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HY Endo Anat&Physio
Day 9
| Question | Answer |
|---|---|
| MC tumor of the adrenal medulla in adults | Pheochromocytoma |
| MC tumor of the adrenals in children | (Adrenal) neuroblastoma |
| Compare the consequences of pheochromocytoma vs. neuroblastoma on blood pressure | Pheo causes episodic HTN. Neuroblastoma does not. |
| What is the path of the L adrenal gland to the IVC? | L adrenal-->L adrenal v--> L renal v--> IVC (same as L gonadal v) |
| What is the path of the R adrenal gland to the IVC? | R adrenal-->R adrenal v-->IVC (same as R gonadal v); remember the R side goes Right to the IVC |
| Where are ADH and oxytocin made? | Hypothalamus |
| What hormones (H) are stored in the neurohypophysis? | ADH/vasopressin and oxytocin are stored in the posterior pituitary/neurohypophysis |
| From which embryonal cells is the posterior pituitary derived? | Neuroectoderm |
| What H are made by the adenohypophysis? | FSH, LH, ACTH, TSH, Prolactin, GH, melanotropin (MSH) are made in the adenohypophysis/anterior pituitary. Mnemonic= FLAT PiG |
| From which embryonal cells is the adenohypophysis derived? | Oral ectoderm (surface ectoderm) aka Rathke's pouch |
| Which subunit is common to TSH, LH, FSH, and hCG? | Alpha subunit |
| Which subunit determines H specificity? | Beta subunit |
| ACTH is synthesized as part of which polypeptide? | POMC |
| Which cells in the pancreas make glucagon? Where are they located? | Alpha cells; peripheral |
| Which cells in the pancreas make insulin? Where are they located? | Beta cells; centrally |
| Which cells in the pancreas make somatostatin? Where are they located? | Delta cells; interspersed |
| What metabolic signal causes beta cells to synthesize insulin? | ATP from glucose metabolism causes K channels to close--> depolarizes cell--> opens Ca channels--> increased intracellular Ca triggers exocytosis of insulin packaged in vesicles |
| Which cells don't need insulin for glucose uptake? Which GLUT transporter are they missing? | Brain, RBCs, Intestine, Cornea, Kidney, Liver (BRICK L). No GLUT 4 receptor. |
| Which cells have GLUT-1 receptor? | RBCs, brain. These tissues can take up glucose regardless of insulin levels. The brain relies on glucose for metabolism under normal circumstances and uses ketones in starvation. RBCs always depend on glucose. |
| Which cells have GLUT-2 receptor? | Beta islet cells, liver, kidney, small intestine |
| Which cells have GLUT-4 (insulin responsive)? | Adipose tissue, skeletal m (these tissues depend on insulin for glucose uptake). |
| How does insulin affect the alpha cells of the pancreas? | Inhibits them from releasing glucagon. |
| How can you differentiate the blood levels of a patient over-injecting insulin from a patient with an insulinoma? | Exogenous insulin has no C-peptide, so the patient who is injecting will have low C peptide levels in their blood while the person with the insulinoma that is secreting endogenous insulin will have sky high C-peptide in their blood. |
| How does insulin affect Na retention in the kidneys? | Increases it |
| What effect does prolactin have on GnRH? | Inhibitory |
| Which hypothalamic H stimulates release of prolactin from the adenohypophysis? | TRH (also stimulates release of TSH) |
| How does prolactin inhibit its own secretion? | Increases dopamine synthesis and secretion from the hypothalamus |
| Stimulates milk production in breast | prolactin |
| Inhibits ovulation in females and spermatogenesis in males by inhibiting GnRH synthesis and release | Prolactin (think of how breastfeeding is like a natural contraceptive) |
| What agent can be used to treat prolactinomas? | Bromocriptine (DA agonists) |
| Via what pathway does DA inhibit prolactin production? | DA comes from the arcuate nucleus to inhibit prolactin production at the anterior pituitary |
| Which pharmacologic agents stimulate prolactin secretion | DA antagonists (most antipsychotics) and estrogens (OCPs, also pregnancy) |
| WHat blocks the last step of cortisol synthesis, resulting in an ACTH surge with a resultant increase in steroid half product excretion? | Metyrapone |
| Hypertension, hypOkalemia, pseudohermaphroditism (ext phenotypic female with no internal reproductive structures) or externally phenotypic female with normal internal sex organs but lacking secondary sexual characteristics | 17 alpha hydroxylase deficiency (1 in first digit= HTN) |
| Masculinization, female psuedohermaphroditism, hypOtension, hyperkalemia, increased plasma renin, and volume depletion; salt wasting may lead to hypovolemic shock in newborn | 21 hydroxylase deficiency (1 in second digit= masculinization) |
| Masculinization, HYPERtension | 11beta-hydroxylase deficiency (1 in first digit=HTN, 1 in second digit=masculinization) |
| What is the precursor to cholesterol? | Acetate |
| What enzyme converts cholesterol to pregnenolone? What substance stimulates this enzyme? What drug inhibits it? | Desmolase. ACTH stimulates desmolase and ketoconazole inhibits it. |
| What enzyme converts testosterone to estradiol? | Aromatase |
| What enzyme converts testosterone to its more active form, DHT? | 5-alpha reductase |
| What drug inhibits 5 alpha reductase? What is its clinical application? | Finasteride; can be used to treat male pattern baldness and BPH |
| Decreased sex hormones, decreased cortisol, increased mineralcorticoids | 17-alpha hydroxylase deficiency |
| Decreased cortisol (increased ACTH), decreased mineralcorticoids, increased sex hormones | 21-hydroxylase deficiency |
| Decreased cortisol, decreased aldosterone and corticosterone, increased sex hormones | 11beta-hydroxylase deficiency |
| Why does 11beta hydroxylase deficiency present with hypertension if aldosterone levels are decreased? | B/c normally the enzyme converts 11-deoxycorticosterone--> corticosterone. Without the enzyme, 11-deoxycorticosterone (a mineralcorticoid itself) builds up and causes HTN. |
| What are the 5 actions of cortisol? | 1. Maintains BP 2. Decreases bone formation (this is why we prophylax with bisphosphonates) 3. Anti-inflammatory 4. Immunosuppressant 5. Increased gluconeogenesis, lipolysis, and proteolysis |
| Why is cortisol said to have a permissive effect with epinephrine? | B/c it upregulates alpha 1 receptors on arterioles to maintain BP. |
| Why are you more likely to get diabetes with long-term cortisol use? | Causes increased gluconeogenesis, lipolysis, and proteolysis |
| Where does PTH come from (which cells)? | Chief cells of parathyroid |
| What does PTH increase production of in osteoblasts? What does this do to osteoclasts? | M-CSF (macrophage colony stimulating factor) and RANK-L. Results in osteoclast stimulation |
| What does a decrease in free Mg do to PTH secretion? What conditions commonly cause Mg to decrease? | Decreases PTH secretion. Decreased Mg can be caused by diarreha, aminoglycosides, diuretics, and alcohol abuse. |
| How does PTH increase 1,25-(OH2) vit D (calcitriol) production? | By stimulating kidney 1-alpha hydroxylase. |
| What does PTH do to urinary cAMP? | Increases it |
| How does PTH affect bone resporption of Ca and Phosphate? | Increases both |
| How does 1,25-(OH2) vitamin D affect calcium and phosphate absorption in the gut? | Increases both |
| Which vitamin D comes from sun exposure? Which vitamin D comes from plant ingestion? | D3= sun; D2= plants |
| What is 24,25-(OH2)? | The inactive form of vitD |
| From which embryonal cells do the calcitonin secreting cells arise? What is the name of these cells? | Parafollicular cells (C cells) of the thyroid derive from the neural crest |
| What causes the secretion of calcitonin? | Increased serum calcium levels. CalciTONin TONes down calcium levels. |
| True or false: Calcitonin is a key hormone in calcium homeostasis. | False. Calcitonin is NOT important in calcium homeostasis. |
| For the most part, all anterior pituitary H use which signaling pathway? | cAMP (FSH, LH, ACTH, TSH, CRH, hCG, ADH- V2 receptor, MSH, PTH, calcitonin, HGRH, glucagon) FLAT CHAMP=mnemonic |
| Vasodilators tend to use which signaling pathway? | cGMP (makes sense); ANP and NO (EDRF) |
| Releasing H tend to use which signaling pathway? | IP3 (GnRH, Oxytocin, ADH-V1 receptor, TRH); GOAT= mnemonic |
| Which H have a cytosolic steroid receptor? | Vitamin D, Estrogen, Testosterone, Cortisol, Aldosterone, Progesterone (VET CAP); VERY important to know these! |
| Which H have a nuclear steroid receptor? | T3/T4; VERY important to know this! |
| Which H receptors have an intrinsic tyrosine kinase (MAP kinase) pathway? | Insulin, IGF-1, FGF, PDGF (remember FGF mutation is assoc'd with achondroplasia/dwarfism); think of growth factors for this one |
| Which H receptors have a receptor associated tyrosine kinase (JAK/STAT pathway)? | GH and prolactin; also cytokine IL-2. Think of the Growth Hormone giant from JAK and the Bean Stalk. |
| In men, what changes in sex hormone binding globulin (SHBG) levels can lead to gynecomastia? | Increased levels of SHBG (lower free testosterone--> gynecomastia) |
| In women, what changes in sex hormone binding globulin (SHBG) levels can lead to hirsuitism? | Decreased levels of SHBG (higher free testosterone--> hirsuitism) |
| What delays the onset of steroid H? | The need for gene transcription and protein synthesis. |
| What is the only purpose of iodine in the body? | To make TH. |
| How does T3/T4 affect the heart? | Upregulates B1 receptors in the heart--> increased CO, HR, SV, and contractility; this is why beta blockers like propanolol are the drug of choice in treating thyroid storm |
| What are the 4 B's of T3 function? | Brain maturation (deficiency is assoc'd w/cretinism), Bone growth (cretins are short), Beta-adrenergic effects, and increased BMR (basal metabolic rate) |
| What happens to thyroxine-binding globulin levels in liver failure? | Decrease |
| What happens to thyroxine-binding globulin levels in pregnancy? | Increase |
| What is the enzyme responsible for oxidation and organification of iodide as well as coupling of MIT and DIT (to make T3 and T4)? | Peroxidase |
| What converts T4 to T3? | Peripheral tissues; most T3 is formed in the blood |
Created by:
sarah3148
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