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Medical Studies 1 > Drug Class Essentials > Flashcards

Drug Class Essentials Flashcards

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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
mechanism of action for P2Y12 inhibitors
-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)
26
common p2Y12 inhibitors
clopidogrel prasugrel ticagrelor
27
whom would you not give P2Y12 inhibitors
-those with bleeding risk for ticagrelor -short half life t/f BD -risk of bradycardia
28
adverse effect of P2Y12 inhibitors
bleeding risk need for compliance shortness of breath
29
monitoring for P2Y12 inhibitors
-ask about SOB for ticagrelor -Hb checks -urate also increases for ticagrelor
30
mechanism for dipyridamole
-inhibit platelet functions by inhibiting phosphodiesterase, which increase platelet cAMP -also inhibits endogenous adenosine re uptake hence results in vasodilatation -given with aspirin
31
whom would you not give dipyridamole to
-those at bleeding risk -due to vasodilatation : pt that have aortic stenosis, recent MI, angina
32
adverse effects for dipyridamole
bleeding vasodilation headache nausea hot flushes
33
monitoring for dipyridamole
-Hb monitoring -ask about dilatation effects
34
Mechanism of action for beta blockers
-act as competitive antagonists -three beta receptors
35
b1 receptors
heart: + chrontotropic effect, dromotropy (conduction) and inotropy kidney: release renin
36
b2 receptors
lungs: relaxation of bronchi and bronchioles skeletal muscle: relaxation of smooth muscle in media metabolic:increase insulin secretion, glycogenolysis, gluconeogensis kidney: increase renin
37
b3 receptors
fat cells: enhance lipolysis detrusor muscle: relax bladder
38
function of selective beta blockers
reduce CO, HR and BP
39
function of non selective beta blockers
-reduce CO, HR and BP -oppose b2 functions (lungs, tunica media, insulin, kidneys)
40
naming convention for beta blockers
end in -lol
41
common beta blockers
atenolol, metoprolol and nebivolol (b1 selective) propranolol and carvedilol (b2 selective)
42
whom would you not give a beta blocker to (absolute contradiction)
-patients with hypotension, bradycardia, second or third degree atrioventricular block, uncontrolled heart failure -airway diseases eg asthma
43
whom would you not give beta blockers to (partial contradiction)
diabetics PVD
44
adverse effects of beta blockers
-dizzines or tiredness initially or dose increased -cant stop treatment suddenly
45
monitoring beta blockers
-changes to HR , BP -ECG if bradycardic -ask for heart failure symptoms
46
how to deprescribe beta blockers
-need to wean dose off slowly to prevent recurrence of angina and tachyarrthymia
47
mechanism of calcium channel blockers
-blocking calcium channels on various muscle cells -eg on heart--> Bp -Gut-->GORD/constipation
48
naming convention for calcium channel blockers
generally end in -dipine
49
common calcium channel blockers
-verapamil: selective for myocardium -dilitiazem: intermediate -dihydropyridine: selective for peripheral vascular tissue
50
whom would you not give calcium channel blockers to
DHP: pt intolerant to previous DHP (dihydropyridine) non DHP: pt with low HR, BP, cardiac conduction defect, systolic heart failure
51
adverse effects of calcium channel blockers
DHP: -flushing, headache, tachycardia (BP drop) -ankle swelling non DHP: constipation, bradycardia
52
monitoring for calcium channel blockers
-BP and HR may vary -ECG if HR low
53
how to deprescribe calcium channel blockers
CAN stop suddenly
54
mechanism of heparin
binds to antithrombin III to enhance anticoagulant effect of antithrombin III
55
types of heparin
unfractioned heparin low molecular weight heparin
56
features of unfractionated heparin
-non linear pharmicokinetics (half life increases w dose) -has anti platelet effect at high doses
57
features of low molecular weight heparin
-no platelet effect -more reliable pharmacokinetics -more reliable efficacy
58
common low molecular weigh heparin
enoxaparin
59
whom would you not give low molecular weight heparin
-those w active bleeding -thrombocytopenia -renal failure
60
adverse effects of low molecular weight heparins
risk of bleeding thrombocytopenia long term: osteoporosis
61
monitoring low molecular weight heparin
-renal function (clearance) -CBE if risk of bleeding -platelets in 2nd week of treatment (check for HITS)
62
whats HITS
heparin induced thrombocytopenia syndrome
63
whole would you not give unfractionated heparin
-those w active bleeding -thrombocytopenia -renal failure
64
adverse effects of unfractionated heparin
risk of bleeding thrombocytopenia need for regular blood test
65
monitoring for unfractionated heparin
-APTT within 6 hours -CBE if risk of bleeding -platelets in second week (checking for HITS)
66
mechanism of statins
-inhibits HMG Co-A reductase enzyme -can reduced LDL cholesterol by -50% -also has modest effect at reducing triglycerides and increasing HDL
67
naming convention for statins
end in -statin
68
common statins
atorvastatin rosuvastatin
69
whole would you not give stains to
those with -renal impairment -hepatic impairment -hepatic drug interactions
70
adverse effects of statin
MSK: aches, inflammation, myopathy, breakdown (less than 1%)
71
monitoring for statin
-lipids at 4 weeks -ask about muscle pain and weakness
72
mechanism of fibrates
-activates proliferator-activated nuclear receptors and modulates lipoprotein and catabolism
73
whom would you not give fibrates to
-renal and hepatic impairment -presence of gall stones or gall bladder disease -pancreatitis
74
adverse effects of fibrates
-Gi adverse effects -rare: gallstones, pancreatitis, DVT
75
monitoring for fibrates
monitor lipids and GI symptoms
76
mechanism of ezetimibe
inhibitor of intestinal sterol absorption and inhibits the absorption of cholesterol and plant sterols
77
whom would you not give ezetimibe to
hepatic impairment and if they use fenofibrate
78
adverse effects of ezetimibe
limited adverse effects except diarrhoea
79
monitoring for ezetimibe
usually used with statins, ask about GI effects and check lipids
80
PCSK9 inhibitors mechanism of action
-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
whom would you give PCSK9 inhibitor to
someone willing to take SC injection every 2 or 4 weeks
82
adverse effects of PCSK9
-injection site reaction -headache,nausea -gastroenteritis etc
83
how to deprescribe lipid lowering drugs
can be stopped suddenly
84
mechanism of nitrates
-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
whom would you not give nitrates to
-pt with phosphodiesterase inhibitor -hypertrophic cardiomyopathy -aortic or mitral stenosis
86
adverse effects of GTN
-at administration, rapid fall in Bp hence must sit -flushing -headache -can get postural hypotension (for long acting nitrate)
87
monitoring GTN
-need at least 8 hours nitrate free period, or can develop tolerance -need to ask about storage, use, postural hypotension, symptoms
88
how to deprescribe nitrate
need to wean gently to avoid rebound effects
89
GTN stands for
Glyceryl trinitrate
90
mechanism of thrombolytics
catalyse the conversion of plasminogen into plasmin, this catalyses the breakdown of fibrin in clot
91
common thrombolytics
alteplase (slower) tenecteplase (only for ST elevation)
92
whom would you not give thrombolytics to
-depends on risk of bleeding -severe HTN -hepatic disease -thrombocytopenia
93
adverse effects of thrombolytics
risk of bleeding vs positive outcomes
94
monitoring thrombolytics
efficacy bleeding outcomes Hb
95
naming convention for ARB
-sartan
96
naming convention for Ca channel blockers
-dipine
97
what are the two main types of valvular dysfunction pathology
regurgitation and stenosis
98
SABA
Mechanism: -Activates beta-2 adrenergic receptors in bronchial smooth muscle. -Causes bronchodilation and rapid relief of bronchospasm. Example: Albuterol (Salbutamol)
99
LABA
Mechanism: -Activates beta-2 adrenergic receptors over a longer duration. -Provides sustained bronchodilation and helps control asthma/COPD symptoms. Example: Salmeterol
100
SAMA
Mechanism: -Blocks muscarinic receptors (M3) in the airways. -Reduces bronchoconstriction and mucus secretion. Example: Ipratropium bromide
101
LAMA
Mechanism: -Blocks muscarinic receptors over an extended period. -Provides prolonged bronchodilation and reduces airway hyperreactivity. Example: Tiotropium
102
anticoagulants vs antiplatelets vs thrombolytics (use)
Anticoagulants: Prevent clot formation (venous) -DVT,PE Antiplatelets: Prevent platelet aggregation (arterial)- prevent MI Thrombolytics: Dissolve existing clots (acute intervention)- Acute MI treatments
103
what are the 4 pillars for HF treatment
SGLT-2, MRA's, BB, Anti hypertensives
104
SGLT-2 Mechanism
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
metformin mechanism
Metformin decreases liver glucose production, improves muscle glucose uptake, and reduces intestinal glucose absorption, effectively lowering blood glucose in diabetes.
106
MRA mechanism
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
Mechanism of corticosteroids
-binds to cytoplasmic receptors and translocates to nucleus, where it alters gene transcription causing large range of effects -onset takes hours
108
suffix of corticosteroids
-sone
109
short side effects of corticosteroids
-increased BGL -fluid retention -hypokalaemia -increased BP -poor sleep, nervousness, altered mood -poor memory -increased peptic ulcers
110
do you need to taper corticosteroids
-if used for <4 weeks systematically then can stop suddenly, otherwise need a taper
111
how to initially prescribe corticosteroids
-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
long term adverse effects of corticosteroids
-proximal myopathy -thin skin -osteoporosis -growth retardation -poor wound healing
113
how does a meter dose inhaler work
-actuation expels fine droplets -patient has to coordinate breath and activation -<10 of drug inhaled -improved with spacer
114
how does dry powder inhaler work
-patient needs to break down powder (can pose issue in pt w dexterity issues ) -does not require coordination with breathing -brisk inspiration needed
115
how does nebuliser work
-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
side effects of SABAs
-allergy -tremor -tachycardia -nervousness -tachyphylaxis
117
side effects of LABAs
-tremor, tachycardia, nervousness
118
contraindications for LABA
-excess beta agonism eg CV, hyperthyroidism -device suitability
119
side effects of SAMA
-dry mouth -systemic anticholinergic effects -allergy
120
side effects of LAMA
-systemic anticholinergic effects -dry mouth
121
side effects of ICS
-dysphonia -candida (fever and chills)

Medical Studies 1 (15 decks)

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