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Cardio > Cardio L26 Drug therapy 3 > Flashcards

Cardio L26 Drug therapy 3 Flashcards

1
Q

Angina definition

A

A condition marked by severe chest pain, often also spreading to the shoulders, arms and neck, caused by an inadequate blood supply to the heart.

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2
Q

Clinical definition of angina

A

Angina is chest pain or discomfort that occurs when an area of your heart muscle doesn’t get enough oxygen-rich blood.

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3
Q

Angina pectoris

A

Pain localized to the chest that can be abrupt (acute) or persistent (chromic)

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4
Q

Causes of angina pectoris

A

Decreasing o2 supply
Increase Cardiac work = o2 consumptions increased
→ Lack of supply and build up of metabolites leads to ischemic pain.

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5
Q

Common Causes of Angina Pectoris

A
  1. Restriction (usually incomplete) in blood supply to working heart muscle.
→ Partial occlusion of blood vessels
Atheroma
Thrombus
→Vasopasm in coronary arteries
Overly reactive vessels
Drugs e.g. cocaine, smoking
→ Severe anaemia
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6
Q

Types pf angina pectoris

A
  1. Chromic stable angina (exercise induced)
  2. Unstable angina (sudden rupture of atherosclerotic plaque)
  3. Prinzmetals (angina inversa)
    • Vasospasm due to oversensitivity to vasoconstrictors
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7
Q

Atheroma process

A

→Damage to endothelium
→ Cholesterol accumulation
→ Monocyte invasion
→ Foam cell degeneration

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8
Q

Foam cell degeneration

A
  • Fibrous tissue, calcium salts
  • Artery narrows
  • Increasing stiffness at margin
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9
Q

Monocyte invasion

A
  • Convert to macrophages

* Convert to foam cells

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10
Q

Cholesterol accumulation

A
  • Oxidation

* Inflammatory response

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11
Q

Damage to endothelium

A

• Exposes intima matrix above smooth muscle layer

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12
Q

Prevent atherosclerosis

A
  1. Statins
  2. Fibrates
  3. Bile acid binding resins
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13
Q

Angina control

A

Nitrates
Beta-blockers
Ca2+ channel blockers
(Aspirin)

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14
Q

Treatment – possibly after first

MI

A
  1. Ranolazine, aspirin

2. Bypass surgery, stents, angioplasty, clot disrupting drugs (enzymes)

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15
Q

Process of cholesterol formation

A

3-Hydroxy-3- methyl-glutaryl-CoA reductase is the rate-controlling enzyme of the mevalonate pathway, which produces cholesterol and other isoprenoids.

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16
Q

Lovastin and Atorvastatin action

A

Inhibit 3-Hydroxy-3- methyl-glutaryl-CoA reductase leading to:

a. Decreased liver cholesterol synthesis
b. Increased VLDL and LDL receptor expression, and decreasing LDL in blood

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17
Q

Side effects: HMG CoA reductase inhibitors:

A

a. Myalgias
b. Muscle cramps
c. Rhabdomyolysis (leading to kidney failure)
d. GI tract disturbances
e. Malabsorption of lipid soluble vitamins (A,D,E,K) and lipid soluble drug

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18
Q

Fibrates: definition

A

Fibrates are amphiphatic carboxylic acids.

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19
Q

Fibrates: Example drugs

A

Bezafibrate

Ciprofibrate

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20
Q

Agonists of the peroxisome proliferator-activated receptor alpha (PPAR – alpha) receptor leads to:

A
  1. Increased Beta-pxidation in the liver
  2. Decreased hepatic triglyceride secretion
  3. Increased lipoprotein lipase activity → increased VLDL clearance
  4. Increased HDL
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21
Q

Main use of fibrates

A

Hypercholesterolemia

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22
Q

Side effects of fibrates

A
  1. Mild stomach upset and myopathy (muscle pain with CPK elevations)
  2. Increased risk for gallstones due to increased cholesterol in bile.
  3. Increased risk of rhabdomyolysis – especially if added to statins.
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23
Q

Bile acid recycling

A

Between intestine and liver

24
Q

What binds bile acid

A

Cholestipol and Cholestyramine in gut leading to increased loss.

25
Q

Cholestipol and Cholestyramine binding leads to:

A
  1. Decreased enterohepatic recirculation of bile salts
  2. Increased synthesis of new bile salts by the liver
  3. Decreased liver cholesterol
  4. Increased LDL receptor expression, and decreasing LDL in blood
26
Q

Side effects of bile acid binding agents

A
  1. Increased in VDLD and triaylglycerides synthesis
  2. GIT disturbances
  3. Malabsorption of lipid soluble vitamins (A,D,E,K) and lipid soluble drugs
27
Q

Nitric oxide is

A

Endothelium-derived relaxing factor

28
Q

What increases NO production

A

Organic nitrates

29
Q

Function of nirtrates

A 
Venous vasodilation/pre-load reduction
Arterial dilation/ after-load reduction
Coronary artery vasodilation
Prevention of coronary vasoconstriction
Enhancement of coronary collateral flow
Antiplatelet and antithrombotic effects
30
Q

Nitrates action

A

All increase NO (EDRF)

31
Q

Types of nitrates

A
  1. Nitroglycerin sI (fast acting)
  2. Isosorbide mononitrate
  3. Isosorbide dinitrate
  4. Transdermal patches (long acting)
  5. Alkyl Nitrates (Poppers)
32
Q

nitrates Side effects

A 
Headaches
Flushing
Palpitations
Tolerance
Major interaction with drugs for impotence (Viagra etc.) leading to hypotensive crisis
33
Q

Nitrates are metabolites to

A

To increase NO

34
Q

NO is

A

EDRF

35
Q

NO stimulates

A

Guanylate cyclase

36
Q

Gaunylate cyclase synthesizes

A

cyclic guanosine monophosphate (cGMP)

37
Q

cGMP activates

A

cCGMP – dependent protein kinase

38
Q

cGMPdK activates

A

Myosin light chain phosphate (s) (MLCP)

39
Q

Myosin light chains in smooth muscle cells are

A

Dephosphorylated

40
Q

The contractile state of smooth muscle depends

A

On phosphorylation if the myosin light chains (calmodulin – dependent kinase phosphorylate)

41
Q

Beta-Blockers: Function

A

Reduce myocardial Oxygen demand

42
Q

Beta-Blockers: Used for

A

First line therapy in the treatment of chronic stable angina (esp, effort-induced angina)

43
Q

Beta-Blockers: Examples

A
  1. Propanolol → non-selective Beta1, Beta2 (not in asthma)
  2. Atenolol →metroprolo more Beta1 – selective
  3. Carvedilol → also block alpha-receptors improving coronary perfusion
44
Q

Beta-Blockers: Side effects

A 
Constipation, indigestion
Hypotension
Sleep disturbance, hallucinations (rare)
Reduce aqueous humour secretion →glaucoma
Skin reactions e.g. hives, psorias
45
Q

Calcium channel blockers: Calcium entry

A

Entry into SM depends on activity of voltage dependent Ca2+ channels (mainly L-type VDCC)

46
Q

Main classes of L-type VDCC antagonists are:

A
  1. Dihyropyridines e.g. Nifedipine (all dipines)
  2. Phenylakyllamines e.g. verapamil
  3. Benzothiazepines e.g. Diltiazem (also non-selective VDCC blockers e.g. Fluspiriline)
47
Q

Side effects calcium channel blockers

A
  1. Peripheral vasodilation: Dizziness, headache, erythema
  2. Constipation
  3. Heart rate changes
  4. Gingival overgrowth
48
Q

calcium channel blockers Reason for use

A

To reduce myocardial oxygen demand and reverse coronary vasospasm.

49
Q

calcium channel blockers Don’t want

A

Reflex sympathetic activation due to peripheral effects.

50
Q

Verapamil

A

Selective for myocardium

→ Hence minimal peripheral vasodilatory effects (compared with dihydropyridines

51
Q

Benzothiazepine calcium channel blocker are

A

Intermediate between phenylalkylamine and dihydropyridines in their selectivity for vascular calcium channels.

→ Cardiac depressant and vasodilator actions
→ Reduce arterial pressure without producing as much reflex cardiac stimulation cause by dihydropyridines

52
Q

Clopidegrel

A

A prodrug, and blocks an ADP receptor on platelet cell membranes.

53
Q

Antiplatelet drugs: Action

A
  • Blockage of this receptor inhibits platelet aggregation by blocking activation of the glycoprotein IIb/IIIa pathway and formation of IIb/IIIa complex.
  • The Iib/ IIIa complex is a receptor mainly for fibrinogen and vitronectin but also for fibronectin and von Willebrand factor.
  • By blocking croos-linking of platelets by fibrin help prevent clot formation
54
Q

Antiplatelet drugs: Side effects

A

Haemorrhage
Severe neutropenia
Thrombotic thrombocytopenic purpura (paradoxical)

55
Q

Ranolazine blocks

A

Late Na+- entry reducing cardiac dysfunction following ischemia.

  1. Increases QT interval
  2. Decreases angina episodes in individuals with coronary artery disease on maximal doses of amlodipine and exercise tolerance in those taking atenolol, amlodipine or diltiazem.
56
Q

Ranolazine side effects

A

Worsen electrical dysfunction in long QT syndrome → risk of sudden cardiac death

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