Endocrine

Front 1

What can TRH stimulate?

Back 1

TSH and Prolactin

Front 2

What is Cortisol's BIG FIB?

Back 2

inc. Blood pressure (up regulating Alpha 1 receptors)
Insulin Resistance (down regulate receptors)
Gluconeogensis (lipolysis and proteolysis for substrates)
dec. Fibroblast act (straie)
Inflammatory modulator (dec. immune cells/response)

Dec. Bone formation (osteoporosis)

Front 3

What are some causes of dramatic losses of Mg2+?

Back 3

Diuretics, Diarrhea, drinking (alcohol), aminoglycosides
paradoxically decreases PTH release (leads to decreases in Ca levels unresponsive to treatment- keep losing it and won't retain any in the kidney without PTH release)

Front 4

What will cause a decrease in serum Ca2+ Acidosis or Alkalosis?

Back 4

Alkalosis- increases the negative charge on albumin and enhancing its binding to calcium= Muscle spasms (tapping on muscle cause contraction) and cramps, parasthesias

Front 5

What are the cAMP signaling hormones, also include the para/sympathetics (Gs)

Back 5

FLAT CAMP ChugG
FSH, LH, ACTH, TSH CRH ADH (V2) MSH PTH Calcitonin hCG GHRH Glucagon

Gs (B1/2, D1, H2, V2) all the evens except D1 (1 daiquiri please) relax SM/stim heart

Front 6

What are the cGMP hormones?

Back 6

Vasodilators (relax SM)
NO (EDRF), ANP

Front 7

What are the IP3 hormones and Para/sympth signaling molecules (Gq)

Back 7

I HAG 3 GOAT

Histamine (1), ATII, Gastrin GnRH, Oxytocin, ADH (v1) TRH

Para/Symp: All the odds M1/3, A1, H1, V1 (constrict SM)

Front 8

What are the Steroid Receptors?

Back 8

VET CAP
Vit. D, estrogen, T3/4 and Testosterone
Cortisol, Androgens, Progesterone

Front 9

What are the intrinsic Tyrosine Kinases?

Back 9

Growth Hormones (MAPK)
Insulin, IGF-1, FGF, EGF, PDGF

Front 10

what are the Receptor associated tyrosine kinases?

Back 10

JAK STAT (acidophils and cytokines)
PIG to associate with That
Prolactin, Immunomodulators (IL2,6,8,IFN), GH

Front 11

What are the molecules that act at Gi?

Back 11

2 MAD, decrease cAMP levels
M2, A2, D2

Front 12

What does an increase in SHBG do in men? Women?

Back 12

high SHBG lowers free T, gynecomastia in men
in women, low SHBG raises free T, hirsutism


increased with Estrogen/ OCP/ pregnancy

Front 13

What are the 4 Ts of Thyroid Hormones?

Back 13

Brain Maturation
Bone Growth
B-Adrenergic Effects (vs. cortisol Alpha 1)
Basal Met. rate (inc. Na/K ATPase)

Front 14

What is the Wolff-Chaikoff effect in the thyroid?

Back 14

Increased Iodine intake actually decreases the organification (by inhibiting thyroid peroxidase) dec. T3/4 production

Front 15

What is the the enzyme responsible for the organifaction and oxidation or Iodine?

Back 15

Thyroid Peroxidase (also couples tyrosine to Iodine)

Propylthiouracil (also decreases 5' deiodinase activity) and Methimazole inhibit peroxidase

Front 16

What can T4 be turned in to?

Back 16

T3 or Reverse T3 (inactive form)
T3 is the active form of thyroxin (binds to TBG) and better affinity for receptor

Front 17

What can inhibit the Na/I transporter?

Back 17

Thiocyanate and perchlorate anions

Front 18

What are the findings in Cushing Syndrome?

Back 18

Hypertension (inc. A1Rs)
Weight Gain, moon facies, Truncal obesity, Buffalo hump (lipodystrophy)
Hyperglycemia (increased gluconeogenisis and insulin resistance)
Skin thinning and purple lines (dec. Fibroblast act.)
Osteoporosis (dec. Bone formation)
Amenorrhea
Immune suppression
Steroids can also lead to Cataract formation from increased glucose
Prox. muscle weakness (inc. Muscle breakdown, peripheral catabolism with liver anabolism)

Front 19

Findings of Addisons

Back 19

Hypotension (dec. Cortisol and Ald)
Hyponatremia
Hyperkalemia and Acidosis
increase ACTH-> MSH-> hyper pigmentation
muscle weakness (hyperkalemia, arrythmias with spiked T waves)

Adrenal atrophy and insufficiency (chronic) all three layers (spares medulla)

secondary will not have skin hyperpigmentation (because due to a DEC. level of ACTH and no hyperkalemia because aldosteron is regulated by the RAA) i.e caused by a dec. Exogenous Steroid use

Front 20

What are the signs of a neuroblastoma in a kid?

Back 20

Malignant tumor of adrenal medulla, most common <4
Abdominal distention
firm, irregular mass, cross midline (vs. Wilms)
Homovanillic acid inc. (dopamine breakdown) in urine
Bombesin +(tumor marker)
N-myc
Less likely to get HTN

Front 21

What is the histology of neuroblastoma?

Back 21

Rossettes and classic, small round/blue nuclei

Dark tumor cells around a pale neurofibril (seen in neuronal blastomas ie. Medulloblastoma, retinoblastoma, neuroblastoma)

Front 22

What is the tumor marker for Neural Crest?

Back 22

S-100, also used in Langerhan cell histocytosis (mesoderm origin, monocyte)

Front 23

What is the Cancer with a rule of 10?

Back 23

Pheochromocytoma (most common adrenal adult, NC origin, chromaffin cells)

Malignant, bilateral, extra-adrenal, calcify, kids

Front 24

What is a pheochromo associated with?

Back 24

MEN 2A/B, vHL


5 Ps
blood Pressue
Pain (HA)
Perspiration
Palpitations
Pallor

increased vanillomalonic acid in urine

Front 25

What are the findings in Hyper and hypo thyroidism

Back 25

Hypo:
Cold, weight gain, fatigue, constipated, DEC REFLEXES, dry, cool skin with brittle hair, low HR/dyspnea
HYPERcholesterolemia (dec. LDL R expression)
High TSH/low T3/4

Hyper:
Heat intolerance, weight loss, hyperactive, diarrhea, INCREASE reflexesm pretibial myxedema (graves), warm moist skin
ARRYTHMIA (elderly pts)
HYPOcholesterolemia
high T3/4, low TSH

Front 26

Findings Hashimotos

Back 26

AntiTPO, thyroglobulin
Hurthle cells (red follicle cells, granular), lymphoid aggregates with germinal centers (increased risk NHL), contender thyroid, atrophic follicles

Front 27

Cretinism

Back 27

6 P's
Pot bellied, Pale, Puffy Face, Protruding umbilicus, Protruding tongue, Poor brain development, Poor Brain development=retarded

most likely small, poor bone growth

Front 28

Findings Subacute De Quervain Thyroditis

Back 28

Inflammed thyroid post flu like illness
Ganulomatous inflammation
Inc. ESR, jaw pain, painful thyroid

Signs of hypothyroid (may show hyper early due to release of colloid from destroyed cells)

Front 29

What is thyroid storm?

Back 29

Sudden release of catacholamines with someone who has hyperthyroid (which increase the the sensitivity to the catacholamines)

Present with Arrythmia, hyperthermia, vomitting, diarrhea, shock (hypovalemic),delirium, coma, inc. HR

Tx: give Steroids (prednisone) Propylthiourical, Propanolol (3 Ps)

Front 30

What is associated with Papillary carcinoma of the thyroid?

Back 30

Orphan annie eye, empty nuclei (annie wants a papi)
Psammoma bodies
Nuclear grooves (coffee beans)
RET/BRAF
Irradiation as a kid

Front 31

What is associated with Follicular Carcinoma/

Back 31

Carcinoma spread past capsule (vs. Adenoma)
Hematogenos spread
good prognosis tho

Front 32

What is ass. with Medullary carcinoma?

Back 32

Parafollicular C cells (NC origin, S-100+)
Make calcitonin- Amyloid stroma with sheets of cells
MEN 2A/B (RET)

Front 33

What are the sings of Psuedohypoparathyroidism?

Back 33

Kidney doesn't respond to PTH (lose Calcium- Receptor abnormality)
Hypocalcemia and tetany
Auto dominant
Short 4/5th digits
Short stature

Front 34

What is the outcome of Sheehan syndrome? Empty Sella Syndrom?

Back 34

Sheehan is an ischemic infart to pituitary following postpartum bleed (pituitary is twice the size in pregnancy but not twice the flow= susceptible to ischemia)

Empty Sella= atrophy of pituitary due to compression, can be due to obesity in women

Both lead to hypopituitarism
Tx: replace the lost hormones

Front 35

What happens in Putuitary Apoplexy?

Back 35

Acute Bleed into an existing adenoma-> cadio collapse from a decrease in ACTH (lack of cortisol and Alpha receptors response) dec. cortisol and adrenal gland (secondary hypo adrenal)

Front 36

What are the bad outcomes for DM 1 and DM 2?

Back 36

DM 1= DKA
DM 2= Hyperosmolar coma

Front 37

What will the eye of a diabetic look like?

Back 37

Retinopathy of NEG
Hemorrhage, exudates, microaneurysms, vessel proliferation

due to osmotic damage to pericytes (microaneurysms) hemorrhages and macular edema

Front 38

What will you see in carcinoid syndrome?

Back 38

Flushing (dilation)
Diarrhea (increased motility)
Right side Valve damage- murmur
Bronchoconstriction- wheezing

increased 5-HIAA (hydroxyindoleacetic acid), niacin deficiency (decreased tryptophan from making serotonin) leads to pellegra= Diarrhea, dementia, dermatitis

tx: somatostatin (octreotide) or resection