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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
So what are the two main systems you want to target in hypertension treatment?
Sympathetic and RAAS.
26
What is the aetiology of hypertension?
Polygenic - major genes, poly genes. | Polyfactorial - environmental, individual and shared.
27
What are the two most likely causes of hypertension?
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.
28
What are some other factors that involved in the aetiology of hypertension?
Age, genetics, family history, environment, weight, alcohol intake, race.
29
BP tends to rise with age, why is this?
Possibly as a result of decreased arterial compliance.
30
How should hypertension be treated in the elderly?
Aggressively, they have more to lose. But must be pragmatic.
31
Discuss how genetics affect the risk of getting hypertension.
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.
32
How many genes are recognised as important in the development of hypertension?
>30 genes, but individually they account for at most 0.5mmHg each.
33
What environmental things can cause hypertension?
Mental/physical stress (removing stress doesn't necessarily return BP to normal).
34
How can salt intake and diet affect hypertension?
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.
35
What is the relationship between alcohol and hypertension?
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.
36
Obese patients have a lower/higher BP.
Higher.
37
What percentage of hypertension is attributable in part or wholly to obesity?
30%.
38
What effect will losing weight have on obese patients BP?
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.
39
What is the MOST important non-pharmacological measure available?
Weight reduction.
40
What other 'weight' is associated with development of hypertension?
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
Living in the same environment, which of Caucasians and Black Populations have a lower BP?
Caucasians. NB. black populations living in rural Africa have lower Bp than those in towns. Reasons unclear (more stress?).
42
Why are black populations more likelihood to have a higher BP than Caucasians?
They are genetically selected to be salt retainers and so are more sensitive to an increase in dietary salt.
43
Will removal of the cause of secondary hypertension return the BP to normal?
Not necessarily. | Sustained hypertension produces end-organ damage to BVs, heart and kidney.
44
What are the main causes of secondary hypertension?
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
What is chronic pyelonephritis?
Continuing pyogenic infection of the kidneys that occurs almost exclusively in patients with anatomic abnormalities.
46
What is fibromuscular dysplasia?
Non-atherosclerotic, non-inflammatory disease of the BVs that causes abnormal growth within the artery wall.
47
What is polycystic kidney disease?
A genetic disorder in which abnormal cysts grow and develop in the kidneys.
48
What must you do before treating hypertension?
Identify TRUE hypertension, by using ABPM - ambulatory BP monitoring or HBPM - home BP monitoring.
49
After making the diagnosis, what is the next step?
``` Assessing risk - Previous MI, stroke, IHD Smoking Diabetes mellitus Hypercholesterolaemia FH Physical examination ```
50
What must you examine if you diagnose hypertension?
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
How can you confirm LVH on ECG?
T wave inversion signifying strain pattern deep S waves in V1 and tall R wave in V5 fulfilling.
52
How can you assess risk carefully?
Assign risk calculator/Q-risk.
53
Once you have assessed risk, what must you do next?
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
Why do we treat hypertension?
To reduce cerebrovascular disease by 40-50%, reduce MI by 16-30%.
55
How do we treat hypertension?
Stepped approach, use low doses of several drugs, this minimises adverse events and maximises patient compliance.
56
What is important to remember in treatment?
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
What do the BHS guidelines say about treatment of hypertension in young people and the elderly?
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
When would you offer treatment to a stage 1 hypertensive?
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
When would you offer treatment to a stage 2 hypertensive?
ABPM >150/95 | Offer anti-hypertensive drug treatment to people of any age with stage 2 hypertension.
60
What would you do for people aged under 40 with stage 1 hypertension?
Seek specialist evaluation of secondary causes of hypertension and a more detailed assessment of potential target organ damage.
61
What can you offer people with hypertension over the age of 80?
Same antihypertensive drug treatment as people aged 55-80 taking into account co-morbidities. BUT BP TARGET IS DIFFERENT = <145/85.
62
What is the white coat effect and how can it be avoided?
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
What is step one of treatment of hypertension?
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
When might you not be able to use a CCB? What would you use instead?
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
Who should not be offered ACEi or ARB?
Pregnant woman or breast feeding woman, if intolerance, if oedema present, certain types of kidney disease.
66
What does step 2 of treatment involve?
Add thiazide-type diuretic e.g. clortalidone or indapamide to CCB or ACEi/ARB.
67
What does step 3 of treatment involve?
Add CCB, ACEi and diuretic together.
68
If diuretic treatment is to be initiated or changed what should be used?
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
What is step 4 treatment of diuretics and what does it involve?
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
Why do you need to be careful in giving spironolactone?
It is a potassium sparing diuretic and so in people with reduced GFR they will have an increased risk of hyperkalaemia.
71
What is the most common ACEi?
Ramipril.
72
What are contraindications for the use of ACEi (ramipril)?
Renal artery stenosis Renal failure Hyperkalaemia
73
What are possible ADRs with ACEis?
Cough, first dose hypotension, taste disturbance, renal impairment, angioneurotic oedema.
74
What are possible D-D interactions of ACEis?
NSAIDS - precipitate acute renal failure Potassium supplements - hyperkalaemia Potassium sparing diuretics - hyperkalaemia.
75
What are the common angiotensin II antagonists (ARB)? What do they do?
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
What are the vasodilating CCBs?
Amlodipine/felodipine
77
What are the rate limiting CCBs?
Verapamil/diltiazem
78
How do CCBs work?
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
Vasodilating CCBs are the antihypertensives of choice in which group of people?
Over 55 yrs. | Women of child bearing age.
80
Why are vasodilating CCBs good?
Compliance is high, benefit in elderly patient with systolic hypertension, rarely can cause postural hypertension.
81
When shouldn't you use CCBs?
Acute MI, HF, bradycardia (don't use rate limiting CCBs).
82
What are possible ADRs with CCBs?
Flushing, headache, ankle oedema, indigestion and reflux oesophagitis. Rate limiting agents can also cause bradycardia and constipation.
83
Name two thiazide type diuretics. When are these commonly used? What can they be used in combination with and what is their proven benefit?
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
Describe how thiazide type diuretics work.
Increase urinary secretion of sodium. Full antihypertensive effect may take weeks. ADRs not common but incl. gout and impotence.
85
What are some less commonly used agents in the treatment of hypertension?
Alpha-adrenoreceptor antagonists (e.g. doxazosin). Central acting agents, e.g. methyldopa, moxonidine Vasodilators, e.g. hydralazine, minoxidil
86
How does doxazosin work in hypertension treatment?
Selectively block post synaptic alpha1-adrenoceptors. Oppose vascular smooth muscle contraction in arteries.
87
What are possible ADRs with doxazosin?
First dose hypotension, dizziness, dry mouth, headache.
88
What is methyldopa mainly used for?
Treatment of hypertension in pregnancy.
89
Explain how methyldopa works.
It is converted to alpha-methynoradrenaline which acts on CNS alpha adrenoreceptors which decrease central sympathetic outflow.
90
What are possible ADRs with methyldopa?
Sedation and drowsiness, dry mouth and nasal congestion, orthostatic hypertension.
91
What is orthostatic hypotension?
A sudden fall in BP when standing up from sitting down or lying down.
92
What is moxonidine?
A centrally acting imidazoline agonist. | Ideal patient population in which it should be used has not been defined.
93
Why is hypertension during pregnancy such a big problem?
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
During normal pregnancy the BP -----, how might it be affected otherwise?
Normally falls unless patient has existing hypertension or primary hypertension develops (gestational hypertension).
95
What is the issue with treating hypertension during pregnancy?
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
Define pre-eclampsia.
BP rises severely from about 20 weeks BP >140/90mmHg and proteinuria >300mg/24h - pre-eclampsia.
97
How is pre-eclampsia treated?
Thiazide diuretic and/or amlodipine plus IV hydrazine, esmolol, labetaolol.

CARD - 1 (28 decks)

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