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LCK STEP > CHAPTER: Endo > Flashcards

CHAPTER: Endo Flashcards

1
Q

Adrenal cortex vs medulla is derived from where

A

Cortex - mesoderm

Medulla - neural crest, makes sense since pre-gang fibers from sympa synapse directly onto medulla

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2
Q

Where are post pit hormones made in the hypothal

A

Supraoptic (ADH) + paraventricular nuclei

Neurophysins to PP

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3
Q

Where is the ant vs post pit + thyroid vs C cells derived from

A

Ant: Rathke pouch of oral ectoderm
Post: neuroectoderm (makes sense!)
Thyroid = endoderm
C cells (parafollicular) = calcitonin = neural crest

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4
Q

Describe cells and layout in the pancreas islet

A

Islet arises from pancreatic bud (embryo)
B = central = insulin
A = peripheral = glucagon
Delta = interspersed = SS

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5
Q

What is the 1 insulin dependent GLUT transporter vs the 4 insulin indep - what tissues are they in

A

Dep: GLUT 4
Insulin + R (tyrosine kinase) -> move GLUT4 to membrane of fat, skeletal muscle
Indep:
GLUT1 - RBC, brain, cornea, placenta
GLUT 2 - B cells islets, liver, kidney, SI
GLUT 3 - brain, placenta
GLUT5 - fructose - spermatocytes, GI
BRICK L = insulin indep glucose uptake
Brain, RBC, intestine, cornea, kidney, liver
RBC = no mito, only use ketones as E source
Brain prefers glucose, but uses ketones during fasting

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6
Q

Fxns PRL

A
  1. Milk production (oxytocin for milk letdown)
  2. X GnRH - X ovulation - makes sense, already thinks your preggo
  3. X spermatogenesis (less libido)
    E increases PRL release in preggo (OCP - why boobs get big)
    Renal failure may get hyperPRL b/c decreased excretion
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7
Q

How does the TRH affect PRL

A

TRH ↑PRL secretion
If dopamine is the off switch for prolaction, TRH is the on! PRL inhibits its own secretion by ↑dopamine synthesis
If TRH builds up in 1ary or 2ary hypoT -> may get prolactin symptoms

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8
Q

How does GH work - what increases and decreases its secretion

A

Via insulin like growth factor 1 IGF1 = analog of somatostatin (somatomedin C)
Released in pulses in response to GHRH
-FB via glucose + somatostatin (now this makes sense!)

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9
Q

Where do endocannabinoids bind in the brain

A

Hypothalamus + nucleus accumbens - areas of appetite regulation

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10
Q

Name receptors at which ADH changes serum osm vs BP

A

V2 for serum osm via aquaporin insertion into CD
Also increases passive urea transporters = moves urea down concentration into medulla -> pulls more water with it (major part of ADH free water mechanism)
V1 for BP

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11
Q

Describe what you get w/ 17 alpha, 11 beta, and 21 OH deficiencies in the adrenals

A

17 = moves across, so only aldo made = high BP, no cortisol, no sex -> M have ambiguous genitalia, undescended testes, W lack 2ary sexual development
21 = down, only sex hormones made
1. Na wasting
2. Early puberty, W virilized
11 = one step further than 21 - get weak aldo made so 21 def w/o Na wasting

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12
Q

Where/how does aromatase vs 5 alpha reductase work

A

Aromotase converts androstenedione and T -> E

5 alpha reductase converts T -> DHT

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13
Q

Mechanism by which cortisol increases BP

A

Increases alpha 1 R -> increased response to NE

Vasoconstrict arteries

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14
Q

Name effects of cortisol: BIG FIB

A

BP up
Insulin resistance up - pro diabetes
Gluconeo, lipolysis up
Fibroblast activity down - why get striae
Inflam/Immune response down (taking exog CS ↓IL2 ↑ing risk of TB + candida infection)
Blasts (osetoblasts) down = less bone formation
Ways cortisol decreases immune:
1. X LT/PG synthesis
2. X histamine release from mast cells
3. X IL 2 for T cell maturation

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15
Q

How does more basic blood pH affect Pca

A

Basic = albumin binds Ca more = hypoCa symptoms

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16
Q

How does Mg effect PTH levels: changes with diarrhea, aminoglycosides, diuretics, alcoholism

A 
↓Mg = ↑PTH
↓↓Mg = ↓PTH 
Causes of ↓Mg: 
Diarrhea
AminoG 
Diuretics 
Alc abuse
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17
Q

Name all the hormones that signal through cAMP receptors: FLAT ChAMP

A 
Gs -> AC -> ↑cAMP -> ↑PKA
FSH
LH
ACTH
TSH
CRH
hCG
ADH - V2
MSH
PTH
Calcitonin, GHRH, glucagon
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18
Q

Name all the hormones that signal through cGMP pathways: BAD GraMPa

A

R w/ CG -> ↑cGMP -> ↑PKG
BNP
ANP
EDRF = NO

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19
Q

Name all the hormones that signal through IP3 pathway: GOAT HAG

A 
Gq -> PLC -> DAG + IP3 = ↑Ca 2+ release ER
GnRH
Oxytocin
ADH - V1
Histamine
AGT 2
Gastrin
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20
Q

Name all the hormones that have intracellular receptors (+/- DNA binding) PET CAT on TV

A 
Prog
Estrogen
T
Cortisol - only active as a dimer
Aldo
T3
T4
Vit D
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21
Q

Name all the hormones that signal through receptor tyrosine kinases aka the MAP kinase pathway

A 
Tyrosine kinases autophos itself then kicks off phos cascade = MAP kinase 
Think growth factors:
Insulin
IGF 1
FGF
PDGF
ECF
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22
Q

Name all the hormones that use the JAK/STAT pathway: PIGGlET

A

JAK STAT = goes into nucleus to act as TF
Prolactin
Immunomodulators: cytokines, IL 2, IL 6, IFN
GH
G CSF
EPO
Thrombopoietin

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23
Q

Treat prolactinoma

A

Dopamine agonist to shrink tumor before surgery
Bromocriptine
Cabergoline

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24
Q

Meds for GH tumor

A

Octreotide = SS analog

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25
Q

Treat SIADH

A

+Na tablet/IV saline
H2O restriction
ADH blocker: vaptans
ADH antag: demeclocycline

26
Q

Treat Graves

A

BB

Thioamide = X peroxide synthesis steps in colloid

27
Q

Thyroid storm meds

A 
4 Ps
Propranolol
Propylthiouracil - X peroxide TH syn steps
Prednisone 
Potassium iodide
28
Q

Treat pheo

A

A antag = phenoxybenzamine

Then BB

29
Q

How does glucose ↑B cell sensitivity? How does TNFa, glucagon, and E cause insulin resistance?

A

PO or IV glucose - ↑GLP1 (incretin) -> ↑B cell sensitivity to glucose -> ↑insulin
TNFa, glucagon, E all has serine kinase activity which blocks the down stream phosphorylation actions of the insulin R

30
Q

Where does PTH cause phos trashing in the nephron

A

PCT ↓P reabsorb

31
Q

4 Bs of TH fxn

A
  1. Bone growth - works with GH
  2. Brain maturation
  3. ↑B1 R @ heart
  4. ↑BMR via ↑Na/K ATPase - ↑O2 consumption, RR, body temp, glycogenolysis, gluconeo, lipolysis
32
Q

Cause of familial hypoCa-uric hyperCa-emia

A

Ca sensing R = GCPR
Defective @ PT + kidneys - always see low Ca - excess reabsorption
ADom

33
Q

What is Addison’s disease

A

Chronic 1ary adrenal insuff - aka intrinsic adrenal problem
Both acute + chronic forms of 1ary will present with skin + mucosal pigmentation
No -FB = ↑POMT -> ↑ACTH + MSH

34
Q

Why are aldosertone levels normal in 2ary or 3ary adrenal insuff?

A

B/c aldo indep regulated via RAAS
2ary = ↓ACTH
3ary = fast withdraw from exog steroids

35
Q

Pts with hyper aldo don’t have edema - why?

A

HTN w/ ↓K + metabolic acidosis
No edema b/c initial ↑BV -> ↑ANP -> diuresis
“Aldosterone escape”

36
Q 
Neuroblastoma
What kind of tumor/mutation
Age group
PE findings
Presentation
Histo
Labs
A

Adrenal medulla (neural crest) tumor of kids
N-myc = oncogene overexpressed
Irreg mass that can cross midline (vs Wilms tumor also ab mass in a kid but unilat)
Present: “dancing eyes + feet” - opsoclonus myoclonus
↑HVA, VMA in urine
HW rosettes, + for Bombesin and NSE

37
Q

Pheo is a adrenal medulla tumor of what cells - most common ectopic site of a pheo

A

Chromaffin cells = neuroendo cells of the adrenal medulla

Bladder wall

38
Q

What are the 2 precurosors and enzyme that break them down to produce VMA

A

E -> metanephrines
NE -> nor-meta
Broken down by MAO -> VMA

39
Q

Describe reflexes, type of muscle weakness, and myxedema and cholesterol status in hypo vs hyperT

A

Hypo: ↓reflexes, prox muscle weakness w/ ↑CK, facial + peri-orbital myx, ↑cholesterol b/c ↓LDL R
Hyper: ↑reflexes, prox muscle weak w/ NORMAL CK, pre-tib + periorbital myx, hypochol b/c ↑LDL R

40
Q

Causes of enlarged thyroid presenting as hypoT that are painful (2) vs non-painful (1)

A

Painful
1. Subacute granulomatous thyroid = post viral infection, also ↑ESR + jaw pain
2. Riedel = fibrotic thyroiditis = rock hard
Nonpainful = Hashimoto

41
Q

Histo + cancer risk Hashimoto

A 
Histo:
1. Hurthle cells = eos cells that line follicles 
2. Germinal centers 
3. Lymphocytic infiltrate... duh
↑risk non-Hod lymphoma thyroid cancer
42
Q

What is toxic mulitnod goiter

A

Focal patches of hyperfxning follicular cells in the thyroid

Hot nodules rarely malig

43
Q

What happens if you quickly replace I in an I deplete person?

A

HyperT

Can also happen if you give I to a person with autonomous thryoid tissue

44
Q

Histo thyroid adenoma

A

Follicular

45
Q

4 types thyroid cancer + histo

A
  1. Papillary - OA eyes, psammoma, nuclear grooves. RET/BRAF mutations. Met via LNs
  2. Follicular - RAS mut, spread through blood (unusual for carcinoma)
  3. Medullary - RET mut - MEN 2A + B, from C cells: ↑calcitonin (↓Pca) “sheets of cells in amyloid stroma”
  4. Anaplastic = “pleomorphic cells w/ irreg giant cells + biphasic spindle cells”
46
Q

Why ↑alk phos w/ ↑PTH?

A

B/c PTH binds blasts - ↑RANKL to bind RANK on clasts

47
Q

State that would have ↑Pca w/ ↓PTH

A

Squamous cell LC - ↑PTrP

48
Q

2 types of hypoPT related to kidney being unresponsive to PTH - name mutation + inheritance patterns + presentation

A

Defect receptor = Gs alpha subunit (kidney resistance to PTH)
Short kid w/ short ring finger + thumb
↓Pca + phos (same thing as having X PTH)
Pseudo - inherited from mom
Pseudo-pseudo = inherited from dad - weird b/c same physical exam findings but not PTH resistance at the kidney

49
Q

Which cause of hyperPT presents with osteitis fibrosa cystica vs renal osteodystrophy

A

1ary hyperPT = hyperCa = osteitis
Cysts in bone filled with brown fibrous tissue (brown tumor of bone”
2ary or 3ary hyperPT = renal disease aka no active vit D = hypoCa = renal osteodystrophy

50
Q

What do you suspect if a patient presents with hyperpig, headache, and bitemp hemianopia after you removed both adrenals for refractory Cushings?

A

The cause of Cushings was a ACTH secreting pit adenoma

You’ve removed the ↑cortisol = no -FB = tumor grows

51
Q

Risk of cancer in acromegaly

A

CR polyps + cancer

52
Q

What is the difference between Laron dwarfism and acondroplasia

A

Laron = X GH R = small head
↑GH but ↓IGF 1
Acromeg = FGF-R mut = large head

53
Q

What is the volume status of SIADH pts // why aren’t they edematous?

A

↑BV -> ↑ANP/BNP -> ↑Na secreted into urine
Normalized blood vol
But makes you HYPOna - worry cerebral edema (water into higher oncotic area)
Euvolemic hypoNa - correct slowly to prevent pons demyelin

54
Q

If a pt presents with sudden onset headache, vision changes, and hypopit features - what are you thinking?

A

Sudden hemm of pit gland (probs pre-exist pit adenoma)

55
Q

What hormone doesn’t drop immediately in Sheehan syndrome?

A

T - existing T4/3 in circulation

Everything else, including PRL drops immediately

56
Q

2 diabetes symptoms due to osmotic damage (sorbitol b/c aldose reductase)

A

Neuropathy

Cataracts

57
Q

Why do diabetics present with nephrotic syndrome?

A

Non-E glycos preferentially thickens efferent art
↑GFR -> microalbuminuria = 1st sign renal damage
Why needs to prescribe ACE - ↓AGT2 = dilate efferent

58
Q

Histo of islet cells in T1 vs T2 diabetes

A 
T1 = leukocyte infiltrate "inflammed"
T2 = amylin (amyloid from insulin)
59
Q

Presentation of a glucagonoma

A 
Dermatitis - necrolytic migratory erythema
Diabetes
DVT
Declining weight
Depression
60
Q

Presentation of somatostatinoma

A

Diabetes
Steatorrhea
Gallstones
↓s insulin, gastrin, CCK, secretin

61
Q

You know the 3 Ps of MEN1 but what does each one present as

A

Menin (tumor supp) chr 11 mut (MEN1)
Pit tumor - prolactinoma, GH-oma
Pancreas - ZE, insulinoma, VIPoma, glucagonoma (rare)
PT adenoma - 1ary hyperPT

LCK STEP (27 decks)

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