Drugs for IHD and Heart Failure Flashcards

1
Q

Core Drug: Digoxin: Mechanism of Action:

A
  • inhibits the Na+/K+ ATPase channel
  • binds to the extracellular K+ binding site
  • increases intracellular Na+
  • Na+ and Ca2+ exchange through
    exchanger (Na+ out, Ca2+ in)
  • increased intracellular Ca2+
  • increased ionotropy
  • increases force of contraction and
    contractility of the heart
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2
Q

Core Drug: Digoxin: What tissues/organs it acts on?

A
  • SA node
  • AV node
  • cardiac muscle
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3
Q

Core Drug: Digoxin: Physiological effects:

A
  • slows the heart rate
  • increases contractility
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4
Q

Core Drug: Digoxin: side effects:

A
  • DOES NOT DECREASE BP
  • arrhythmias especially with hypokalaemia
  • xanthopsia = colour vision deficiency,
    mostly see yellow
  • anorexia
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5
Q

Core Drug: Digoxin: Interactions:

A
  • many drugs increase toxicity
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6
Q

Core Drug: Digoxin: Pharmacokinetics:

A
  • orally active
  • requires loading dose
  • half life c. 36 hours
  • narrow therapeutic window
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7
Q

Core Drug: Digoxin: Clinical Use:

A
  • end stage heart failure sometimes
  • to slow heart rate in atrial fibrillation, very
    commonly
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8
Q

Core Drug: “Digoxin Effect”:

A

reverse tick on ECG
not necessarily toxic

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9
Q

Core Drug: Digoxin: specific antidote:

A

Digibind
for too much digixin causing toxicity

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10
Q

Digoxin is from which plant

A

foxglove

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11
Q

Core Drug: digoxin: Mechanism of action diagram:

A
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12
Q

Heart Failure Pathophysiology:

A

INSERT DIAGRAM

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13
Q

Therapeutic Targets for heart Failure Drugs:

A

insert slide

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14
Q

Therapeutic Targets for angina drugs:

A

insert slide

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15
Q

Core Drug: Furosemide: Mechanism of action:

A
  • blocks Na+/K+/Cl co transporter in the thick ascending limb of the loop of henle
  • blocks the Cl- channel of the cotransporter
  • increased loss of: Na+, K+, Cl- and WATER
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16
Q

Core Drug: Furosemide: clinical uses:

A
  • much more powerful than other diuretics
  • used to clear peripheral oedema
  • used intravenously for acute pulmonary
    oedema
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17
Q

Core Drug: Furosemide: Pharmacokinetics:

A
  • “Lasix” = lasts for 6 hours
  • route of administration?
  • therapeutic window?
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18
Q

Core Drug: Furosemide: Side Effects:

A
  • dehydration
  • renal impairment
  • hypokalaemia
  • hyponatraemia
  • hypomagnesaemia
  • hyperuricaemia (high uric acid, causes
    gout)
  • auditory nerve damage (especially high
    doses and renal impairment)
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19
Q

Core Drug: Ramipril: mechanism of action:

A
  • ACE inhibitors (improves prognosis,
    mortality and quality of life)
  • blocks conversion of angiotensin I to
    angiotensin II
  • and blocks break down of Bradykinin
    (vasoactive peptide)
  • hence decrease in angiotensin II and increase in bradykinin peptide
20
Q

Core Drug: Ramipril: Physiological effects:

A
  • arteriolar dilation:
    - decreases after load, left
    ventricle has to pump more, increases
    speed of contraction
  • venodilation:
    - decreases preload
    - descending LA pressure
  • decrease in aldosterone and ADH, hence
    decrease in fluid retention
21
Q

Core Drug: Ramipril: clinical uses:

A
  • most commonly used drug to treat heart
    failure
  • also used for hypertension
22
Q

Core Drug: Ramipril: side effects:

A
  • dry cough (bradykinin accumulation in
    lungs)
  • renal impariment
  • hyperkalaemia: commonly given with a
    diuretic
23
Q

Core Drug: Ramipril: pharmacokinetics:

A
  • route of administration?
  • dosage: once daily dosage
  • therapeutic window?
  • half life?
24
Q

Core Drug: Losarten/Candesarten: mechanism of action:

A
  • blocks action of angiotensin II on the
    angiotensin I receptor
25
Core Drug: Losarten/Candesarten: physiological effects:
- arteriolar dilation: - decreases after load, left ventricle has to pump more, increases speed of contraction - venodilation: - decreases preload - descending LA pressure - decrease in aldosterone and ADH, hence decrease in fluid retention SAME AS ACE INHIBITORS
26
Core Drug: Losarten/Candesarten: side effects:
- DECREASE IN DRY COUGH COMPARED TO ACE-Is - renal impariment - hyperkalaemia: commonly given with a diuretic SIMILAR TO ACE INHIBITORS
27
Core Drug: Losarten/Candesarten: pharmacokinetics:
- route of administration - dosage - half life - therapeutic window - used in a fixed dose combination
28
Core Drug: Losarten/Candesarten: clinical uses:
- most commonly used for heart failure - alternative for patients intolerant of ACE inhibitors
29
Core Drug: Spironalactone: Mechanism of action:
- blocks the upregulation of Na+ channels in the DCT by aldosterone
30
Core Drug: Spironalactone: physiological effects:
31
Core Drug: Spironalactone: side effects:
- impaired renal function - hyperkalaemia - glynaecomastia (structurally similar to oestregen) - causes men to grow breasts
32
Core Drug: Spironalactone: clinical uses:
- prognostic benefit in: - very poor LV function - post MI (esp with acute heart failure)
33
Core Drug: Spironalactone: pharmacokinetics:
- route of administration - dosage - half life - therapeutic window
34
Eplerenone vs spironolactone
fewer side effects in eplerenone
35
over activation of sympathetic nervous system in heart failure results in (3) physiological processes
insert diagram
36
Positive ionotropes associated with what in heart failure
increased mortality
37
Heart failure and the adrenergic system:
- positive inotropes uniformly associated with increased mortality - malignant arrhythmias - catecholamine cardiotoxicity: - structural/functional cardiomyocyte changes - LV dilation and adverse remodelling - some are pressors = cause vasoconstriction - activate RAAS
38
adrenoreceptor activation
insert slide
39
Core Drug: Bisoprolol & Propranolol : Mechanism of action:
40
Core Drug: Bisoprolol & Propranolol: physiological effects:
- slow heart rate <70bpm - increased diastolic filling time - reduced afterload (lower BP) - reduced renin release: reduces RAAS activation - do not affect contractility (once patient is stabalised): - no effect on contractility in the absence of catecholamines (NAdr, Adr) - unlike calcium channel blockers - substantial mortality benefit (35% reduction)
41
Core Drug: Bisoprolol & Propranolol: clinical uses:
42
Core Drug: Bisoprolol & Propranolol: side effects:
43
Core Drug: Bisoprolol & Propranolol: pharmacokinetics:
- route of administration - dosage - half life - therapeutic window
44
Ivabradine used for and how
- heart failure - slows the heart by blocking the i (small f) channel in the SA node
45
Sacubitril used for, how take, what does it do
- neprilysin inhibitor - used with valsartan in fixed dose combination - slows heart rate?
46
Dapaglifozin used for and what does it do
- heart failure - inhibits glucose reabsorption in the kideny