Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 2 > Pharmacology Of Cardiac Disease > Flashcards

Pharmacology Of Cardiac Disease Flashcards

1
Q

Define acute coronary syndromes.

A

A set of cardiovascular conditions wherein blood supply to the heart muscle is suddenly blocked via occlusion of coronary arteries by thrombus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What symptoms characterise acute coronary syndromes?

A

Severe chest pain

SOB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some specific examples of acute coronary syndromes?

A

ST-segment elevated myocardial infarction (STEMI)
Non-ST segment elevated (NSTEMI)
Unstable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why is urgent treatment required for acute coronary syndromes?

A

They are life-threatening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 2 basic principles for the treatment of acute coronary syndromes?

A
  1. Increase O2 supply of myocardium: improve coronary blood flow + administer O2
  2. Reduce O2 demand of myocardium: reduce HR + force of contraction, cardiac preload + afterload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define heart failure.

A

Inability of the heart to deliver O2 at a sufficient rate to metabolising tissues throughout the body caused by abnormality of cardiac structure or function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

If hypertension is left untreated, what can occur?

A

Atherosclerosis which reduces blood flow to heart

Structural abnormalities in the heart e.g. L ventricular hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the treatment strategies for chronic heart failure?

A
  1. Improve contractility with positive ionotropes e.g. sympathomimetics (Dobutamine)
  2. B-blocker to modulate enhanced/sustained cardiac adrenergic drive
  3. Reduce oedema with diuretics e.g. loop (Furosemide)
  4. Reduce preload + afterload e.g. ACEi (Ramipril) or ARB (Losartan)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some other important targets, especially for preventing cardiovascular disease?

A
  1. Platelets: regulate blood clotting to prevent coronary thrombosis
  2. Hepatocytes: regulate cholesterol production + uptake by liver reducing atherosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the main blood vessel cells?

A
  1. Fibroblasts: connective tissue outer layer
  2. SMCs: contractile vascular smooth muscle layer
  3. Endothelial cells: lining of blood vessel lumen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the signal transduction occurring in vascular smooth muscle cells allowing them to contract.

A
  1. Angiotensin II binds to its receptor which stimulates IP3
  2. IP3 mobilises Ca2+ stores in SR
  3. Ca2+ also comes in through L-type channels on the cell membrane
  4. Ca2+ binds calmodulin which stimulates MLCK
  5. MLCK + ATP phosphorylate MLC causing contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the signal transduction occurring in vascular smooth muscle cells allowing them to relax.

A
  1. NO diffuses through the SMC membrane
  2. cGMP is stimulated
  3. cGMP stimulates MLCP
  4. MLCP dephosphorylates MLC causing relaxation releasing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do ACE inhibitors do?

A

Block conversion of angiotensin I to angiotensin II by ACE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do angiotensin receptor blockers (ARBs) do?

A

Directly block activation of the angiotensin II receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What physiological effect do both ACE inhibitors and ARBs have?

A

Decreased vasoconstriction in peripheral blood vessels leading to reduced peripheral resistance, reduced cardiac afterload + lowers BP

Aldosterone secretion is reduced leading to less H2O retention, lower plasma volume + lower cardiac preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the key side effect of ACE inhibitors that ARBs do not really cause?

A

Persistent cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the mechanism of action of calcium channel blockers?

A
  1. Prevent opening of voltage-gated L-type Ca2+ channels
  2. Reduced Ca2+ influx into SMCs
  3. Vasodilator effect on resistance in vessels decreasing cardiac afterload
  4. Drive coronary artery dilation + improve blood flow
  5. Some can affect heart directly with -ve chronotropic + inotropic effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the key side effects of calcium channel blockers?

A

Ankle-swelling

Palpitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Do calcium channel blockers act on veins?

A

Generally not

20
Q

What are the common calcium channel blockers?

A 
Nifedipine
Amlodipine (dihydropyridine subclass)
21
Q

What are the key examples of nitrate vasodilators?

A 
Glyceryl Trinitrate (GTN)
Isosorbide Mononitrate (ISMN)
22
Q

What is the mechanism of action of nitrate vasodilators?

A
  1. Metabolised to release NO
  2. NO stimulates sGC
  3. Increased cGMP in vascular SMCs
  4. Drives dephosphorylation of MLC via activation of MLCP
  5. Inhibits influx of Ca2+ into SMCs
  6. Drives vascular SMC relaxation
23
Q

What is the key side effect of nitrate vasodilators?

A

Headache

24
Q

What effects so nitrate vasodilators have on the heart?

A

Dilates arteries AND veins:

  • Venodilation reduces cardiac preload
  • Coronary artery vasodilation increases blood + O2 supply to myocardium
  • Moderate arteriolar dilation reduces cardiac afterload
25
Q

Describe the signal transduction in cardiomyocytes causing contraction.

A
  1. B1-adrenoceptor stimulation
  2. G proteins activate AC
  3. AC converts ATP to cAMP
  4. cAMP stimulates PKA
  5. PKA increases free Ca2+ levels inside cell via activation of channels on membrane + release from SR
  6. Ca2+ causing contraction
26
Q

What is the mechanism of action of beta-blockers?

A
  1. Competitive inhibitors of A + NA at B-adrenoceptor sites inhibiting sympathetic stimulation of heart muscle
  2. -ve chronotropes + inotropes so decrease HR + cardiomyocyte contractility
  3. Reduce workload of the heart relieving O2 demand
27
Q

What types of beta-blockers are selective for the heart?

A

B1-antagonists e.g. Atenolol

28
Q

What are the key side effects of beta-blockers?

A

Dizziness

Constipation

29
Q

What do diuretics do?

A

Act in kidney on renal tubular epithelial cells to increase H2O + Na output in urine, reduce plasma volume reducing cardiac preload + thus oedema

30
Q

What are key diuretic examples which can be used for cardiac diseases? What does each one do?

A
  1. Loop e.g. Furosemide inhibits renal Na/K/2Cl transporter
  2. Thiazide e.g. hydrochlorothiazide inhibit renal Na/Cl symporter
  3. K-sparing e.g. spironolactone inhibit aldosterone activity
31
Q

What are neprilysin inhibitors? Give an example.

A

New + promising treatment for heart failure with reduced EF

E.G. Sacubitril

32
Q

What is the mechanism of action of neprilysin inhibitors?

A
  1. Neprilysin is major enzyme involved in breakdown of NPs
  2. Inhibition of neprilysin prolongs presence + activity of NPs
  3. NPs promote H2O + Na excretion
33
Q

What drugs should neprilysin inhibitors be given with to be effective?

A

ARBs e.g. Valsartan

34
Q

What can IV adrenaline be used for?

A

Treatment for cardiac arrest (acute heart failure)

35
Q

What is the mechanism of action of adrenaline?

A

A is a powerful sympathomimetic + positive inotrope:

  • Binds + stimulates cardiomyocyte B1-adrenergic receptors
    2. Drives heart muscle contraction to restore heart function
36
Q

What can IV atropine be used for?

A

Treatment for sinus bradycardia (acute heart failure)

37
Q

What is the mechanism of action of atropine?

A
  1. Blocks M2 ACh receptors on cardiomyocytes
  2. Inhibits PS effects, cholinergic vagus nerve transmission which normally exert negative chronotropy
  3. Accelerates repolarisation rate in cardiac muscle
  4. Heart rate increased
38
Q

Define sinus bradycardia.

A

Dangerously slow HR

39
Q

Why can antiplatelet drugs be used to treat or prevent cardiovascular disease?

A

Platelet activation can drive thrombus formation leading to ACS

40
Q

What are the major antiplatelet drugs?

A

Aspirin (COX inhibitor)

Clopidogrel (ADP receptor inhibitor)

41
Q

What is the mechanism of action of ADP receptor inhibitors?

A
  1. Binds to + blocks function of ADP receptors on platelet surfaces
  2. Inhibits platelet activation + subsequent thrombus formation
42
Q

What is the mechanism of action of COX inhibitors?

A
  1. Blocks enzyme action of platelet COX enzyme
  2. COX required for synthesis of TXA2 production
  3. Reduced TXA2 synthesis inhibits platelet activation + thrombus formation
43
Q

What is the benefit of antiplatelet drugs and HMG-CoA reductase inhibitors used in the prevention or treatment of cardiovascular disease?

A

They do not affect BP

44
Q

How do HMG-CoA reductase inhibitors (Statins) prevent cardiovascular disease?

A

Reduce circulating cholesterol levels + promote uptake of excess cholesterol from the bloodstream into the liver -> effective protection against atherosclerosis development

45
Q

How is HMG-CoA reductase involved in cholesterol production?

A

Liver hepatocytes is main site of cholesterol production + it is secreted as LDL

HMG-CoA reductase is essential + rate-limiting step in cholesterol synthetic pathway

Block 2 (45 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions