions of parasitosis, factitional disorders, and endogenous pruritus [kidney, liver, thyroid, anemia, lymphoma, parasites, other])
irregular presentation
linear heme crusts
post inflammatory changes
Neurodermatitis (Neurodermatitis/Neurodermatology includes delusions of parasitosis, factitional disorders, and endogenous pruritus [kidney, liver, thyroid, anemia, lymphoma, parasites, other])
Neurodermatitis
(Neurodermatitis/Neurodermatology includes delusions of parasitosis, factitional disorders, and endogenous pruritus [kidney, liver, thyroid, anemia, lymphoma, parasites, other])
old scarring from past flares
angulated
upper back only
Neurodermatitis (Neurodermatitis/Neurodermatology includes delusions of parasitosis, factitional disorders, and endogenous pruritus [kidney, liver, thyroid, anemia, lymphoma, parasites, other])
Neurodermatitis
(Neurodermatitis/Neurodermatology includes delusions of parasitosis, factitional disorders, and endogenous pruritus [kidney, liver, thyroid, anemia, lymphoma, parasites, other])
linear scratches
DIFFERENTIAL contact dermatitis
Neurodermatitis (Neurodermatitis/Neurodermatology includes delusions of parasitosis, factitional disorders, and endogenous pruritus [kidney, liver, thyroid, anemia, lymphoma, parasites, other])
Neurodermatitis
(Neurodermatitis/Neurodermatology includes delusions of parasitosis, factitional disorders, and endogenous pruritus [kidney, liver, thyroid, anemia, lymphoma, parasites, other])
bizarre ulceration pattern
Pityraisis Rosea (Appears as *classically well circumscribed papules and plaques* in a
Pityraisis Rosea
(Appears as *classically well circumscribed papules and plaques* in a “Christmas” or “fir” tree appearance on back, upside down on chest; primarily involves trunk. The primary plaque is referred to as a herald patch.)
sharply demarcated, erythematous papules, plaques, some annular (central clearing)
not very much scaling
truncal predominance
Pityriasis Rosea (Appears as *classically well circumscribed papules and plaques* in a
Pityriasis Rosea
(Appears as *classically well circumscribed papules and plaques* in a “Christmas” or “fir” tree appearance on back, upside down on chest; primarily involves trunk. The primary plaque is referred to as a herald patch.)
sharply demarcated annular and erythematous papules and plaques
truncal distribution
Psoriasis (Appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
Psoriasis
(Appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
papulosquamous eruption at scalp
thick scaling
Psoriasis (Appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
Psoriasis
(Appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
papulosquamous eruption
sharply demarcated
scaly
Psoriasis (Appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
Psoriasis
(Appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
very erythematous
swollen joints with potential arthritic changes
Psoriasis (Appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
Psoriasis
(Appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
*nail pitting*
plaque on right
Psoriasis (Appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
Psoriasis
(Appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
onycholysis
*oil drop*
Psoriasis (Dermatologic appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
Psoriasis
(Dermatologic appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
club shaped
equal levelNOTE compare to histology of lichen simplex chronicus

Psoriasis (Appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)
Psoriasis
(Appearance is a classic papulosquamous eruption favoring elbows, knees, scalp, and sacral area, *usually sparing the face*. Nail findings [onycholysis, pits, oil drop (most specific] are highly correlated with arthritis.)

*Monroe’s microabscess*

NOTE compare to histology of lichen simplex chronicus

Mycosis Fungoides, a cutaneous T cell lymphoma (Erythrodermic patch progresses to intensely pruritic, well-developed plaques in a *bathing trunk distribution* [clinically diagnostic]. These then progress to low grade, insidious tumors. Less developed lesions are typically not pruritic. Median duration from onset to definitive diagnosis is 4-6 years. Dermatopathic lymphadenopathy usually present.)
Mycosis Fungoides, a cutaneous T cell lymphoma
(Erythrodermic patch progresses to intensely pruritic, well-developed plaques in a *bathing trunk distribution* [clinically diagnostic]. These then progress to low grade, insidious tumors. Less developed lesions are typically not pruritic. Median duration from onset to definitive diagnosis is 4-6 years. Dermatopathic lymphadenopathy usually present.)
plaques, slightly scaly
buttocks and lower trunk most affected
Mycosis Fungoides, a cutaneous T cell lymphoma (Erythrodermic patch progresses to intensely pruritic, well-developed plaques in a *bathing trunk distribution* [clinically diagnostic]. These then progress to low grade, insidious tumors. Less developed lesions are typically not pruritic. Median duration from onset to definitive diagnosis is 4-6 years. Dermatopathic lymphadenopathy usually present.)
Mycosis Fungoides, a cutaneous T cell lymphoma
(Erythrodermic patch progresses to intensely pruritic, well-developed plaques in a *bathing trunk distribution* [clinically diagnostic]. These then progress to low grade, insidious tumors. Less developed lesions are typically not pruritic. Median duration from onset to definitive diagnosis is 4-6 years. Dermatopathic lymphadenopathy usually present.)
orange/salmon color
some scaling
Tinea (Use
Tinea
(Use “capitis” for scalp, “manum” for hand, “pedis” for foot, “cruris” for groin area, “ungium” for nail, “corporis” for body- location ‘not otherwise specified’.)
Tinea (Use
Tinea
(Use “capitis” for scalp, “manum” for hand, “pedis” for foot, “cruris” for groin area, “ungium” for nail, “corporis” for body- location ‘not otherwise specified’.)
annulare with scaling
Tinea (Use
Tinea
(Use “capitis” for scalp, “manum” for hand, “pedis” for foot, “cruris” for groin area, “ungium” for nail, “corporis” for body- location ‘not otherwise specified’.)
Tinea (Use
Tinea
(Use “capitis” for scalp, “manum” for hand, “pedis” for foot, “cruris” for groin area, “ungium” for nail, “corporis” for body- location ‘not otherwise specified’.)
Tinea (Use
Tinea
(Use “capitis” for scalp, “manum” for hand, “pedis” for foot, “cruris” for groin area, “ungium” for nail, “corporis” for body- location ‘not otherwise specified’.)
Tinea (Use
Tinea
(Use “capitis” for scalp, “manum” for hand, “pedis” for foot, “cruris” for groin area, “ungium” for nail, “corporis” for body- location ‘not otherwise specified’.)
segmented; hyphae in fungus
Note that this is on the cheek in a child approximately <2 months. Psoriasis does not “like” the face.
(Most common form of eczema is atopic dermatitis; appearance is classically more ill-defined scaly erythematous coalescing papules and plaques; *infantile form favors face*, scalp and extensors; 80% develop allergic rhinitis)” alt=”C. Eczema
Note that this is on the cheek in a child approximately <2 months. Psoriasis does not “like” the face. (Most common form of eczema is atopic dermatitis; appearance is classically more ill-defined scaly erythematous coalescing papules and plaques; *infantile form favors face*, scalp and extensors; 80% develop allergic rhinitis)”>
C. Eczema
Note that this is on the cheek in a child approximately <2 months. Psoriasis does not “like” the face.
(Most common form of eczema is atopic dermatitis; appearance is classically more ill-defined scaly erythematous coalescing papules and plaques; *infantile form favors face*, scalp and extensors; 80% develop allergic rhinitis)
What is the most likely diagnosis?
A. Allergic contact dermatitis
B. Candidiasis
C. Eczema
D. Psoriasis
E. Tinea
Aphthous Stomatitis (Affects 20-60% of the population and manifests as recurrent, idiopathic oral ulcers commonly called
Aphthous Stomatitis
(Affects 20-60% of the population and manifests as recurrent, idiopathic oral ulcers commonly called “canker sores”
with a whitish, yellow necrotic surface/base and surrounding erythema;
variants include herpetiform and major aphthae [1-3 cm; may be an initial manifestation of Behcet’s, but this is rare in Lubbock].)
round, “punched out” ulcers
yellow/white necrotic base with surrounding erythema
Histoplasmosis
Histoplasmosis
uncommon oral ulcer
Pemphigus Vulgaris (90% will develop oral ulcers, and 50% present with oral ulcers, may involve buccal mucosa or tongue.)
Pemphigus Vulgaris
(90% will develop oral ulcers, and 50% present with oral ulcers, may involve buccal mucosa or tongue.)
uncommon oral ulcer
Mucosal/Cicatricial Pemphigoid
Mucosal/Cicatricial Pemphigoid
uncommon ulcerative scarring of mucosa
Herpes Labialis
Herpes Labialis
blister on erythematous base
Hand, Foot, Mouth Disease (Diagnosis especially likely if dermatologic findings are in a child.)
Hand, Foot, Mouth Disease
(Diagnosis especially likely if dermatologic findings are in a child.)
blisters, erythema around it on hand
Squamous Cell Carcinoma of the Lip
Squamous Cell Carcinoma of the Lip
Squamous Cell Carcinoma of the Tongue
Squamous Cell Carcinoma of the Tongue
Leukoplakia (Appearance is a
Leukoplakia
(Appearance is a “white-plaque” that does not scrape off, commonly seen in the middle aged and elderly with history of gradual onset, smoking, snuff, dentures. Biopsy shows hyperkeratosis, acanthosis, dysplasia and atypia, lymphocytic infiltrate, carcinoma in-situ.)
plaque
Leukoplakia (Appearance is a
Leukoplakia
(Appearance is a “white-plaque” that does not scrape off, commonly seen in the middle aged and elderly with history of gradual onset, smoking, snuff, dentures. Biopsy shows hyperkeratosis, acanthosis, dysplasia and atypia, lymphocytic infiltrate, carcinoma in-situ.)
plaque
Geographic tongue (Occurs after eating hot foods or drinking hot beverages; benign finding that will heal.)
Geographic tongue
(Occurs after eating hot foods or drinking hot beverages; benign finding that will heal.)
histologically appears like psoriasis
C. Herpes virus infection
C. Herpes virus infection
What is the best diagnosis?
A. Candidiasis
B. Cicatricial pemphigoid
C. Herpes virus infection
D. Pemphigus vulgaris
E. Syphilis
A. True Note the pearly color and presence of telangiectasias. This is a basal cell carcinoma.
A. True
Note the pearly color and presence of telangiectasias. This is a basal cell carcinoma.
Is this lesion malignant?
A. True
B. False
Verruca Vulgaris, the Common Wart
(Caused by multiple types of human papilloma virus infecting epidermal cells. Appears as flesh-colored firm papule or nodule with hyperkeratotic (corrugated) surface with black dots, interrupting normal skin lines. Commonly found on hands, fingers. Treat with *non-specific destruction*.)
flesh-colores firm papules/nodules
interrupts normal skin lines
usually on hands, fingers
Verruca Vulgaris, the Common Wart
(Caused by multiple types of human papilloma virus infecting epidermal cells. Appears as flesh-colored firm papule or nodule with hyperkeratotic (corrugated) surface with black dots, interrupting normal skin lines. Commonly found on hands, fingers. Treat with *non-specific destruction*.)
flesh-colores firm papules/nodules
interrupts normal skin lines
usually on hands, fingers
Flat Warts
Flat Warts
Slightly raised, flat surfaced papule
Plantar Warts
Plantar Warts
often covered by callus
can be painful
Condyloma Acuminatum, the Venereal Wart (Appears as a soft, moist papule or plaque, can be sessile or pedunculated and is often cauliflower-like.)
Condyloma Acuminatum, the Venereal Wart
(Appears as a soft, moist papule or plaque, can be sessile or pedunculated and is often cauliflower-like.)
soft, moist papule
cauliflower-like
Corn (Clavus or Heloma) (Localized thickening of epidermis caused by pressure or friction, appears as white-gray or yellow-brown, well circumscribed, scaly papules or nodules that *do not interrupt skin lines*; most commonly involving toes. )
Corn (Clavus or Heloma)
(Localized thickening of epidermis caused by pressure or friction, appears as white-gray or yellow-brown, well circumscribed, scaly papules or nodules that *do not interrupt skin lines*; most commonly involving toes. )
yellow-brown, well circumscribed, scaly papules
not interrupting skin lines
usually on feet and toes
Seborrheic Keratosis (Arises as benign neoplasm of epidermal cells; appearance varies in size and color: flesh, tan, brown, occasionally black; oval to round, waxy, well-demarcated, *
Seborrheic Keratosis
(Arises as benign neoplasm of epidermal cells; appearance varies in size and color: flesh, tan, brown, occasionally black; oval to round, waxy, well-demarcated, *”stuck on”* appearance; may have *verrucous* or crumbly surface, occasionally with keratin-filled pits. Spares palms and soles.)
tan to dark brown; round and waxy
*”stuck on”*, like you could peel it off
Seborrheic Keratosis (Arises as benign neoplasm of epidermal cells; appearance varies in size and color: flesh, tan, brown, occasionally black; oval to round, waxy, well-demarcated, *
Seborrheic Keratosis
(Arises as benign neoplasm of epidermal cells; appearance varies in size and color: flesh, tan, brown, occasionally black; oval to round, waxy, well-demarcated, *”stuck on”* appearance; may have *verrucous* or crumbly surface, occasionally with keratin-filled pits. Spares palms and soles.)
tan to dark brown; round and waxy-appearing
*”stuck on”*, like you could peel it off
Skin Tag (An extremely common benign fleshy tumor; appears as a tan- to flesh-colored, soft *pedunculated* papule with smooth, folded surface. Commonly found on the eyelids, neck, and skin folds (inframammary, axilla, inguinal). No therapy is necessary.)
Skin Tag
(An extremely common benign fleshy tumor; appears as a tan- to flesh-colored, soft *pedunculated* papule with smooth, folded surface. Commonly found on the eyelids, neck, and skin folds (inframammary, axilla, inguinal). No therapy is necessary.)
soft, *pedunculated* papule
Skin Tag (An extremely common benign fleshy tumor; appears as a tan- to flesh-colored, soft *pedunculated* papule with smooth, folded surface. Commonly found on the eyelids, neck, and skin folds (inframammary, axilla, inguinal). No therapy is necessary.)
Skin Tag
(An extremely common benign fleshy tumor; appears as a tan- to flesh-colored, soft *pedunculated* papule with smooth, folded surface. Commonly found on the eyelids, neck, and skin folds (inframammary, axilla, inguinal). No therapy is necessary.)
flesh-colored papules with smooth, folded surface in the axilla
Molluscum Contagiosum (Caused by *poxvirus infection* of epidermal cells, common in childhood; also venereal transmission as an adult; *suspect HIV if 100s of persistent lesions*; will commonly see pontaneous *remission* over several months. Appears as 2-5mm hard, smooth, dome-shaped flesh colored or translucent papules demonstrating *central umbilication with 'cheesy' core content*.)
Molluscum Contagiosum
(Caused by *poxvirus infection* of epidermal cells, common in childhood; also venereal transmission as an adult; *suspect HIV if 100s of persistent lesions*; will commonly see pontaneous *remission* over several months. Appears as 2-5mm hard, smooth, dome-shaped flesh colored or translucent papules demonstrating *central umbilication with ‘cheesy’ core content*.)
hard, smooth, dome-shaped flesh-colored
central *umbilication with “cheesy” core*
Molluscum Contagiosum (Caused by *poxvirus infection* of epidermal cells, common in childhood; also venereal transmission as an adult; *suspect HIV if 100s of persistent lesions*; will commonly see pontaneous *remission* over several months. Appears as 2-5mm hard, smooth, dome-shaped flesh colored or translucent papules demonstrating *central umbilication with 'cheesy' core content*.)...
Molluscum Contagiosum
(Caused by *poxvirus infection* of epidermal cells, common in childhood; also venereal transmission as an adult; *suspect HIV if 100s of persistent lesions*; will commonly see pontaneous *remission* over several months. Appears as 2-5mm hard, smooth, dome-shaped flesh colored or translucent papules demonstrating *central umbilication with ‘cheesy’ core content*.)…
hard, smooth, dome-shaped flesh-colored
central *umbilication with “cheesy” core*
(Precancerous epidermal neoplasm caused by exposure to UV light. Appears as 1-10-mm wide reddish, ill-defined indistinct borders with rough, yellowish adherent scale. Often easier felt than seen. Small number (~< 1/1000 per year) develop into squamous cell carcinoma.)” alt=”Actinic Keratoses (“Sun Spots”)
(Precancerous epidermal neoplasm caused by exposure to UV light. Appears as 1-10-mm wide reddish, ill-defined indistinct borders with rough, yellowish adherent scale. Often easier felt than seen. Small number (~< 1/1000 per year) develop into squamous cell carcinoma.)”>
Actinic Keratoses (“Sun Spots”)
(Precancerous epidermal neoplasm caused by exposure to UV light. Appears as 1-10-mm wide reddish, ill-defined indistinct borders with rough, yellowish adherent scale. Often easier felt than seen. Small number (~< 1/1000 per year) develop into squamous cell carcinoma.)
rough, yellowish adherent scale
(Precancerous epidermal neoplasm caused by exposure to UV light. Appears as 1-10-mm wide reddish, ill-defined indistinct borders with rough, yellowish adherent scale. Often easier felt than seen. Small number (~< 1/1000 per year) develop into squamous cell carcinoma.)…” alt=”Actinic Keratoses (“Sun Spots”)
(Precancerous epidermal neoplasm caused by exposure to UV light. Appears as 1-10-mm wide reddish, ill-defined indistinct borders with rough, yellowish adherent scale. Often easier felt than seen. Small number (~< 1/1000 per year) develop into squamous cell carcinoma.)…”>
Actinic Keratoses (“Sun Spots”)
(Precancerous epidermal neoplasm caused by exposure to UV light. Appears as 1-10-mm wide reddish, ill-defined indistinct borders with rough, yellowish adherent scale. Often easier felt than seen. Small number (~< 1/1000 per year) develop into squamous cell carcinoma.)…
rough, yellowish adherent scale
Squamous Cell Carcinoma (Malignancy of *keratinocytes caused by UV light with potential to metastasize* [2% overall], appearing as a scaling, indurated plaque or nodule that sometimes bleeds or ulcerates. Persistent ulceration or bleeding warrants a biopsy. *Treat by surgical excision*)
Squamous Cell Carcinoma
(Malignancy of *keratinocytes caused by UV light with potential to metastasize* [2% overall], appearing as a scaling, indurated plaque or nodule that sometimes bleeds or ulcerates. Persistent ulceration or bleeding warrants a biopsy. *Treat by surgical excision*)
scaling, indurated nodule
Squamous Cell Carcinoma (Malignancy of *keratinocytes caused by UV light with potential to metastasize* [2% overall], appearing as a scaling, indurated plaque or nodule that sometimes bleeds or ulcerates. Persistent ulceration or bleeding warrants a biopsy. *Treat by surgical excision*)
Squamous Cell Carcinoma
(Malignancy of *keratinocytes caused by UV light with potential to metastasize* [2% overall], appearing as a scaling, indurated plaque or nodule that sometimes bleeds or ulcerates. Persistent ulceration or bleeding warrants a biopsy. *Treat by surgical excision*)
scaling plaque
Bowen's Disease (Squamous Cell Carcinoma in Situ)
Bowen’s Disease (Squamous Cell Carcinoma in Situ)
red, scaly, crusted and well-defined plaque
Keratoacanthoma (May involute, but difficult to differentiate from SCC, so treat regardless.)
Keratoacanthoma
(May involute, but difficult to differentiate from SCC, so treat regardless.)
rapidly growing, crater-like nodule
Basal Cell Carcinoma (Malignancy of the *epidermal basal cell* that rarely metastasizes, but can be *locally destructive*; caused most commonly by *UV radiation*, nodular subtype most common. Appears as a *pearly*, semitranslucent papule or nodule, often with central depression and *telangiectasias*. Borders are rolled and waxy or cratered. *Treat with surgery.*(
Basal Cell Carcinoma
(Malignancy of the *epidermal basal cell* that rarely metastasizes, but can be *locally destructive*; caused most commonly by *UV radiation*, nodular subtype most common. Appears as a *pearly*, semitranslucent papule or nodule, often with central depression and *telangiectasias*. Borders are rolled and waxy or cratered. *Treat with surgery.*(
pearly, semitranslucent nodules
central depression
Basal Cell Carcinoma with Rodent Ulcer (Malignancy of the *epidermal basal cell* that rarely metastasizes, but can be *locally destructive*; caused most commonly by *UV radiation*. Appears as a *pearly*, semitranslucent papule or nodule, often with central depression and *telangiectasias*. Borders are rolled and waxy or cratered. *Treat with surgery.*)
Basal Cell Carcinoma with Rodent Ulcer
(Malignancy of the *epidermal basal cell* that rarely metastasizes, but can be *locally destructive*; caused most commonly by *UV radiation*. Appears as a *pearly*, semitranslucent papule or nodule, often with central depression and *telangiectasias*. Borders are rolled and waxy or cratered. *Treat with surgery.*)
ulceration and crusting
pearly appearance with telangiectasias
Pigmented Basal Cell Carcinoma
Pigmented Basal Cell Carcinoma
pearly with rolled margin
shiny blue-black color, speckled
Pigmented Basal Cell Carcinoma
Pigmented Basal Cell Carcinoma
pearly with telangiectasias
blue-black color, speckled
Superficial Basal Cell Carcinoma
Superficial Basal Cell Carcinoma

red, slightly scaling, well-demarcated plaque

DIFFERENTIAL eczema

Superficial Basal Cell Carcinoma
Superficial Basal Cell Carcinoma

red, slightly scaling, well-demarcated plaque

DIFFERENTIAL eczema

Sclerosing (Scarring) Basal Cell Carcinoma (Least common and most aggressive.)
Sclerosing (Scarring) Basal Cell Carcinoma
(Least common and most aggressive.)
atrophic white plaque that looks like scar
Sclerosing (Scarring) Basal Cell Carcinoma (Least common and most aggressive.)
Sclerosing (Scarring) Basal Cell Carcinoma
(Least common and most aggressive.)
atrophic white plaque that looks like scar
Epidermal Inclusion Cyst / Epidermoid Cyst
(Derived from the upper portion of the hair follicle lining and commonly located in the mid and lower dermis. *Discharges cheesy, foul-smelling macerated keratin*. Appears as a flesh-colored, firm, but often malleable, solitary nodule with central punctum or pore. *Multiple epidermal inclusion cysts are a feature of Gardner’s syndrome.*)
flesh-colored solitary nodule with central pore
Epidermal Inclusion Cyst / Epidermoid Cyst
(Derived from the upper portion of the hair follicle lining and commonly located in the mid and lower dermis. *Discharges cheesy, foul-smelling macerated keratin*. Appears as a flesh-colored, firm, but often malleable, solitary nodule with central punctum or pore. *Multiple epidermal inclusion cysts are a feature of Gardner’s syndrome.*)
flesh-colored solitary nodule with central pore
Hemangioma, Superficial
(Benign proliferation of blood vessels in dermis and subcutis, most commonly arising in infancy and regressing spontaneously after first year of life; color depends on size and depth of vessels.)
bright red lesion
Hemangioma, Subcutaneous
(Benign proliferation of blood vessels in dermis and subcutis, most commonly arising in infancy and regressing spontaneously after first year of life; color depends on size and depth of vessels.)
bluish lesion
Hemangioma, Mixed
(Benign proliferation of blood vessels in dermis and subcutis, most commonly arising in infancy and regressing spontaneously after first year of life; color depends on size and depth of vessels.)
bright red, dome-shaped lesion
Dermatofibroma
(Dermal fibrotic papule or small nodule of unknown origin, possibly trauma; appears as a slightly elevated area ~5mm, often with overlying hyperpigmentation and epidermal thickening. When palpated, these are firm and indurated; demonstrate *”dimple sign.”*)
Pinching shows central dimpling
Light tan to dark brown
Dermatofibroma
(Dermal fibrotic papule or small nodule of unknown origin, possibly trauma; appears as a slightly elevated area ~5mm, often with overlying hyperpigmentation and epidermal thickening. When palpated, these are firm and indurated; demonstrate *”dimple sign.”*)
dark brown, overlying hyperpigmentation and thickening
Keloids (Exuberant scar tissue due to *excessive proliferation of collagen*, most common in young black people. Appear as *overgrown scars*; pink to dark brown, elevated, firm, protuberant nodules/plaque; *more extensive than the original wound*; irregular claw-like borders. New and active lesions *often itch*. Treat these cautiously due to their high recurrence rate.)
Keloids
(Exuberant scar tissue due to *excessive proliferation of collagen*, most common in young black people. Appear as *overgrown scars*; pink to dark brown, elevated, firm, protuberant nodules/plaque; *more extensive than the original wound*; irregular claw-like borders. New and active lesions *often itch*. Treat these cautiously due to their high recurrence rate.)
dark brown elevated, firm, protuberant nodules/plaque
usually appearing on earlobes, shoulders, upper chest, and back
Keloids (Exuberant scar tissue due to *excessive proliferation of collagen*, most common in young black people. Appear as *overgrown scars*; pink to dark brown, elevated, firm, protuberant nodules/plaque; *more extensive than the original wound*; irregular claw-like borders. New and active lesions *often itch*. Treat these cautiously due to their high recurrence rate.)
Keloids
(Exuberant scar tissue due to *excessive proliferation of collagen*, most common in young black people. Appear as *overgrown scars*; pink to dark brown, elevated, firm, protuberant nodules/plaque; *more extensive than the original wound*; irregular claw-like borders. New and active lesions *often itch*. Treat these cautiously due to their high recurrence rate.)
pink elevated, firm, protuberant nodules/plaque
usually appearing on earlobes, shoulders, upper chest, and back
Lipoma (Benign subcutaneous *fat* tumor, most common in midlife. Appears as freely mobile, rubbery, flesh-colored nodules, only slightly elevated above the skin's surface, but easily palpable deep in skin. Biopsy if rapidly growing; therapy is usually not required, but if desired can be excised.)
Lipoma
(Benign subcutaneous *fat* tumor, most common in midlife. Appears as freely mobile, rubbery, flesh-colored nodules, only slightly elevated above the skin’s surface, but easily palpable deep in skin.
Biopsy if rapidly growing; therapy is usually not required, but if desired can be excised.)
rubbery, flesh-colored nodule
usually seen on trunk, neck, and upper extremities
Lipoma (Benign subcutaneous *fat* tumor, most common in midlife. Appears as freely mobile, rubbery, flesh-colored nodules, only slightly elevated above the skin's surface, but easily palpable deep in skin. Biopsy if rapidly growing; therapy is usually not required, but if desired can be excised.)
Lipoma
(Benign subcutaneous *fat* tumor, most common in midlife. Appears as freely mobile, rubbery, flesh-colored nodules, only slightly elevated above the skin’s surface, but easily palpable deep in skin.
Biopsy if rapidly growing; therapy is usually not required, but if desired can be excised.)
rubbery, flesh-colored nodule
usually seen on trunk, neck, and upper extremities
Neurofibroma (Focal proliferation of neural tissue in the dermis; multiple lesions are seen in Neurofibromatosis Type 1 [von Recklinghausen's disease]; appear as soft, flesh colored *protruding papule* or nodule which demonstrate characteristic *
Neurofibroma
(Focal proliferation of neural tissue in the dermis; multiple lesions are seen in Neurofibromatosis Type 1 [von Recklinghausen’s disease]; appear as soft, flesh colored *protruding papule* or nodule which demonstrate characteristic *”buttonhole sign”* [when compressed, the papule feels like it can be pushed through a defect in the skin]; less often, these can be deep, firm nodule [plexiform neurofibroma] and be tender; “feels like bag of worms.”)

soft, flesh-colored, protruding papule or nodule

DIFFERENTIAL skin tags

Plexiform Neurofibroma (Focal proliferation of neural tissue in the dermis; multiple lesions are seen in Neurofibromatosis Type 1 [von Recklinghausen's disease]; most commonly appear as soft, flesh colored *protruding papule* or nodule which demonstrate characteristic *
Plexiform Neurofibroma
(Focal proliferation of neural tissue in the dermis; multiple lesions are seen in Neurofibromatosis Type 1 [von Recklinghausen’s disease]; most commonly appear as soft, flesh colored *protruding papule* or nodule which demonstrate characteristic *”buttonhole sign”* [when compressed, the papule feels like it can be pushed through a defect in the skin]; less often, these can be deep, firm nodule [plexiform neurofibroma] and be tender; “feels like bag of worms.”)
large, deep, firm nodule
“feels like a bag of worms”
Xanthelasma (Focal collection of *lipid-laden histiocytes* in dermis or tendons with yellow appearance due to fat composition; *usually a skin sign of hyperlipidemia* [not always in case of xanthelasma]. All xanthomas except tendon types are yellow papules, plaques, and nodules.)
Xanthelasma
(Focal collection of *lipid-laden histiocytes* in dermis or tendons with yellow appearance due to fat composition; *usually a skin sign of hyperlipidemia* [not always in case of xanthelasma]. All xanthomas except tendon types are yellow papules, plaques, and nodules.)
yellowish plaques on eyelids
Eruptive Xanthomas (*due to very high triglycerides* (Focal collection of *lipid-laden histiocytes* in dermis or tendons with yellow appearance due to fat composition; *usually a skin sign of hyperlipidemia* [not always in case of xanthelasma]. All xanthomas except tendon types are yellow papules, plaques, and nodules.)
Eruptive Xanthomas (*due to very high triglycerides*
(Focal collection of *lipid-laden histiocytes* in dermis or tendons with yellow appearance due to fat composition; *usually a skin sign of hyperlipidemia* [not always in case of xanthelasma]. All xanthomas except tendon types are yellow papules, plaques, and nodules.)
reddish-yellow papules and plaques
Tuberous Xanthoma (Focal collection of *lipid-laden histiocytes* in dermis or tendons with yellow appearance due to fat composition; *usually a skin sign of hyperlipidemia* [not always in case of xanthelasma]. All xanthomas except tendon types are yellow papules, plaques, and nodules.)
Tuberous Xanthoma
(Focal collection of *lipid-laden histiocytes* in dermis or tendons with yellow appearance due to fat composition; *usually a skin sign of hyperlipidemia* [not always in case of xanthelasma]. All xanthomas except tendon types are yellow papules, plaques, and nodules.)
potato-like nodules
commonly seen on elbows, buttocks
Tendon Xanthomas (*due to very high cholesterol) (Focal collection of *lipid-laden histiocytes* in dermis or tendons with yellow appearance due to fat composition; *usually a skin sign of hyperlipidemia* [not always in case of xanthelasma]. All xanthomas except tendon types are yellow papules, plaques, and nodules.)
Tendon Xanthomas (*due to very high cholesterol)
(Focal collection of *lipid-laden histiocytes* in dermis or tendons with yellow appearance due to fat composition; *usually a skin sign of hyperlipidemia* [not always in case of xanthelasma]. All xanthomas except tendon types are yellow papules, plaques, and nodules.)
deep, flesh-colored, hard nodules located within peripheral tendons
most commonly involving Achilles tendon and extensor fingers
Kaposi's Sarcoma (Malignant *vascular tumor caused by HHV8*; appears as *purple* macules, papules, plaques and nodules. In classic Kaposi's Sarcoma (elderly men of Mediterranean descent), it appears as lower leg lesions. If AIDS-associated, the lesions may appear anywhere.)
Kaposi’s Sarcoma
(Malignant *vascular tumor caused by HHV8*; appears as *purple* macules, papules, plaques and nodules. In classic Kaposi’s Sarcoma (elderly men of Mediterranean descent), it appears as lower leg lesions. If AIDS-associated, the lesions may appear anywhere.)
purple macules, papules, plaques, and nodules
Kaposi's Sarcoma (Malignant *vascular tumor caused by HHV8*; appears as *purple* macules, papules, plaques and nodules. In classic Kaposi's Sarcoma (elderly men of Mediterranean descent), it appears as lower leg lesions. If AIDS-associated, the lesions may appear anywhere.)
Kaposi’s Sarcoma
(Malignant *vascular tumor caused by HHV8*; appears as *purple* macules, papules, plaques and nodules. In classic Kaposi’s Sarcoma (elderly men of Mediterranean descent), it appears as lower leg lesions. If AIDS-associated, the lesions may appear anywhere.)
purple macules, papules, plaques, and nodules
Freckle/Ephelis (Sun-induced hyperpigmented macules that only occur in sun-exposed areas; very common. *Amount of melanin is increased*, but number of melanocytes stays the same.)
Freckle/Ephelis
(Sun-induced hyperpigmented macules that only occur in sun-exposed areas; very common. *Amount of melanin is increased*, but number of melanocytes stays the same.)
hyperpigmented macules
Lentigo (Hyperpigmented macule caused by *increased number of melanocytes* Two main types: (1) Lentigo simplex: childhood, idiopathic, few in number, (2) Actinic lentigo: adults, *sun induced*, often numerous, more common.)
Lentigo
(Hyperpigmented macule caused by *increased number of melanocytes*
Two main types: (1) Lentigo simplex: childhood, idiopathic, few in number, (2) Actinic lentigo: adults, *sun induced*, often numerous, more common.)
hyperpigmented macules
Lentigo (Hyperpigmented macule caused by *increased number of melanocytes* Two main types: (1) Lentigo simplex: childhood, idiopathic, few in number, (2) Actinic lentigo: adults, *sun induced*, often numerous, more common.)
Lentigo
(Hyperpigmented macule caused by *increased number of melanocytes*
Two main types: (1) Lentigo simplex: childhood, idiopathic, few in number, (2) Actinic lentigo: adults, *sun induced*, often numerous, more common.)
hyperpigmented macules
Junctional Nevus (Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
Junctional Nevus
(Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
light to dark brown macule
Compound or Intradermal Nevus (Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
Compound or Intradermal Nevus
(Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
brown, rough-surfaced papule
Compound or Intradermal Nevus (Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
Compound or Intradermal Nevus
(Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
flesh-colored smooth-surfaced papule
Dysplastic Nevus (Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
Dysplastic Nevus
(Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
variegated in color; irregular, indistinct border
erythematous background
Dysplastic Nevus (Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
Dysplastic Nevus
(Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
variegated in color; irregular, indistinct border
Congenital Nevus (Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
Congenital Nevus
(Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
elevated, dark brown papule or plaque with discrete borders
Cognenital Nevus (Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)
Cognenital Nevus
(Benign common neoplasm of pigment-forming cells [*the nevus cell*], generally having uniform color, surface, and border [changing or symptomatic nevi are suspicious!]. Note that darkening, itching, and development of new nevi are common during pregnancy and adolescence. Types of nevi: (1) Junctional: nevus cells confined to base of epidermis, (2) Compound: nevus cells in epidermis and dermis, (3) Intradermal: nevus cells in dermis only. They vary greatly in appearance and may be any of the following: flat or elevated, smooth or verrucoid, polypoid or sessile, flesh colored to tan to dark brown to blue, often contains hair.)

elevated, dark brown papule or plaque with discrete borders

NOTE large congenital nevi (> 20cm) have increased chance of developing into melanoma

Superficial Spreading Melanoma (Malignant neoplasm of pigment-forming cells [melanocytes and nevus cells] demonstrating an increasing incidence [1 in 70 lifetime risk]. 50% of melanomas are associated with a nevus. Note that *superficial spreading melanoma is the most common type.*)
Superficial Spreading Melanoma
(Malignant neoplasm of pigment-forming cells [melanocytes and nevus cells] demonstrating an increasing incidence [1 in 70 lifetime risk]. 50% of melanomas are associated with a nevus. Note that *superficial spreading melanoma is the most common type.*)
irregular in color, surface, border
may occur anywhere on body but show predilection for upper back in males and lower legs in females
Superficial Spreading Melanoma (Malignant neoplasm of pigment-forming cells [melanocytes and nevus cells] demonstrating an increasing incidence [1 in 70 lifetime risk]. 50% of melanomas are associated with a nevus. Note that *superficial spreading melanoma is the most common type.*)
Superficial Spreading Melanoma
(Malignant neoplasm of pigment-forming cells [melanocytes and nevus cells] demonstrating an increasing incidence [1 in 70 lifetime risk]. 50% of melanomas are associated with a nevus. Note that *superficial spreading melanoma is the most common type.*)
irregular in color, surface, border
may occur anywhere on body but show predilection for upper back in males and lower legs in females
Nodular Melanoma (Malignant neoplasm of pigment-forming cells [melanocytes and nevus cells] demonstrating an increasing incidence [1 in 70 lifetime risk]. 50% of melanomas are associated with a nevus.)
Nodular Melanoma
(Malignant neoplasm of pigment-forming cells [melanocytes and nevus cells] demonstrating an increasing incidence [1 in 70 lifetime risk]. 50% of melanomas are associated with a nevus.)
rapidly growing, blue-black, eroded nodule
occur anywhere on the body
Nodular Melanoma (Malignant neoplasm of pigment-forming cells [melanocytes and nevus cells] demonstrating an increasing incidence [1 in 70 lifetime risk]. 50% of melanomas are associated with a nevus.)
Nodular Melanoma
(Malignant neoplasm of pigment-forming cells [melanocytes and nevus cells] demonstrating an increasing incidence [1 in 70 lifetime risk]. 50% of melanomas are associated with a nevus.)
rapidly growing, blue-black, smooth nodule
occur anywhere on the body
Lentigo Maligna Melanoma
(Malignant neoplasm of pigment-forming cells [melanocytes and nevus cells] demonstrating an increasing incidence [1 in 70 lifetime risk]. 50% of melanomas are associated with a nevus.)
multicolored patch with some elevated areas; changes in size, growing slowly; darkening is insidious (years)
occurs on sun-exposed skin
Lentigo Maligna Melanoma
(Malignant neoplasm of pigment-forming cells [melanocytes and nevus cells] demonstrating an increasing incidence [1 in 70 lifetime risk]. 50% of melanomas are associated with a nevus.)
multicolored patch with some elevated areas; changes in size, growing slowly; darkening is insidious (years)
occurs on sun-exposed skin
Acral Lentiginous Melanoma
(Malignant neoplasm of pigment-forming cells [melanocytes and nevus cells] demonstrating an increasing incidence [1 in 70 lifetime risk]. 50% of melanomas are associated with a nevus. *Note that acral lentiginous melanoma is most frequent in blacks and Asians.*)
irregular, enlarging, black growth
occurs on palms, soles, toes or fingersDIFFERENTIAL lentigo maligna melanoma

Acral Lentiginous Melanoma
(Malignant neoplasm of pigment-forming cells [melanocytes and nevus cells] demonstrating an increasing incidence [1 in 70 lifetime risk]. 50% of melanomas are associated with a nevus. *Note that acral lentiginous melanoma is most frequent in blacks and Asians.*)
irregular, enlarging, black growth
occurs on palms, soles, toes or fingersDIFFERENTIAL lentigo maligna melanoma

Survival Statistics Based on Melanoma Depth
Survival Statistics Based on Melanoma Depth
Main treatment is surgical excision, with increasing margins for increasing thickness.
Pigmented Basal Cell Carcinoma
Pigmented Basal Cell Carcinoma
shiny, blue-black color, speckled
rolled borders; waxy and cratered
Superficial Spreading Melanoma
Superficial Spreading Melanoma
irregular in color, surface, border
Combined Melanocytic Nevus
Combined Melanocytic Nevus
variegated in color; irregular, indistinct border
C. Poison Ivy Linear and geometric patterns usually have their source outside the body.
C. Poison Ivy
Linear and geometric patterns usually have their source outside the body.
This vesicular eruption is caused by:
A. HSV
B. VZV
C. Poison Ivy
D. Streptococcus
HSV (Grouped vesicles on erythematous base; can quickly become pustules that rupture and crust, which may result in ulcers.)
HSV
(Grouped vesicles on erythematous base; can quickly become pustules that rupture and crust, which may result in ulcers.)
grouped vesicles on erythematous base
Herpetic Whitlow (Grouped vesicles on erythematous base; can quickly become pustules that rupture and crust, which may result in ulcers.)
Herpetic Whitlow
(Grouped vesicles on erythematous base; can quickly become pustules that rupture and crust, which may result in ulcers.)
grouped vesicles on erythematous base
fingers
Eczema Herpeticum (Grouped vesicles on erythematous base; can quickly become pustules that rupture and crust, which may result in ulcers.)
Eczema Herpeticum
(Grouped vesicles on erythematous base; can quickly become pustules that rupture and crust, which may result in ulcers.)
generalized skin infection with predisposing skin disease
HSV
HSV
Tzanck smear
multinucleated giant cells
Chronic HSV
Chronic HSV
grouped vesicles in plaque
Varicella<br />
(Caused by primary VZV infection. Crops of macules develop into papules --> vesicles --> pustules --> crust. Typically all types of lesions seen at the same time<br />
'Dewdrop on a rose petal' is classic.)
Varicella
(Caused by primary VZV infection. Crops of macules develop into papules –> vesicles –> pustules –> crust. Typically all types of lesions seen at the same time
‘Dewdrop on a rose petal’ is classic.)
generalized, pruritic vesicular eruption
various lesions (macules, papules, vesicles)
“dewdrop on a rose petal”
Zoster (Caused by reactivation of VZV in sensory nerve; can involve adjacent [*but not bilateral*] dermatomes. Post-herpetic neuralgia is more common in elderly and can be severe.)
Zoster
(Caused by reactivation of VZV in sensory nerve; can involve adjacent [*but not bilateral*] dermatomes. Post-herpetic neuralgia is more common in elderly and can be severe.)
unilateral eruption of groups of vesicles along dermatome
Zoster (Caused by reactivation of VZV in sensory nerve; can involve adjacent [*but not bilateral*] dermatomes. Post-herpetic neuralgia is more common in elderly and can be severe.)
Zoster
(Caused by reactivation of VZV in sensory nerve; can involve adjacent [*but not bilateral*] dermatomes. Post-herpetic neuralgia is more common in elderly and can be severe.)
unilateral eruption of groups of vesicles along dermatome
Superficial desquamation beginning.
Superficial desquamation beginning.
Superficial desquamation after toxic erythema.
Superficial desquamation after toxic erythema.
erythematous plaques, violaceous hue; sun exposure
DIFFERENTIAL drug reaction
sparing of the nasolabial folds; “butterfly rash”
Cellulitis (displaying the four cardinal signs)
Cellulitis (displaying the four cardinal signs)
redness, warmth, swelling, pain
intact epidermis
blisters occur only rarely
Fungal Cellulitis (cannot determine cause by observation)
Fungal Cellulitis (cannot determine cause by observation)
sharply demarcated red plaque with orange peel appearance (follicles accentuated)
Furuncle
Furuncle
associated hair follicle
Abscess
Abscess
no associated hair follicle
fluctuates when pressed
Erythema Nodosa (Causes: Strep, OCPs, Pregnancy, or idiopathic)
Erythema Nodosa
(Causes: Strep, OCPs, Pregnancy, or idiopathic)
red, ill-defined nodules with bruise-like appearance on shins
will be painful when touched
Fixed Drug Eruption (Causes: *NSAIDs, sulfonamides,* tetracyclines, carbamazepine)
Fixed Drug Eruption
(Causes: *NSAIDs, sulfonamides,* tetracyclines, carbamazepine)
sharply demarcated red plaques, later dusky
same lesion can reappear
prefers the distal extremities, face, lips, and genitalia
Carcinoid Syndrome
Carcinoid Syndrome
persistent flushing of the face due to high levels of 5HT
Carcinoma Erysipeloides
Carcinoma Erysipeloides
cutaneous metastases mimicking cellulitis
painful, hot
Urticaria<br />
(*Individual lesions last <24 hours*)
Urticaria
(*Individual lesions last <24 hours*)
slightly raised, some blanching at border
edematous plaques
Uritcaria
Uritcaria
localized, acute dermal edema
Urticaria, cold induced
Urticaria, cold induced
localized, acute dermal edema
geographic patterns
Urticardia, cold induced
Urticardia, cold induced
localized, acute dermal edema
Urticaria, pressure induced
Urticaria, pressure induced
localized, acute dermal edema
(*Most often caused by HSV*)
(*Most often caused by HSV*)
target lesions with rim of pallor and outermost zone of red
(*Most often caused by HSV*)
(*Most often caused by HSV*)
target lesions with rim of pallor and outermost zone of red
Erythema migrans (*Caused by Borrelia burgdorferi transmitted by Ixodes*, treat with doxycycline, amoxicillin, or ceftriaxone)
Erythema migrans
(*Caused by Borrelia burgdorferi transmitted by Ixodes*, treat with doxycycline, amoxicillin, or ceftriaxone)
slowly expanding, >5 cm red expanding plaque
Erythema migrans (*Caused by Borrelia burgdorferi transmitted by Ixodes*, treat with doxycycline, amoxicillin, or ceftriaxone)
Erythema migrans
(*Caused by Borrelia burgdorferi transmitted by Ixodes*, treat with doxycycline, amoxicillin, or ceftriaxone)
slowly expanding, >5 cm red expanding plaque
Ixodes tick
Ixodes tick
Erythema migrans (*Caused by Borrelia burgdorferi transmitted by Ixodes*, treat with doxycycline, amoxicillin, or ceftriaxone)
Erythema migrans
(*Caused by Borrelia burgdorferi transmitted by Ixodes*, treat with doxycycline, amoxicillin, or ceftriaxone)
slowly expanding, >5 cm red expanding plaque
Erythema gyratum repens
Erythema gyratum repens
reaction to internal malignancy
Erythema annular centrifugum
Erythema annular centrifugum
reaction to distal infection?
scaling trailing behind red border

Lippincott’s Pharmacology Chapter 1

Passive Diffusion
High conc. -> low
majority of drugs work this way
does not involve carrier, is not saturable, and shows a low structural specificity

Facilitated Diffusion
involves carrier proteins
High conc -> low
no energy required, an be saturated, may be inhibited by compounds that compete for the carrier

Active Transport
Shows saturation kinetics for the carrier
drugs closely resemble naturally occurring metabolites that are actively transported across cell membranes
may be competitively inhibited

exo/endocytosis
B12 is absorbed by endocytosis; some neurotransmitters (e.g., norepinephrine) are stored in vesicles and released by exocytosis

Distribution equilibrium
when the permeable form of a drug achieves an equal concentration in all body water space

P-glycoprotein
a multidrug transmembrane transporter protein responsible for transporting various molecules , including drugs, across cell membranes; in areas of high expression, it reduces drug absorption

bioavailability
the fraction of administered drug that reaches the systemic circulation

bioequivalence
when two related drugs show comparable bioavailability and similar times to achieve peak blood concentrations

therapeutic equivalence
when two similar drug products that are pharmaceutically equivalent with similar clinical safety profiles

Pharm – General Principles of Pharmacology

What are the four (4) types of names assigned to drugs?
1) Chemical name
2) Generic name
3) Official name
4) Trade name (brand name)

What are the three (3) key features of a drug’s chemical name?
1) Exact chemical makeup of the drug
2) Placement of the atoms or molecular structure
3) No capitalization

What are the four (4) key features of a drug’s generic name?
1) Non-proprietary
2) Name given to drug before it becomes official
3) May be used in all countries by all manufacturers
4) No capitalization

What are the two (2) key features of a drug’s official name?
1) Name listed in “The United States Pharmacopeia National Formulary”
2) May not be the same as the generic name

What are the four (4) key features of a drug’s trade name (brand name)?
1) Name is registered by the manufacturer and is followed by the trademark symbol
2) Can be used only by the manufacturer
3) Any given drug may have several trade names
4) First letter of the name is capitalized

What is the largest category of drugs?
Prescription

Prescription drugs require a prescription by a ________.
Licensed health care provider

Prescription drugs are also called ________ drugs.
Legend

Prescriptions must have 1) the ________ of the drug, 2) the ________ of the drug, 3) the ________ of administration, 4) the ________ of administration, and 5) the ________.
1) name
2) dose
3) number of times
4) route
5) amount to be dispensed

Non-prescription drugs may be obtained without a ________.
Prescription

What is another name for non-prescription drugs?
OTC (over the counter)

Name two general conditions under which risks may be associated with non-prescription drugs.
1) When directions are not followed
2) When adverse reactions occur

What is a controlled substance?
A controlled substance is a drug or chemical whose use, ownership, or manufacture is regulated by law — particularly the federal Controlled Substances Act.

Drugs, substances, and certain chemicals used to make drugs are classified into ________ distinct categories or schedules.
Five

Drugs, substances, and certain chemicals used to make drugs are classified into distinct categories or schedules depending upon 1) ________ and 2) ________.
1) the drug’s acceptable medical use
2) the drug’s abuse or dependency potential

The schedule numbering for controlled substances ranges from ________ to ________.
I to V

A schedule V drug has a [higher or lower] potential for abuse or dependency than a schedule I drug.
Lower

What are the two key features of a schedule I drug?
1) High abuse potential
2) No accepted medical use in the U.S.

What are the two examples of a schedule I substance listed in the PowerPoint presentation?
1) Heroin
2) LSD

Schedule II substances are characterized by potential for abuse with ________ physical or psychological ________.
Severe
Dependence

Schedule III substances have [more or less] abuse potential than schedule II substances.
Less

Schedule III substances are characterized by ________ physical or psychological dependence.
Moderate

Non-barbiturate sedatives, non-amphetamine stimulants, and limited amounts of certain narcotics are examples of schedule ________ drugs
III

Schedule III substances have [more or less] abuse potential than schedule IV substances.
More

Schedule IV substances are characterized by ________ dependence.
Limited

What are the two (2) general categories the PowerPoint presentation gives as examples of schedule IV substances?
1) Sedatives and anxiety agents
2) Non-narcotic analgesics

Schedule ________ substances are characterized by limited abuse potential.
V

Anti-________ and anti-________ medications are categorized as schedule V substances because they contain small amounts of ________.
(Anti)-tussives
(Anti)-diarrheals
Narcotics

Drugs taken by mouth (except liquids) go through how many phases?
Three

Drugs taken by ________ (except liquids) go through three (3) phases.
Mouth

The three (3) phases of drugs taken my mouth (except liquids) are:
1) Pharmaceutic phase
2) Pharmacokinetic phase
3) Pharmacodynamic phase

The ________ phase involves the dissolution of the drug.
Pharmaceutic

Drugs must be in ________ to be absorbed.
Solution

Liquid drugs and ________ drugs do not go through the pharmaceutic phase because they are already in solution.
Parenteral

________ administration involves the esophagus, stomach, and small and large intestines (i.e., the gastrointestinal tract).
Enteral

Oral, sublingual (dissolving the drug under the tongue), and rectal are ________ methods of administration.
Enteral

________ administration literally means to avoid the gut (gastrointestinal tract) and refers to any route of administration outside of or beside the alimentary tract.
Parenteral

________ tablets do not dissolve until reaching the small intestine.
Enteric-coated

Metabolic activities of the drug within the body after it is administered relate to the ________ phase.
Pharmacokinetic

The pharmacokinetic phase relates to how many different features or actions of the drug?
Six (6)

The six drug features or actions that figure into pharmacokinetics are:
1) Bioavailability
2) Absorption
3) Distribution
4) Metabolism
5) Excretion
6) Drug half-life

Mnemonic: BAD MED

Absorption is the process by which a drug ________.
Becomes available for use in the body

In ________ absorption, a carrier molecule moves the drug across a membrane.
Active

Passive absorption occurs when the drug moves from an area of ________ concentration to ________ concentration. This transport mechanism is known as ________.
Higher
Lower
Diffusion

________ is a method of absorption in which cells engulf the drug particle, causing movement across the cell.
Pinocytosis

________, ________, and ________ affect the rate of absorption.
Route of administration
Solubility of the drug
Certain body conditions

What are the two (2) PowerPoint examples of body conditions that affect the rate of absorption?
1) Lipodystrophy
2) Food in the stomach

Whether a drug is ________ soluble or ________ soluble can affect its rate of absorption.
Water
Lipid

IV, IM, SC, and PO are examples of ________, which affects the rate of absorption.
Route of administration

________ is the fraction of the drug that reaches systemic circulation chemically unchanged.
Bioavailability

Protein binding refers to the fact that drugs travel in the system circulation bound to ________ and are ________ when bound to protein.
Albumin
Inactive

Protein molecules release the drug, which diffuses through the tissue, interacts with receptors, and produces the desired ________.
Therapeutic effect

________ drug levels must be maintained in order for the drug to be effective.
Therapeutic

If the drug level [increases or decreases], the drug will not produce the desired effect.
Decreases

If the drug level increases, ________ symptoms may occur.
Toxic

________ is the chemical reaction that occurs in the liver and converts a drug to an inactive compound.
Biotransformation

The ________ effect applies to drugs that are absorbed in the small intestines and are transported to the liver via portal circulation. There they are metabolized by the liver before release into the circulatory system.
First-pass

The first-pass effect applies to drugs that are absorbed in the ________ and are transported to the liver via portal circulation. There they are metabolized by the liver before release into the circulatory system.
Small intestines

The first-pass effect applies to drugs that are absorbed in the small intestines and transported to the ________ via portal circulation. There they are metabolized by the ________ before release into the circulatory system.
Liver
Liver

The first-pass effect can ________ the bioavailability of a drug.
Decrease

The first-pass effect can decrease the ________ of a drug.
Bioavailability

Only ________ drugs undergo the first-pass effect.
PO

________ refers to elimination of a drug from the body.
Clearance

In the process of excretion, the ________ renders the drug inactive and the ________ excretes the inactive compounds.
Liver
Kidney

Some drugs are excreted by the kidney unchanged and without ________ involvement.
Liver

What are the six (6) PowerPoint examples of routes of excretion?
1) Kidney
2) Sweat
3) Breast milk
4) Respiratory
5) Feces
6) Bile

The ________ phase refers to drug actions and effects on the body.
Pharmacodynamic

As part of a drug’s pharmacodynamics, primary and secondary effects may alter the cellular ________ or the cellular ________.
Environment
Function

Alteration in ________ function can increase or decrease physiologic function.
Cellular

Physical changes in the cellular environment include what three (3) alterations listed in the PowerPoint?
1) Osmotic pressure
2) Lubrication
3) Absorption

________ refers to the intended effect of the drug on the body.
Therapeutic response

________ are drugs that bind with a receptor to produce results.
Agonists

Drugs that bind with a receptor and prevent another molecule from binding to the same receptor and producing some result are called ________
Antagonists

What are the six (6) main categories of drug reactions?
1) Toxic reactions
2) Drug tolerance
3) Drug idiosyncrasy
4) Allergic drug reactions
5) Adverse drug reactions
6) Cumulative drug effect

Mnemonic: Tall Talking Idiots Alert Comatose Advisors
Tolerance, Toxic, Idiosyncrasy, Allergic, Cumulative, Adverse

Adverse reactions are often called ________ when they are mild.
Side effects

________ reactions are often called side effects when they are mild.
Adverse

Allergic reactions can be called ________ reactions.
Hypersensitivity

________ can be called hypersensitivity reactions.
Allergic reactions

________ may prompt the body to produce antibodies against what it perceives as an antigen.
Allergic reactions

Allergic reactions may prompt the body to produce ________ against what it perceives as an ________.
Antibodies
Antigen

________ is an extremely serious allergic reaction and can be life-threatening if not recognized and treated immediately.
Anaphylactic shock

Anaphylactic shock is an extremely serious ________ and can be life-threatening if not recognized and treated immediately.
Allergic reaction

________ refers to any abnormal or unusual drug reaction of unknown cause and with no predictability.
Drug idiosyncrasy

________ refers to decreased response to a drug requiring increase in dosage.
Tolerance

[Increased or decreased] response to drug requiring [increase or decrease] in dosage is referred to as tolerance, which is a sign of ________.
Decreased
Increase
Drug dependence

________ refers to increased response to a drug because of decreased metabolism and excretion (usually secondary to ________ or ________ disease).
Cumulative effect
Liver
Kidney

Cumulative effect refers to [increased or decreased] response to a drug because of [increased or decreased] metabolism and excretion (usually secondary to liver or kidney disease).
Increased
Decreased

________ refers to poisoning of the system secondary to overdose of chemical resulting in elevated blood concentration.
Toxic reaction

Toxic reaction refers to poisoning of the system secondary to ________ of chemical resulting in ________ blood concentration.
Overdose
Elevated

________ refers to a genetically caused abnormal response to a drug.
Pharmacogenetic reaction

What are the two (2) main types of drug interactions from the PowerPoint?
1) Drug-drug
2) Drug-food

What are the three (3) basic types of drug-drug reactions?
1) Additive drug reaction
2) Synergistic drug reaction
3) Antagonistic drug reaction

________ is the term used when two or more drugs are taken at the same time and the action of one plus the action of the other results in an action as if just one drug had been given. This could be represented by 1+1= 2. An example would be a barbiturate and a tranquilizer given together before surgery to relax the patient.
Additive drug reaction

________ occurs when two drugs are taken together that are similar in action, such as barbiturates and alcohol, which are both depressants, resulting in an effect that is exaggerated out of proportion to that of each drug taken separately at the given dose. This could be expressed by 1+1= 5. An example might be a person taking a dose of alcohol and a dose of a barbiturate. Normally, taken alone, neither substance would cause serious harm in this example, but if taken together, the combination could cause coma or death.
Synergistic drug reaction

________ occurs when two drugs given together have an opposite effect on the body. This could be expressed by 1+1=0. An example might be the use of a tranquilizer to stop the action of LSD. Some stimulants will counteract the effects of depressants and thus are used to treat overdoses of barbiturates and narcotics.
Antagonistic drug reaction

What are the five (5) chief factors influencing drug response?
1) Age
2) Weight
3) Gender
4) Disease
5) Route of administration

________ refers to taking of multiple drugs and creates potential for ________
Polypharmacy
Interactions

Polypharmacy is often practiced by ________, who have more conditions for which to be medicated.
the elderly

Polypharmacy increases the possibility of ________ reactions.
Adverse

Oral Pathology – Exam 1

Lichen

Primitive plants composed of symbiotic algae and fungi

Grow on tree trunks or rocks

Pathology: any of various skin diseases characterized by patchy eruptions of small, firm papules

Lichen Planus
Chronic immunologically-mediated disease
Oral lesions; +/- lesions on skin, other mucosae
Oral lesions more persistant than skin lesions
Middle age onset
Slight greater predilection in females over males

Lichen Planus – Skin Lesions
Most on flexor surfaces
Plaques or papules
Purple, flat-topped with white (Wickham’s) striae
Pruritic
Wax and wane and often subside in 2 years
Oral Lichen Planus – Types
White adherent
Erosive (e.g. desquamative gingivitis)
Vesiculobullous
White Adherent Lesions
Reticular striae
Plaques
Papules
White Adherent Lesions – Reticular Type
Asymptomatic
Interlacing white lines
Bilateral and symmetrical
Buccal mucosa > tongue > gingivae, lips, etc.
White Adherent Lesions – Plaques

Tongue and buccal mucosa

*The most common site for plaque is the dorsum of the tongue

Erosive Lichen Planus
E.g. Desquamative gingivitis (slide 120)
Symptomatic
Atrophy, erythema around central ulceration
Peripheral radiating white striae
Rare malignant transformation
Thick fibrinous exudate gives an appearance suggesting a bulla
Erosive Lichen Planus – Clinical Differential Diagnosis
Hypersensitivity reactions:
Systemic (e.g. drugs)
Local or contact (e.g. amalgam, cinnamon)Lupus erythematosus

Chronic ulcerative stomatitis

Oral graft-versus-host disease

Lichen Planus – Management
******
In general, monitor for iatrogenic candidiasis
Reticular Type
No treatment needed after diagnosis
Clinical monitoring
Erosive
Topical corticosteroids
Systemic immunosuppressive, if necessary
Monitor for potential dysplasia, SCC
Oral Lichen Planus – Histology
Orthokeratosis or parakeratosis
Uneven acanthosis (diffuse epidermal hyperplasia)
Rete ridges prominent, sharp (“saw tooth”), or absent (due to lymphocyte “remodeling” rete ridges)
T-LYMPHOCYTE zone in UPPER LAMINA PROPRIA (immediately below the epithelium)
Loss of basal cells (lymphocytes attack basal cell layer; apoptotic bodies left behind)
Immunofluorescence non-specific: shaggy fibrinogen band along BMZ
Oral Lichen Planus – Histology, cont’d.
Colloid, cytoid or Civette bodies (apoptotic basal cells are eosinophilic degenerating keratinocytes)
Lichen mucositis may have similar features
“Lichen Mucositis”
Lesions with clinical and/or histological resemblance to classical lichen planus
May exhibit some variation from classical features*See slide 24 for picture

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Pemphigus – Types
Vulgaris
Vegetans
Foliaceus
Erythematosus
Paraneoplastic
Drug induced*Foliaceus and erythematosus do not affect the oral cavity

Pemphigus Vulgaris – Clinical Features
Autoimmune vesiculobullous mucocutaneous disease
Appears first in mouth in some cases
Childhood to old age, but most occur between 30-50 years old
Pemphix (Greek) = bubble or blister
Skin lesions appear as flaccid blisters*Autoantibody against Desmoglein 3 triggers response and destroys epithelial cells

*See slides 26-28 for pictures

Pemphigus Vulgaris – Clinical Features
Oral mucosa:
Positive Nikolsky signOral lesions:
Painful
Vesicles rupture rapidly
Ulcers with irregular outlines
Spread peripherally and coalesce

Positive Nikolsky Sign
Pemphigus vulgaris
Paraneoplastic pemphigus
Pemphigoid (all types)
Bullous lichen planus
Erythema multiforme
Epidermolysis bullosa
Hypersensitivity reactions*May not be demonstrable in all cases

Pemphigus Vulgaris – Histology
Autoantibodies against desmoglein 3
Acantholysis (“acantho” = prickle)
Suprabasilar cleft with tombstone basal cells:
Cleft contains Tzanck cells (float off into space)*Basal cells lose attachment to the cells above them, but remain attached to the basement membrane

Pemphigus Vulgaris – Diagnosis

Exfoliative cytology: acantholytic round epithelial (Tzanck) cells

Histology: suprabasilar cledft with tombstone basal cells (cleft contains Tzanck cells)

DIF: Labelled Igs attached to autoantibodies against desmoglein 3 around epithelial cells in specimen (creates fishnet pattern)

IIF: Labelled CIRCULATING AUTOANTIBODIES to desmoglein 3 create same pattern on animal mucosa

Pemphigus Vulgaris – Management
Diagnosis ASAP
Prescriptions by experienced physician
Systemic corticosteroids
Other immunosuppressive agents
Monitor for iatrogenic candidiasis
Monitor disease by indirect immunofluorescence: circulating Igs correlate with disease activity
Serious drug side effects
10% fatal due to treatment
Systemic Corticosteroid Side Effects
Diabetes mellitus
Adrenal suppression
Weight gain
Osteoporosis
Peptic ulcers
Severe mood swings
Increased susceptibility to infections
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******
Perilesional Biopsy – Chronic Blisters, Erosions and Ulcers

Perilesion = tissue around the lesion

Diagnosis of immunologically-mediated ulcerative conditions (e.g. PV, MMP, BP, LP, LE)

Biopsy specimen should include perilesional (clinically normal) tissue

One-half in 10% formalin for routine H & E stain
Other half in Michel’s (preservative) solution

Incubated with FLUORESCIN-LABELED KNOWN PREPARED ANTIBODY against tissue-bound autoantibody or tissue antigen (C3, fibrinogen)

Bound fluorescin emits bright yellow-green light when tissue is exposed to UV light

Direct Immunofluorescence

Identifies factors in fresh (or preserved) patient tissue

Patient tissue incubated with F-LABELED KNOWN, PREPARED ANTIBODY against:
Tissue bound autoantibody (in PV, MMP, BP, LE)
PV: autoantibody to desmoglein 3
Tissue antigen (C3, fibrinogen)
Foreign (e.g. viral) antigen

Bound fluorescein emits bright yellow-green light when tissue is exposed to UV light

Indirect Immunofluorescence

Identifies circulating autoantibody in patient’s serum

Monkey mucosa is incubated with patient’s serum

Autoantibody in serum attaches to corresponding structure in the mucosa

F-LABELED KNOWN PREPARED ANTIBODY against the antibody is incubated with tissue section

Bound fluorescein emits bright yellow-green light when tissue is exposed to UV light

Pemphigus Vegetans
Variant of pemphigus vulgaris (less serious form)
Oral involvement in a few cases
Acantholytic bullae followed by epithelial hyperplasia and intraepithelial abscess
Pustular vegetations may look verrucous
Many eosinophils present
Vegetans type may occur in lull in pemphigus vulgaris
Can spontaneously remit
Paraneoplastic Pemphigus
Mucocutaneous disease associated with lymphoma (or benign lymphoprolifierative disease)
May appear before lymphoma diagnosis
Sudden onset of multiple vesiculobullous lesions on skin and mucosae
Also seen in erythema multiforme
Paraneoplastic Pemphigus, cont’d.
Cicatricial conjunctivitis in some cases
Skin lesions papular and pruritic (like lichen planus)
Lips resemble erythema multiforme (crusting)
Corticosteroids controls this disease but make malignancy worse
Paraneoplastic Pemphigus – Pathogenesis
Tumor causes host lymphocytes to release IL-6
IL-6 stimulates Igs against basement membrane antigens
Cytotoxic T lymphocytes presentThis multifaceted immunologic attack produces a variety of clinical, histologic and immunologic changes

Paraneoplastic Pemphigus – Histology

Lichenoid mucositis with subepithelial cleft or intraepithelial cleft

Some cases are only lichenoid

DIF: Weak deposition of immunoreactions (IgG and C); between epithelial cells and/or linear deposits at the basement membrane zone

IIF (using patient serum and epithelium from rat bladder): Igs between epithelial cells against desmogleins 1 and 3; Igs in BMZ against desmoplakin I and II, BPAG-1, etc.

***REVIEW CASES***
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Mucous Membrane Pemphigoid – Clinical Features
Chronic vesiculobullous disease
Most often affects females greater than 40 years old
Vesicles rupture: painful ulcers may persist for months
Positive Nikolsky sign
Usually exclusive to the mucous membrane of the oral mucosa; much lesser extent in the skin
Causes desquamative gingivitis
Desquamative Gingivitis
Gingivae red, edematous and glazed
Superficial ulceration or desquamation/peeling
Occurs more on the buccal gingiva than the lingual
Vesiculobullous conditions: MMP, ELP, PV, CUS, EBA, SLE, drug reactions, LIgA, paraneoplastic pemphigus
Mucous Membrane Pemphigoid – Clinical Features, cont’d.

Conjunctival involvement may lead to scarring

Symblepharon
Ankyloblepharon
Entropion

Symblepharon
Adhesions between bulbar and palpebral conjunctivae
Ankyloblepharon
Adhesion of ciliary edges of eyelids to each other
Entropion
Scarring may cause eyelids to turn inward
Mucous Membrane Pemphigoid – Histology
Subepithelial cleft
Entire epithelium lifts off the surface; looks like “unzipping”
Separation of epithelium from connective tissue at the BMZ results in vesicle formation
Subepithelial Vesicles in Oral Vesiculo-Ulcers
Pemphigoid (all types)
Epidermolysis bullosa (some types)
Linear IgA disease
Angina bullosa hemorrhagica
Dermatitis herpetiformis
Mucous Membrane Pemphigoid – Immunofluorescence
Homogeneous linear fluorescence at BMZ on DIF (IgG, C3, etc.)
See a definite line along the basement membrane zoneCIRCULATING IGs IN ONLY 5-30% OF CASES (this is IIF)

Mucous Membrane Pemphigoid – Pathogenesis and Histology
AUTOANTIBODIES (IgG etc.) TO BMZ ANTIGENS:
Hemidesmosome: BPAG (230kd) in plaque (in BP and MMP); BPAG2 (180kd) TRANSMEMBRANE PROTEIN (in MMP); Integrin alpha-6, beta-4 (in MMP)
Lamina lucida: LAMININ (EPILIGRIN) IN ANCHORING FILAMENTS (in MMP)Binding of IgG triggers reaction involving C and PMNs

Weakens basement membrane

Homogenous linear fluorescence at BMZ in DIF

Circulating Igs in only 5-30% of cases

Mucous Membrane Pemphigoid – Management

Removal of drug-induced disease

Ophthalmic consult

Topical corticosteroids:
Increase potency as necessary

Systemic:
Corticosteroids
Steroid sparing immunosuppressives
Tetracycline or minocycline
Dapsone

Bullous Pemphigoid – Clinical Features
Most common autoimmune blistering disease
Occurs in older people (60-80)
Starts with pruritus
Multiple tense bullae on normal or erythematous skin
Bullous Pemphigoid – Clinical Features, cont’d.
Bullae rupture, producing crust
Heal without scars
Oral lesions uncommon
Clinical course shorter than MMP
Bullous Pemphigoid – Histology
Subepithelial cleavage
Antigens: BP180 and BP230
Eosinophils within bullae
DIF positive in 90-100% of cases
IIF positive in 50-90% of cases
Titers don’t correlate with disease activity
Bullous Pemphigoid – Management
Removal of drug-induced disease
Systemic immunosuppresive agents
Lower doses of prednisone than for pemphigus
Better prognosis
Spontaneous remission in 2 to 5 years in some
Mortality due to treatment in older patients
Systemic Lupus Erythematosus – Pathogenesis
Antibodies against host cell antigens:
Nuclear (seem to do the most damage)
Cytoplasmic
Cell surfaceGenetic, environmental and hormonal factors trigger:
Increased B cell function
Abnormal T cell activity

*Patients most often die from renal failure

Discoid Lupus Erythematosus
******
Organs Involved
Skin and oral only
Symptoms
NO
Serology
NO DETECTABLE ANTIBODIES
Histopathology
Basal cell loss
Lymphocytes at interface and perivascular
Keratosis
DIF
Granular/linear basement membrane deposits of IgG and C3
Systemic Lupus Erythematosus
******
Organs Involved
Skin, oral, heart, kidneys, joints
Symptoms
Fever, malaise, weight loss
Serology
Positive ANA
Anti-DNA antibodies
Histopathology
Similar to discoid
DIF
Similar to discoid
Systemic Lupus Erythematosus – Clinical Features
Young adult females
Erythematous cutaneous rash (“butterfly” pattern on face)
Fever, weight loss, malaise
Glomerulonephritis
Damage to: joints, heart, lungs
Oral Lesions – LE
White plaques +/- ulceration
Erythema
Erosions
Ulcers
Desquamative gingivitis*Classical lesion: central red area or ulcer with white spots and peripheral radiating white lines

*Oral lesions may occur in SLE and CCLE

Systemic Lupus Erythematosus – Laboratory Abnormalities
Hematologic changes:
Anemia
Leukopenia
ThrombocytopeniaReduced serum complement concentration

ANTINUCLEAR ANTIBODIES

SLE – Antinuclear Antibodies

IIF is the most common technique to detect ANAs

Pattern of nuclear fluorescence suggests type of antibody

Homogenous/diffuse: antibodies to chromatin, histones and ds-DNA

Rim: antibodies to ds-DNA

Speckled: antibodies to non-DNA antigens (histones and RNP):
Sm
RNP
SS-A (Ro)
SS-B (La)

Nucleolar: antibodies to nucleolar RNP

Lupus Erythematosus – Histology
Hyperkeratosis:
Follicle keratin plugging in skin in CCLE, but nor in SLEAlternating epithelial atrophy/acanthosis

Basal cell degeneration (apoptotic bodies)

Subepithelial edema (+/- vesicles)

Thick PAS + BMZ

Lupus Erythematosis – Histology, cont’d.

Subepithelial, perivascular and adnexal lymphocytes

Intense inflammation in superficial lamina propria; inflammatory cells in deeper connective tissue (perivascular tissue)

See bulging of rete ridges due to attacking lymphocytes

*See zone of lymphocytes attacking the basal cells
*Looks like lichen planus, until you see deeper perivascular inflammation

Lupus Erythematosus – Histology, cont’d.
IF shows shaggy, granular-linear deposits in BAND along mucocutaneous BMZ:
IgG (IgM and IgA), C3 and fibrinogen
Band along BMZ is LUPUS BAND TEST
Positive in clinically normal skin in SLE (not CCLE)*In patients with CCLE, will only see the bands in the lesions; in SLE patients, will see the bands even in normal skin

Systemic Sclerosis
Probable autoimmune pathogenesis
Occurs much more in females than males
Insidious onset
INCREASED COLLAGEN (produces a mask-like facies)
Microstomia
Sclerodactyly (fingers with tightly bound skin)
Systemic Sclerosis – Scleroderma
Fibrosis of lungs, heart, kidneys, GI tract
Fibrosis also causes atrophy of the ramus, coronoid process or condyle; PDL space around mandibular molar is widened (with intact lamina dura)
Interstitial pulmonary disease, which leads to pulmonary hypertension and heart failure
Localized Scleroderma

Morphea

The cutaneous alteration (from a limited form of scleroderma) called en coup de sabre because the lesion resembles a scar that might result from a cut with a sword

Raynaud’s Phenomenon

Arterial insufficiency of acral parts SECONDARY to another disorder that causes arterial narrowing (e.g. SLE, systemic sclerosis, etc.)

Claudication (limping), color and temperature changes

Chronic ulcerations and eventual gangrene

See breakdown and resorption of digits (fingers may be fixed in a claw-like position; shortening may occur from acro-osteolysis; ulcerated fingertips)

Raynaud’s Disease
Vasospasm and its consequences are primary (increased response to stimuli has no known cause
Systemic Sclerosis – Diagnosis

Histology

Rheumatoid factor (antibody against Fc fragment of human IgG)

ANAs (including Anto-Scl-70; Scl-70 is a centromere antigen)

Systemic Sclerosis – Management

D-penicillamine inhibits collagen formation

Surgery (esophageal dilation)

Calcium channel blockers (increase peripheral blood flow and reduce Raynaud’s)

ACE inhibitors (reduce hypertension if kidneys severely affected)

Oral hygiene instruction

Poor long-term prognosis

CREST

Mild form of systemic sclerosis

C: calcinosis cutis
R: Raynaud’s phenomenon
E: esophageal dysfunction
S: sclerodactyly
T: telangiectasia

Mostly affects 50-70 year old females

Erythema Multiforme
Vesiculo-ulcerative mucocutaneous disease
Mostly affects the lips
Occurs in young adults
Occurs in males more than females
Prodrome: fever, malaise, headache
Abrupt onset; usually resolves in four weeks
Recurrence linked to HSV
Erythema Multiforme – Pathogenesis
Self-limiting hypersensitivity reaction
Precise mechanism unknown
Possible involvement of both cell-mediated and humoral immune systems
Ag-Ab complexes target small mucocutaneous vessels
Some drugs may cause EM: Sulfas, Penicillin, Dilantin, Barbiturates, Iodines, Salicylates
Erythema Multiforme – Clinical
Usually acute, self-limited
Some cases chronic or recurring acute
Headache, fever, lymphadenopathy
Target skin lesions (concentric erythematous rings)
Skin macules, papules, vesicles, bullae, etc
Oral ulcers
Erythema Multiforme – Oral Lesions
Painful
Aphthous-type ulcers
Multiple superficial extensive ulcers
Bullae soon rupture*Destruction of epithelium that is superficial, but deeper than pemphigus vulgaris

Erythema Multiforme – Types
Minor
Major
Stevens Johnson syndrome (oral, eye and genital lesions)
*These three may overlapToxic epidermal necrolysis (usually caused by drugs; patients look like they have extensive burns)

Erythema Multiforme – Histology
Necrotic keratinocytes
Spongiosis
Vesicles in epithelium may extend to the subepithelium
Necrosis of vesicle roof
Interface infiltrate lymphohistiocytic
Perivascular inflammation
IF nonspecific*Histology is characteristic but not pathognomonic

Erythema Multiforme – Management
Eliminate triggers (antiviral agents in cases triggered by HSV)
Early corticosteroids (topical, systemic)
Rehydrate
TEN (toxic epidermal necrolysis): burn unit, avoid corticosteroids, pooled IgGs (blocks Fas ligand, which caused epithelial destruction)
Reactive Arthritis (Reiter’s Syndrome)
Abnormal immune reaction to microbial antigen (STD or dysentery)
See 1-4 weeks after exposure
Acute onset of triad: non-specific urethritis, conjunctivitis, arthritis
Skin lesions in some (histology is psoriasiform)
Reactive Arthritis (Reiter’s Syndrome), cont’d.
Oral in less than 20% of cases:
Ulcers (RAU)
Papules
Erythema migrans?Most affects young adult males

HLA-B27 phenotype

Lasts weeks to months with recurrences

NSAIDS for arthritis