Hypertension Flashcards

1
Q

Hypertension definition

A

Pressure on arterial walls exceeding a defined threshold

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2
Q

What does isolated hypertension mean?

A

Just one particular artery or vein/region, i.e. renovascular, portal

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3
Q

Normotension, according to the slide, is what range

A

<120 over <80

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4
Q

Pre-hypertension is what range

A

120-139 / 80-89

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5
Q

Stage I HTN range

A

140-159 / 90-99

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6
Q

Stage II HTN range

A

sys > 160 / dia > 100

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7
Q

Isolated systolic HTN range

A

sys >140 and dia < 90

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8
Q

When in the day is blood pressure normally higher?

A

Morning

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9
Q

What happens to the systolic vs diastolic value with age?

A

Systolic increases with age, diastolic decreases with age

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10
Q

At what age do women meet or surpass the systolic blood pressure of men? (before this age, women have lower BP than men)

A

60-70 years old

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11
Q

What percentage of all death is related to HTN?

A

13-15%

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12
Q

What does essential HTN mean?

A

no clear etiological factor, and describes 80-90% of all HTN patients. all others are “secondary” and have a clear cause

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13
Q

Two things that affect peripheral resistance (from slide)

A

Vessel wall function

Vessel wall structure

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14
Q

Two things that affect cardiac output (again just from slide, not the formula or whatever)

A

Intravascular volume

Contractility

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15
Q

How does increased NaCl intake lead to increased BP?

A

“In order to increase Na+ excretion, BP must increase some too”
Increases glomerular filtration, decreases renal tubule Na+ absorption

Also ANF
(one single mech not clear, but effects of high NaCl uptake are very clear)

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16
Q

What is the guideline for sodium intake in the average population?

A

2300 mg sodium (5.8g NaCl)

17
Q

What is the guideline for sodium intake in the >51 y/o, diabetic, or hypertensive population?

A

1500 mg sodium (3.8g NaCl)

18
Q

Main effects of Angiotensin:

A

vasoconstriction, stimulation of aldosterone secretion, stimulation of vessel wall smooth muscle proliferation

19
Q

Main effects of aldosterone (relevant to this lecture anyway)

A

Stimulation of Na reabsorption

20
Q

How do alterations in RAS relate to essential and secondary hypertension?

A

Essential hypertension: RAS is a consequence, not a cause

Secondary htn: may be from renin-secreting tumors, renovascular HTN, primary or secondary aldosteronism

21
Q

In sustained HTN, what may happen to the baroreceptor set-point?

A

It may be altered, and symp activity is too high. Increased symp tone is related to obesity, sleeping disorders etc. May be more of a “permissive effect” than a cause of hypertension

22
Q

What is arteriosclerosis?

A

Decreasing in elasticity of vessel walls

23
Q

How do ion transport changes in smooth muscle cells lead to HTN?

A

Intracellular Ca2+ increases, causing increased contractile activity in arterioles and vasoconstriction

24
Q

How does endothelin affect vascular compliance?

A

It’s a vasoconstrictor

25
Q

HTN causes weakened vessel walls. What are 3 possible pathologies resulting from this?

A
  1. Cerebral vessel weakening -> hemorrhagic stroke
  2. Renal vessel weakening -> nephrosclerosis and renal failure
  3. Opthalmic vessel weakening -> retinopathy
26
Q

HTN causes accelerated atherosclerosis. What are 3 major risks from this?

A

AMI, ischemic stroke, and aneurysms/dissections

27
Q

HTN causes an increase in afterload. What are 2 major risks from this?

A

Heart failure and AMI due to increased myocardial O2 demand

28
Q

What are two cerebral problems from hypertension that are not a form of stroke?

A

Hypertensive encephalopathy: loss of cerebral autoregulation, etc..

Hypertension-associated Dementia

29
Q

What are 3 manifestations of hypertension in the heart?

A

LVH, CHF, and coronary artery disease

30
Q

What is the most frequent cause of secondary hypertension?

A

Kidney disease

31
Q

What part of the kidney is primarily affected by HTN?

A

Glomeruli primarily affected.

Tubular damage develops at a later stage

Combined glomerular and tubular damage makes the vessels leaky (?)

32
Q

What is the threshold for microalbuminuria vs clinical albuminuria? (check this when suspecting kidney damage from HTN)

A

Micro: 30-300 mg/24 hours
Clinical: >300 mg/24 hours

33
Q

What’s a good early, non-invasive diagnostic of peripheral vascular disease?

A

Dilated fundoscopic examination

34
Q

What are the two kidney secondary hypertension entities?

A

Parenchymal and Renovascular

35
Q

What are some endocrine causes of HTN?

A

Primary aldosteronism, Cushing’s syndrome, Pheochromocytoma, Hyperthyroidism, Acromegaly

36
Q

What are some drugs that may cause secondary HTN?

A

Estrogen/androgen hormone supplements, NSAIDS, chronic alcohol intake, antidepressants, immunosupressive agents

37
Q

How do you test kidney function in diagnostic laboratory test of HTN?

A

Urine sediment, albumin, potassium

Serum creatinin

38
Q

How do you test endocrine function in diagnostic laboratory test of HTN?

A

Serum sodium, potassium, calcium, TSH

39
Q

What are 3 ways to reduce intravascular volume by medication?

A

Diuretics
ACE inhibitors
Aldosterone antagonists