W2: Hypertension Flashcards

PBL 2 Drugs Vascular changes

1
Q

What are the 3 layers of blood vessels and describe them briefly

A

Tunic Externa: layer of loose, thick connective tissue which has elastic and collagen fibres. It has a supporting function.

Tunica media:
(External elastic lamina: provides recoil to arteries)
circular layer of Smooth Muscle: controls vessel diameter

Tunica intima:
(internal elastic lamina - only in larger arteries)
lamina propria
basement membrane
Endothelial cell: flattened, thin layer which allows blood to flow smoothly.

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2
Q

what are 2 important functional properties of arteries ?

A

Their elasticity and contractility - comes from elastic tissue

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3
Q

What are the 3 types of arteries? give examples

A

Elastic arteries: large and bendy, they propel high pressure blood out of the heart. e.g. aorta, common carotid, common iliac, subclavian

Muscular arteries: are less bendy (less elastic fibres and more smooth muscle), Smooth muscle allows them to contract to maintain blood pressure further away from the heart. They are distributing arteries since they repeatedly branch. e.g. radial, ulnar, , femoral, axillary.

Arterioles: resistance vessels which branch not capillaries

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4
Q

Describe some differences between veins and arteries?

A

Arteries: thickest layer is the tunica media, small lumens

Veins: thickest layer is tunica adventitia, large lumens

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5
Q

What is the cell type found in endothelium?

A

Simple squamous

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6
Q

What do large veins usually have?

A

Valves to prevent back flow of blood

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7
Q

Define blood pressure

A

The hydrostatic pressure of blood exerted against the walls of a blood vessel or heart chamber.

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8
Q

What is systolic blood pressure?

A

The maximum arterial pressure resulting from the ejection of blood during ventricular contraction.

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9
Q

What is Diastolic pressure?

A

Arterial blood pressure during ventricular relaxation

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10
Q

What is the calculation for Mean Arterial Pressure?

A

MAP = Diastolic BP + 1/3 Pulse Pressure

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11
Q

What is the calculation for pulse pressure?

A

PP = systolic - diastolic

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12
Q

Define MAP

A

MAP = average pressure in arteries during one cardiac cycle

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13
Q

Describe haemodynamic factors affecting blood pressure

A

Cardiac Output

Total peripheral resistance:
Blood vessel diameter (smaller the lumen, the greater the resistance)
Blood vessel length (longer the vessel, the greater the resistance)
blood viscosity
Compliance (stretchiness) of blood vessel
Pressure gradient

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14
Q

Describe the neurohormonal factors that affect blood flow?

A

Autonomic nervous system:
When sympathetic activity is increased, this increases release of noradrenaline. This induces vasoconstriction of blood vessels and increases HR and BP. Parasympathetic activity is inhibited.

Hormonal control: renin-angiotensin-aldosterone system
E.g. if blood pressure is low:
Beta 2 receptors on Juxtaglomerular cells respond to sympathetic nerve stimulation.
They increase Renin secretion in the kidneys which is involved in the conversion of angiotensinogen (produced by the liver) to angiotensin I.
Angiotensin convening enzyme (ACE) which is found in vascular endothelium converts angiotensin I to angiotensin II.

AII has very important functions:
Increases sympathetic activity

Increases tubular Na and Cl reabsorption and H20 retention to increase blood volume and therefore BP.

Increases aldosterone secretion from the adrenal gland
which stimulates tubular Na and H20 reabsorption.

Increases arteriole vasoconstriction to increase BP.

Increases ADH secretion from the pituitary gland which increases water reabsorption from the collecting duct.

If the blood pressure is HIGH:
Atrial-natriuretic peptides: are released form the right atrium. They induce vasodilation and promote Na and water excretion which lowers blood volume and therefore BP.

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15
Q

Define hypertension

A

Hypertension is a long term medical condition in which arterial blood pressure is persistently elevated

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16
Q

describe the stages of hypertension

A

Normal BP range: 90-119 / 60-79
Prehypertension 120-139 / 80-89
Stage 1: 140-159 / 90-99
Stage 2: >160 / >100

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17
Q

Describe the 2 types of hypertension and their causes

A

Primary (95% of cases):
no direct cause but closely linked with poor lifestyle choices e.g. lack of exercise, alcohol, high salt diet, obesity

Secondary: (5% fo cases)
usually due to an underlying condition e.g. 
endocrine issues (Cushing's disease)
Renal parenchymal disease
Renal artery stenosis 
Drugs e.e.g NSAIDs
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18
Q

What are the effects of hypertension on the body?

A

Increased CO
Increased sympathetic activity, particularly in kidneys
increased renin release, angiotensin II, aldosterone etc.

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19
Q

What are the severe consequences of hypertension?

A

Damages endothelial cells

Increases risk of:
Atherosclerosis 
Stroke
Cerebral haemorrhage
Heart failure 
Myocardial infarction 
Renal failure 
Retinopathy 

Heart disease
 Peripheral artery disease
 Vascular dementia
 Premature death

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20
Q

Describe the responses to changes in posture

A

When someone goes form supine (lying down) to standing position, the effects of gravity cause venous pooling in the vessels below the heart. This increase venous pressure and, to compensate, the veins dilate and the CO, SV and cardiac filling is reduced.

This hypotension is only transient as the baroreceptor reflex detects the change in pressure.

The baroreceptors decrease their firing rate in response to the low blood volume.. This increases sympathetic activity and the HR increases.
Peripheral vasoconstriction increases TPR which helps restore blood pressure.

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21
Q

Define and describe postural hypotension

A

Postural hypotension is a condition where a person’s blood pressure drops abnormally when they stand up form lying down/sitting.

It occurs use to the fair of the baroreceptor reflex and is defined by a decrease in systolic blood pressure of > 15 mmHg

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22
Q

What drug can cause postural hypotension?

A

Alpha adrenoreceptor blocker drugs affect the baroreceptor reflex. They inhibit vasoconstriction which is usually initiated by the baroreceptor reflex upon postural hypotension change.

23
Q

What is rational prescribing?

A

Principles of Drug selection

24
Q

What are causes of poor drug compliance?

A
Poor eyesight
Culture and personal beliefs
Large number of tablets
Side effects
Forgetfulness 
Patients Lack information about the disease
25
Q

Consequences of poor drug compliance?

A
  • Reduction in cost effectiveness of medical care
  • Reduced quality of life
  • Effect on health and well-being – worsening of condition
  • Increased risk of morbidity
  • Excess hospital admissions
  • More likely to be placed in nursing home
26
Q

What are the risk factors of hypertension?

A
Smoking
Obesity
Diet (salt)
Genetic factors
Exercise 

SODGE

27
Q

List the antihypertensive drugs

A
ACE inhibitor 
Angiotensin II receptor inhibitor 
Alpha Adrenoreceptor blocker
Beta adrenoreceptor blocker
Calcium channel blockers 
Diuretics
28
Q

For Alpha Adrenoreceptor blockers: give 2 examples, mechanism of action and its side effects

A

e.g. phentolamine (a1 and a2) doxazosin (a1 selective)
Effect:
• Reduce BP by lowering sympathetic tone in arterioles
• Reduce peripheral resistance

Side effects:
• Postural hypotension (loss of sympathetic vasoconstriction)
• Reflex tachycardia (as BP drops, detected by baroreceptors = abnormally fast HR)
• Increased closure of internal sphincter of bladder which can cause Benign Prostatic Hyperplasia

29
Q

For Beta Adrenoreceptor blockers: give 2 examples, mechanism of action and its side effects

A

e.g. propranolol and atenolol

Effect:
Reduces sympathetic tone in heart and renin release from kidneys
This decreases HR, CV and CO

Side effects: HIVE
Hypoglycaemia
Intolerance to exercise 
Vivid dreams
Exacerbates asthma
30
Q

Where is ACE usually found?

A

On vascular endothelium , particular on lungs

31
Q

what are beta and alpha receptor blocker described as?

A

Competitive reversible antagonists

32
Q

For ACE inhibitors: give 2 examples, mechanism of action and its side effects

A

e.g. captiprol and enalapril

Mechanism: Reduce production of angiotensin II so decreased renal reabsorption so lower blood volume. Decreased aldosterone and ADH secretion, sympathetic tone and arterial vasoconstriction.

Side effects:
Persistent irritant cough (due to reduced breakdown of bradykinin, a peptide that activates sensory nerves in lung tissue )
Sudden drop in BP after first dose

33
Q

For Angiotensin II receptor blockers: give 2 examples, mechanism of action and its side effects

A

e.g. losartan and candesartan
Blocks At2 receptor so reduces vasoconstriction and decreased blood pressure.

Side effects:
better than ACE inhibitors as no persistent, irritant cough
But they are more expensive so only used if ACE inhibitors don’t work

34
Q

What are the differences between the two ATII receptors?

A

AT1 receptor: mediates vasoconstriction and aldosterone releasing effects

AT2 receptor: mediates vasodilation (DON’T WANT TO BLOCK)

35
Q

For diuretics: give AN example, mechanism of action and its side effects

A

e.g. bendroflumethiazide
Decreases blood volume by decreasing renal reabsorption of Na and H2O. Also vasodilator so reduces peripheral resistance.

Side effects:
Lowers plasma K levels so need to take K supplements

36
Q

For Calcium Channel blockers: give AN example, mechanism of action and its side effects

A

e.g. diltiazem, verapamil and nifedipine

Mechanism:

a) Open channel block - cork in the bottle = directly goes into channel and blocks e.g. verapamil and diltiazem work this way
b) Allosteric modulation - binds to another site on the calcium channel and reduces channel opening. e.g. nifedipine

Effect:
blocking calcium entry in vascular smooth muscle: reduces vasoconstriction so = vasodilation
Blocking calcium entry in cardiac muscle: reduces contraction, HR and SV so = reduces CO

Side effects:
Headache
Constipation
Cardiac dysrhythmias

37
Q

What are the NICE guidelines for prescribing anti-hypertensive drugs?

A

If person is aged under 55 years: ACE inhibitor or low-cost Angiotensin II receptor blocker

If person is aged above 55 OR of African/Caribbean origin of any age: Calcium Channel blocker

Next step: Combine

Next step: add a thiazide-like diuretic

Next step: consider adding another diuretic OR alpha blocker OR beta blocker

Seek expert advice

38
Q

Which sex is usually more prone to hypertension and why?

When does this answer change?

A

Males are more likely to have hypertension as females releases oestrogen which is a vasodilator and keeps blood pressure low.

After menopause, oestrogen levels decrease and women become more hypertensive than men.

39
Q

What are the gross structural changes that occur in the vascular wall as a result of hypertension?

A
  • Thickening of tunica media
  • Increased wall to lumen ratio (media gets thicker and lumen gets smaller which contributes to TPR)
  • Lengthening of small arteries
40
Q

What is Pulse Wave Velocity?

A

The velocity at which blood pressure pulse propagates through the circulatory system

41
Q

How does hypertension change the PWV?

A

Increases the PWV. As arteries reduce their compliance and stiffen, this means that pressure waves are not reduced by their stretch.

42
Q

What’s the difference between inward and outward normal remodelling?

A

Inward has a smaller lumen and outward has a larger lumen

43
Q

What’s the difference between hypertrophic and hypotrophic remodelling?

A

Hypertrophic has more growth in the vessel wall compared to hypotrophic

44
Q

What type of vessel remodelling is likely in patients with hypertension?

A

Eutrophic/hypertrophic inward remodelling

45
Q

How effective are different hypertensive drugs at restoring vascular structural changes?

A

Beta Blocker: not effective
ACE inhibitor: slightly helps to improve the media-lumen ratio
Angiotensin II receptor blocker: slightly helps to improve the media-lumen ratio
Renin inhibitor: improves the Media to Lumen Ratio

46
Q

How does hypertension affect the fenestrae in endothelium ?

A

The inner surface of the internal elastic lamina has fenestrae which are small holes that are the only way endothelial cells can communicate with the smooth muscle that lies in tunica media.

Endothelial cells allow flow mediated vasodilation. The action of blood against the endothelial cells triggers the formation of Nitric Oxide which is an important vasodilator. it goes through the fenestrae and relaxes the smooth muscle.

Hypertension causes changes in the diameter and number of small holes. This reduces the contact point so smooth muscle doesn’t relax as much and there is less vasodilation.

47
Q

What hypertensive therapy can normalise flow mediated vasodilation?

A

ACE inhibitors

48
Q

What is the effect of angiotensin II on vascular structure?

A

In hypertension, there is more AGT II in blood plasma so more vasoconstriction. AGT II also has mitogenic effects which stimulates smooth muscle growth and MMPs. This causes vascular structural changes.

49
Q

What increases formation of tissue fluid (oedema) ?

A

Increased permeability of capillary wall

Dilatation on arterioles with a constant Mean Arterial Pressure.

50
Q

Where is ADH synthesised and released from?

A

Synthesised in Hypothalamus and released from posterior pituitary gland

51
Q

What is the relationship of “resistance to flow” to vessel length, viscosity and radius?

A

Directly proportional to viscosity and blood vessel length.

Indirectly proportional to radius

52
Q

What effects does high blood pressure have on Potassium levels?

A

Decrease in potassium (hypokalaemia)

53
Q

What effect does vasodilation have on capillary pressure and interstitial fluid?

A

Vasodilation increases capillary pressure and interstitial fluid formation.