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Block 2 Week 3 > BP Regulation: Hormone Control > Flashcards

BP Regulation: Hormone Control Flashcards

1
Q

Neuronal control of Bp?

A

1) regulate CO via SV & HR by changing preload and contractility
2) controls distribution of blood between body and heart
3) re-allocate the CO from ischemic tolerant organs to critical organs
4) regulate EDV (preload)

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2
Q

Hormonal control of BP?

A

1) catelchoamines
2) Neuronotic Peptides (ANP/BNP)
3) Renin-Angiotensin- Aldosterone system
4) Anti-Diuretic hormone (vasopressin)

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3
Q

What is the sympathy-adrenal system and what does it respond to?

A
  • when SNS fires onto adrenal medulla (on top of both kidneys) and causes releases of catelchoamines
  • in response to stress, exercise, hypovolemia, hypoglycemia
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4
Q

How does norepinephrine effect the body?

A
  • preferentially acts on alpha 1 receptors, causes vasoconstriction in skin/gut arterioles
  • can work on beta 1 receptors of SA & myocardium to promote increased HR, contractility, and diastolic reaction
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5
Q

how does epinephrine effect the body?

A

1) preferentially acts on beta 1 in SA & myocardium
2) can work on beta-2 and cause vasodilation in heart & sk muscles, main effect though is metabolic not vasculutre
3) pharm doses can act on alpha 1, causes systemic vasoconstriction to increase SVR & arterial pressure

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6
Q

Ionotropic agent

A

affects contractility

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7
Q

lusiotropic agent

A

affects diastolic relaxation (positive increases, negative decreases)

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8
Q

Adrenal gland structure/histology and secretions? (2 main structures)

A
  • located at top of kidneys has outer cortex & central medulla
  • medulla- secretes catelchoamines
  • zona glomerulosa: secretes aldosterone in response to AT-II
  • zona fasciculata: secretes cortisol in response to ACTH from pituitary
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9
Q

How do heart transplants experience increased HR and contractility during exercise w/o innervation from SNS or PNS?

A

-due to catelchoamine release during exercise from the adrenal medulla

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10
Q

hormone vasoconsctiors?

A
  • NE binds alpha 1, promotes constriction in gut/skin
  • AT-II initiates vasoconstriction when released
  • ADH-vasopressin
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11
Q

hormonal vasodilators?

A

-Epi acting on Beta-2 receptor prominent in heart & sk. muscle for fight/flight response

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12
Q

What is the Natriuretic peptide family?

A

-fam of peptides that promote exertion of Na and urine
-consist of ANP and BNP both in cardiac myocytes
-are cardiopulmonary vol receptors, decrease SNS when activated
-

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13
Q

How are natriuretic peptides activated? What else is activated in this process?

A
  • when cardiac myocytes are over stretched (hypervolumia) ANP/BNP released to tell body have too much blood/pressure
  • hypervolumia also stimulates cardiopulmonary vol receptors to decrease SNS
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14
Q

What are renal & vascular effects of ANP/BNP release?

A

1) inhibit RAA to increase Na and urine excretion
2) causes vasodilation & decreased SVR
3) decrease salt & h20 appetite & ADH secretion
* ANP/BNP= Anti-RAA, do everything to decrease blood volume by decreasing the BP

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15
Q

Natriuresis? Diuresis?

A
  • Naturesis= Na excretion

- Diuresis= urine output

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16
Q

CHF patients and natriuretic peptides?

A
  • have significantly elevated ANP/BNP since have poor kidney profusion due to poor heart functioning
  • kidneys take poor profusion as sign of low BP and BV so excrete less fluid to increase preload
  • now heart OVERFILLED (hypervolumia), myocytes stretching & releases ANP/BNP
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17
Q

What does anti-diuretic hormone (vasopressin) do?

A
  • regulates H20 permeability of kidney distal tubule & collecting ducts
  • causes decreases urine output, vaso/venoconstriction both compensatory for hypovolemia, hypotension & plasma hyper-osmolarity
18
Q

What controls ADH release?

A

1) hypotension (from medullary CV center)
2) hypovolemia (atrial vol receptors)
3) plasma hyperosmolarity (hypothalmic osmoreceptors)
* plasma= strongest signal for ADH release*

19
Q

Renin-Angiotensin- Aldosterone (RAA) System? How activated?

A
  • a hormone cascade that increases BP & blood volume

- activated in response to hypotension, hypovolemia, SNS activity

20
Q

What RAA mechanisms?

A

a) decreases arterial pressure causes JG cells to release renin
b) proteolytic enzyme renin cleaves angiotensinogen–> AT-I
c) AT-I –> AT-II via ACE converting enzymes in lungs
d) AT-II acts on hypothalmus to stimulate thirst & aldosterone release from adrenal cortex

21
Q

AT-II effects (6)?

A

a) vasoconstriction
b) increase brain thirst response
c) aldosterone release from adrenal cortex
d) ADH secretion from pituitary
e) increased SNS
f) increase Na/ H20 retention

22
Q

aldosterone effects?

A

-released from adrenal cortex, causes decreases urine output by increases Na and H20 reabsorption

23
Q

Juxtaglomerular Renal Barorecrptors and main goal?

A
  • JG cells (juxtaglomerular cells) compose juxtaglomerular apparatus (JGA)
  • they are in afferent renal arterioles & deceit changes in wall dissension or Renal Perfusion Pressure
  • release renin is response to hypovolemia, hypotension or increased SNS signaling

-to increase BP back to normal

24
Q

JG cells release?

A

1) renal hypoperfuson (decreased MAP) causes JG cells to release renin
2) Hypotension in body causes SNS activation & it stimulates JG cells to release renin
- when blood flow & pressure restored, JG cells loose stretch & SNS signals and release is halted
- this

25
Q

1) lisinopril

2) losartan

A

1) ACE inhibitor (pri=ACE inhibitor); AT-I can’t convert to AT-II so RAA response blunted
2) angiotensin receptor blocker (ARB); (artan= ARB)
- similar effects as ACE inhibitor

26
Q

what happens if have persistent RAA activation?

A

-results in hypertension

27
Q

What is shock? 4 types of circulatory shock? common feature for all of them?

A
  • shock= when BP is inadequate to support critical organs
    1) cariogenic shock
    2) hypovoluminc
    3) obstructive
    4) distributive
  • all have common feature of atrial hypotension
28
Q

cariogenic shock

A
  • issue w/ hearts ability to contract (decreased contractility)
  • due to MI, ischemic heart disease, arrhythmia causing uncoordinated ventricle contraction
29
Q

Hypovolumic shock?

A
  • inadequate filling of heart due to low EDV (preload), not enough blood to fill vessels
  • due to hemorrhage (also called hemorrhagic shock)
30
Q

obstructive shock?

A
  • when heart can’t contract (Cardiac tamppenade) or when have a pulmonary embolism (obstruction) so blood flow is blocked
  • only 2% of shock cases
31
Q

distributive shock

A
  • lumps together septic and anaphylactic shock, is when CO is normal but loose SVR
  • most common type of shock
32
Q

septic shock

A

-gram negative bacteria release endotoxins, causes macrophages to release cytokines that cause systemic vasodilation & failure of SVR

33
Q

anaphylactic shock

A
  • allergic rxt causes cytokine release that increases mast cell granulation and causes vasodilation & a loss of SVR
34
Q

what are the effects of arterial hypo perfusion?

A

a) brain:altered mental status/ thirst
b) skin: cool, clammy, since baroreflex diverting blood from skin
c) kidney: oliguria (few urine), baroreflex causes blood to divert from kidneys so retain fluids
d) heart: tachycardia due to baroreflex trying to increase CO

35
Q

how long until brain/heart, kidney/lung/liver, and sk. muscle/gut/skin have irreversible ischemic damage?

A

a) brain/heart: 2-5 min
b) kidney/lung/liver: 120-150 min
c) sk muscle, gut, skin= 360-600 min

36
Q

4 stages of shock (due to blood loss)?

A

a) compensated (initial)
b) compensated (non-progressive)
c) decompensated
d) irreversible

37
Q

compensated (initial) shock?

A
  • loose 0-15% of blood volume
  • may have no symptoms
  • compensatory systems activated and working
  • MAP drops below 5mm HG
  • -treat aggressively,s top bleeding, keep warm, give fluids & O2
38
Q

compensated (non-progressive) shock?

A
  • loose 15-25% of blood volume
  • compensatory mechanisms are failing
  • thirsty
  • anxious, restless weak
  • cool, clammy skin
  • decreased PP
  • tachycardia/tachypena
  • treat aggressively,s top bleeding, keep warm, give fluids & O2
39
Q

decompensated shock

A

-25-35% blood volume lost
-absent or weak pulse
-altered mental status (maybe unconscious)
-acidosis
-slow breathing
-toxin accumualtion
is reversible if act quickly if not start positive feedback spiral towards death

40
Q

irreversible

A
  • organ failure
  • heart failure
  • collapse of SVR
  • widespread cell death
  • is a positive feedback spiral that instigated by low MAP and propagated by low MAP to cause even lower MAP and lead to death since organs no longer professed*
41
Q

how is blood volume restored after hemorrhage?

A
  • renal fluid conservation
  • drink water (thirst)
  • transcapillary refil

Block 2 Week 3 (6 decks)

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