10 Endocrine

q123456's version from 2016-06-01 17:21


Question Answer
temporal arteritisgranulomatous inflammation of media

headache, difficulty chewing, facial pain, vision deterioration/blindness, High ESR, multinuclear giant cells in arterial biopsy, prednisone therapy

a 64 year old caucasian female presents to your office with headache followed by sudden onset of blindness in her right eye. she was recently admitted to the hospital for fever, pelvic and shoulder girdle pain and weight loss
High eosinophil, wrist drop(mononeuropathy), adult onset asthma, p-ANCAChurg-Strauss vasculitis
polyarteritis nodosa(PAN)
systemic necrotizing vasculitis
fever, weight loss, myalgias, abdominal pain
segmental, transmural, necrotizing inflammation of arteries
what of arteries will be spared by polyarteritis nodosa? pulmonary
hepatitis B infection
buergersegmental thrombosing vasculitis
***berger: IgA
Wegener's, C-ANCANASAL mucosal ulceration+glomerulonephritis


Question Answer
bacterial endocarditisvalvular damage

S aureus-acute
S sanguis (viridans): subacute
S bovis in colon cancer
S epidermidis on prosthetic valves
Intercalated discgap junctions
action potentials to spread between cardiac cells KA8-45
atherosclerosisendothelial cell damage>>>macrophage infiltrate the intima and platelet adhere to damaged endothelium>>>PDGF release>>>hyperplasia of SM cells, SM cells migrate to the intima>>>foam cells, ECM collegen elastin

macrophages in the intima
secret metalloproteinases>>>degrade collagen>>>reduce plaque stability

atherosclerosis involves intestnal arteries>>>intestinal hypoperfusion>>>Epigastric pain after meal+no abnormalities in GI
fibrous plaqueSMCs, foam cells, inflammatory cells and ECM
the vascular reaction to endothelial and intimal injury isintimal hyperplasia and fibrosis
injured endothelial cells releasePDGF>>>SMC migration and proliferation
180/70mmHg in old peopleisolated systolic hypertension, SBP>160, DBP<90, Aortic stiffening
increased AST without accompanying elevation of ALTmyocardial infarction KA26/17
graft vascular diseasegraft arteriosclerosis, intimal thickening of coronary arteries due to proliferation of fibroblasts and myocytes KA32-11

adrenal KA32-6

Question Answer
PheochromocytomaEpisodic hypertension, sudden onset headache, heart palpitations, diaphoretic
benign tumor
usually seen in adults
malignant tumor in children.
adrenal medulla or any other side,
not present as episodic hypertension

***both have hypersecretion of cathecolamines.
progesterone>>>11-deoxycorticosterone21 hydroxylase
17a hydroxylase
13 year old girl, 152/91, lack of 2rd sexual characteristics, a blind vigina, hypokalemia, low testosterone and estradiol, 46 xy
Metyrapone testing: reversibly inhibiting steroid 11β-hydroxylase>>>block cortisol synthesis>>>stimulates ACTH>>>Stimulates adrenal glands to produces hormones
hyperaldosteronismhypertension+low renin+hypoK+
low K+, high HCO3-, Metabolic alkalosis Na+ normal not very high
treatment:aldosterone antagonist>>>eplerenone/spironolactone
eplerenone/spironolactone Side effects: gynecomastia

conn's syndrome: adosterone secreting adrenal adenomas>>>excess K+secretion, Na+retention>>>hypertesnion, metabolic alkalosis, muscle weakness and paresthesias
acute adrenal insufficiencywaterhouse friderichsen syndrome
Adrenal hemorrhage: Meningococcal meningitis/low Na+/high K+
addison diseasechronic adrenal insufficiency


patients with advanced metastatic aquamous cell lung cancer feels weak, fatigues and diarrhea/constipation, hyperpigmentation of the skin

the most common cause of adrenal insufficiency: glucocorticoid therapy>>>depression of hypothalamus-pituitary-adrenal axis. e.g. SLE patients treat with prednisone: hypotension>>>nausea, abdominal pain and dizziness after infection or sugery (under stressful situations)

type I diabetes, hyperpigmentaion,hypotension/hyponatremia/hyperkalemia/Metabolic acidosis, weight loss/decreased insulin requirement

an ACTH stimulation test fails to elicit a significant increase in serum cortisol levels
cushing syndromehigh cortisol-->obesity+hypertension+Hirsutism
obesity especially centrally, hirsutism in women, infection, menstrual irregularities in women, decreased libido and erectile dysfunction in men, high blood pressure, DM and week and brittle bones (osteoporosis)
cushing disease: excess cortisol is excess ACTH made by a pituitary tumor

most common cause of cushing syndrome: prolonged corticosteroid therapy
SLE >>>excess steroid medications>>>cushing syndrome

low dose dexamethasone suppression testing, measurement of late-night salivary cortisol levels or 24 hour urinary cortisol excretion

cushing disease: plasma levels of ACTH and cortisol are both increased, an overnight high dose dexamethasone test produces at least 50% suppression of cortisol levels.
Adrenal cortical hyperplasiaKids, developing pubic hair, tall, high testosterone
Administering low doses of exogenous corticosteroids to suppress ACTH secretion
prolonged corticosteroid therapyadrenal insufficiency and Cushing's syndrome

hypothalamus and pituitary

Question Answer
posterior pituitaryNeurophysins(carrier ADH and oxytocin)
Acidophils of pituitaryGH and prolactin
Basophils of pituitaryFSH/LH, ACTH and TSH
Remnants of Rathke's pouchrathke's pouch: anterior pituitary(ectodem)
Craniopharyngiomas: brain tumor most commonly in children compress optic chiasm
Growth hormone from the anterior pituitaryincreases production of insulin like growth factor-1 (IGF-1) from liver>>> stimulate the proliferation of cartilage in bone>>>bone growth
anatomy of long bone epiphysis>epiphyseal plate(metaphysis)>diaphysis
estrogen effect on the long boneepiphyseal plate (a hyaline cartilage plate in the metaphysis at each end of a long bone)
osteoporosis: decreased bone mass with a normal ratio of mineral to matrix.
All low of CRH, ACTH, cortisolprolonged corticosteroid therapy
Cortisol suppresses both ACTH and CRT: prolonged corticosteroid therapy>>>All low of CRH, ACTH, cortisol
increased CRH/ACTH, decreased cortisolprimary hypoadrenalism, autoimmune, damage to the adrenal glands
increased CRH/ACTH/Cortisolincrease in CRH>>>hypercortisolism (CUSHING)
increased CRH, decreaed ACTH/CortisolDamage to the pituitary
decreased CRH/ACTH, increased cortisoladrenal adenoma>>>excessive cortisol production
prolactinprolactin secretion: inhibitory via dopamine secreted from hypothalamus
osteoporosis: prolactin inhibits GnRH>>>low estrogen>>>bone loss
1) postmenopausal women: headache, visual field defects, low estrogen-->bone loss and vaginal
2) men: lowTestosterone-->erectile dysfunction
3) female of repruductive age: galactorrhea and amenorrhea and infertility
Anorexia nervosa-Amenorrhealoss of pulsatile GnRH release from the hypothalamus (due to body fat falls)
low levels of LH, FSH and estradiol


Question Answer Column 3
Insulininsulin resistance:activation of serine kinases. meals>>>parasympathetic: ACh stimulates muscarinic ACh receptors to cause a depolarization>>>secretion of insulin

sympathetic axons>>>Norepinephrine, somatostatin>>>inhibit insulin secretion (repolarization)promotes glucagon secretion>>>hyperglycemia

glucagon and epinephrine>>>stress hyperglycemia

the interstinal hormones stimulate insulin secretion?glucagon like polypeptide 1 (GLP-1) and glucose dependent insulinotropic polypeptide (GIP)

glucose dependent insulinotropic polypeptide (GIP): secreted by the duodenum.
glucagon like polypeptide 1 (GLP-1): secreted by ileum

the primary target of insulin:skeletal muscles

type I DM: Autoimmune response against pancreatic beta cells that leads to progressive loss of beta cell mass.
pseudomonas aeruginosa
ecthyma gangrenosum
exotoxin A >>>EF-2
a 54 year old man with a history of type 2 DM comes to the physician because of an unresolved skin lesion on his foot. the lesion appeared several weeks ago, but recently has expanded and become painful. physical examination shows a 5 cm lesion with a black, necrotic center and raised erythematous edges. which of the following toxins has a mechanism of action most similar to the toxin most likely responsible for this patient's skin lesion? Diphtheria toxin. KA23-16
diabetic ketoacidosis>>>low K+ and MAcidosisglycosuria>>>osmotic diuresis>>>water loss (hypovolemia)>>>increase aldosterone>>>total body K+ deficit>>>decreased intracellular potasium
Maternal diabeteslarge but immature for age babies, transposition of the great vessels KA23-18
hypoglycemic neonate:
gestational diabetes
diffuse hyperplasia of the islets
GLUTGlucose transport: facilitated diffusion (carrier proteins without energy)
Glut4: skeletal muscle and adipocytes
glucose trasport into skeletal/cardiac muscle, adipose tissue and liver: facilitated diffusion/GLUT4
Glut2: pancreatic beta cells/bidirectional transporter
liver cells to uptake glucose for glycolysis, and release of glucose during gluconeogenesis: Glut2
Glut2: renal, liver, pancreatic and small interstine.
glucose and excess ketone bodies excreted in the urineosmotic diuretics>>>excessive excretion of water in the urine>>>dehydration
postabsorptive state fastingliver store glycogen
glucogenogenesis from non carbohydrate (amino acid from skeletal mucles)
stored triglyceride and ketone bodies in the liver (lipolysis and ketogenesis)
insulin resistancefree fatty acid>>>serne phosphorylation of the insulin receptor
DM type II: pancreatic islet amyloid deposition
Glucagonoma syndromeNecrolytic migratory erythema+Diabetes mellitus+anemia
Necrolytic migratory erythema: The most characteristic clinical sign of glucagonoma syndrome.Most often affects the genital and anal region, the buttocks, groin and lower legs
falsely high values of HbA1cred cell turnover is low e.g. vitamin B12/folate deficiency anemia KA9-7

Parathyroid and thyroid

Question Answer
primary hyperparathyroidismMENI/IIa, kidney stone, hypercalcemia>>>peptic ulcer/acute pancreatitis and increased osteoclastic activity>>>bone resorption>>>cortical thinning (subperiosteal resorption)
Hypoparathyroidism1) primary: most common cause, accidental damage to or removal during surgery.
2) functional hypoparathyroidism: Low levels of magnesium>>>low PTH>>>low serum calcium>>>weakness, tremors, muscle fasciculations and seizures. Trousseau sign of latent tetany positive (It is distinct from the Trousseau sign of malignancy).
thyroid cancerPapillary thyroid cancer: Psammonma bodies
Follicular thyroid cancer: hurthle cells
Medullary thyroid carcinoma: polygonal tumor cells and amyloid
MENParathyroid+Pancreatic+Pituitary MEN1
e.g. A 37 year old man comes to the physician because of fatigue and a 6lb weight loss over the last 3 months. He also has experienced watery diarrhea and occasional nausea after large meals. He says he has not had any vomiting or dysphagia. physical examination reveals a soft abdomen with mild epigastric tenderness. lab studies of serum show: calcium 11.4 mg/dl, phosphate 2 mg/dl. abdominal CT scan shows a 3 cm lesion in the head of the pancreas. the serum concentration of which of the following hormones is most likely to be decreased? testosterone.
Medullary+Parathyroid MEN2a
Medullary+Mucosal neuromas MEN2b
adrenal medulla-->pheochromocytomas-->epinephrine ***carotid body tumor (paraganglioma)-->NE (Another catecholamines not Epi)
hypothyroidismweight gain+constipation+dry skin+delayed relaxation of knee and ankle reflexes
hypothyroid myopathy: muscle pain/cramps/weakness, weight gain/fatigability, elevated creatine kinase

1)subacute granulomatous thyroiditis:KA34-9
extremely tender, enlarged,
increased thyroid hormone levels and decreased TSH for 6-8 weeks >>>followed by a hypothyroid state for 2-4 months
viral infection,
granulomatous inflammation
can spontaneously remit.
neutrophil infiltration>>> mixed cellular infiltration with occational multinucleate giant cells
elevated ESR
reduced radioactive iodine
2)riedel thyroiditis: extensive fibrosis involving the thyroid gland
3)hashimoto's thyroiditis>>> chronic lymphocytic thyroiditis>>>diffuse mononuclear infiltration with formation of germinal centers
testicular tumorshCG can mimic TSH , causing the thyroid gland to become hyperstimulated increased T3/T4
hyperthyroidismgraves disease: pretibial myxederma and exophthalmos
rT3: Inactive form of thyroid hormone, T4 is converted to rT3
thyroid peroxidase:thyroglobuline iodination
treated with hormone replacement therapy containing estrogen and progesteronethyroid binding globulin TBG increase with estrogen use>>>increased bound T4>>>Free thlyroid hormones remains norml>>>increase in total T4, normal T3, TSH
diffuse nontoxic goiterno hyperthyroidism, no painful