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Biomedical Pharmacology > Lecture 12 - Cardiovascular Pharmacology > Flashcards

Lecture 12 - Cardiovascular Pharmacology Flashcards

1
Q

What is hypertension?

A

Elevated blood pressure

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2
Q

What is the blood pressure of a healthy person?

A

120/80

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3
Q

Why does blood pressure increase with age?

A

Lifestyle effects
Natural aging process
Hardening of arteries (less distensible)

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4
Q

What is blood pressure controlled by?

A

Integrated system P

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5
Q

What are the primary contributors of blood pressure?

A

Cardiac output
Stroke volume
Heart rate
Total peripheral resistance

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6
Q

What can each of the factors that contribute to blood pressure be manipulated by?

A

Drug therapy

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7
Q

What happens when blood pressure goes down?

A

The sympathetic vasomotor centre activity increases in the brain due to activation of baroreceptors

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8
Q

What elevates blood pressure?

A

Cardiac stimulation
Activation of sympathetic nervous system
Venous constriction
Increasing venous rerun
Increase preload and force of contractility

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9
Q

How does cardiac stimulation increase cardiac output?

A

In terms of heart rate and force of contraction

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10
Q

What happens when blood pressure decreases?

A

Cause renin release

Due to reduced blood flow through juxtaglonerular apparatus

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11
Q

What are the effects of Angiotensin II?

A 
Venous constriction (elevate venous return)
Arterial constriction 
Knock on effect of aldosterone
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12
Q

What are the processes that bring BP down?

A

Arterial constriction
Increase in sympathetic vasomotor centre activity
Renin release
Venous constriction

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13
Q

What is the vasomotor centre?

A

Influences sympathetic outflow
Alpha 2 adrenoceptor agonist
Presynaptic modulation of neurotransmitter release

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14
Q

What does the sympathetic nerve terminal release?

A

Noradrenaline

Influences postsynaptic receptors

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15
Q

Where are alpha 2 adrenoceptor located?

A

Sympathetic nerve terminal

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16
Q

What happens when alpha 2 adrenoceptor is stimulated?

A

Negative effect mediated via influence on ca2+ channel opening
Decreases continued release of noradrenaline

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17
Q

What is Beta receptor antagonist (blockers)?

A

Direct effect on the heart (Beta 1 receptors)

Reduce contractility of the heart (reduce cardiac output - reduce BP)

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18
Q

What is vascular smooth muscle?

A

Vasodilators
Ca2+ channel antagonist
Angina and treatment of hypertension
Some diuretics - some vasodilatory effect

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19
Q

What is AT1 receptors?

A

Block synthesis of Angiotensin II or blocking the receptors itself

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20
Q

What is the effect of ACE inhibitors?

A

Influence adrenal cortex

Reduce effect of Angiotensin II

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21
Q

In the kidney, what does diuretics have an effect in?

A

Reducing overall circulating blood volume

Reduce blood pressure

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22
Q

What is the therapeutic approaches to treatment of hypertension?

A 
Vasomotor centre 
Sympathetic nerve terminals
Beta-adrenoceptors on heart 
Sympathetic Ganglia 
Angiotensin receptors on vessels 
Alpha-adrenoceptors on vessels
Vascular smooth muscle 
Adrenal cortex 
Kidney tubules 
Juxtaglomerular cells that release renin
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23
Q

Vasomotor centre

A

Alpha 2- Adrenoceptor agonists

Imidazoline receptor agonist

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24
Q

Sympathetic nerve terminals

A

Adrenergic neuron Antagonist

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25
Q

Beta-adrenoceptors on heart

A

B-adrenoceptor Antagonist

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26
Q

Sympathetic Ganglia

A

Ganglion blockers

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27
Q

Angiotensin receptors on vessels

A

ACE inhibitors

AT1 receptor antagonist

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28
Q

Alpha- Adrenoceptor on vessels

A

Alpha 1 Antagonist

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29
Q

Vascular smooth muscle

A 
Diuretics 
Vasodilators 
Nitrovasodilafors 
Calcium channel Antagonist 
Potassium channel openerds
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30
Q

Adrenal cortex

A

ACE Inhibitors of Angiotensin II formation

AT1 receptor antagonist

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31
Q

Kidney tubules

A

Diuretics

ACE inhibitors

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32
Q

Juxtaglomerular cells that release renin

A

B-Adrenoceptor Antagonist

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33
Q

B-adrenoceptor Antagonist

A

Pindolol
Atenolol
Propranolol

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34
Q

What is B-adrenoceptor Antagonist most important actions

A

B1 receptor blockade
Decreased heart rate and cardiac output
Reduced renin secretion

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35
Q

What is adrenoceptor Antagonist aided by?

A

Vasodilation of blood vessels supplying skeletal muscle

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36
Q

What happens when Beta receptors are stimulated?

A

Vascular muscle relaxation

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37
Q

What does some of Beta adrenoceptor agonist have?

A

Partial antagonist and partial agonist activity

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38
Q

What is pindolol?

A

Used for hypertension

Beta 1 Antagonist and Beta 2 partial agonist

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39
Q

What are some examples of alpha-adrenoceptor Antagonist?

A

Prazosin
Doxazosin
Phenoxybenzamine

40
Q

What is alpha-adrenoceptor Antagonist?

A

Involves the reduction of arteriolar resistance
By reducing sympathetic input
Mediated by alpha 1 receptors

41
Q

What is the result of stimulating alpha 1 receptors?

A

Contract smooth muscle

42
Q

What is the result of blocking alpha 1 receptors?

A

Relaxation

Dilation of venous capacitance vessels

43
Q

What happens at rest of alpha-adrenoceptor antagonist?

A

Ongoing sympathetic tone

Governing the overall diameter of blood vessels

44
Q

What is the problem of alpha-adrenoceptor Antagonist?

A

Induce a reflex tachycardia
Marked with non-selective compounds
Can increase HDL

45
Q

What is prazosin?

A

Short acting

46
Q

What is doxazosin?

A

Long acting

47
Q

What are the side effects related to the relaxtory effect upon smooth muscle (alpha-adrenoceptor Antagonist)

A

Postural hypotension (venous pooling)
Legarthy (drowsy and dull)
Palpitations

48
Q

What are ACE inhibitors?

A

Reduce circulatory level of Angiotensin II

Block conversion from Angiotensin

49
Q

What are examples of ACE inhibitors?

A

Captopril

Enalapril

50
Q

What are the therapeutic effect of ACE inhibitors?

A

Hypotensive effect without reflex tachycardia (through relaxation of smooth muscle)
Reduced aldosterone release
Reversal of left ventricular hypertrophy
Prevention of vascular changes by inhibition of cellular growth
Reduced degradation of vasodilator kin in

51
Q

What does Kinin have and is responsible for?

A

Vasodilatory effect

Responsible for inhibiting cough

52
Q

What is Angiotensin receptor antagonist?

A

Block what Angiotensin II does at relevant receptor

AT1 receptor seen in vascular smooth muscles

53
Q

What are examples for Angiotensin receptor antagonist?

A

Losartan

Valsartan

54
Q

What are the side effects of Angiotensin receptor antagonist?

A

Headache

Legarthy

55
Q

What is ACE inhibitor

A

Enalapril

56
Q

What is Angiotensin inhibitor?

A

Valsartan

57
Q

What are examples of directly acting vasodilators?

A

Calcium channel antagonist

Potassium channel activators

58
Q

What does minoxidil lead to?

A

Hair growth

59
Q

What are side effects of directly acting vasodilators?

A 
Flushing and headache 
Reflex tachycardia 
Palpitations 
Salt and water retention 
Hirsutism (abnormal growth of hair on a woman’s face and body)
60
Q

What is Hydralazine?

A

Produces relaxation

61
Q

What are the side effects of Hydralazine?

A

Side effects include reflex sympathetic activation and SLE like syndrome

62
Q

When is borderline hypertension more likely to be treated?

A

If patient has renal impairment
Ischaemic heart disease
Diabetes
Previous stroke

63
Q

Young: treatment of hypertension

A

B-adrenoceptor antagonist/ACE inhibitors

64
Q

Elderly: treatment of hypertension

A

Ca2+ channel antagonist

Diuretics

65
Q

What is an example of centrally active hypertensive ?

A

Methyldopa

66
Q

What are the approaches to treating hypertension?

A

Step 1: one/two drug in the young beta-blocker or ACE inhibitor
Step 2: getting no response, look at combining
Step 3: if there is still no response, combine 2-3 compounds
Step 4: look g at putting in another drug

67
Q

What is the best approach to treating hypertension?

A

Single pill combining many different active compounds

68
Q

What is Atherosclerosis?

A

Plaque formation
Plaque rupture
Thrombus formation
Death and disability caused by heart attack

69
Q

How is Atherosclerosis formed?

A

Cholesterol ridge core

70
Q

Where is cholesterol embedded in?

A

Plaque because of removal from circulation

71
Q

Where does plaque protrude as it grows?

A

Lumen of the blood vessels
Reduces diameter of the blood vessel
Reducing BF to one region

72
Q

What happens when cap is eroded and exposed to the core?

A

Aggregation and activation of platelets which adhere to the Atherosclerosis plaque

73
Q

Why is platelet aggregation a problem?

A

Blood clotting mechanism get involved

74
Q

Why is cholesterol important?

A

Constituent of cell membrane

Precursor of many important steroids (bile salt, steroid hormones)

75
Q

Where is cholesterol mainly synthesised?

A

Liver

HMG-CoA reductase

76
Q

Where are LDL taken up by?

A

Liver (receptor mediated l)

Taken up into peripheral tissues (non-receptor mediated)

77
Q

Why are HDL classified as good cholesterol?

A

Promote transport from peripheral tissues to liver
Promote storage of LDL
Removal from circulation

78
Q

What are two pathways by which cholesterol accumulates in the liver?

A

Exogenous pathway

Endogenous pathway

79
Q

Where does cholesterol come from?

A

Diet (direct circulation through portal system)

Or with fatty acids in diet combined with glycerol and cholesterol which are absorbed into bloodstream

80
Q

What does chylomicrons contain?

A

Both cholesterol and triglycerides

81
Q

What are chylomicrons?

A

Lipoprotein lipase which acts upon triglycerides breaking them down into free fatty acids which can be absorbed into peripheral tissue

82
Q

How is cholesterol moved out of the liver?

A

In the form of very low LDL

83
Q

Why is the endogenous pathway favoured?

A

Majority of cholesterol is synthesised from acetyl cOA

84
Q

What is Dyslipidaemia?

A

Condition where lipid processing is disrupted
Inherited disorder - altered synthesis of cholesterol familial hypercholesterolmia
Diseases affecting lipid metabolism

85
Q

What does Frederickson classification define?

A

Six groups based on which lipoprotein is elevated

86
Q

What groups are most at risk of atheroma?

A

Groups IIa and IIb

87
Q

What groups are triglyceride elevated in?

A

Type IIb but not in type 2a

88
Q

When are Statins prescribed?

A

When there is an incidence of increased LDL cholesterol

89
Q

What are examples of statin?

A

Simvastatin
Lovostatin
Pravastatin
Atorvastatin

90
Q

What does station reduce?

A

LDL cholesterol

Risk of death from cardiovascular events

91
Q

Who should statins be considered for?

A

All patients at risk of any cardiovascular disease

92
Q

When are Fibrates used?

A

Where there is an issue with cholesterol and triglycerides

93
Q

What does fibrates have an influence upon?

A

Certain nuclear receptors

94
Q

What is example of nuclear receptor?

A

PPARa
These nuclear receptors will translocate to the nucleus when a relevant agonist binds to them
Alteration in transcription of genetic material

95
Q

What are examples of Fibrates?

A

Bezafibrate
Gemfibrozil
Ciprofibrate

96
Q

What does Bezafibrate have significant effect upon?

A

Genes that code for lipases that can break down Chylomicrons

Biomedical Pharmacology (19 decks)

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