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Medical Studies 1 > Pharmacology > Flashcards

Pharmacology Flashcards

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USMLE® Step 1 flashcards
1
Q

describe beta blockers

A

competitive antagonists

acts on beta 1, 2 and 3 receptors

reduced Q, HR, BP, decrease renin secretion, constriction of smooth muscle in arteries

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2
Q

who should you definitely not give beta blockers to

A

patients where cardiac effects are undesirable e.g patient w hTN or bradycardia

contraindicated in severe or poorly controlled reversible airways disease e.g asthma

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3
Q

who should you be cautious abt when giving beta blockers

A

diabetes w hypoglycaemia as may mask symptoms of this

can lower walking distance in peripheral vascular disease

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4
Q

what should you communicate when prescribing beta blockers

A

dizziness or tiredness at start of Rx or when dose increased

do not stop Rx suddenly

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5
Q

what should you monitor when prescribing beta blockers

A

HR

BP

ECG if bradycardic

HF symptoms

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6
Q

how should you deprescribe beta blockers

A

need to wean off slowly to prevent recurrence of angina, tachyarrhythmia

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7
Q

what effect do calcium channel blockers have on vascular smooth muscle

A

relaxation of arterioles > decrease vascular resistance > decrease BP

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8
Q

what effect do calcium channel blockers have on myocardium

A

decrease force of contraction > decrease BP or worsening of HF in those who are prone (negative inotropy)

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9
Q

what effect do calcium channel blockers have on cardiac conduction tissue

A

decrease HR > negative chronotropy

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10
Q

what are 2 main classes of calcium channel blockers

A

non-dihydropyridine

dihydropyridine

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11
Q

who is not suitable for dihydropyridines

A

low BP

intolerance to previous DHP

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12
Q

who is not suitable for non-dihydropyridines

A

low HR

low BP

cardiac conduction defect

systolic HF

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13
Q

what should you communicate when prescribing dihydropyridines

A

flushing, headache, tachycardia

swelling of ankles (DONT GIVE DIURETIC FOR THIS)

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14
Q

what should you communicate when prescribing non-dihydropyridines

A

constipation

bradycardia

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15
Q

what should you monitor when prescribing calcium channel blockers

A

BP

HR (up or down depending on class)

ECG if low HR

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16
Q

how do nitrates work

A

they dilate the veins, which reduces venous return, hence reduced preload, which then reduces the amount of work for the heart

arteriolar dilation which lowers BP hence lower afterload and less work

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17
Q

who should you not give nitrates to

A

ppl on phosphodiesterase inhibitors

ppl w hypertrophic cardiomyopathy, aortic, or mitral stenosis

ppl who cannot keep nitrate free period

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18
Q

what should you communicate when prescribing short acting nitrates

A

fall in BP when first take so need to sit down
when to take
how many to take
when to call ambulance
flushing
headache

need at least 8 hour nitrate free period

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19
Q

what should you monitor for nitrates

A

effect on angina symptoms

postural BP effects for long acting nitrate

how many times, when taking etc for short acting GTN

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20
Q

how should you deprescribe nitrates

A

need to wean off gently

usually reduce dose by 30 mg at a time

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21
Q

how do ACE inhibitors work

A

ACE in RAAS system blocked

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22
Q

who would you not give ACE inhibitors to

A

absolute contraindications:
history of intolerance to ACE
history of hereditary/idiopathic angioedema
pregnancy
renal artery stenosis

relative contraindications:
hTN
hyperkalaemia
renal impairment

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23
Q

what should you communicate when prescribing ACE inhibitors

A

cough (due to accumulation of bradykinin)

angioedema

hyperkalaemia

dizziness

renal impairment

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24
Q

what should you monitor when prescribing ACE inhibitors

A

within 1-2 wks of commencing or dose escalation, should have K, renal function, and BP checked

should ask abt cough, swelling of angioedema

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25
Q

what should you communicate when prescribing long acting nitrates

A

initially get headache, flushing

postural hTN

need at least 8 hr nitrate free period

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26
Q

what are 3 types of antiplatelets

A

aspirin

P2Y12 inhibitors

dipyridamole

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27
Q

how does aspirin work

A

inhibits cox-1 enzyme as well as cox-2

results in reduced thromboxane A2 production (which is inducer of platelet aggregation hence get platelet inhibition)

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28
Q

who should you not give aspirins to

A

patients where there is active bleeding or serious risk of bleeding

aspirin allergy

aspirin sensitive asthma

aspirin induced peptic ulcer disease

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29
Q

what should you communicate when prescribing aspirin

A

main risk is bleeding

additional risk of causing GI ulcers

small risk of intracerebral haemorrhage

simple bruising in skin

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30
Q

what should you monitor when prescribing aspirin

A

ask about adverse effects

hematology performed routinely in this population

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31
Q

how do P2Y12 inhibitors work

A

binds to P2Y12 receptor and inhibits ADP mediated platelet aggregation

32
Q

who should you not give P2Y12 inhibitors to

A

bleeding risk - age, weight, drug interactions etc.

33
Q

what should you communicate when prescribing P2Y12 inhibitors

A

need for compliance

shortness of breath

34
Q

what should you monitor when prescribing P2Y12 inhibitors

A

check Hb

ask abt shortness of breath for ticagrelor

urate also increases for ticagrelor

35
Q

how does dipyridamole work

A

inhibits platelet function by inhibiting phosphodiesterase which increases platelet cAMP

also inhibits endogenous adenosine reuptake hence results in vasodilation

36
Q

who should you not give dipyridamole to

A

there is a bleeding risk so should not give to ppl w aortic stenosis, recent MI or angina

37
Q

what should you communicate when prescribing dipyridamole

A

headache

nausea

hot flushes

38
Q

what should you monitor when prescribing dipyridamole

A

Hb

ask about dilatation effects

39
Q

how does heparin work

A

binds to antithrombin lll to enhance anticoagulant effect of antithrombin lll

40
Q

what is unfractionated heparin

A

mix of diff chain lenght heparins 5-30K dalton

given intravenously and subcutaneously

half life of 30-90 minutes

has antiplatelet effect at high doses

41
Q

what is low molecular weight heparin (LMWH)

A

only includes the low molecular weight fragments - 5-10K dalton

more of an effect on factor Xa than thrombin, no platelet effect

given subcutaneously

half life of 4 hrs

more reliable efficacy and fewer bleeding complications and thrombocytopenia

42
Q

who should you not give LMWH to

A

patients w active bleeding

patients w thrombocytopenia or other bleeding disorder

patients w renal failure

previous heparin induced thrombocytopenia

43
Q

what should you communicate when prescribing LMWH

A

risk of bleeding

thrombocytopenia

long term: osteoporosis

44
Q

what should you monitor when prescribing LMWH

A

renal function

platelets in second week of treatment (looking for HITS)

CBE if risk of bleeding

45
Q

what is HITS

A

heparin induced thrombocytopenia syndrome

IgG antibodies against complexes of heparin and platelets which results in platelet aggregation and thrombin generation hence can get thromboses as well as bleeding due to thrombocytopenia

46
Q

who should you not give unfractionated heparin to

A

active bleeding

thrombocytopenia or other bleeding disorders

previous heparin induced thrombocytopenia

47
Q

what should you communicate when prescribing unfractionated heparin

A

risk of bleeding

thrombocytopenia

need for regular blood tests

48
Q

what should you monitor when prescribing unfractionated heparin

A

APTT within 4-6 hrs then every 4-6 hrs if dose adjustment needed then at least daily

CBE if risk of bleeding

platelets in second week of Rx (looking for HITS)

49
Q

if LMWH is more effective and has a lower risk of bleeding, then why would you use unfractionated heparin in some cases

A

we use it in situations where we want to be able to monitor effect e.g in patients w severe peripheral edema or ascites

we also use it in patients who have a high risk of bleeding, as the infusion of unfractionated heparin can be stopped faster as it has a half life of only 30-90 mins while LMWH is 4 hrs

50
Q

how do statins work

A

inhibit HMG Co-A reductase enzyme which limits the rate of cholesterol synthesis

51
Q

who should you not give statins to

A

those w previous intolerance contraindicated

renal impairment

hepatic impairment

hepatic drug interactions

52
Q

what should you communicate when prescribing statins

A

may experience musculoskeletal problems such as muscle aches, myositis, myopathy

53
Q

what should you monitor when prescribing statins

A

lipids at 4 weeks

CK/ALT+AST at baseline and if clinically indicated

ask about muscle pain/weakness

54
Q

how do fibrates work

A

activate peroxisome proliferator-activated nuclear receptors and modulate lipoprotein synthesis and catabolism

55
Q

who should you not give fibrates to

A

renal/hepatic impairment

presence of gallstones or gallbladder disease

pancreatitis

56
Q

what should you communicate when prescribing fibrates

A

GI adverse effects

very rare:
gallstones
pancreatitis
DVT

57
Q

what should you monitor when prescribing fibrates

A

GI symptoms

lipids

58
Q

how does ezetimibe work

A

inhibitor of intestinal sterol absorption and inhibits the absorption of cholesterol and plant sterols

59
Q

who should you not give ezetimibe to

A

discouraged in moderate and severe hepatic impairment

60
Q

what should you communicate when prescribing ezetimibe

A

some diarrhoea potentially

61
Q

what should you monitor when prescribing ezetimibe

A

ask abt GI effects

usually used w statin so same monitoring as statin ie lipids and 4 weeks and ask abt muscle pain

62
Q

how to PCSK9 inhibitors work

A

inhibit PCSK9 degradation of LDL receptors which increases the number of LDL receptors which increases the hepatic LDL uptake and reduces serum LDL

63
Q

who should you not give a PCSK9 inhibitor to

A

those who cannot tolerate getting a subcutaneous injection every 2 to 4 weeks

64
Q

what should you communicate when prescribing PCSK9 inhibitor

A

injection site reactions

nasopharyngitis

URTI

influenza

65
Q

describe deprescribing of lipid lowering drugs

A

medication can be stopped suddenly

66
Q

how do thrombolytic drugs work

A

break down plasminogen into plasmin, which catalyses breakdown of fibrin in clot

67
Q

who should you not give thrombolytic drugs to

A

those at a bleeding risk

e.g severe uncontrolled HTN, severe hepatic disease, severe thrombocytopenia

68
Q

what should you communicate when prescribing thrombolytic drugs

A

risk of bleeding

69
Q

what should you monitor when prescribing thrombolytic drugs

A

efficacy

bleeding outcomes

Hb

70
Q

how does amiodarone work

A

decreases sinus node and junctional automacity

slows AV and bypass tract conduction

prolongs refractory period of myocardial tissues

71
Q

who should you not give amiodarone to

A

ppl w lung disease

ppl w hepatic disease

ppl w neurological disease

ppl w thyroid dysfunction

72
Q

what should be communicated when prescribing amiodarone

A

acute - nausea, vomitting, taste disturbance

chronic toxicity - pulmonary issues, thyroid dysfunction, hepatic issues, skin photosensitivity, ocular issues, neurotoxicity, bradycardia

73
Q

what should be monitored with amiodarone

A

ECG / holter cardiac monitoring

liver function tests

thyroid function tests

lung function assessment

74
Q

how does digoxin work

A

increases vagal tone which slows HR and reduces AV conduction

75
Q

who should you not give digoxin to

A

ppl w hypothyroidism

hyperkalemia

low Mg

high Ca

heart block

wolff-parkinson white syndrome

76
Q

what should you communicate when prescribing digoxin

A

at higher concentrations - may get anorexia, nausea

77
Q

what should you monitor when prescribing digoxin

A

ECG or rhythm monitoring

ask abt anorexia or nausea

electrolytes

renal function

Medical Studies 1 (16 decks)

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