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126 Cards in this Set
- Front
- Back
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Location of cortisol synthesis
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adrenal zona fasciculata
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cortisol function
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BBIIG
1. blood pressure- maintains blood pressure, via upregulation of alpha1 receptors on arterioles, allowing epi to have better effect 2. bone- decreased bone formation 3. anti-Inflammatory 4. decreased immune function 5. increased gluconeogenesis, lipolysis, proteolysis |
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regulation of cortisol
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CRH from hypothalamus stimulates ACTH production from anterior pituitary
cortisol has negative feedback on hypothalamus and pituitary (decreased CRH and ACTH) |
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causes of Cushing's syndrome
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1. iatrogenic- steroids
2. cushing's disease- ACTH secretion from pituitary adenoma 3. ectopic ACTH- other tumor makes ACTH (small cell lung, bronchial carcinoids) 4. adrenal tumor- adenoma, carcinoma, or nodular hyperplasia |
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clinical presentation of Cushing's
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moon face
buffalo hump HTN weight gain truncal obesity hyperglycemia insulin resistance striae skin thinning osteoporosis amenorrhea immune suppression |
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results of dexamethasone suppression test in normal person
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decreased cortisol
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results of dexamethasone suppression test in Cushing's disease
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increased cortisol after low dose, decreased cortisol after high dose
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results of dexamethason suppression test in ectopic ACTH syndrome
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increased cortisol after low and high dose
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resutls of dexamethasone suppression test in cortisol producing tumor
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increased cortisol after low and high dose
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What is Addison's disease
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primary adrenal insufficiency- via atrophy or destruction
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causes of primary adrenal insufficiency
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addison's
TB metastasis |
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clinical presentation of primary adrenal insufficiency
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hypotension (decreased aldosterone)
hyperkalemia acidosis hyperpigmentation (increased MSH from POMC) |
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what is secondary adrenal insufficiency
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decreased pituitary ACTH
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clinical presentation of secondary adrenal insufficiency
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hyponatremia from increased ADH
normal aldo- no hyperkalemia no hyperpigmentation |
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Waterhouse-Friderichsen syndrome
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acute primary adrenal insufficiency due to adrenal hemorrhage- associated with N. meningitidis septicemia, DIC and septic shock
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signs and symptoms of hypothyroidism
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cold intolerance
weight gain lethargy, fatigue, weakness constipation hyporeflexia myxedema (facial, periorbital) dry, cool skin coarse brittle hair bradycardia dyspnea on exertion |
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signs and symptoms of hyperthyroidism
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heat intolerance
weight loss hyperactivity diarrhea hyperreflexia pretibial myxedema warm moist skin fine hair chest pain, palpitations, arrhythmias |
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lab findings in hypothyroidism
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↑ TSH
↓ total T4 ↓ free T4 ↓ T3 uptake |
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lab findings in hyperthyroidism
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↓ TSH
↑ total T4 ↑ free T4 ↑ T3 uptake 3 |
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most common cause of hypothyroidism
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Hashimoto's thyroiditis
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Hashimoto's associated with ...
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HLA-DR5
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antibodies in Hashimoto's
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antimicrosomal
antithryoglobulin |
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early Hashimoto's
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may by hyperthyroid briefly during thyrotoxicosis, follicle rupture
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notable Hashimoto's histology
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Hurthle cells, lymphocytic infiltrate, germinal centers
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cause of cretinism
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severe fetal hypothyroidism- generally from iodine deficiency
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clinical presentation of cretinism
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pot bellied, puffy faced, protruding umbilicus, protuberant tongue, mentally retarded
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sporadic cretinism
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defect in T4 formation or from failure of thyroid to develop
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subacute thyroiditis (de Quervain's)
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self-limited hypothyroidism after flu-like illness
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clinical presentation in subacute thyroiditis
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↑ ESR
jaw pain tender thyroid early inflammation |
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notable histology features of subacute thyroiditis
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granulomatous inflammation
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riedel's thyroiditis
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thyroid replaced by fibrous tissue
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clinical findings in riedel's thyroiditis
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fixed, hard, painless goiter
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Grave's disease
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autoimmune hyperthyroidism with TSAb
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clinical features of Grave's disesase
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opthalmopathy (proptosis, EOM swelling)
pretibial myxedema diffuse goiter |
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hypersensitivity reaction of Grave's disease
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type II
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toxic multinodular goiter
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focal patches of hyperfunctioning follicular cells working independently of TSH due to TSH R mutation
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lab findings in toxic multinodular goiter
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↑ T3, T4
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Jod Basedow phenomenon
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thyrotoxicosis that occurs after repleting iodine stores post-deficiency
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most common thyroid cancer
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papillary carcinoma
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papillary thyroid carcinoma
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most common, good prognosis, ground glass nuclei, psammoma bodies, nuclear grooves, Orphan Annie eye, increased risk with childhood radiation
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follicular thyroid carcinoma
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good prognosis, uniform follicles
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medullary thyroid carcinoma
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tumor of C cells that make calcitonin, sheets of tumor cells in stroma
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medullary thyroid carcinoma associated with...
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MEN2A, MEN2B
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anaplastic thyroid carcinoma
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older patients, very poor prognosis
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Hashimoto's thyroiditis is associated with future disease...
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B cell lymphoma
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most common pituitary adenoma
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prolactinoma
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clinical findings in pituitary adenoma
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amenorrhea, galactorrhea, low libido, infertility (decreased GnRH), bitemporal hemianopsia (impingement on optic chiasm)
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clinical presentation of DI
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polydipsia
polyuria dillute urine |
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lab findings in DI
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plasma osm > 290
urine specific gravity <1.006 |
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central DI causes
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pituitary tumor, trauma, surgery, histiocytosis X
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nephrogenic DI causes
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hereditary
secondary to hypercalcemia lithium demeclocycline (ADH antagonist) |
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diagnosis of DI
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water deprivation- no increase in urine osm
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treatment of central DI
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adequate fluid intake
desmopressin |
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treatment of nephrogenic DI
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adequate fluid intake
HCTZ indomethacin amiloride |
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clinical presentation of SIADH
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hyponatremia
high urine osm (>serum osm) water retention |
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causes of SIADH
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1. ectopic secretion- small cell lung cancer
2. CNS disorders, trauma 3. pulmonary disease 4. drugs- cyclophosphamide |
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body response to SIADH
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decreased aldosterone, exacerbates hyponatremia
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treatment of SIADH
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demeclocycline and water restriction
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Signal for beta cell to secrete insulin...
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ATP from glucose metabolism closes the K channel
this depolarizes the cell which opens Ca channels Ca facilitates insulin exocytosis |
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C peptide
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released with endogenous insulin secretion (proinsulin = insulin + C peptide)
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insulin effects
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1. ↑ glucose transport
2. ↑ glycogen synthesis 3. ↓ gluconeogenesis 4. ↑ TG synthesis 5. ↑ Na retention (kidney) 6. ↑ protein synthesis (muscle) 7. ↑ K uptake in cells |
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Cells that don't require insulin
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Brain
RBC Intestine Cornea Kidney Liver (BRICKL) |
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location of GLUT-1
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RBC
Brain |
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GLUT-2 location
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kidney
liver pancreatic beta islet cells small intestine |
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GLUT 4 location
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muscle adipose
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PTH source
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chief cells of parathyroid
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PTH actions
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1. ↑ bone resorption- direct osteoblast stimulation, indirect osteoclast stimulation
2. ↑ Ca reabsorption in kidney 3. ↓ PO4 reabsorption in kidney 4. ↑ 1,25 (OH)2 Vitamin D production by stimulating kidney's 1a-hydroxylase |
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regulation of PTH
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↓ serum calcium increases PTH
increased serum Mg increases PTH |
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Vitamin D2 source
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plant ingestion
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Vitamin D pathway
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D3 and D2 converted to 25 OH vitamin D in liver
then to 1,25 (OH)2 vitamin D in kidney (this is active) |
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vitamin D function
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1. increased intestinal Ca and PO4 absorption
2. increased bone resorption of Ca and PO4 |
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regulation of vitamin D
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increased production- PTH, decreased Ca, decreased phosphate
decreased production- feedback inhibition |
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calcitonin source
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parafollicular/C cells of thyroid
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function of calcitonin
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↓ bone resorption of Ca
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regulation of calcitonin
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↑ Ca causes ↑ calcitonin
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T3/T4 function
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4xB = brain, bone, BMR, beta receptors
1. bone growth 2. CNS maturation 3. ↑ beta receptors in heart - causes ↑ CO, HR, SV, contractility 4. ↑ BMR via ↑ Na/K activity (↑ body temp, O2 consumption) 5. ↑ glycogenolysis, gluconeogenesis, lipolysis |
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thyroid hormone regulation
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TRH from hypothalamus stimulates pituitary
TSH from pituitary stimulates follicular cells T3 is negative feedback to pituitary |
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causes increased TBG
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estrogen (OCP, pregnancy)
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causes decreased TBG
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liver failure
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symptoms of hyperparathyroidism
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1. stones- kidney stones
2. bones- bone cysts 3. groans- constipation 4. psych overtones- depression, weakness |
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primary hyperparathyroidism cause
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usually adenoma
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labs for primary hyperparathyroidism
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1. ↑ serum Ca
2. ↑ urine calcium 3. ↑ AP 4. ↓ serum phosphate 5. ↑ urine cAMP 6. ↑ PTH |
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secondary hyperparathyroidism cause
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hyperplasia due to decreased dietary Ca and increased phosphorous, often in CRF
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labs for secondary hyperparathyroidism
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1. ↓ serum Ca
2. ↑ serum phosphate 3. ↑ AP 4. ↑ PTH |
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tertiary hyperparathyroidism
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from chronic renal disease
really high PTH high Ca |
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causes of hypoparathyroidism
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excision during thyroid surgery
autoimmune destruction DiGeorge syndrome |
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clinical findings in hypoparathyroidism
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hypocalcemia
tetany Chvostek's sign Trousseau's sign |
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pseudohypoparathyroidism
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autosomal dominant kidney unresponsiveness to PTH
hypocalcemia short stature short 4th, 5th digit |
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acromegaly
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excess GH in adults
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acromegaly findings
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large tongue with deep furrows
deep voice large hands large feet coarse facial features impaired glucose tolerance |
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diagnosis of acromegaly
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increased IGF-1 and failure to suppress GH following oral GTT
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acute manifestations of DM
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polyuria
polydipsia weight loss DKA in type 1 hyperosmolar coma in type 2 |
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DM retinopathy
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hemorrhage
exudates microaneurysms vessel proliferation |
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DM nephropathy
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nodular sclerosis
progressive proteinuria CRF atherosclerosis leading to HTN |
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DM CVD
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large vessel atherosclerosis, CAD, peripheral vascular occlusive disease, gangrene
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DMT1 gene association
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HLA DR3, 4
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signs and symptoms of DKA
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Kussmaul respirations
n/v abdominal pain psychosis/delirium dehydration fruity breath |
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labs in DKA
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↑ urine ketones
hyperkalemia hyperglycemia ↑ H, ↓ HCO3 - anion gap met ac ↑ blood ketone leukocytosis |
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DKA complications
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mucormycosis
rhizopus infection cerebral edema cardiac arrhythmias HF |
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treatment of DKA
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fluid
insulin K (replete intracellular stores) perhaps glucose to prevent hypoglycemia |
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MEN 1
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3xP
parathyroid tumor pituitary tumor (prl or GH) pancreatic endocrine tumor (ZE syndrome, insulinoma, VIPoma, glucagonoma) often have kidey stones and stomach ulcers on presentation |
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MEN2A
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medullary thyroid carcinoma (secretes calcitonin)
pheochromocytoma parathyrroid tumor |
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MEN2B
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medullary thyroid carcinoma
pheochromocytoma oral/intestinal gnaglioneuromatosis |
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MEN inheritance
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autosomal dominant
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gene associated with MEN2A, 2B
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ret gene
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rapid acting insulins
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normal
lispro aspart |
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long acting insulins
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detemir
glargine |
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intermediate acting insulins
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NPH
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insulin therapy adverse effects
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weight gain
hypoglycemia |
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first generation sulfonylurea
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chlorpropramide
tolbutamide |
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second generation sulfonylurea
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glyburide
glimepiride glipizide |
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sulfonylurea mechanism of action
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close ATP dependent K channel in beta cells, which depolarizes the cell, causing Ca channel to open and then Ca causes insulin release
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sulfonylurea adverse effects
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hypoglycemia for second generation
disulfuram like effects for first generation |
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biguanides
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metformin
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metformin mechanism of action
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decrease gluconeogenesis
increase glycolysis increase peripheral glucose uptake (IS) |
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bad side effect of metformin
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lactic acidosis (beware in renal and liver disease)
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thiazolidiendiones
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rosiglitazone
pioglitazone |
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thiazolidinedione mechanism of action
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increase insulin sensitivity
via PPARy |
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thiazolidinedione adverse effects
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weight gain
edema hepatotoxicity CV toxicity |
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a-glucosidase inhibitors
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acarbose
miglitol |
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a-glucosidase inhibitor mechanism of action
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inhibit intestinal brush border a-glucosidase, prevents disaccharide breakdown, decreased post prandial hyperglycemia
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a-glucosidase inhibitor adverse effects
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GI disturbances
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incretin mimetics
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pramlintide
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GLP-1 analogs
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exenatide
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pramlintide mechanism of action
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decrease glucagon
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exenatide mechanism of action
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increase insulin
decrease glucagon |
