CVS

Question 1

First line antihypertensive drugs: What does ABCD stand for

Answer 1

ACE inhibitor, Beta Blocker, Calcium Channel Blocker, Diuretics

Question 2

ACE inhibitors: class, suffix, MOA, ADR, contraindications

Answer 2

Antihypertensive
"-pril"s 
Short-acting: Enalapril, Captopril
Long-acting: Benazepril
Decrease Na, H2o retention by decreasing aldosterone
Block bradykinin breakdown (by AGII), bradykinins cause the release of NO for vasodilation
ADR: Angioedema and dry cough
Contraindicated in pregnancy

Question 3

Ag II T1 blockers: class, suffix, MOA, ADR, contraindications

Answer 3

Antihypertensive
“-sartan”s
Direct blockage of AT1 receptors
Contraindicated in pregnancy

Question 4

B-Blockers: class, suffix, MOA, ADR, contraindications

Answer 4

Antihypertensive, ischemic HD, anti-arrythmia
Cardioselective B1 blockers (MANBABE)
HTN, Ischemia: Block cAMP, decrease Myocin-LC activation, decrease Ca2+ influx to decrease contractility
Arrythmia: Negative inotropic effect (prolongs AV conduction)
Bradycardia, bronchoconstriction, cardiac depression
Contraindicated in diabetics, asthmatics

Question 5

CCB: class, name, MOA, ADR, contraindications

Answer 5

Antihypertensives, ischemic heart disease

Inhibit channel to decrease Ca influx and calmodulin signalling, decreases Myosin LC activation

Nifedipine- DHP more vascular selective
Decrease vascular smooth muscle tone, vasodilation decrease oxygen requirement and BP

Verapamil- NDHP more cardiac muscle selective
Decrease SA, AV nodal conduction, decrease contractility
Used for supraventricular tachycardia, arrythmia because of negative chronotropic effect

Cannot use on HF patients because cardiac depression. Only for angina and hypertension

Question 6

Loop diuretics: class, suffix, MOA, ADR, contraindications

Answer 6

Antihypertensives, HF
Sulfonamide derivatives (furosemide)
Act at ascending limb, selectively inhibit Na/K/Cl cotransporter at luminal side to prevent Na reabsorption
Increase renal blood flow to increase GFR
Hypokalemic alkalosis because of more K+, H+ excretion
Ionic imbalance of Mg, Ca because less driving force
Ototoxicity, cannot take with aminoglycosides

Question 7

DCT diuretics: class, suffix, MOA, ADR, contraindications

Answer 7

Antihypertensives, HF
Thiazides
Act at DCT. Blocks Na/Cl cotransport but enhance Ca2+ reabsorption
Hypokalemic alkalosis, more K+, H+ secretion

Question 8

Potassium-sparing diuretics: class, suffix, MOA, ADR, contraindications

Answer 8

HF
SEAT: Spironolactone, Eplerenone, Amilioride, Triamterene
Target K+ secretion at collecting duct. To decrease Na+ reabsorption and K+ secretion.
S and E inhibit aldosterone receptor and T and A inhibit Na+ channel protein.
Hyperkalemia, metabolic acidosis, gynaecomastia

Question 9

Type I hyperlipoproteinemia

Answer 9

Familial hyperchylomicronemia, raised CM levels

Due to LPL deficiency

Question 10

Type II hyperlipoproteinemia + tx

Answer 10

IIa: f. hypercholesterolemia, raised LDL.
IIb: mixed hyperlipidemia, raised VLDL and LDL.

tx: Statin

Question 11

Type IV hyperlipoproteinemia + tx

Answer 11

Familial hypertriglyceridemia, raised VLDL tx: niacin, vit B3

Question 12

First line drug for Type II (TG<4.5mmol/L)

Answer 12

Statins

Question 13

First line drug for Type II (TG>4.5mmol/L)

Answer 13

Fibrates to lower risk of pancreatitis, niacin if severe

Question 14

Niacin: class, MOA, ADR, contraindications

Answer 14

Lipid-lowering by inhibiting HSL
Inhibiting HSL to prevent lipolysis in tissues. Hence, lower amount of VLDLs needed to transport TGs out of liver
Most potent in increasing HDL
Flushing (first few days), hyperuricemia and GOUT

Question 15

Cholestyramine, Cholestipol: class, MOA, ADR, contraindications

Answer 15

Lipid-lowering by lowering bile acid concentration (+ve bind to -ve salts), liver uses more cholesterol to produce bile acids
Useful in isolated LDL increase only, causes HMG-CoA reductase to be upregulated so often used with statin
Cause bloating and abdominal discomfort
May cause impaired vitamin ADEK absorption
Contraindicated in pregnancy

Question 16

Ezetimibe: class, MOA, ADR, contraindications

Answer 16

Lipid-lowering by impairing cholesterol absorption
Selectively inhibits cholesterol transport protein NPC1L1
Often combined with statin
Contraindicated in pregnancy

Question 17

Gemfibrozil: class, MOA, ADR, contraindications

Answer 17

Lipid-lowering by increasing LPL activity
Fibrates
Peripheral clearance effect because act as ligands for PPAR-a, increasing FFA uptake and decreasing liver TG levels, less VLDL needed
Upregulate Apo-A proteins (on HDL)
Contraindicated in pregnancy
DDI: Displace warfarin in albumin-binding, interferes with clearance of statins

Question 18

Statins: class, MOA, ADR, contraindications

Answer 18

Lipid-lowering by inhibiting HMG-CoA reductase
Competitive inhibitor at rate-limiting step of cholesterol synthesis
Peripheral clearance effect as LDL receptors upregulated to take in more cholesterol
**Fibrinolytic, helps with atherosclerosis
Take in evening, cholesterol levels highest in fasting state
Contraindicated in pregnancy
Hepatotoxicity, myotoxicity, nausea, cataracts, rash, headache
Metabolised by CYP450

Question 19

Mode of administration: Lipid-lowering drugs

Answer 19

Oral, except PCSK9 antibodies (subq)

Question 20

Only lipid-lowering drug that is not contraindicated in pregnancy

Answer 20

Omega 3 FA

Question 21

What are the factors affecting cardiac oxygen requirement?

Answer 21

Preload (which depends on blood volume and venous tone), afterload (which depends on arterial BP), heart rate, contractility

Question 22

Nitrates: class, name, MOA, ADR, contraindications

Answer 22

Ischemic heart disease
Nitroglycerin, nitroprusside (SNP)
Donates nitrite which is converted to NO needed for guanylyl cyclase pathway, cGMP needed to dephosphorylate myosin LC.
Smooth muscle relaxation causes vasodilation to decrease preload and afterload. Vein dilation reduces preload and arterial dilation reduces TPR (afterload). Coronary artery dilation also increases oxygenation.
Tachycardia baroreflex (temporary), hypotension, headache (meningeal artery dilation)
Long term: Tolerance (tissue thiols depleted)

SNP produces cyanide as by-product, risk of poisoning

Question 23

NSAIDs: class, name, MOA, ADR, contraindications

Answer 23

Antiplatelet
Aspirin
Irreversible COX inhibitor, prevent TXA2 synthesis by platelets when they want to aggregate
Bleeding and peptic ulcers because inhibitory towards PG synthesis

Question 24

GPIIb/IIIa fibrinogen receptor antagonists: class, name, MOA, ADR, contraindications

Answer 24

Antiplatelet
Abciximab
mAb against receptor found on platelet membrane
For high risk angioplasty patients, given with aspirin and heparin
Bleeding, thrombocytopenia

Question 25

aPTT vs PT

Answer 25

aPTT: activated partial thromboplastin time, intrinsic pathway (damage to endothelium). Used to monitor heparin
PT: prothrombin time, extrinsic pathway (external trauma causing tissue factor release). Used to monitor warfarin

Question 26

Vit K dependent factors

Answer 26

2, 7, 9, 10

Question 27

Heparin: class, MOA, ADR, contraindications

Answer 27

Anticoagulant
AT3 potentiator, enhances binding to clotting factors 2a, 9a, 10a by 1000x
Given with GP11b/IIIa blockers for angioplasty
Short term: allergy
Long term: osteoporosis, transient reversible hair loss

Question 28

Warfarin: class, MOA, ADR, contraindications

Answer 28

Anticoagulant
Inhibit Vit K reductase, factor 2, 7, 9, 10 cannot be activated as reduced bit K is used as a cofactor for gamma carboxylation for these factors
Contraindication: PREGNANCY
Narrow TI, albumin-bound (risk of bleeding)
Metabolised by CYP450
Teratogen, risk of cutaneous necrosis

Question 29

Difference in use of heparin and warfarin (hint: difference in onset time, mode of administration and side effects)

Answer 29

Heparin used to induce anticoagulation especially in DVT and PE (immediate onset, administer via subq), warfarin to maintain in the long run.

Question 30

When can reduced and oxidised vit K be administered?

Answer 30

Reduced vit k needed for clotting (activate factors 2, 7, 9, 10), can be used to treat bleeding caused by warfarin. Oxidised vit k given to “overwork” vit K reductase to slow down carboxylation of glutamate residues of the clotting factors.

Question 31

Tissue plasminogen activators: class, names, MOA, ADR, contraindications

Answer 31

Thrombolytic agents
t-PA, Urokinase, streptokinase
Essentially all are t-PA, converts plasminogen to plasmin which degrades fibrin. For emergency use to lyse clots

Question 32

Diuretics in edematous patient with CHF

Answer 32

Thiazide if not severe, furosemide if severe. Need to manage hypokalemia by using potassium-sparing diuretic or potassium supplement

Question 33

First line drug in non-edematous patient with CHF

Answer 33

ACE Inhibitors decrease preload and afterload.

Question 34

Pathophysiology of CHF

Answer 34

Causes of LHF: IHD, aortic stenosis, CoA, pericardial effusion
As heart becomes less effective, preload increases as more blood remains in heart after each cycle. Heart becomes overstretches because it cannot fully compensate

Question 35

Classes of anti-arrhythmics

Answer 35

Class 1: SCB
Class 2: BB
Class 3: PCB
Class 4: NHDPCCB
Adenosine

Question 36

Which class of anti-arrhythmics is used for supraventricular tachycardia?

Answer 36

Class 4 NHDPCCB- Verapamil, Diltiazem are more myocardial selective
Reduces AV conductivity, prolongs phase 4 depolarisation

Adenosine also used, but half like only 10s and for emergency use

Question 37

Which class of anti-arrythmics is used for atrial fibrillation?

Answer 37

On top of Beta Blockers,
Class 3 PCB- Amiodarone
Prolongs phase 3 repolarisation, no phase 0 effect (phase 0 only sodium channels open)
Increases ERP and APD

Question 38

3 sodium channel blockers

Answer 38

Class 1A: Procainamide
Class 1B: Lidocaine
Class 1C: Flecainide (last resort, may increase mortality)

Question 39

GTN vs SNP: Mode of administration

Answer 39

GTN : Oral

SNP: IV