Hypertension Patho Flashcards

1
Q

Does goal BP = ideal BP?

A

No

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2
Q

BP = ….

A

CO * PVR

CO - Cardiac output (SV * HR)
SV - stroke volume
HR - heart rate
PVR - peripheral vascular resistance

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3
Q

PVR Factors

A
  • vascular tone

- resistance arteriole diameter

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4
Q

Cardiac Output Factors

A
  • Blood volume - renal Na+/H2O absorption

- Symp. NS - cardiac HR and contractility

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5
Q

Blood Volume

A
  • Regulates CO
  • long term regulation controlled by kidneys
  • Hypertension clinics are run by nephrologists
  • Dehydration: decreases ECF, decreases BP, decreases Na+/H2O excretion
  • Too much salt: opposite effects
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6
Q

Glomerulus

A
  • controls blood volume by regulating Na+/H2O exretion
  • Macula densa cells - regulations Na+/H2O excretion
  • Juxtaglomerular cells - regulate aldosterone which effects Na+/H2O retention
  • Ascending loop of Henle and distal tubule are CRITICAL segments for Na+/H2O absorption, therefore critical for BV
  • Ascending loop - large amounts of sodium, distal tubule - modest amounts of sodium
  • More dietary Na+ increases your BP
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7
Q

Arteriolar Diameter

A
  • Regulates PVR
  • resistance vessels
  • Contriction/dilation regulates peripheral bascular resistance
  • Increase in endogenous vasoconstrictors increases BP
  • Decrease in endogenous vasodilators increases BP
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8
Q

Endogenous Vasoconstrictors

A
  • NE
  • Epi
  • Angiotensin II
  • Thomboxane A2
  • Endothelin-1
  • Serotonin
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9
Q

Endogenous Vasodilators

A
  • Prostacyclin
  • Bradykinin
  • NO
  • EDHF
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10
Q

Renin-Angiotensin-Aldosterone System

A
  • *OFTEN ACTIVATED IN HTN PATIENTS**
  • Liver - releases angiotensinogen into blood vessels
  • Renin from the kidney interacts with it and make Angiotensin I
  • ACE from lungs interacts with Angiotensin I and makes Angiotensin II
  • Angiotensin II acts on AT Receptors and causes vasoconstrictions and the release of aldosterone
  • Aldosterone then causes sodium retention (increases BP overall)
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11
Q

Which hypertensive drugs are less effective in black patients?

A
  • ARBs

- ACE-Is

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12
Q

SNS

A

-Activation increases BP by increasing HR and contractility force

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13
Q

Are body systems highly integrated??

A

YES

  • Dramatic increases in vasodilation activates the SNS
  • Dramatic increases in vasoconstriction increases Na+/H2O excretion
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14
Q

Secondary HTN

A
  • Needs workup for secondary causes when newly diagnosed for HT
  • Renal artery stenosis, adrenal disease, medication
  • Treating secondary causes fixes the hypertension
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15
Q

Promoting Na/H2O Excretion

A
  • Possible HTN drug target
  • Block Na+ absorption in renal excretion
  • Diuretics
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16
Q

Blocking Vasoconstriction/Stimulating Vasodilation

A
  • Possible HTN drug target
  • Blocks calcium channels on anterior, smooth muscle
  • Block Ang II synthesis/signaling
  • Block alpha-1 receptors
  • Stimulate NO release/signaling
17
Q

Block SNS

A
  • Possible HTN drug target
  • Block Alpha1/Beta1 receptors (one or both)
  • Blocks sympathetic outflow in CNS