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Dermatology > stuff I forget from skin as an immune organ > Flashcards

stuff I forget from skin as an immune organ Flashcards

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Dermatology Board Prep flashcards
1
Q

what are the inherent physical nonimmune skin defenses?

A

Physical Resistance to mechanical trauma Relatively water impermeable Physical separation between self and nonself

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2
Q

what are the inherent chemical nonimmune skin defenses?

A

Chemical Free fatty acids Free radical trapping Antimicrobial peptides

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3
Q

what molecule responsible for photoprotective nature of skin?

A

Melanin as a UV chromophore

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4
Q

t/fSkin is capable of both innate and adaptive immune responses

A

true

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5
Q

what is the old view of keratinocytes? 2 components?

A

Old view: Keratinocytes… Are passive barrier cells

Are passive victims of immune attack

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6
Q

Keratinocytes as immune cells

which cytokines do they produce?

which cytokines do they repond to?

which intracellular adhesion molecule do they upregulate?

when can they present antigen?

A

**Produce cytokines: ** IL-1, TNF-, chemokines
**Respond to cytokines: **IFN, IL-1
Upregulate ICAM-1
Present antigen:Particularly when stimulated

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7
Q

t-lymphs in the skin. how many are there?

A

Although not readily visible in normal skin, there are many lymphocytes in both epidermis and dermis
Estimated normal adult skin has 20 billion T cells
Twice that in normal circulation

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8
Q

skin immune team:

role of keratinocytes?

role of dendritic cells?

role of t-cells?

A

Keratinocytes sense pathogens and “danger signals”

Migratory dendritic cells (including Langerhans cells) take up pathogens and initiate a wide range of immune responses

T cells that live in skin (tissue-resident memory T cells) respond and perform effector functions

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9
Q

Two major adhesion molecules of clinical significance include

A

Desmosomes
Hemidesomsomes

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10
Q

define pemphis vulgaris

A

Disorder of adhesion of one keratinocyte to another

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11
Q

pemphis vulgaris:

epidemiology:

who does it affect?

KNOW:HOW does it start?

what phyiscal finding are you most likely to see?

what happens if it is untreated?

A

epi: Rare, chronic and progressive
whoAffects adults, rarely children
starts:Often starts with mucosal erosions
Because of the depth of blistering process, more likely to see erosions rather than blisters
If untreated, high mortality

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12
Q

which conditon?

A

pemphisgus vulgaris

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13
Q

what is the pathogenesis of pemphigus vulgaris?

KNOW: what is the target antigen?

A

Autoantibodies to molecule in the desmosome, which mediates adhesion of one keratinocyte to another
_Target antigen is desmoglein 3
Remember: “PV=DG3”_

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14
Q

KNOW: pemphigus vulgaris: can circulating antibodies be detected? do they correlate with disease progress?

KNOW: prognosis w/tx? how about w/o tx?

A
  • *Circulating antibodies can usually be detected in the blood (serum)**
  • *The amount usually correlates with the disease progress and can be followed**
  • *With treatment, disease usually remits in several years**
  • *If untreated, mortality up to 30-70%**
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15
Q

define bullous pemphigoid?

what type of disease is ti?

how many cases?

onset?

which gender more likely affected?

A

Disorder of adhesion of the epidermis to the underlying dermis

type: Autoimmune blistering disease
epi: 6-7 new cases per million
Onset usually after age 60
Men > women

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16
Q

which condition?

A

bullous pemphigoid

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17
Q

what is the clinical presentation of bullous pemphigoid?

A

Fairly sudden onset of very itchy wheals and tense blisters on trunk and extremities
Mouth and oral mucosa affected in some

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18
Q

What causes bullous pemphigoid?

KNOW: which drug in particular associated with bullous pemphigoid?

can pregnant women have this condition?

A

Uncertain “why”
In some cases is caused by drugs with BP including furosemide(must know), ibuprofen (NSAIDS), captopril, penicillamine, and antibiotics.
Pregnant women have version of condition called “gestational pemphigoid” or pemphigoid gestationis

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19
Q

KNOW: what is the pathogenesis of bullous pemphigoid?

KNOW: what are the target antigens?

A

Production of autoantibodies to molecules that make up hemidesomsome
This prevents epidermis from binding to dermis
Target antigens are:
Bullous pemphigoid antigen-230 (BPAg1)
Bullous pemphigoid antigen-180 (BPAg2

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20
Q

Can detect circulating autoantibodies on blood of some patients. Do titers correlate with disease activity?

which cells are elevated in BP?

A

titer does not correlate with disease activity (but in pemphigus vulgaris, titers do correlate)

Some patients also have elevated eosinophils

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21
Q

fyi: both pemphigus and pemphigoid:

Can be serious or life-threatening
Require treatment with immunosuppressant agents
Last months to years, even with treatment
Mortality is fortunately now low, but not zero

A

fyi

22
Q

epidemiology of drug rxns:

  1. how often do they occur?
  2. which drugs(2 in particular) have higher rates of ADEs.
A
  1. Most drugs result in adverse reactions only rarely (1/1000 exposures)
  2. sulfonamides, penicillins have much higher rates of adverse reactions (30 to 50/1000).
    Incidence of fatalities due to drug reactions among inpatients is between 0.1% and 0.3%
23
Q

what is the pathogeneisis of drug eruptions?

KNOW: what which two compoundsproduces cell damage?

A

Most cases: unknown
May be immunologic (allergic reactions) but most are COMPLEX

Drug-hapten presented by Langerhans cells to T cells
perforin and granzyme are produced –>cell damage

24
Q

KNOW: Patient’s __________ of the drug and generation of toxic metabolites plays a large role

A

Patient’s metabolism of the drug and generation of toxic metabolites plays a large role

(P-450 metabolism is significant in drug reactions to sulfas and anticonvulsants)
Organ failure affects clearance

25
Q

the presence of which immunodefiency predisposes to drug reaction?

which two infections predispose to drug rxn?

A

immunodeficiency: acquired glutathione deficiency

infection: HIV or EBV

(P-450 metabolism is significant in drug reactions to sulfas and anticonvulsants)
Organ failure affects clearance

26
Q

chart to be aware of

A

look over a few times

27
Q

what is the most common type of drug rxn? how does it present?

when does it start?

where on body does it start?

which class of drugs most likely to cause this rxn?

A

morbilliform (aka maculopapular) eruptions

Itchy, red, often with small papules throughout
Typically starts within first 2 wks of treatment, but possible up to 10 days after drug is stopped
Proximally first (groin/axillae) then generalize within 1-2 days
Most commonly: Antibiotics- semisynthetic penicillins and Bactrim

28
Q

which condition?

A

morbillifomr eruption

29
Q

which three drug groups commonly cause drug reactions?

A

An anticonvulsant
A sulfa antibiotic
Any drug that starts with “p”

30
Q

what are the 6 drugs that start with P that can cause rnxn??

A

penicillamine
procainamide
phenytoin
PTU
piroxicam
polymyxin

31
Q

More complicated drug rashes: drug hypersensitivity syndromes

most commonly seen with which drugs?

A

Most commonly seen anticonvulsants and long acting sulfonamides

32
Q

More complicated drug rashes: drug hypersensitivity syndromes

KNOW:what are symptoms(6- REF LH)? which one is life threatening?

KNOW:what should be done to tx rxn?

A

fever, rash, eosinophilia, enlarged lympadenopathy, hepatitis and nephritis
Hepatitis may be life threatening
the drug should be stopped immediately/ without debate

33
Q

Anticonvulsant Hypersensitivity Syndrome

seen with which 3 drugs?

A

Seen with phenytoin, phenobarbitol, carbamazepine and others.
With the exception of valproic acid, cross reactions are common.

34
Q

Anticonvulsant Hypersensitivity Syndrome

KNOW: what is it due to?

A

Due to deficiency of epoxide hydrolase and inability to detoxify arene oxide metabolites
Metabolites bind to proteins and elicit an immune response

35
Q

KNOW: Immunologic urticaria or hives is most commonly associated with ________and related beta-lactam antibiotics

A

Immunologic urticaria or hives is most commonly associated with penicillin and related beta-lactam antibiotics (associated with IgE antibodies to PCN or its metabolites)

36
Q

KNOW: which tissues does angioedema usually affect?

A

eyelids, lips, lobes of the ears, and external genitalia

mucous membranes of the mouth, tongue, or larynx

37
Q

angioedema sometimes a complication of which drugs?

A

Sometimes a complication of ACE- inhibitors (Lisinopril and enalapril > captopril)

38
Q

angioedema?

which race 5x at greater risk?

KNOW: what causes angioedema

KNOW: what does it depend on?

KNOW: recurrence?

A

Blacks are at five times greater risk than whites

Thought to be related to blocking of kinase II increasing tissue kinin

Episodes may be severe (45% require hospitalization)

  • *Dose dependent** (may resolve with decreased dose but I’d probably stop the drug)
  • *Patients with one episode of angioedema have a tenfold risk of a second episode **
39
Q

is redman syndrome an allergic rxn?

A

NO

40
Q

At any time during infusion of ___________, a macular eruption appears initially on the back of the neck and sometimes spreads to the upper trunk, face and arms

A

At any time during infusion of vancomycin, a macular eruption appears initially on the back of the neck and sometimes spreads to the upper trunk, face and arms

41
Q

what is red man syndrome associated with?

what are symptoms due to?

how do you prevent redman syndrome?

A

Associated pruritus, “heat” and hypotension
Caused by elevated blood histamine
Prevented by slow infusion and pretreatment with antihistamines

42
Q

Most medication-related photosensitivity is caused by _______. why?

A

Most medication-related photosensitivity is caused by UVA as drugs absorb in UVA range and UVA is able to penetrate into the dermis where UVA is present

43
Q

___________reactions are eczematous, pruritic, involve the immune system

do the occure b4 or after photosensitive?

A

Photoallergic reactions are eczematous, pruritic, involve the immune system

happen later

44
Q

KNOW: Most common causes of photosensitivity? (which three drugs highligted in lecture)

A

NSAIDs, Bactrim, thiazide diuretics

others: Most common causes of photosensitivity are NSAIDs, Bactrim, thiazide diuretics, related sulfonylureas, quinine, quinidine, and certain Tetracyclines.

45
Q

KNOW: phototoxicity

what is it related to?

is prior sensitization required?

3 drugs that commonly cause?

when after insult does it happen?

clinical presentation?

A

Related to both dose of medication and UVR
Prior sensitization is not required (can potentially occur in anyone)
Tetracyclines(think doxy), amiodarone, nonsteroidal agents are common culprits
Happens fast
Stinging and burning occurs after 30 minutes of sun exposure.
Dusky, blue-red erythema of face and dorsal hands is seen.
Desquamation is not seen

46
Q

pathogenesis of toxic epidermal necrolysis?

what happens to keratinocytes?

is there inflammation?

A

Thought to be an immune-related cytotoxic reaction aimed at destroying keratinocytes that express a foreign antigen

Keratinocytes undergo apoptosis and die, allowing epidermis to slough off dermis

There is usually minimal inflammation seen

47
Q

KNOW: what is the most serious of drug rxns?

how does it usually start?

are mucous membranes involved?

how do pts present? what is mortality?

A

toxic epidermal necrolysis

Usually starts with a widespread rash, which over several days starts blistering and peeling

Mucous membranes usually involved

Patients are sick; mortality up to 30%

48
Q

KNOW: 4 drugs that cause toxic epidermal necrolysis?

A

_Anticonvulsants
Antibiotics_
Even nonsteroidal antiflammatory agents like ibuprofen

49
Q

how do you tx toxic epidmeral necrolysis? (4)

A

Stop the drug immediately
Supportive care
Management in burn unit where available

  1. Use IV: Ig to bind/block apoptosis
50
Q
A

Widespread Lesions Characteristic of
Stevens-Johnson Syndrome

Dermatology (18 decks)

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