L10 Hypertension 1 Flashcards

1
Q

Define hypertension.

A

Sustained increases in systemic blood pressure > 140/90mm Hg

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2
Q

define the 2 cases of hypertension:

A

Essential/primary hypertension: cause in unknown, due to genetic and environmental factors. 90-95% of patients.
Secondary hypertension: secondary to another disease or the use of medications. 5-10% of patients.

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3
Q

List factors associated with primary hypertension.

A
age
salt intake
weight
race
potassium concentration
alcohol
exercise
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4
Q

What are some causes of secondary hypertension?

A
kidney disease
analgesic neuropathy
adrenocorticol hypertension (cushiness disease and primary aldosteronism)
cerebral tumour
pre-eclampsia
renal artery stenosis
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5
Q

What are some drugs that can cause hypertension?

A
Alcohol
effervescent antacids
NSAIDs
corticosteroids
OCs and oestrogen
sympathomimetics
MAOIs
venlafaxine
eryhtropoetin
cyclosporin
licorice
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6
Q

What is myocardial infarction?

A

the death of an area of heart muscle as a result of being deprived of its blood supply.
Characterised by severe chest pain.
AKA Heart attack.

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7
Q

What is proteinuria?

A

Protein is allowed to leak into the urine as a result of a defect in the glomerular capillary.

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8
Q

What is the target BP for patients with hypertension? What is the target BP for patients with CHD, diabetes, renal disease or stroke?

A

140/90

130/80

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9
Q

What are some non-pharmacological therapy of hypertension?

A
Diet: low KCl and saturated fats
Weight reduction
Cessation of smoking
reduce excessive alcohol consumption
30 minutes of moderate intensity on 5 or more days per week
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10
Q

When should treatment for hypertension be commenced?

A

Depends on level of BP and patients risk level and response to lifestyle changes.
Low risk: try lifestyle changes and reassess after 2 years. treat if BP> 160/100
med risk: try lifestyle changes for 3-6 months and treat if no improvement, high BP or family history of CVD, indigenous. reassess after 6-12 months.
High risk: treat promptly with lifestyle changes AND drugs. reassess frequently.

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11
Q

How is blood pressure regulated?

A

Baroreceptors in the carotid arteries and aortic arch detect drop in BP. Impulses sent to brain and increased sympathetic outflow to the heart, blood vessels and adrenal gland. Increased release of NA activates beta-1 receptors in the heart, and alpha-1 receptors in the blood vessels to cause vasoconstriction.

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12
Q

what are the two mechanisms by which blood pressure is increased?

A

Increased cardiac output

increased total peripheral resistance

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13
Q

how is systolic blood pressure controlled?

A

bardiac output: depends on venous return

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14
Q

how is diastolic blood pressure controlled?

A

Total peripheral resistance

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15
Q

describe the renin-angiotensin-aldosterone system

A

Important role in maintaining BP, blood volume and electrolyte balance.
Renin is secreted by the kidney in response to decreased renal blood flow, decreased salt intake and stimulation from the sympathetic nervous system.

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16
Q

What is the role of renin in the RAAS?

A

Catalyses conversion of angiotensin to angiotensin 1.

17
Q

Outline the steps in RAAS control of BP.

A

Renin catalyses conversion of angiotensin to angiontensin 1.
angiotensin 1 is converted to angiotensin 2 by angiotensin-converting enzyme (ACE)
angiotensin 2 stimulates AT(II)1 and AT(II)2 receptors to cause vasoconstriction and aldosterone secretion.
Aldosterone secretion increases sodium excretion, increasing blood volume –> increased CO and BP.

18
Q

What are the 3 mechanisms of action of angiotensin II?

A
  1. vasoconstriction, particularly in efferent arterioles of kidney. Due to increased release of noradrenaline from sympathetic nerves increasing vasoconstriction (indirect effect)
  2. salt retention: angiotensin II stimulates proximal tubular reabsorption of sodium ions. initiates secretion of aldosterone from adrenal cortex, thus stimulating reabsorption of sodium ions.
  3. cardiovascular growth: cell growth in the left ventricle and arteriolar wall.
19
Q

What are the target tissues for antihypertensives?

A

Heart: cardiac output
Arterioles: determine peripheral resistance
Kidney: blood volume
CNS: baroreceptors and set point
Sympathetic nerves: relase NA
Endothelial cells: regulate levels of angiotensin II, ET-1 (vasoconstrictor) and NO (vasodilator).

20
Q

List the 5 major drug classes of antihypertensives, and their general mechanism of action.

A
  1. ACE inhibitors and angiotensin receptor antagonists (sartans)
  2. beta blockers
  3. thiazide and related diuretics
  4. calcium channel blockers
  5. selective alpha-blockers
21
Q

What are some other antihypertensives?

A
  1. centrally-acting alpha-2 agonists
  2. arteriolar vasodilator
  3. nonselective arteriolar and venous vasodilator
22
Q

What are the first choice drugs for hypertension?

A

an ACE inhibitor or saran, or,
a dihydropyradine calcium channel blocker, or,
low dose thiazide diuretic if over 65 years

23
Q

Why are thiazides not recommended as a first line mono therapy in younger patients?

A

Assosciation with new onset diabetes.

24
Q

What are the rationale for staged introduction of drugs?

A

High doses of antihypertensives are often not effective during chronic use, and often result in side effects.
Blood pressure can be controlled without side effects by combining low doses of different drugs with complimentary mechanisms of action.
the dose of a single agonist is often limited by homeostatic mechanisms.

25
Q

What are the preferred drug combinations for hypertension?

A

ACE inhibitor with a thiazide diuretic or calcium channel blocker.
Calcium channel blocker with a thiazide diuretic.