Fa Bros - End

Front 1

what is the most common tumor of adrenal medulla in adults?

Back 1

pheochromocytoma

Front 2

what is the most common tumor of adrenal medulla in children

Back 2

neuroblastoma

Front 3

which adrenal medulla tumor causes episodic HTN?

Back 3

pheochromocytoma

Front 4

capsule --> medulla

1)layers
2)secretory products
3)regulatory control

Back 4

GFR - "salt, sugar, and sex"

Glomerulosa - aldosterone
renin-angiotensin

Fasciculata - glucocorticoids


Reticularis - androgens
ACTH, hypothalamic CRH

Medulla - catecholamines (epi, NE)
preganglionic sympathetic products

Front 5

drainage of adrenal gland

Back 5

L adrenal --> L adrenal vein --> L renal vein --> IVC

R adrenal --> R adrenal vein --> IVC

Front 6

where does the post pit derive from?

Back 6

neuroectoderm

Front 7

hormones of post pit

Back 7

vasopressin + oxytocin

made in hypothal, shipped to post pit.

Front 8

hormones of anterior pituitary?

Back 8

FLAT PiG

FSH
LH
ACTH
TSH

PROLACTIN
GH

MELANOTROPIN

Front 9

where does the ant pit derive from

Back 9

oral ectoderm

Front 10

pancreas cell types

what do they secrete

Back 10

alpha - glucagon

beta - insulin

delta - somatostatin

Front 11

prolactin regulatory pathway

Back 11

prolactin increase Dopamine synthesis + Dopamine release from hypothalamus

Dopamine inhibits prolactin secretion

TRH increases prolactin secretion

Dopamine agonists inhibit prolactin secretion

Front 12

fxn prolactin

Back 12

inhibits GnRH synthesis/release

inhibits ovulation

commonly see amenorrhea

Front 13

souce of PTH

Back 13

parathyroid - chief cells

Front 14

fxn PTH

Back 14

PHOSPHATE TRASHING HORMONE

net: increase serum Ca, decrease serum PO4, increase urine PO4

1) increase bone resorption of Ca and PO4

2) increase kidney reabsorption of Ca in DCT

3) decrease kidney reabsorption of PO4

4) increase 1, 25OH vit D production by stimulating kidney 1 alpha hydroxylase

Front 15

what stimulates PTH secretion

Back 15

decrease free serum Ca

Front 16

where is the inactive vit D converted, what is it?

Back 16

liver - 24, 25 OH vit D

Front 17

where is active vit D converted, what is it?

Back 17

kidney - 1, 25 OH vit D

Front 18

Fxn vit D

Back 18

increase absorption of dietary Ca, P

increase bone resorption of Ca and PO4

Front 19

what increases vit D formation

Back 19

increased PTH

decrease Ca

decrease P

Front 20

Ca, P, ALP levels

in hyperparathyroidism

Back 20

hyperPTH

high Ca, low P, high alkaline phosphate

Front 21

Ca, P, ALP levels

in paget's disease of bone

Back 21

Paget's bone

Normal/increased Ca, normal P, high high high alkaline phosphate

Front 22

Ca, P, ALP levels

in Vit D intoxication

Back 22

Vit D intoxification

high Ca, high P, normal/increased ALP

Front 23

Ca, P, ALP levels

in Osteoporosis

Back 23

osteoporosis

all normal

Front 24

Ca, P, ALP levels

in renal insufficiency

Back 24

renal insufficiency

decreased Ca, high P, normal ALP

Front 25

source of calcitonin

Back 25

parafollicular cells of thyroid

Front 26

fxn calcitonin

Back 26

*OPPOSES PTH*

decrease bone resorption of Ca

Front 27

regulation calcitonin

Back 27

increase serum Ca causes calcitonin secretion

Front 28

what are steroid/thyroid hormones

Back 28

PET CAT

Progesterone
Estrogen
Testosterone

Cortisol
Aldosterone
Thyroxine, T3

Front 29

how do steroid hormones circulate?

Back 29

bound to specific binding globulins

they are lipophilic

Front 30

what hormone mechs causes gynecomastia

Back 30

increased sex hormone binding globulin lowers free testosterone

Front 31

what horman mechs cause hirsuitism

Back 31

decreased sex hormone binding globulin raises free testosterone

Front 32

fxn thyroid

Back 32

4 B's

BRAIN MATURATION
BONE GROWTH (WITH GH)
BETA ADRENERGIC EFFECTS (INCREASE CO, SV, HR CONTRACTILITY)
BMR INCREASE (INCREASE O2 CONSUMPTION, RR, INCREASE BODY TEMP)
INCREASE GLYCOGENOLYSIS, GLUCONEOGENESIS, LIPOLYSIS

Front 33

WHAT STIM THYROID HORM

Back 33

TRH FROM HYPOTHAL

Front 34

WHAT DECREASES THYROID BINDING GLOBULIN

Back 34

HEPATIC FAILURE

Front 35

WHAT INCREASES THYROID BINDING GLOBULIN

Back 35

PREGNANCY

Front 36

WHAT ARE INSULIN DEPENDENT ORGANS

Back 36

SKELETAL MUSCLE, ADIPOSE

Front 37

WHAT ARE INSULIN INDEPENDENT ORGANS THAT TAKE UP GLUCOSE

HOW?

Back 37

BRAIN, RBC

USE GLUT-1

Front 38

SYMPTOMS OF CUSHING'S

Back 38

HTN, WEIGHT GAIN, MOON FACIES, TRUNCAL OBESITY, BUFFALO HUMP, HYPERGLYCEMIA, SKIN CHANGES (THINNING/STRIAE), OSTEOPOROSIS, AMENORRHEA, IMMUNE SUPPRESSION

Front 39

CUSHING'S ETIOLOGIES

Back 39

PRIMARY PIT ADENOMA - INCREASE ACTH

PRIMARY ADRENAL - DECREASE ACTH

ECTOPIC ACTH PROD (SMALL CELL LUNG CANCER)- INCREASE ACTH

IATROGENIC (CHRONIC STEROIDS) - DECREASED ACTH

Front 40

CUSHING DIAGNOSIS:

WHAT TEST USE?

Back 40

INCREASED CORTISOL

TEST: DEXAMETHASONE SUPPRESSION TEST
1)HEALTHY
LOW DOSE: DECREASED CORTISOL

2) ACTH PRODUCING TUMOR
LOW DOSE: INCREASED CORTISOL
HIGH DOSE: DECREASED CORTISOL

3) CORTISONE PRODUCING TUMOR
LOW DOSE: INCREASED CORTISOL
HIGH DOSE: INCREASED CORTISOL

Front 41

HYPERALDOSTERONISM

1A) PRIMARY CAUSED BY?
B) RESULTS IN?

2A) SECONDARY CAUSED BY?
B) RESULTS IN?

Back 41

PRIMARY HYPERALDOSTERONISM

1A) CAUSED BY ALDOSTERONE SECRETING TUMOR

B) RESULTS IN HTN, HYPOKAL, METABOLIC ALKALOSIS, LOW PLASMA RENIN

2A) CAUSED BY RENAL ARTERY STENOSIS, CHRONIC RENAL FAILURE, CHF, CIRRHOSIS, NEPHROTIC SYNDROME
B) RESULTS IN: KIDNEY PERCEPTION OF LOW INTRAVASCULAR VOLUME --> OVERACTIVE RENIN-ANGIOTENSINOGEN SYSTEM

HIGH RENIN

Front 42

RX HYPERALDOSTERONISM

Back 42

SPIRONOLACTONE

K SPARING DIURETIC

ACTS AS ALDOSTERONE ANTAGONIST

Front 43

ADDISON'S DISEASE

1) CAUSE?

2) CHARACTERIZED BY?

Back 43

1) PRIMARY DEFICIENCY OF ALDOSTERONE, CORTISOL - ADRENAL ATROPHY

2) HYPOTENSION
SKIN HYPERPIGMENTATION (INCREASED ACTH PRODUCTION FROM POMC)

ADRENAL ATROPHY/ABSENCE OF HORMONE PRODUCTION - ALL 3 CORTICAL DIVISIONS

SECONDARY: NO SKIN HYPERPIGMENTATION - DECREASED PIT ACTH PRODUCTION

Front 44

pheochromocytomas are associated with what 3 diseases

Back 44

neurofibromatosis

MEN II

MEN III

Front 45

what do most pheochromocytomas secrete

Back 45

epi

NE

Dopamine

Front 46

what do you use to rx pheochromocytomas

Back 46

alpha antagonists (phenoxybnenzamine)

plus

non-selective, irreversible alpha blocker

Front 47

episodic hyperadrenergic symptoms of pheochromocytoma

Back 47

5P's

pressure (high bp)
pain (headache)
perspiration (tachycardia)
palpitations
pallor

Front 48

what are the 3 Multiple Endocrine Neoplasias (MEN) -

what do they all have in common

Back 48

MEN I, II, III

ALL AD

MEN II/III associated with "ret" gene

Front 49

MEN I symptoms

Back 49

presents with kidney stones and stomach ulcers

3P's
Pancreas - ZE syndrome, insulinoma, VIPomas

Parathyroid

Pituitary

Front 50

MEN II symptoms

Back 50

medullary carcinoma of thyroid, pheochromocytoma, parathyroid tumor

Front 51

MEN III symptoms

Back 51

medullary carcinoma of thyroid, pheochromocytoma, ORAL AND INTESTINAL GANGLIONEUROMATOSIS (mucosal neuromas)

Front 52

Hypothyroidism symptoms

Back 52

cold intolerance, hypoactivity, weight gain, fatigue, lethargy, decreased appetite, constipation, weakness, decreased reflexes, myxedema (facial/periorbital), dry cool skin, coarse brittle hair

Front 53

hyperthyroidism symptoms

Back 53

heat intolerance, hyperactivity, wt loss, chest pain/palpitations, arrhthymias, diarrhea, increased reflexes, warm moist skin, fine hair

Front 54

graves' disease is what kind of disease?

what kind of antibodies?

symptoms?

when does it present

Back 54

autoimmune hyperthyroidism

thyroid-stimulating/TSH receptor antibodies

opthalmopathy (proptosis, EPM swelling), pretibial myxedema, diffuse goiter

presents during stress (childbirth)

Front 55

lab findings in hypothyroidism

Back 55

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

Front 56

lab findings in hyperthyroidism

Back 56

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

Front 57

what type of hypersensitivity rxn is Graves' disease

Back 57

type II

Front 58

pathology of riedel's thyroiditis

what kind of thyroid disease

Back 58

thyroid replaced by fibrous tissue

hypothyroid

Front 59

hashimoto's thyroiditis

1)what kind of thyroid disease

2) symptoms

3) histologic findings

4) what kind of antibodies

Back 59

1)autoimmune hypothyroidism

2) moderately enlarged, nontender thyroid

3) lymphocytic infiltrate with germinal centers

4) antimicrosomal ab + antithyroglobulin ab

Front 60

subacute thyroiditis

1) cause?

2) findings?

3) early in course can be what?

Back 60

1) self-limited hypothyroidism after flu-like illness

2) elevated ESR, jaw pain, early inflammation, very tender thyroid gland

3) hyperthyroid

Front 61

4 types of thyroid cancer are

Back 61

papillary carcinoma - MC, excellent prognosis, ground glass nuclei, psammoma bodies

follicular carcinoma - good prognosis, uniform follicles

medullary carcinoma - parafollicular C cells, produces calcitonin, sheets of cells in amyloid stroma, MEN types II and III

undifferentiated/anaplastic - older pt, very poor prognosis

Front 62

endemic vs sporadic cretinism

Back 62

endemic - occurs where endemic goiter prevalent (lack Iodine)

sporadic - cause by defect T4 formation or developmental failure in thyroid formation

Front 63

cretinism findings

Back 63

pot bellied, pale, puffy faced child with protruding umbilicus and protuberant tongue

Front 64

cause of acromegaly

Back 64

excess GH in adults

increased GH is normal in stress, exercise, hypoglycemia

Front 65

acromegaly findings

Back 65

large tongue w/ deep furrow
deep voice
large hands and feet
coarse facial features
impaired glucose tolerance (insulin resistance)

Front 66

cause of gigantism

Back 66

increased GH in children

Front 67

rx acromegaly

Back 67

octreotide

Front 68

primary hyperPTH

lab findings?

Back 68

hypercalcemia

hypercalciuria (renal stones)

hypophosphatemia

high PTH

high cAMP in urine

asymptomatic or present with weakness and constipation "groans"

Front 69

secondary hyper PTH

lab findings?

Back 69

low serum Ca (most from chronic renal dz)

hypocalcemia,
hypophosphatemia
high PTH

Front 70

what is osteitis fibrosa cystica?

Back 70

cystic bone bone spaces filled with brown fibrous tissue

Front 71

what is renal dystrophy?

Back 71

bone lesions due to secondary hyperparathyroidism due to renal disease

Front 72

phrase of hyperPTH?

Back 72

STONES, BONES, GROANS

Front 73

hypoPTH

1) cause

2) symptoms

Back 73

accidental surgical excision or DiGeorge syndrome

hypocalcemia, tetany

Front 74

what is chvostek's sign

what is it indicative of

Back 74

tap facial nerve, get contraction of facial muscles

hypoPTH

Front 75

what is trousseau's sign?

what is it indicative of

Back 75

occlusion of brachial artery with BP cuff --> carpal spasm

hypoPTH

Front 76

what causes hypercalcemia

Back 76

CHIMPANZEES

Calcium ingestion (milk-alkali syndrome)

HyperPTH, Hyperthyroid

Iatrogenic (thiazide)

Multiple myeloma

Paget's disease

Addison's disease

Neoplasms

Zollinger-Ellison syndrome,

Excess Vit D

Excess Vit A

Sarcoidosis

Front 77

acute manifestation diabetes mellitus

Back 77

polydipsia
polyuria
polyphagia
wt loss
DKA (type 1)
hyperosmolar coma (type 2)
unopposed secretion of GH/epi (exacerbating hyperglycemia

Front 78

chronic manifestation diabetes mellitus

Back 78

nonenzymatic glycosylation
small vessel dz-> retinopathy
large vessel atherosclerosis, CAD, periph vasc occlusive dz, gangrene, CVD

osmotic damage
neuropathy (motor, sensory, autonomic degeneration)
cataracts (sorbitol accum)

Front 79

what tests would you order with diabetes mellitus

Back 79

fasting serum glucose
glucose intolerance test
HbA1c

Front 80

insulin deficiency effects

Back 80

decrease glucose uptake ->
hyperglycemia, glucosuria, osmotic diuresis, electrolyte depletion

increase protein catabolism -> increase plasma aa, lose N in urine -> hyperglycemia

increased lipolysis -> increase plasma FFA, ketogenesis, ketonuria, ketonemia

all go to dehydration, acidosis -> coma, death

Front 81

what is the most important complication of type 1 diabetes

Back 81

ketoacidosis

Front 82

causes of DKA

Back 82

increase insulin requirements from increase in stress

excess fat breakdown and increase ketogenesis from the increase in FFA, which are made to ketone bodies

Front 83

signs/symptoms DKA

Back 83

Kussmaul respiration (rapid/deep breathing),
hyperthermia,
N/V,
abdominal pain, psychosis/dementia, dehydration,
fruity breath odor

Front 84

DKA labs

Back 84

hyperglycemia
high H+
low HCO3 (anion gap metabolic acidosis)
high blood ketone levels
leukocytosis
hyperkalemia but depleted intracell K

Front 85

DKA complication

Back 85

life threatening mucormycosis, rhizopus infection, cerebral edema, cardiac arrhythmias, heart failure

Front 86

rx DKA

Back 86

fluids,
insulin,
K,
glucose if necessary to prevent hypoglycemia

Front 87

cause of diabetes insipidus

Back 87

lack of ADH

central DI - pit tumor, trauma, surgery, histiocytosis X

lack of renal response to ADH

hereditary/ secondary to hypercalcemia nephrogenic DI, Li, Demeclocycline

Front 88

symptom DI

Back 88

intensive thirst

polyuria

inability to [] urine b/c lack of ADH or renal response to ADH

Front 89

Diag DI

Back 89

water deprivation test - no increase in urine osmolality

Front 90

lab finding DI

Back 90

<1.006 urine specific gravity

serum osmolality >290 mOsm/L

Front 91

Rx DI

Back 91

adequate fluid intake

central - intranasal desmopressin

nephrogenic - HCTZ, indomethicin, amiloride

Front 92

Causes SiADH

Back 92

ectopic ADH (small cell lung cancer)

CNS disorder/head trauma

pulmonary dz

drugs (cyclophosphamide)

Front 93

SiADH labs

Back 93

excessive water retention

hyponatremia (very low lead to seizure)

urine osmolarity > serum osmolarity

Front 94

SiADH rx

Back 94

demeclocycline or H20 restriction

Front 95

what is carcinoid syndrome caused by

Back 95

neuroendocrine cell carcinoid tumor

metastatic small bowel tumor

secrete high levels 5HT

Front 96

symptoms of carcinoid syndrome

Back 96

diarrhea,
cutaneous flushing,
asthmatic wheezing,
right sided valvular dz

Front 97

what is a gastrin-secreting tumor of the pancreas or duodenum?

what does it cause?

what is most associated with?

Back 97

Zollinger-Ellison syndrome

causes recurrent ulcers

most associated with MEN type 1

Front 98

Insulin

Lispro, Insulin (short)

NPH (intermediate)

Lente, ultralente (long)

Back 98

Insulin

MOA: BINDS INSULIN RECEPTOR
liver - increase glucose stored as glycogen
muscle - increase glycogen and protein synthesis, K uptake
fat - aids TG storage

USE: TYPE 1 DM, life threatening hyperkal, stress induced hyperglycemia

Tox: hypoglycemia, hypersensitivity rxn (rare)

Front 99

Sulfonylureas

1st gen: Tolbutamide, Chlorpropamide

Back 99

1st gen Sulfonylureas

MOA: close K channel in beta cell membrane so cell depolarizes -> triggers insulin release via increase in Ca influx

USE: stim release of endogenous insulin in Type 2 DM *REQUIRE ISLET FXN*

TOX: disulfiram-like effect

Front 100

Sulfonylureas

2nd Gen: Glyburide, Glimepiride, Glipizide

Back 100

2nd gen Sulfonylureas

MOA: close K channel in beta cell membrane so cell depolarizes -> triggers insulin release via increase in Ca influx

USE: stim release of endogenous insulin in Type 2 DM *REQUIRE ISLET FXN*

TOX: hypoglycemia

Front 101

Biguanides

Metformin

Back 101

MOA: decrease gluconeogenesis

USE: oral hypoglycemic, used in pt w/o islet cell fxn

TOX: lactic acidosis

Front 102

Glitazone

Pioglitazone

Rosiglitazone

Back 102

Glitazones

MOA: increase target cell response to insulin

USE: type 2 DM

TOX: weight gain, hepatotoxicity

Front 103

alpha glucosidase inhibitors

acarbose
miglitol

Back 103

alpha glucosidase inhibitors

MOA: INHIBIT INTESTINAL BRUSH BORDER ALPHA GLUCOSIDASE, delayed sugar hydrolysis and glucose absorption leads to lower postprandial hyperglycemia

USE: type 2 DM

TOX: GI

Front 104

Orlistat

Back 104

Orlistat

MOA: alter fat metab - inhibit pancreatic lipase

USE: long term obesity management

TOX: steatorrhea
GI
reduced absorption fat-soluble vitamin
headache

Front 105

Sibutramine

Back 105

Sibutramine

MOA: sympathomimetic serotonin, norepi reuptake inhibitor

USE: short/long term obesity management

TOX: HTN, tachycardia

Front 106

Propylthiouracil, Methimazole

Back 106

PTU, Methimazole

MOA: inhibit organification and coupling of thyroid hormone synthesis.
PTU decreases peripheral conversion T4->T3

USE: hyperthyroid

TOX: skin rash, agranulocytosis (rare, aplastic anemia

Front 107

GH Somatostatin use

Back 107

GH def

Turners

Front 108

Octreotide use

Back 108

acromegaly,
carcinoid,
gastrinoma,
glucagonoma

Front 109

oxytocin use

Back 109

stim labor

uterine contraction

milk letdown

control uterine hemorrhage

Front 110

desmopressin (ADH) use

Back 110

pituitary (central) DI

Front 111

Levothyroxine
Triiodothyronine

Back 111

Levothyroxine, Triiodothyroxine

MOA: thyroxine replacement

USE: hypothyroidism, myxedema

TOX: tachy, heat intolerance, tremors

Front 112

Glucocorticoids

HYDROCORTISONE, PREDNISONE, TRIAMCINOLONE, DEXAMETHASONE, BECLOMETHASONE

Back 112

GLUCOCORTICOIDS

MOA: decrease LT and PG production by inhibit Phospholipase A2 and expression of COX

USE: addison's, inflammation, immune suppression, asthma

TOX: Iatrogenic Cushing's - buffalo hump, moon facies, truncal obesity, peptic ulcer, muscle wasting, thin skin, easy buisability, osteoporosis, adrenocortical atrophy