Pharmacology 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
what should you communicate when prescribing long acting nitrates
initially get headache, flushing postural hTN need at least 8 hr nitrate free period
26
what are 3 types of antiplatelets
aspirin P2Y12 inhibitors dipyridamole
27
how does aspirin work
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)
28
who should you not give aspirins to
patients where there is active bleeding or serious risk of bleeding aspirin allergy aspirin sensitive asthma aspirin induced peptic ulcer disease
29
what should you communicate when prescribing aspirin
main risk is bleeding additional risk of causing GI ulcers small risk of intracerebral haemorrhage simple bruising in skin
30
what should you monitor when prescribing aspirin
ask about adverse effects hematology performed routinely in this population
31
how do P2Y12 inhibitors work
binds to P2Y12 receptor and inhibits ADP mediated platelet aggregation
32
who should you not give P2Y12 inhibitors to
bleeding risk - age, weight, drug interactions etc.
33
what should you communicate when prescribing P2Y12 inhibitors
need for compliance shortness of breath
34
what should you monitor when prescribing P2Y12 inhibitors
check Hb ask abt shortness of breath for ticagrelor urate also increases for ticagrelor
35
how does dipyridamole work
inhibits platelet function by inhibiting phosphodiesterase which increases platelet cAMP also inhibits endogenous adenosine reuptake hence results in vasodilation
36
who should you not give dipyridamole to
there is a bleeding risk so should not give to ppl w aortic stenosis, recent MI or angina
37
what should you communicate when prescribing dipyridamole
headache nausea hot flushes
38
what should you monitor when prescribing dipyridamole
Hb ask about dilatation effects
39
how does heparin work
binds to antithrombin lll to enhance anticoagulant effect of antithrombin lll
40
what is unfractionated heparin
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
what is low molecular weight heparin (LMWH)
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
who should you not give LMWH to
patients w active bleeding patients w thrombocytopenia or other bleeding disorder patients w renal failure previous heparin induced thrombocytopenia
43
what should you communicate when prescribing LMWH
risk of bleeding thrombocytopenia long term: osteoporosis
44
what should you monitor when prescribing LMWH
renal function platelets in second week of treatment (looking for HITS) CBE if risk of bleeding
45
what is HITS
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
who should you not give unfractionated heparin to
active bleeding thrombocytopenia or other bleeding disorders previous heparin induced thrombocytopenia
47
what should you communicate when prescribing unfractionated heparin
risk of bleeding thrombocytopenia need for regular blood tests
48
what should you monitor when prescribing unfractionated heparin
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
if LMWH is more effective and has a lower risk of bleeding, then why would you use unfractionated heparin in some cases
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
how do statins work
inhibit HMG Co-A reductase enzyme which limits the rate of cholesterol synthesis
51
who should you not give statins to
those w previous intolerance contraindicated renal impairment hepatic impairment hepatic drug interactions
52
what should you communicate when prescribing statins
may experience musculoskeletal problems such as muscle aches, myositis, myopathy
53
what should you monitor when prescribing statins
lipids at 4 weeks CK/ALT+AST at baseline and if clinically indicated ask about muscle pain/weakness
54
how do fibrates work
activate peroxisome proliferator-activated nuclear receptors and modulate lipoprotein synthesis and catabolism
55
who should you not give fibrates to
renal/hepatic impairment presence of gallstones or gallbladder disease pancreatitis
56
what should you communicate when prescribing fibrates
GI adverse effects very rare: gallstones pancreatitis DVT
57
what should you monitor when prescribing fibrates
GI symptoms lipids
58
how does ezetimibe work
inhibitor of intestinal sterol absorption and inhibits the absorption of cholesterol and plant sterols
59
who should you not give ezetimibe to
discouraged in moderate and severe hepatic impairment
60
what should you communicate when prescribing ezetimibe
some diarrhoea potentially
61
what should you monitor when prescribing ezetimibe
ask abt GI effects usually used w statin so same monitoring as statin ie lipids and 4 weeks and ask abt muscle pain
62
how to PCSK9 inhibitors work
inhibit PCSK9 degradation of LDL receptors which increases the number of LDL receptors which increases the hepatic LDL uptake and reduces serum LDL
63
who should you not give a PCSK9 inhibitor to
those who cannot tolerate getting a subcutaneous injection every 2 to 4 weeks
64
what should you communicate when prescribing PCSK9 inhibitor
injection site reactions nasopharyngitis URTI influenza
65
describe deprescribing of lipid lowering drugs
medication can be stopped suddenly
66
how do thrombolytic drugs work
break down plasminogen into plasmin, which catalyses breakdown of fibrin in clot
67
who should you not give thrombolytic drugs to
those at a bleeding risk e.g severe uncontrolled HTN, severe hepatic disease, severe thrombocytopenia
68
what should you communicate when prescribing thrombolytic drugs
risk of bleeding
69
what should you monitor when prescribing thrombolytic drugs
efficacy bleeding outcomes Hb
70
how does amiodarone work
decreases sinus node and junctional automacity slows AV and bypass tract conduction prolongs refractory period of myocardial tissues
71
who should you not give amiodarone to
ppl w lung disease ppl w hepatic disease ppl w neurological disease ppl w thyroid dysfunction
72
what should be communicated when prescribing amiodarone
acute - nausea, vomitting, taste disturbance chronic toxicity - pulmonary issues, thyroid dysfunction, hepatic issues, skin photosensitivity, ocular issues, neurotoxicity, bradycardia
73
what should be monitored with amiodarone
ECG / holter cardiac monitoring liver function tests thyroid function tests lung function assessment
74
how does digoxin work
increases vagal tone which slows HR and reduces AV conduction
75
who should you not give digoxin to
ppl w hypothyroidism hyperkalemia low Mg high Ca heart block wolff-parkinson white syndrome
76
what should you communicate when prescribing digoxin
at higher concentrations - may get anorexia, nausea
77
what should you monitor when prescribing digoxin
ECG or rhythm monitoring ask abt anorexia or nausea electrolytes renal function