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204 theme 1 > 14. pharmacological aspects and immunology > Flashcards

14. pharmacological aspects and immunology Flashcards

1
Q

discovery of aspirin

A

white willow, bark used to treat fever and joint pain

hoffman: acetylsalicylic acid (aspirin)

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2
Q

NSAID examples

A 
aspirin 
paracetamol 
propionic acid derivative, eg ibuprofen, naproxen
arylakanoic acid derivatives, eg indometacin, diclofenac 
oxicams
fanatic acid derivatives
betazones  
coxibs, eg celecoxib
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3
Q

eicosanoid pathway

A

during tissue injury
phospholipids converted by phospholipase to arachidonic acid
converted to leukotrienes (lipoxygenases) or prostaglandin H2 (cyclo-oxygenases)
tissue specific syntheses convert prostaglandin H2 into: thromboxane, prostaglandins or prostacyclins

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4
Q

NSAID mechanism of action

A

all inhibit cycle-oxygenase enzymes
3 isoforms of cycle oxygenase exist
precent prostaglandin H2 formation and thus thromboxanes, prostaglandins and prostacyclins

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5
Q

COX-1

A

constitutive expression
in stomach, kidney, platelets, vascular epithelium
inhibition leads to anti platelet activity
side effects

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6
Q

COX-2

A

induced in inflammation (by IL-1)
injury, infection, neoplasia
inhibition leads to analgesia and anti-inflammatory actions

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7
Q

COX-3

A

in CNS only (?)
specifically inhibited by paracetamol
antipyretic and analgesic actions

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8
Q

indications for NSAID therapy

A

mild analgesics
potent analgesics
anti-inflammatories

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9
Q

NSAIDs as mild analgesics

A 
orally and topically 
mechanical pain of all types
minor trauma 
headaches, dental pain  
dysmenorrhoea
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10
Q

NSAIDs as potent analgesics

A

orally, parentally, rectally
peri-operative pain
ureteric colic

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11
Q

NSAIDs as anti-inflammatories

A

not great anti inflammatory action, most of the time
gout
inflammatory arthritis, eg ankylosing spondylitis, rheumatoid arthritis

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12
Q

aspirin

A

used for pain and inflammation

anti platelet effect: prophylaxis for ischaemic heart disease, treatment of acute MI

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13
Q

aspirin is limited by

A

GI toxicity
tinnitus (mechanism obscure, usually reversible)
Reye’s syndrome (fulminant hepatic failure in children)

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14
Q

non-NSAID anti-platelet drugs

A

clopidogrel

dipyrimidole

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15
Q

paracetamol

A 
only binds COX3
no significant anti-inflammatory action 
no significant GI  toxicity 
analgesic/anti-pyretic 
dangerous in overdose
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16
Q

paracetamol metabolism under normal circumstances

A

paracetamol conjugated in the liver with glucoronide and sulphate
minority is oxidised by microsomal enzymes to toxic intermediary - rapidly self-neutralised by conjugation with glutathione

17
Q

paracetamol metabolism when present in excess

A

conjugation reactions overwhelmed
toxic intermediaries accumulate
can cause potentially fatal hepatic necrosis

18
Q

NSAID GI toxicity - prostaglandins

A

prostaglandins E2 and I2 lost
decreases acid production
increases mucus production
increases blood supply

19
Q

NSAIDs - effect on stomach and duodenum (and colon)

A

irritation
ulcers (gastric 15-30%, duodenal 10%)
bleeding
similar effect in colon - colitis

20
Q

risk factors for NSAIDs and GI

A 
relative risk 4.7 for all - higher for some NSAIDs (piroxicam = 18) 
previous GI bleed  
age 
chronic disease
steroid use
21
Q

NSAID nephrotoxicity

A

primarily related to changes in glomerular blood flow
decreased glomerular filtration rate, sodium retention, hyperkalaemia, papillary necrosis
acute renal failure 0.5-1%

22
Q

asthma and aspirin

A

about 10% asthmatics experience bronchospasm following NSAIDs
perhaps because arachidonic acid is shunted down 5-lipoxygenase pathway to form leukotrienes

23
Q

non selective NSAIDs - least to most potent

A

ibuprofen
naproxen
diclofenac (voltarol)
indometacin - reserved fro specialist diseases

24
Q

preventing NSAID toxicity

A

use sparingly - paracetamol or opioids

GI toxicity - use gastroprotective drugs (PPIs, misoprostil - PGE1 analogue)

25
Q

selective COX-2 inhibitors

A

anti-inflammatory and analgesic in humans
objective evidence of selectivity - less side effects than non-selective NSAIDs
coxibs - celecoxib, rofecoxib, etoricoxib

26
Q

coxibs efficacy

A

numerous clinical trials - data
comparable efficacy to non-selective NSAIDs - for acute pain, dysmenorrhoea, inflammatory joint disease etc
less side effects

27
Q

celecoxib

A

only current coxib prescribed

indicated for patients at risk for GI bleed

28
Q

corticosteroids

A

cortisol (hydrocortisone)
have many effects on:
carb, protein and lipid metabolism, fluid and electrolyte balance, bone metabolism, psychological
modulates immune respnose

29
Q

how do steroids modulate the immune responses?

A

reduce immune activation
alter gene expression by binding to steroid receptor which activates transcription
onset of action is delayed
effects T and B cells and cells of the innate immune system

30
Q

immunomodulation by steroids

A

cell trafficking

cell function

31
Q

steroids and cell trafficking

A

lymphopenia, monocytopenia

neutrophilic and impaired phagocyte migration

32
Q

steroids and cell function

A

T cell hyper-responsiveness
inhibited B cell maturation
decreased IL1, IL6 and TNF alpha production
inhibits COS
widespread inhibition of Th1 and Th2cytokines
impaired phagocyte killing

33
Q

clinical uses of steroids

A

suppress inflammation
asthma, Crohn’s, UC, eczema, MS, sarcoid, allergy, rheumatoid arthritis, SLE
suppress specific immunity - graft refection
replacement therapy in hypoadrenalism

34
Q

steroid preparation

A

different routes of administration-systemic or topical

different drugs - potencies, pharmacokinetics

35
Q

early side effects of steroid therapy

A

weight gain
glucose intolerance
mood change
suppression fo ACTH release

36
Q

later side effects of steroid therapy

A 
proximal muscle weakness
osteoporosis
skin changes (striae)
body shape changes (buffalo hump, central obesity)
hypertension
cataracts 
adrenal suppression
37
Q

adrenal suppression during corticosteroid therapy

A

high dose corticosteroids suppress endogenous production within 1 week
adrenal cortex atrophies afternoon prolonged therapy - endogenous production takes time to recover upon cessation
abrupt withdrawal reduces ability to deal with physiological stress - may precipitate adrenal crisis

38
Q

steroids and risk of infection

A

phagocytic defects
bacterial - S. aureus, enteric bacteria
fungal - candida, aspergillus

cell mediated
intracellular pathogens - TB, varicella, listeria, pneumocystis

204 theme 1 (12 decks)

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