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Endocrine
Pathology: Endocrine
| Question | Answer |
|---|---|
| 1. Most common hormone secreted by pituitary adenoma 2. Central diabetes insipidus vs Nephrogenic diabetes insipidus | 1. prolactin 2. ADH deficiency vs impaired renal response to ADH |
| 1. Poor lactation, loss of pubic hair and fatigue following pregnancy. 2. What is the pathologenesis of this disorder? | 1. Sheehan syndrome 2. pituitary doubles in size during pregnancy, but blood supply does not → infarction |
| Treatment of: 1. central diabetes insipidus 2. prolactinoma | 1. desmopressin (ADH analog) 2. bromocriptine (dopamine agonist) |
| Drug related to: 1. SIADH 2. Nephrogenic diabetes insipidus | 1. Cyclophosphamide 2. Lithium |
| What is responsible for the following findings in hyperthyroidism? 1. increased basal metabolic rate 2. increased sympathetic nervous system activity 3. hypocholesterolemia 4. finger clubbing | 1. increased synthesis of Na+-K+ ATPase 2. increased expression of β1 adrenergic receptors 3. increased LDL receptor synthesis 4. (acropachy) subperiosteal new bone formation |
| Which type of hypersensitivity reaction: 1. Graves disease 2. Type 1 diabetes | 1. type II - autoantibody stimulates TSH receptor 2. type IV |
| What is the cause of exophthalmos and pretibial myxedema seen in Graves disease? | 1. TSH binds fibroblast TSH receptors → glycosaminoglycans buildup 2. immune reaction → inflammation, edema, and fibrosis |
| What are the lab levels of T4 and TSH in: 1. primary hypothyroidism 2. secondary hypothyroidism 3. hyperthyroidism | 1. ↓ T4, ↑ TSH (thyroid gland problem) 2. ↓ T4, ↓ TSH (pituitary problem) 3. ↑ T4, ↓ TSH |
| Patient with long-standing Hashimoto thyroiditis now presents with an enlarging thyroid. What is the most likely diagnosis? | B-cell (marginal zone) lymphoma |
| Hypothyroidism in: 1. neonates and infants 2. children or adults | 1. Cretinism 2. Myxedema |
| Patient with hyperthyroidism, tender thyroid following a viral infection. What is the cause of thyrotoxicosis? | Subacute (De Quervain) Thyroiditis. increased T4 release after gland destruction |
| What is the most likely diagnosis when investigating a thyroid nodule with radioactive iodine uptake: 1. Increased uptake 2. Decreased uptake | 1. Graves disease or nodular goiter 2. Adenoma and carcinoma |
| 1. Genetic mutation associated with multiple endocrine neoplasia 2. 1. What is the outcome of a water deprivation test administered to a patient with diabetes insipidus? | 1. RET oncogene 2. no increase in urine osmolality |
| Pathogenesis of renal osteodystrophy | 1. kidney failure → ↓ phosphate secretion and ↓ vitamin D activation 2. ↑ phosphate binds free calcium → ↓ ionized calcium 3. ↓ free calcium stimulates PTH secretion 4. ↑ PTH leads to bone resorption |
| 1. ↑ serum PTH, ↑ serum calcium, ↓ serum phosphate. Diagnosis? 2. Most likely cause? | 1. Primary hyperparathyroidism 2. Parathyroid adenoma |
| 1. Trousseau sign 2. Chvostek sign | 1. hand spasm after inflation of BP cuff during hypocalcemia 2. contraction of facial muscle after tapping on masseter during hypocalcemia |
| 1. What is the differential for: ↑ serum PTH, ↓ serum calcium, ↑ serum phosphate 2. What is the most likely cause of each differential? | 1. Secondary hyperparathyroidism - chronic renal failure 2. pseudohypoparathyroidism - defective Gs protein at PTH receptor |
| Which major histocompatability complex is associated with: 1. Type 1 diabetes 2. Hashimoto thyroiditis | 1. HLA-DR3 and HLA-DR4 2. HLA-DR5 |
| Why are ketones absent in type 2 diabetes mellitus | insulin is present in DM2 (as opposed to DM1) and counteracts glucagon mediated lipolysis |
| 1. Abdominal mass with episodic hypoglycemia and mental status changes 2. What is a gastrinoma? 3. Where is gastrin produced? | 1. insulinoma 2. tumor secreting excess gastrin 3. G cells in the antrum of the stomach, duodenum, and the pancreas |
| What is the pathogenesis of diabetic retinopathy? | 1. pericytes lining retinal blood vessels take up glucose and incur osmotic damage 2. pericytes die and blood vessels weaken leading to aneurysm, hemorrhage and blindness |
| 1. Most common cause of primary hyperaldosteronism (Conn's syndrome) 2. Common cause of secondary hyperaldosteronism | 1. adrenal adenoma 2. renovascular hypertension leading to activation of RAAS (e.g. fibromuscular dysplasia) |
| 1. In congential adrenal hyperplasia (CAH), what is the cause of adrenal hyperplasia? 2. Most common cause of CAH? | 1. increased ACTH secretion 2. 21-hydroxylase deficiency |
| Which adrenal cortex hormones are able to be produced in the following enzyme deficiencies: 1. 21-hydroxylase 2. 17-hydroxylase 3. 11-hydroxylase | 1. sex steroids 2. mineralocorticoids 3. sex steroids and a metabolite with mineralocorticoid activity |
| Which mineralocorticoid like metabolite is produced in 11-hydroxylase deficiency? | 11-deoxycorticosterone |
| Exacerbation of hypotension is children with N meningitidis infection | Waterhouse-Friderichsen syndrome - hemorrhagic necrosis of adrenal glands due to DIC from N meningitidis - leads to lack of cortisol |
| 1. What is the cause of Addison disease? 2. Embryologic origin of adrenal medulla | 1. progressive autoimmune destruction of the adrenal glands 2. neural crest |
| 1. Anosmia and hypogonadism 2. What is the defect? | 1. Kallmann syndrome 2. Failure of GnRH neurons to migrate from the olfactory placode to the hypothalamus; failure of olfactory bulb to form |
| 1. Embryologic origin of the majority of pineal gland tumors 2. Craniopharyngioma is derived from: | 1. germ cell (germinoma) 2. Rathke's pouch remnants |
| What are the symptoms of a prolactinoma and why are these symptoms seen? | 1. galactorrhea (overproduction of breast milk) 2. inhibition of ovulation and spermatogenesis by inhibiting GnRH |
| 1. usual cause of death from acromegaly 2. Best screening test for thyroid dysfunction | 1. cardiomyopathy 2. TSH |
| How does estrogen increase serum T4 but there is no thyrotoxicosis? | 1. estrogen ↑ thyroid binding globulin (TBG) 2. free T4 (FT4) binds TBG and the thyroid replaces FT4 3. total T4 (bound and free) is ↑ but FT4 remains normal |
| Extensive fibrosis of the thyroid gland presenting as a 'hard as wood'gland in young female. | Reidel fibrosing thyroiditis |
| Autoimmune thyroiditis that develops post partum | Subacute painless lymphocytic thyroiditis |
| 1. How does growth hormone excess lead to hyperglycemia? 2. Thyroid neoplasm associated with empty-appearing nuclei (Orphan Annie nuclei) | 1. GH increased gluconeogenesis 2. papillary adenocarcinoma |
| 1. How is toxic multinodular goiter differentiated from Grave's disease on physical exam? 2. Why is this distinction seen? | 1. lack exophthalmos and pretibial myxedema 2. while both have ↑ T4 therefore ↓ TSH, Grave's has autoantibody stimulation of fibroblast TSH receptors and inflammation |
| What are glucose and cholesterol levels in hypothyroidism | 1. hypoglycemia (decreased glycogenolysis) 2. hypercholesterolemia (decreased LDL receptor synthesis) |
| What is the cause of a nontoxic goiter? | ↓ thyroid hormone → ↑ TSH → hyperplasia/hypertrophy of gland |
| How does metabolic alkalosis effect free and total serum calcium and PTH? | due to few H+ ions, the COOH group of albumin is mostly COO- and binds more ionized Ca2+ 1. free, ionized calcium decreased 2. total serum calcium normal 3. PTH increased |
| How does liver cirrhosis effect free and total serum calcium and PTH? | liver cirrhosis leads to ↓ albumin production and less calcium binding 1. free, ionized calcium normal 2. total serum calcium decreased 3. PTH normal |
| What is DiGeorge's syndrome | failure of descent of 3rd/4th pharyngeal pouches leading to absent thymus and parathyroid |
| 1. cystic and hemorrhagic bone lesion seen with ↑ PTH 2. Why is metabolic acidosis seen with hyperparathyroidism? | 1. osteitis fibrosa cystica (caused by ↑ osteoclast activity) 2. decreased proximal tubule reclamation of bicarbonate |
| How does sarcoidosis lead to hypercalcemia? | macrophages in granulomas synthesize 1α-hydroxylase, causing hypervitaminosis D |
| How does respiratory/metabolic alkalosis lead to hypophosphatemia | 1. ↑ intracellular pH activates phosphofructokinase 3. ↑ phosphate uptake into cells to create ATP 2. ↑ Glycolysis leads to phosphate consumption as glucose phosphorylation increases |
| 1. Most common cause of hyperphosphatemia 2. What is the likely cause of ectopic Cushing syndrome? | 1. renal failure 2. ACTH production by a small cell carcinoma |
| 1. What disorder is the Metyrapone test used to diagnose? 2. What does it do? | 1. adrenal insufficiency (Addison's disease) 2. blocks cortisol synthesis by inhibitng 11β-hydroxylase thus stimulating ACTH secretion by pituitary |
| What is the cause of weight gain in Cushing syndrome? | 1. cortisol causes gluconeogenesis → hyperglycemia 2. insulin increases storage of fat in adipose |
| What is the cause of the following clinical findings in Cushing syndrome: 1. muscle weakness 2. purple abdominal striae 3. hirsutism | 1. gluconeogenesis leads to breakdown of type II (fast twitch) muscles 2. cortisol weakens collagen, causing blood vessel rupture and stretch marks 3.↑ DHEA and androstenedione |
| Patient with palpitations, sweats, anxiety and headache. | Pheochromocytoma (half have sustained or paroxysmal hypertension) |
| Most common tumor of the adrenal medulla 1. adults 2. children | 1. pheochromocytoma 2. neuroblastoma |
| What urine epinephrine metabolites are used to diagnose pheochromocytoma and neuroblastoma? | 1. vanillylmandelic acid (VMA) 2. homovanillic acid (HVA) |
| 1. Which type of diabetes is hereditary and manifests when patients are < 25? 2. What is the inheritance patter? | 1. Maturity onset diabetes of the young (MODY) 2. autosomal dominant |
| 1. How does obesity effect insulin resistance? 2. Why are triglyceride levels high in type 2 DM? 3. Why are triglyceride levels high in type 1 DM? | 1. increased adipose downregulates insulin receptor synthesis 2. hyperinsulinemia increases synthesis of VLDL 3. decreased insulin → ↓ action of lipoprotein lipase; fatty acids cannot be hydrolyzed off of VLDL |
| Pathogenesis for diabetic nodular glomerulosclerosis | 1. hyaline arteriosclerosis of efferent arterioles ↑ GFR 2. leads to hyperfiltration damage to mesangium 3. ↑ deposition of type IV collagen |
| Mechanism for gestational diabetes | most likely human placental lactogen (HPL), cortisol and progesterone have anti-insulin effects |
| 1. Do newborns of mothers with gestational diabetes experience hypoglycemia or hyperglycemia? 2. How does respiratory distress syndrome occur following gestational diabetes? | 1. hypoglycemia; high levels of insulin at birth drives glucose into hypoglycemic range 2. insulin inhibits fetal surfactant production |
| How does diabetic ketoacidosis (DKA) lead to hyperkalemia? | 1. DKA is an increase in ketone bodies and lactic acid leading to metabolic acidosis 2. the body ↑ H+ uptake in exchange for K+ in attempt to raise pH 3. leads to hyperkalemia |
| For the clinical diagnosis of hypoglycemia, what triad of findings must be present? | Whipple triad: 1. symptoms consistent with hypoglycemia 2. low plasma glucose concentration (<50mg/dL) 3. relief of symptoms after plasma glucose is normalized |
| What is postprandial (reactive) hypoglycemia? | (postprandial means after a meal) exaggerated insulin secretion after a meal leading to transient hypoglycemia |
| What is required for a diagnosis of metabolic syndrome? | Three of the following: 1. ↑ waist circumference 2. ↑ triglycerides 3. ↑ LDL 4. ↑ blood pressure 5. ↑ fasting glucose |
| What is the cause of hypotension seen in patients with Addison's disease? | 1. ↓ cortisol → ↓ α1 receptors in vasculature 2. ↓ aldosterone → hypovolemia |
| Which type of acidosis is associated with hypoaldosteronism (Addison's disease)? | Type IV renal tubular acidosis - ↓ aldosterone → ↑ K+ → inhibits NH3 secretion - NH3 combined with the H+ that is also not secreted (from ↓ aldosterone) - NH4+ accumulates → metabolic acidosis |
| What would glucose levels be expected to be in Congenital Adrenal Hyperplasia? | ↓ cortisol → ↓ in gluconeogenesis and hypoglycemia |
| Cause for pathology in diabetes type 2 1. resistance of peripheral tissues to the action of insulin 2. peripheral neuropathy 3. cataracts | 1. high free fatty acids 2. uptake of glucose by Schwann cells, conversion to sorbitol and osmotic injury 3. same as neuropathy but uptake of glucose by lens of eye |
| 1. Most common cause of hypocalcemia? 2. Tetany with normal calcium level | 1. hypoalbuminemia (cirrhosis, nephrosis, burns) 2. metabolic alkalosis or ↑ albumin |
| 1. Which diuretic drug can cause hypercalcemia? 2. Which hypertensive drug can cause hypocalcemia? | 1. thiazide 2. furosemide |
| What are some causes of hyperprolactinemia? | 1. oral contraceptives 2. prolactinoma 3. hypothyroidism 4. breast feeding (suckling stimulus) 5. severing hypothalamic-hypophysial tract from injury (loss of dopamine connection) |
| How does Cushing's disease lead to hypertension? | 1. ↑ ACTH → ↑cortisol and aldosterone 2. ↑ cortisol → ↑α1 adrenergic receptors in vasculature 3. ↑ aldosterone → Na and water retention |
| What is the effect of a dexamethasone suppression test on cortisol (low dose/high dose): 1. ACTH-producing pituitary adenoma 2. Ectopic ACTH-producing tumor 3. Adrenal adenoma | (low/high) 1. no change/↓ cortisol 2. no change/no change 3. no change/no change |
| Why are sodium levels normal with hyperaldosteronism? | 1. initially ↑ aldosterone leads to Na retention followed by ↑ osmolality 2. ADH release and water reabsorption to compensate 3. osmolality back to normal |
| Treatment for pheochromocytoma | phenoxybenzamine, a nonselective α-blocker, followed by surgery to remove tumor |
| Which antibodies are present in Hashimoto's thyroiditis? | antimirosomal and antithyroglobulin |
| Thyroid neoplasms: 1. proliferation of follicles surrounded by fibrous capsule 2. ↑ risk with childhood irradiation 3. proliferation of follicles with invasion through capsule 4. proliferation of parafollicular cells | 1. follicular adenoma 2. papillary carcinoma 3. follicular carcinoma 4. medullary carcinoma (secrete calcitonin) |
| Thyroid neoplasms: 1. seen in elderly 2. amyloid tumor marker 3. associated with Hashimoto's thyroiditis 4. psamomma bodies | 1. anaplastic carcinoma 2. medullary carcinoma 3. Lymphoma 4. papillary carcinoma |
| 1. Primary hyperparathyroidism 2. Secondary hyperparathyroidism | 1. parathyroid gland adenoma 2. ↓ Ca2+ → ↑PTH (most often from chronic renal disease → ↓ vitamin D activation) |
| Characteristics of MEN 1 | 3P's 1. Parathyroid tumor 2. Pancreatic tumor (gastrin) 3. Pituitary adenoma |
| Characteristics of MEN 2A | MPM 1. Medullary carcinoma of thyroid 2. Pheochromocytoma 3. Parathyroid tumor |
| Characteristics of MEN 2B | MPM 1. Medullary carcinoma of thyroid 2. Pheochromocytoma 3. Marfanoid habitus/Mucosal neuromas |
| Cardiovascular drug associated with hypothyroidism | Amiodarone |
| How does SIADH effect sodium levels? | ↑ ADH → hypervolemia → ↓ aldosterone and hyponatremia |
| How does ethanol lead to hypoglycemia? | inhibition of gluconeogenesis during fasting |
| How do the following effect glucose levels: 1. Cortisol 2. Growth hormone 3. T4 | 1. ↑ gluconeogenesis 2. ↑ gluconeogenesis 3. ↑ glycogenolysis |
Created by:
amichael87
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