First Aid - Pathology

Front 1

Cushing's syndrome

Back 1

increased cortisol due to a variety of causes
primary pituitary adenoma (Cushing's disease) (increased ACTH)
primary adrenal hyperplasia/neoplasia (decreased ACTH)
ectopic ACTH production (e.g., small call lung cancer) (increased ACTH)
iatrogenic (decreased ACTH)

Front 2

Cushing's disease

Back 2

primary pituitary adenoma (increased ACTH)

Front 3

What are the clinical features of Cushing's syndrome?

Back 3

HTN, wt. gain, moon facies, truncal ovesity, buffalo hump, hyperglycemia (insulin resistance), skin changes (thinning, striae), osteoperosis, amenorrhea, innume suppression

Front 4

primary hyperaldosteronism
(Conn's syndrome)

Back 4

aldosterone-secreting tumor -> HTN, hypokalemia, metabolic alkalosis, low plasma renin

Front 5

secondary hyperaldosteronism

Back 5

due to renal artery stenosis, chronic renal failure, CHF, nephrotic syndrome

Front 6

What type of hyperaldosteronism is associated w/ high renin levels?

Back 6

secondary

Front 7

What type of hyperaldosteronism is associated w/ low renin levels?

Back 7

primary (Conn's)

Front 8

primary aldosterone and cortisol insufficiency
(Addison's disease)

Back 8

adrenal atrophy -> deficiency of aldosterone and cortisol -> hypotension and skin hyperpigmentation

Front 9

secondary aldosterone and cortisol insufficiency

Back 9

similar to Addison's except w/o skin hyperpigmentation

Front 10

What is the most common tumor of the adrenam medulla in adults?

Back 10

pheochromocytoma

Front 11

pheochromocytoma

Back 11

neoplasm that secretes epinerphrine and NE intermittently -> episodes of increased BP accompanied w/ headache
(rules of 10; 10% malignant, 10% bilateral, 10% extraadrenal, 10% calcify, 10% occur in kids, 10% familial)

Front 12

What is the most common tumor of the adrenal medulla in children?

Back 12

neuroblastoma

Front 13

What diseases is pheochromocytoma associated with?

Back 13

neurofibromatosis, MEN types II & III

Front 14

What is the treatment for pheochromocytoma?

Back 14

alpha-antagonists (esp. phenoxybenzamine)

Front 15

What are the hyperadernergic symptoms of pheochromocytoma?

Back 15

(5 P's)
Pressure (elevated)
Pain (headache)
Perspiration
Palpitations
Pallor/diaphoresis

Front 16

MEN type I

Back 16

pancreas, parathyroid, pituitary tumors
presents w/ kidney stones and stomach ulcers

Front 17

MEN type II

Back 17

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

Front 18

MEN type III
(aka MEN IIb)

Back 18

medullary carcinoma of the thyroid, pheochromocytoma, and oral and intestinal ganglioneuromatosis (mucosal neuromas)

Front 19

MEN types are associated w/ the ret gene?

Back 19

MEN types II and III

Front 20

What MEN types include pheochromocytoma?

Back 20

MEN types II and III

Front 21

What MEN types present w/ kidney stones and stomach ulcers?

Back 21

MEN type I

Front 22

Which MEN types include pancreatic tumors?

Back 22

MEN type I

Front 23

Which MEN types include medullary carcinoma of the thyroid?

Back 23

MEN types II and III

Front 24

Which MEN types include parathyroid tumor?

Back 24

MEN type I and II

Front 25

Which MEN types include oral and intestinal ganglioneuromatosis (mucosal neuromas)?

Back 25

MEN type III

Front 26

MEN syndromes have what kind of inheritance?

Back 26

autosomal dominant

Front 27

hypothyroidism

Back 27

high TSH, low total T4, low free T4, low T3 uptake

Front 28

hyperthyroidism

Back 28

low TSH (if primary), high total T4, high free T4, high T3 uptake

Front 29

Grave's disease

Back 29

autoimmune hyperthyroidism w/ thyroid stimulating/TSH antibodies

Front 30

What is the clinical presentation of hypothyroidism?

Back 30

cold intolerance , hypoactivity, wt. gain, fatigue, lethargy, decreased appetite, constipation, weakness, decreased reflexes, myxedema, dry, cool skin, coarse-brittle hair

Front 31

What is the clinical presentation of hyperthyroidism?

Back 31

heat intolerance, hyperactivity, wt. loss, hest pain/palpitations, arrhythmias, diarrhea, increased reflexes, warm-moist skin, fine hair

Front 32

What is the clinical presentation of Grave's disease?

Back 32

ophthalmopathy, pertibial myxedema, diffuse goiter
often presents during stress

Front 33

What is the treatment for Grave's disease?

Back 33

propylthiouracil - inhibits production of thyroid hormone as well as peripheral conversion of T4 to T3

Front 34

Is Grave's disease hyper- or hypothyroid?

Back 34

hyperthyroid

Front 35

Is Riedel's thyroiditis hyper- or hypothyroid?

Back 35

hypothyroid

Front 36

Riedel's thyroiditis

Back 36

thyroid replaced by fibrous tissue (hypothyroid)

Front 37

Hashimoto's thyroiditis

Back 37

autoimmune disorder resulting in hypothyroidism
60-80x risk of developing thyroid lymphoma compared to normal controls

Front 38

Subacute thyroiditis
(de Quervain's)

Back 38

Self-limited hypothyroidism often following a flulike illness
(may be hyperthyroid early in course)

Front 39

Is Hashimoto's thyroiditis hyper- or hypothyroid?

Back 39

hypothyroid

Front 40

Is subacute thyroiditis hyper- or hypothyroid?

Back 40

hypothyroid, however may be hyperthyroid early in course

Front 41

What are the 4 types of thyroid cancer?

Back 41

papillary
follicular
medullary
undifferentiates/anaplastic

Front 42

Which type of thyroid cancer has excellent prognosis?

Back 42

papillary

Front 43

Which type of thyroid cancer has good prognosis?

Back 43

follicular

Front 44

Which is the most common type of thyroid cancer?

Back 44

papillary

Front 45

What is the origin of medullary thyroid cancer?

Back 45

parafollicular "C cells"

Front 46

Which type of thyroid cancer produces calcitonin?

Back 46

medullary

Front 47

Which type of thyroid cancer has horrible prognosis?

Back 47

undifferentiated/anaplastic

Front 48

Which type of thyroid cancer has psammoma bodies?

Back 48

papillary

Front 49

Which type of thyroid cancer has "ground-glass" nuclei?

Back 49

papillay

Front 50

Which type of thyroiod cancer has uniform follicles?

Back 50

follicular

Front 51

endemic cretinism

Back 51

lack of dietary iodine

Front 52

sporadic cretinism

Back 52

caused by defect in T4 formation or developmental failure in thyroid formation

Front 53

What are the clinical findings of cretinism?

Back 53

mentally retarded, pot-bellied, pale, puffy-faced child w/ protuding umbilicus and protuberant tongue

Front 54

acromegaly

Back 54

excess GH in adults

Front 55

What are the clinical findings of acromegaly?

Back 55

large tongue w/ deep furrows, deep voice, large hands and feet, coarse facial features

Front 56

gigantism

Back 56

excess GH in children

Front 57

What are the acute manifestations of diabetes mellitus?

Back 57

polydipsia, polyuria, polyphagia, wt. loss, DKA (type 1), hyperosmolar coma (type 2), unopposed secretion of GH and epinephrine (exacerbating hyperglycemia)

Front 58

What are the chronic manifestations of diabetes mellitus?

Back 58

1) small vessel disease -> retinopathy, glaucoma, nephropathy
2) large vessel atherosclersis, CAD, peripheral vascular occlusive disease and gangrene, cerebrovascular diseaes
3) neuropathy
4) cataracts (sorbitol accumulation)

Front 59

What are the tests used to diagnose diabetes mellitus?

Back 59

fasting serum glucose
glucose tolerance test
HbA1c (measures long-term diabetic control)

Front 60

diabetic ketoacidosis

Back 60

usually due to an increase in insulin requirements from an increase in stress (e.g., infection)
excess fat breakdown and the increase in free fatty acids, which are then made into ketone bodies

Front 61

What are the signs/symptoms of diabetic ketoacidosis?

Back 61

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

Front 62

What are the lab values in diabetic ketoacidosis?

Back 62

hyperglycemia
increased H
decreased HCO3
increased blood ketone levels
leukocytosis
hyperkalemia (but depleted intracellular K)

Front 63

What are the complications of diabetic ketoacidosis?

Back 63

life-threatening mucormycosis, Rhizopus infection, cerebral edema, cardiac arrhythmias, heart failure

Front 64

What is the treatment for diabetic ketoacidosis?

Back 64

fluids, insulin, potassium
glucose to prevent hypoglycemia

Front 65

central diabetes insipidus

Back 65

lack of ADH
(pituitary tumor, trauma, surgery, histocytosis X)

Front 66

nephrogenic diabetes insipidus

Back 66

lack of renal response to ADH
(hereditary or secondary to hypercalcemia, lithium demeclocycline)

Front 67

What are the lab findings for diabetes insipidus?

Back 67

urine spec. gravity < 1.006
serum osmolality > 290 mOsm/L

Front 68

What is the treatment for central diabetes insipidus?

Back 68

intranasal desmopressin (ADH analog)

Front 69

What is the treatment for nephrogenic diabetes insipidus?

Back 69

hydrochlorothiazide (diauretic - paradoxical effect)
indomethacin
amiloride

Front 70

SIADH

Back 70

excessive ADH secretion caused by
1) ectopic ADH (small cell lung cancer)
2) CNS disorders/head trauma
3) pulmonary disease
4) drugs (e.g., cyclophosphamide)

Front 71

What are the symptoms of SIADH?

Back 71

excessive water retention
hyponatremia
urine osmolarity > serum osmolarity

Front 72

What are the causes of hypercalcemia?

Back 72

(CHIMPANZEES)
Calcium ingestion
Hyperparathyroid
Hyperthyroid
Iatrogenic (thiazides)
Multiple myeloma
Paget's disease
Addison's disease
Excess vit. D
Excess vit. A
Sarcoidosis

Front 73

hyperparathyroidism

Back 73

excessive PTH

Front 74

What are the causes of primary hyperparathyroidism?

Back 74

usually an adenoma

Front 75

What are the lab findings of primary hyperparathyroidism?

Back 75

increased PTH
hypercalcemia
hypercalciuria
hypophosphatemia
increased cAMP in urine

Front 76

What are the lab findings of secondary hyperparathyroidism?

Back 76

increased PTH
hypocalcemia
hyperphosphatemia

Front 77

osteitis fibrosa cystica
(aka von Recklinghausen's syndrome)

Back 77

cyctic bone spaces filled w/ brown fibrous tissue

Front 78

renal osteodystrophy

Back 78

bone lesions due to secondary hyperparathyroidism due in turn to renal disease

Front 79

hypoparathyroidism

Back 79

low PTH -> hypocalcemia, tetany
due to accidental surgical excision or DiGeorge syndrome

Front 80

pseudohypoparathyroidism

Back 80

kidney unresponsive to PTH -> hypocalcemia, shortened 4th/5th digits, short stature
autosomal recessive

Front 81

carcinoid syndrome

Back 81

recurrent diarrhea, cutaneous flushing, asthmatic wheezing, right-sided valvular disease

Front 82

Why is carcinoid syndrome not seen if carcinoid tumor is limited to the GI tract?

Back 82

b/c serotonin undergoes 1st pass metabolism in the liver

Front 83

What is the most common tumor of the appendix?

Back 83

carcinoid tumor

Front 84

What is the cause of carcinoid syndrome?

Back 84

carcinoid tumors (neuroendocrine cells) which secrete high levels of serotinin

Front 85

What is the treatment for carcinoid syndrome?

Back 85

octreotide

Front 86

What fraction of carcinoid tumors metasitasize?

Back 86

1/3

Front 87

Zollinger-Ellison syndrome

Back 87

gastrin-secreting tumor of pancreas -> recurrent ulcers
may be assoc. w/ MEN type I

Front 88

osteoperosis

Back 88

reduction of bone mass in spite of normal mineralization

Front 89

type I osteoperosis

Back 89

postmenopausal
increased bone resorption due to decreased estrogen levels

Front 90

type II osteoperosis

Back 90

senile osteoporosis
affects men and women > 70 years old

Front 91

Osteoperosis affects what population the most?

Back 91

whites > blacks > Asians

Front 92

What is the cause of type I osteoperosis?

Back 92

decreased estrogen levels -> increased bone resorption
postmenopausal