Hypertension Flashcards

1
Q

What is ambulatory blood pressure monitoring?

A

Two measurements per hour taken, average reading used

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2
Q

Describe the different classifications/stages of Hypertension?

A
  1. Stage 1 hypertension:
    • Clinic blood pressure: 140/90 mmHg or higher
    • Ambulatory bp monitoring or home bp monitoring: 135/85 mmHg or higher.
  2. Stage 2 hypertension:
    • Clinic blood pressure:160/100 mmHg or higher
    • ABPM/HBPM average blood pressure is 150/95 mmHg or higher.
  3. Severe hypertension:
    • Clinic systolic blood pressure:180 mmHg or higher
    • Clinic diastolic blood pressure is 110 mmHg or higher.
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3
Q

What diseases does hypertension predispose to?

A

Atherosclerotic changes:

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

Aneurysms:

  • 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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4
Q

Define accelerated/malignant hypertension?

A
  • A rapid sustained increase in blood pressure that is associated with target organ damage
  • Diagnosed if there is SBP>200 or DBP>120 and bilateral retinal haemorrhages/exudates

Untreated mortality of 20%

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

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5
Q

What is primary hypertension?

A

Primary or essential hypertension is hypertension of an unknown cause and accounts for 95% of cases

Likely to be multifactorial

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6
Q

What is secondary hypertension?

A

Secondary hypertension is secondary to a known cause.

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7
Q

What are the causes of secondary hypertension?

(7)

A
  1. Adrenal cortical diseases:
    • Primary hyperaldosteronism (e.g.Conn’s) - most common secondary cause
    • Cushing’s, Acromegaly
  2. Renal aa stenosis
    • Second most common secondary cause
  3. CKD:
    • Reduced perfusion causes stimulation of the RAAs.
  4. Pheochromocytoma
    • adrenal gland tumour will secrete all the hormones including aldosterone
  5. Coarctation of the aorta
  6. Neurogenic causes
    • Raised ICP
  7. Pregnacy
    • Pre-eclampsia
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8
Q

Which drugs can cause hypertension?

A

Recreational:

  • Cocaine
  • Amphetamines
  • Alcohol
  • Caffeine
  • Corticosteroids
  • Cyclosporin
  • Oestrogen
  • NSAIDs
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9
Q

Describe the RAA system?

A

Think Renin angiotensin aldosterone system

  1. Low renal perfusion stimulates the release of renin from the kidneys.
  2. Renin converts angiotensinogen (which is produced in the liver) into angiotensin I.
  3. ACE* converts angiotensin I into angiotensin II.
  4. Angiotensin II causes vasoconstriction of arterioles and stimulates release of aldosterone from the adrenal gland.
  5. 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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10
Q

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

A

Patient should be given ambulatory monitoring before any treatment (two measurements per hour taken, average reading used)

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11
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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12
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 or renal disease
  • High CV risk (>20% over 10 years)

All patients with Stage 2

*Stage 1: 140/90

*Stage 2: 160/100

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13
Q

Describe the drug regimen for hypertension?

A
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14
Q

Describe the actions of ACEI and give examples of these drugs and side effects?

A
  • Act via RAA system
  • 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+.

Examples are ramipril or lisonopril

First line in those <55 and also in diabetics (renoprotective)

S/Es:

  • Dry cough (10% of pts)
  • Hyperkalamia
  • First dose hypotension (give at night)
  • Worsened renal function in those with preiously ‘normal’ GFR - monitor U&Es
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15
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 or if hyperkalaemic, or in severe aortic stenosis

In AKI

Paradoxically it is 1st line in diabetic nephropathy.

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16
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!

Examples: (Suffix = pine)

  • Verapamil (Rate limiting)
  • diltiazem (rate limiting)
  • Dihydropyridines (Smooth muscle)
  • Felodopine
  • Amlodopine
  • Nifedipine
17
Q

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

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

Examples:

  • Thiazides: Bendroflumethazide
  • Thiazide like: chloratidone and linapamide
18
Q

What are statins?

A

HMG-CoA reductase inhibitors, thus stop the first step in the cholesterol synthesis pathway

19
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.

20
Q

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

A

Primary: 20mg od

Secondary: 80mg od

21
Q

What are the main side effects of statins?

A

Liver dysfunction.

Headache, GI and Nausea, Myalgia (common)

Myopathy and rhabdomyolysis (rare, dose related)