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94 Cards in this Set
- Front
- Back
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What is the major problem in Cushing's syndrome?
What is the #1 cause? |
too much cortisol
iatrogenic sterioids (lowers ACTH) |
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What are the three major endogenous causes of Cushing's syndrome
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1. Cushing's (70%) - ACTH secretion from pituitary ademona
2. Ectopic ACTH - from non piutitary source (small cell lunger cancer, bronchial carcinoids) 3. Adrenal (15%) - adeoma, carcinoma, nodular hyperplasia (lowers ACTH) |
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Adrenocortical ademoa can cause what two conditions
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1. cushing's (hypercortisolism)
2. Conn's (hyperaldosteronism) |
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Patient comes in with
-HTN -wt gain -moon facies -truncal obesity -buffalo hump -hyperglycemia (insulin resistance) -skin changes (thinning striae) -osteoperosis -amenorrhea -immune suppression dx? |
Cushing's syndrome
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Interpret results
give dexamethasone cortisol decreases after low dose |
Healthy
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Interpret results: I give dexamethasone
patient has high cortisol after a low dose, low cortisol after a high dose |
ACTH-producing pituitary tumor
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Interpret results: I give dexamethasone
Patient has high cortisol after both a low and a high dose |
Ectopic ACTH-producing tumor or cortisol-producing tumor
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HTN, hypokalemia, metabolic alkalosis, LOW plasma renin
what's the dx? |
primary hperaldosteronism (Conn's)
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Patient has HTN, metabolic alkalosis, hypokalemia, and HIGH plasma renin
dx? 5 possible causes? |
secondary hyperaldosteronism
Renal artery stenosis, Chronic renal failure, CHF, cirrhosis, nephrotic syndrome Kidney percieves low intravascular volume--> activatse RAAS |
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2 treatment options for hyperaldosteronism
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1. surgery to remove tumor and/or spironolactone
2. K sparing diuretic (aldosterone antagonist) |
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What is the pathology in addison's disease?
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chronic primary adrenal insufficiency due to adrenal atrophy or destruction by disease (TB, autoimmune, metastasis)
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Patient comes in with
-hypotension -hyperkalemia -acidosis -skin hyperpigmentation dx? what causes skin hyperpigmentation? |
Addison's disease
adrenal insufficiency --> loss of aldosterone and cortisol hyperpigmentation from elevated ACTH (by product is MSH from POMC) |
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What is the cause of secondary adrenal insufficiency?
How can you tell it apart from pirmary? |
decreased pituitary ACTH production
no skin hyperpigmentation, no hyperkalemia |
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Addison's disease
what layers of the adrenal does it affect? Which does it spare? |
affects 3 cortical divisions
spares medulla |
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What is waterhouse-friderichesen syndrome?
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acute primary adrenal insufficiency due to adrenal hemorrhage associated with Niesseria meningitides septicemia, DIC, and endotoxic shock
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What is the most common tumor of the adrenal medulla in adults?
from what cells is it derived? From what cells are THESE cells derived? |
Pheochromocytoma
chromaffin cells Neural crest |
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On looking at an EM of a pheochromocytoma, one can see blue-back granules within tumor cells?
What are these granules |
dense-core neurosecretory granules
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Patient experiences spells of:
-elevated blood Pressure -Pain (headache) -Perspiration -Palpitation (tachycardia) -Pallor -see elevated urine vanillyl mandelic acid and catecholamines dx? what are 2 conditions associated with this? -how do you treat |
Pheochromocytoma
Neurofibromatosis, MEN2A and 2B treat with: 1. phenoxybenzamine (nonselective, irreversible alpha blocker) 2. Surgery to remove tumor |
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What is the rule of 10s for pheochromocytomas?
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10% of cases are each of these:
-malignant -bilateral -extra-adrenal -calcify -kids -familial |
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Elevated in urine - signifies what
a. elevated HVA b. VMA c. metanephrine what condition do you see elevations of these in urine |
a. dopamine
b. NE c. epi pheochromocytoma |
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Most common adrenal medulla tumor in children?
From where can it arise? |
Neuroblastoma
From any neural crest element of sympathetic chain - |
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Neuroblastoma
what will you see in urine? What is associated with rapid tumor progression? |
See elevated HVA (from dopamine)
Overexpression of N-myc oncogene |
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Signs/Symptoms of what?
-Cold intolerance (low heat production) -wt. gain, decr. appetitie -hypoactivity, lethargy, fatigue -constipation -dec. reflexes -facial/periorbital myxedema -dry, cool skin, coarse brittle hair bradycardia, dyspnea orn exertion High TSH, Low T3 and T4 |
Hypothyroidism
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Patient has
-heat intolerance -wt loss -hyperactivity -diarrhea -inc. reflexes -pretibial myxedema -warm, moist skin, fine hair -chest pain, palpitations, arrhythmias -low tsh -high T3/T4 dx? |
primary hyperthyroidism
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Test that is sensitive for primary hypothyroidism
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high TSH
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Most common cause of hypothyroidism
a. type of disorder b. assoc. with what HLA subtype c. what might you see early in course |
Hashimoto's thyroiditis
a. autoimmune (antimicrosomial, antithyroglobulin) b. HLA-DR5 c. hyperthyroid early (thyrotoxicosis secondary to follicular rupture) |
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Pt has large, nontender thyroid
-histo: hurthle cells, lymphycytic infiltrate with germinal centers dx? |
Hashimoto's thyroiditis
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Child in China born with
-pot belly -pale -puffy face -protruding umbilicus -protuberant tongue dx? cause? what is the cause if it is endemic? if it is sporadic? |
Cretinism from severe fetal hypothyroidism
endemic = lack of iodine (goiter) sporadic = defect in T4 formation or developmental failure in thyroid formation |
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Patient has flu-like illness, gets
-hypothyroidism -high ESR, jaw pain, early inflammation, tender thyroid -see granulomatous inflammation dx? early in course? |
subacute thyroiditis (de Quervain's)
may be hyperthyroid early |
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Patient has hypothyroid symptoms
find fixed, hard, painless goiter dx? what is happening? |
Riedel's thyroiditis
thyroid replaced by fibrous tissue |
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Type of myxedema seen in
a. hypothyroid b. hyperthyroid |
a. facial/periorbital
b. pretibial |
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Patient presents in childbirth with
-proptosis, periorbital edema -pretibial myxedema -diffuse goiter dx? What is happening? What kind of disease is this? |
Graves' disease (presents during stress times)
autoimmune hyperthyroidism --> thyroid or TSH-receptor stimulating antibodies Type II hypersensitivity |
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A patient with graves' experiences major stress, dies from arrhythmia
what is one probable cause? |
stress --> catecholamine surge
coupled with hyperthyroidism, led to arrhythmia |
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What is a toxic multinodular goiter
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Focal patches of hyperfunctioning follicular cells producing T3 and T4 independent of TSH
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You have a toxic multinodular goiter
It is "hot" on thyroid scan implications of it being hot? what does it mean to be hot? |
hot nodule = not malignant
hot = takes up lots of radioactive iodine on thyroid scan |
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When a patient with iodine deficienc goiter is made iodine replete, what must you watch out for
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thyrotoxicosis
Jod-Basedow Phenomenon |
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Thyroid Cancer
What is the most common what is it's prognosis |
papillary carcinoma
excellent |
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Thyroid Cancer
Patient had childhood irradiation, now has histo: -ground glass nuclei (orphan annie) -psammoma bodies -nuclear grooves on biopsy of thyroid dx? |
papillary carcinoma
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On histological specimen, you see follicles distended with colloid and lined by flattened epithelium, areas of fibrosis and hemorrhage
hyperplasia --> involution of thyroid gland dx? |
multinodular goiter
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Thyroid Cancer
Histo: uniform follicles dx? prog? |
follicular carcionoma
good |
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Thyroid Cancer
Patient with parathyroid tumor and pheochromocytoma has - increased production of calcitonin from parafollicular C cells -sheets of cells in amyloid stroma dx? associated condition |
medullary carcinoma
associated with MEN2A/2B |
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Thyroid Cancer
Seen in older patients, carries a poor prognosis |
undifferentiated, anaplastic
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Thyroid Cancer
Associated with Hashimoto's thyroiditis |
Lymphoma
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Patient presents with
history: -weakness and constipation -bone pain labs: -hypercalcemia -hypercalciuria -hypophosphatemia -elevated PTH -elevated alkaline phosphatase -elevated cAMP in urine dx? Usually etiology? Source of bone pain? |
primary hyperparathyroidism
adenoma Osteitis fibrosa cystica - cystic spaces in bone are filled with brown fibrous tissue |
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Patient presents with
-hypocaclemia -hyperphosphatemia -increased alkaline phosphatase -increased PTH dx? most common cause and pathogenesis? |
secondary hyperparathyroidism
chronic renal disease --> low excretion of phosphorus, low conversion to active vitamin D --> low intestinal absorption of Ca, buildup of Calcium phosphate --> LOW Ca activates parathyroid gland |
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What is the difference in lab values between primary and secondary hyperparathyroidism
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primary = hypercalcemia
secondary = hypocalcemia |
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Patient has high Ca and VERY high PTH
also has chronic renal disease what is the dx? pathogenesis? |
Tertiary hyperparathyroidism
chronic stimulation of PTH --> autonomous secretion of PTH |
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Patient presents with
-tetanic contracions -hypocalcemia -when you tap on the facial nerve, facial muscles contract -when you occlude the brachial artery with a bp cuff, you get carpal spasm dx? 3 common causes |
hypoparathyroidism (Chvostek's sign, Trousseau's sign)
accidental surgical incision (thyroid surgery), autoimmune destruction, DiGeorge Syndrome |
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Parathyroid pathologies - what is the condition if you see:
a. high PTH, high Ca b. high PTH, low Ca c. low PTH, high Ca d. low PTH, low Ca |
a. primary hyperparathyroidism
b. secondary hyperparathyroidism (chronic renal failure) c. PTH-independent hypecalcemia (Ca intake, cancer) d. hypoparathyroidism |
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Patient comes in with
-amenorrhea -galactorrhea -low libido -infertility -bitemporal hemoanopia dx? treat? |
prolactinoma (impinging on optic chiasm)
dopamine agonst - bromocriptine or cabergoline |
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Most common pituitary adenoma
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prolactinoma
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Patient is an adult who comes in with
-large tongue with deep furrows -deep voice -large hands and feet -coarse facial features -impaired glucose tolerance (insulin resistance) -increase in serum IGF-1 dx? treatment |
acromegaly due to excess GH in adults
pituitary adenoma resection followed by octreotide administration |
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Child has gigantism (increased linear bone growth)
2 things to confirm diagnosis? |
Excess GH in kids
1. increase IGF-1 2. failure to suppress serum GH following oral glucose tolerance test |
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Patient has intense thirst and polyuria +
-lack of ADH --> cannot concentrate urine -urine specific gravity < 1.006; serum osmolality >290 2 things on differential? How do you tell them apart? |
Central and nephrogenic DI
give desmopressin (ADH analog) --> if it helps fluid retention --> central DI -if it does not help --> nephrogenic DI |
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4 causes of central DI
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-pituitary tumor
-trauma -surgery -histiocytosis X |
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4 causes of nephrogenic DI
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-hereditary
-secondary to: hypercalcemia, Lithimum, demeclocycline (ADH antag.) |
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Treatment
a. central DI b. nephrogenic DI |
a. intra-nasal desmopresin (ADH analog)
b. nephrogenic DI = hydrochlorotiazide, indomethacin, amiloride |
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Patient comes in with
-excessive water retention -hyponatremia -urine osmolarity > serum osmolarity -see very low aldosterone levels dx? Why low aldo? what is one complication? treat? (2) |
SIADH
low aldo as a compensation for hyponatremia very low serum Na --> seizures (correct slowly) demeclocycline or H20 restriction |
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4 causes of SIADH
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1. ecotpic ADH (small cell lung disorder)
2. CNS disorders/head trauma 3. pulmonary disease 4. drugs (cyclophosphamide) |
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Patient has polydipsia, polyuria, polyphagia + wt. loss
dx? 3 associated manifestations acutely |
DM
1. DKA (type 1) 2. Hyperosmolar coma (type 2) 3. unopposed secretion of GH and epi (exacerbating hyperglycemia) |
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3 effects of insulin deficiency (glucagon excess)
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1. increased glucose uptake --> hyperglycemia --> dehydration, acidosis --> coma, death
2. increased protein catablism --> plasma aa, nitrogen loss in urine --> hyperglycemia c. increased lipolysis --> increased plasma FFAs, ketogenesis, ketonuria, ketonemia |
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2 major chronic manifestations of diabetes mellitus
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1. nonenzymatic glycosylation
2. osmotic damage |
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Patient with DM gets hemorrhage, exudates, microaneurysms and vessel proliferation in eye
what is going on |
nonenzymatic glycosylation of small vessels
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Patient with DM gets glaucoma
what is going on |
nonenzymatic glycosylation of small vessels
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Patient with DM gets
-nodular sclerosis -progressive proteinuria -chronic renal failure -arteriosclerosis --> HTN -kimmelstiel-Wilson nodules mechanism for what is going on? |
nonenzymatic glycosylation --> diabetic nephropathy
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2 chronic manifestations of osmotic damage caused by DM
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1. neuropathy (motor, sensory, autonomic degeneration)
2. Cataracts (sorbitol accum.) |
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3 tests for diabetes mellitus
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-fasting serum glucose
-glucose tolerance test -HbA1c (measures long term diabetic control) |
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Type 1 vs. Type 2 DM
onset, insulin-dependence |
1 = juvenile, dependent
2 = adult, non-insulin dependent |
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Type 1 DM
what do you see on histology |
autoimmune attack on pancreatic b-cells ==> chronic inflammation --> fibrosis
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Type 1 vs. Type 2 DM
primary defect |
1 = viral or autoimmune destruction of beta cells
2 = increased resistance to insulin |
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Type 1 vs. Type 2 DM
insulin necessary in treatment |
1 = yes
2 = sometimes |
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Type 1 vs. Type 2 DM
age |
1 = <30
2 = >40 |
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Type 1 vs. Type 2 DM
Associated with obesity |
1 = no
2 = yes |
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Type 1 vs. Type 2 DM
genetic predisposition |
1 = weak, polygenic
2 = strong, polygenic |
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Type 1 vs. Type 2 DM
association with HLA system |
1 = yes (HLA DR3 and 4)
2 = No |
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Type 1 vs. Type 2 DM
Glucose intolerance |
1 = severe
2 = mild/mod |
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Type 1 vs. Type 2 DM
insulin sensitivity |
1 = high
2 = low |
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Type 1 vs. Type 2 DM
ketoacidosis |
1 = common
2 = rare |
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Type 1 vs. Type 2 DM
b cell numbers in islets |
1 = low
2 = variable (with amyloid deposits) |
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Type 1 vs. Type 2 DM
serum insulin level |
1 = low
2 = variable |
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Type 1 vs. Type 2 DM
classic symptoms of polyuria, olydipsia, thirst, wt. loss |
1 = common
2 = sometimes |
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Type 1 vs. Type 2 DM
histology |
1 = islet leukocyte infiltrate
2 = islet amyloid deposit |
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Patient with DM gets
-rapid, deep breathing -nausea/vomiting -abdominal pain -psychosis/delirium -dehyrdation -fruity breath labs: -hyperglycemia -high H, low HCO3 (anion gap acidosis) -high blood ketone levels -leukocytosis -hyperkalemia, but depleted intracellular K dx? What is going on??? |
Diabetic ketoacidosis seen in DM1
stress increases need for insulin --> excess fat breakdown --> ketogenesis --> ketone bodies (b-hydroxybutyrate >acetoacetate) |
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5 possible complications of diabetic ketoacidosis
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1. life-threatening mucormcosis
2. rhizopus infection 3. cerebral edema 4. cardiac arrhythmias 5. heart failure |
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Treatmet for diabetic ketoacidosis
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fluids, insulin, K (to replete intracellular stores)
glucose to prevent hypoglycemia |
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Patient has recurrent
-diarrhea -cutaneous flushing -asthmatic wheezing -right sided valvular disease increased 5-HIAA in urine dx? what is going on? |
carcinoid syndrome
carcinoid tumor (neuroendocrine cells) --> secrete high serotonin |
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Where do you see carcinoid most often?
When do you not see sympotms, even with the presence of a tumor? |
metastatic small bowel tumors
Not if tumor is limited to GI because serotonin undergoes first pass metabolism in liver |
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most common tumor of appendix?
Derived from what? treat? |
carcinoid syndrome
Derived from neuroendocrine cells of GI tract octreotide |
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Rule of 1/3 for carcinoids
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1/3 metastasize
1/3 present with second malignancy 1/3 multiple |
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Patient gets recurrent ulcers
-see rugal thickening with acid hypersecretion one possible tumor etiology? Associated with what condition |
Zollinger Ellison
Gastrin-secreting tumor of pancreas or duodenum MEN1 (Pancreatic component) |
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3 Tumors of the MEN 1 syndrome
How does it commonly present |
3P's
Parathyroid Pituitary (PRL or GH) Pancreatic (ZE, insuolinoma, VIPoma, glucagonoma) commonly presents with kidney stones (Parathyroid ^ PTH --> ^Ca), stomach ulcers (ZE) |
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3 tumors of MEN 2A
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2P's
Pheocrhomocytoma Parathyroid Medullary thyroid carcinoma (secretes calcitonin) |
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3 tumors of MEN 2B syndrome
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1P
Pheochromocytoma Medullary thyroid carcinoma (calcitonin) Oral/intestinal ganglioneuromatosis (associated with marfinoid habitus) |
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Type of inheritance of MEN syndromes?
gene? |
autosomal dominant
ret gene (2A and 2B) |
