Step 1 Endo

Front 1

what does each layer make?
1) Glomerulosa
2) Fasiculata
3) Reticularis
4) Medulla

Back 1

1) aldo
2) Cortisol (can make sex hormones too)
3) androgen
4) Catecholamines (NEURAL CREST ORIGIN for the chromaffin cells)

Front 2

What is the adenhypophysis derived from

Back 2

Oral ectoderm (rathkes pouch - choriocarcinoma, rathkes pouch cyst)

Front 3

Where do the islets arise from?

Back 3

Pancreatic buds

Front 4

Where are alpha and beta islet cells located within the islet

Back 4

Glucagon - peripheral
Insulin - central

Front 5

What are the 6 anabolic effects of insulin?

Back 5

1) inc glucose transport
2) Inc glycogen synthesis and storage
3) inc triglyceride syn and storage
4) inc na retention
5) inc prot syn
6) inc cellular uptake of K and aa

Front 6

Where are the following transporters found?
1) GLUT 1
2) GLUT 2
3) GLUT 3
4) GLUT 4

Back 6

1) RBCs and Brain
2) Bidirectional - Liver, and B iselt cell, kidney and SI
3) Placenta, brain, kidney
4) mucle and adipose (insulin responsive)

** These channels do facilitated diffusion, they prefer D isomers,

Front 7

What mediator decreases GH and TSH secretion?

Back 7

Somatostatin

Front 8

TRH increases the secretion of what two horomones?

Back 8

TSH and PRL

Front 9

Prolactin increases release of what regulatory hormone

Back 9

DA

Front 10

What is the enzyme deficiency? Symptoms: Hypotenion, hyperkalemia, inc PRA, volume depletion. Masculinization, female pseudohermaphroditism

Back 10

This is CAH with a 21 alpha hydroxylase deficiency you would also see a bulid up of 17 hydroxyprogesterone, and progesterone

Front 11

What is the enzyme deficiency: Hypertension, hypokalemia...XY - pseduohermaphroditis external female, no internal repro orgs due to MIF, XX - eternal femal with normal insides but no secondary sex char

Back 11

CAH deficiency in 17 alpha hydroxylase no sex hormones or cortisol...lots of aldo

Front 12

Whats the enzyme deficiency? Hypertension, masculinization see and increase in 11deoxycorticosterone and 11 deoxycortisol,

Back 12

11 beta hydroxylase (CAH)

Front 13

What are the five functions of cortisol?

Back 13

1) Maintains BP (permissive with epi, upregs a1 receptors on arterioles)
2) dec bone formation
3) anti inflamm
4) dec immune function
5) inc gluconeogenesis, lipolysis, proteolysis

* exogenous corticosteriods can cause an increase in serum PMNs due to demarginalization

Front 14

Where in the kidney does PTH inc reabsorption of calcium

Back 14

DCT

Front 15

What two ions alter PTH secretion

Back 15

Mg (dec causes dec pth) causes: alco abuse, diarrhea, aminoglycosides, diuretic
Ca (dec cause inc)

Front 16

How does PTH cause inc bone reabsorp

Back 16

Cause inc production of M-CSF and RANKL in OBs that stimbulates OCs

Front 17

what enzyme does phosphate inhibit (in ca homeostasis)

Back 17

1 alpha hydroxylase

Front 18

What hormones use cAMP
"Flat Champ"

Back 18

FSH, LH, ACTH, TSH CRH, HcG, ADH (V2), MSH, PTH, GHRH, Calcitonin, GLUCAGON

Front 19

What hormones use cGMP

Back 19

NO (aka EDGF), ANP
Vasodilators

Front 20

What hormones use IP3

Back 20

GnRH, OCT, ADH (V1), TRH

Front 21

What hormones use steriod receptors
1) cytosolic
2) nucelar

Back 21

1) Vit D, cortisol, aldosterone, Estrogen, Testosterone, Progesterone,
2) T3/T4

Front 22

Which hormones use intrinsic typrosine kinase receptors
(mapk pathway)

Back 22

Insulin, IGF-1 , FGF, PDGF

** The insulin Y kinase phosphorylates insulin response substrates and activates them, things that P serine residues on the same targets will block the effects of insulin. TNF alpha is a serine kinase.

Front 23

Which hormones use receptor associated tyrosine kindases
(jak/stat)

Back 23

GH, PRL, IL2

Front 24

In men what does increased levels of sex hormone binding globulin do?

Back 24

It lowers free testosterone --> gynectomastia

Front 25

In women what does decreased SHBG do?

Back 25

Raises free testosterone --> hirsutism (think menopause - dec estrogen --> dec binding globins from liver --> hirsutism in menopause)

Front 26

Where is most t3 formed

Back 26

Blood

Front 27

what are the 5 functions of thyroid homrone

Back 27

1) Bone growth (synergistic with GH)
2) CNS maturation (think cretenism)
3) inc B1 receptors in the heart
4) inc BMR via inc na/k transporter activity
5) inc glycogenolysis, gluconeogenesis, lipolysis

Front 28

what decreases TBG and what increases it

Back 28

Dec - liver failure
Inc - Pregnancy and OCP (free t4 will be the same, total T4 will increase)

Front 29

What are the three functions of thyroid peroxidase

Back 29

Oxidation and organifiation of iodide, as well as coupling of MIT and DIT

Front 30

What cell makes thyroglobulin? What hormone increases its production?

Back 30

Thyroid epithelium, TSH

Front 31

#1 cause of cushings syndrome

Back 31

Exogenous (iatrogenic) steroids

Front 32

What is cushings DISEASE

Back 32

due to ACTJ secretion from a pituitary adenoma (inc ACTH)

Front 33

What type of cushings does not respond to dexamethasone suppression at high or low doses

Back 33

Ectopic CTH (small cell lung cacer, bronchial carcinoids

Front 34

Endogenous causes of Cushings (3)

Back 34

1) cushings disease (pituitary will respond to high dose of dex)
2) ectopic ACTH
3) adeoma (dec acth)

Front 35

What are the S/Sx of Conn syndrome

Back 35

Hyperaldosteronism: Hypokalemia (muscle weakness, parasthesia, acidosis (transcellular shift)) low plasma renin, hypertension...aldo secreting tumor. Can be bi or unilateral.
**Hypernatremia is rare due to aldo escape

Front 36

What hormone is responsible for the aldosterone escape in conns

Back 36

ANP (promotes naturiesis)

Front 37

What are the S/Sx of Addisons disease?

Back 37

Def of aldo and cortisol causing hypotension, hyperkalemia, acidosis, skin hyperpigmentation,, involves all 3 cortical divisions but spares the medulla. Secondary adrenal insufficiency should have dec pituaitary acth prouction and should have no skin hyperpigmention or hyperkalemia

Front 38

What happens in adrenal crisis

Back 38

You get hypotension, tachycardia, hypoglycemia in someone with a history consistent with adrenal insufficiency (see vomiting abd pain, weight loss, and hyperpigmentation)

Front 39

What are causes of addisons

Back 39

Autoimmune destruction of the adrenal, TB, metastasis, Waterhouse-fridreichsen

Front 40

What are the three components of a craniopharyngioma (grossly)

Back 40

Solid (actual cells), filled with a machinery oil like liquid, and calicifications. Tumor of rathkes pouch(oral ectoderm)

Front 41

What do most Pheochromocytomas secrete

Back 41

NE, Epi, and DA see and increase in urinary VMA, and elevated plasma catecholamines

Front 42

What is the treatment for Pheo

Back 42

a1 block followed by surgery....I remember they said you could use a BB after a1 but first aid only mentions the alpha block. SHould use phenoxybenzamine (irreverse) but can use phentoamine (revers)

Front 43

what are the 5 ps of episodic symtoms of pheo?

Back 43

Pressure (^ bp)
Pain (HA)
Perspiration
Palpitations (tachy)
Pallor

Front 44

What is the most common tumor of the adrenal medulla in children? What is the Urine marker for it?

Back 44

Neuroblastoma, HVA. Due to urine overexpression of N-myc

Front 45

What are the break down products of DA, NE, and Epi

Back 45

HVA, VMA, Metanephrine

Front 46

Constipation, dec reflexes and nyxedema (facia/periorbital) are seen in what thyroid disorder?

Back 46

hypothyroidism

Front 47

How do you treat radiation poinsoning

Back 47

KI, perchlorate they use the same transporter as Radioactive I so they competitively inhibit one another

Front 48

What is the antibody seen in hashimotos

Back 48

Anti-thyroglobulin

Front 49

What is the HLA association with Hashimotos?

Back 49

HLA DR5 (also pernicious anemia)

Front 50

What is the histo finding in hashimotos

Back 50

Hurthle cells lymphocytic infilatrate with germinal centers

Front 51

What are the s/sx of cretinism

Back 51

Pot belly, pale, puffy face kid with protruding umbilicus and protuberant tongue (also MR, and I think growth retarded)

Front 52

Subacute thyroiditis s/sx

Back 52

Painful thryoid, granulomatous inflamm

Front 53

What is the etiology of riedels thyroiditis

Back 53

Thyroid replaced by fibrous tissue

Front 54

Why type of hypersensitivity is Graves

Back 54

II

Front 55

Thyrotoxicosis

Back 55

Catecholamine surge leadsto death by arrhythmia (Inc thyroid increases the B receptors if you surge the epi then you will get over stimulation!) Can tx wtih B blockers

Front 56

What symptom of graves will not resolve with BB

Back 56

Exopthalmos

Front 57

What is the pathophys of toxic multinodular goiter

Back 57

Focal patches of Hyperfunctioning follicular cells working indp of TSH due to a mutation of the TSH recepto. ***Hot nodules are rarely malignant

Front 58

What is the jod basedow phenomenon

Back 58

Thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete

Front 59

Most common thyroid tumor? What are the histo signs?

Back 59

Papillary carinoma...Ground glass nuclei (orphan annie) psammoma bodies, inc risk with childhood irradiation.

Front 60

What thyroid cancer has uniform follicles

Back 60

Follicular (dur) you cannot diagnose this by cytology (IF?)

Front 61

What thyroid carcinoma originates from C cells? What are the histo signs?

Back 61

Medullary, makes calcitonin, sheets of cells in amyloid stroma. Assoc w/ Men 2a and 2b (ret gene muts)

Front 62

What thyroid cancer has a very poor prognosis?

Back 62

Undifferentiated/anaplastic (often see n in the elderly)

Front 63

What thyroid cancer is associated with hashimotos

Back 63

Lymphoma

Front 64

Whats the common cause of primary hyperparathyroidism

Back 64

Adenoma

Front 65

What is osteitis fibrosa cystica

Back 65

Cystic bone spaces filled with brown fibrous tissue (chronically elevated PTH)

Front 66

What is renal osteodystrophy

Back 66

Bone lesions due to 2 or 3 hyperparathyroidism due in turn to renal disease.

Front 67

What is the cause of tertiary hyperparathyroidism

Back 67

Refractory hyperparathyroidism resulting form chrnic renal disease - see inc PTH inc CA

Front 68

What are the labs in secondary Hyperparathyroidism

Back 68

Inc PTH, hypocalcemia, hypophos, this is due to hypovitaminosis D

Front 69

Causes of hypoparathyroidsim

Back 69

accidental surgical excision, AI destruction, or digeorge

Front 70

Pseudohypoparathyroidism

Back 70

Albrights hereditary osteodystrophy - autodom kidney unresponsiveness to PTH, hypocalc shortened 4th and 5th digits, short stature

Front 71

Whats is chvosteks sign and what does it suggest

Back 71

Tapping of facial nerve = contraction of facial muscles sign of hypocalcemia

Front 72

how do you treat a prolactinoma

Back 72

Bromocriptine or cabergoline (DA agonists)

Front 73

What happens to the glucose in acromegaly

Back 73

Impaired glucose tolerance (insulin resistance)

Front 74

Tx for acromegaly

Back 74

resection followed by octreotide

Front 75

What are some causes of central DI

Back 75

Trauma, pit tumor, surgery, or histiocytosis X

Front 76

What are some causes of nephrogenic DI

Back 76

Hereditary, hypercalcemia, lithium,demeclocycline (ADH antag), hypokalemia (mostly cAMP inhibition is the key)

Front 77

What are the urine osm and spec gravity for DI

Back 77

<1.006, and >290

Front 78

How do you treat central and peripheral DI

Back 78

1) central - intranasal desmopressin
2) peripheral - HCTZ, indomethacin, amiloride (esp good for Li tox)

Front 79

What are the signs of SIADH

Back 79

excessive water retention, hyponatremia, urine osmolarity>serum osm...Body responds with dec aldo (hyponat) to maintain near normal vol status. Very low serum sodium levels can lead to seizure

Front 80

How do you treat SIADH

Back 80

Demeclocyline or H2O restriction

Front 81

What are some causes of SIADH

Back 81

Small cell lung cancer, CNS disorders/head trauma, pulmonary disease, drugs (CYCLOPHOSPHAMIDE)

Front 82

What are the acute manifestations of DM1 and DM2

Back 82

DM1 - DKA
DM2 - hyperosmolar coma (inc hemoconcentration and volume depletion, don't see elevated ketones) Ketosis is absent bc there is insulin inhibiting lipolysis

** Presence of unopposed secretion of GH and epi can exacerbate hyperglycemia

Front 83

what are the HLA association in DM1

Back 83

DR3 and DR4

Front 84

In what condition do you see amyloid deposits in the B islets

Back 84

DM2, not seen in one

Front 85

What are the S/Sx of DKA

Back 85

Kussmaul resp (rapid deep breathing due to reflex response of the chemo receptors to acidosis), N/V, abd pain, psychosis/delirium, fruity breath. Hyperkalemia but there is depleted intracellular K due to transcellular shift from dec insulin (BE CAREFUL WHEN GIVING INSULIN WATCH K)

Front 86

S/SX of carcinoid syndrome

Back 86

Diarrhea, cutaneous flushing, asthmatic wheezing, and right sided valvular dz, most common tumor of the appendix!!!!!!!!!!!!!!

Front 87

Men 1 characteristics

Back 87

Parathyroid tumors
Pituitary tumor (PRL or GH)
Pancreatic endocrine (ZE, vipoma, glucagonoma)

Front 88

Men 2A

Back 88

Parathyroid, Pheochromocytoma, Medullary thyroid

Front 89

Men 2B

Back 89

Pheo, Medullary thyroid, Marfainoid habius and ORAL/INTESTINGAL GANGLIONEUROMATOSIS (flesh colored nodules)

Front 90

What are the signs and symptoms of zollinger ellison

Back 90

Stomach shows rugal thickening with acid hypersecretion. Causes recurrent ulcers - may be associated wtih MEN I