Brainscape's Knowledge GenomeTM

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


See full index

PT3001: Introduction to Pharmacology > Heart & Diabetes Pharmacology I: Drugs and the Heart I > Flashcards

Heart & Diabetes Pharmacology I: Drugs and the Heart I Flashcards

1
Q

What are the FOUR major components of Cardiomyocyte cells?

A
  1. Sarcolema
  2. T-tubules
  3. Sarcoplasmic Reticulum
  4. Myofibrils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the mechanism of action of Cardiomyocyte Contraction?

A
  • Membrane depolarisation - Ca2+ entry through channels
  • Ca2+ release from SR
  • Actin-Myosin contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the FOUR key elements of healthy vascular function?

A
  1. Vascular Tone (vT)
  2. Integrity of the vascular barrier (vB)
  3. Vascular Content (vC)
  4. Blood Flow (BF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is Ischaemic Heart Disease (IHD)?

A

Inadequate supply of oxygenated blood to heart tissue

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

What are some of the characteristics of IHD?

A
  • Narrowing of coronary arteries supplying blood to heart
  • Decreased vessel tone (vT)
  • Decreased integrity (vB)
  • Decreased blood flow (BF)
  • Atherosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Angina?

A

Restricted flow of oxygenated blood to cardiac muscle

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

What is a major symptom of Angina?

A

Chest pain radiating to neck, jaw, back, and arms

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

What causes Stable Angina Pectoris?

A
  • Brought on by exertion: physical, cold, excitement, stress
  • Goes away with rest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes Unstable Angina?

A
  • Transient formation / dissolution of blood clot in artery
  • Severe pain with little exertion, no warning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes Variant (Prinzmetal) Angina?

A
  • Caused by coronary artery spasm
  • Uncommon episodic angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Heart Failure (HF)?

A

Impaired or damaged myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes Heart Failure?

A

CAD -> Myocardial hypoxia -> Tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the effects of HF?

A
  • Inadequate pumping of blood to meet metabolic demand
  • Reduced cardiac output
  • Fluid build up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the symptoms of HF?

A
  • Oedema
  • Tiredness
  • Shortness of breath
  • Cough
  • Swelling of abdomen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the compensatory mechanisms of HF?

A
  • INCREASED sympathetic activity
  • INCREASED RAAS
  • Cardiac remodelling (hypertrophy)

(Compensation leads to progressive heart disease)

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

What type of drugs are most used for the treatment of both angina and HF?

A
  • RAAS inhibitors
  • β blockers
  • Organic nitrates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why is Nitric Oxide (NO) used to treat Ischaemia?

A

Potent vasodilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

TRUE OR FALSE:
Nitric Oxide acts on both veins and arteries equally?

A

False.
Acts on veins, less so on arteries

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

What is the mechanism of action for Organic Nitrites?

A
  • Organic nitrates biotransformed into NO
  • NO activates guanyl cyclase
  • Increase in cGMP
  • Protein kinase activation
  • Light chain myosin dephosphorylated
  • Relaxation of Actin-Myosin
  • Smooth muscle relaxation
  • Vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is PRELOAD?

A

Venous return of blood volume
* causes filling pressure on heart (muscle stretching)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is AFTERLOAD?

A

Vascular resistance the ventricles must overcome to push blood into arteries

22
Q

What is the vasodilatory effect of Organic Nitrates on Veins?

A
  • Dilation of veins
  • Reduces venous blood pressure and workload on the heart (PRELOAD)
23
Q

What is the vasodilatory effect of Organic Nitrates on Arteries?

A
  • Dilation of larger arteries
  • Reduced aortic pressure (AFTERLOAD)
  • Increases flow of oxygenated blood to heart
24
Q

How does decreased Preload and Afterload help the heart?

A

Decreased preload & afterload reduces workload on the heart and myocardial O2 demand

25
Q

Why is Glyceryl Trinitrate NOT given orally?

A
  • Extensive first-pass hepatic metabolism
  • Short plasma half-life (minutes)
26
Q

Why is Glyceryl Trinitrate given sublingually?

A
  • Rapidly absorbed into systemic circulation
  • Rapidly metabolised (EXTRAHEPATIC HYDROLYSIS)
  • Rapidly cleared
  • Renal secretion - GTN metabolites
27
Q

Which type of Voltage Gated Ca2+ Channel is important in cardiac & VSMC?

A

L-type

28
Q

Which subunit is pore-forming on L-VGCCs?

A

α1 subunit

29
Q

Which L-type Calcium Channel Blocker (CCB) drugs is selective to blood vessels?

A

Dihydropyridines

30
Q

How do Dihydropyridines work?

A
  • Vasodilatory
  • Decrease arterial VSMC contraction
31
Q

What is the mechanism of action of RAAS Inhibitors?

A
  • ACE inhibitors REDUCE Angiotensin II
  • ARBs inhibitors BLOCK AT 1-R binding to Angiotensin II
  • Aldosterone antagonists BLOCK ALD-R binding to Aldosterone
32
Q

What is the effect of reducing Angiotensin II?

A

Decreased VSMC constriction in arterioles (vasodilatory)
* SVR & BP reduced

33
Q

What are the effects of reducing Angiotensin II AND Aldosterone?

A
  • Decrease renal Na+ and water reabsorption - reduced blood volume & BP
  • Decrease cardiac remodelling (hypertrophy)
  • Decrease RAAS-induced sympathetic activity - reduced HR, contractility, renin
34
Q

What are TWO examples of ACE Inhibitors?

A
  1. Ramipril
  2. Captopril
35
Q

What are TWO examples of ARBs Inhibitors?

A
  1. Valsartan
  2. Losartan
36
Q

What is an example of an Aldosterone Antagonist?

A

Spironolactone

37
Q

What is the rationale for use of RAAS Inhibitors to treat Heart Failure and Angina?

A
38
Q

What subtype of adrenoceptors are found in heart tissue?

A

Mainly β1
* increase HR and cardiomyocyte contraction

39
Q

What subtype of adrenoceptors are found in vascular smooth muscle cell (VSMC) tissue?

A

β2
* stimulate VSMC relaxation

40
Q

Which type of adrenoceptor blocking drugs are used to treat Angina?

A
  • 1st generation: Non-selective β blockers
  • Act at both β1 and β2 adrenoceptors
41
Q

Which type of adrenoceptor blocking drugs are used to treat Heart Failure?

A
  • 2nd generation: Cardio Selective β1 blockers
  • Greater selectivity for β1 over β2 adrenoceptors
42
Q

What is an example of a 1st Generation: Non-Selective β blocker drug?

A

Propanolol

43
Q

What are TWO examples of 2nd Generation: Cardio Selective β1 blocker drugs?

A
  • Metoprolol
  • Bisoprolol
44
Q

Which neurotransmitter do 2nd Generation: Cardio Selective β1 blocker drugs block the binding of?

A

NA

45
Q

What is the mechanism of action of Non-Selective β blocker drugs?

A
  • DECREASES negative regulation
  • Active MLCK
  • INCREASE in VSMC contraction
  • Vasoconstriction
  • Increase of hypertension (BP)
46
Q

What is the rationale for the use of Selective β blocker drugs to treat Heart Failure and Angina?

A
47
Q

What are TWO Positive Inotrope drugs used in the treatment of chronic heart failure?

A
  • Cardiac glycoside
  • β-agonist
48
Q

What Cardiac glycoside drug is used in the treatment of chronic heart failure, and what does it do?

A

Digoxin
* Increases cellular Ca2+ concentration
* Increases contractility

49
Q

What β-agonist drug is used in the treatment of chronic heart failure, and what does it do?

A

Dobutamine
* Increase sympathetic activity on heart
* Increase heart rate
* Increase myocardial contractility

50
Q

What is the mechanism of action of Digoxin?

A
  • Inhibition of Na+/K+ ATPase
  • Increase levels of cellular Na+
  • Slows inward Na+ in exchange for outward Ca2+ (Increasing cellular Ca2+)
  • Increases actin-myosin contraction

PT3001: Introduction to Pharmacology (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions