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127 Cards in this Set
- Front
- Back
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What blocks 11beta hydroxylation?
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Metyrapone
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What is pendrin? Where is it located? How is this related to Pendred's Syndrome?
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On the apical border of the follicular cells, another transport protein, called pendrin, transports iodide out of the cells, into the follicular lumen, to be oxidized and coupled to tyrosine.
Pendrin is an I/Cl cotransporter. In addition to thyroid cells, it's also expressed in the kidneys and inner ear. Pendred's Syndrome--a hereditary sensorineural hearing loss, with associated impaired thyroid function and goiter. |
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Where is the posterior pituitary derived from?
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Neuroectoderm
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Where is the anterior pituitary derived from?
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Oral ectoderm (Rathke's pouch)
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How is insulin made?
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ATP glucose metabolism closing K channels and depolarizing cells leads to production in b cells.
required for adipose and skeletal muscle uptake of glucose |
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Where do GLUT-1 receptors work?
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RBCs (always depends on glucose)
brain (can depend on ketones during starvation) (independent of insulin) |
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Where do GLUT-2 receptors work?
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b cells
liver kidney small intestine |
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Where do GLUT-4 receptors work?
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adipose tissue
skeletal muscle (dependent on insulin) |
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What does somatostatin inhibit?
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GH
TSH |
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Which two hormones are within the same family and can cause lactation?
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GH
prolactin |
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How is prolactin regulated?
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1. prolactin secretion from anterior pit is tonically inhibited by dopamine from hypothalamus
2. prolactin in turn inhibits its own secretion by increasing dopamine synthesis and secretion from hypothalamus 3. TRH stimulates prolactin secretion |
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What does prolactin inhibit besides itself?
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GnRH, leading to inhibition of ovulation and spermatogensis
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What happens when there is 17a-hyroxylase deficiency?
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pregnenolone and progesterone are unable to form cortisols and sex hormones, leading to
XY -- pseudohermaphrodism XX -- sexual infantilism Aldosterone will be increased, leading to hypertension, hypokalemia. |
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What happens when there is an 21-hydroxylase deficiency?
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Inability for progesterone to progress to aldosterone; cortisol pathway blocked, leading to decreased aldosterone (hypotension, hyperkalemia) and decreased cortisol.
Testosterone increase, leading to masculinization |
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What happens when there is an 11b-deoxycorticosterone deficiency?
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Aldosterone, cortisol pathways inhibited but b/c 11-deoxycorticosterone can act like aldosterone, there is hypertension.
Testosterone pathway unaffected, increased --> masculinization |
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What is the function of cortisol?
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1. Blood pressure maintenance (permissive effect with epinephrine -- upregulates a1 receptors)
2. decreased Bone formation 3. anti-Inflammatory effect 4. decreased Immune function 5. increased Gluconeogenesis, lipolysis, proteolysis |
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How is cortisol regulated?
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CRH stimulates ACTH release, causing cortisol production
excess cortisol leads to decreased CRH, ACTH, cortisol |
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Where is the source of PTH?
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Chief cells of parathryroid
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What is the function of PTH?
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1. Increased bone resorption of Ca and PO4
2. Increased kidney reabsorption of Ca in DCT 3. Decreased kidney reabsorption of PO4 4. Increased 1,25-(OH)2 vitamin D production by activating 1a-hydroxylase (increases intestinal Ca absp) |
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How is PTH regulated?
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Decreased free serum Ca in increased PTH secretion
Decreased free serum Mg in decreased PTH secretion |
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What are common causes of decreased Mg?
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Diarrhea
Aminoglycosides Diuretics Alcohol abuse |
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How is PTH regulated?
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increased PTH
decreased Ca, phosphate = increase in vit D production |
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What is the source of calcitonin? What is its function? How is it regulated?
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From the parafollicular cells (C cells) of thyroid
Function -- decrease bone resorption of Ca Regulation -- increased serum Ca causes calcitonin secretion |
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Which endocrine hormones utilize IP3?
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GnRH
oxytocin ADH TRH |
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What is the function of the thyroid hormones?
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1. bone growth
2. CNS maturity 3. increased b1 receptors in the heart = increased CO, HR, SV, contractility 4. increased basal metabolic rate via increased Na/K-ATPase activity = increased O2 consumption, RR, body temp 5. increased glycogenolysis, gluconeogenesis, lipolysis |
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How are thyroid hormones regulated?
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TRH stimulates TSH, which stimulates follicular cells.
T4/T3 made. Increased T3 will negative feedback TRH. |
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What are the drugs that can be used to stop organification of I in thyroid hormone synthesis?
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perchlorate
pertechnetate |
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What are the drugs that interfere with the coupling of DIT, MIT?
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propylthiouracil
methimazole |
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What pathologies can cause ectopic ACTH?
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small cell carcinoma
bronchial carcinoids |
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What happens in primary hyperaldosteronism? (Conn's)
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- aldosterone secreting tumor
--> hypertension (Na retention) --> hypokalemia (K excretion) --> metabolic alkalosis (H excretion) --> low plasma renin |
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What happens in secondary hyperaldosteronism?
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- kidney perceives low intravascular volume
--> increased renin to make aldosterone --> hyertension, hypokalemia, metabolic alkalosis (renal artery stenosis, chronic renal failure, CHF, cirrhosis, nephrotic syndrome) |
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How to treat hyperaldosteronism?
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surgery to remove tumor and/or spironolactone (K-sparing diuretic) that works by acting as an aldosterone antagonist
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What is Addison's Disease?
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Chronic adrenal insufficiency
low aldosterone --> hypotension, hyperkalemia, acidosis low cortisol |
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How to differentiate b/w primary and secondary Addison's?
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Primary due to trauma/destruction of adrenal (autoimmune, TB, mets)
Low cortisol levels lead to increased ACTH = hyperpgimentation Secondary is due to decreased ACTH in brain...no hyperpigmentation |
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What is Waterhouse-Friderichsen Syndrome? What is it associated with?
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Acute, primary adrenal insufficiency due to bilateral infarction, leading to adrenal hemorrhage.
Associated with Nisseria meningisits septicemia, DIC, and endotoxic shock. |
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Compare pheochromocytoma and neuroblastoma.
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Pheo
- episodic hypertension - urinary VMA (NE) - increase catacholamines - a/w neurofibromatosis, MEN2A/B Neuro - bombesin - urinary HVA (DA) - overexpression of N-myc a/w rapid tumor progression |
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What are the 5 P's of episodic hyperadregenic symptoms of pheochromocytoma?
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Pressure (BP)
Pain (headache) Perspiration Palpatations (tachy) Pallor |
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What is the HLA association in Hashimoto's? How to treat?
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DR5
levothyroxine |
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What is causes painful hypothyroidism, self-limited following a flu-like illness?
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Subacute granulomatous thyroiditis (de Quervain)
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What is the HLA association with Graves Disease? How to treat?
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D3
B8 radioactive iodine or antithryroid drugs (PTU) |
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What is thyrotoxicosis?
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Stress-indused catecholamine surge leading to death by arrhythmia
Seen as a serious complication of Graves' and other hyperthyroid disorders |
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What is a toxic multinodular goiter? What is seen in terms of levels?
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Focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor.
See increase in release of T3/4. Hot nodules rarely malignant. |
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What is Jod-Basedow phenomena?
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thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete.
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What are the key features of papillary carcinoma?
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- most common (80%)
- excellent prognosis - orphan Annie "ground glass" nuclei - spreads through cervical lymph nodes - can be caused by an inversion of ch 1 (reversal of the order of DNA b/w two breaks in a chromosome), resulting in fusion protein |
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What are the key features of follicular carcinoma?
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- good prognosis
- uniform follicles - spread hematogenously (mets to lung, brain) - 15% |
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What are the key features of medullary carcinoma?
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- from parafollicular C cells
- produces calcitonin - sheets of cells in amyloid stroma - associated with MEN 2A/B |
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What are the key features of anaplastic carcinoma?
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- older patients
- very poor prognosis - invades soft tissue |
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What is primary hyperparathryoidism?
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- usually an adenoma
--> hypercalcemia, leading to bone pain (Ca resorption) --> hypercalciuria, leading to renal stones --> hypophosphatemia |
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What is secondary hyperparathyroidism?
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Due to decreased gut Ca reabsorption and increased phosphorus (e.g. chronic renal disease causing hypovitaminosis D)
--> increased PTH b/c want more Ca --> hypocalcemia (b/c can't reabsorb any) --> hyperphosphatemia (b/c increased phosphorus) --> renal osteodystrophy |
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What is tertiary hyperparathyroidism?
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refractory (autonomous) hyperparathyroidism resulting from chronic renal disease
increased PTH, Ca |
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What are reasons for hypoparathyroidism?
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surgery (accident)
DiGeorge autoimmune destruction |
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What are symptoms of hypocalcemia?
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Trousseau's sign -- occlusion of brachial artery with BP cuff -- carpal spasm
Chvostek's -- tapping of facial nerve -- contraction of facial muscles |
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What is psuedohypoparathyroidism?
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Unresponsiveness to PTH
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What are some dopamine agonists?
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Bromocriptine
Cabergoline |
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What types of pathologies can cause panhypoparathyroidism?
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Any pituitary tumor that destroys 75% of the pituitary may result in panhypoparathyroidism.
Characterized by abnormalities of the thyroid, adrenal gland, and repro organs. 1. pituitary adenoma 2. sheehan syndrome 3. craniopharyngioma |
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How to diagnose acromegaly/gigantism?
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increase in IGF-1 and failure to suppress serum GH following oral glucose tolerance test
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What drugs can cause diabetes insipidus?
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lithium
demeclocycline (ADH antagonist) |
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What drugs can be used to treat diabetes insipidus?
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1. Central -- intranasal desmopressin
2. Nephrogenic -- hydrochlorothiazide, indomethacin, amiloride |
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How to treat SIADH?
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demeclocycline
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What are acute manifestations of diabetes mellitus?
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Polydipsia (thirst)
Polyuria Polyphagia (eat too much) Weight loss DKA (type 1) hyperosmolar coma (type 2) unopposed secretion of GB and epinephine (exacerbation of hyperglycemia) |
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What does insulin deficiency lead to?
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1. decreased glucose uptake
- hyperglycemia, glycosuria, osmotic diuresis, electrolyte depletion 2. increased protein catabolism - increased plasma amino acids, nitrogen loss in urine 3. increased lipolysis - increased plasma FFAs, ketogenesis, ketouria, ketonemia |
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What are chronic manifestations of diabetes mellitus?
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1. small vessel disease --> retinopathy, glaucoma, nephropathy
2. large vessel atherosclerosis --> CAD, peripheral vascular occlusive disease, gangrene 3. neuropathy (motor, sensory, autonomic degeneration) 4. cataracts due to sorbitol accumulation (lacking in sorbitol dehydrogenase) |
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What is the HLA association with Type 1 DM?
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HLA-DR3/4
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What is diabetic ketoacidosis?
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One of the most important complications of type 1 diabetes. Usually due to increased insulin requirements from increased stress.
Excess fat breakdown andincreased ketogenesis from increased free fatty acids, which are then made into ketone bodies |
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What are the signs of DKA?
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- Kussmaul respirations (rapid/deep breathing)
- nausea/vomitting - ab pain - psychosis/delirium - dehydration - fruity odor breath |
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What are the lab findings in DKA?
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- hyperglycemia
- increased H - HCO3 (anion gap metabolic acidosis) - increased blood ketone levels - leukocytosis - hyperkalemia, but depleted intracellular K due to transcellular shift from decreased insulin |
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What are the complication sof DKA?
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- life-threatening mucor
- rhizopus infection - cerebral edema - cardiac arrhythmias - heath failure |
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What is the treatment for DKA?
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fluid
insulin K glucose if necessary to prevent hypoglycemia |
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What is carcinoid syndrome?
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Rare syndrome caused by carcinoid tumors (neuroendocrine cells), especially metastatic small bowel tumors, which secrete high levels of serotonin (5-HT). Not seen if tumor is limited to GI tract (5-HT undergoes first-pass metabolism in liver).
Results in recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and right-sided valvular disease Most common tumor of the appendix Increased 5-HIAA in urine |
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What is the rule of 1/3s in carcinoid syndrome?
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1/3 multiple
1/3 mets 1/3 present with 2nd malignancy treat with octreotide |
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What is Zollinger-Ellison?
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gastrin-secreting tumor of the pancreas of duodenum
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What is the inheritance of MEN? What is the mutation in MEN 2A/B?
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AD
ret gene mutation |
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How does TRH affect prolactin?
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increases prolactin secretion
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cAMP signalling pathway?
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FSH
LH ADH (V2) TSH CRH hCG ACTH MSH PTH calcitonin, GHRH, glucagon |
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IP3 signalling pathway?
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GnRH
Oxytocin ADH (V1) TRH |
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What is sex-binding hormone?
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binding globulin that increases solubility and allows for increased delivery of steroid to the target organ.
In men, increased levels of sex hormone-binding globulin (SHBG) lower free testosterone --> gynecomastia In women, decreased SHBG raises free testosterone --> hirutism |
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How do thyroid hormones function on the body other than bone growth and CNS maturation?
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1. increased b1 receptors in the heart = increased CO, HR, SV, contractility
2. increased basal metabolic rate via increased Na/K ATPase activity = increased O2 consumption, RR, body temp |
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Can beta blockers be utilized in hyperthyroidism?
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b-blcoker ipodate blocks peripheral conversion of T4 --> T3
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Where is a prolactinoma usually located?
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In the sphenoid (where the sellica turcica grows)
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Does a lack of GH lead to fasting hypoglycemia in an adult? What amino acids stimulate GH?
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Yes
Arginine & Histidine |
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What inflammatory disorders result in hypothalamic funciton?
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sarcoidosis
meningitis |
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What are the causes for increased and decreased TBG? How does this affect T4?
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Increase in TBG synthesis increases T4
- estrogen: pregnancy, OCP, hormone replacement decreases in TBG lead to decrease in T4 - anabolic steroids, nephrotic syndrome |
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What is the pathogenesis for Hashimoto's thyroiditis?
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1. cytotoxic T cells destroy the parenchyma (type IV hypersensitivity) -- initial thyrotoxicosis, eventual hypothyroidism
2. blocking antibodies against TSH receptor (type II HSR) -- decrease hormone synthesis 3. helper T cells release cytokines attracting macrophages that damage tissue (type IV HSR) 4. antimicrosomal and thyroglobulin antibodies destroy prenchyma (type II HSR) -- develop as a result of gland injury, no causal role |
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What are complications of Graves disease involving the heart? How to treat the ridic catacholamines?
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A fib,
b-blocker |
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Where is a prolactinoma usually located?
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In the sphenoid (where the sellica turcica grows)
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What can happen with a craniopharyngioma?
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remnants of Rathke's pouch, visual field defect, suprasellica
can be confused with prolactinoma |
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Does a lack of GH lead to fasting hypoglycemia in an adult? What amino acids stimulate GH?
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Yes
Arginine & Histidine |
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What inflammatory disorders result in hypothalamic funciton?
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sarcoidosis
meningitis |
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What are the causes for increased and decreased TBG? How does this affect T4?
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Increase in TBG synthesis increases T4
- estrogen: pregnancy, OCP, hormone replacement decreases in TBG lead to decrease in T4 - anabolic steroids, nephrotic syndrome |
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What is the pathogenesis for Hashimoto's thyroiditis?
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1. cytotoxic T cells destroy the parenchyma (type IV hypersensitivity) -- initial thyrotoxicosis, eventual hypothyroidism
2. blocking antibodies against TSH receptor (type II HSR) -- decrease hormone synthesis 3. helper T cells release cytokines attracting macrophages that damage tissue (type IV HSR) 4. antimicrosomal and thyroglobulin antibodies destroy prenchyma (type II HSR) -- develop as a result of gland injury, no causal role |
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What are complications of Graves disease involving the heart? How to treat the ridic catacholamines?
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A fib,
b-blocker |
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How do sulfonylureas work?
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stimulate insulin secretion by closing K channel
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How does FSH act in men?
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acts on Sertoli cells to maintain spermatogenesis
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How does LH act in men?
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acts on Leydig cells to promote testosterone
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How to sulfonylureas work? What are the different types?
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Close K channel in b-cell membrane, so cell depolarizes --> trigering of insulin release via increased Ca influx
-- requires endogenous insulin, so works only in Type 2 Diabetes prolong binding of insulin to target tissue receptors,reduce serum glucagon receptors. First gen -- tolbutamide Second gen -- glyburide, glipizide |
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What are the side effects of tolbutamide? Contraindicated in pregnancy?
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disulfram-like reactions (flushing after alcohol)
contraindicated in pregnancy and use with caution in renal/hepatic insufficiency |
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What are the biguanides? How does metformin work?
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decrease in gluconeogenesis, increase in glycolysis, increase in peripheral glucose uptake (increases insulin activity)
reduces LDL, TG -- DOES NOT CAUSE HYPOGLYCEMIA |
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What is metformin used to treat? What are the side effects?
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first choice for Type 2 DM, though can be used in both. Used for PCOS.
Side effects -- lactic acidosis (contraindicated in renal failure) |
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How do glitazones work? When is it used? What are the sid eeffects?
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increase insulin sensitivity in peripheral tissue. binds to PPAR-gamma nuclear transcription regulator.
used as monotherapy in DM2 or in combo Side effect -- weight gain, edema; hetpatotoxicity (trogliatzone), CV toxicity |
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How do a-glucosidase inhibitors work? What are the side efects?
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inhbit intestinal brush-border a-gluocosidases. delayed sugar hydrolysis and glucose absorption lead to decreased postprandial hyperglycemia.
used or monotherapy DM2 or combined. Side -- Aracarbose, MiglitolGI disturbances |
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What are mimetics? How do they work? What are the side effects?
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Pramlintide decreases glucose. For type 2DM
hypoglycemia, nausea, diarrhea |
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How do the GLP-1 analogs work?What are side effects?
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GLP=1 is an incretin hormone secreted by intestinal L cells in response to food intake. decreases glucose by nducing satiety, decreasing gastric emptying, increasing insulin resistance.
exanitide increases insulin, decreases glucagon. Type 2DM Side -- nausea, vomiting, pancreatitis |
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How does meglintide work?
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type 2DM
binds to K channel on pancreatic b-cell = inhibition --> depolarization, opening Ca channels --> increase insulin release |
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How do DPP-4 inhibitors work?
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sitagliptin inhibits GLP-1
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How does PTU work? What are the side effects?
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Inhibits organification of iodide and coupling of thyroid hormone synthesis.
Toxicity -- skin rash, agranulocytosis (rare), aplasic anemia. |
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What is demeclocycline? What does it treat? What are the side effects?
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ADH antagonist
treat SIADH tox -- nephrogenic DI, photosensitivity, abnormalities of bone and teeth |
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What is the function of 17a-hydroxylase? What levels are seen in serum?
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decreased sex hormones and cortisol, increased mineralcorticoids.
17A-hydroxylase converts pregnelone and progesterone into its next phases to become cortisols and sex hormones. |
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What is the clinical presentation of 17a-hydroxylase? What are the specific presentations in XY and XX? What are the ACTH levels?
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- hypertension, hypokalemia
- XY: decreased DHT → pseudohermaphrotism (externally phenotypic female, no internal reproductive structures due to MIF) - XX: externally phenotypic female with normal internal sex organs but lacking secondary characteritics (sexual infantilism – lack of pubic and axillary hair) - ACTH levels are increased due to negative feedback effect of decreased cortisol |
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What are the precursors of estrogen? How is it made?
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The precursors of estrogen are products of the zona reticularis, dehydroepiandrosertone –(B-HYDROXYSTEROID DEHYDROGENASE)-->androstenedione, which can either be made into estrone, then estradiol OR made into testosterone, which is then converted by AROMATASE into estradiol.
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What is the function of 21b-hydroxylase? What levels are seen?
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decreased cortisol and mineralcorticoids, increased sex hormones.
21b-hydroxylase converts pathways to corticosterone (to make aldosterone) and cortisol |
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What is the clinical presentation of 21b-hydroxylase deficiency? What are the ACTH levels?
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- hypotension, hyperkalemia,
- increased plasma renin activity, volume depletion - masculinization, female pseudohermaphrotism - early appearance of pubic and axillary hair - ACTH levels are increased due to negative feedback effect of decreased cortisol |
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What is female psuedohermaphrodism?
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46, XX
Sex chromatin-positive CAH is common cause (excessive androgens) Virilization of female embryo Clitoral hypertrophy Partial fusion of labia majora Persistent urogenital sinus |
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What is the adult remnant of the gubernaculum in females? in males?
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Ovarian ligament & round ligament of uterus
(in males, anchors testes in scrotum) |
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What is the adult remnant of the processus vaginalis in males? in females?
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Ovarian ligament & round ligament of uterus
(in males, anchors testes in scrotum) |
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What are the types of tumors associated with MEN 1 (Werner's Syndrome)?
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Parathyroid tumors
Pituitary tumors (prolactin or GH) Pancreatic endocrine tumors – Zollinger-Ellison, insulinoma, VIPoma, glucagonoma (rare) |
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What are the types of tumors associated with MEN 2A (Sipple's Syndrome)?
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Medullary thyroid carcinoma (secretes calcitonin)
Pheochromocytoma Parathyroid tumors |
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What are the types of tumors associated with MEN 2B?
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Medullary thyroid carcinoma (secretes calcitonin)
Pheochromocytoma Oral/intestinal ganglioneuromatosis (associated with marfanoid habitus) |
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Which neoplasm is most commonly responsible for ACTH --> Cushing's Syndrome?
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small cell carcinoma
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What neoplasms are responsible for ADH --> SIADH?
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smell cell lung carcinoma
intracranial neoplasm |
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What is Lambert-Eaton? What can it be caused by?
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Lambert Eaton (muscle weakness at the beginning of the day) attacks the presynaptic Ca2+ receptors. It can be caused by a thymoma or small cell lung carcinoma.
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What is ADH? What is its purpose?
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retains water
stimulates reabsorption by renal collecting ducts, increases permeability of late distal tubules and collecting ducts an increase in serum osmolarity will lead to an increased in ADH, a decrease in serum osmolarity (or the presence of ethanol in the system) will lead a a decrease in ADH (OMGZ THERE IS TOO MUCH WATER, WE NEED TO STOP ABSORBING THIS SHIT) |
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What is central diabetes insipidus?
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problem within the brain, usually to a head trauma – there is no/decreased production of ADH
tumor, trauma, autoimmune, familial |
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What is nephrogenic diabetes insipidus?
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problem with receptors in the kidney – no response to ADH
can be acquired, due to drugs (lithium), familial water deprivation test is used to see the osmolarity of the urine – URINE OSMOLARITY WILL NOT INCREASE |
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A patient complains of intense thirst and profuse urination. After further testing, you suspect diabetes insipidus. What urine specific gravity and serum osmolality findings would you see in a patient with diabetes insipidus?
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Urine specific gravity > 1.006
Serum osmolarity > 290 mOsm/L |
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What is Lambert-Eaton syndome? Which neoplasms can cause?
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(a) Antibodies against presynaptic Ca channel at NMJ, leading to decreased Ach release
(b) thymoma, small cell lung carcinoma (c) Lambert-Eaton muscle weakness at the beginning of the day |
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What are all of the possible side-effects of glucocorticoid use?
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(a) Cushing-like symptoms
(b) immunosuppression (c) cataracts (d) acne (e) osteoporosis (f) hypertension (g) peptic ulcers (h) hyperglycemia (i) psychosis |
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What are the functions of cortisol?
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15. Cortisol is BBIIG – maintains blood pressure (premissive effect with epinephrine – upregulates a1 receptors, decreased bone formation, anti-inflammatory, decreased immune funtion, increased gluconeogensis, lipolysis, proteolysis
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