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First Aid Diseases > Endo > Flashcards

Endo Flashcards

1
Q

Most common tumor of ad med in kids?

- can it cause episodic HTN?

A

Neuroblastoma

- No, but a pheo in adults can

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2
Q

Post pit:

  • derived from?
  • how to hormones get to it?
A
  • neuroectoderm

- via neurophysins (carrier pr’s), from the hypo

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3
Q

Ant pit is derived from?

  • a-subunit of hormone is same in?
  • which hormones are acidophils?
  • which are basophils?
  • what are the hormones it secretes?
A

Oral ectoderm (Rathke’s pouch)

  • TSH, LH, FSH, hCG
  • GH, PRL
  • B-FLAT: Baso’s-FSH, LH, ACTH, TSH
  • FLAT PiG: FSH, LH, ACTH, TSH, GH, PRL
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4
Q

Islet of Langerhans in panc contain what 3 cells? which make what?

A

a-cells: glucagon (on periph)
b-cells: insulin (centrally located)
gamma-cells: somatostatin (interspersed)

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5
Q

How does Glc stim insulin release?

A

Glc metab’n -> ATP which closes K+ ch’s and depol’s b-cell mem -> opens V-gated Ca ch’s -> Ca influx stim’s exocytosis of insulin granules

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6
Q

Which body parts don’t need insulin to take up Glc?

- GLUT-1, 2, 4 =

A

BRICK L: Brain, RBCs, Intestine, Cornea, Kidney, Liver

  • 1=insulin indepen. (RBCs, brain)
  • 2=bidirec (b-cells, liver, kidney, smI)
  • 4=insulin dep (adipose, SkM)
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7
Q

How do these affect insulin release:

  • high Glc
  • somatostatin
  • b2-agonists
  • GH
  • a2-agonists
A
  • incr insulin
  • decr
  • incr
  • incr (bc incr’s insulin resistance)
  • decr
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8
Q

What 2 paths does insulin binding its R take?

A

1) TK phos’n -> PI3-kinase pthwy -> GLUT-4 to surface, also syn of glycogen, lipids and pr
2) RAS/MAP kinase pthwy -> cell growth, DNA syn

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9
Q

Somatostatin inhib’s which 2 hormones?

A

TSH and GH release from ant pit

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10
Q

PRL

  • stim’d by?
  • inhib’d by?
A
  • TRH

- DA from hypo, PRL also stim’s DA -> less PRL

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11
Q

GH

  • works thr?
  • secretion stim’d by? inhib’d by?
A
  • IGF-1/somatomedin secretion

- exercise and sleep; glc and somatostatin

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12
Q

17a-hydroxylase defic =

XY and XX effects?

A

Can only make mcc’s -> HTN and hypoK
XY: decr’d DHT -> pseudohermaph.
XX: nl F but no 2* sex charac’s

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13
Q

3 types of congenital bilat ad hyperplasia?

A

17a-hydroxylase defic (only mcc’s)
21-hydroxylase defic (only androgens) (most common)
11b-hydroxylase defic (androgens + 11-deoxycorticosterone)

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14
Q

21-hydroxylase defic =

- in Females?

A

Can only make androgens -> hypotension, hyperK, incr’d RAAS, vol depletion
- masculinization -> pseudohermaph

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15
Q

11b-hydroxylase defic =

- in Females?

A

Can only make androgens, 1 step further than 21-hydrox though so do make 11-deoxycorticosterone
- HTN from 11-deoxycorticosterone (mcc) and masculinization

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16
Q

Cortisol

  • functions?
  • get striae from?
A

BBIIG = BP (upreg’s a1Rs so incr’s sensitivity on vessels), decr’s Bone formation, anti-Inflamm/Immsupp’ive, Insulin resistance (diabetogenic), Gluconeogenesis (also lipolysis and proteolysis)
- inhib’s fibrobl’s

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17
Q

PTH

  • effect on Ca and phos
  • effect on VitD
  • how do Ca and Mg affect its release? what about phosphate?
A
  • incr bone resorption of them, incr Ca reab’n in DCT, decr phos reab’n in PT (phos trashing hormone!)
  • incr 1,25-(OH)2D (calcitriol) prod in kidney by stim’ing 1a-hydroxylase
  • decr’d Ca/Mg incr’s PTH, but very decr’d Mg decr’s PTH; incr’d phos -> incr’d PTH, decr’d phos -> decr’d PTH
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18
Q

Get decr’d Mg from?

- effect on PTH?

A

D, aminoglycosides, diuretics, EtOH abuse

- incr’d PTH secretion, unless it’s really low then it decr’s PTH

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19
Q

1,25-(OH)2 D3

  • made where?
  • stim’d by?
  • actions?
A
  • kidney
  • low phosphate or Ca and high PTH upreg the NZ that makes it
  • incr’s ab’n of dietary Ca and PO4 in GI, incr’s bone resorption of Ca and PO4
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20
Q

Calcitonin

  • func
  • stim’d by
A

decr bone resorption of Ca (opposes actions of PTH) [incr’s bone mineralization]
- incr’d serum Ca (not imp in nl Ca homeostasis)

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21
Q

Which hormones act via cAMP?

Which act via cGMP?

A
  • FLAT ChAMP: FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2 R), MSH, PTH + calcitonin, GHRH, glucagon
  • Vasodilators: ANP, NO (EDRF)
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22
Q

Which hormones act via IP3?

A
  • GGOAT: GnRH, GHRH (minor role), Oxytocin, ADH (V1 R), TSH + hist (H1), ATII, gastrin
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23
Q

Which hormones act via a steroid R?

A

VETTT CAP: VitD, Estrogen, Testos, T3/T4, Cortisol, Aldosterone, Progesterone

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24
Q

Which hormones signal thr a intrinsic TK R?

Which hormones have a R-assoc’d TK?

A
  • GFs and MAP kinase pthwy: insulin, IGF-1, FGF, PDGF, EGF

- PIG + JAK/STAT: PRL, Immunomodulators (cytokines IL-2,6,8, IFN), GH

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25
Q

Wolff-Chaikoff effect =

A

excess iodine temp’ly inhib’s thyroid peroxidase -> decr’d iodine organification -> decr’d T3/T4 production

26
Q

T3 functions?

A

4 B’s: Brain maturation, Bone growth, b-adrenergic effects (incr’s b1Rs on heart -> works better and harder), Basal metab rate (incr’s Na/K ATPase so incr’d O2 consump) (also incr’s E by glycogenolysis, gluconeogenesis, lipolysis)

27
Q

TBG incr’s/decr’s when?

  • T4 -> T3 by?
  • which NZ
A

TBG decr’s in hep failure, also w/ anabolic steroids or nephrotic synd (lost in urine) -> more free T3 to work (decr’d total serum T4, but nl FT4 and nl TSH)
TBG incr’s in preg and w/ OCP use (estrogen!) -> less free T3 (more T4 bound to more TBG, but FT4 is still the same even though more T4 overall -> nl TSH)
- 5’-deiodinase in periph

28
Q

How does body keep euvol state in SIADH?

  • If Na gets really low, what happens?
  • What drug can cause SIADH?
A

Decr’d aldos -> decr’d water retention to maintain near-nl vol status

  • seizures
  • cyclophosphamide
29
Q

Craniopharyngioma =

- causes?

A

benign tumor from Rathke’s pouch remnants

- most common cause of hypopit in kids

30
Q

Empty sella synd

  • usu occurs in who?
  • what happens?
A

obese women w/ HTN

- subarachnoid space extends into sella and fills up with CSF -> compresses pit gl

31
Q

Cretinism findings?

A

5Ps: Pot-bellied, Pale, Puffy-faced child w/ Protruding umbilicus and Protuberant tongue

32
Q

Nontender hypothyroidism?
Tender hypothyroid?
Fixed, hard (rock-like) and painless goiter?
Painless thyroiditis?

A
  • Hashimoto’s thyroiditis
  • Subacute thyroiditis (de Quervain’s) (self-limited, post viral illness)
  • Riedel’s thyroiditis (replaced by fibrous tissue)
  • Autoimm, usu post partum w/ no germinal follicles in gland
33
Q

Jod-Basedow phenomenon =

A

thyrotoxicosis if a patient w/ severe iodine defic goiter is made iodine replete

34
Q

Thyroid storm =

- may see incr’d ALP from?

A

stress-induced catecholamine surge -> death by arrhythmia, also high F, shock from V, coma (serious comp of Graves and other hyperthyroid d/o’s)
- incr’d bone turnover

35
Q

Papillary ca of thyroid
- on histo see?
- incr’d risk w/?
Follicular ca of thyroid, on histo see?

A
  • empty-appearing nuc (Orphan Annie’s eyes), psammoma bodies, and nuc grooves
  • childhood radiation
  • uniform follicles
36
Q

Why does resp/metab alkalosis give you tetany?

A

Alkalosis incr’s (-) on alb (H+ leave it) -> binds more Ca2+ -> same serum Ca level but less free Ca (and thus incr’d PTH) -> partial depol of n’s and m’s bc lower threshold potential

37
Q

Effect of PTH on bicarb?

A

Incr’d PTH decr’s bicarb reab’n -> nl anion gap metabolic acidosis (type II RTA)

38
Q

How is VitD act’d?

A

In liver by 25-hydroxylase to 23-(OH)D

Then in kidney by 1a-hydroxylase to 1,25-(OH)2D

39
Q

Why do you get hypoPT from hypoMg?

A

Need Mg as cofactor for cAMP, which need for PTH act’n

40
Q

1* HyperPT

  • Ca, phos, cAMP?
  • sx?
A
  • incr’d Ca, decr’d phos, incr’d urinary cAMP
  • stones (Ca renal stones), bones (osteitis fibrosa cystica: cysts filled w/ brown fibrous tissue), groans (constipation) and moans (psychosis, confusion, anxiety, coma)
41
Q

2* HyperPT

- Ca, phos, alk phos?

A
  • decr’d Ca, incr’d phos if CKD or decr’d if anything else (more PTH, less phos reab’d), incr’d ALP (more bone brkdwn)
42
Q

Renal osteodystrophy =

A

bone lesions from 2/3* hyperPT due to renal dz (no VitD, so low Ca, so incr’d PTH)

43
Q

3* HyperPT =

A

refractory (autonomous) hyperPT from CKD, incr’d PTH even though incr’d Ca

44
Q

HypoPT sx?
PseudohypoPT =
- sx?

A
  • hypoCa, tetany
  • AD kidney unresponsiveness to PTH (mutation in Gs R)
  • hypoCa, short 4/5th digits, short stature
45
Q

Chvostek’s sign =

- sign of?

A

tapping of facial n. -> contraction of facial m’s

- tetany from hypoCa in hypoPT

46
Q

Trousseau’s sign =

- sign of?

A

occlusion of brachial a. w/ BP cuff -> carpal spasm

- tetany from hypoCa in hypoPT

47
Q

HTN, hypoK, metab alkalosis, low pl renin =

A

1* hyperaldosteronism (Conn’s synd)

HTN from incr’d Na, alk from incr’d H+ out, low pl renin bc neg fdbk from high aldos levels

48
Q

HTN, hypoK, metab alkalosis, high pl renin =

A

2* hyperaldos from renal perception of low IV vol -> incr’d RAAS

49
Q

Hypotension, hyperK, metab acidosis =

- also have?

A 
Addison's dz (no aldos nor cortisol)
Low Na (hypotension, high K, high H+ from no aldos to run proton pump
- skin pigmentation
50
Q

Waterhouse-Friderichsen synd =

A

acute 1* ad insuff from bilat ad hemorrhage, usu from N.meningitidis septicemia, DIC and endotoxic shock

51
Q

What do you have to give to a pt before removing a pheo?

A

Irreversible a-blockers (phenoxybenzamine) -> so no HTN crisis
Then b-blockers to slow HR

52
Q

Pheo sx:

A

5Ps: P (high BP), pain (HA and ileus), Perspiration, Palpitations (tachy), Pallor

53
Q

Pheo rule of 10s:

A

10% malg, bilat, extra-ad, calcify, kids

54
Q

Neuroblastoma oncogene?

- what is high in urine?

A

overexp’n of N-myc oncogene assoc’d w/ rapid tumor progression
- HVA (DA brkdwn product)

55
Q

Histo of islet cells in DM type 1 vs. 2?

A

T1DM - islet leukocytic infiltrate

T2DM - islet amyloid (AIAPP) deposit

56
Q

Kussmaul respirations =

- seen in?

A

Rapid and deep breathing

- DKA

57
Q

Sx of DKA?

- trtmt?

A

Kussmal resp’s, N/V, ab pain, psychosis/delirium, dehydration, fruity breath odor (due to exhaled acetone)
- IV fluids and IV insulin, K+ (to replete IC stores), glc if needed to prevent hypoGlc

58
Q

Carcinoid synd, rule of 1/3 = ?

- most common location

A

1/3 met, 1/3 present w/ 2nd malig, 1/3 mult

- appendix

59
Q 
MEN 1 (Wermer's synd) =
- presents w/?
A

PT, pit (PRL or GH) and panc endo tumors (ZES, insulinomas, VIPomas, glucagonomas)
- kidney stones and stomach ulcers (ZES)

60
Q

MEN 2A (Sipple’s synd) =

A

Medullary thyroid ca (calcitonin), pheo, PT tumor

61
Q

MEN 2B =

A

Medullary thyroid ca, pheo and oral/GI ganglioneuromatosis (marfanoid habitus)

First Aid Diseases (16 decks)

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