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Flashcards in Random Organ systems - endo Deck (105)
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Define osteitis fibrosa cystica

cystic bone spaces w/ brown fibrous tissue => bone pain


Labs of primary hyperparathyroidism

increased serum PTH, Ca+, alk phos (due to osteoblast turned on)
decreased serum phosphate

increased urinary cAMP (PTH stimulates Gs receptor)


What is MCC of secondary hyperparathyroidism?

chronic renal failure => excess PTH extrinsic to parathyroid gland


Labs of secondary hyperparathyroidism

increased PTH, phosphate, alk phos
decreased serum Ca+


What are causes of hypoparathyroidism?

AI damage, surgical excision, DiGeorge syndrome


Presentation of hypoparathyroidism?

numbness/tingling & muscle spasms (tetany) => Trousseau's sign (BP cuff), Chavsofic sign (tap on jaw)


Labs for hypoparathyroidism

low PTH & low serum Ca+


What is the cause of pseudohypoparathyroidism?

organs not responding to PTH so hypocalcemia w/ elevated PTH


The end organ resistance of pseudohypoparathyroidism is due to what?

AD mutation in Gs protein assoc w/ short stature & short 4th & 5th digits


What causes type I DM? What is it associated with?

autoimmune destruction of Beta cells of T lymphocytes => Ab against insulin leading to inflammation of islets

Assoc w/ HLA-DR3 & DR4


What are the clinical features of a type I DM patient in DKA?

hyperglycemia (>300)
anion gap metabolic acidosis due to ketoacids in blood
hyperkalemia but getting losses in urine so ends in low body potassium bc it is not in cells
Kussmaul respirations, mental change, fruity breath


Tx of DKA

replacement of electrolytes w/ K+


What is the mechanism of insulin resistance in type II DM?

decreased numbers of insulin receptors on skeletal muscle & adipose tissue


How does insulin concentration change during the course of type II DM?

rises due to resistance then very decreased bc of Beta cell exhaustion

amyloid deposits


Tx of type II DM

weight loss (1st always);
Rx to counter insulin resistance;
end stage is insulin dependent


What is a risk for uncontrolled type II DM? How does it present?

hyperosmolar non-ketotic coma => very very high glucose leading to life threatening diuresis causing hypoTN & coma w/ absent ketones (small amounts of insulin counteracts glucagon)


Vascular complications of DM?

NEG of vascular BM =>

NEG of large/medium vessels leads to atherosclerosis;
NEG of small vessels leads to hyaline arteriosclerosis;
NEG of Hgb leads to HbA1c (marker of glycemic control)


What cells/structures are at risk for osmotic damage due to high sugar?

Schwann cells => basis of neuropathy in diabetics
Pericytes in retina blood vessels => aneurysm causing rupture to blindness


Pancreatic endocrine tumors are associated with what?

MEN 1 => parathyroid hyperplasia & pituitary adenoma


How does an insulinoma present? what relieves Sx? What are the labs?

episodic hypoglycemia w/ mental changes relieved by glucose

low glucose;
high insulin & C peptide


Patient w/ Treatment resistant PUD. what is Dx?

Gastrinoma => ZE syndrome

can be multiple & extend into jejunum


Patient w/ low stomach pH along with gallstones & steatorrhea. Dx? Why the Sx?

inhibits gastrin so achlorhydria
inhibits CCK => cholelithiasis & steatorrhea


Patient w/ watery diarrhea, hypokalemia, achlorhydria. Dx?



How does cortisol raise the blood sugar? What are the effects of the elevated blood glucose?

breakdown muscle causing weakness w/ thin extremities;

insulin is released to store fat on face, back, trunk


What is the mechanism of abdominal striae in Cushings?

ruptured blood vessels due to collagen damage


How does stress or any increase in cortisol raise HTN?

upregulate alpha-1 receptors on arterioles thus increasing effect of catecholamines (esp NE)


What are the 3 mechanisms by which cortisol leads to immune suppression?

1) inhibits phospholipase A2 => cannot produce arachidonic acid metabolites
2) inhibits IL-2
3) inhibits histamine release from mast cells


What are the 4 major causes of cushing syndrome?

MCC=> exogenous corticosteroids;
Primary adrenal adenoma, hyperplasia, or CA (one large & one atrophic adrenal gland)
ACTH secreting pituitary adenoma (hyperplastic adrenals);
paraneoplsatic ACTH secretion (bilateral hyperplastic adrenals)


Prolonged exogenous corticosteroids will result in what grossly?

atrophy of both adrenals


How would ATCH pituitary adenoma be differentiated from paraneoplastic ACTH secretion?

High dose dexamethasone (cortisol analog) then measure cortisol levels

If ACTH is suppressed then pituitary adenoma;

If no ACTH suppression then small cell lung CA