Lecture 8: Hypertension Flashcards

1
Q

What is hypertension?

A
  • Persistent raised blood pressure
  • Normal blood pressure: 120/80 mm Hg
  • Treat when systolic > 140
  • Diastolic > 90
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2
Q

How do we measure BP?

A

Measure in the brachial artery in the arm

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3
Q

What is white coat hypertension?

A
  • BP may be artificially high bc you are being checked medically, making you nervous
  • Can be circumvented via ambulatory blood pressure monitoring (ABPM)
    • Inflates once an hour during the day n night
    • BP measured automatically n transferred onto a disk
  • Can also be overcome w home BP measurement but they’re not calibrated
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4
Q

Describe the diagnosis of hypertension in the clinic

A
  • High BP -> 140/90 mmHg or higher
  • ABPM: ensure at least 2 measurements per hour during person’s waking hours
    • Average value of at least 14 measurements taken during person’s waking hours
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5
Q

Describe the diagnosis of hypertension in the home blood pressure monitoring (HBPM)

A
  • For each BP recording, 2 consecutive measurements are taken, at least 1 minute apart n with the person seated
  • BP is recorded twice daily, morning n evening
  • BP recording continues for at least 4 days, ideally for 7 days
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6
Q

What are you measuring when you take a blood pressure?

A
  • Ausculation
    • Listening to any sounds from the body (e.g. heart)
  • Korotkoff sounds
  • Inflate cuff n use statoscope to listen to brachial artery
    • Inflate cuff so high to stop blood flow -> no sound
    • Slowly let pressure off -> pressure falls
    • Point when you hear the first sound (systolic BP)
    • Pressure in cuff is low enough to allow blood to go thru = systolic BP
  • Sound increases in volume [more blood blow]
  • Turn pressure down further -> hear no more sound [no more turbulence] = diastolic pressure
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7
Q

What is mean arterial pressure?

A
  • MAP = (SP + (2 * DP)/3)
  • Not just average BP as uneven amount of time spent at rest
  • ~2/3 diastolic and ~1/3 systolic
  • Mean closer to diastolic
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8
Q

What are the causes of hypertension?

A
  • 90-95% primary essential hypertension
    • Probably a complex genetic disorder
  • Secondary hypertension
    • Renal causes [increase BP -> not providing volume of liquid]
    • Endocrine disorders [hormones that cauese artery restriction]
    • Aortic coarctation [part of the aorta is occluded]
    • Preeclampsia (pregnancy)
    • Neurogenic hypertension (overactivity of the SNS)
    • Endocrine tumours: primary hyperaldosteronism, phaeochromocytoma, renin secreting tumour
    • Drug induced: amphetamines, NSAIDS, steroids
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9
Q

Why treat hypertension?

A
  • Hypertension increases the risk of
    • Stroke (occlusion in the brain)
    • Coronary events (myocardial infarction, angina)
    • Aortic aneurysm (bulging in blood vessel, aorta [pressure] -> fatal)
    • Heart failure
    • Renal failure
    • End organ damage
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10
Q

Symptoms of hypertension

A
  • Headaches [high pressure]
  • Dizzy
  • Flushing
  • Awareness of heart beat
  • Nosebleeds
  • None (most common): silent killer
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11
Q

Signs of hypertension

A
  • Level of blood pressure
  • Cardiomegaly/left ventricular hypertrophy [heart has to work w high pressure -> increase in muscle mass]
    • Can be observed in an echocardiogram
  • Abnormal renal function
    • Blood test
  • Proteinuria or haematuria
    • Urine test
  • Hypertensive retinopathy
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12
Q

How is hypertension managed?

A
  • Patient education/lifestyle changes
    • Stop smoking
    • Loss of weight
    • Exercise
    • Reduce salt intake
    • Diet
    • Relaxation therapy
  • Drug treatment
  • Surgery
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13
Q

What is the effect of excess weight on BP?

A
  • Weight n BP are linked
  • Likely that wight interacts w various factors controlling BP at different points over lifetime
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14
Q

What determines BP?

A
  • How much blood is ejected
    • Determined by cardiac output
      • Heart rate
      • Stroke volume
        • Filing pressure (Starling Law’s: more blood that comes back to heart, stretches the fibers in heart -> bigger CO)
        • Contractility (determined by SNS)
    • Total peripheral resistance
      • Diameter of arterioles
      • Small lumen -> higher pressure
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15
Q

What are the 2 major mechanisms for controlling BP?

A
  • Baroreceptor/SNS
    • Controls BP minute to minute
  • ECF volume/plasma renin activity
    • Longer term effects
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16
Q

Describe the baroreceptor reflex

A
  • Baroreceptors are located in the carotid sinus n aortic arch
  • When there is a fall in BP -> decrease frequency of nerve impulse in baroreceptors -> inhibit parasympathetic nervous system n stimulate SNS -> increase in heart rate
  • RESULT
    • Increases heart rate n artery contraction [β receptors in the heart] ->increase in CO n total periphery resistance -> increase in BP
    • Increase in venous return -> stretching of heart muscle -> increase cardiac output
  • EXAMPLE
    • Hemorrhage/loss of blood, baroreceptors keep alive
      • Fast heart rate -> try to increase BP to maintain organs
17
Q

What things can you aim to change to reduce BP?

A
  • Cardiac output (stroke volume * heart rate)
    • Diuretics: reduce BP
    • ACE inhibitors: reduce blood volume
    • Angiotensin II receptor antagonists: reduce blood volume
    • β-blockers: reduce heart rate n contractility
  • Reduce total peripheral resistance
    • Vasodilators
    • Calcium channel antagonists
    • ACE inhibitors
    • Angiotensin II receptor antagonists
    • α-adrenoreceptor blockers
  • Some drugs do both: ACE inhibitors, angiotensin II receptor antagonists
18
Q

How do ACE inhibitors n angiotensin II receptor antagonists work?

A
  • Renin-angiotensin-aldosterone system
  • Liver secretes angiotensinogen (inactive) into blood stream
  • Converted by renin, which is secreted by the kidney, into angiotensin I (inactive)
  • Angiotensin I converted to angiotensin II (active)
  • Causes adrenal cortex to cause aldosterone release
  • Acts on BP
19
Q

What are the effects of angiotensin II?

A
  • Vasoconstriction of arterioles
  • Stimulates Na+ reabsorption in PCT
    • Cl- and water follow passively
  • Stimulates aldosterone secretion (adrenal cortex)
  • Stimulates vasopressin secretion from posterior pituitary gland
  • Stimulates thirst
20
Q

What are ACE inhibitors?

A
  • All ACE inhibitors end w “pril” suffix
  • Reduce arterial resistance n blood volume
  • Causes rapid fall in BP n persistent dry cough
    • Block the breakdown of bradykinin (mediator released in response to inflammation)
    • Bradykinin is broken down to inactive peptides via ACE
    • Thus ACE inhibitors block this process -> buildup of bradykinin -> can persist in throat -> dry cough
21
Q

What are angiotensin II receptor antaogonists?

A
  • Angiotensin II receptor antagonists
  • End w “sartan” suffix
    • Osartan, candesartan, valsartan
  • Well tolerated side effect profile
  • Once daily dosing
  • No significant adverse effects
  • Cost effects
22
Q

What are Ca channel antagonists?

A
  • Block L-type Ca channels
  • Dihydropyridines end w “dine”
    • Vasodilators -> reduce TPR
    • Blocking Ca channels in muscles -> prevents contractions
  • Unwanted side effects
    • Headaches
    • Flushing
    • Ankle swelling
23
Q

What are β-adrenoreceptor blockers?

A
  • e.g. atenolol (lol suffix)
  • Used to be first line therapy but not anymore [significant reduction in blood pressure but ppl were still dying, other agents are more effective at reducing the incidence of stroke n CVS mortality]
  • Mode of action unclear but reduce cardiac output, alter baroreceptor reflex sensitivity
  • May also suppress renin secretion
  • Contra-indicated: asthma sufferers
    • β-receptors in lungs that cause dilation in bronchioles, block receptors -> more likely to get asthma attack
  • Can cause peripheral vasoconstriction -> cold hands n feet
23
Q

Explain the reflex tachycardia

A
  • Alpha 1 are in blood vessels
  • Alpha 2 are presynaptic n inhibit noradrenaline release
  • Non-selective alpha antagonists block both alpha 1 n alpha 2 -> more noradrenaline -> activates β receptors -> increase in heart rate
23
Q

What are thiazide diuretics?

A
  • Cause mild diuresis
    • Bendroflumethiazide
  • Work at the beginning of the distal convoluted tubule in kidneys to increase water n sodium loss
  • Work to reduce blood volume, CO n mean arterial pressure [more excretion from the kidney]
    • Take in the morning to avoid nocturnal diuresis
  • Use low doses
  • Cause hypokalemia
  • Most effective in elderly or patients of African origin
24
Q

What is malignant (accelerated) hypertension?

A
  • V high BP (diastolic > 140 mm Hg)
  • Medical emergency
  • Symptoms
    • Nausea
    • Dizziness
    • Headache
    • Blurred vision
    • Kidney failure
    • Retinopathy
    • Heart failure
  • Treatment
    • IV vasodilators
    • Oral β blockers
    • Calcium antagonists
    • Not ACE inhibitors (immediately) as rapid fall in BP could lead to cerebral infarction n blindness