Week 1: Pathophysiology of hypertension Flashcards

1
Q

Define hypertension

A

Hypertension = high blood pressure, blood vessels have persistently raised pressure

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2
Q

How does blood pressure relate to risk of CV events?

How do drugs alter this risk?

How do we know which patients to give drug therapy to?

A

The higher the BP the greater the risk of CV events (Stroke and MI).

Blood pressure lowering drugs reduce that risk accordingly, however need a clinical definition to know which patients to give drug therapy to.

Drug vs non drug approach –> high risk vs population approach

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3
Q

Why do we treat Hypertension?

A

3/5 deaths in UK from vascular disease

Blood pressure predicts the risk of vascular disease

Risks of hypertension can be reversed by treatment

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4
Q

List different types of hypertension

A
  • Essential or Primary hypertension
  • Secondary hypertension
  • Pesudo resistant –> sever High BP on several drugs and remains uncontrolled (often due to lack of adherence)
  • Resistant or refractory –> does not respond well to drugs
  • Isolated systolic hypertension –> only high systolic common in ageing population, reflective of stiffening of large arteries
  • In pregnancy
  • Paedatric hypertension
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5
Q

What are the stages of essential or primary hypertension?

Reference figures

A

Stage 1:

  • Clinic BP : 140 / 90 mmHg or ABPM under 135/85 mmHg

Stage 2:

  • Clinic BP 140/90 to 179/119 mmHg or ABPM of 135/85 to 149/94 mmHg

Severe:

  • Clinic BP: 180/ 120 mmHg or more, ABPM 150/95 mmHg or more
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6
Q

How should you manage stage 1 hypertension?

A

Check BP every 5 yrs and more often if close to 140/ 90 mmHg

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7
Q

How should you manage stage 2 hypertension?

A

Offer ABPM

investigate for target organ damage (includes both micro (retinopathy, vascular dementia) and macrovascular damage (stroke, myocardial infarction)

Assess cardiovascular risk

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8
Q

How should you manage severe hypertension?

A

assess for target organ damage as soon as possible

Consider starting drug treatment immediately without ABPM if target organ damage

Repeat clinic BP in 7 days if no target organ damage

Refer for same day specialist if retinal haemorrhage, papilloedema or life threatening sx

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9
Q

What is ABPM?

How does BP change over 24 hrs?

A

Ambulatory blood pressure monitoring:

Top = systolic, bottom = diastolic

Middle line = heart rate

Two lines = boundaries for normal blood pressure

Often have a nocturnal dip which is a normal physiological variation in blood pressure. 10% or more drop in BP at night compared to the day. Drops due to low activity and posture, increased parasympathetic output.

Also morning rise in BP

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10
Q

What is labile hypertension?

A

24HR monitoring, BP often normallu fluctuates but more than normal and above normal blood pressure

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11
Q

What is non dipping?

How does this affect risk for cardiovascular disease?

A

Non dipping is when an individuals blood pressure does not drop overnight, pt’s have increased risk of cardiovascular disease than others.

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12
Q

What are some causes of secondary HTN?

A

1) Primary hyperaldosteronism (Conn’s syndrome) –> e.g. due to adrenal adenoma or adrenal bilateral hyperplasia
2) renovascular disease –> Fibromuscular dysplasia and atherosclerotic
3) Obstructive Sleep Apnoea
4) Chronic Kidney disease
5) Phaeochromocytoma –> rare but lethal, overproduction of Adrenaline and NA from the medulla, intermittent HTN, can be highly severe
6) Aortic coarctation –> narrowing of aorta congential or sclerotic, upper body HTN (measure BP in both arms)
7) Cushing’s disease
8) Hyperparathyroidism

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13
Q

What is Conn’s syndrome?

Causes?

How can electrolytes be affected?

How do you treat?

A

Conns syndrome = HTN difficult to control with standard therapy ass. with tendency to hypokalemia and hypernatraemia. If pt presenting with hypoK, HTN in abscence of other factors e.g. diuretic then refer

1-5% of causes of secondary HTN

50% adrenal adenoma, 50% bilateral adenoma

Treatment –> spironolactone plus/ minus surgery (Surgery only if discrete adeonma, not if bilateral adrenal hyperplasia, surgical removal would cause Addison’s disease).

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14
Q

Describe some of the key investigations of Conn’s syndrome

What other condition may be found during these investigations?

A

Conn’s syndrome: measure plasma aldosterone, need to find if it is raised in the supine position vs standing position. (In this patient it is raised).

Measure Renin angiotensin system by measurin the Renin production. If there is a volume expansion you will suppress Renin, as primary production of aldosterone will suppress Renin. Primary production of Aldosterone should be matched by a suppression of Renin. This is diagnostic of Conn’s syndrome.

High aldosterone and high renin means secondary hyperaldosteronism due to something else e.g. heamorrhage, low salt etc.

Can also measure 24 hr urine exrection of k+ –> will be very high when there is a lot of aldosterone, leads to hypokalaemia.

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15
Q

What is shown in this patient’s CT?

A

Bilateral adenoma:

12 mm nodule in root of lateral limb of R adrenal gland

11 mm nodule in the body of the L adrenal gland

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16
Q

What is adrenal venous sampling?

A

Adenal venous sampling is a key diagnostic test which measures the concentration of aldosterone coming from both adrenal veins to diagnose the source of adrenal secretion.

This is important as unilateral adrenal disease may be surgically resected, whereas bilateral cannot. (Would lead to total loss of adrenal secretion –> Addison’s disease (Adrenal insufficiency).

17
Q

Describe adrenal venous sampling and potential results you could acquire.

A

Taking sample of both veins coming off adrenal glands (R and L adrenal veins). Measure aldosterone above the vena cava and below from R and L adrenal veins to understand where aldosterone is coming from.

Left lateralisation:

  • Measure both aldosterone (1560) and cortisol (100) and calculate the ratio.
  • Left A/C ration 15.6 and right A/C ratio is 2.4
  • Left side divided by right side =15.6/ 2.4 = 6.5
  • therefore aldosterone secretion is significantly predominant at the left side

Contralateral suppression:

  • Right A/C ration is 2.4 and peripheralA/C ratio is 3.2
  • Right side presents a phenomenon of contralateral suppression
18
Q

What is renal artery stenosis?

When is it common?

What is the risk?

A

Renal artery stenosis = development of an atheroma in the renal artery

Common when multiple CV risk factors are present

Occurs in 50% of patients with clinical vascular disease

Early risk of vascular death

19
Q

How would you pick up renal artery stenosis?

How is it treated?

A
  • Hypertension, possible resistant to tx, renal angiogram or MRI angiogram
  • Renal artery angioblasty
20
Q

What is fibromuscular dysplasia?

Who does it affect mostly?

How does it appear on an angiogram?

A

Fibromuscular dysplasia is a non atherosclerotic genetic disease in which there is abnormal growth in the wall of an artery. Most commonly affects renal and carotid arteries.

Affects mostly younger, female population. Suspect in younger hypertensive patients that are resistant to tx.

Often looks like “beads on a string” on angiogram.

21
Q

What is phaeochromocytoma?

How does it present?

A

Phaemochromocytoma is a rare tumour of the adrenal gland.

Severe hypertension appears intermittently, it will not be continuous

Other sx: Hot flushes, palpitations, sweating attacks, chest pain, headache, blurred vision

Odd descriptions e.g. patient describes headache during sneeze/ defecation (anything that increases abdominal pressure).

This syndrome is due to an overproduction of Adrenaline/ Noradrenaline intermittently. Can be bilateral or unilateral. Other adrenaline/ NA cells can be found within the ganglia and within the bladder.

22
Q

What are key diagnostic tests with phaechromocytoma?

A

Measure catecholamines and metabolites: plasma adrenaline, plasma noradrenaline, urinary adrenaline, urinary noradrenaline, urine VMA’s (vanillylmandelic acid = metabolite of catecholamine).

Protocol requires 3 consecutive tests to ensure you dont catch only inbetween crises. Rise of catecholamine needs to be well above the upper limit, 2-3x larger. (to ensure not just anxiety during dr appt.).

23
Q

What is the tx for a patient with suspected pheomchromocytoma?

A

Pt given phenoxybenzamine which is an alpha blocker to block the activity of NA, and blood pressure will fall dramatically.

Pt then given Beta blocker (atenolol), still high level of adrenaline present but the blood pressure is controlled.

Surgical removal of the tumour is required (in most tumour is benign but can become malignant).

24
Q

What is shown within this patients CT? (need to add picture slide 22)

A

Bilateral pheochromocytoma, enlarged masses of adrenal glands plus some haemorrhaging.

25
Q

What is an iodine 123 MIBG scan?

A

Radioactive iodine is given which is taken up by the chromaffin cells within adrenal medulla that secrete adrenaline/ NA etc. When scanned they light up as “hot spots” of overactivity within the adrenal glands. In this patient bilateral enlargement seen.

26
Q

What are the characteristic features of phaeochromocytoma?

A
  • 10% is extra adrenal (hence whole body scan)
  • 10% is bilateral
  • 10% is familial (MEN 2a)
  • 10% malignant
  • key: sweats, headaches, with or without palpitations
  • Paroxysmal hypertension
  • Risk of cardiomyopathy when undiagnosed and malignancy
27
Q

Describe the histopathology of pheochromocytoma

A

Compared to normal adrenal gland a pheochromocytoma is composed of spindle shaped chromaffin cells and supporting sustentacular cells which aggregrate into small nest known as zenballen with rich vascular network.

28
Q

How is a patient with phaeochromocytoma tx?

A

BP shown pre and post tx: tumour surgically removed, then given flurocortisone and hydrocortisone replacement therapy (cortisol and aldosterone replaced). Blood pressure returns to normal, long term follow up again shown to be normal.

29
Q

What is pseudo resistant hypertension?

What can be the cause/s?

A

Pseudoresistant HTN –> is HTN that appears to be resistant to tx but is due to other factors.

Could be white coat hypertension, misleads you into thinking pt needs tx. High BP only within the clinic, to diagnose requires 24 monitoring

Could also be due to an inaccurate measurement e.g. cuff size.

Could also be due to poor adherence to tx.

30
Q

Define resistant HTN

A

Resistant HTN defined when a pt’s BP is not controlled to recommended BP goals despite tx with an appropriate combinations of 3 drug therapies prescribed at their max recommended and or tolerated doses.

31
Q

What is most resistant HTN due to?

A

Most resistant HTN is due to systolic HTN

32
Q

What are the charactersistics of resistant HTN?

A
  • Older age (above 75 yrs)
  • high baseline BP
  • chronicity of uncontrolled HTN
  • target organ damage (LVH or CKD)
  • diabetes
  • obesity atherosclerotic vascular disease
  • aortic stiffening
  • women
  • black african origin
  • excessive dietary sodium and alcohol consumption
  • drugs
33
Q

What are some drugs known to raise BP?

A
  • NSAIDS
  • Sympathomimetic amines
  • Estrogen and analogues (COCP & HRT)
  • Methylxanthines (theophyliine and theobromine, caffeine)
  • Cyclosporine
  • Erythropoetin
  • venlafaxine
  • Cocaine
  • Nicotine
  • Phencyclidine (angel dust)
  • herbal ectasy
  • plus withdrawal from certain drugs (beta blocker, alpha antagonist, opiods, ethanol, calcium antagonist)
34
Q

Approach to prevention and tx of HTN?

A

Tx pts extensively to prevent high risk of continued uncontrolled high BP

Non pharmacological tx promoted due to population effect and high risk pts

First use primary prevention and disease management strategy by:

  • Reducing salt intake
  • high potassium diet
  • weight reduction
  • regular dynamic exercise
  • moderate alcohol consumption
35
Q

What is the effect of dietary salt reduction on blood pressure?

A

Global policy to reduce salt consumption, majority hidden in processed food.

RCT showed levels of salt reduction lowers BP in dose response pattern.

Low BP sustained for 1 yr as long as they maintained low salt consumption

36
Q

What is the equation for BP?

A

BP = CO X SVR