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Fall'20 A&P III > cvs 4 previous semester > Flashcards

cvs 4 previous semester Flashcards

1
Q

BF to an organ is proportional to its metabolic activity. IE more blood flow to exercising muscles is an example of

A

active hyperemia

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2
Q

is an increase in blood flow to an organ to occurs after a period of occlusion of flow

A

reactive hyperemia

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3
Q

what three organs exhibit auto-regulation

A

heart, brain, kidneys

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4
Q

blood flow to an organ remains constant over a wide range of perfusion pressures- this is called

A

auto regulation

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5
Q

what is used to explain autoregulation

A

myogenic hypothesis

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6
Q

vascular smooth muscle contracts when it is stretched

A

myogenic hypothesis

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7
Q

example of myogenic hypothesis

A

increase perfusion pressure to an organ increases stretch of vascular smooth muscle leads to contraction. the resulting vasoconstriction will maintain a constant flow.

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8
Q

tissue supply of 02 is matched to tissue demand for 02

A

metabolic hypothesis

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9
Q

in metabolic hypothesis vascular metabolites are produced as a result of metabolic activity in tissue. what are the vasodilators

A

c02
H+
K+
adenosine

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10
Q

during exercise the increase metabolism leads to what

A

increase production of vasodilators, increase blood flow, increase 02 delivery to the tissue

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11
Q

increase sympathetic tone causes

A

vasoconstriction

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12
Q

decrease sympathetic tone causes

A

vasodilation

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13
Q

what is bradykinin similar to

A

histamine

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14
Q

what causes arteriolar constriction helps to prevent blood loss

A

serotonin 5-ht

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15
Q

what is implicated in the vascular spasm of migraine headache

A

serotonin 5ht

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16
Q

what are the effects of histamine

A

arteriolar dilation and venous constriction leads to increased capillary hydrostatic pressure and increased filtration out of the capillaries resulting in local edema

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17
Q

how does histamine create local edema

A

artery dilation venous constriction
increase cap hydrostatic pressure
increased filtration out of the capillaries

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18
Q

prostacyclin is a

A

vasodilator

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19
Q

thromboxane A2 is a

A

vasoconstrictor

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20
Q

what do baroreceptors do

A

alerts brain in case of low blood pressure

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21
Q

what are baroreceptors

A

stretch receptor

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22
Q

where are baroreceptor located

A

carotid sinus near the bifurcation of common carotid arteries

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23
Q

what is responsible for the minute to minute regulation of arterial BP

A

baroreceptor

24
Q

what accounts for vasomotor tone and produces vasoconstrictor activity tonically

A

baroreceptor

25
Q

what controls circulation

A

sympathetic nervous system

26
Q

what controls the heart function via vagus nerve

A

parasympathetic nervous system

27
Q

where does the vasomotor center transmit its impulses

A

down the cord to almost all blood vessels

28
Q

where is the VMC located?

A

bilaterally in the reticular substance of the medulla and the lower third of the pons

29
Q

what is the vmc composed of

A

a vasoconstrictor area, vasodilator area, and sensory area.

30
Q

decrease stretch on the baroreceptors - what happens

A

the firing rate of the carotid sinus nerve hering nerve, CN IX, which stimulates the VMC in the brain

31
Q

The responses of VMC to a decrease MAP are:

A

Decrease parasympathetic (vagal) outflow to the heart

Increase sympathetic outflow to the heart and blood vessels

32
Q

The following four effects attempts to increase the arterial pressure to normal

A

increase Heart rate ,resulting from decrease parasympathetic tone and increase sympathetic tone to the SA node
increase Contractility and SV which produces increase in cardiac output
increase vasoconstriction of arterioles; as a result TPR will increase , increasing arterial pressure
increase vasoconstriction of veins resulting increase venous return

33
Q

A decrease in renal perfusion pressure causes the juxtaglomerular cells to secrete

A

renin

34
Q

ACE catalyzes the conversion of angiotensin I to angiotensin II in the

A

lungs

35
Q

ace inhibitors

A

e.g. captopril) blocks the conversion of angiotensin I to angiotensin II and therefore, BP

36
Q

arb action

A

Angiotensin receptor (AT1) antagonist (e.g. Losartan) block the action of angiotensin II at its receptor and decrease blood pressure.

37
Q

what does angiotensin 2 have for effect on aldosterone

A

synthesis and secretion of aldosterone by the adrenal cortex

38
Q

aldosterone increases what to be reabsorbed

A

Na+ reabsorption by the renal distal tubular, thereby increasing extracellular fluid volume

39
Q

increase HR= means? treatment?

A

increase 02 consumption
decrease coronary blood flow

give beta blockers

40
Q

increase BP

increase Wedge

A

increase afterload
increase work of heart
increase 02 consumption

increase depth of anesthesia
nitroglycerin

41
Q

decrease blood pressure

decrease or normal wedge

A

decrease TPR
decrease BP and coronary blood flow

decrease anesthesia
fluids
phenylephrine to improve BP and coronary circulation

42
Q

decrease BP

increase wedge

A

heart is failing
intros
phenylephrine
nitroglycerine

43
Q

normal hemodynamics

A

ng and CA channel blockers

44
Q

Loss of circulating volume %

< 20 %

A

Skin changes
BP normal
Thirsty , cold , wake and alert

45
Q

20-40%

A

Oliguria (20 ml/hr)
Restlessness
decrease BP, weak pulse >120
Confusion

46
Q

> 40 %

A

Very low BP, no pulse >140
EKG changes
Lethargic, coma
No urine output

47
Q

Coronary Circulation %

A

5% of cardiac output (250 ml/min)

48
Q

Coronary Circulation

vasodilation

A

hypoxia and adenosine

49
Q

Bainbridge Reflex

A

Increase in atrial pressure increases heart rate
Stretch of atria sends signals to VMC via vagal afferents to increase heart rate and contractility.
Prevents damming of blood in veins atria and pulmonary circulation.

50
Q

Cushing reaction:

A

increased ICP causes compression of cerebral blood vessels leading to cerebral ischemia and increase cerebral PCO2 .The VMC directs an increase in sympathetic outflow to the heart and blood vessels, which cause a profound hypertension, bradycardia and irregular respiration (Cushing triade; opposite to shock !)

51
Q

Cerebral ischemia

A

Cerebral ischemia
When the brain is ischemic the conc. of CO2 and H+ in brain tissue increases
Chemoreceptor in the VMC respond by increasing sympathetic flow to heart and blood vessel
Constriction of arterioles causes intense peripheral vasoconstriction and increase TPR
Blood flow to other organs (e.g. kidneys) is significantly reduce in an effort to keep blood flow to brain
MAP can increase to life-threatening levels

52
Q

Angiotensin II has four effects

A

It stimulates the synthesis and secretion of aldosterone by the adrenal cortex
Aldosterone increases Na+ reabsorption by the renal distal tubule, thereby increasing extracellular fluid volume, blood volume and arterial pressure
This action of aldosterone is slow because it requires new protein synthesis
It increases Na+-H+ exchange  contraction alkalosis
It increases thirst
It causes vasoconstriction of the arterioles, thereby increasing the TPR and MAP

53
Q

Steps in the renin-angiotensin-aldosterone system

A

A decrease in renal perfusion pressure causes the juxtaglomerular cells to secrete renin
Renin catalyzes the conversion of angiotensinogen to angiotensin I in plasma
ACE catalyzes the conversion of angiotensin I to angiotensin II in the lungs
ACE inhibitors (e.g. captopril) blocks the conversion of angiotensin I to angiotensin II and therefore, BP
Angiotensin receptor (AT1) antagonist (e.g. Losartan) block the action of angiotensin II at its receptor and decrease blood pressure.

54
Q

Renin-angiotensin-aldosterone system

A

Is a slow, hormonal mechanism
Is used in long-term blood pressure regulation by adjustment of blood volume
Renin is an enzyme that catalyzes the conversion of angiotensinogen to angiotensin I in plasma
Angiotensin I is inactive
Angiotensin I is converted into Angiotensin II by ACE in lung
Angiotensin II is physiologically active

55
Q

Valsalva maneuver

A

expiring against a closed glottis)
Tests the integrity of baroreceptor mechanism
Causes  intrathoracic pressure which  venous return
The  venous return causes  in cardiac output and arterial pressure (Pa)
If the baroreceptor reflex is intact, the decrease in Pa is sensed by the baroreceptor, leading to  in sympathetic flow to the heart and blood vessels. In the test,  in heart rate would be noted.
When the person stops the maneuver, there is a rebound increase in venous return, cardiac output and Pa. The  in Pa is sensed by the baroreceptor, which direct a  in heart rate.

Fall'20 A&P III (13 decks)

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