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autonomic final > lecture 20 > Flashcards

lecture 20 Flashcards

1
Q

how does exercise causes the loss of homeostasis

A

increased production of CO2, body temp and affects BP

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2
Q

how does the ANS help maintain homeostasis

A

increase RR, sweat rate, heart rate

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3
Q

what is produced by skeletal muscles during exercise and how does the body deal with these compounds

A

CO2 + lactic acid = lots decrease pH of blood > peripheral and central chemosensors activates project to DRG to VRG > increase RR

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4
Q

what is produced by working muscles during exercise and how does the body deal with this

A

muscles generate heat > increase body temp > activates pre-optic area of hypotha > causes vasodilation of blood ves near skin (heat dissipation + decrease total peripheral resis) + causes production of sweat (contain water and sodium so > heat dis + decrease BV + decrease Na levels)

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5
Q

what happens to BP during exercise

A
  • BP increases to deliver o2 to working muscles
  • set point for baroR increased
  • lactic acid and other metabolites are released from working muscles which are sensed and act to cardiovas center in medulla > SNS act increased to heart and vasculature = trigger muscle chemoreflex
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6
Q

how does exercise effect SNS output to heart and vasculature

A

increases SNS output
- PNS outflow to heart decreased
- SNS outflow to vasculature may still be increased in non-exercising tissue if BP does not meet higher baroR set point

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7
Q

what is the result of chronic exercise training

A
  • causes adaptation
  • muscle increase capacity to produce ATP
  • less lactic acid produced > less stim of muscle chemoreflex = lesser increase in HR by SNS so increased cardiac output is maintained by increased SV
  • less stim of respiration
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8
Q

how does autonomic output help maintain water and sodium balance

A
  • volumetric thirst
  • activation of renin-angiotensin system
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9
Q

how is volumetric thirst elicited

A
  • carotid sinus (baroR)
  • heart and large blood ves (atrial baroR)
  • kidneys (JG cells)
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10
Q

how is RAS elicited

A
  • decrease blood flow to kidneys causes release of renin > increases production of ang2 (direct + indirect effects to maintain water and sodium levels)
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11
Q

what are the direct effects of ang2 to maintain water and sodium levels

A

Angiotensin II has direct effects
- At circumventricular organs: increases thirst At SFO + Increases sodium appetite At OVLT
- In the vasculature: Increases vasoconstriction
- In the kidneys: Increases retention of sodium

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12
Q

what are the indirect effects of ang2 to maintain water and sodium levels

A
  • At the posterior pituitary > Increased vasopressin release = increases vasoconstriction + Increases reabsorption of water in kidneys
  • At the anterior pituitary > Increased ACTH release > Increases release of aldosterone = Increases reabsorption of sodium in kidneys + Increases salt appetite
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13
Q

what is shock

A
  • condition in which the body tissues do not receive adequate perfusion > decrease blood supply = less oxygen + glucose and less removal of metabolic waste > cell death, organ failure, death
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14
Q

what are the stages of shock

A
  • Initial shock
  • Compensatory shock
  • Decompensatory shock
  • Refractory shock
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15
Q

describe initial shock

A

blood flow is shifted to vital organs so blood flow to cap beds is severely restricted

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16
Q

describe compensatory shock

A
  • different compensatory mechanisms activate in order to increase perfusion
  • chemosensors, SNS, RAS, hypothalamus
    1) anerobic metabolism > decrease pH (lactic acid) > sensed by chemo sensors > activate DRG + VRG = increase RR
    2) SNS activate > increases HR and vasocon to support BP + increase NE + epi to increase cardiac contractility and vasocon
    3) activation of RAS > decreased blood flow to kidneys = release renin > ang2 produced = vasocon + thirst and salt app + release of aldosterone (Na reabsorp and salt app) + vasopressin (incr reabsorp water and vasocon)
    4) hypothalamus act > release CRF > release ACTH = increase cortisol and blood glu + release aldosterone
    also vasopressin from posterior pit = reabsorp water + vasocon
17
Q

describe decompensatory shock

A

body cannot maintain perfusion > lysosome break down > more acid
Na K pump begins to fail > sodium retention and osmotic pressure inside cells rise = swell and may burst

18
Q

describe refractory shock

A

multi organ failure

19
Q

what is the 4 kind of shock

A

cardiogenic + distributive + hypovolemic + obstructive

20
Q

describe cardiogenic shock + symptoms

A
  • intracardiac causes of decreased cardiac output
  • heart func can be decr by several conditions:
    myocar infarc = decrease SV
    CHF = decrease SV
  • symptoms = SoB/swelling of lower extremities
  • treatment = O2 + determination of cause so other appropriate treatment can be used
21
Q

describe distributive shock

A

Severe peripheral vasodilation
2 kinds: neurogenic and anaphylatic

anaphylactic = allergic reaction lead to vasodil and leakage of fluid from blood ves

22
Q

describe neurogenic shock

A

neurogenic = loss of autonomic tone > vasodil (like from dmg to spinal column so symp outflow is blocked = Prohibits sympathetic postganglionic release of NE + Prohibits sympathetic activation of adrenal glands = Blocks release of epi, NE into bloodstream)
symptoms: Warm, dry skin
Redness of the skin
Low blood pressure
Slow pulse
Treatment includes: Administration of iv fluids
Administration of norepinephrine, epinephrine

23
Q

describe anaphylactic shock

A

Exposure to an antigen that an individual is
sensitized to causes a massive response which
includes the release of vasoactive substances > Vasodilation = Decreased blood pressure
Increased permeability of the capillaries = Movement of fluid from blood vessels to interstitial space
(edema) > Causes relative hypovolemia
Symptoms of anaphylactic shock include
Redness of skin
Itching, hives
Swelling
Difficulty breathing
Increased heart rate
Decreased blood pressure
Treatment includes
Maintenance of airway
Administration of
medications including
Antihistamines
Corticosteroids
Epinephrine
Inhaled albuterol

24
Q

describe hypovolemic shock

A
  • Reduced intravascular volume
    decrease blood volume which could be from several factors:
  • Internal bleeding (stomach or duodenal ulcers + Colon cancer)
  • External bleeding
  • Dehydration (Vomiting or diarrhea + Heat exhaustion)
  • Plasma loss in burn patients

Symptoms of hypovolemic shock include
Increased heart rate
Feeling weak
Decreased urination
Low blood pressure

Treatment includes
Determining the cause
Halting any bleeding
Administration of i.v. fluids
Administration of oxygen
Elevation of lower extremities

25
Q

describe obstructive shock

A
  • Physical obstruction of ventilation or blood flow
    results in insufficient oxygen delivery to tissues
  • Inadequate blood oxygenation may be the
    result of several conditions:
    Pneumonia = Infection of the lung
    Trauma ie. Collapse of the lungs
    Congestive heart failure
    n = Failure of the left ventricle causes an accumulation of blood in the pulmonary circulation > Impairs gas exchange

Treatment depends on cause but includes
aggressive ventilation with high flow O2

26
Q

what are the neurotransmitters involved in feeding behavior

A

Classical Neurotransmitters:
Serotonin (5-HT)
Norepinephrine (NE)

Neuropeptides:
- Neuropeptide Y (NPY) = Agouti-Related Peptide (AgRP)
- POMC peptides = Melanocortins (MSHs)

27
Q

what is the effect of serotonergic tone on food intake

A
  • Increased serotonergic tone leads to decreased food intake (anorectic agent)
  • Administration of serotonin precursor decreases food intake in food-deprived rats
  • 5-HTP decreases stress-induced feeding
28
Q

what is fenfluramine + mec

A

Indirect agonist = Promotes release of serotonin + Inhibits reuptake of serotonin > Decreases rate and duration of feeding (Decreases food intake by 10-25%)
- Chronic administration leads to weight loss
- Cessation of administration leads to weight regain

mechanism = increases feeling of satiety
- Peripheral effect: decreased gastric emptying
- Rats display thermogenic effect

Clinical Trial of fenfluramine/phentermine
Phentermine is stimulant
Acts at catecholamine sites

29
Q

does high protein diet increase serotonin levels and decrease feeding?

A

no
- serotonin precursor is essential aa tryptophan - cannot be synthesized in body however high protein diet also increases diff aa (L-valine) that competes for transport across BBB
- L-valine decrease anorectic effects of 5HTP

30
Q

describe high carb diet

A

fasted rats given high carb display increase in brain serotonin (possible that insulin release > uptake of aa into muscle > depletion from plasma = uptake trypto into cns)
- high carb leads to higher tryp/LNAA ratio vs high protein in human
- low carb weight loss diet decrease serotonin in CNS (decrease sero associated with aggression and depression)

31
Q

to be cont

A

autonomic final (8 decks)

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