Hypertension pathophysiology Flashcards

1
Q

Primary hypertension etiology? can it be cured?

A

Polygenetic HTN (more common than monogenetic)
- genetic defects related to sodium imbalance, NO release, aldosterone excretion, angiotensinogen physiology
most patients
- cannot cure but can control
- population studies guide choice of therapy (ex. stroke with black people, europeans CHD)

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2
Q

Secondary hypertension etiology? can it be cured?

A

Could be disease, drug, combo
Technically “yes”

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3
Q

Which drugs are secondary causes for HTN

A
  • Alcohol/Ethanol (excessive)
  • NSAIDs
  • cyclosporine, tacrolimus
  • COCs
  • Corticosteroids
  • Salt (high sodium intake)
  • SSRIs/SNRIs/MAOIs
  • Licorice root/ephedra alkaloids/St. John’s Wort
  • Stimulants (cocaine, nicotine)
  • Sympathomimetic decongestants
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4
Q

What disease can cause secondary HTN

A
  • Chronic kidney disease
  • Cushing’s syndrome
  • Obstructive sleep apnea
  • Parathyroid disease
  • Pheochromocytoma
  • Primary aldosteronism
  • Renovascular disease
  • Thyroid disease
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5
Q

What are the studies for black patients?

A

ACEi believed to be less effective for black patients
- not first line for black patients

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6
Q

Systolic BP
What occurs?
What is it determined by?
Equation?

A

When heart is contracting
- determined by Cardiac output CO
- CO = stroke volume x Heart rate

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7
Q

Dystolic BP
What occurs?
What is it determined by?

A

Heart is relaxing
- determined by total peripheral resistance

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8
Q

What is mean arterial pressure?
When is it used?
Equation?

A

MAP: 1/3 of SBP and 2/3 of DBP
- body spends more time in diastole

Used in hypertensive emergency

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9
Q

What is pulse pressure a measure of?
Equation?
Used for?
Directly correlated to?

A

Measures arterial wall tension
SBP - DBP
- used for isolated systolic HTN
- Directly correlated to CV morbidity/mortality

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10
Q

What is total peripheral resistance determined by? (2)

A

Functional constriction
Structural vascular hypertrophy

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11
Q

What is blood pressure the product of?

A

increase cardiac output and increased total peripheral resistance

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12
Q

what are causes of increased cardiac output

A
  • increased cardiac preload
  • increased fluid volume (from excess sodium/renal sodium retention)
  • Venous constriction
  • Excess stimulation of the renin-angiotensin-aldosterone system RAAS
  • Sympathetic nervous system overactivity
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13
Q

what are causes of increased peripheral resistance

A
  • Functional vascular constriction
  • Excess stimulation
  • SNS overactivity
  • Excess stimulation of RAAS
  • genetic alterions
  • structural hypertrophy
  • hyperinsulinemia resulting from metabolic syndrome
  • endothelial derived factors
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14
Q

When is BP the lowest?
When does it rise sharply?
When is the highest BP?
When is BP increased acutely?

A

When is BP the lowest?
- during sleep

When does it rise sharply?
- few hours prior to awakening

When is the highest BP?
- midmorning

When is BP increased acutely?
- during physical activity or emotional stress

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15
Q

Define isolated systolic hypertension. What does it result from?

A

SBP value elevated and DBP are not <90 and <80
- result from changes in the arterial vasculature consistent with aging (decrease the compliance of arterial wall due to both structural and functional changes)

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16
Q

What is the most important regulator of BP

A

Renin-angiotensin-aldosterone system RAAS

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17
Q

How is BP detected?

A

Located in the afferent arterioles in the baroreceptor sensing device of the kidney

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18
Q

Which intra-renal factors is renin regulated by?

A
  • renal perfusion pressure
  • level of catecholamines
  • angiotensin II
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19
Q

Which extra-renal factors is renin regulated by?

A
  • level of sodium
  • chloride
  • potassium
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20
Q

What other things do the RAAS regulate?

A
  • Na
  • K
  • blood volume
  • vascular tone
  • SNS
21
Q

What does upregulation of RAAS do to BP?

A

Increase BP

22
Q

What natriuretic hormone do?

A

Inhibits Na/K-ATPase
- interferes with Na transport

23
Q

What does an increased NH cause?

A

MORE NH should reduce Na and water in the system

Since NH also interferes with Na transport out of smooth muscle cells
- more NG causes INC intracellular Na + Ca –> Inc vascular tone

24
Q

How is hyperinsulinemia caused?

A

Combo of multiple CV insulin resistance and metabolic syndrome

25
Q

How does hyperinsulinemia affect BP?

A

inc insulin causes inc in sodium retention and sympathomimetic effects
- insulin has some growth hormone effects –> hypertrophy of vascular walls –> inc TPR

26
Q

How do baroreceptors react to changes in BP?
how does this affect BP/

A

Decreased BP -> vasoconstriction + increased HR
Increased BP -> vasodilation + decreased HR

Not as effective in elderly

Any defect in autonomic nerve fibers, adrenergic receptors, baroreceptors, CNS cause HTN

27
Q

How should kidneys respond to decrease and increased BP?

What do defects in this cause?

A

Normal
Low BP: dec Na excretion and inc water volume = inc blood volume
High BP: inc Na excretion and dec water volume - dec blood volume

Defects
- chronic dec Na excretion and inc water volume –> inc blood volume and sodium in smooth muscle –> inc TPR

28
Q

How should vascular endothelium respond normally to low and high BP ?

Which system is defective?

A

Low BP: secrete vasoconstricting substances
- angiotensin II
- endothelin I

High BP: secrete vasodilating substances
- prostacyclin
- bradykinnin
- nitric oxide

Ex. dec NO = inc vasoconstriction and inc BP

29
Q

Which electrolytes effect BP?

A

Sodium
- inc Na = inc BP

Calcium
- inc Ca = dec BP

Potassium
- inc K = dec BP

30
Q

Starting at what BP does the risk of CVD increase? At what incrament?

A

starting at 115/75
- increases with 20/10

31
Q

Which BP number should be used to predict CHD complications? at what age?

A

<50yo = DBP
50-59yo: SBP, BDP, pulse
60+: SBP, pulse

32
Q

Who should we screen for hypertension that may have additional CV risk factors?

A
  • Age Men 55+, women 65+
  • DM
  • Dyslipidemia
  • Albuminuria
  • Family history of premature CV disease
  • Obesity BMI 30+
  • Physical inactivity
  • Tobacco use
33
Q

How do we diagnose hypertension?

A

The average of 2+ measurements taking during 2+ clinical encounters

34
Q

What is BP measured in practice with?

A

Indirect measurement using sphygmomanometer
- Automated office blood pressure (AOBP)

35
Q

How to prepare patient for BP measurement?

A
  • Avoid nicotine, caffeine, meals, exercise, for 30 min before
  • remove clothing that covers cuff
  • Comfortably sit
  • uncross legs
  • back and arm supported
  • middle of the cuff is at level with the right atrium
  • relax for 5 min and do not talk
36
Q

How does the automated office blood pressure device work (AOBP). How to record BP?

A

Measures at 1-2 min intervals
- HCP should be there for the first measurement only to verify cuff size

Measure 3 times
- discard first measurement, average the last 2

To record
- Average BP
- Arm used
- Patient position (supine, sitting or standing)

37
Q

How does Non-AOBP work? How do you measure BP?

A
  1. Select a cuff size recommended by manufacturer
  2. Place the bell or diaphragm of the stethoscope on the BRACHIAL artery
  3. Increase pressure to 30 mmHg above the level when the pulse disappears
  4. Open control valve at 2mm Hg/heart beat
38
Q

How do you read systolic and diastolic BP in a non-AOBP?

A

Systolic
- at first appearance of clear tapping sound

Diastolic
- point at which the sounds disappear

39
Q

How many times do you record for non-AOBP?
Which values do you use

A

Measure at least 3 times, on the SAME ARM
- Discard the first 1 measurement, average the rest

Perform same steps on other arm
- use the arm with HIGHER values

40
Q

How does ambulatory BP monitoring work? When is it used?

A

If office-induced increase in BP is suspected

Device remains on patient for 24 hours and measured every 20-30 min during day and 30-60 at night
- THRESHOLD IS LOWER (more strict test)

41
Q

Does the non-AOBP overestimate or underestimate BP?

A

Sphygmomanometer Will produce slightly higher BP values (5/5 higher) - overestimate

42
Q

How does the AOBP in the pharmacy compare to physicians office?

A

It is comparable
- pharmacies need to go through calibration and adjustment of cuff sizes

43
Q

Are AOBP affected by the setting in which BP is recorded?

A

No

44
Q

Are ambulatory BP monitoring similar to automated office monitoring

A

Yes

45
Q

What BP qualifies as a hypertensive crisis?

A

Systolic BP 180+
Diastolic BP 120+

46
Q

Differentiate between the 2 types of hypertensive crises?

A

Urgency:
- no end-organ damage (not progressing, chronic)
- Optic disc edema
- Reduction in BP over several hours/days using oral therapy

Emergency
- acute/progressive organ damage
- CNS/Eyes/Cardiac/Renal insufficiency
- Treatment: within hours using parenteral therapy

47
Q

What are risk factors for hypertensive crisis? (4)

A
  • Medication non-adherence
  • cocaine use
  • drug interactions
48
Q

What IV BP meds are used for emergency crisis? (3)
At what rate should it work

A

Labetalol
Nitroprusside
Nitroglycerin

Reduce initially by 25%
over next 2 hours target 160/100
Over 24 hours should be “normal”

49
Q

What oral BP meds are used for urgency crisis? (3)
At what rate should it work

A

Clonidine
Labetalol
Captopril

Reduction must be slow and gradual (24-48 hr)