Upgrade to remove ads
Patho integrative body functions review
Terms in this set (82)
goals of acute stress
survival, vigilance, alertness, arousal, aggression
(fight or flight SNS activation)
chronic stress results
-state of exhaustion
-may exacerbate diseases (ex: CAD, IBS, PTSD, DM)
what does the adrenal cortex release in response to stress?
hypothalamus-anterior pituitary adrenal axis
stress/circadian rhythm->hypothalamus releases corticotropin-releasing hormone to enter the anterior pituitary->this stimulates the ant. pit. to secrete adrenocorticotropic hormone->which acts directly on adrenal cortex to promote synthesis and release of cortisol
Do adrenals store glucocorticoids?
NO, they synthesize them when needed and this is regulated by negative feedback loop
when do cortisol levels peak?
in the morning (decrease throughout the day)
what are glucocorticoids?
-cortisol (stress hormone)
-diverts metabolism from building proteins TO supplying energy for dealing with stress
-causes signs and symptoms of chronic stress
what are mineralocorticoids?
-promotes renal reabsorption of sodium (therefore water too)
-promotes renal secretion of potassium and hydrogen
-increases BV and BP
-decreases urine output
what is the goal of physiologic glucocorticoids?
to get more glucose to the brain
metabolic effects of physiologic glucocorticoids
-increases gluconeogenesis (formation of glucose)
-decreases peripheral glucose utilization (sp glucose goes to brain)
-decreases glucose uptake by muscles and adipose tissue
-increases glucose storage (glycogen)
-suppression of protein synthesis
-stimulation of lipolysis and fat redistribution
cardiovascular effects of physiologic glucocorticoids
-maintenance of vascular integrity
-increases RBCs, decreases WBSs (suppresses immune system)
effects of cortisol release
-increases blood glucose
-stronger sympathetic system effect on heart rate
-decreases non-essential energy-using activities (like hormone, bone, RBC and WBC formation
what bone production cell does cortisol inhibit?
OSTEOBLAST (bc they are responsible for building bone and reinforcing bone matrix)
what bone production cell does cortisol further stimulate?
OSTEOCLAST (bc they are responsible for breaking down bone)
too much cortisol (therefore increased blood glucose)
Primary Cushing's Syndrome
-abnormal growth/hypersecretion of ACTH and glucocorticoids
Secondary Cushing's Syndrome
-chronic administration of pharmacologic glucocorticoids (autoimmune diseases, rheumatoid arthritis, organ transplant etc.)
signs and symptoms of Cushing's syndrome
-osteoporosis (weak bones)
fluid and electrolyte disturbances
-fat redistribution (think buffalo hump, pot belly)
-decreased resistance to infection
-hirsutism (weird hair growth)
too little cortisol
-Addison's disease (problem with adrenals
-caused by infection, removal of adrenals, hemorrhage
-results in glucocorticoid deficiency (and possibly mineralocorticoid)
-ABRUPT discontinuation of chronic pharmacologic glucocorticoids (MOST COMMON)
-hypopituitarism-> deficiency in cortisol due to insufficient ACTH secretion (glucocorticoid deficiency NOT mineralocorticoid)
signs and symptoms of adrenal glucocorticoid deficiency
-decreased gluconeogenesis (hypoglycemic)
-nausea, vomiting, diarrhea
signs and symptoms of adrenal mineralocorticoid deficiency
-decreased potassium excretion (hyperkalemia)
-decreased sodium reabsorption (hyponatremia)
how do you treat adrenal insufficiency?
-take physiologic steroid replacement (glucocorticoids for cortisol deficiency and mineralocorticoids from aldosterone deficiency)
how is physiologic steroid treatment different from pharmacologic steroid treatment?
-physiologic: low doses to produce normal responses
-pharmacologic: higher doses to treat more serious immune disorders
what is Addisonian Crisis?
-abrupt discontinuation of pharmacologic steroids or failure to give ppl more steroids who are under extra stress/trauma
signs and symptoms of Addisonian Crisis
how would you treat a patient with Addisonian Crisis?
-immediate replacement of cortisol (hydrocortisone)
what happens if you have long-term adrenal suppression?
the pituitary gland loses its ability to manufacture ACTH
what happens if you have prolonged absence of ACTH?
the adrenals atrophy and lose their ability to synthesize cortisol
increased glucocorticoids activate the negative feedback loop and suppress the release of what?
-corticotropin-releasing hormone (CRH from hypothalamus)
-adrenocorticotropic hormone (ACTH from anterior pituitary)
Result of sudden withdrawal of glucocorticoids
acute adrenal insufficiency (prevent this with gradual weaning of glucocorticoid over long time)
what happens if you discontinue prolonged glucocorticoid treatment?
there will be a period where adrenals are unable to produce cortisol
this condition affects infants and is possible with adrenal insufficiency
what are the functions of the thyroid?
-stimulates energy use (increases metabolic rate=increased O2 consumption and heat production)
-stimulates cardiac function (increases rate and force of cardiac contractility-> increased CO and O2 demand)
-promotes growth and development (of brain and nervous system and skeletal maturation)
thyroid gland produces 2 active hormones?
-T4 (thyroxine) (precursor of T3)
most T3 and T4 are bound to what?
what are thyroid hormones eliminated by?
thyroid dysfunction and increased TSH
anterior pituitary dysfunction and decreased TSH with presence of decreased T3 or T4
where does T4 undergo conversion to T3?
T3 vs. T4 amount and half life duration
T3: 10% and 1 day half life
T4: 90% and 7 day half life
What needs to be presents in the serum to diagnose hyperthyroidism?
When do you order tests for T3 and T4?
when TSH levels are abnormal
what is the difference between hypothyroidism and hyperthyroidism?
hypo- LOW T3/T4
hyper- HIGH T3/T4
Hypothalamic-Pituitary-Thyroid Feedback Loop
Sleep/cold temp./stress->trigger hypothalamus to release Thyrotropin-releasing hormone (TRH)->which stimulates the anterior pituitary to secrete Thyroid-stimulating hormone (TSH)->stimulates thyroid gland to increase in size and synthesize/release T3/T4
Hyperthyroidism with low TSH
-thyroid cause bc thyroid gland is producing too much T3/T4 (negative feedback loop and ant. pit. suppress secretion of TSH)
Hyperthyroidism with high TSH
-pituitary cause bc pituitary releases TSH and it should be lower here
Hypothyroidism with low TSH
-pituitary cause bc pituitary releases TSH and it should be higher here
Hypothyroidism with high TSH
-thyroid cause bc thyroid gland is trying to produce T3/T4 by over compensating and releasing extra TSH, but ant. pit. is not kicking in
Hypothyroidism clinical manifestations
-pale, puffy face
-cold, dry skin
-brittle hair/hair loss
-decreased heart rate and temperature
-lethargy, fatigue, cold intolerance
how do you treat hypothyroidism?
lifelong hormone replacement
Why is hypothyroidism most significant in first trimester of pregnancy?
fetus does not have developed thyroid gland therefore they are dependent on mom's hormones
what can hypothyroidism in pregnancy cause?
-permanent neuropsychological changes
-impaired development of CNS, bones and muscles
Hyperthyroidism clinical manifestations
-increased metabolism, heat production and body temp
-increased HR and contractility
-CNS stimulation- nervous, insomnia, rapid speech and thoughts
-skeletal muscle weakening
-heightened sensitivity to catecholamines (bc SNS is so activated)
-exophthalmos (eye ball protrusion)
How do you treat hyperthyroidism?
-surgical ablation (achieve normal T3/T4 prior to removal)
-radioactive iodide (gradual decrease in thyroid function- make damage stay limited to thyroid only)
-anti-thyroid drugs (only treatment for kids)
Thyrotoxic crisis (thyroid storm)
-life threatening medical emergency
-increased release of thyroid hormones
-caused by surgery or severe illness
-treat with high doses of iodide and propylthiouracil
what do excessive thyroid hormone levels cause (as seen in a thyroid storm)?
-restless, coma maybe
what are the normal body temperatures?
If body temp is greater than thermostatic set point
heat dissipating behaviors (to get rid of excess body heat)
if body temp is less than thermostatic set point
heat producing behaviors (to increase body temp)
what regulates our core body temp via nervous system feedback?
thermoregulatory center in hypothalamus
What are heat dissipating behaviors?
-superficial vasodilation (flushing)
-diaphoresis (SWEATING- heat loss through evaporation)
What are heat producing behaviors?
-superficial vasoconstriction (to shunt blood back to core to maintain/increase body temp)
-goosebumps (pilomotor contraction)
-increased production of epinephrine and thyroid hormones
what is pyrexia?
fever (body temp is less than thermoregulatory set point)
how is our thermoregulatory set point increased?
prostaglandin E2 (which leads to hypothalamus initiating heat-producing behaviors until core body temp reaches new set point)
endogenous pyrogen that can induce fever
exogenous pyrogens that can induce fever
polysaccharides from bacterial cell wall, toxins
what is the purpose of pyrexia?
-to improve immune function by increasing activity of WBCs (stimulates interferon production and t cell activation)
-to inhibit microbial growth at higher temps
(with every temp degree increase comes HR increase)
stages of fever development
1. prodrome (mild headache, fatigue, pains)
2. chill (try to increase temp until it reaches new set point- heat producing behaviors- shivers)
3. flush (new set point is reached- vasodilation, warm/red skin, temp begins to fall- start heat dissipating behaviors)
4. defervescence- initiation of sweating
manifestations of fever
malaise, anorexia, muscle ache, headache, fatigue, increased HR and RR, dehydrated, increased metabolic rate bc increased oxygen demand
how to treat a fever
-resolves itself once underlying cause of increased set point is removed
-cool baths and cooling blankets
-drink fluids (restore fluid loss, prevent tissue breakdown and support hypermetabolic state)
What do you have to be extra cautious of when considering the elderly and fevers?
-elderly have lower temps thus slight elevations indicate fever
what individuals cannot mount a full fever response?
-newborns and infants
-immunocompromised (HIV, chemotherapy, organ transplant)
How is hyperthermia different from having a fever?
-thermostatic set point is unchanged
-body cannot maintain temp within normal range
-heat exhaustion or heat stroke
difference between heat exhaustion and heat stroke
-heat exhaustion: loss of Na+ and water through SWEAT, temp between 37.8 and 40, treat with cooling and rehydration
-heat stroke: life threatening rise on body temp, NO sweating, loss of consciousness, temp over 40 (ex: elderly in no AC, working out in hot weather)
-thermostatic set point unchanged
-core temp <35
-post cardiac arrest, surgery, ice environment etc.
individuals at increased risk for accidental hypothermia
passive treatment of hypothermia
-remove from cold environment
-cover with blankets
-warm fluids to drink
active treatment of hypothermia
-immerse in warm water
-slowly use warming blankets (to avoid inducing seizures)
As the severity of hypothermia increases, what happens to ability to shiver?
ability to shiver decreases bc they get weaker (same with metabolic rate which increases initially to generate heat but then decreases overtime)
signs of hypothermia
-vasoconstriction, pale, blue cyanotic
-dehydration and increased blood viscosity
THIS SET IS OFTEN IN FOLDERS WITH...
Nutrition 7 - Kwashiorkor & Marasmus
Chapter 9: Stress and Adaptation
Nutrition (10) - Kwashiorkor and marasmus
Marasmus & Kwashiorkor Presentation
YOU MIGHT ALSO LIKE...
Gould's Pathophysiology Chapter 16 Endocrine System
Pathophysiology: Week 3: Endocrine & Diabetes
OTHER SETS BY THIS CREATOR
Med Surge Exam 5 Kidney Review
Med Surge Exam 5 HIV/Cancer Review
Exam 4 Burn Review
Exam 4 Endocrine Review