lecture 20 Flashcards
how does exercise causes the loss of homeostasis
increased production of CO2, body temp and affects BP
how does the ANS help maintain homeostasis
increase RR, sweat rate, heart rate
what is produced by skeletal muscles during exercise and how does the body deal with these compounds
CO2 + lactic acid = lots decrease pH of blood > peripheral and central chemosensors activates project to DRG to VRG > increase RR
what is produced by working muscles during exercise and how does the body deal with this
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)
what happens to BP during exercise
- 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
how does exercise effect SNS output to heart and vasculature
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
what is the result of chronic exercise training
- 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
how does autonomic output help maintain water and sodium balance
- volumetric thirst
- activation of renin-angiotensin system
how is volumetric thirst elicited
- carotid sinus (baroR)
- heart and large blood ves (atrial baroR)
- kidneys (JG cells)
how is RAS elicited
- decrease blood flow to kidneys causes release of renin > increases production of ang2 (direct + indirect effects to maintain water and sodium levels)
what are the direct effects of ang2 to maintain water and sodium levels
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
what are the indirect effects of ang2 to maintain water and sodium levels
- 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
what is shock
- 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
what are the stages of shock
- Initial shock
- Compensatory shock
- Decompensatory shock
- Refractory shock
describe initial shock
blood flow is shifted to vital organs so blood flow to cap beds is severely restricted
describe compensatory shock
- 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
describe decompensatory shock
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
describe refractory shock
multi organ failure
what is the 4 kind of shock
cardiogenic + distributive + hypovolemic + obstructive
describe cardiogenic shock + symptoms
- 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
describe distributive shock
Severe peripheral vasodilation
2 kinds: neurogenic and anaphylatic
anaphylactic = allergic reaction lead to vasodil and leakage of fluid from blood ves
describe neurogenic shock
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
describe anaphylactic shock
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
describe hypovolemic shock
- 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
describe obstructive shock
- 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
what are the neurotransmitters involved in feeding behavior
Classical Neurotransmitters:
Serotonin (5-HT)
Norepinephrine (NE)
Neuropeptides:
- Neuropeptide Y (NPY) = Agouti-Related Peptide (AgRP)
- POMC peptides = Melanocortins (MSHs)
what is the effect of serotonergic tone on food intake
- 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
what is fenfluramine + mec
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
does high protein diet increase serotonin levels and decrease feeding?
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
describe high carb diet
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)
to be cont
