Drug Class Essentials Flashcards
common ACE
perindopril
ramipril
naming convention for ACE
end in -pril
what does ACE ARB ARNI stand for
-angiotensin converting enzyme inhibitor
-angiotensin II receptor blockers
-Angiotensin Receptor-Neprilysin Inhibitors
mechanism of ACE inhibitors
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.
whom would you not give ACE inhibitors to (absolute contradictions)
-history of intolerance to ACE
-history of hereditary/idiopathic angiodema
-pregnancy
-renal artery stenosis to all renal function
whom would you not give ACE inhibitors to (relative contradictions)
hypotension (<90 systolic)
hyperkalaemia (K>6)
renal impairment
adverse effects of ACE inhibitors
*cough (due to build up of bradykinin)- 5-10%
*angioedema- 1 in 1000
*hyperkalaemia
*dizziness (lower BP)
*renal impairment
monitoring for ACE inhibitor
-within 1-2 weeks of commencing dosing or dose escalation, pt should have K, renal function and BP checked
-ask about cough and angioedema
naming convention for ARB
end in -sartan
Common ARB
candesartan and irbesartan
mechanism of action for ARB
-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
whom should you not give ARB to
-hypotension (<90 systolic)
-hyperkalaemia (K>6)
-renal impairment
-history of intolerance to ARB
-pregnancy
-renal artery stenosis to all renal function
adverse effects of ARB
*hyperkalaemia
*dizziness (lower BP)
*renal impairment
* NOT angioedema or cough
monitoring for ARB
-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
mechanism of ARNI
-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.
ARNI example
sarcubtril/valsartan
whom should you not give ARNI to
-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
important monitoring for ARNI
-emphasise angioedema risk
-instruction on separating ACE and ARNI use (when swapping)
Deprescribing considerations for ACE, ARB, ARNI
-can be stopped immediately (no taper)
-change in pt circumstance may make drugs less appropriate
other name for aspirin
acetylsalicylic acid
mechanism of aspirin
-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)
Whom should you not give asprin to
-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
adverse effects of aspirin
-bleeding
-GI ulcers (uncommon 1%)
-intracerebral hameorrhage
-simple bruising (common)
-GI pain or dyspepsia
-allergy
monitoring for aspirin
-ask about adverse effects
-routine haematological checks
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)
common p2Y12 inhibitors
clopidogrel
prasugrel
ticagrelor
whom would you not give P2Y12 inhibitors
-those with bleeding risk
for ticagrelor
-short half life t/f BD
-risk of bradycardia
adverse effect of P2Y12 inhibitors
bleeding risk
need for compliance
shortness of breath
monitoring for P2Y12 inhibitors
-ask about SOB for ticagrelor
-Hb checks
-urate also increases for ticagrelor
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
whom would you not give dipyridamole to
-those at bleeding risk
-due to vasodilatation : pt that have aortic stenosis, recent MI, angina
adverse effects for dipyridamole
bleeding
vasodilation
headache
nausea
hot flushes
monitoring for dipyridamole
-Hb monitoring
-ask about dilatation effects
Mechanism of action for beta blockers
-act as competitive antagonists
-three beta receptors
b1 receptors
heart: + chrontotropic effect, dromotropy (conduction) and inotropy
kidney: release renin
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
b3 receptors
fat cells: enhance lipolysis
detrusor muscle: relax bladder
function of selective beta blockers
reduce CO, HR and BP
function of non selective beta blockers
-reduce CO, HR and BP
-oppose b2 functions (lungs, tunica media, insulin, kidneys)
naming convention for beta blockers
end in -lol
common beta blockers
atenolol, metoprolol and nebivolol (b1 selective)
propranolol and carvedilol (b2 selective)
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
whom would you not give beta blockers to (partial contradiction)
diabetics
PVD
adverse effects of beta blockers
-dizzines or tiredness initially or dose increased
-cant stop treatment suddenly
monitoring beta blockers
-changes to HR , BP
-ECG if bradycardic
-ask for heart failure symptoms
how to deprescribe beta blockers
-need to wean dose off slowly to prevent recurrence of angina and tachyarrthymia
mechanism of calcium channel blockers
-blocking calcium channels on various muscle cells
-eg on heart–> Bp
-Gut–>GORD/constipation
naming convention for calcium channel blockers
generally end in -dipine
common calcium channel blockers
-verapamil: selective for myocardium
-dilitiazem: intermediate
-dihydropyridine: selective for peripheral vascular tissue
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
adverse effects of calcium channel blockers
DHP:
-flushing, headache, tachycardia (BP drop)
-ankle swelling
non DHP: constipation, bradycardia
monitoring for calcium channel blockers
-BP and HR may vary
-ECG if HR low
how to deprescribe calcium channel blockers
CAN stop suddenly
mechanism of heparin
binds to antithrombin III to enhance anticoagulant effect of antithrombin III
types of heparin
unfractioned heparin
low molecular weight heparin
features of unfractionated heparin
-non linear pharmicokinetics (half life increases w dose)
-has anti platelet effect at high doses
features of low molecular weight heparin
-no platelet effect
-more reliable pharmacokinetics
-more reliable efficacy
common low molecular weigh heparin
enoxaparin
whom would you not give low molecular weight heparin
-those w active bleeding
-thrombocytopenia
-renal failure
adverse effects of low molecular weight heparins
risk of bleeding
thrombocytopenia
long term: osteoporosis
monitoring low molecular weight heparin
-renal function (clearance)
-CBE if risk of bleeding
-platelets in 2nd week of treatment (check for HITS)
whats HITS
heparin induced thrombocytopenia syndrome
whole would you not give unfractionated heparin
-those w active bleeding
-thrombocytopenia
-renal failure
adverse effects of unfractionated heparin
risk of bleeding thrombocytopenia
need for regular blood test
monitoring for unfractionated heparin
-APTT within 6 hours
-CBE if risk of bleeding
-platelets in second week (checking for HITS)
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
naming convention for statins
end in -statin
common statins
atorvastatin
rosuvastatin
whole would you not give stains to
those with
-renal impairment
-hepatic impairment
-hepatic drug interactions
adverse effects of statin
MSK: aches, inflammation, myopathy, breakdown (less than 1%)
monitoring for statin
-lipids at 4 weeks
-ask about muscle pain and weakness
mechanism of fibrates
-activates proliferator-activated nuclear receptors and modulates lipoprotein and catabolism
whom would you not give fibrates to
-renal and hepatic impairment
-presence of gall stones or gall bladder disease
-pancreatitis
adverse effects of fibrates
-Gi adverse effects
-rare: gallstones, pancreatitis, DVT
monitoring for fibrates
monitor lipids and GI symptoms
mechanism of ezetimibe
inhibitor of intestinal sterol absorption and inhibits the absorption of cholesterol and plant sterols
whom would you not give ezetimibe to
hepatic impairment and if they use fenofibrate
adverse effects of ezetimibe
limited adverse effects except diarrhoea
monitoring for ezetimibe
usually used with statins, ask about GI effects and check lipids
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
whom would you give PCSK9 inhibitor to
someone willing to take SC injection every 2 or 4 weeks
adverse effects of PCSK9
-injection site reaction
-headache,nausea
-gastroenteritis etc
how to deprescribe lipid lowering drugs
can be stopped suddenly
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
whom would you not give nitrates to
-pt with phosphodiesterase inhibitor
-hypertrophic cardiomyopathy
-aortic or mitral stenosis
adverse effects of GTN
-at administration, rapid fall in Bp hence must sit
-flushing
-headache
-can get postural hypotension (for long acting nitrate)
monitoring GTN
-need at least 8 hours nitrate free period, or can develop tolerance
-need to ask about storage, use, postural hypotension, symptoms
how to deprescribe nitrate
need to wean gently to avoid rebound effects
GTN stands for
Glyceryl trinitrate
mechanism of thrombolytics
catalyse the conversion of plasminogen into plasmin, this catalyses the breakdown of fibrin in clot
common thrombolytics
alteplase (slower)
tenecteplase (only for ST elevation)
whom would you not give thrombolytics to
-depends on risk of bleeding
-severe HTN
-hepatic disease
-thrombocytopenia
adverse effects of thrombolytics
risk of bleeding vs positive outcomes
monitoring thrombolytics
efficacy
bleeding outcomes
Hb
naming convention for ARB
-sartan
naming convention for Ca channel blockers
-dipine
what are the two main types of valvular dysfunction pathology
regurgitation and stenosis
SABA
Mechanism:
-Activates beta-2 adrenergic receptors in bronchial smooth muscle.
-Causes bronchodilation and rapid relief of bronchospasm.
Example:
Albuterol (Salbutamol)
LABA
Mechanism:
-Activates beta-2 adrenergic receptors over a longer duration.
-Provides sustained bronchodilation and helps control asthma/COPD symptoms.
Example:
Salmeterol
SAMA
Mechanism:
-Blocks muscarinic receptors (M3) in the airways.
-Reduces bronchoconstriction and mucus secretion.
Example:
Ipratropium bromide
LAMA
Mechanism:
-Blocks muscarinic receptors over an extended period.
-Provides prolonged bronchodilation and reduces airway hyperreactivity.
Example:
Tiotropium
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
what are the 4 pillars for HF treatment
SGLT-2, MRA’s, BB, Anti hypertensives
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.
metformin mechanism
Metformin decreases liver glucose production, improves muscle glucose uptake, and reduces intestinal glucose absorption, effectively lowering blood glucose in diabetes.
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.
Mechanism of corticosteroids
-binds to cytoplasmic receptors and translocates to nucleus, where it alters gene transcription causing large range of effects
-onset takes hours
suffix of corticosteroids
-sone
short side effects of corticosteroids
-increased BGL
-fluid retention
-hypokalaemia
-increased BP
-poor sleep, nervousness, altered mood
-poor memory
-increased peptic ulcers
do you need to taper corticosteroids
-if used for <4 weeks systematically then can stop suddenly, otherwise need a taper
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
long term adverse effects of corticosteroids
-proximal myopathy
-thin skin
-osteoporosis
-growth retardation
-poor wound healing
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
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
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
side effects of SABAs
-allergy
-tremor
-tachycardia
-nervousness
-tachyphylaxis
side effects of LABAs
-tremor, tachycardia, nervousness
contraindications for LABA
-excess beta agonism eg CV, hyperthyroidism
-device suitability
side effects of SAMA
-dry mouth
-systemic anticholinergic effects
-allergy
side effects of LAMA
-systemic anticholinergic effects
-dry mouth
side effects of ICS
-dysphonia
-candida (fever and chills)
