Fa Endocrinolgy

Front 1

Cushing's syndrome: What are etiologies of Cushing’s syndrome? Is ACTH always elevated?

Back 1

increased cortisol due to:, 1. Cushing’s disease (primary pituitary adenoma) increased ACTH, 2. Primary adrenal (hyperplasia/neoplasia) decreased ACTH, 3. Ectopic ACTH production (ie- small cell lung ca) increased ACTH, 4. Iatrogenic, decreased ACTH

Front 2

Cushing's syndrome: Describe the clinical picture of Cushings.

Back 2

HTN, wt gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin change (thinning, striae), osteoporosis, immune supression

Front 3

Hyperaldosteronism: T/F Conn’s syndrome is secondary hyperaldosteronism.

Back 3

False. Conn’s syndrome is primary hyperaldosteronism, caused by an aldosterone-secreting tumor. Results in HTN, hypokalemia, metabolic alkalosis, low plasma renin.

Front 4

Hyperaldosteronism: Which hyperaldosteronism is associated with high plasma renin?

Back 4

Secondary hyperaldosteronism. It is due to renal artery stenosis, chronic renal failure, CHF, cirrhosis, or nephrotic syndrome. Kidney perception of low intravascular volume results in an overactive renin-angiotensin sysem.

Front 5

Hyperaldosteronism: What is the tx for hyperaldosteronism?

Back 5

Spironolactone, a diuretic that works by acting as a aldosterone antagonist.

Front 6

Addison's Disease: What characterizes addison’s disease? (which hormones are elevated or deficient)? Is it associated with HTN or hypotension?

Back 6

Primary deficiency of aldosterone and cortisol due to adrenal atrophy, causing hypotension and skin hyperpigmentation. Adrenal atrophy, absence of hormone production, involves all 3 cortical divisions.

Front 7

Addison's Disease: T/F In primary insufficiency decreased pituitary ACTH production is characterized by skin hyperpigmentation.

Back 7

False: increased ACTH causes MSH activity & hyperpigmentation

Front 8

Tumors of adrenal medulla: T/F Neuroblastoma is the most common tumor of adrenal medulla in adults.

Back 8

False. Pheochromocytoma is the most common tumor of adrenal medulla in adults. It is derived from chromaffin cells (arise from neural crest). It is associated with neurofibromatosis MEN types II and III.

Front 9

Tumors of adrenal medulla: Where does neuroblastoma occur?

Back 9

Neuroblastoma is the most common tumor of adrenal medulla in children. It can occur anywhere along the sympathetic chain.

Front 10

Tumors of adrenal medulla: AUTHOR

Back 10

Jason Lee

Front 11

Pheochromocytoma: secrete combination of two molecules

Back 11

epinephrine and norepinephrine

Front 12

Pheochromocytoma: epidemiology (rule of 10's)

Back 12

10% malignant, 10% bilateral, 10% extra-adrenal, 10% calcify, 10% kids, 10% familial

Front 13

Pheochromocytoma: symptoms - 5 P's

Back 13

(elevated blood) Pressure, Pain (headache), Perspiration, Palpitations, Pallor/diaphoresis --> relapsing and remittant

Front 14

Pheochromocytoma: elevations in two lab values

Back 14

urinary VMA and serum catecholamines

Front 15

Pheochromocytoma: association with two other endocrine diseases

Back 15

MEN II and III

Front 16

Pheochromocytoma: treatment

Back 16

alpha-antagonists

Front 17

Multiple Endocrine Neoplasia: type I (Wermer's syndrome) - 3 P's

Back 17

Pancreas, Pituitary, and Parathyroid tumors

Front 18

Multiple Endocrine Neoplasia: type II (Sipple's syndrome)

Back 18

medullary carcinoma of thyroid, pheochromocytoma, parathyroid tumor, or adenoma

Front 19

Multiple Endocrine Neoplasia: type III

Back 19

medullary carcinoma of thyroid, pheochromocytoma, oral/intestinal ganglioneuromatosis

Front 20

Hypothyroidism and hyperthyroidism: myxedema is prominent in which one

Back 20

hypothyroidism

Front 21

Hypothyroidism and hyperthyroidism: chest pain, palpitations, arrhythmias

Back 21

hyperthyroidism

Front 22

Hypothyroidism and hyperthyroidism: TSH is (increased/decreased) in primary hyperthyroidism? In primary hypothyroidism?

Back 22

hyper - decreased, hypo - increased

Front 23

Hypothyroidism and hyperthyroidism: Graves' disease involves autoantibodies with what mechanism of action?

Back 23

stimulation of TSH receptors

Front 24

Hypothyroidism and hyperthyroidism: three symptoms of Graves'

Back 24

ophthalmopathy, pretibial myxedema, diffuse goiter

Front 25

Hypothyroidism and hyperthyroidism: Graves' is a type __ hypersensitivity

Back 25

type II

Front 26

Hashimoto's thyroiditis: thyroid is (enlarged/not enlarged) and (tender/nontender)

Back 26

enlarged, nontender

Front 27

Hashimoto's thyroiditis: autoimmune antibodies directed against ---

Back 27

microsomes

Front 28

Hashimoto's thyroiditis: histology shows (type of cell) infiltrate

Back 28

lymphocytes (with germinal centers)

Front 29

Subacute thyroiditis (de Quervain's): self-limited (hyper/hypo)thyroidism following ---

Back 29

hypothyroidism following flu-like illness

Front 30

Subacute thyroiditis (de Quervain's): symptoms include

Back 30

jaw pain, tender thyroid gland, early hyperthyroidism

Front 31

Thyroid cancer: most common, good prognosis, "ground glass" nuclei, psammoma bodies

Back 31

papillary carcinoma

Front 32

Thyroid cancer: poor prognosis, uniform follicles

Back 32

follicular carcinoma

Front 33

Thyroid cancer: calcitonin producing (C cells), sheets of cells

Back 33

medullary carcinoma (MEN II and III)

Front 34

Thyroid cancer: older patients, horrible prognosis

Back 34

undifferentiated/anaplastic

Front 35

Cretinism: caused by a lack of dietary --- or defect in --- formation

Back 35

iodine (endemic), T4 (sporadic)

Front 36

Cretinism: symptoms include

Back 36

pot-belly, paleness, puffy face, protuberant tongue, protruding umbilicus

Front 37

Acromegaly: caused by excess --- in adults

Back 37

growth hormone

Front 38

Acromegaly: symptoms include

Back 38

large furrowed tongue, deep voice, large hands and feet, coarse facial features

Front 39

Acromegaly: in children, leads to ---

Back 39

gigantism

Front 40

Diabetes mellitus: acute symptoms common to both types

Back 40

polydipsia, polyuria, polyphagia, weight loss

Front 41

Diabetes mellitus: match: (DKA/hyperosmolar coma) with (type I/type II)

Back 41

DKA=type I, hyperosmolar coma=type II

Front 42

Diabetes mellitus: effects (increased/decreased) of insulin deficiency and glucagon excess on 1) glucose uptake, 2) protein catabolism, 3) lipolysis

Back 42

1) decreased, 2) increased, 3) increased

Front 43

Diabetes mellitus: increased plasma free fatty acids leads to

Back 43

ketogenesis

Front 44

Diabetes mellitus: hyperglycemia has what effect on blood volume and electrolytes

Back 44

decreased volume (osmotic diuresis), electrolyte depletion

Front 45

Diabetes mellitus: three chronic manifestations

Back 45

retinopathy (hemorrhage, exudate, microaneurysm), nephropathy (nodular sclerosis), neuropathy (sensory, motor, autonomic)

Front 46

Diabetes mellitus: sorbitol accumulation leads to what sequelae in the eye

Back 46

cataracts, glaucoma

Front 47

Diabetes mellitus: three tests - what are they? which one measures long-term glucose control?

Back 47

fasting glucose, glucose tolerance test, HbA1c

Front 48

Diabetes mellitus: AUTHOR

Back 48

Jacob Pugsley

Front 49

Type 1 - juvenile onset: % of diabetes

Back 49

0.15

Front 50

Type 1 - juvenile onset: Insulin necessary in treatment

Back 50

Always

Front 51

Type 1 - juvenile onset: Age

Back 51

<30

Front 52

Type 1 - juvenile onset: Association with obesity

Back 52

No

Front 53

Type 1 - juvenile onset: Genetic predisposition

Back 53

weak, polygenic

Front 54

Type 1 - juvenile onset: Association with HLA system

Back 54

Yes (HLA-DR3 & 4)

Front 55

Type 1 - juvenile onset: Glucose intolerance

Back 55

Severe

Front 56

Type 1 - juvenile onset: Ketoacidosis

Back 56

Common

Front 57

Type 1 - juvenile onset: B-cell numbers in the islets

Back 57

decreased

Front 58

Type 1 - juvenile onset: Serum insulin levels

Back 58

decreased

Front 59

Type 1 - juvenile onset: Classic symptoms of polyuria, polydipsia, thirst, weight loss

Back 59

Common

Front 60

Type 1 - juvenile onset: Theorized cause

Back 60

viral or immune destruction of B cells

Front 61

Type 2 - adult onset: % of diabetes

Back 61

0.85

Front 62

Type 2 - adult onset: Insulin necessary in treatment

Back 62

Sometimes

Front 63

Type 2 - adult onset: Age

Back 63

>40

Front 64

Type 2 - adult onset: Association with obesity

Back 64

Yes

Front 65

Type 2 - adult onset: Genetic predisposition

Back 65

Strong, polygenic

Front 66

Type 2 - adult onset: Association with HLA system

Back 66

No

Front 67

Type 2 - adult onset: Glucose intolerance

Back 67

mild to moderate

Front 68

Type 2 - adult onset: Ketoacidosis

Back 68

Rare

Front 69

Type 2 - adult onset: B-cell numbers in the islets

Back 69

Variable

Front 70

Type 2 - adult onset: Serum insulin levels

Back 70

Variable

Front 71

Type 2 - adult onset: Classic symptoms of polyuria, polydipsia, thirst, weight loss

Back 71

Sometimes

Front 72

Type 2 - adult onset: Theorized cause

Back 72

increased resistance to insulin

Front 73

Diabetic Ketoacidosis (type 1): What precipitates this

Back 73

Increase in insulin requirements from increase in stress (e.g. infection)

Front 74

Diabetic Ketoacidosis (type 1): Ketone bodies from where

Back 74

Excess fat breakdown, increase ketogenesis from increased free fatty acids which are made into ketone bodies

Front 75

Diabetic Ketoacidosis (type 1): Signs/Symptoms

Back 75

Kussmaul respirations (rapid/deep breathing), hyperthermia, nausea/vomiting, abdominal pain, psychosis/dementia, dehydration, fruity breath odor

Front 76

Diabetic Ketoacidosis (type 1): Labs

Back 76

Hyperglycemia, high H+, low HCO3- (anion gap metabolic acidosis), high blood ketone levels, leukocytosis

Front 77

Diabetic Ketoacidosis (type 1): Complications

Back 77

Life threatening mucormycosis, Rhizopus infection, cerebral edema, cardiac arrhythimias, heart failure

Front 78

Diabetic Ketoacidosis (type 1): Treatment

Back 78

Fluids, insulin, and potassium; glucose if necessary to prevent hypoglycemia.

Front 79

Diabetes insipidus: summary

Back 79

intensive thirst, polyuria, inability to concentrate urine with fluid constriction owing to lack of ADH (central DI) or to lack of renal response to ADH (nephrogenic DI). Caused by lithium or demeclocycline

Front 80

Diabetes insipidus: Findings

Back 80

Urine specific gravity < 1.006; serum osmolality > 290 mOsm/L

Front 81

Diabetes insipidus: Treatment

Back 81

adequate fluid intake; Central DI - intranasal desmopressin (ADH analog); nephrogenic DI - hydrochlorothiazide, indomethacin, or amiloride

Front 82

SIADH: what does it stand for

Back 82

Syndrome of inapropriate ADH

Front 83

SIADH: finds

Back 83

1) excess water retention 2) hyponatremia [may lead to seizures - correct slowly] 3) urine osmolarity > serum osmolarity

Front 84

SIADH: causes

Back 84

1) Ectopic ADH [small cell lung cancer] 2) CNS disorders/head trauma 3) pulmonary disease 4) Drugs

Front 85

Hyperparathyroidism: What causes primary hyperparathyroidism?

Back 85

Usually an adenoma

Front 86

Hyperparathyroidism: What are the findings of primary disease?

Back 86

hypercalcemia, hypercalciuria, hypophosphatemia, high parathyroid hormone, high cAMP in urine; often asymptomatic, may present with weakness and constipation

Front 87

Hyperparathyroidism: what is osteitis fibrosa cystica? (von Recklinghausen's syndrome)

Back 87

cystic bone spaces filled with non-neoplastic fibrous tissue

Front 88

Hyperparathyroidism: What causes secondary hyperparathyroidism?

Back 88

low serum Ca++, most often chronic renal disease.

Front 89

Hyperparathyroidism: What are the findings of secondary hyperparathyroidism?

Back 89

hypocalcemia, hyperphosphatemia, high parathyroid hormone

Front 90

Hypoparathyroidism: findings

Back 90

hypocalcemia, tetany.

Front 91

Hypoparathyroidism: causes

Back 91

accidental surgical excision (thyroid surgery) or DiGeorge syndrome

Front 92

Hypoparathyroidism: note: pseudohypoparathyroidism

Back 92

autosomal recessive kidney unresponsiveness to PTH. Hypocalcemia, shortened 4th/5th digits, short stature

Front 93

Carcinoid syndrome: frequency

Back 93

rare

Front 94

Carcinoid syndrome: cause

Back 94

carcinoid tumors (neuroendocrine cells), especially those of the small bowel; they secrete high levels of serotonin (5-HT) that does not get metabolized by the liver due to liver metastases.

Front 95

Carcinoid syndrome: symptoms

Back 95

recurrent diarhea, cutaneous flushing, asthmatic wheezing, and right-sided valvular disease.

Front 96

Carcinoid syndrome: most common tumor of what?

Back 96

apendix

Front 97

Carcinoid syndrome: lab

Back 97

high 5-HIAA in urine

Front 98

Carcinoid syndrome: Rule of 1/3s:

Back 98

1/3 metastasize; 1/3 present with second malignancy; 1/3 multiple

Front 99

Carcinoid syndrome: Treatment?

Back 99

Octreotide

Front 100

Carcinoid syndrome: What is this medication?

Back 100

synthetic octapeptide analog of somatostatin (growth hormone-inhibiting hormone)

Front 101

Zollinger-Ellison syndrome: What kind of tumor causes this?

Back 101

Gastrin secreting tumor (usually) of the pancreas

Front 102

Zollinger-Ellison syndrome: what does it cause?

Back 102

recurrent ulcers

Front 103

Zollinger-Ellison syndrome: may be associated with what?

Back 103

MEN type I

Front 104

Osteoporosis: what is this?

Back 104

reduction in bone mass in spite of normal bone mineralization

Front 105

Osteoporosis: what characterizes type 1?

Back 105

Postmenopausal (10-15 years after menopause); increased bone reabsorption due to low estrogen levels. Treated with estrogen replacement

Front 106

Osteoporosis: what characterizes type 2?

Back 106

Senile osteoporosis - affects men and women > 70 y/o

Front 107

Osteoporosis: what races are affected most?

Back 107

whites>blacks>asians

Front 108

Osteoporosis: symptoms of vertebral crush fractures

Back 108

acute back pain, loss of height, kyphosis

Front 109

Osteoporosis: other

Back 109

distal radius (Colles') fracures, vertebral wedge fracures.