Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Endocrine PPPP
Pass clues
| Question | Answer |
|---|---|
| The endocrine system is composed of glands, hrms are prod and actions are performed, which of the glands is considered the "master switchboard?" | Hypothalamus |
| Notes: It is important to know that the endocrine system cephalo caudal follows this arrangement. | Hypthalamus, pituitary both in the brain. then thyroid, adrenals, gonads (testes/ovaries). |
| The Hypothalamus secretes hrm that tell the pituitary to either release or inhibit hrm., which hrm are released that cause release of others from anterior pituitary? | GnRH, CRH, TRH, GHRH these go to the gonads, adrenals, thyroid, liver respectively notice all have "R" and "H" in them. |
| What hrm are released from the Post. pituit? | Oxytocin (milk letdown and baby letdown by uterine cx) and Vasopressin aka ADH work at vessels and kidneys constriction and water reabsorption respectively. |
| When talking about GH, what is the stimulus for release and the inhibitory for release? | Stimulus is GHRH and inhibitory is Somatostating |
| When GH is released from the Anter.pituit, where does it go next and how does it influence long bone growth, name all hrms that lead to bone growth? | The GHrH is released from the hypothalamus to the anterior pituitary which releases GH from there the GH travels to the Liver where it releases Somatomedins travel to the Somatomedin receptors on bones and cartilage and bone growth ensues |
| ACTH is stimulated to be released by what and what is the organ targeted and final prod. made and what is fxn of that final prod? | ACTH is stimulated by the hypothalamic release of CRH goes to ant. pituit release of ACTH to adrenals for prod of Cortisol in response to stress. |
| Somatostatin is a negative feedback hrm for which hrm prod by anterior pituitary? | GH |
| PRL is inhibited by which Tyrosine breakdown product? | Dopamine (DA) |
| What drug may cause the sureptitious release of PRL leading to milk production? | DA antagonists like antipsychotics |
| What pathology may lead to the sureptitious release of PRL leading to milk production? | Pituitary infarct s/p childbirth or mass effect on DA fibers where in both the DA effect of inhibiting PRL is taken away=PRL release. |
| Notes:PRL is inhibitory to the entire axis it is the exception to the rule. | Shuts down the entire axis. |
| GnRH causes the production of which 2 hrms? | FSH and LH |
| FSH is responsible for which job? | Spermatogenesis and follicular developement |
| LH is responsible for which job? | Testosterone release and Prod and release of estrogen and progesterone |
| What does TRH do at the anterior pituitary? | Release of TSH which allows the thyroid to release T3 and T4 |
| Which of the following hrm. deal with mild let down, PRL or Oxytocin and the correct one is released from which part of the pituitary? | Oxytocin (milk letdown and baby letdown) and released form post. pituit. |
| What is inhibin, who prod it and what does it do? | Inhibin is prod by the sertoli cells under the direction of FSH and it's action is to inhibit prod of FSH. |
| Notes:hrms and 2nd messengers- 2nd messengers are like the "doorbell" that let in water soluble products into the cell.90% of hrms use the 2nd messengers cAMP. | If a hrm requires a 2nd messenger then it is water soluble. If not then it is likely a steroid hrm and those go right through the membrane. |
| What are the other 2nd messengers besides cAMP? | IP3, Dag and Calcium |
| Notes: when considering hrms, it is important to keep the following in mind. | 1.Name and where it comes from. 2. main stimulus 3. Main inhibitor 4. Where does it go 5. Main action 6. 2nd messenger 7. miscellaneous syndromes |
| Which of the following is the main stimulus of erythropoietin productino (EPO)anemia or hypoxia? | Hypoxia not anemia (anemia is Hgb< 6) |
| EPO is made where and works where to prod what? | made in kidneys works at bone to prod erythropoiesis (RBC) life of an RBC is 120 days. |
| What is the 2nd messenger of EPO? | TK (tyrosine kinase) anytime you build something you go to Lowes when the body does it it used TK as a 2nd messenger like insulin & GH |
| Remembering the phrase Salt Sugar and Sex applly this to the adrnal cortex? | GFR salt/sugar/sex respectively. Zona Glomerulosa reabsorbs salt by hrm aldosterone, Z. fasiculata deals with Cortisol dealing with sugar increase all stress hrm increase glucose release and z. reticularis is the sex steroids prod |
| What is another name for ADH and where does it work in r/t kidney? | vasopressin (DDAVP) works at CT to increase pure water reabsorption by direct action on aquaporin receptors |
| How does aldosterone work? | increases the reabsorption of Na thus bringing in water in cases dehydration. |
| What is the main action of aldosterone? | makes more Na/K pumps! |
| what if one has too much aldosterone production, what is that condition called? | Conns syndrome |
| How would the overproduction of aldosterone be exhibited on a chemistry panel specifically to Na, K, acid/base balance and symptom? | hyper-Na-tremia, Hypo-K-alemia, alkalosis, HTN. |
| Aldosterone deficiency can be MC d/t adrenal insufficiency congenitally or in adults d/t abrupt withdrawal of steroids or AI adrenalitis, which enzymes are implicated in adrenal insuff? | 21 beta hydroxylase deficiency some call it alpha 11 beta hydroxyalase deficiency some call it alpha |
| What B/P problem does 21 beta hydroxylase deficiency lead to and why? | Hypotension the pathway does not get to prod 11 deoxycorticosterone a prod that acts much like aldosterone that increase Na and water uptake. |
| What B/P problem can arise from 11 beta hydroxyalase deficiency and why? | Hypertension, the pathway prod 11 deoxycorticosterone a prod that acts much like aldosterone that increase Na and water uptake therefore increase vol = increase B/P |
| notes: cortisol, aldosterone and testosterone have no 2nd messengers | no 2nd messengers |
| what is the pos and neg feedback to cortisol production. | pos feedback is hypoglycemia and stress neg feedback is hyperglycemia as you become more stressed, you increase cortisol and an increase in cortisol affects memory it blocks memory. |
| too little cortisol prod as in adrenal insufficiency is called what? | Addisons-JFK had this! |
| Too much cortisol prod is known as Cushing's syndrome or disease what are the causes of cushings (3 of them) and which are dis or syndr? | Pituitary ademona-Cushings dis Small cell CA-Cushings dis. Adrenal adenoma-Cushings syndrome (affect many organs) diseases affect one organ |
| What character from TV could be classified as cushing's? | M&M man |
| What importance is the measurement of cortisol on pt suspected of having cushing's? | NONE, we never meas cortisol directly, has no clinical significance. We use the Dexamethasone suppression test. |
| The Dexamethasone suppression test is an important diagnostic test of cushing's if suppression occurs in the low dose test, what is that indicative of? | Obesity, depression or normal variant aka idiopathic or we don't know |
| What is the dose of the low dose Dexamethasone test? | 0.5 mg IV Q 6hr x 4 doses |
| What is the dose of the high does Dexamethasone test? | 1.0 mg IV Q 6hr x 4 doses |
| If suppression of Dexamethasone occurs on the high dose, what do we suspect? | Pituitary adenoma |
| What unusual complaint from a patient can lead you to suspect and test for a pituitary adenoma? | Sudden blindness or any issue of visual field disturbances. A pt may state that she had many close calls on the road while driving where she almost crashed or will not drive at night now d/t visual changes this is a macrotumor. |
| If no suppression of Dexamethasone occurs on the high dose, what is the next step? | Check the ACTH levels |
| After no suppression of Dexamethasone occurs on the high dose and we check ACTH levels what would a high ACTH indicate? | small cell CA step II next step chest xray and bronchcoscopy get biopsy |
| After no suppression of Dexamethasone occurs on the high dose and we check ACTH levels what would a low ACTH indicate? | adrenal adenoma step II next step MRI MRI if its squishy. |
| Pheochromocytoma is a very rare tumor (1-3%) but d/t the fact it will kill the pt, it is important, where is it and what can kill the pt if not tx promptly? | Adrenals or suprarenal gl, release of both NE and EPI cause a surge of catecholamines leading to CNS stimulation (rage and HA), CV stimulation (HTN and tachy) can lead to stroke. |
| What is contraindicated in the treatment when a pheochromocytoma is suspected? | Beta blocker because alpha stimulation is unblocked can kill pt by stroke. can give phentolamine short axn or long axn phenoxybenzamine these are 2 alpha blockers. |
| What key to dx a pt with this (clinical history) will lead you to suspect pheochromcytoma? | bouts of rage, episodes of rage, rage in general, pt may say this or loved ones may mention it. |
| What is the best dx test for pheochromocytoma? | 24 hr collection you can also order a KUB and blood catecholamines for preliminary dx but best is 24 hr urine. |
| What are we looking for in the 24 hr urine collection of pheochromocytoma? | urine metanephrines, VMA (vanellyl mandellic acid), catecholamines |
| which common abd mass seen in children resembles pheochromocytoma? | neuroblastoma. < 5 yo higher in males. |
| step II: once you have a positive lab for pheochromo after 24 hr urine collection, what is the next step in dx? | MRI or CT it's squishy |
| Which GLUT receptor allows glucose into a Beta cell of the pancreas? | GLUT 2 |
| what is the importance of allowing glucose into a pancreatic beta cell? | the glucose is important in prod ATP |
| The prod of ATP in the pancr beta cell has what axn directly as it aides in the release of insulin? | blocking K channels causing depolarization allowing Ca to enter the cell |
| What is the stimulus of insulin release by the beta cells of the pancreas? | Ca influx |
| Which mineral imbalance can affect the release of insulin? | Calcium hypocalcemia can impede release. |
| sulfonylureas like glipizide and glyburide help the beta cell release insulin, how does it do this? | Blocks the K channels allowing depolarization hence moving Ca in to the cell increasing release of insulin. |
| which tissues do not need insulin for glucose entrance into the cell? | BRICKLE-Brain, RBC, Intestine, Cornea, Kidney, Liver, Exercising muscle |
| Insulinomas act very much like sulfonylureas as they sureptitiously release insulin regardless of pt being well fed or starving, besides hypoglycemia, what else would you see in respect to insulin and c-peptide? | High in both insulin and c-peptide CT to dx and surg to tx it. |
| What condition seen in infants mimics s/s seen in insulinoma? | nessidioblastosis tx pancreatectomy partial |
| We learned that somatostatin inhibits GH release,and essentially is inhibitory in axn but also made in the pancreas, what does it inhibit there and who prod it? | prod by the delta cells of the pancreas and inhibits both insulin and glucagon. somatostatinoma cause overprod of somatostatin |
| What other GI hrm are affected by somatostatin? | VIP, GIP, CCK, Secretin, Motilin |
| What is drug that works like somatostatin? | Octreotide |
| What is the action of CCK and what stimulates it's release? | amino acids and FA in the duodenum stimul it and it cause GB contraction to release bile |
| What is the actual function of Gastric Acid (HCl)? | To breakdown proteins to their smallest form AA so the body can absorb and use to build proteins. |
| What is the action of Gastrin and what stimulates it's release? | Causes HCl secretion may respond to increase pH, gastric distention, AA in stomach. inhibited by low pH. |
| What is the action of Secretin and what stimulates it's release? | when hydrogen ions (HCL) enter the duodenum or FA and works at pancreas to release bicarb. to alkalinize the chyme. 2nd messenger is cAMP. |
| When a 2nd messenger is cAMP, what does that say about the solubility of the hormone, water soluble or fat soluble? | Water soluble |
| VIP does what? | Stop prod of hydrogen ions so no gastric acid and stiumlates the release of bicarb. main action is to relax GI Sm. Muscle. 2nd messenger is cAMP. |
Created by:
sxirsrick
Popular USMLE sets