CAD, HF, Acute CS & AF Flashcards

1
Q

What is the role of GTN?

A
  • Vasodilator, given for angina pectoris
  • Causes venous dilatation to reduce cardiac preload
  • Decreasing cardiac oxygen demand
  • GTN is metabolised into NO in smooth muscle cells
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2
Q

What are the adverse effects of Nitrate drugs?

A
  • venous pooling
  • leads to postural hypotension, from supine to sitting position
  • dizziness and headaches
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3
Q

What are the types of Angina?

A
  • Stable angina (most common)
  • Unstable Angina
  • Prinzmetal Angina
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4
Q

What is stable angina?

A
  • Most common type of angina
  • Induced by exercise, heavy meals, cold and emotional stress
  • Controlled well by GTN & other anti-anginal drugs
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5
Q

What is unstable angina?

A
  • Occurs at rest
  • May be induced by little exercise or stress
  • Occurs due to possible thrombus formation on ruptured atheromatous plaque
  • Causing partial occlusion of CA
    -Patient at risk of full occlusion of CA and MI
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6
Q

What is prinzmetal angina?

A
  • rare form of angina
  • spasm of CA’s
  • may occur in patient’s with minimal atherosclerotic damage and rarely progresses to MI
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7
Q

Why is GTN administered as sublingual, skin patch or buccal spray and NOT as a tablet to swallow?

A
  • Absorption of the drug in the gut will lead to metabolisation by the liver
  • Limits the drug availability
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8
Q

Can a patient with Asthma be prescribed with Beta Blockers for angina (non-selective & selective)?

A

-No
- B- blockers have affinity for both B1 (cardiac) & B2 receptors (airways) on bronchial muscles
- This can lead to bronchoconstriction
- Even selective B- blockers can have some effect

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9
Q

What is the mechanism of action of Beta Blockers e.g. Propranolol?

A
  • act on B1 and B2 receptors
  • cause vasoconstriction & bronchoconstriction
  • Block sympathetic effects on B1 & B2 receptors
  • Causes small reduction in HR and CO; little effect on BP
  • May be beneficial for some angina patients; reduces the response of B1 receptors to sympathetic stimulation during exercise, stress etc.
  • Selective & Non-selective B-Blockers
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10
Q

How can you distinguish between Angina & MI?

A
  • Angina goes away after rest and taking medication e.g. GTN
  • MI patient still presents with symptoms
  • Pain, pallor, sweating, nausea, hypotension with shock suggest complete occlusion of CA
  • MI patient will have increased Troponin I & T with increased creatine phosphokinase
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11
Q

What is the MOA of Calcium Channel blockers (CCB’s)?

A
  • Block L type Ca channels of vascular smooth muscles
  • Reduces Ca concentration in smooth muscles
  • Leads to dilation of arteries due to reduced contractile activity
  • CCB’s mainly act on arteries
  • Dihydropyridines, e.g. Nifedipine, is useful for CA dilation
  • Commonly used for prinzmetal angina
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12
Q

What ECG changes will be expected in Angina?

A
  • ST segment depression
  • Severe Angina may present with ST segment elevation for short duration
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13
Q

What is Angina Pectoris?

A
  • Paroxysmal attacks of retrosternal chest discomfort, tightness, or pressure due to myocardial ischemia
  • Pain may radiate to left arm, chin and jaw area
  • Narrowed CA’s may not be able to dilate upon exercise, stress, cold etc
  • Therefore, increased oxygen demand of cardiac muscles are not met, leading to ischemia
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14
Q

What is heart failure?

A

-heart is unable to pump enough blood
-Unable to meet the metabolic needs
- Ventricular dysfunction results in low cardiac output
-congestion of blood (backward failure) and poor systemic perfusion (forward failure)
-Disturbance of tissue fluid management; increased venous pressure
- therefore swelling of ankles is presented in patients

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15
Q

What is the significant underlying cause of Heart Failure?

A

Hypertension- leads to increased afterload which causes hypertrophy of ventricles and increased O2 consumption
- reducing cardiac efficiency

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16
Q

What are Thiazides? MOA?

A
  • Thiazides are diuretics
  • Reduce Na and Water reabsorption by acting on distal tube of Nephrons
  • Block NaCl transporters
  • This ultimately reduces blood volume
  • Diuretics also act on vascular smooth muscles to cause dilation
  • Both of these reduce BP and reduce peripheral edema
  • Preload and afterload is also reduced
17
Q

What are the symptoms of Right Sided Heart Failure?

A
  • Abdominal bloating
  • Nausea
  • Loss of appetite
  • Reduced tolerance to exercise
  • Breathlessness
18
Q

What are adverse effects of thiazide’s?

A
  • hypokalaemia, hyperglycaemia & hyperurecaemia
19
Q

What type of diuretics are prescribed when thiazides are not functioning well?

A
  • Loop diuretics (stronger diuretic than thiazides)
  • Better to introduce a stronger diuretic than increase dose of thiazides
  • As therapeutic effect is lower and increased events of adverse effects
20
Q

What is the MOA of loop diuretics?

A
  • Blockage of Na+, K+, 2Cl-cotransporter in the thick ascending loop of Henle
    -Diminishing concentration gradient between the (usually hypertonic) renal medulla and the cortex → concentration of urine is no longer possible → increased diuresis
    -Decreased reabsorption of Ca2+ and Mg2+
  • Increased PGE release (can be inhibited by NSAIDs)
    Dilation of renal afferent arterioles → diuresis
  • General venodilation (rapid venous pooling) → ↓ cardiac preload
21
Q

What are the adverse effects of Loop Diuretics?

A
  • Similar to thiazides
    -Hypokalaemia, Hyperglycaemia and Hyperurecaemia
  • Some patients may also present with hypovolemia & hypotension, which can develop to CV collapse
22
Q

Define Myocardial Infarction

A

-obstruction of blood flow to cardiac muscles
-due to occluded CA’s leading to ischemia
-Interruption of blood flow to that area causes potential cell death of affected cardiac muscles

23
Q

What is the MOA of Epinephrine on the heart?

A
  • non-selective A & B receptor agonist
  • acts on B1 receptors on cardiac muscles to stimulate contractions to increase CO
  • doesn’t cause bronchoconstriction, as it relaxes airways
24
Q

What is the MOA of aspirin?

A
  • Aspirin is a NSAID which inhibits COX enzyme
  • This prevents the release of PGs
  • Whom are responsible for inflammation, temperature regulation, blood clotting etc.
  • Aspirin aids to reduce fever, pain and stops blood clotting
25
Q

Why is aspirin administered to patients after an MI?

A
  • prevent risk of blood clotting in the circulation
26
Q

What are the MOA of thrombolytic agents and use in MI e.g. streptokinase?

A
  • “dissolve’ clots obstructing blood flow in CA’s to cardiac muscles
  • Activates plasminogen to plasmin conversion; lyses clots
  • Should be administered within 12 hours of infarction; ideally within 1st hour
    -Given IV
27
Q

What are the contraindications for thrombolytic agents?

A
  • allergy to medication
  • recent hemorrhage e.g. recent head injury with intracranial hemorrhage or had surgery
28
Q

What is Furosemide? MOA?

A
  • Loop diuretic
  • Acts on ascending thick loop of Henle
  • Acting on Na/Cl transporters
  • Reduces Na and water reabsorption in collecting duct
  • Large amounts of salt and water is excreted by the kidney
  • Strong class of diuretics, able to improve pulmonary edema
29
Q

What is atrial fibrillation?

A
  • Common type of supraventricular tachyarrhythmia

-Characterized by uncoordinated atrial activation that results in an irregular ventricular response

30
Q

What type of drug is Digoxin and what is its MOA?

A
  • Cardiotonic agent
  • Increases contractility of cardiac muscles
  • Increases Ca concentration in cardiac muscles
  • Acts on Na/K pumps in cardiac muscle; competes on K binding site
31
Q

What are the adverse effects of Digoxin use?

A

-narrow therapeutic index
-therapeutic dosage is close to dosage causing toxicity
-may cause cardiac rhythm abnormalities
- GI disturbances, anorexia, nausea, CNS effects e.g. confusion and visual disturbances

32
Q

What is the MOA of warfarin?

A
  • Anticoagulant
  • Structurally similar to Vit K which is needed for synthesis of prothrombin and other clotting factors
  • Interferes with actions of Vit K and reduces risk of clotting
  • Given for anticoagulant therapy for atrial fibrillation