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HY Endo Path&Pharm
Day 9
| Question | Answer |
|---|---|
| Increased cortisol due to a variety of causes | Cushing's syndrome |
| What is the MCC of Cushing's syndrome? | Exogenous (iatrogenic) steroids |
| What is the MCC of endogenous Cushing's syndrome? | Cushing's disease |
| Increased ACTH secretion from pituitary adenoma | Cushing's disease |
| What happens to the adrenal cortex in Cushing's disease? | Hyperplasia of the zona fascicularis |
| What are 2 potential ectopic sources of ACTH (ACTH from non-pituitary tissue)? | Small cell lung cancer, bronchial carcinoids |
| In what instance of Cushing's syndrome would you see low ACTH? | With an adrenal adenoma; low ACTH is caused by negative feedback from cortisol that is being secreted by the adenoma |
| What causes the hyperpigmentation seen in Cushing's disease? | ACTH is synthesized as part of POMC, which also makes MSH. As ACTH synth increases, MSH also increases, stimulating melanocytes to make more pigment. May be seen in small cell lung CA and bronchial carcinoids. |
| Dexamethasone test results: Decrease in cortisol after low dose | Healthy individual |
| Dexamethasone test results: Cortisol levels cannot be suppressed after low dose, but decrease after a high dose | ACTH-producing pituitary tumor (subject to negative feedback from cortisol); Cushing's disease |
| Dexamethasone test results: Cortisol cannot be suppressed by a low or high dose; ACTH is high | Ectopic ACTH producing tumor (not coming from pituitary, so not subject to neg feedback from cortisol); small cell lung CA, bronchial carcinoids |
| Dexamethasone test results: Cortisol cannot be suppressed by a low or high dose; ACTH is low | Adrenal adenoma producing cortisol; part of normal axis, so excess cortisol feedsback to inhibit ACTH; cortisol cannot be suppressed b/c it is not the result of ACTH stimulation from the pituitary |
| Aldosterone-secreting tumor resulting in HTN, hypokalemia, metabolic alkalosis, and low plasma renin | Primary hyperaldosteronism/Conn's syndrome (HTN with LOW plasma renin? think Conn's; aldosterone has neg feedback on renin) |
| How does secondary hyperaldosteronism differ from Conn's syndrome (primary hyperaldosteronism)? | Secondary is caused by the kidney perceiving a low intravascular volume and overactivating the renin-angio system. Renin will be high (Conn's has low renin). |
| What is the tx for primary hyperaldosteronism? | Surgery to remove the tumor or spironolactone (K sparing diuretic that acts as an aldosterone antagonist); remember hyperaldosteronism causes hypokalemia |
| Deficiency of aldosterone and cortisol causing hypotension, hyperkalemia, acidosis, and skin hyperpigmentation. | Addison's disease (adrenal insufficiency); may be due to adrenal atrophy or destruction by disease |
| What part of the adrenals does Addison's involve? What part is spared? | Involves all 3 layers of cortex; medulla is spared |
| How is secondary adrenal insufficiency different from Addison's? | Secondary is caused by decreased ACTH stimulation from the pituitary; it has no hyperpigmentation b/c there is a LOWER level of ACTH (so lower levels of POMC and MSH) |
| What causes hyperpigmentation in Addison's? | ACTH production is upregulated to try and get adrenals going, and in the process, the increase in POMC also results in an increase in MSH |
| What infection is assoc'd with Waterhouse Friedrichsen syndrome? | Neisseria meningitidis septicemia; causes acute primary adrenal insufficiency due to adrenal hemorrhage; DIC and endotoxic shock |
| Patient presents with hypOtension, tachycardia, and hypoglycemia with a h/o vomiting, abdominal pain, weight loss, and hyperpigmentation. | Adrenal insufficiency; treat immediately with corticosteroids |
| Virilization (pubic and axillary hair), increased linear growth, and elevated levels of 17-hydroxyprogesterone and testosterone. Salt wasting may be present. | Congenital adrenal hyperplasia due to 21-hydroxylase deficiency |
| Pheochromocytomas arise from which adrenal cells? From which embryonic cells? | Chromaffin cells of the medulla; neural crest cells |
| How are the symptoms of a pheo (elevated BP, HA, perspiration, palpitations, pallor, panic attack) different from those of hyperthyroidism? | Pheo symptoms are episodic; hyperthyroid symptoms are continuous |
| What H are secreted by pheos? | epi, NE, and DA |
| What syndromes are pheos assoc'd with? | Neurofibromatosis, MEN 2A, MEN 2B |
| What are the urinary markers for adult pheos? | Elevated urinary VMA, HVA, and metanephrines (plasma will have elevated catecholamines) |
| What is the treatment for pheos? | Alpha antagonists like phenoxybenzamine (irreversible) followed by surgery to remove the tumor; NEVER give beta blocker b/c it can worsen HTN; phentolamine is a reversible alpha blocker |
| What is the rule of 10s with pheo? | 10%: malignant, bilateral, extra-adrenal, calcify, kids, familial |
| What is the urinary marker for adrenal neuroblastoma in children? | Elevated urinary HVA |
| What is HVA? VMA? Metanephrine? | HVA is a breakdown product of dopamine. VMA is a breakdown product of norepinephrine. Metanephrine is a breakdown product of epinephrine. |
| Facial/periorbital myxedema is seen in which thyroid disease? | HypOthyroidism |
| Pretibial myxedema is seen in which thyroid disease? | Hyperthyroidism (Graves' disease) |
| What are the lab findings for hypOthyroidism (TSH, T4, T3 uptake)? | TSH is high (trying to stim thyroid to make TH), T4 is low, T3 uptake is low |
| Which test is most sensitive for hypOthyroidism? | TSH; TSH elevation can be detected before all other lab abnormalities |
| What are the lab findings for hyperthyroidism (TSH, T4, T3 uptake)? | Low TSH (neg feedback), T4 is high, T3 uptake is high |
| What is the MCC of a goiter? | Iodine deficiency |
| What does hot/cold thyroid nodule refer to? | Hot nodule takes up radioactive iodine; cold nodule does not |
| A cold thyroid nodule on a woman-- benign or malignant? | Probably benign |
| A cold thyroid nodule on a man or child-- benign or malignant? | Probably malignant |
| Hashimoto's thyroiditis is assoc'd with with HLA? | HLA-DR5 |
| Hurthle cells (enlarged epithelial cells with excessive eosinophilic granular cytoplasm), lymphocytic infiltrates, with germinal centers | Hashimoto's thyroiditis |
| What can cause hyperthyroidism early on in the course of Hashimoto's? | Thyrotoxicosis during follicular rupture (think of antibodies running around the follicles destroying them and letting out H) |
| Pot-bellied, pale, puffy-face child with protruding umbilicus and protruberant tongue. Short stature and mental retardation ensue. | Cretinism; due to severe fetal hypothyroidism |
| What are the 2 types of cretinism and their causes? | 1. Endemic: occurs wherever endemic goiter is prevalent (lack of dietary iodine). 2. Sporadic: defect in T4 formation or developmental failure in thyroid formation |
| Increased ESR, jaw pain, very tender thyroid following a flu-like illness. What is the disease and what would you expect to find on histology? | Subacute deQuervain's thyroiditis. See granulomatous inflammation. |
| Fixed, hard (rock-like) thyroid with painless goiter. What is the disease and its pathogenesis, and what would you expect to see histologically? | Riedel's thyroiditis; thyroid replaced by fibrous tissue (may be hypO or euthyroid); see fibrosis, macrophages, and eosinophilic infiltrate |
| Autoimmune hyperthyroidism. What disease? What type hypersensitivity? | Graves' disease. Type 2 |
| Stress induced catecholamine surge leading to death by arrhythmia. What disease? Which arrhythmia? | Thyrotoxicosis (thyroid storm); afib |
| How is thyroid storm treated? | With beta blockers and an anti-thyroid agent (propylthiouracil, methimazole) |
| What is the mechanism of action of antithyroid agents like propylthiouracil and methimazole? | Inhibit iodination of tyrosyl groups (can't put an iodine on thyroid hormone) |
| Which antithyroid agent can also decrease peripheral conversion of T4 to T3? | Propylthiouracil (give PROPs to propylthiouracil for all its extra work!); glucocorticoids can also do this |
| Which antithyroid agent is teratogenic? Which agent is given to pregnant women instead? | Methimazole is a possible teratogen. Pregnant women are given propylthiouracil instead. |
| Beta blockers can treat all of the symptoms of thyroid storm except for? | Sweating and exophthalmos (glucocorticoids can be used to treat exophthalmos and decrease peripheral conversion of T4-->T3) |
| What are the toxic SE of anti-thyroid agents? | Skin rash, agranulocytosis, and aplastic anemia. (HIV drugs like zidovudine have the same set of SE) |
| What drugs are used to treat hypothyroidism? | Leveothyroxine and triiodothryonine (thyroxine replacement is MOA) |
| What causes periorbital myedema in hypothyroidism? | Deposition of GAGs (similar pathogenesis to development of mitral valve prolapse) |
| Focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor. | Toxic multinodular goiter. Increased release of T3/T4. Hot nodules are rarely malignant. |
| Thyroid storm-like symptoms in a patient with iodine deficiency after being given a radiocontrast dye for a procedure. | Jod-Basedow phenomenon |
| Woman with increased total T4 with normal TSH. | On estrogen (OCPs or pregnancy) |
| Man with low T4 and normal TSH. | Taking anabolic steroids |
| MC thyroid cancer with ground glass (Orphan Annie) nuclei, psammoma bodies, and nuclear grooves. Increased risk with childhood irradiation. | Papillary CA |
| Thyroid cancer from parafollicular C cells; produces calcitonin, sheets of cells in amyloid stroma. What MEN syndromes is it assoc'd with? | Medullary CA; assoc'd with MEN 2A and 2B |
| Undifferentiated thyroid cancer with very poor prognosis; typically seen in elderly | Anaplastic thyroid CA |
| Which thyroid cancer is assoc'd with Hashimoto's? | Lymphoma (non-Hodgkin's) |
| Bone lesions due to secondary or tertiary hyperparathyroidism due in turn to renal disease | Renal osteodystrophy |
| What causes primary hyperparathyroidism? | Usually an adenoma |
| What causes secondary hyperparathyroidism? | Decreased gut Ca absorption and increased phosphorous retention, mostly due to renal disease |
| What causes tertiary hyperparathyroidism? What are the lab findings? | Refractory (autonomous) hyperparathyroidism results from chronic renal disease. Greatly increased PTH, increased Ca |
| What are the causes of hypOparathyroidism? | Accidental surgical excision, autoimmune destruction, or DiGeorge syndrome. |
| What two signs are indicative of hypocalcemia (serum Ca <7mg/dL)? | Chvostek's sign (tapping of facial n--> facial m twtiching) and Trousseau's sign (Tighten the BP cuff--> occlusion of brachial a--> carpal spasm) |
| AD kidney unresponsiveness to PTH at the level of the renal tubule; hypocalcemia, shortened 4th/5th digits, short stature. What will the PTH level be? | PseudohypOparathryoidism (Albright's hereditary osteodystrophy). PTH will be high b/c it's desperately trying to wake up the kidney, but the kidney can't hear it. |
| Low PTH levels with high calcium | PTH-independent hypercalcemia (excess calcium ingestion, cancer) |
| What causes amenorrhea in anorexics? | Decreased body fat--> loss of pulsatile GnRH release from the hypothalamus (so no FSH and LH changes necessary for cycle) |
| Overstimulation of the zona reticularis will lead to what physical presentation? | Hirsuitism (hyperandrogens) |
| Parasthesias and weakness in the setting of hyperaldosteronism | Conn's |
| Weight gain, easy bruising, high cortisol. | Cushing's syndrome (too much cortisol) |
| Diarrhea, flushing, excess 5HT | Carcinoid syndrome |
| What hormonal therapy can be used to treat both growth hormone deficiency and Turner's syndrome? | GH |
| What hormonal therapy can be used to treat acromegaly, carcinoid, gastrinomas, and glucagonomas? | Octreotide (SST- the grand inhibitor) |
| What hormonal therapy can be used to stimulate lab, uterine contractions, and milk letdown. What gynecologic emergency is it used to control? | Oxytocin; controls uterine hemorrhage |
| What is the MC pituitary adenoma? | Prolactinoma |
| Amenorrhea, galactorrhea, low libido, infertility, bitemporal hemianopia; low GnRH | Prolactinoma |
| What is the treatment for prolactinomas? | Bromocriptine or cabergoline (DA agonists; DA inhibits prolactin) cause shrinkage of tumor |
| Excess GH in adults | acromegaly |
| Excess GH in children | gigantism (epiphyseal plates have not yet fused--> increased linear bone growth) |
| In what conditions is GH secretion normally increased? | Stress, excercise, and hypOglycemia |
| How is GH excess diagnosed? | Increased serum IGF-1 (insulin-like growth factor); failure to suppress serum GH following oral glucose tolerance test. |
| Older woman with large tongue with deep furrows, deep voice, large hands, and insulin resistance. | Acromegaly (excess GH) |
| Intense thirst and polyuria together with an inability to concentrate the urine owing to a lack of ADH. | Central Diabetes Insipidus (pituitary tumor, trauma, surgery, histiocytosis X) |
| Intense thirst and polyuria together with an inability to concentrate the urine owing to a lack of renal response to ADH. | Nephrogenic Diabetes Insipidus (hereditary or secondary to hypercalcemia or drugs) |
| Which drugs can cause nephrogenic diabetes insipidus? | Demeclocycline (an ADH antagonist used to treat SIADH), lithium, and tetracycline |
| How can the water deprivation test be used to distinguish between nephrogenic and central diabetes insipidus? | Water deprivation: If you give ADH and they can concentrate their urine, you know it's central (due to lack of ADH). If you give ADH and they still can't concentrate their urine, you know it's nephrogenic (problem is the kidneys, not a lack of ADH). |
| How is urine osmolality related to urine concentration? | Large values indicate concentrated urine (>300) and small values indicate dilute urine. |
| Excessive water retention, hyponatremia, urine osmolarity > serum osmolarity. | SIADH |
| Name 4 causes of SIADH. | 1. Ectopic ADH (small cell lung CA) 2. CNS disorders/head trauma 3. Pulmonary disease 4. Drugs (e.g., cyclophosphamide) |
| What is a potentially serious complication of SIADH? | Seizures due to very low serum Na levels (body tries to compensate for SIADH by decreasing aldosterone to maintain near-normal volume status) |
| What is the treatment for central diabetes insipidus? | Intranasal desmopressin (ADH analog) |
| What is the treatment for nephrogenic diabetes insipidus? | hydrochlorothiazide, indomethacin, and amiloride (good for lithium-induced DI) |
| What is the treatment for SIADH? | Demeclocycline or H2O restriction |
| Name 3 side effects of demeclocycline. | 1. Nephrogenic DI 2. Photosensitivity 3. Bone/teeth abnormalities (similar to tetracycline) |
| Fatigue, anorexia, poor lactation, loss of pubic and axillary hair postpartum. | Sheehan's postpartum pituitarism; caused by pituitary infarct due to hemorrhage or postpartum bleeding |
| Polydipsia, polyuria, polyphagia, weight loss, DKA | Diabetes Mellitus type 1 |
| Hyperosmolar coma is assoc'd with which type of diabetes? | Type 2 |
| What cardiovacsular drug can decrease diabetic nephropathy? | ACE-i |
| What process leads to the chronic manifestations of diabetes? | Nonenzymatic glycosylation |
| Which diabetic test measures long-term glucose control? | HbA1c |
| What drug can be used to treat neuropathic pain in diabetes? | Gabapentin or pregabalin |
| Why are Schwann cells, lens, retina, and kidneys preferentially damaged in diabetes? | B/c they only have aldose reductase. Without sorbitol dehydrogenase, cells can only convert glucose to sorbitol which has osmotic properties. Pulls in water and damages cell. |
| Type 1 or Type 2 DM: weak, polygenic genetic predisposition | Type 1 |
| Type 1 or Type 2 DM: HLA-D3, D4 assoc'n | Type 1 |
| Type 1 or Type 2 DM: strong, polygenic genetic predisposition | Type 2 |
| Type 1 or Type 2 DM: High insulin sensitivity | Type 1 (Type 2 is insulin resistant) |
| Type 1 or Type 2 DM: Islet cell leukocytic infiltrate | Type 1 |
| Type 1 or Type 2 DM: Islet cell amyloid deposit | Type 2 |
| Excess fat breakdown and increased ketogenesis from increased free fatty acids which are then made into ketone bodies. | DKA (normally insulin inhibits lipolysis which is what creates the ketones) |
| Kussmaul respiration (rapid/deep breathing), nausea/vomiting, abdominal pain, psychosis/delirium, dehydration. | DKA |
| What are the lab findings in DKA? | Hyperglycemia, increased H+, decreased HCO3- (anion gap metabolic acidosis), increased blood ketone levels, leukocytosis, and hyperkalemia with depleted intracellular K |
| What cardiovascular complications may be seen with DKA? | Cardiac arrhythmias and heart failure (from K depletion) |
| Why is carcinoid syndrome only symptomatic when it occurs outside of the GI tract? | B/c in the GI tract, it undergoes significant first pass metabolism in the liver. |
| Recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and R sided valvular disease. | Carcinoid syndrome. Be FDR (Bronchospasm, Flushing, Diarrhea, Right sided heart valve disease/murmur) |
| From where are carcioid tumors derived? What is the urinary marker? | Derived from neuroendocrine cells of GI tract; elevated 5-HIAA in urine |
| What is the treatment for carcinoid syndrome? | Octreotide |
| Gastrin secreting tumor of pancreas or duodenum; stomach shows rugal thickening with acid hypersecretion. What is the disease and what MEN syndrome is it assoc'd with? | Zollinger-Ellison syndrome; MEN type 1 |
| What is the treatment for Zollinger-Ellison syndrome? | PPI and octreotide (need PPI b/c not all gastrinomas respond to octreotide) |
| Which thyroid CA-- papillary or follicular-- tends to metastasize to the cervical lymph nodes? | Papillary. Follicular actually avoids the lymph nodes. |
| It's raining MEN! Hallelujah!: Pancreas, Pituitary, Parathyroid | MEN 1 (3 P's) |
| It's raining MEN! Hallelujah!: Medullary and thyroid CA, Pheochromocytoma, Parathyroid | MEN 2A (2 P's) |
| It's raining MEN! Hallelujah!: Medullary and thyroid CA, Pheochromocytoma, and mucosal neuroma | MEN 2B (1P) |
| All MEN syndromes have what type of inheritance? | Autosomal dominant (men are dominant, or at least they think they are...) |
| Which MEN syndromes would have a ret-protooncogene assoc'd tumor that secretes a substance which can be converted into amyloid? | MEN 2A and 2B: medullary thyroid CA secretes calcitonin which can be converted into amyloid |
| How do glucocorticoids work? | Decrease production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX2. |
| How do cortisol injections treat keloids? | Decrease excess collagen production |
| Person being treated with propylthiouracil for hyperthyroidism presents with fever and sore throat. | Agranulocytosis complication (low neutrophils). Discontinue meds and get a WBC. |
| What is the treatment of choice for DKA? | Short acting insulin (6-8hr) |
| What is the treatment of choice in a non-medical setting for a person who loses consciousness due to hypOglycemia? | IM or subQ injection of GLUCAGON by an informed friend or relative. IN a medical setting, IV dextrose is used (contains glucose) |
| Name three rapid acting insulins. | Lispro, aspart, and regular insulin. |
| What are the toxicities of insulin use? | Hypoglycemia, and hypersensitivity rxn. |
| Which insulin is intermediate acting? | NPH |
| Which insulins are long-acting? | Glargine and determin |
| What class of diabetic drugs works by closing K channels in the Beta cell membrane, triggering insulin release via increased Ca influx? | Sulfonylureas |
| Which sulfonylureas are 1st generation? What are their toxic SE? | Tolbutamide and chlorpropamide. Disulfiram-like reactions. |
| Which sulfonylureas are 2nd generation? What are their toxic SE? | Glyburide, glimepiride, and glipizide. Hypoglycemia. |
| Which diabetic drug acts primarily in the liver to decrease gluconeogenesis? | Metformin (biguanide) |
| What is the difference in clinical use between sulfonylureas and metformin? | Sulfonylureas require functional islet cells to work, whereas metformin does not require any islet cell function to work. |
| Why is metformin contraindicated in renal failure? | Increased risk of lactic acidosis, the most feared toxic SE. Creatinine levels should be checked yearly in patients on metformin. |
| What procedure requires temporary cessation of metformin treatment? | Procedures using IV contrast; increases risk of developing lactic acidosis |
| What is the mechanism of glitazones/thiazolidinediones? | Increase insulin sensitivity in the peripheral tissues by binding to the PPAR gamma nculear transcription regulator |
| What are the glitazones/thiazolidinediones? | Pioglitazone, rosiglitazone |
| What are the toxic SE of glitazone/TZD therapy? | Weight gain, edema (CHF exacerbation), hepatotoxicity (check LFTs yearly), and CV toxicity (mostly with rosiglitazone) |
| Which class of diabetic drugs inhibits intestinal brush border alpha glucosidases? What are the names of the individual drugs in this class? | Alpha glucosidase inhibitors. Acarbose and miglitol. |
| Which diabetic drug class can be used in a type 2 DM patient who has problems with very high blood sugar right after a meal? | Alpha glucosidase inhibitors (acarbose or miglitol). |
| Which diabetic drug decreases glucagon? | Pramlintide (mimetic); not commonly used |
| Which GLP-1 analog increases insulin and decreases glucagon release? What potentially toxic SE is it assoc'd with? | Exenatide; assoc'd with pancreatitis (also n/v) |
| Type 1 or Type 2 DM: Low sugar diet and insulin replacement therapy | Type 1 |
| Type 1 or Type 2 DM: DIetary modification and exercise for weight loss as first recommendation; also oral hypoglycemics and insulin replacement | Type 2 |
| What is one of the main ways to reduce insulin resistance in type 2 diabetes? | Increase adiponectin levels (tend to be low in type 2 DM) |
Created by:
sarah3148
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