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Human Pathophyisology: Midterm > Lecture 4: CV Pathophysiology II > Flashcards

Lecture 4: CV Pathophysiology II Flashcards

1
Q

CO = ?

A

HR * SV

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2
Q

What is a normal MAP?

A

100 mmHg

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3
Q

factors that increase heartrate

A

positive chronotropic effect

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4
Q

factors that decrease heartrate

A

negative chronotropic effect

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5
Q

factors that increase contractility

A

positive inotropic effect

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6
Q

factors that decrease contractility

A

negative inotropic effect

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7
Q

increased EDV leads to increased SV

A

Frank-Sterling mechanism

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8
Q

stretching of muscle cells allows more actin/myosin cross bridges to form, causing more tension and increasing contractility

A

length-tension relationship

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9
Q

the degree of stretch of the muscle prior to contraction

A

preload

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10
Q

What does increasing EDV do to the preload?

A

increases it

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11
Q

What does hypertension do the contractility and SV?

A

decreases both (heart must pump against higher arterial pressure)

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12
Q

the load that the heart must pump against

A

afterload

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13
Q

Which receptors monitor BP?

A

venous, atrial, and arterial baroreceptors

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14
Q

What are some problems that can arise with the electrical system of the heart?

A
  • SA node irregularities
  • AV blocks
  • abnormal activation of SNS or PNS
  • atrial fibrillation
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15
Q

What are some problems that can arise with the cardiac muscle of the heart?

A
  • unable to relax or expand

- unable to generate sufficient force to eject blood

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16
Q

What are some of the problems that can arise with venous return (preload)?

A
  • central venous pressure too low due to abnormal vasodilation
  • low blood volume
  • high blood volume (kidney reacting to heart failure)
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17
Q

What are some of the problems that can arise with afterload?

A
  • stiffening of large arteries with age (arteriosclerosis)

- increase in resistance in smaller arteries

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18
Q

How does the filtrate in the glomerulus compare to plasma?

A

its much lower in concentration of proteins

19
Q

What are some factors that alter GFR?

A
  • changes in MAP

- contraction of renal arteries

20
Q

How does contraction of afferent and efferent arterioles affect GFR?

A
  • contraction of AFFERENT decreases GFR by decreasing pressure
  • contraction of EFFERENT increases GFR by increasing pressure
21
Q

when the macula densa cells in the nephron detect a change in Na+/Cl- levels and triggers vasodilation/vasoconstriction of the afferent arteriole to compensate

A

tubuloglomerular feedback

22
Q

Describe the differences of sodium and water reabsorption across the nephron.

A

proximal tubule - 65-75% of sodium reabsorbed; water follows
loop of Henle - 15-20% of sodium reabsorbed (only sodium)
distal tubule - variable; controlled by aldosterone and ADH

23
Q

What are the most important sensors of BP?

A
  • carotid baroreceptors
  • juxtaglomerular apparatus
  • macula densa
24
Q

What is the pathway for renin?

A

juxtaglomerular apparatus –> renin + angiotensinogen (from liver) –> angiotensin I + ACE (on endothelial cells) –> angiotensin II

25
Q

What are the effects of angiotensin II?

A
  • increases thirst
  • vasoconstriction (decreased blood flow to kidneys)
  • increases levels of ADH and aldosterone
26
Q

What can trigger renin release?

A
  • SNS activity
  • decrease in intrarenal BP
  • input from macula densa (decreased Na+/Cl- levels)
  • angiotensin II (negative feedback)
27
Q

What are the functions of aldosterone and where does it come from?

A
  • produced by adrenal cortex
  • controls activity of Na+/K+/ATPase pumps on the distal tubes and collecting duct
  • increases ion reabsorption thus water retention
  • aldosterone is also triggered by high extracellular K+ levels
28
Q

What is atrial natriuretic hormone and what is its function?

A
  • made by atria of the heart (response to stretch/increase blood volume)
  • cardio-protective –> lowers plasma volume
  • dilates glomerular afferent arterioles = increased Na+ excretion
  • inhibits Na+ reabsorption in collecting ducts
29
Q

Where does ADH/vasopressin come from and what is its function?

A
  • produced by posterior pituitary
  • increases reabsorption of water in the distal tubules and collecting ducts by making them permeable to water (aquaporins)
  • contraction of smooth muscle throughout body increases MAP
30
Q

What stimulates/inhibits the release of ADH?

A

Stimulates: increase in plasma osmolarity, decrease in blood volume, angiotensin II, certain drugs

Inhibits: decrease in plasma osmolarity, increase in blood volume, atrial natriuretic peptide, certain drugs/alcohol

31
Q

What controls thirst centers in the brain?

A
  • activity of osmoreceptors
  • activity of blood volume receptors and baroreceptors
  • angiotensin II
32
Q

What is autotransfusion?

A
  • a decrease in capillary hydrostatic pressure causes fluid to move from interstitium to capillaries; automatic
  • activation of SNS –> mobilizes glucose stores –>increase osmolarity promoting fluid reabsorption
33
Q

How does the baroreceptor reflex kick in during a hemorrhage?

A
  • detects a drop in BP

- increases HR/SV and increases vasoconstriction

34
Q

How do the kidneys react to a hemorrhage?

A
  • drop in blood pressure decrease GFR
  • increase in vasoconstriction also decreases GFR
  • ALSO macula densa senses decrease in Na+/Cl- levels
  • stimulates renin release
  • leads to increase aldosterone/ADH/angiotensin II
  • increased thirst
35
Q

How do kidneys respond to heart failure?

A
  • initially, react same as hemorrhage
  • overtime, heart cannot keep up with increase preload
  • leads to peripheral and pulmonary edema
36
Q

How can heart failure be managed/treated?

A
  • low sodium diet (reduces fluid retention
  • diuretic drugs
  • vasodilators (decrease afterload)
  • ionotropic drugs (increase SV, stresses heart)
  • synthetic atrial natriuretic hormone (ANP, reduces blood volume)
37
Q

when someone feels like they are going to pass out but then recover

A

perisyncope

38
Q

MAP = ?

A

CO * TPR

39
Q

syncope due to blood loss, loss of other fluids, or heat stress

A

hypovolemic hypotension

40
Q

syncope due to a fall in BP after standing up, triggering the baroreceptor reflex (response does not occur properly)

A

postural hypotension

41
Q

syncope triggered by strong emotion; decrease in SNS and increase in PSN lowers MAP

A

vasovagal syncope

42
Q

syncope due to problems with cardiac rhythm and electrical conduction pathways; most worrisome

A

cardiogenic syncope

43
Q

What happens during syncope?

A
  • drop in blood pressure leads to disruption of oxygen/nutrient/blood delivery to reticular activating system
  • RAS is responsible for keeping you “awake”
44
Q

What are symptoms of syncope?

A
  • light-headedness
  • blurry or dark vision
  • fainting
  • symptoms disappear/get better when changing posture
  • paleness
  • clammy and cold hands
  • sweating

Human Pathophyisology: Midterm (6 decks)

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