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Scientific Basis of Medicine > The Case Of The Red-skinned Man > Flashcards

The Case Of The Red-skinned Man Flashcards

1
Q

2 types of adverse drug reactions

A

type A

type B

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2
Q

type A

type B

A

dose and pharmacology related reaction, predictable, low mortality

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3
Q

Type B adverse drug reactions

A

dose and pharmacology independent, unpredictable, high mortality
aka drug hypersensitivity reactions

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4
Q

Types of drug hypersensitive reaction

A

immediate

non-immediate

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5
Q

time frame of immediate DHR

A

within an hour, often faster esp if IV treatment

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6
Q

symptoms of immediate DHR

A 
urticaria
angioedema
rhinitis
laryngeal oedema
bronchospasm
cardiovascular collapse
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7
Q

2 types of immediate DHR (mediators)

A

IgE mediated

non IgE mediated

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8
Q

How are mast cells activated?

A

sensitised IgE binds specific allergen

cross-linking and clustering of FceR1 receptors, receptor phosphorylation, mast cell degranulation

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9
Q

is DHR related to atopic phenotype?

A

no, independent, having atopy does NOT make you more likely to have a DHR

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10
Q

when does immediate DHR occur related to dose?

A

after the 1st dose in a course, may have had previous course of same/similar drug when sensitisation occurred

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11
Q

non IgE mediated DHR

A

non-specific mast cell activation, more likely in people with spontaneous urticaria

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12
Q

what types of drugs cause non IgE mediated immediate DHR?

A

opiates
radiocontrast media
vaccines
myorelaxants

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13
Q

high risk drugs for immediate DHR?

A

antibiotics
NSAIDs
taxane chemo
myorelaxants

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14
Q

serum mast cell tryptase

A

investigation used to confirm acute anaphylaxis

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15
Q

how to do mast cell tryptase test?

A

take blood sample 1-2hrs after symptom onset, again after 24hrs - should see rise followed by normalisation

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16
Q

non-immediate DHR time-frame

A

typically 3-5 days into drug course, 5-8 if never had it before, continue after drug stopped

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17
Q

which drugs cause the most non-immediate DHRs?

A

anti-microbial

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18
Q

Stevens-Johnson Syndrome

A

dangerous DHR on a spectrum with toxic epidermal necrolysis

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19
Q

symptoms of SJS

A 
fever
cough
conjuctivitis
mucositis
erythema multiforme
epidermal necrolysis
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20
Q

symptoms of SJS

A

drug induced skin reaction involving at least 30% of skin

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21
Q

epidemiology of SJS

A

affects men more, 3-8 days after dose

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22
Q

most common drugs causing SJS

A

antibiotics
anticonvulsants
allopurinol
(can also be infection induced)

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23
Q

type 4 hypersensitivity to drugs

A

occurs 3-8 days into course, get macula-papular rash, no systemic upset

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24
Q

true prevalence of beta lactam allergy

A

1-2% population although 1-% report it

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25
Q

why is true prevalence of beta lactam allergy lower?

A

sensitisation lost at a rate of 10% a year

original symptoms caused by something else

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26
Q

can you test for drug allergy?

A

only reliable antigen test is for beta-lactam allergy

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27
Q

challenge test

A

gradually increase dose under observation until therapeutic dose reached, watch for side effects

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28
Q

management of a probable type 1 DHR

A

avoid entire class

29
Q

management of a probable type 4 DHR

A

avoid index drug, may be able to use others in class

30
Q

red man syndrome

A

erythematous pruritic rash that involves the face, neck, and upper torso, caused by vancomycin

31
Q

types of ANCA-associated vasculitis

A

granulomatosis with polyangiitis
microscopic polyangiitis
Churg-Strauss syndrome

32
Q

Vasculitis symptoms

A 
fever
myalgia
weight loss
haematuria
proteinuria
haemoptysis
dyspnoea
vasculitic rash
33
Q

Goodpasture syndrome

A

small vessel vasculitis with anti-GBM antibodies which attack type 4 collagen

34
Q

Symptoms of Goodpasture’s Syndrome

A 
cough
SOB
hamoptysis
proteinuria
haematuria
*pulmonary haemorrhage major complication*
35
Q

Treating Goodpasture’s syndrome?

A

immunosuppression and plasma exchange

36
Q

symptoms of SLE

A

fever, fatigue, weight loss, Reynaud’s, malaria rash, discoid rash, polyarthritis, pericarditis, glomerulonephritis

37
Q

treating lupus nephritis

A

ACEi

prednisolone with mycophenolate

38
Q

antibodies found in SLE

A

anti-dsDNA

ANA

39
Q

which SLE antibodies are more specific?

A

anti-dsDNA

40
Q

treating SLE generally

A

suncream

hydroxychloroquine

41
Q

Causes of drug-induced SLE (4)

A

procainamide
hydralazine
isoniazid
phenytoin

42
Q

5 types of cardiorenal syndrome

A 
1 - acute cardiac cause with AKI
2 - chronic cardiac cause with CKD
3 - AKI causes acute cardiac disorder
4 - CKD causes chronic HF
5 - systemic condition causes cardiac and renal dysfunction
43
Q

how does cardiac disease lead to renal disease?

A

impaired cardiac output leads to reduced renal perfusion, reduced GFR so impaired renal function, RAAS activated, volume expansion which further injures cardiac tissue

44
Q

Hepatorenal syndrome (HRS)

A

Acute renal failure occurs because of a decrease in renal blood flow secondary to liver disease

45
Q

pathophysiology of hepatorenal syndrome

A

Portal hypertension –> vasodilator and angiogenic factor production –> splanchnic/systemic vasodilation –> decreased effective arterial blood volume –> increased cardiac output, neurohumoral activation –> renal vasoconstriction

46
Q

Type 1 hepatorenal syndrome

A

rapid progression
creatinine doubles
caused by alcohol or sepsis
prognosis 2wks

47
Q

Type 2 hepatorenal syndrome

A

develops slowly, caused by refractory ascites, prognosis 4-6 months

48
Q

diagnostic criteria for hepatorenal syndrome

A 
cirrhosis with ascites
creatinine > 133
no shock
no hypovolaemia
no renal disease
no nephrotoxic drugs
49
Q

why is there low urine sodium in hepatorenal syndrome?

A

excess aldosterone from RAAS causes extreme sodium retention, very low urine sodium indicates severe disease

50
Q

Treating HRS

A

sodium and water restriction
treat reversible causes
liver transplant

51
Q

which infections are linked to glomerular disease? (4)

A

Hepatitis C
malaria
HIV
bacterial infections

52
Q

which cancers are associated with glomerular disease? (3)

A

lymphoma
leukaemia
myeloma

53
Q

what is the most common glomerular disease?

A

IgA nephropathy (Berger disease)

54
Q

typical presentation of IgA nephropathy

A

frank haematuria following an URTI

55
Q

pathophysiology of IgA nephropathy

A

autoimmune condition where IgA immune complexes are deposited in the kidney

56
Q

treating IgA nephropathy

A

ACEi
steroids
maybe immunosuppression
outcomes very variable

57
Q

IgA vasculitis (Henoch-Schonlein purpura)

A

excess IgA production and deposition w/in blood vessel

58
Q

Symptoms of IgA Vasculitis

A

palpable purpuric rash over buttocks and limbs
abdominal pain
arthralgia
haematuria

59
Q

treating IgA vasculitis

A

steroids
analgesia
mostly self-limiting, better prognosis than IgA nephropathy

60
Q

most common cause of nephrotic syndrome in children

A

minimal change disease

61
Q

histological hallmark of minimal change disease

A

normal on light microscopy

effacement and fusion of podocytes on electron microscopy

62
Q

treating suspected minimal change disease in a child

A

empirical steroids, can give before the biopsy result

63
Q

nephrotic syndrome

A

Proteinuria, hypoalbuminemia, oedema

hypercholesterolaemia

64
Q

complications of nephrotic syndrome

A

Hypercoagulability, increased infection

65
Q

treating nephrotic syndrome

A

salt and fluid restriction
diuretics
ACEi

66
Q

membranous nephropathy biopsy result

A

spike and dome appearance of basement membrane

67
Q

how does membranous nephropathy present?

A

nephrotic syndrome
most common in males in 40s and 50s
commonest glomerulonephritis in adults

68
Q

treating membranous nephropathy

A

ACEi
immunosuppression
consider anticoagulation

Scientific Basis of Medicine (35 decks)

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