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Hypertension Flashcards

1
Q

What do you use to measure blood pressure

A

Sphygmomanometer

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2
Q

How do you measure blood pressure

A

seated for at least 5 min, no caffeine or nicotin before 30 min of measurement, no feet dangling, arm elevated to heart lvl, 2 measurement 5 min apart , before hypertension diagnosis, repeated at 3 times at least 2 weeks apart.

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3
Q

Systolic BP

A

Contract and pump out

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4
Q

Diastole BP

A

when chamber is relax and it is filling

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5
Q

Hypertension

A

Elevated systemic arterial blood pressure

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6
Q

Normal blood pressure

A

<120, <80

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7
Q

Pre hypertension

A

120-139, 80-89

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8
Q

Stage 1 Hypertension

A

140-159 , 90-99

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9
Q

Stage 2 Hypertension

A

> 160, >100

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10
Q

Two type of Hypertension

A

Primary- no known cause, majority cases.

Secondary - with cause (kidney disease, hyperthyroidism, pregnancy, erythropoietin, Pheochromocytoma, sleep apnea, oral contraceptive use)

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11
Q

What are causes of hypertension? What are the risk factor of hypertension and meds causes hypertension?

A

amt of water and salt in body, condition of kidneys, nervous system, blood vessels, hormones.
Risk factor- obesity, smoking, stress, high salt diet, diabetes, african descent.
Meds - NSAID, oral contraceptive, cold med that contain pseudoephedrine

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12
Q

Determinant of Blood Pressure

A

Blood pressure = Cardiac output x peripheral resistance

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13
Q

What is cardiac output determined by

A
  • heart rate, contractility, blood volume and venous return
  • increase in these will increase cardiac output, and caused higher blood pressure
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14
Q

What is peripheral resistance determined by

A

arteriole constriction

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15
Q

What body system regulate blood pressure

A
  1. Sympathetic nervous system
  2. RAAS
  3. Kidney
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16
Q

Baroreceptor things to know

A

on aortic arch and carotid sinus - sense bp and relay to bp, if it is too lower, brain stem send impulse along sympathetic neuron stimulate heart - cause increase cardiac output and vice versa.
Respond rapidly
can oppose drug attempts due to higher set point

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17
Q

RAAS

A
  • blood volume and electrolyte balance
  • activation of RAAS - takes hours or days to influence blood pressure.
    Angiotensin -> (renin) Angiotensin 1(inactive) -> ACE–>Angiotensin 2( active) – Aldosterone, ADH (vasopressin)
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18
Q

Renin

A

Cleave angiotensinogen to angiotensin 1

RATE limiting step

synthesize and secreted by juxtaglomerular cell

Will be increase in release - if there is - low bp, decrease blood volume, stimulation of beta 1 adrenergic receptor on juxtaglomerular cells of kidney

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19
Q

ACE

A

ACE convert inactive Angiotensin 1 to 2

Angiotensin 2 is very good vasoconstrictor - bind to AT1 receptor and increase bp

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20
Q

Aldosterone what does it do

A

increase sodium and water retention- increase blood volume, increase BP

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21
Q

ADH, what does it do?

A

Posterior pituitary gland- ADH - vasopressin - water retention - increase bp

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22
Q

Renal BP regulation

A
  • by retaining water
  • increase blood volume
23
Q

Non drug treatment for hypertension

A
  • initial recommendation
  • decreasing body weight
    -restrict sodium
  • exercise
  • potassium supplementation
    -DASH diet
    -smoking cessation
    -Alcohol restriction
24
Q

How does obesity cause hypertension

A
  • increase insulin secretion- cause tubular reabsorption of NA and create extracellular volume
  • increase sympathetic nervous system -> activate heart –> increase contractility and vasoconstriction of arteries
25
Salt lvl to help decrease bp
limit to 5 g per day
26
Potassium
Inversely correlated with bp High potassium diet DO NOT do high potassium diet ifACE inhibitor taking
27
Sites of Action for Antihypertensive med
Vascular Smooth Muscles - calcium channel blockers -Thaizide Diuretics RAAS -Beta Blocker -Direct Renin Inhibitor - ACE inhibitor - ARBs -Aldosterone Receptor antagonists Brain Stem -Centrally Acting Alpha 2 Agonist Heart -Beta Blocker -Calcium Channel Blocker Kidney - Thiazide Diuretic - Loop Diuretics - Potassium Sparing Diuretics
28
Diuretics
Mainstay therapy -3 main classes : Thiazide Diuretic, Loop Diuretics, Potassium Sparing Diuretics - Block sodium and chloride reabsorption from nephron of kidney - prevent reabsorption of water , lower cardiac output and decrease bp
29
Diuretic Site of Action
Loop - Thick ascending limp, 20% of Na+ and Cl- reabsorbed Thiazide - Distal tubules, 10% of Na+ and Cl- Potassium Sparing - Collecting duct , 1-5% Na+ reabsorbed
30
Adverse Effect of Loop Diuretic
- Hypokalemia (fatal due to cardiac dysrhythmia) - Hyponatremia - Dehydration - Hypotension
31
When do you use loop diuretic
- needs rapid loss of fluid - edema - severe hypertension - severe renal failure
32
Thiazide Diuretic
- Most common to use - Act by two mechanism 1. block Na and Cl in distal tubules 2. Decrease vascular resistance, we don't know how. Adverse affect - Hypokalemia (fatal due to cardiac dysrhythmia) - Hyponatremia - Dehydration - Hypotension
33
Potassium Sparing Diuretic/ Aldosterone Inhibitor
- minimal lowering of bp - never use alone - inhibit aldosterone receptor in collecting duct - aldosterone normally cause sodium uptake and potassium secret - blocking does the opposite effect - secrete sodium and retain potassium - combo with thiazide and loop diuretic - Should not be used with ACE or ARBs due to conservation of K with these drugs. - Adverse effect : hyperkalemia
34
Beta blockers how does it work (olol)
2 mechanisms 1. block cardiac beta 1 receptor (normally binding of catecholamine cause increase cardiac output) 2. Blocking beta 1 receptor on juxtaglomerular cell ( release renin to cause RAAS and vasoconstrictor)
35
1st gen beta blocker
- non selective block of beta blocker - beta 1 in heart and juxtaglomerular cell) and also beta 2 receptor in lung (could be an issue with resp diseases)
36
2nd gen beta blocker
selective block of beta 1
37
Beta blocker adverse effect
- bradycardia - decrease cardiac output - hf -rebound hypertension (cardiac excitation ) need to wean off over 10-14 days - non selective beta blocker --> bronchoconstriction Inhibition of hepatic and muscle glycogenolysis
38
ACEI MOA ends with -Pril
1. Decrease production of Angiotensin ii 2. Inhibit breakdown of bradykinin ( ACE breaks down bradykinin and bradykinin cause vasodilation)
39
Adverse effect of ACEI
- 1st dose hypotension - hyperkalemia ( decrease in angiotensin ii cause decrease aldosterone causes potassium retention) - persistent cough - Angioedema - NSAID decrease affect of ACEI
40
ARBs Ends with -sartin
similar to ACEI - block binding of Angiotensin ii to receptor AT1 receptor - Do not effect angiotensin ii synthesis - cause vasodilation - abrs decrease aldosterone release from adrenal cortex - don't break down bradykinin so no cough - lower angioedema risk
41
Direct Renin Inhibitor How does it work?
Bind to renin block conversion of angiotensinogen to angiotensin 1 (rate limiting step) - bp lowering affect is the same as other classes of drugs
42
Adverse effects of Direct Renin Inhibitor
Hyperkalema Lower incident of cough and angioedema Diarrhea
43
Calcium role in heart
- important for contraction - outside cell to inside cell via calcium channel
44
Calcium Channel Blockers MOA
Important for contractility and vasoconstriction of arterioles
45
Two type of Calcium Channel
- Dihydropyridine Calcium Channel Blocker - Non-dihydropyridine Calcium Channel Blocker
46
Dihydropyridine Calcium Channel Blocker ends with -dipine
- decrease calcium influx into arteriolar smooth muscle - result in relaxing of muscles around the arteries and cause vasodilation - at therapeutic dose won't act on heart
47
Adverse Effect of Dihydropyridine Calcium Channel Blocker
flushing, dizziness, headache, peripheral edema, rash, reflex tachycardia
48
Non-Dihydropyridine Calcium Channel Blocker
- both heart and smooth muscle of arteries - vasodilation and also decrease cardiac output
49
Adverse Effect of non-Dihydropyridine Calcium Channel Blocker
Flushing, headache, dizziness, edema, constipation, compromise cardiac function use with care for people with hf.
50
Centrally Acting Alpha 2 receptor agonist
- decrease sympathetic outflow to heart and blood vessel ( normally it increase cardiac output and vasoconstriction)
51
Centrally Acting Alpha 2 receptor agonist Adverse Effect
- Drowsiness - dry mouth - rebound hypertension (taper off slowly over time)
52
Treatment algorithms
- targe bp lvl (<140 over <90) -pt with diabetic or chronic kidney disease (130/80 or less) With renal disease - can't use thiazide, need loop
53

Pharm (10 decks)

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