Step 1 - Endocrine 2

denniskwinn's version from 2015-04-25 16:00



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Hypothyroidism signs/symptomsCold intolerance (⇣ heat production), Weight gain, ⇣ appetite, Hypoactivity, lethargy, fatigue, weakness, Constipation, ⇣ reflexes, Myxedema (facial/periorbital), Dry, cool skin; coarse, brittle hair
Hypothyroid lab findings⇡TSH, ⇣Total T4, ⇣free T4,⇣T3 uptake
Hyperthyroid sxHeat intolerance ( heal production), Weight loss, ⇡ appetite, Hyperactivity, Diarrhea, ⇡ reflexes, Chest pain, palpitations, arrhythmias, Warn, moist skin; fine hair
Hyperthyroid lab findings⇣TSH (if primary), ⇡ Total T4, ⇡Free T4, ⇡T3 uptake
Acute thyroiditisBact infection→fever, pain, cervical adenopathy, initial↑T4,↓TSH,↓I123 uptake - tx: Penicillin
(Pumping what it has out)
HashimotosAutoimmune hypothyroidism - can have hyperthyroid early when follicles rupture - slow course - antimicrosomal and anti-thyroglobulin antibodies. Assoc w/DR5 and hurthle cell in histology ..
↑ incidence in Turners, Down and Klinefelters
Goiter formation(3)Incre Thyroid stim:
1) Graves(AB)
2)Abnorm Pituatary(incre TSH)
3) Hashimoto's(Primary dysfunc)


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CretinismSevere fetal hypothyroidism
-endemic where endemic goiter happens.
Sporadic cretinism caused by defect in T4 formation or developmental failure in thyroid formation
Cretinism findingspot-bellied, pale, puffy faced child with protruding umbilicus and protuberant tongue
Subacute thyroiditisDe quervains
- self limited hypothyroid often following a flu-like illness/URI
- ⇡ESR, jaw pain, early inflammation and very tender thyroid
- granulomatous inflammation
- no lymphadenopathy
Riedel’sThyroid replaced by fibrous tissue (hypothyroid)
- presents w/fixed, hard(rock like) and painless goiter
- can produce tracheal obstruction
- treat with corticosteroids
GravesAutoimmune hyperthyroid
-TSH receptor antibodies
- is a type II hypersensitivity reaction
Graves sxProptosis, EOM swelling, pretibial myxedma, diffuse goiter, often presents during stress
Graves complication(thyroid storm)stress induced catecholamine surge leading to death by arrhythmia - also in other hyperthyroid
Graves TxBeta blocker, thionamides, Ablative I123 if refractive
Toxic multinodular goiterFocal patches of hyperfunctioning folliclular cells independent of TSH due to mutation in TSH receptor
- nodules are not malignant -


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Jod-Basedow phenomenonThyrotoxicosis if a pt w/iodine deficiency goiter is given iodine
Thyroid cancer (5)1)Papillary
4) Undifferentied/Anaplastic
5) Lymphoma
Thyroid Papillary carcinomaMC, excellent prognosis
-"ground-glass" nuclei (Orphan Annie), -psammoma bodies, nuclear grooves.
- ⇡ risk with childhood irradiation.
Thyroid Follicular carcinoma-Good prognosis, uniform follicles.
Thyroid Medullary carcinoma-From parafollicular "C cells"; produces calcitonin -Sheets of cells in amyloid stroma
. Associated with MEN types 2A and 2B.
Thyroid Undifferentiated/anaplastic-Older patients; very poor prognosis.
Thyroid Lymphoma-A/w Hashimoto's thvroiditis
Hypercalcemia causesCalcium ingestion. Hyperparathyroid, Hyperthyroid, Iatrogenic (thiazides), Multiple myeloma, Paget’s disease, Addison’s disease, Neoplasms, Z-E syndrome, Excess vitamin d, Excess vitamin a, Sarcoidosis (CHIMPANZEES)
Primary HyperParathyroidismusually and adenoma
Primary hyperparathyroidism sx⇡PTH, ⇡Alkaline phosphatase, ⇡cAMP in urine - stones, bones, groans
Secondary hyperparathyroidism-Due to low gut calcium absorption and high phosphorus ( most often in CRD)
CRD= hypocalcemia, hyperphosphatemia, high alkaline phosphatase, high PTH


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Osteitis fibrosa cystica (von Recklinghausen's syndrome)Cystic bone spaces filled with brown fibrous tissue (bone pain).
Renal osteodystrophy-Bone lesions due to 2° hyperparathyroidism due in turn to renal disease.
Hypoparathyroidism causesDue to surgical excision, autoimmune destruction, or digeorge syndrome
Hypoparathyroidism findings-Hypocalcemia, tetany
Chvostek’s sign
Trousseau’s sign
HypomagnesiaSecondary cause of hypoparathyroidism - caused by diarrhea, aminoglycosides, diuretics, alcoholism
PseudohyperparathyroidismAlbright’s hereditary osteodystrophy
-AD kidney unresponsive to PTH
- hypocalcemia
-shortened 4th/5th digits
-short stature
Most common Pituitary adenomaprolactinoma,
Prolactinoma findingsamenorrhea, galactorrhea, low libido, infertility, Can impinge on optic chiasm causing bitemporal hemianopia
Prolactinoma tx Bromocriptine or cabergoline (dopamine agonists) causes shrinkage(in 50% of patients, but FIXES sexual dysfunction in 70%).


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Acromegalyexcess GH in adults
Acromegaly findingsLarge tongue with, deep furrows, deep voice, large hands and feet, coarse facial features, impaired glucose tolerance (insulin resistance)
Gigantismexcess GH in children
Excess GH treatmentpituitary adenoma resection followed by octreotide administration
Normal times for increased GHstress, exercise and hypoglycemia
Excess GH diagnosis⇡ serum IGF-1, failure to suppress serum GH following oral glucose tolerance test
Sheehan’s syndromePostpartum hypopituitarism - enlargement of anterior pituitary (⇡ lactotrophs) during pregnancy without corresponding ⇡ blood supply leads to ⇡ risk of infarction of the pituitary gland following severe bleeding and hypoperfusion during delivery. May cause fatigue, anorexia, poor lactation and loss of pubic and axillary hair.
Diabetes insipidusintense thirst and polyuria with inability to concentrate urine (lack of ADH = central, lack of response to ADH=nephrogenic)
Diabetes insipidus diagnosiswater deprivation test - urine osmolality doesn’t ⇡. Response to desmopression distinguishes b/w central and nephrogenic -if there is a response then its central
Diabetes insipidus findingsurine specific gravity <1.006, serum osmoalilty >290mOsm/L
Diabetes insipidus treatmentadequate fluid intake, for central DI - intranasal desmopressin - for nephrogenic DI - HCTZ, Indomethacin, amiloride


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SIADH sxExcessive water retention, hyponatremia, urine osmolarity> serum osmolarity - very low serum sodium can lead to seizure (correct slowly)
SIADH txDemeclocycline or water restriction
SIADH causes1)Ectopic ADH (small cell lung cancer)
2) CNS disorders/head trauma
3) Drug (cyclophosphamide)
DM acute manifestations1)Polydipsia, polyuria, polyphagia, weight loss
2)DKA (type I), hyperosmolar coma (type 2)
3)Unopposed secretion of GH and epinephrine (exacerbating hyperglycemia).
Insulin induced hypoglycemiaSweat, tachycardia, palpitations, tremulous, nausea, hunger, focal neuro deficits -tx with glucagon IV and glucose
DM chronic manifestations (2)Nonenzymatic glycosylation:
1. Small vessel disease (diffuse thickening of BM)⇢ retinopathy (hemorrhage, exudates, microaneurysms, vessel proliferation), glaucoma, nephropathy (nodular sclerosis, progressive proteinuria, chronic renal failure, arteriosclerosis⇢HTN, Kimmelstiel-Wilson nodules
2. Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease and gangrene, cerebrovascular disease. . Osmotic damage: 1. Neuropathy, Cataracts
DM testsFasting serum glucose, glucose tolerance test, HbA1c (measures long-term diabetic control)
Dm1 primary defectViral or immune destruction of beta cells
Dm2 primary defectincreased insulin resistance


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Aldose reductaseConverts glucose into sorbitol which leads to osmotic damage
Metabolic syndromeInsulin resistance, high TAG, HTN, CAD, obesity, low HDL, Fasting gluc>110
Metabolic syndrome treatmentstatins, ACEI, diuretics, treat insulin resistance w/pharm and weight loss
Dm1 HLA assocDR3 and DR4
Diabetic ketoacidosis sxKussmaul respirations ( rapid/deep breathing) nausea/vomiting, abdominal pain, psychosis/delerium, dehydration, fruity breath odor (due to exhaled acetone)
Diabetic ketoacidosisDMI complication, usually due to stress causing increased insulin requirement - increased liploysis increasing ketone bodies in blood
Diabetic ketoacidosis labsHyperglycemia, High H+, Low bicarb(Anion gap metabolic acidosis), high blood ketone, leukocytosis, Hyperkalemia(relatively, but overall losing potassium)
Diabetic ketoacidosis complications-Life-threatening mucormycosis, Rhizopus infection(fungal infection)
-Cerebral edema, cardiac arrhythmias, heart failure
Diabetic ketoacidosis TxFluids, insulin and K+ (to replete intracellular stores) glucose if necessary to prevent hypoglycemia


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CarcinoidNeuroendocrine cell tumors - from neuroendocrine cells of GI tract - especially metastatic, small bowel tumors, which secrete high levels of serotonin (5-HT)
- most common tumor in appendix
Carcinoid sxResults in recurrent diarrhe, cutaneous flushing, asthamatic wheezing and right sided valvular disease. ⇡ 5-HIAA in urine
Carcinoid rule of thirds1/3 metastasize, 1/3 present with 2nd malignancy, 1/3 multiple


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Zollinger-Ellison syndromeGastrin-secreting tumor of pancreas or duodenum. Causes recurrent ulcers. May be associated with MEN 1
MEN I (Wermer’s syndrome)1)Parathyroid tumors
2)Pituitary tumors (prolactin or GH)
3)Pancreatic endocrine tumors (ZE, insulinoma, VIPomas, glucagonoma(rare) - 3 P’s - autosomal dominant
MEN I presentationcommonly with kidney stones and stomach ulcers
MEN 2A (Sipple’s syndrome)1)Medullary thyroid carcinoma (secretes calcitonin)
3)PTH tumors
- 2 P/ M - autosomal dominant - ret gene
MEN 2B1)Medullary thyroid carcinoma (secretes calcitonin)
3) Oral/Intestinal ganglioneuromatosis aka mucosa neuroma (a/w marfanoid habitus)
- autosomal dominant - assoc w ret gene


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Hypoglycemia diagnosisprolonged fast - must satisfy whipple's triad - sx occur, hypoglycemia demonstrated, sx relieved by glucose
Hypoglycemia sxadrenergic sx, dizziness, confusion, headache, inability to concentrate
Hypoglycemia causes1)MC=excess insulin, also alcohol, renal failure, malnutrition, kidney disease.
2)Congenital include:
- Maple syrup urine disease
-Carnitine deficiency(can't use certain fats for energy if needed)
Tx strategy for DM Ilow sugar diet, insulin replacement
Tx strategy for DM IIdietary modification and exercise for weight loss, oral hypoglycemia and insulin replacement
Fast acting insulinsLispro, Aspart
Intermediating acting insulinsNPH
Long acting insulinsGlargine, Detemir
Insulin actionsBind insulin receptor - increase glucose stored as glycogen in liver, increased glycogen in muscle and increase protein synth. In fat, aid in TG storage
Insulin clinical useDMI, DM II - also life threatening hyperkalemia and stress-induced hyperglycemia
Insulin toxicityHypoglycemia, hypersensitivity rxn (very rare)


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SulfonylureasGlyburide, Glimepiride, Glipizide
Sulfonylureas actionClose K+ channel in beta cell membrane triggering insulin release via Ca++ influx
Sulfonylureas clincal usestimulate release of endogenous insulin in DM2. Require some islet function so useless in DM I
Sulfonylurea toxicitieshypoglycemia
Biguanides actionunknown mechanism - possibly ⇣ gluconeogenesis, ⇡ glycolysis, ⇣serum glucose levels. Overall acts as insulin sensitizer.
Biguanide clinical useused as oral hypoglycemic - can be used in patients w/out islet function
Biguanide toxicitiesMost grave adverse effect is lactic acidosis (contraindicated in renal failure)
TZDs(Thiazolidinediones)pioglitasone, rosiglitazone
TZD actionincrease insulin sensitivity in peripheral tissue
TZD indicationsmonotherapy in DM2 or combined therapy
TZD toxicitiesweight gain, edema, hepatotoxicity, CV toxicity


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A-glucosidase inhibitorsacarbose - not really used
Alpha glucosidase inhibitor mechanismDelayed glucose absorption
Alpha glucosidase toxicitiesGI disturbances
Mimetics mechanismDecrease glucagon
Mimetics indicationsDM 2
Mimetics toxicitieshypoglycemia, nausea, diarrhea
GLP-1 mimeticsExenatide
GLP-1 mimetic mechanismIncrease insulin, decrease glucagon release
GLP-1 indicationDM 2
GLP-1 toxicitiesNausea, vomiting, pancreatitis


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Orlistat mechanismAlters fat metabolism by inhibiting pancreatic lipases
Orlistat clinical uselong-term obesitymanagement (in conjunction with modified diet)
Orlistat toxicitiessteatorrhea, GI discomfort, reduced absorption of fat-soluble vitamins, headache
Sibutramine mechanismSympathomimetic serotonin and norepinephrine reuptake inhibitor
Sibutramine clinical useshort-term and long-term obesity management
Sibutramine toxicityHTN and tachycardia
Propylthiouracil, methimazole mechanismInhibit organification of iodide and coupling of thyroid hormone synthesis
Propylthiouracil, methimazole clincal usehyperthyroidism
Propylthiouracil, methimazole Toxicityskin rash, agranulcytosis(rare) aplastic anemia


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Levothyroxine, triiodothyronine mechanismThyroxine replacement
Levothyroxine, triiodothyronine clinical useHypothyroidism, myxedema
Levothyroxine, triiodothyronine toxicitytachycardia, heat intolerance, tremors, arrhythmias
GH clinical indicationsGH deficiency, Turner’s syndrome
Somatostatin (ocreotide) indications-Acromegaly
-Carcinoid, gastrinoma, glucagonoma
1)Inhibits GH and TSH
Oxytocin indicationsstimulates labor, uterine contractinos, milk let-down, controls uterine hemorrhage
ADH (desmopressin) indicationsPituitary (central) DI


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Demeclocycline mechanismADH antagonist (member of the tetracycline family)
Demeclocycline clinical useSIADH
Demeclocycline toxicitiesNephrogenic DI, photosensitivity, abnormalities of bone and teeth
GlucocorticoidsHydrocortisone, prednisone, triameinolone, dexamethasone, beclomethasone
Glucocorticoids mechanismdecrease production of leukotrienes and prostaglandin by inhibitingphospholipase A2 and COX-2 expression
Glucocorticoid clinical useAddison’s, inflammation, immune suppression, asthma
Glucocorticoid toxicityIatrogenic cushing’s, OSTEOPOROSIS