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CARD - 1 > Hypertension - Aetiology, Pathophysiology and Treatment > Flashcards

Hypertension - Aetiology, Pathophysiology and Treatment Flashcards

1
Q

What is the no. 1 cause of preventable mortality/morbidity in the world?

A

Hypertension.
2mmHg rise in BP:
7% increased risk mortality from IHD
10% increased risk mortality from stroke.

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2
Q

Most —-/—— treatment ever reviewed by nice.

A

Cost effective.

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3
Q

What are the end organ damage complications of hypertension?

A

Brain - haemorrhage, stroke, cognitive decline.
Retinopathy
Peripheral vascular disease
Kidney - renal failure, dialysis, transplantation, proteinuria.
Heart - LVH, coronary heart disease, congestive heart failure, MI.

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4
Q

When does BP vary?

A

Physical and mental stress cause it to rise.

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5
Q

Define hypertension.

A

That blood pressure above which the benefits of treatment outweigh the risks in terms of morbidity and mortality.

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6
Q

What is BP distribution like in the population?

A

Exhibits a normal distribution within the population (bell shaped curve).

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7
Q

What did the Framingham study find?

A

Increasing BP is associated with a progressive increase in the risk of stroke and CV disease.
Risk rises exponentially not linearly with pressure. Age plays significant role also.

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8
Q

At what blood pressure is a patient hypertensive?

A

Different guidelines.
BHS 140/90
JNC 140/90 opt <120/<80
WHO-ISH 140/90

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9
Q

What are the NICE definitions for the three stages of hypertension?

A

Stage 1 hypertension - clinical BP is 140/90mmHg +. ABPM daytime average 135/85mmHg +.

Stage 2 hypertension - clinical BP is 160/100mmHg +. ABPM daytime average 150/95mmHg +.

Severe hypertension - clinical systolic BP is 180mmHg or diastolic BP is 110mmHg +.

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10
Q

What is the aetiology in the majority of cases?

A

In 90% cases no cause can be found.

Primary hypertension.

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11
Q

What is the aetiology in the rest of the cases?

A

Secondary hypertension as a result of:

chronic renal disease, renal artery stenosis, endocrine disease, Cushings, Conn’s syndrome, Pheochromocytoma, GRA…

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12
Q

What factors increase risk of morbidity in hypertension?

A 
Smoking (adds 10/20 mmHg)
Diabetes mellitus (5-30x inc MI)
Renal disease
Male (x2)
Hyperlipidaemia
Previous MI/stroke
LVH (x2).
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13
Q

Say the risk factors for CV disease in order of their risk.

A

Low fitness, hypertension, smoking, diabetes, obesity, high cholesterol.

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14
Q

Blood pressure is controlled by an integrated system, what are the prime contributors to blood pressure?

A

CO, HR, SV and peripheral vascular resistance.

All of which can be manipulated by drug therapy.

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15
Q

What is the effect of the sympathetic system on the CV system?

A

Vasoconstriction, reflex tachycardia, increased CO.

Action of sympathetic system are rapid and account for second to second BP control.

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16
Q

Which system is pivotal in long term BP control?

A

The Renin-Angiotensin-Aldosterone system.

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17
Q

What is the RAAS responsible for?

A

Maintenance of sodium balance

Control of BP and blood volume.

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18
Q

What is the RAAS stimulated by?

A

Fall in BP
Fall in circulating volume
Sodium depletion.

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19
Q

Where is renin released from?

A

Juxtaglomerular apparatus.

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20
Q

What does renin do?

A

Converts angiotensinogen to angiotensin I.

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21
Q

What converts angiotensin I into angiotensin II?

A

Angiotensin converting enzyme (ACE).

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22
Q

What is the role of angiotensin II?

A

It is a potent vasoconstrictor, anti-natriuretic peptide, stimulator of aldosterone release from adrenal glands.
Also a potent hypertrophic agent which stimulates myocyte and smooth muscle hypertrophy in the arterioles.

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23
Q

What is aldosterone?

A

A potent anti-natriuretic and antidiuretic peptide.

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24
Q

What are poor prognostic indicators in hypertensive patients?

A

Myocyte and smooth muscle hypertrophy.

Partially explains why hypertension and risks of hypertension persist in some patients despite treatment.

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25
Q

So what are the two main systems you want to target in hypertension treatment?

A

Sympathetic and RAAS.

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26
Q

What is the aetiology of hypertension?

A

Polygenic - major genes, poly genes.

Polyfactorial - environmental, individual and shared.

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27
Q

What are the two most likely causes of hypertension?

A

Increased reactivity of resistance vessels –> increase in peripheral resistance (as a result of a hereditary defect of smooth muscle lining arterioles).

A sodium homeostatic effect - in essential hypertension, kidneys unable to excrete right amount of sodium, so sodium and fluid retained –> BP increases.

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28
Q

What are some other factors that involved in the aetiology of hypertension?

A

Age, genetics, family history, environment, weight, alcohol intake, race.

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29
Q

BP tends to rise with age, why is this?

A

Possibly as a result of decreased arterial compliance.

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30
Q

How should hypertension be treated in the elderly?

A

Aggressively, they have more to lose. But must be pragmatic.

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31
Q

Discuss how genetics affect the risk of getting hypertension.

A

A history of hypertension tends to run in family. Closest correlation between sibs rather than parent and child. Possible that environmental factors common have a role.

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32
Q

How many genes are recognised as important in the development of hypertension?

A

> 30 genes, but individually they account for at most 0.5mmHg each.

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33
Q

What environmental things can cause hypertension?

A

Mental/physical stress (removing stress doesn’t necessarily return BP to normal).

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34
Q

How can salt intake and diet affect hypertension?

A

Strong relationship between hypertension, stroke and salt intake. Reducing salt intake in hypertensive individuals does lower BP. However reducing salt in normotensives appears to have little effect.

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35
Q

What is the relationship between alcohol and hypertension?

A

One of the commonest causes of hypertension in the young scot. Affects 1% population. Small amounts of alcohol tend to decrease BP, large amounts tend to increase BP. If alcohol is reduced BP will fall over several days to weeks. Average fall is 5/3mmHg.

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36
Q

Obese patients have a lower/higher BP.

A

Higher.

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37
Q

What percentage of hypertension is attributable in part or wholly to obesity?

A

30%.

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38
Q

What effect will losing weight have on obese patients BP?

A

BP will fall.
If untreated patient loses 9Kg has been reported to produce fall in BP of 19/18 mmHg.
In treated patients a fall of 30/21 mmHg reported.

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39
Q

What is the MOST important non-pharmacological measure available?

A

Weight reduction.

40
Q

What other ‘weight’ is associated with development of hypertension?

A

Birth weight associated with development of hypertension in later life.

The lower the birth weight the higher the likelihood of developing hypertension and heart disease.

41
Q

Living in the same environment, which of Caucasians and Black Populations have a lower BP?

A

Caucasians.

NB. black populations living in rural Africa have lower Bp than those in towns. Reasons unclear (more stress?).

42
Q

Why are black populations more likelihood to have a higher BP than Caucasians?

A

They are genetically selected to be salt retainers and so are more sensitive to an increase in dietary salt.

43
Q

Will removal of the cause of secondary hypertension return the BP to normal?

A

Not necessarily.

Sustained hypertension produces end-organ damage to BVs, heart and kidney.

44
Q

What are the main causes of secondary hypertension?

A

Renal disease (20% of resistant hypertension) - chronic pyelonephritis, fibromuscular dysplasia, renal artery stenosis, polycystic kidneys.

Drug induces - NSAIDs, OCP, corticosteroids.

Pregnancy - pre-eclampsia.

Endocrine - Conn’s syndrome, Cushings disease, Pheochromocytoma, Hypo/hyperthyroidism, acromegaly.

Vascular - coarctation of the aorta.

Sleep apnoea.

45
Q

What is chronic pyelonephritis?

A

Continuing pyogenic infection of the kidneys that occurs almost exclusively in patients with anatomic abnormalities.

46
Q

What is fibromuscular dysplasia?

A

Non-atherosclerotic, non-inflammatory disease of the BVs that causes abnormal growth within the artery wall.

47
Q

What is polycystic kidney disease?

A

A genetic disorder in which abnormal cysts grow and develop in the kidneys.

48
Q

What must you do before treating hypertension?

A

Identify TRUE hypertension, by using ABPM - ambulatory BP monitoring or HBPM - home BP monitoring.

49
Q

After making the diagnosis, what is the next step?

A 
Assessing risk - 
Previous MI, stroke, IHD
Smoking
Diabetes mellitus
Hypercholesterolaemia
FH
Physical examination
50
Q

What must you examine if you diagnose hypertension?

A

Assess end organ damage
ECG and echocardiogram to check for LVH
Proteinuria
Renal US and function

Screen for treatable causes
Renal artery stenosis/FMD
Cushings disease
Conn's syndrome
Sleep apnoea
51
Q

How can you confirm LVH on ECG?

A

T wave inversion signifying strain pattern deep S waves in V1 and tall R wave in V5 fulfilling.

52
Q

How can you assess risk carefully?

A

Assign risk calculator/Q-risk.

53
Q

Once you have assessed risk, what must you do next?

A

Set a target BP to be obtained.

BHS suggests <135/80-85mmHg.

Treatment should be started at an overall CVD risk of 20%/10 yrs.

54
Q

Why do we treat hypertension?

A

To reduce cerebrovascular disease by 40-50%, reduce MI by 16-30%.

55
Q

How do we treat hypertension?

A

Stepped approach, use low doses of several drugs, this minimises adverse events and maximises patient compliance.

56
Q

What is important to remember in treatment?

A

All drugs have side effects so use stepped approach.
Do not continuously change antihypertensive medication and add new medication to current therapy until target BP achieved.

57
Q

What do the BHS guidelines say about treatment of hypertension in young people and the elderly?

A

Young people have high renin levels so can give ACEi/ARB.

Elderly have low renin levels so better to give calcium channel blocker or thiazide-type diuretic.

58
Q

When would you offer treatment to a stage 1 hypertensive?

A

Offer antihypertensive drug treatment to people aged under 80 and with ABPM >135/85 with one or more of the following:
target organ damage, established VC disease, renal disease, diabetes, 10 year CV risk equiv. to 20%+.

59
Q

When would you offer treatment to a stage 2 hypertensive?

A

ABPM >150/95

Offer anti-hypertensive drug treatment to people of any age with stage 2 hypertension.

60
Q

What would you do for people aged under 40 with stage 1 hypertension?

A

Seek specialist evaluation of secondary causes of hypertension and a more detailed assessment of potential target organ damage.

61
Q

What can you offer people with hypertension over the age of 80?

A

Same antihypertensive drug treatment as people aged 55-80 taking into account co-morbidities. BUT BP TARGET IS DIFFERENT = <145/85.

62
Q

What is the white coat effect and how can it be avoided?

A

Raised BP because stressed in hospital.

Need to identify it and consider ABPM or HBPM as an adjunct to clinical BP to measure response to treatment.

63
Q

What is step one of treatment of hypertension?

A

Offer step 1 antihypertensive treatment with calcium channel blocker (CCB) to >55 years and to black people from Africa/Caribbean of any age.

If patient <55 yrs offer ACEi or ARB.

64
Q

When might you not be able to use a CCB?

What would you use instead?

A

If there is oedema or if the patient is intolerant or if evidence of HF or high risk of HF.

Offer thiazide-like diuretic.

65
Q

Who should not be offered ACEi or ARB?

A

Pregnant woman or breast feeding woman, if intolerance, if oedema present, certain types of kidney disease.

66
Q

What does step 2 of treatment involve?

A

Add thiazide-type diuretic e.g. clortalidone or indapamide to CCB or ACEi/ARB.

67
Q

What does step 3 of treatment involve?

A

Add CCB, ACEi and diuretic together.

68
Q

If diuretic treatment is to be initiated or changed what should be used?

A

Thiazide-like diuretic e.g. chlortalidone (12.5-25.0mg once daily) or indapamide (1.5mg modified release or 2.5mg once daily) in preference to a conventional thiazide diuretic.

69
Q

What is step 4 treatment of diuretics and what does it involve?

A

Treatment of resistant hypertension.
Consider further diuretic therapy with low-dose spirnolactone (25mg once daily) if the blood K level is 4.5mmol/l or less.
Consider higher dose thiazide like diuretic treatment if blood K level greater than 4.5mmol/l.

70
Q

Why do you need to be careful in giving spironolactone?

A

It is a potassium sparing diuretic and so in people with reduced GFR they will have an increased risk of hyperkalaemia.

71
Q

What is the most common ACEi?

A

Ramipril.

72
Q

What are contraindications for the use of ACEi (ramipril)?

A

Renal artery stenosis
Renal failure
Hyperkalaemia

73
Q

What are possible ADRs with ACEis?

A

Cough, first dose hypotension, taste disturbance, renal impairment, angioneurotic oedema.

74
Q

What are possible D-D interactions of ACEis?

A

NSAIDS - precipitate acute renal failure
Potassium supplements - hyperkalaemia
Potassium sparing diuretics - hyperkalaemia.

75
Q

What are the common angiotensin II antagonists (ARB)? What do they do?

A

Losartan, valsartan, candesartan, irbesartan.
Angiotensin II antagonists competitively block the actions of angiotensin II at the angiotensin AT1 receptor.

They show advantage over ACEi - no cough.

76
Q

What are the vasodilating CCBs?

A

Amlodipine/felodipine

77
Q

What are the rate limiting CCBs?

A

Verapamil/diltiazem

78
Q

How do CCBs work?

A

By blocking the L type calcium channels. Selectivity between vascular and cardiac L type channels. Relax large and small arteries and reduce peripheral resistance, reducing CO.

79
Q

Vasodilating CCBs are the antihypertensives of choice in which group of people?

A

Over 55 yrs.

Women of child bearing age.

80
Q

Why are vasodilating CCBs good?

A

Compliance is high, benefit in elderly patient with systolic hypertension, rarely can cause postural hypertension.

81
Q

When shouldn’t you use CCBs?

A

Acute MI, HF, bradycardia (don’t use rate limiting CCBs).

82
Q

What are possible ADRs with CCBs?

A

Flushing, headache, ankle oedema, indigestion and reflux oesophagitis.

Rate limiting agents can also cause bradycardia and constipation.

83
Q

Name two thiazide type diuretics. When are these commonly used? What can they be used in combination with and what is their proven benefit?

A

Indapamide, clortalidone.

First line treatment in mild-moderate hypertension in afro-caribbean.

Can be used in combo with any other antihypertensives.

Proven benefit in stroke and MI reduction.

84
Q

Describe how thiazide type diuretics work.

A

Increase urinary secretion of sodium. Full antihypertensive effect may take weeks.

ADRs not common but incl. gout and impotence.

85
Q

What are some less commonly used agents in the treatment of hypertension?

A

Alpha-adrenoreceptor antagonists (e.g. doxazosin).

Central acting agents, e.g. methyldopa, moxonidine

Vasodilators, e.g. hydralazine, minoxidil

86
Q

How does doxazosin work in hypertension treatment?

A

Selectively block post synaptic alpha1-adrenoceptors. Oppose vascular smooth muscle contraction in arteries.

87
Q

What are possible ADRs with doxazosin?

A

First dose hypotension, dizziness, dry mouth, headache.

88
Q

What is methyldopa mainly used for?

A

Treatment of hypertension in pregnancy.

89
Q

Explain how methyldopa works.

A

It is converted to alpha-methynoradrenaline which acts on CNS alpha adrenoreceptors which decrease central sympathetic outflow.

90
Q

What are possible ADRs with methyldopa?

A

Sedation and drowsiness, dry mouth and nasal congestion, orthostatic hypertension.

91
Q

What is orthostatic hypotension?

A

A sudden fall in BP when standing up from sitting down or lying down.

92
Q

What is moxonidine?

A

A centrally acting imidazoline agonist.

Ideal patient population in which it should be used has not been defined.

93
Q

Why is hypertension during pregnancy such a big problem?

A

Hypertension during pregnancy is the second most common cause of maternal and fetal death.

Approx. 30% of women who have hypertension before pregnancy will develop pre-eclampsia.

94
Q

During normal pregnancy the BP —–, how might it be affected otherwise?

A

Normally falls unless patient has existing hypertension or primary hypertension develops (gestational hypertension).

95
Q

What is the issue with treating hypertension during pregnancy?

A

Many medications are teratogenic.

Pre-pregnancy don’t use ACEi or ARB
USE nifedipine MR, Methylodopa, atenolol, labetalol.

During pregnancy add thiazide diuretic and/or amlodipine.

96
Q

Define pre-eclampsia.

A

BP rises severely from about 20 weeks BP >140/90mmHg and proteinuria >300mg/24h - pre-eclampsia.

97
Q

How is pre-eclampsia treated?

A

Thiazide diuretic and/or amlodipine plus IV hydrazine, esmolol, labetaolol.

CARD - 1 (28 decks)

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