Physio 2 - Endocrinology 4

drraythe's version from 2015-06-09 01:44

Growth hormone

Question Answer
Growth hormone aka? produced where by what? affects what?aka somatotropin. produced in anterior pituitary by acidophils as a protein hormone. It affects nearly all tissues capable of growth (hyperplastic and hypertrophic)
how is somatotropin a partially tropic hormone? it stimulates the liver to produce SOMATOMEDINS (or insulin-like growth factors= IGF)
how does somatropin DIRECTLY affect metabolism?(just somatotropin, not somatomedins/insulin-like-growth- factors aka IGFs, so is direct) means it goes DIRECT--> LYPOLYTIC and glucose sparing--> inc lipolysis, causes insulin resistance (diabetogenic)
how does somatotropin INDIRECTLY affected metabolism?(IGFs aka insulin-growth-like-factors/somatomedins, which are STIMULATED by somatotropin. Hence, indirect) IGFs--> PROTEIN ANABOLIC (mm, bone, liver)--> inc. AA uptake, inc DNA/RNA synth, inc protein synth, inc mitotic rates
Summary of metabolic effects of growth hormone (3)(1) promotion of growth via stim of protein synth, esp during adolescent phase (esp somatomedins here) (2) inc fat utilization/mobilization (3) dec glucose utilization (esp somatotropins for 2+3)
growth hormone forces body to use ____ for energy by reducing ____ availabilitylipids, glucose
how is release of growthhormone (somatotropin) controlled?by hypothalamic GH releasing hormone and GH inhibiting hormone
which repro hormone is known to cause a release of GH in (which animals?)progesterone stims GH release in dogs and cats
how is GH related to tissue ageing? life-long production of GH decreases in old age--> mitotic tissues are not maintained--> tissue ageing
what two things can happen with a GH deficiency?dwarfism and early ageing (dwarfs do have a shorter life span)
explain how GH is related to dwarfismdwarfism is a INHERITED deficiency of GH and/or somatomedins
explain how GH is related to early aging. what might cause this?if the deficiency in GH happens later in life (as opposed to dwarfism). Could be due to damaged pituitary cells (tumor, hemorrhage, radiation) or liver damage (reduces somatomedins)
what two things can happen with a GH excess?(1) before sexual maturity= true gigantism (v. rare) (2) after sexual maturity= acromegaly
explain acromegaly (caused by what in who)excess GH AFTER sexual maturity, usually caused by GH prducing TUMORS in CATS. and in DOGS, continuously high PROGESTERONE levels
signs of acromegaly include? inc bone/cartilage growth (face/joints), cardiac hypertrophy, secondary diabetes mellitus

Adrenal cortex-- glucocorticoids

Question Answer
adrenal cortex vs medulla?cortex= produces >30 steroid hormones (adrenocortical hormones). Medulla= related to the symp. nervous system, secretes catecholamines
name the 4 layers of the adrenal gland and what they secrete(first three= cortex). (capsule of gland)--> (1) zona glomerulosa (mineralocorticoids- 90% aldosterone!) --> (2) zona fasciculata (glucocorticoids- 95% cortisol) --> (3) zona reticularis (androgens) --> medulla (epi, norepi, neuropeptide) [to remember, it's "GFR" and the deeper you go, the sweeter it gets]
cortisol is the ___ hormone. Walk through the path for its release.STRESS hormone. Stress stim hypothalamus to release corticotropin releasing hormone --> CRH stim release of corticotropin (ACTH) from anterior pituitary --> ACTH stim release of cortisol (and androgens) --> cortisol exerts neg feedback on CRH and ACTH release
aside from under stress, when/how else is cortisol secreted? ACTH and cortisol secretion also follow a circadian rhythm. highest concentrations are seen during an animals activity phase (diurnal vs nocturnal species)
a stress hormone provides what in times of need to vital tissues?glucose!
glucocor have anabolic affect on what tissue, and catabolic affect on what tissue?anabolic on liver and catabolic on extra-hepatic tissue
look at the damn graph on 6.2.2fack
what do glucocor do to the liver? (6)(anabolic) (1) REALLY inc gluconeogenesis (from AAs) (2) inc glycogenesis (prereq for glucagon's glycogenolytic effects) (3) inc plasma glucose (4) inc AA uptake (5) inc protein synth (6) inc ketone bodies and VLDLs
what do glucocor do to the extra-hepatic tissues? (3)(1) dec glucose uptake/metabolism, in mm and fat this is an anti-insulin effect (this inc the plasma glucose, as seen on hepatic effects) (2) inc proteolysis (this inc AA uptake, gluconeogenesus, and protein synth in the liver) (3) inc lipolysis, which redistributes fat (abdomen) (this inc ketone body and VLDL formation in the liver)
what do glucocor do (in general, briefly) to...The liver? GI? blood glucose? CNS/Pituitary? blood pressure?LIVER= inc weight (glycogen and fat). GI= inc appetite, inc stomach HCl, dec mucus. BLOOD GLUCOSE= inc hyperglycemia and steroid daibetes. CNS/PITUITARY= dec ACTH, ADH, TSH, GH, FSH/LH. BLOOD PRESSURE= sensitization to NE/E
what do glucocor do (in general, briefly) to...MM tissue? fat tissue? blood cells? inflammation?MM TISSUE= dec mm tissue, connective tissue, and bone matrix. FAT TISSUE= dec or redistribute. BLOOD= inc neutrophils and RBCs, dec lymphocytes, eos=> STRESS LEUKOGRAM (Stress means LEss happy). INFLAMMATION= dec
how are glucocor anti-inflammatory?(they prevent the release of inflammatory mediatiors eg from lysosomes, macrophages, monocytes) **reduce/prevent inflammations and resolve existing inflammations, probably by deactivating inflammatory mediators= PHYSIOLOGICAL CONTROLLER OF INFLAMMATORY PROCCESSES.
what are the long-term effects of glucocorticoids depressing inflammatory processes? (2 major things)IMMUNE DEPRESSIVE (depress lymphocyte proliferation, atrophy of lymphatic tissue, depression of antibody production) and DEPRESS WOUND HEALING (dec collagen synth)
what is POMC? what is its purpose?the pre-pro-hormone of ACTH. "pro-opio-melanoCortin". The cleaving of POMC gives rise to several ACTIVE polypeptides
What are the 4 active polypeptides produced from the cleaving of POMC?(1) alpha-MSH (melanocyte stimulating hormone-> darken skin and mucosa) (2) beta-endorphin (modulates pain perception and affective b/h) (3) CLIP= corticotropin-like intermediate peptide (pathological effects in horses) (4) ACTH= adrenalcorticotropic hormone (controls release of cortisol, also NECESSARY TO MAINTAIN VIABILITY OF ENTIRE ADRENAL CORTEX)
what hormone is crucial to maintain viability of entire adrenal cortex?ACTH
what happens to the adrenal gland in long-standing elevated cortisol levels (could be endogenous or exogenous)?can lead to ATROPHY of adrenal cortex through SUPPRESSION OF ACTH---> can impair gluco AND mineralocorticoids
what is hyperadrenocortisism also called? what is it an excess of?aka cushings, and excess of GLUCOcorticoids
4 causes of hyperadrenocortisism?(1) adenomas of adrenal glands --> excess cortisol (rare). (2) adenomas of ant. pituitary--> excess ACTH--> cortisol (common) (3) iatrogenic= prolonged glucocorticoid therapy (4) HORSES-> pituitary pars intermedia tumors produce POMC= (a. MSH b. beta-endorphine c. CLIP d. VERY LITTLE ACTH --> CLIP is thought to inc. the ACTH efficiency 6x's)
what animals is hyperadrenocortisism common in? type? which animals is it rare in?common in (1) middle aged to old dogs (boxer, terrier, poodle, dachshund) and 90% are pituitary dependent (2) in middle aged to old horses (ponies > horses) usually pituitary pars intermedia tumor. RARE IN CATS.
hyperadrenocortisism has what effect on proteins? explain the pathophysiology of this.PROTEOLYSIS leads to mm atrophy, weakness, osteoporosis, slow wound healing, reduced collagen (thin skin). Bilateral hair loss and discoloration in dogs. in HORSES is slow hair shedding (hirsutism)
what is the hair symptom horses get in hyperadrenocorticism? what is it called?slow hair shedding= HIRSUTISM
how does hyperadrenocorticism affect fat tissue/ related stuff?LIPOLYSIS with typical fat re-distribution, which can lead to hepatomegaly and an enlarged abdomen and weakened abdominal mm, which leads to a POTBELLY (but no weight loss)
how does hyperadrenocorticism affect blood sugar levels? what does this result in?HYPERGLYCEMIA (because of inc gluconeogenesis) + insulin resistance --> steroid diabetes --> PU/PD (often "prediabetic")
PU/PD happens in hyperadrenocorticism. what are the 3 reasons it can happen?(1) from hyperglycemia b/c of the inc gluconeogenesis (inc gluconeogenesis b/c proteolysis leads inc AA so the liver makes them into glucose) leads to "steroid diabetes" (2) can be caused by compression of the posterior pituitary (lack of ADH=antidiuretic hormone) (3) or inhibition of renal ADH receptors
what does cushings do to the immune system?immunodepression
what does cushings do to appetite?inc
what does cushings do to the pituitary?it depresses the pituitary gland (dec. TSH, FSH, LH, GH)= panhypopituitarism
does cushings cause b/h changes?in horses, they become docile b/c of inc endorphins
how does cuhings affect gastric mucosa?can get ulcers
how does cushings affect the look of the skin? why is this?hyperpigmentation (if ACTH is inc), thin skin from proteolysis
what horse disease can hyperadrenocorticism cause?LAMINITS
how does one treat PDH?PDH= pituitary dependent hyperadrenocorticism. surgical removal of tumors is difficult, so treat with MITOTANE (this is an insecticide (DDD) which suppresses the adrenocortex)
what happens to cortisol and ACTH in an adrenal gland adenoma?inc cortisol. dec ACTH (neg feedback makes it dec)
what happens to cortisol and ACTH in PDH?(pituitary dependent hyperadrenocorticism) cortisol inc and ACTH inc (b/c pituitary makes ACTH a LOT and then the adrenal gland makes more in response)
what happens to cortisol and ACTH in iatrogenic hyperadrenocorticismDEC cortisol (ENDOGENOUS-- not the given stuff) and dec ACTH (neg feedback)
if you saw a dog with untreated hyperadrenocortisism, what symptoms would you be likely to see?Potbelly, alopecia, thin skin, muscle wasting, PU/PD, recurrent infections (UTI), ulcers
What other endocine disorders can happen if a dog has untreated hyperadrenocortisism? (5)type III steroid diabetes, panhypopituitarism, hypothyroidism (the neg feedback suppresses the entire ant. pituitary), repro failure (neg feedback suppression), GH deficiency/early aging (neg feedback suppression)

Adrenal Cortex-- mineralocorticoids

Question Answer
what is the main stimulus for mineralocorticoid secretion? (pathway). (the other two, lesser stims?)HYPOVOLEMIA and low blood pressure. --> renin --> angiotensin --> ALDOSTERONE (also stim by hyperkalemia and moderately by hyponatremia)
aldosterone is the ___ saver and the ___ and ___ looser hormonesodium saver and a K+ and H+ looser
what happens in the kidney with aldosterone, and the results of it (when it is a "sodium saver")?hypovolemia--> aldosterone release--> inc Na+ absorption (via the Na/K pump)--> inc osmotic absorption of water. So, Na+ AND water are retained. Plasma Na+ conc. is unchanged, but ECF is increased, which means= normovolemia.
what happens in the kidney with aldosterone, and the results of it (when it is a "K/H loser")?aldosterone stims renal K+ excretion (via the Na/K pump) and aldosterone stims renal H+ excretion (via Na/H exchanger)
what other systems aside from the kidney assist with K+/Na+ balance?INC Na+ absorption / K+ secretion in sweat glands, salivary glands, intestines
what is uncontrolled/excessive aldosterone secretion called?hyperaldosteronism
what are the causes of hyperaldosteronism? (3)(1) aldosterone-secreting tumors (rare) (2) potentially any condition that leads to chronic hypovolemia (3) MOST OFTEN seen with renal tissue damage with localized ischemic areas (= low blood volume) so those ischemic areas have continued stim of renin-angiotensin system (angiotensin II stims aldosterone release from adrenal cortex)
explain "renal hypertension" pathogenesis. how common is it in cats and dogs?common! Excessive aldosterone release (most common cause= kidney damage)--> continually inc Na and H2O retention--> hypervolemia (inc ECF)--> inc arterial pressure-->pressure diuresis-->Na+ and water excretion inc-->overall, intravascular fluid volume remains slightly above normal and animal develops permanent HYPERTENSION (RENAL HYPERTENSION)
explain what happens in terms of K and H with hyperaldosteronismuncontrolled loss of K/H (via Na/K pump and Na/H exchanger)--> hypokalemia+metabolic alkalosis which leads to hyperpolarization of membranes (mild alkalosis stimulates Na/K pumps)--> retards action potential transmission in nn+mm--> neuromuscular excitability decreases--> mm weakness, hyporeflexia, lethargy
what is addisons disease? what is affected first, and what is affected second?HYPO-ADRENO-CORTICISM. First to go are the glucocorticoids (think cortisol) and THEN mineralocorticoids (think aldosterone)
causes of hypoadrenocorticism? (3)(1) immune-mediated destruction of adrenal cortex (youngish female dogs) (2) mitotane induced adrenocortical necrosis (from mitotane therapy) (3) long standing cortisol therapy--> depression of ACTH--> cortex atrophy [2+3 from trying to fix cushings]
signs of glucocorticoid deficiency? (2)USUALLY UNSPECIFIC SIGNS! (1) pts unable to cope w/stressful situations (2) pts unable to maintain blood glucose levels between meals ( dec(?) gluconeogenesis) --> hypoglycemia, lethargy
what is a normal Na/K plasma ratio? what is the level you'd see in Addison's disease?normal= 30-40, but in addisons the Na:K ratio is <20. (less sodium retained means smaller ratio)
What happens in an addison's crisis (acute)? how about chronic?Acute= ACUTE Na+H2O LOSS. means hypovolemia-->shock/collapse/death. in CHRONIC is it a chronic loss of Na/H2O. it is called the "great pretender" where theyre "not doing so well", PU/PD, diarrhea, vomiting
In addisons, what happens with K/H? What are the results of this?RETAIN K/H--> acidosis/hyperkalemia--> depolarization--> mm shivering, *paradoxically inc. K conductivity of heart pacemaker cells--> flattens prepotential-->bradycardia, arrythmia, CARDIAC ARREST
how does PU/PD + chronic renal failure lead to hypertension?Constant PU → general hypovolemia →constant renin/angiotensin/aldosterone release→ Na and water retention → normovolemia but often renin is secreted in excess of actual need → hypervolemia → increased CO and BP = hypertension (Localized ischemia depending on underlying cause of renal failure → more renin release etc etc)
how/when/why can PU/PD + chronic renal failure + hypertension affect the pt's erythrocytic system in the long run?When: more than 75% of renal tissue is malfunctioning. Why: decreased EPO release, anemia of chronic disease (ACD) due to renal inflammation. How: dyshempoietic, non-regenerative, normocytic, normochromic anemia.