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Medical Studies 1 > Drug Class Essentials > Flashcards

Drug Class Essentials Flashcards

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USMLE® Step 1 flashcards
1
Q

common ACE

A

perindopril
ramipril

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2
Q

naming convention for ACE

A

end in -pril

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3
Q

what does ACE ARB ARNI stand for

A

-angiotensin converting enzyme inhibitor
-angiotensin II receptor blockers
-Angiotensin Receptor-Neprilysin Inhibitors

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4
Q

mechanism of ACE inhibitors

A

Inhibit the enzyme ACE, which converts angiotensin I to angiotensin II.
Angiotensin II is a potent vasoconstrictor that increases blood pressure and stimulates aldosterone secretion.
Reducing angiotensin II levels leads to vasodilation and decreased blood pressure, as well as reduced aldosterone secretion, which lowers sodium and water retention.

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5
Q

whom would you not give ACE inhibitors to (absolute contradictions)

A

-history of intolerance to ACE
-history of hereditary/idiopathic angiodema
-pregnancy
-renal artery stenosis to all renal function

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6
Q

whom would you not give ACE inhibitors to (relative contradictions)

A

hypotension (<90 systolic)
hyperkalaemia (K>6)
renal impairment

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7
Q

adverse effects of ACE inhibitors

A

*cough (due to build up of bradykinin)- 5-10%
*angioedema- 1 in 1000
*hyperkalaemia
*dizziness (lower BP)
*renal impairment

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8
Q

monitoring for ACE inhibitor

A

-within 1-2 weeks of commencing dosing or dose escalation, pt should have K, renal function and BP checked
-ask about cough and angioedema

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9
Q

naming convention for ARB

A

end in -sartan

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10
Q

Common ARB

A

candesartan and irbesartan

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11
Q

mechanism of action for ARB

A

-Block the angiotensin II receptors
-Prevents angiotensin II from exerting its vasoconstrictive and aldosterone-secreting effects.
-Similar end effect to ACE inhibitors, with vasodilation and reduced blood pressure
-does not lead to bradykinin accumulation

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12
Q

whom should you not give ARB to

A

-hypotension (<90 systolic)
-hyperkalaemia (K>6)
-renal impairment
-history of intolerance to ARB
-pregnancy
-renal artery stenosis to all renal function

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13
Q

adverse effects of ARB

A

*hyperkalaemia
*dizziness (lower BP)
*renal impairment
* NOT angioedema or cough

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14
Q

monitoring for ARB

A

-within 1-2 weeks of commencing dosing or dose escalation, pt should have K, renal function and BP checked
-don’t ask about cough and angioedema

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15
Q

mechanism of ARNI

A

-Combination of an ARB and a neprilysin inhibitor.
-Neprilysin is an enzyme that breaks down neutral endopeptidases
-neutral endopeptidases promote vasodilation and natriuresis (excretion of sodium in urine).
By inhibiting neprilysin, these beneficial peptides remain active longer.
The ARB component blocks the effects of angiotensin II.

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16
Q

ARNI example

A

sarcubtril/valsartan

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17
Q

whom should you not give ARNI to

A

-hypotension (<90 systolic)
-hyperkalaemia (K>6)
-renal impairment
-history of intolerance to ARB
-pregnancy
-renal artery stenosis to all renal function
-history of hereditary/idiopathic/ ACE induced angiodema
-pt using ACE inhibitor

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18
Q

important monitoring for ARNI

A

-emphasise angioedema risk
-instruction on separating ACE and ARNI use (when swapping)

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19
Q

Deprescribing considerations for ACE, ARB, ARNI

A

-can be stopped immediately (no taper)
-change in pt circumstance may make drugs less appropriate

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20
Q

other name for aspirin

A

acetylsalicylic acid

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21
Q

mechanism of aspirin

A

-inhibits Cox-1 enzyme predominantly (also Cox-2)
-this decreases prostglandins for inflammation
-inhibition is irreversible
-leads to reduced thromboxane A production (leads to platelet inhibition)

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22
Q

Whom should you not give asprin to

A

-pt with serious risk of bleeding
-aspirin or NSAID allergy
-aspirin sensitive asthma
-aspirin or NSAID induced peptic ulcer disease, erosive gastritis
-pt with severe renal disease, hepatic disease

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23
Q

adverse effects of aspirin

A

-bleeding
-GI ulcers (uncommon 1%)
-intracerebral hameorrhage
-simple bruising (common)
-GI pain or dyspepsia
-allergy

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24
Q

monitoring for aspirin

A

-ask about adverse effects
-routine haematological checks

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25
Q

mechanism of action for P2Y12 inhibitors

A

-binds to P2Y12 receptor and inhibits adenosine diphosphate (ADP)-receptor
-decreasing platelet aggregation
-clopidogrel has irreversible effect (needs bio activation)
-ticagrelor is reversible
-adherence is important (short half life)

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26
Q

common p2Y12 inhibitors

A

clopidogrel
prasugrel
ticagrelor

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27
Q

whom would you not give P2Y12 inhibitors

A

-those with bleeding risk

for ticagrelor
-short half life t/f BD
-risk of bradycardia

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28
Q

adverse effect of P2Y12 inhibitors

A

bleeding risk
need for compliance
shortness of breath

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29
Q

monitoring for P2Y12 inhibitors

A

-ask about SOB for ticagrelor
-Hb checks
-urate also increases for ticagrelor

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30
Q

mechanism for dipyridamole

A

-inhibit platelet functions by inhibiting phosphodiesterase, which increase platelet cAMP
-also inhibits endogenous adenosine re uptake hence results in vasodilatation
-given with aspirin

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31
Q

whom would you not give dipyridamole to

A

-those at bleeding risk
-due to vasodilatation : pt that have aortic stenosis, recent MI, angina

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32
Q

adverse effects for dipyridamole

A

bleeding
vasodilation
headache
nausea
hot flushes

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33
Q

monitoring for dipyridamole

A

-Hb monitoring
-ask about dilatation effects

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34
Q

Mechanism of action for beta blockers

A

-act as competitive antagonists
-three beta receptors

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35
Q

b1 receptors

A

heart: + chrontotropic effect, dromotropy (conduction) and inotropy
kidney: release renin

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36
Q

b2 receptors

A

lungs: relaxation of bronchi and bronchioles
skeletal muscle: relaxation of smooth muscle in media
metabolic:increase insulin secretion, glycogenolysis, gluconeogensis
kidney: increase renin

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37
Q

b3 receptors

A

fat cells: enhance lipolysis
detrusor muscle: relax bladder

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38
Q

function of selective beta blockers

A

reduce CO, HR and BP

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39
Q

function of non selective beta blockers

A

-reduce CO, HR and BP
-oppose b2 functions (lungs, tunica media, insulin, kidneys)

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40
Q

naming convention for beta blockers

A

end in -lol

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41
Q

common beta blockers

A

atenolol, metoprolol and nebivolol (b1 selective)
propranolol and carvedilol (b2 selective)

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42
Q

whom would you not give a beta blocker to (absolute contradiction)

A

-patients with hypotension, bradycardia, second or third degree atrioventricular block, uncontrolled heart failure
-airway diseases eg asthma

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43
Q

whom would you not give beta blockers to (partial contradiction)

A

diabetics
PVD

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44
Q

adverse effects of beta blockers

A

-dizzines or tiredness initially or dose increased
-cant stop treatment suddenly

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45
Q

monitoring beta blockers

A

-changes to HR , BP
-ECG if bradycardic
-ask for heart failure symptoms

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46
Q

how to deprescribe beta blockers

A

-need to wean dose off slowly to prevent recurrence of angina and tachyarrthymia

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47
Q

mechanism of calcium channel blockers

A

-blocking calcium channels on various muscle cells
-eg on heart–> Bp
-Gut–>GORD/constipation

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48
Q

naming convention for calcium channel blockers

A

generally end in -dipine

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49
Q

common calcium channel blockers

A

-verapamil: selective for myocardium
-dilitiazem: intermediate
-dihydropyridine: selective for peripheral vascular tissue

50
Q

whom would you not give calcium channel blockers to

A

DHP: pt intolerant to previous DHP (dihydropyridine)
non DHP: pt with low HR, BP, cardiac conduction defect, systolic heart failure

51
Q

adverse effects of calcium channel blockers

A

DHP:
-flushing, headache, tachycardia (BP drop)
-ankle swelling
non DHP: constipation, bradycardia

52
Q

monitoring for calcium channel blockers

A

-BP and HR may vary
-ECG if HR low

53
Q

how to deprescribe calcium channel blockers

A

CAN stop suddenly

54
Q

mechanism of heparin

A

binds to antithrombin III to enhance anticoagulant effect of antithrombin III

55
Q

types of heparin

A

unfractioned heparin
low molecular weight heparin

56
Q

features of unfractionated heparin

A

-non linear pharmicokinetics (half life increases w dose)
-has anti platelet effect at high doses

57
Q

features of low molecular weight heparin

A

-no platelet effect
-more reliable pharmacokinetics
-more reliable efficacy

58
Q

common low molecular weigh heparin

A

enoxaparin

59
Q

whom would you not give low molecular weight heparin

A

-those w active bleeding
-thrombocytopenia
-renal failure

60
Q

adverse effects of low molecular weight heparins

A

risk of bleeding
thrombocytopenia
long term: osteoporosis

61
Q

monitoring low molecular weight heparin

A

-renal function (clearance)
-CBE if risk of bleeding
-platelets in 2nd week of treatment (check for HITS)

62
Q

whats HITS

A

heparin induced thrombocytopenia syndrome

63
Q

whole would you not give unfractionated heparin

A

-those w active bleeding
-thrombocytopenia
-renal failure

64
Q

adverse effects of unfractionated heparin

A

risk of bleeding thrombocytopenia
need for regular blood test

65
Q

monitoring for unfractionated heparin

A

-APTT within 6 hours
-CBE if risk of bleeding
-platelets in second week (checking for HITS)

66
Q

mechanism of statins

A

-inhibits HMG Co-A reductase enzyme
-can reduced LDL cholesterol by -50%
-also has modest effect at reducing triglycerides and increasing HDL

67
Q

naming convention for statins

A

end in -statin

68
Q

common statins

A

atorvastatin
rosuvastatin

69
Q

whole would you not give stains to

A

those with
-renal impairment
-hepatic impairment
-hepatic drug interactions

70
Q

adverse effects of statin

A

MSK: aches, inflammation, myopathy, breakdown (less than 1%)

71
Q

monitoring for statin

A

-lipids at 4 weeks
-ask about muscle pain and weakness

72
Q

mechanism of fibrates

A

-activates proliferator-activated nuclear receptors and modulates lipoprotein and catabolism

73
Q

whom would you not give fibrates to

A

-renal and hepatic impairment
-presence of gall stones or gall bladder disease
-pancreatitis

74
Q

adverse effects of fibrates

A

-Gi adverse effects
-rare: gallstones, pancreatitis, DVT

75
Q

monitoring for fibrates

A

monitor lipids and GI symptoms

76
Q

mechanism of ezetimibe

A

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

77
Q

whom would you not give ezetimibe to

A

hepatic impairment and if they use fenofibrate

78
Q

adverse effects of ezetimibe

A

limited adverse effects except diarrhoea

79
Q

monitoring for ezetimibe

A

usually used with statins, ask about GI effects and check lipids

80
Q

PCSK9 inhibitors mechanism of action

A

-inhibit PCSK9
-human MAB that binds to PCSK9
-inhibits PCSK9 degradation of LDL receptors, increasing LDL receptors, increasing hepatic LDL uptake, decreasing serum LDL

81
Q

whom would you give PCSK9 inhibitor to

A

someone willing to take SC injection every 2 or 4 weeks

82
Q

adverse effects of PCSK9

A

-injection site reaction
-headache,nausea
-gastroenteritis etc

83
Q

how to deprescribe lipid lowering drugs

A

can be stopped suddenly

84
Q

mechanism of nitrates

A

-they are a source of NO
-results in relaxation of smooth muscle in tissues
-has effect of dilating veins
-decreased venous return, decreased preload, decreased work
-increases arteriolar dilation, decreasing preload, decreasing work

85
Q

whom would you not give nitrates to

A

-pt with phosphodiesterase inhibitor
-hypertrophic cardiomyopathy
-aortic or mitral stenosis

86
Q

adverse effects of GTN

A

-at administration, rapid fall in Bp hence must sit
-flushing
-headache

-can get postural hypotension (for long acting nitrate)

87
Q

monitoring GTN

A

-need at least 8 hours nitrate free period, or can develop tolerance
-need to ask about storage, use, postural hypotension, symptoms

88
Q

how to deprescribe nitrate

A

need to wean gently to avoid rebound effects

89
Q

GTN stands for

A

Glyceryl trinitrate

90
Q

mechanism of thrombolytics

A

catalyse the conversion of plasminogen into plasmin, this catalyses the breakdown of fibrin in clot

91
Q

common thrombolytics

A

alteplase (slower)
tenecteplase (only for ST elevation)

92
Q

whom would you not give thrombolytics to

A

-depends on risk of bleeding
-severe HTN
-hepatic disease
-thrombocytopenia

93
Q

adverse effects of thrombolytics

A

risk of bleeding vs positive outcomes

94
Q

monitoring thrombolytics

A

efficacy
bleeding outcomes
Hb

95
Q

naming convention for ARB

A

-sartan

96
Q

naming convention for Ca channel blockers

A

-dipine

97
Q

what are the two main types of valvular dysfunction pathology

A

regurgitation and stenosis

98
Q

SABA

A

Mechanism:
-Activates beta-2 adrenergic receptors in bronchial smooth muscle.
-Causes bronchodilation and rapid relief of bronchospasm.
Example:
Albuterol (Salbutamol)

99
Q

LABA

A

Mechanism:
-Activates beta-2 adrenergic receptors over a longer duration.
-Provides sustained bronchodilation and helps control asthma/COPD symptoms.
Example:
Salmeterol

100
Q

SAMA

A

Mechanism:
-Blocks muscarinic receptors (M3) in the airways.
-Reduces bronchoconstriction and mucus secretion.
Example:
Ipratropium bromide

101
Q

LAMA

A

Mechanism:
-Blocks muscarinic receptors over an extended period.
-Provides prolonged bronchodilation and reduces airway hyperreactivity.
Example:
Tiotropium

102
Q

anticoagulants vs antiplatelets vs thrombolytics (use)

A

Anticoagulants: Prevent clot formation (venous) -DVT,PE
Antiplatelets: Prevent platelet aggregation (arterial)- prevent MI
Thrombolytics: Dissolve existing clots (acute intervention)- Acute MI treatments

103
Q

what are the 4 pillars for HF treatment

A

SGLT-2, MRA’s, BB, Anti hypertensives

104
Q

SGLT-2 Mechanism

A

SGLT-2 inhibitors block glucose reabsorption in the kidneys’ proximal tubules, increasing urinary glucose excretion, which lowers blood glucose and BP + aids diabetes control.

105
Q

metformin mechanism

A

Metformin decreases liver glucose production, improves muscle glucose uptake, and reduces intestinal glucose absorption, effectively lowering blood glucose in diabetes.

106
Q

MRA mechanism

A

Mineralocorticoid receptor antagonists (MRAs) block aldosterone receptors in the kidneys, reducing sodium and water reabsorption while promoting potassium retention, lowering blood pressure and fluid overload.

107
Q

Mechanism of corticosteroids

A

-binds to cytoplasmic receptors and translocates to nucleus, where it alters gene transcription causing large range of effects
-onset takes hours

108
Q

suffix of corticosteroids

A

-sone

109
Q

short side effects of corticosteroids

A

-increased BGL
-fluid retention
-hypokalaemia
-increased BP
-poor sleep, nervousness, altered mood
-poor memory
-increased peptic ulcers

110
Q

do you need to taper corticosteroids

A

-if used for <4 weeks systematically then can stop suddenly, otherwise need a taper

111
Q

how to initially prescribe corticosteroids

A

-give short Rx and monitor for effects and adverse effects
-once re evaluated, and reviewed diagnosis and treatment options consider long term Rx
-try to use lowest dose effective

112
Q

long term adverse effects of corticosteroids

A

-proximal myopathy
-thin skin
-osteoporosis
-growth retardation
-poor wound healing

113
Q

how does a meter dose inhaler work

A

-actuation expels fine droplets
-patient has to coordinate breath and activation
-<10 of drug inhaled
-improved with spacer

114
Q

how does dry powder inhaler work

A

-patient needs to break down powder (can pose issue in pt w dexterity issues )
-does not require coordination with breathing
-brisk inspiration needed

115
Q

how does nebuliser work

A

-liquid dispersed into aerosol by rapid steam of air or oxygen
-requires no coordination but gives rise to systemic exposure (adverse)
-used in those with very poor coordination

116
Q

side effects of SABAs

A

-allergy
-tremor
-tachycardia
-nervousness
-tachyphylaxis

117
Q

side effects of LABAs

A

-tremor, tachycardia, nervousness

118
Q

contraindications for LABA

A

-excess beta agonism eg CV, hyperthyroidism
-device suitability

119
Q

side effects of SAMA

A

-dry mouth
-systemic anticholinergic effects
-allergy

120
Q

side effects of LAMA

A

-systemic anticholinergic effects
-dry mouth

121
Q

side effects of ICS

A

-dysphonia
-candida (fever and chills)

Medical Studies 1 (15 decks)

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