Endocrine Flashcards
primary damage:
damage to the endocrine gland
secondary damage
damage to pituitary or thalamus
primary glands
only job is hormone secretion
- pineal, hypothalamus, pituitary, parathyroid, thymus, adrenals, ovaries, testes
autocrine signalling
cell releases a hormone—> targets the same cell to make more molecules ( local)
paracrine signalling
1 cell secretes hormones that interacts w neighbouring cells to influence their activity
ex: ecosinoids
secondary hormones:
heart–> ANP
Kidneys__> bicarb, erythropoiten,
cortisol, ALDO, E/P/T are examples of ….
steroid hormones
- hydrophobic molecules
can diffuse across cells membranes to transcript MRNA
glycoproteins, AA derivaties, and ionated AA=
nonsteriodal hormones
upregulation
when there is a decreased amount of hormone in the blood the target ell will make more receptors to pick up more hormones
down regulations
when there is too much hormones in the blood and the target cells reduce its amount of receptors to take up less hormone
neurohypophysis secretes…..
vasopression, oxytocin
adenohypophysis secretes…
TRH, CRH, TSH, ACTH, LH & GNRH, prolactin, somatostatin
short loop feedback:
when the pituitary hormone changes the secretion of the hypothalamic hormone
long loop feedback
target organ changes the hormone secretion of the hypothalamic/pituitary hormones
circadian rhythms….
influences the production of CRH in blood
GH=++ secretion @ 12am–>4am
adrenal cortex layers
zona glomerulosa: outermost, secretes mineralcorticoids ex:ALDO
Zona fasiculata: middle zone which secretes glucocorticoids, ex: cortisol
ZOna reticularis: inner most layer that secretes gonadococorticoidsex:androgens
adrenal medulla secretes…
catechoalmines like norepinephrine
ALDO functions:
regulates ECF fluid vol by reabsorbing Na+ & H2O in the nephron of the kidneys
-regulates ECF K+ Na+/K+
- release stimmed by ++ANG2 when Bp= low–> travels through caps & diffuse through nephrons cells—>bids to cell receptor & alters mrna transcription to ++ expression of NA+/K+ pumps= more K+ excreted +Na+ reabsorbed
glucocorticoid functions:
+BGL, aa/FA , gluconeogenesis, anti-inflammatory
neg feedback loop for hypothalamic- pituitary pathway:
1 hypothalamus = stimmed by stress/circadian rhythm–>anteiror pituitary–> secretes acth (influencescells of zona fasiculata to secrete more cortisol
(as CRH increases—> cortisol +/as Cortisol +—> CRH decreases)
cushings diease
primary/secondary hypercortisol secretion, onset=40yrs, can be iatrogenic due to excessive use of glucocorticoids & can completely stop the production of CRH/ACTH
s/s:Fat depositions, Decreased muscle mass: muscle weakness
Bone demineralization
aldosterone(like effects)
Increased production of androgens
Hyperglycemia ( loss of sensitivity to insulin)
Poor concentration & memory
Addisons disease
primary hypocortiso; secretion & low ALDO, hypovolemia, hyponatremia, hyperkalemia, decreases BGL, N/V/D/C, +pigmentation
general adaption syndrome (GAS)
1) ALARM: stress activity of hypothalamus ++ cotrisol/+SNS, 2)resistance–> maintenance of alarms, allostasis, if stress not managed body compensates( counter productive) 3) exhaustation: body resources are depleted ++ risk of infection
thyroid hormone fucntions…
T3/T4–> ++ SNS response
- ++BMR, +protein synthesis/degradation, glycogenolysis, gluconeogenesis, + lypolysis, +Hr/FOC/CO
secretion regulation of t3-t4:
1) hypothalamus–> tonic release of TRH 2)anteiror pituitary release TSH–> TSH binds to receptors on follicular cells (thyroid) to make more T3/T4 3) T3/T4: metabolic effects & TSH secretion fro anterior pituitary ( neg feedback)
PTH
+ ECF Ca2+–> +bone reabsorption Ca2+, activates osteoclasts break down matrix and reabsorb Ca2+ through the nephrons
Vit D
influences Ca2+ diet & synthesis (food/skin)—> liver–>kidneys
Calcitonin:
secreted when blood Ca2+= too high, secreted by the thyroid cells, osteoclasts stop break-down normal levels Ca2+
melatonin
secreted by the pineal gland/ circadian cycle
-amino acid derivative
GH
regulated by somtotropin pr GnRH, levels ++ at night, + muscle mass, ++ Ca2= retention, + osteoblasts, -BGL,
pancreatic hormones
alpha- glucagon
beta-insulin
delta-somatostatin
episonlin- gherlin
pp cell- pancreatic polypeptide
acini: exocrine pancreas funftion
what hormone do neonates need for proper neuro development?
T3/T4–> for myelin sheath/axon development
Hypothyroidism
- congenital, due to lack of precursors/non-ionated salts
manifestations: - -BMR, bradycardia, -BP, weight gain despite appetitie, hyperlipidemia, lethargy, bad memory, low t3/t4, + TSH/TRH, cold intolerance
cretinism….
hypothyroidism in neonates, s/s: 1 month old, thickened tongue/lips, poor muscle tone, jaundice, neuro delays, irreversible damage
myxedema
ptolonged lack of t3/t4, non pitting edema, alt mental state, cold intolerance
lack of iodine ( goiters)
TSH stim thyroid to make T3/T4
No iodine so no T3/T4 but thyroglobulin continues ot be produced—> colloid
No T3/T4 thus TSH remains High
hyperthyroidism( primary/secondary)
primary: graves disease antibiody produced to stim TSH receptor on follicularcells produce more t3/t4
secondary: usually related to tumour of the anteriori pittuitary gland, affects the secretion of TRH/YSH by having an + secretion of both
manifestations: +BMR, +SNS, weight loss, Heat intlerance, amenorrhea, thyroidmegally
congenital adrenal hyperplasia
autosomal recessive condition ( can not make enzye necessary for cortisol/ALDO production)
-turns htem into progesteron ( androgens
- enhances maleness, lack of cortisols, +CRH/ACTH, virillization of females:
giantism
pituitary tumour thats benign before the epiphyseal plates stop growing, +GH/IGF secretion–> + bone growth/cartillage, extremely tall individuals, delayed puberty, excessive face bones
hyposecretion of GH
congenital/can be aquired, lack of gh production, receptors dont respond/lack of IGF
- normal Birthweight tho no long bone growth
diabetes mellitus: typ1
pancreas does not make insulin anymore due to beta cell destruction, (can be auto immune)
tx: insulin
hypersecretion of GH/acromegaly
begnin tumour on pituitary after epipheals plate stops growing (20-40 y/o)
TSH stim thyroid to make T3/T4
No iodine so no T3/T4 but thyroglobulin continues ot be produced—> colloid
No T3/T4 thus TSH remains High
3 p’s of hyperglycemia
polyphagia, polyuria, polydispia
kussmals respirations can occur in what kind of diabetes…
hyperglycemia, type 1 diabetes mellitus.
NIDDM
skeletal muscle cells/liver is less reactive to insulin & pancreas does not secrete enough insulin
factors: age, lifestye, obesity, genetics
Tx for HHS
- Regular exercise and healthy diet
- Oral hypoglycemic meds
Increased insulin secretion ( incretins, sulfonylureas, meglitinides)
Drugs that increase receptor sensitivity ( Biguanides)
Drugs that reduce CHO absorption ( alpha glucosidase inhibitors)
Drugs that promote satiety ( Amylin) - Insulin
NKHH?
non-ketoitic hyperosmolar syndrome–> DKA in NIDDM, 20% higher mortality compared to DKA
neuropathy
due to glomerulosclerosis ( initial increased filtering—> damage to glomeruli through I/N/F process); hypertension
why do diabetics have ++ risk for infection?
Poor circulation, increased glucose supports bacteria, poor healing due to reduced insulin
diabetes insipidus:
-Central inability to make and secrete ASH- idiopathic tumor, surgery, trauma
-Nephrogenic: inability to respond to the ADH; lack of reabsorption of H2O
-Dipsogenic- constant thirst→ big water load= lots of pee
Gestational: w/ pregnancy, placenta produces enzymes that metabolize ADH
