bp regulation & htn Flashcards

1
Q

Difference in bp between a patients right and left arm is a sign of

A

vascular disease!

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2
Q

Why is hypertension bad?

A

It damages blood vessels throughout the entire body, affecting multiple systems.

Ex) Heart, brain, renal failure, retinopathy, peripheral vascular disease

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3
Q

Mechanisms of hypertension

A
  • Chronic positive salt & water balance
    • Excessive salt; diseased kidney; messed up hormones; etc
  • Overactive nervous system sending signals to heart, kidney, and blood vessels to retain salt
  • Incorrect responses of hormones that normally regulate salt and water balance & cardiovascular system
    • Increased heart contractility; vasoconstriction; decreased blood flow to kidney reducing salt excretion
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4
Q

Most monogenetic causes of hypertension involves

A

Inappropriate Na+ reabsorption by the kidneys

Ex) Aldosteronism, liddle’s syndrome (excess Na+ channel activity), etc

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5
Q

Hypertension & Kidney disease can cause each other.

How does eating excessively salty food cause hypertension?

A

Eating too much salt can decrease your kidney’s Na+ excretory capability –> increased ECFV & BV

–> chronic increases in ECFV & BV or decreases in vascular capacitance will cause hypertension

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6
Q

How does increased [NaCl] lead to concentrated urine and thirst?

A

ADH gets released –> thirst & concentrated urine

Whereas, if [NaCl] drops, then ADH gets inhibited.

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7
Q

Osmolality is rapidly regulated by adjusting

A

the ECFV by peeing

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8
Q

Salt-resistant patients

A

When they increase their salt intake, they do have increased cardiac output since their ECFV increases (like normal).

However, they have decreased vascular resistance to accommodate for this increased cardiac output –> won’t develop hypertension

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9
Q

The most important regulatory mechanism of Na+ excretion is

A

GFR

  • Autoregulatory mechanisms: higher bp, the greater afferent arteriole resistance to maintain RBF and GFR.
  • NO from vascular smooth muscle cells maintains RBF and normal salt excretion
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10
Q

What stimulates reabsorption at the proximal tubule?

A

Ang II

Adrenergic agents

Increased luminal flow or solute delivery

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11
Q

What stimulates reabsorption at the thick ascending limb?

A

ADH

Adrenergic agents

Mineralcorticoids

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12
Q

What diuretics work at the distal tubule and connecting tubule cells?

A

Thiazides block the Na/Cl cotransporter

Amiloride blocks the apical Na+ channels, and at higher concentrations, the Na/H exchanger

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13
Q

What stimulates reabsorption at the collecting duct?

A

Aldosterone

Antidiuretic hormone

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14
Q

Pressure natriuresis

A

The higher your blood pressure, the higher Na+ excretion.

However, whether your salt status (deplete or replete) determines how much Na you’ll excrete at any given pressure.

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15
Q

The impact of nitric oxide on pressure natriuresis

A

It promotes sodium excretion when bp is high

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16
Q

COX1 & 2 are constitutively expressed in the kidney.

What upregulates COX2?

A
  • Volume restriction
  • High renin states ( need to compensate)
    • Salt restriction
    • ACE inhibition
    • diuretic therapy
    • renovascular htn
17
Q

Giving an NSAID would have what effect on GFR and renal plasma flow?

A

Decreases both GFR & RBF because you don’t have prostaglandins to vasodilate. Thus, the RAS system is unopposed and going to vasoconstrict, decreasing both.

18
Q

ANP

A
  • Vasodilates
  • Decreases aldosterone, renin, and Na reabsorption
19
Q
A
20
Q

Beta blockers & calcium blockers

A

reduce blood vessel constriction

(remember that the sympathetic mechanism relies on norepi workign on a B receptor)