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Bloc C - Exam 2 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are the mechanisms of action of Unfractionated Heparin?

A
  1. Mixture of sulphated mucopolysaccharides from mast cells, acts on antithrombin IIa and Xa.
  2. Unfractionated heparin: obtained from the mast-cells of animals
  3. Given parentally (IV and subcutaneous)
  4. Zero order kinetics
  5. Monitoring is essential: Activated partial thromboplastin time (aPTT) and platelet count as used
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2
Q

What is the antagonist of Unfractionated Heparin?

A

Protanime Sulfate (when significant bleeding only)

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3
Q

What are the clinical uses of Unfractionated and Low Molecular Weight Heparin?

A
  1. Pulmonary embolism
  2. Deep vein thrombosis above knee joint
  3. Unstable angina in myocardial infarction
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4
Q

What are the secondary effects of Unfractionated Heparin?

A
  1. Bleeding
  2. Thrombocytopenia (HIT)
  3. Allergies
  4. Hair loss
  5. Osteoporosis
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5
Q

What secondary effect is less important in Low Molecular Weight Heprain compared to Unfractionated Heparin?

A

Thrombocytopenia (HIT)

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6
Q

What are the constraindications of Unfractionated and LMW Heparin?

A
  1. Thrombocytopenia
  2. Bleeding disorders
  3. Active peptic ulcer disease
  4. Severe hypertension
  5. Use in pregnancy should be restricted to when really needed (but doesn’t cross placenta)
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7
Q

What is the mechanism of action of Low molecular weight heparins?

A
  • Main action through a catalytic effect on the inhibition of factor Xa by antithrombin III. Thus, less monitoring.
  • Shorter effect.
  • Given subcutaneously.
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8
Q

What are the types of LMWH?

A
  1. Enoxaparin
  2. Dalteparin
  3. Fondaparinux
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9
Q

What are the types or new oral anticoagulants?

A
  • Warfarin (Coumadin and Sintrom)
  • Dabigatran
  • Rovaroxaban (Xa)
  • Edoxaban (Xa)
  • Apixaban (Xa)
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10
Q

What are the mechanisms of action of Wafarin?

A
  1. Vitamin K antagonist, makes it impossible for coagulant factors to work
  2. Full antithrombotic takes 2-5 days (long), half-life varies a lot
  3. Crosses placenta
  4. Monitor with prothrombin time (PT) and it’s important to maintain therapeutic international normalized ratio (INR)
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11
Q

What are the clinical uses of Wafarin?

A
  1. Long-term
  2. Best to prevent strokes in patients with valve problems (used indefinitely)
  3. AF
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12
Q

What are the mechanisms of action of Dabigatran?

A
  1. Oral direct thrombin inhibitor (prodrug)
  2. Rapid onset action but $$
  3. No need for lab monitoring
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13
Q

What are the mechanisms of action of Rovaroxaban, Apixaban and Edoxaban?

A

Oral direct factor Xa inhibitor Most used of new oral anticoagulants

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14
Q

What is the antagonist of Wafarin?

A

Fresh frozen plasma + Vitamin K1

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15
Q

What is the antagonist of Dabigatran?

A

Idarucizumab (when major bleeding)

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16
Q

What is the antagonist of Rovaroxaban, Apixaban and Edoxaban?

A

Andexanet alfa

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17
Q

What are the clinical uses of Dabigatran, Rovaroxaban, Apixaban and Edoxaban?

A
  1. Prevention of stroke with AF
  2. Prevention of PE and deep vein thrombosis (PTH/PTG)
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18
Q

What are the secondary effects of all oral anticoagulants?

A
  1. Bleeding
  2. Drug interactions
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19
Q

What are the contraindications of all oral anticoagulants?

A
  • Pregnancy (bleeding and foetal malformation)
  • Patient must be educated to report any change in medication, including non-prescription drugs and even food supplements
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20
Q

Name one important fibrinolytic drug?

A
  1. Alteplase (short)
  2. Tenecteplase (long)
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21
Q

What is the antagonist of Fibrinolytic drugs?

A

ε-Aminocaproic

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22
Q

What are the mechanisms of fibrinolytic drugs?

A
  1. Catalyze the formation of plasmin from plasminogen, leading to the lysis of thrombi
  2. Tenecteplace have longer half-life
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23
Q

What are the clinical uses of fibrinolytic drugs?

A
  • Acute myocardial infarction with ST elevation: first 3 hours
  • Clots in catheter
  • Large PE
  • Ischemic strokes
  • Patients are then treated with aspirin and clopidogrel
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24
Q

What are the secondary effects of fibrinolytic drugs?

A
  • Bleeding caused by lysis of physiological thrombi and induction of a systemic lytic state
  • Conversion of ischemic to haemorrhagic stroke
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25
Q

What are the contraindications of fibrinolytic drugs?

A
  • Hypertension
  • Recent surgery
  • Active bleeding
  • Previous CC incident
  • Aortic dissection or acute pericarditis
  • Gastro-intestinal bleeding (3 months)
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26
Q

What’s the pharmacological name of Aspirin?

A

Acetylsalicylic acid

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27
Q

What is the mechanism of action of Aspirin?

A

Drugs that block Thromboxane synthesis:

  • Blocks the production of thromboxane A2 by covalently acetylating the serine residue near the active site of cyclooxygenase-1
  • Irreversible, taken orally
  • Higher doses of aspirin when used as an NSAID may paradoxically have less anti-platelet effect
  • O order: half-life 15 minutes
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28
Q

What are the clinical uses of Aspirin?

A
  • Decrease incidence of cerebral and cardiac ischemic symptoms
  • Coronary bypass
  • Unstable angina
29
Q

What are the side effects of Aspirin?

A
  • Liver overdose (Salicylism) = hearing problems/dizziness
  • Gastro-intestinal symptoms
  • Asthma exacervation
  • Liver toxicity
  • Bleeding
  • Resistance
30
Q

What are the contraindications of Aspirin use ?

A
  • Bleeding disorder
  • Interaction with anticoagulants
  • Ulcers
  • Asthma
  • Pregnancy
  • Aspirin allergy
31
Q

What are the drugs that block irreversibly platelet ADP receptors P2Y12?

A
  1. Clopidogrel
  2. Prasugrel
  3. Ticagrelor
32
Q

What are the mechanisms of action of Clopidogrel and Prasugrel?

A
  • ADP activates platelets by binding to two membrane purine receptors, P2Y1 and P2Y12 (simultaneously)
  • Long-term effects on platelet function (like for aspirin, new platelets required)
  • Genetic variability because of enzyme activation (prodrug), taken orally
  • Prasugrel less affected by genetic variations of the metabolizing enzymes (to be preferred over clopidogrel in case of loss of function of the CYP2C19
33
Q

What are the clinical uses of Clopidogrel?

A
  • Superior to aspirin in secondary prevention of stroke
  • MI
  • Alternative to Aspirin when allergy
34
Q

What are the clinical uses of Prasugrel?

A

Acute coronary syndrome

35
Q

What are the side effects of Clopidogrel?

A
  • Nausea
  • Diarrhea
  • Bleeding
  • Resistance
  • Possible TTP
36
Q

What are the side effects of Prasugrel?

A

Higher risk of bleeding than Clopidogrel

37
Q

What are the contraindications of Prasugrel?

A
  • If previous stroke or transient ischemic attack
  • Older (>75) patients
38
Q

What is Ticagrelor?

A

A drug not used anymore

Mechanisms of action:

  • Not related to the other inhibitors of ADP pathway
  • Reversible inhibitor of P2Y12 receptors
  • Faster and more predictable effects

Was used for

  • Greater reduction in CV death, MI and stroke than with clopidogrel
  • Lower dose for long-term for high risk of recurrent ischemic events post-MI

Side effects

  • Dyspnea
  • Bradycardia
  • Minor bleeding more often

Contraindications

Previous intracranial bleeding

39
Q

What are the drugs that are platelet glycoprotein IIB/IIIA inhibitors?

A
  1. Abciximab
  2. Eptifibatide
  3. Tirofiban
40
Q

What are the mechanisms of action of drugs that are platelet glycoprotein IIB/IIIA inhibitors?

A
  • Abciximab = antibody against the glycoprotein IIB/IIIA receptor
  • Eptifibatide and Tirofiban = fibrinogen blocker
  • Extremely powerful blockers of platelet aggregation
  • Given by injection
  • Inactivation of transfused platelets with Eptifibatide and Tirofiban because of long half-lives of these drugs
41
Q

What are the clinical uses of drugs that are platelet glycoprotein IIB/IIIA inhibitors?

A
  • Their use is in major decline: ticagrelor and prasugrel are replacing them
  • Used in percutaneous coronary interventions
42
Q
A
43
Q

What are the side effects of drugs that are platelet glycoprotein IIB/IIIA inhibitors

A
  • Bleeding
  • Thrombocytopenia
44
Q

What is the most used anti-platelet drug ?

A

Aspirin

45
Q

What 2 drugs are commonly associated ?

A

Aspirin and clopidogrel after an episode of CAD

46
Q

What drug do you give to a patient resistant to Clopidogrel?

A

prasugrel or ticagrelor

47
Q

What is the effect of inotropes drugs ?

A

Increase the availability of intra-cellular calcium

  • ↑ force of contraction
  • ↑ Frank-Starling curve
  • ↑ stroke volume (and cardiac output) at any given EDV
48
Q

What are the 3 main types of inotropes drugs?

A
  1. Cardiac glycosides - Digitalis (digoxin)
  2. Sympathomimetic amines (dopamine, dobutamine, norepinephrine, epinephrine, isoproterenol)
  3. Phosphodiesterase inhibitors (milrinone)
49
Q

What is the mechanism of action of Cardiac glycosides - Digitalis (digoxin)?

A
  • Change the K+ CA2+ Na+ pump (↓ K+ and ↑ Na+)
  • ↑ contractility and CO
  • ↓ cardiac enlargement, symptoms, baroreceptor sensitivity, AV node conduction, HR
  • NO EFFECT ON MORTALITY
  • Side effects and interactions: different arrhythmias, nausea, anorexia, hallucinations
  • Narrow therapeutic window that requires a lot of monitoring (++ with renal diseases)
50
Q

What is the uses of Sympathomimetic amines (dopamine, dobutamine, norepinephrine, epinephrine, isoproterenol)?

A
  • Dobutamine for cardiogenic shock without significant hypotension,
  • Norepinephrine for septic and cardiogenic shock with hypotension
  • Epinephrine for anaphylactic shock.
51
Q

What is the mechanism of action of Phosphodiesterase inhibitors (milrinone)?

A
  1. → cAMP → Ca2+
52
Q

What is a vasopressine drug and its effects?

A

Induce vasoconstriction and thereby elevate mean arterial pressure (MAP), differ from inotropes, which increase cardiac contractility; however, many drugs have both vasopressor and inotropic effects.

  • Indicated for a decrease of >30 mmHg from baseline systolic blood pressure, or a mean arterial pressure <60 mmHg when either condition results in end-organ dysfunction due to hypoperfusion
  • Avoid in those with active organ ischemia
53
Q

What is a vasodilator?

A

Vasodilators help reverse the adverse consequences of neuro-hormonal compensatory mechanisms in HF and hypertension:

  • Excessive vasoconstriction
  • Volume retention
  • Ventricular remodelling with progressive deterioration of LV function
54
Q

What are the 4 main types of vasodilators?

A
  1. Venous Dilators (nitrates, nitroglycerin)
  2. Pure Arterial vasodilators (hydralazine)
  3. Mixed balanced vasodilators (nitroprusside, ACE ihbibitors α-blockers)
  4. Calcium channel blockers (Verapamil and diltiazen)
55
Q

How do Venous Dilators (nitrates, nitroglycerin) act?

A
  1. Are used for angina
  2. Acts through NO in the endothelial cells
  3. ↓ venous return and LV preload
  4. ↓ LV diastolic pressure and pulmonary capillary hydrostatic pressure
56
Q
A
57
Q

How do Pure Arterial vasodilators (hydralazine) act?

A
  1. Acts through the endothelial cells to release NO too and needs an intact endothelium
  2. ↓ systemic vascular resistance and LV afterload
  3. ↑ stroke volume (shifts cardiac output curve upwards)
58
Q

How do mixed balanced vasodilators (nitroprusside, ACE ihbibitors α-blockers) act?

A
  1. Vasodilation of both venous and arterial circuits
  2. Inhibitors of the renin-angiotensin-aldosterone system
  3. Angiotensin Converting Enzyme (ACE) inhibitors that blocs the effect of angiotensine II

STANDARD FIRST-LINE CHRONIC THERAPY IN PATIENTS WITH LV SYSTOLIC DYSFUNCTION and used to manage hypertension because it decreases mortality

Adverse effect: cough

  1. Angiotensin 2 (Type 1) receptor Blockers (ARB)

Is a biased ligand

Ex: Entresto is acombination of valsartan (ARB) and sacubitril (neprilysin inhibitor)

59
Q

How do Calcium channel blockers (Verapamil and diltiazen) act?

A
  1. CCBs are often used to treat hypertension
  2. CCBs are particularly effective in elderly patients
  3. CCBs are usually administered orally as long-acting once-a-day formulations
60
Q

How do diuretics act?

A

Diuretics eliminate excess sodium and water through renal excretion thus they are often used in the treatment of hypertension. Diuretics similarly reduce intravascular volume and in some cases promote vascular dilation.

61
Q

What are the 3 types of diuretic drugs?

A
  1. Loop diuretics (Na+K+ receptor in proximal glomerulus tubule)
  2. Thiazides (Na+Cl receptor in distal glomerulus tubule)
  3. Potassium-sparing diuretics (receptor in most distal part of glomerulus)
62
Q

How do Loop diuretics (Na+K+ receptor in proximal glomerulus tubule) act?

A
  1. Used in the acute management of pulmonary oedema and in the treatment of chronic HF or peripheral oedema (orally)
  2. They are effective in the setting of impaired renal function
  3. The mechanism of venous vasodilation appears to involve drug-induced prostaglandin and NO generation from endothelial cells, which act to relax vascular smooth muscle.
  4. Most commonly used loop diuretic is furosemide, the oral form of which demonstrates reliable gastrointestinal absorption but a short duration of action (4 to 6 hours) that limits its usefulness in the chronic treatment of hypertension
  5. Adverse effects include hypokalemic metabolic alkalosis, ototoxcity (hearing loss), gout…
63
Q

What are the types of Thiazides (Na+Cl receptor in distal glomerulus tubule)?

A
  1. Indapamide is unique among this class in that it displays a particularly prominent vasodilating effect
  2. Chlorothiazide, the parent compound, has low lipid solubility and hence low bioavailability; higher doses are therefore required to achieve therapeutic levels
  3. Metolazone, is sometimes effective in patients with reduced renal function

Adverse effects: hypokalemia, metabolic alkalosis, hyponatremia, hyperuricemia, hyperglycemia, weakness, fatigability, and paresthesias

64
Q

How do Potassium-sparing diuretics (receptor in most distal part of glomerulus) act?

A
  1. Potassium-sparing diuretics prevent K+ secretion by antagonizing the effects of aldosterone in collecting tubules.
  2. Serum potassium level must be closely monitored.
  3. Adverse effects include hyperchloremic metabolic acidosis and gynecomastia
65
Q

True of false: there is evidence-based therapy for HF with preserved EF?

A

FALSE, NOT YET.

66
Q

All the hypertension drugs, do they treat symptoms or the disease ?

A

Symptoms !!

67
Q

What is the best treatment for hypercholesterolymia?

A

STATINS

High-risk patients or familial: health behavior modifications + statins

Low/moderate-risk patients: health behavior modifications + optional secondary testing + maybe statins

  • Statins lower risk to the same relative degree independent of baseline risk and baseline LDL-C
  • The absolute risk benefit with statins is greatest in the highest risk patients
  • High intensity vs. lower intensity statin therapy further lowers risk
  • No RCT tested a specific strategy of dosing statin to achieve a pre-specified LDL-C target. However, evidence to date suggests that lower is better
68
Q

What are the other non-statins treatment that we use for hypercholesterolymic patients?

A
  • Bile Acid Binding Resins (used with pregnant woman)
  • Fibrates: not recommended for patients on statins that reached the LDL targets
  • Niacin: not recommended for patients on statins that reached the LDL targets
  • Ezetimibe: second-line therapy to lower LDL-C in patients with ASCVD if targets are not reached on maximally tolerated statin therapy
  • PCSK9 inhibitors: directly binds to the LDLR, very safe, IT IS THE FUTUR
69
Q

What were the recommendations of Fourier and Odyssey trials?

A

The use of PCSK9 inhibitors drugs for:

  • ASCVD with sub-optimal LDL-C despite taking maximally tolerated statin ± ezetimibe
  • Heterozygous FH with sub-optimal LDL-C despite taking maximally tolerated statin ± ezetimibe

Bloc C - Exam 2 (7 decks)

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