Hypertension Flashcards

1
Q

Describe the different classifications of Hypertension?

A

Stage 1 hypertension:
Clinic blood pressure: 140/90 mmHg or higher
Ambulatory pressure: 135/85 mmHg or higher.

Stage 2 hypertension:
Clinic blood pressure:160/100 mmHg or higher
HBPM average blood pressure is 150/95 mmHg or higher.

Severe hypertension:
Clinic systolic blood pressure:180 mmHg or higher
Clinic diastolic blood pressure is 110 mmHg or higher.

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2
Q

What diseases does hypertension predispose to?

A

Atherosclerotic:
Hypertension damages the blood vessels therefore allowing for the 1st stages in plaque formation, increasing the risk of MI’s, strokes, peripheral arterial disease.

Aneurysm:
Due to the increased pressure the aa must withstand

Cardiac Failure
Due to the increased afterload on the heart.

Retinopathy
High pressure causing damage to the small aa supplying the retina.

CKD
Raises interglomerular pressure therefore protein is filtered and patients may have proteinuria.
Also damages the vasculature of the kidney.
As kidney perfusion is reduced there is increased activation of the RAAS causing increased circulating volume and BP.

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3
Q

Define accelerated/malignant hypertension?

A

Severe hypertension >200mg systolic >130mg diastolic accompanied with end organ failure/ bilateral retinal haemorrhages

Untreated mortality of 20%

Urgent treatment is needed to reduce the patients hypertension the same day.

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4
Q

What is primary hypertension?

A

Primary or essential hypertension: is hypertension of an unknown cause and accounts for 75% of cases.

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5
Q

What is secondary hypertension?

A

Secondary hypertension: is secondary to a known cause.

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6
Q

What are the causes of secondary hypertension?

A

Renal disease: (75% of secondary cases)
CKD: Reduced perfusion causes stimulation of the RAAs.
Renal aa stenosis

Endocrine conditions:
Cushing's Syndrome (can also cause raised aldosterone a mineralocorticoid)
Conn's (hyperaldosteronism)
Acromegaly
Phaeochromocytoma (adrenal gland tumour will secrete all the hormones including aldosterone)

Coarctation of the aorta.

Pre-eclampsia in utero.

Obstructive sleep apnoea

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7
Q

Which drugs can cause hypertension?

A
Recreational:
Cocaine
Amphetamines
Alcohol
Caffeine

Corticosteroids

Cyclosporin

Oestrogen

NSAIDs

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8
Q

Describe the RAA system?

A

Low renal perfusion stimulates the release of renin from the kidneys.

Renin converts angiotensinogen (which is produced in the liver) into angiotensin I.

ACE* converts angiotensin I into angiotensin II.

Angiotensin II causes vasoconstriction of arterioles and stimulates release of aldosterone from the adrenal gland.

Aldosterone causes reabsorption of Na+ and secretion of K+ from the distal convoluted tubule and collecting ducts.

(water follows Na+ therefore increasing circulating volume)

*released from the surface of the pulmonary and renal epithelium

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9
Q

Describe the management of a patient with a high clinic blood pressure reading?

A

Patient should be given ambulatory monitoring before any treatment.

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10
Q

What are the lifestyle changes that should be advised for a patient with hypertension?

A
Smoking cessation
Weight reduction
Increase exercise
Reduce excess caffeine intake
Reduce alcohol intake
Diet (reduce fats and salt eat more fruit + veg)
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11
Q

Describe who should receive pharmacological management for hypertension?

A

Stage 1 with one or more of the following:
End organ damage
Diabetes
CV disease
High CV risk (>20% over 10 years – see rear of BNF)

All patients with Stage 2

Stage 1: 140/90
Stage 2: 160/100

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12
Q

Describe the drug regimen for hypertension?

A

Not black and younger than 55yo:
A then C

  1. ACE inhibitor or Angiotensin II receptor antagonist
  2. Ca channel blocker
  3. Thiazide like diuretic
  4. Add alpha blocker
    or spironolactone (aldosterone receptor antagonist)
    or other diuretic or beta blocker

Black or older than 55
C then A

  1. Ca channel blocker
  2. ACE inhibitor or Angiotensin II receptor antagonist
  3. Thiazide like diuretic
  4. Add alpha blocker or spironolactone (aldosterone receptor antagonist)or other diuretic or beta blocker

Statins should be considered for all patients with a high risk of developing CVD.

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13
Q

Describe the actions of ACEI and give examples of these drugs, side effects and important adverse drug reactions?

A

Blocks angiotension converting enzyme and stops bradykinin be converted into an inactive metabolite.
They reduce arteriole vasoconstriction and reduce circulating volume by reducing the reabsorption of Na+.

Egs:
Ramipril Lisinopril Enalopril Catopril

S/e: Dry cough, 1st dose hypotension.
Adverse effects: Hyperkalaemia and hyponatraemia. Angioedema (rare)

GOOD for diabetic nephropathy
Take at night, start low go slow

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14
Q

When is using an ACE Inhibitor not recommended?

A

In renovascular disease as it can cause a drop in renal function due to under perfusion.

Dont use in pregnancy of if hyperkalaemic, or in severe aortic stenosis

In AKI.

Paradoxically it is 1st line in diabetic nephropathy.

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15
Q

Describe the mechanism of action of Ca channel blockers and give examples?

A

They act on the voltage gated channels on vascular smooth muscle leading to vasodilation and a drop in BP.

In rate limiting Ca channel blockers affects the voltage gated channels of the heart, slows the heart rate NEVER GIVE WITH B BLOCKERS!

Verapamil (Rate limiting), diltiazem (rate limiting)

Dihydropyridines (Smooth muscle)
Felodopine
Amlodopine
Nifedipine

Suffix = pine

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16
Q

Describe the use of thiazide and thiazide like diuretics in the treatment of hypertension, examples and contraindications?

A

Third line: Thiazide like diuretics

Reduces reabsorption of Na+ and Cl- from the distal convoluted tubule.

Important considerations:
Doesn’t work in moderate renal failure
Avoid if patient has gout or hypokalaemia

Side effects:
Hypotension
Hypokalaemia
Impaired glucose tolerance
Makes gout worse

Eg:

Thiazides: Bendroflumethazide
Thiazide like: chloratidone and linapamide

17
Q

What are the indications for starting lipid lowering therapy?

A

Anybody post MI.
Anyone with a 10% 10 year CVD risk.
Anyone with high cholesterol.

18
Q

What are the treatment doses of Atorvastatin for primary and secondary prevention?

A

Primary: 20mg od
Secondary: 80mg od

19
Q

What are the main side effects of statins?

A

Liver dysfunction.
Headache, GI and Nausea, Myalgia (common)
Myopathy and rhabdomyolysis (rare, dose related)