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112 Cards in this Set

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what is the most common tumor of adrenal medulla in adults?
pheochromocytoma
what is the most common tumor of adrenal medulla in children
neuroblastoma
which adrenal medulla tumor causes episodic HTN?
pheochromocytoma
capsule --> medulla

1)layers
2)secretory products
3)regulatory control
GFR - "salt, sugar, and sex"

Glomerulosa - aldosterone
renin-angiotensin

Fasciculata - glucocorticoids


Reticularis - androgens
ACTH, hypothalamic CRH

Medulla - catecholamines (epi, NE)
preganglionic sympathetic products
drainage of adrenal gland
L adrenal --> L adrenal vein --> L renal vein --> IVC

R adrenal --> R adrenal vein --> IVC
where does the post pit derive from?
neuroectoderm
hormones of post pit
vasopressin + oxytocin

made in hypothal, shipped to post pit.
hormones of anterior pituitary?
FLAT PiG

FSH
LH
ACTH
TSH

PROLACTIN
GH

MELANOTROPIN
where does the ant pit derive from
oral ectoderm
pancreas cell types

what do they secrete
alpha - glucagon

beta - insulin

delta - somatostatin
prolactin regulatory pathway
prolactin increase Dopamine synthesis + Dopamine release from hypothalamus

Dopamine inhibits prolactin secretion

TRH increases prolactin secretion

Dopamine agonists inhibit prolactin secretion
fxn prolactin
inhibits GnRH synthesis/release

inhibits ovulation

commonly see amenorrhea
souce of PTH
parathyroid - chief cells
fxn PTH
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
what stimulates PTH secretion
decrease free serum Ca
where is the inactive vit D converted, what is it?
liver - 24, 25 OH vit D
where is active vit D converted, what is it?
kidney - 1, 25 OH vit D
Fxn vit D
increase absorption of dietary Ca, P

increase bone resorption of Ca and PO4
what increases vit D formation
increased PTH

decrease Ca

decrease P
Ca, P, ALP levels

in hyperparathyroidism
hyperPTH

high Ca, low P, high alkaline phosphate
Ca, P, ALP levels

in paget's disease of bone
Paget's bone

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

in Vit D intoxication
Vit D intoxification

high Ca, high P, normal/increased ALP
Ca, P, ALP levels

in Osteoporosis
osteoporosis

all normal
Ca, P, ALP levels

in renal insufficiency
renal insufficiency

decreased Ca, high P, normal ALP
source of calcitonin
parafollicular cells of thyroid
fxn calcitonin
*OPPOSES PTH*

decrease bone resorption of Ca
regulation calcitonin
increase serum Ca causes calcitonin secretion
what are steroid/thyroid hormones
PET CAT

Progesterone
Estrogen
Testosterone

Cortisol
Aldosterone
Thyroxine, T3
how do steroid hormones circulate?
bound to specific binding globulins

they are lipophilic
what hormone mechs causes gynecomastia
increased sex hormone binding globulin lowers free testosterone
what horman mechs cause hirsuitism
decreased sex hormone binding globulin raises free testosterone
fxn thyroid
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
WHAT STIM THYROID HORM
TRH FROM HYPOTHAL
WHAT DECREASES THYROID BINDING GLOBULIN
HEPATIC FAILURE
WHAT INCREASES THYROID BINDING GLOBULIN
PREGNANCY
WHAT ARE INSULIN DEPENDENT ORGANS
SKELETAL MUSCLE, ADIPOSE
WHAT ARE INSULIN INDEPENDENT ORGANS THAT TAKE UP GLUCOSE

HOW?
BRAIN, RBC

USE GLUT-1
SYMPTOMS OF CUSHING'S
HTN, WEIGHT GAIN, MOON FACIES, TRUNCAL OBESITY, BUFFALO HUMP, HYPERGLYCEMIA, SKIN CHANGES (THINNING/STRIAE), OSTEOPOROSIS, AMENORRHEA, IMMUNE SUPPRESSION
CUSHING'S ETIOLOGIES
PRIMARY PIT ADENOMA - INCREASE ACTH

PRIMARY ADRENAL - DECREASE ACTH

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

IATROGENIC (CHRONIC STEROIDS) - DECREASED ACTH
CUSHING DIAGNOSIS:

WHAT TEST USE?
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
HYPERALDOSTERONISM

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

2A) SECONDARY CAUSED BY?
B) RESULTS IN?
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
RX HYPERALDOSTERONISM
SPIRONOLACTONE

K SPARING DIURETIC

ACTS AS ALDOSTERONE ANTAGONIST
ADDISON'S DISEASE

1) CAUSE?

2) CHARACTERIZED BY?
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
pheochromocytomas are associated with what 3 diseases
neurofibromatosis

MEN II

MEN III
what do most pheochromocytomas secrete
epi

NE

Dopamine
what do you use to rx pheochromocytomas
alpha antagonists (phenoxybnenzamine)

plus

non-selective, irreversible alpha blocker
episodic hyperadrenergic symptoms of pheochromocytoma
5P's

pressure (high bp)
pain (headache)
perspiration (tachycardia)
palpitations
pallor
what are the 3 Multiple Endocrine Neoplasias (MEN) -

what do they all have in common
MEN I, II, III

ALL AD

MEN II/III associated with "ret" gene
MEN I symptoms
presents with kidney stones and stomach ulcers

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

Parathyroid

Pituitary
MEN II symptoms
medullary carcinoma of thyroid, pheochromocytoma, parathyroid tumor
MEN III symptoms
medullary carcinoma of thyroid, pheochromocytoma, ORAL AND INTESTINAL GANGLIONEUROMATOSIS (mucosal neuromas)
Hypothyroidism symptoms
cold intolerance, hypoactivity, weight gain, fatigue, lethargy, decreased appetite, constipation, weakness, decreased reflexes, myxedema (facial/periorbital), dry cool skin, coarse brittle hair
hyperthyroidism symptoms
heat intolerance, hyperactivity, wt loss, chest pain/palpitations, arrhthymias, diarrhea, increased reflexes, warm moist skin, fine hair
graves' disease is what kind of disease?

what kind of antibodies?

symptoms?

when does it present
autoimmune hyperthyroidism

thyroid-stimulating/TSH receptor antibodies

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

presents during stress (childbirth)
lab findings in hypothyroidism
high TSH,
low total T4,
low free T4,
low T3 uptake
lab findings in hyperthyroidism
low TSH (if primary)
high total T4,
high free T4
high T3 uptake
what type of hypersensitivity rxn is Graves' disease
type II
pathology of riedel's thyroiditis

what kind of thyroid disease
thyroid replaced by fibrous tissue

hypothyroid
hashimoto's thyroiditis

1)what kind of thyroid disease

2) symptoms

3) histologic findings

4) what kind of antibodies
1)autoimmune hypothyroidism

2) moderately enlarged, nontender thyroid

3) lymphocytic infiltrate with germinal centers

4) antimicrosomal ab + antithyroglobulin ab
subacute thyroiditis

1) cause?

2) findings?

3) early in course can be what?
1) self-limited hypothyroidism after flu-like illness

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

3) hyperthyroid
4 types of thyroid cancer are
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
endemic vs sporadic cretinism
endemic - occurs where endemic goiter prevalent (lack Iodine)

sporadic - cause by defect T4 formation or developmental failure in thyroid formation
cretinism findings
pot bellied, pale, puffy faced child with protruding umbilicus and protuberant tongue
cause of acromegaly
excess GH in adults

increased GH is normal in stress, exercise, hypoglycemia
acromegaly findings
large tongue w/ deep furrow
deep voice
large hands and feet
coarse facial features
impaired glucose tolerance (insulin resistance)
cause of gigantism
increased GH in children
rx acromegaly
octreotide
primary hyperPTH

lab findings?
hypercalcemia

hypercalciuria (renal stones)

hypophosphatemia

high PTH

high cAMP in urine

asymptomatic or present with weakness and constipation "groans"
secondary hyper PTH

lab findings?
low serum Ca (most from chronic renal dz)

hypocalcemia,
hypophosphatemia
high PTH
what is osteitis fibrosa cystica?
cystic bone bone spaces filled with brown fibrous tissue
what is renal dystrophy?
bone lesions due to secondary hyperparathyroidism due to renal disease
phrase of hyperPTH?
STONES, BONES, GROANS
hypoPTH

1) cause

2) symptoms
accidental surgical excision or DiGeorge syndrome

hypocalcemia, tetany
what is chvostek's sign

what is it indicative of
tap facial nerve, get contraction of facial muscles

hypoPTH
what is trousseau's sign?

what is it indicative of
occlusion of brachial artery with BP cuff --> carpal spasm

hypoPTH
what causes hypercalcemia
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
acute manifestation diabetes mellitus
polydipsia
polyuria
polyphagia
wt loss
DKA (type 1)
hyperosmolar coma (type 2)
unopposed secretion of GH/epi (exacerbating hyperglycemia
chronic manifestation diabetes mellitus
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)
what tests would you order with diabetes mellitus
fasting serum glucose
glucose intolerance test
HbA1c
insulin deficiency effects
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
what is the most important complication of type 1 diabetes
ketoacidosis
causes of DKA
increase insulin requirements from increase in stress

excess fat breakdown and increase ketogenesis from the increase in FFA, which are made to ketone bodies
signs/symptoms DKA
Kussmaul respiration (rapid/deep breathing),
hyperthermia,
N/V,
abdominal pain, psychosis/dementia, dehydration,
fruity breath odor
DKA labs
hyperglycemia
high H+
low HCO3 (anion gap metabolic acidosis)
high blood ketone levels
leukocytosis
hyperkalemia but depleted intracell K
DKA complication
life threatening mucormycosis, rhizopus infection, cerebral edema, cardiac arrhythmias, heart failure
rx DKA
fluids,
insulin,
K,
glucose if necessary to prevent hypoglycemia
cause of diabetes insipidus
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
symptom DI
intensive thirst

polyuria

inability to [] urine b/c lack of ADH or renal response to ADH
Diag DI
water deprivation test - no increase in urine osmolality
lab finding DI
<1.006 urine specific gravity

serum osmolality >290 mOsm/L
Rx DI
adequate fluid intake

central - intranasal desmopressin

nephrogenic - HCTZ, indomethicin, amiloride
Causes SiADH
ectopic ADH (small cell lung cancer)

CNS disorder/head trauma

pulmonary dz

drugs (cyclophosphamide)
SiADH labs
excessive water retention

hyponatremia (very low lead to seizure)

urine osmolarity > serum osmolarity
SiADH rx
demeclocycline or H20 restriction
what is carcinoid syndrome caused by
neuroendocrine cell carcinoid tumor

metastatic small bowel tumor

secrete high levels 5HT
symptoms of carcinoid syndrome
diarrhea,
cutaneous flushing,
asthmatic wheezing,
right sided valvular dz
what is a gastrin-secreting tumor of the pancreas or duodenum?

what does it cause?

what is most associated with?
Zollinger-Ellison syndrome

causes recurrent ulcers

most associated with MEN type 1
Insulin

Lispro, Insulin (short)

NPH (intermediate)

Lente, ultralente (long)
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)
Sulfonylureas

1st gen: Tolbutamide, Chlorpropamide
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
Sulfonylureas

2nd Gen: Glyburide, Glimepiride, Glipizide
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
Biguanides

Metformin
MOA: decrease gluconeogenesis

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

TOX: lactic acidosis
Glitazone

Pioglitazone

Rosiglitazone
Glitazones

MOA: increase target cell response to insulin

USE: type 2 DM

TOX: weight gain, hepatotoxicity
alpha glucosidase inhibitors

acarbose
miglitol
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
Orlistat
Orlistat

MOA: alter fat metab - inhibit pancreatic lipase

USE: long term obesity management

TOX: steatorrhea
GI
reduced absorption fat-soluble vitamin
headache
Sibutramine
Sibutramine

MOA: sympathomimetic serotonin, norepi reuptake inhibitor

USE: short/long term obesity management

TOX: HTN, tachycardia
Propylthiouracil, Methimazole
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
GH Somatostatin use
GH def

Turners
Octreotide use
acromegaly,
carcinoid,
gastrinoma,
glucagonoma
oxytocin use
stim labor

uterine contraction

milk letdown

control uterine hemorrhage
desmopressin (ADH) use
pituitary (central) DI
Levothyroxine
Triiodothyronine
Levothyroxine, Triiodothyroxine

MOA: thyroxine replacement

USE: hypothyroidism, myxedema

TOX: tachy, heat intolerance, tremors
Glucocorticoids

HYDROCORTISONE, PREDNISONE, TRIAMCINOLONE, DEXAMETHASONE, BECLOMETHASONE
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