Shit - Endo Flashcards
MSH
from intermediate lobe of AP
AP vs PP origins
AP = oral ectoderm PP = neuroectoderm
Increase C-peptide via
Insulinoma
Sulfonyluras (chlorpromazine, tolbutamide, Glimeperide, glipizide, glyburide)
insulin effects on the kidney:
increase Na+ resorption
Insulin-independent glucose transporters:
1 = brain, RBC, cornea 2 = liver, panc, kidney, GIT 3 = brain, placenta, neurons 5 = fructose @ spermatocytes, GIT
Adrenergics on insulin release
a2 = decrease insulin release (stronger) (b2 = increase insulin release)
Effect of drugs that open K+ channels (diazoxide) or cause decreased EC K+ (thiazides)
Can;t close b-cell K+ channels .: can’t release insulin .: hyperglycaemia
CRH effects
ACTH, MSH, b-endorphins
Tesamorelin
GHRH analog to treat lipodystrophy in HIV
GnRH regulated by:
prolactin (i.e. breastfeeding stops GnRH release; prolactinoma causes infertility, OP, galactorhea)
delta cells in pancreas secrete + function
somatostatin; inhibits GH and TSH release in HPA (also many GIT actions).
Somatostatin role in HPA
inhibit GH and TSH release
Somatostatin role in GIT
INHIBITS RELEASE OF: Gastrin Cholecystokinin (CCK) Secretin Motilin Vasoactive intestinal peptide (VIP) Gastric inhibitory polypeptide (GIP) Enteroglucagon Decrease rate of GE
Panc:
Insulin
GCG
Exocrine function
TRH effects
increases TSH and prolactin release.
[so 1’ or 2’ hypothyroidism would cause hyperprolactinemia]
How is prolactin regulated
Increase: TRH
Decrease: DA, Prolactin (increases DA synthesis)
Somatomedin C =
IGF-1 (muscle mass, linear growth) [GH = InsResistance]
GH: increased and decreased by:
Increased:
GHRH
Sleep
Exercise
Decreased:
somatostatin
glucose
somatomedin negative feedback
Ghrelin function:
induce hunger
cause HG release
Conditions that increase ghrelin release
Sleep deprivation
Prader-willi
Regulation of AHD
1' = osmo-Rs in hypothalamus (most important job is osmolarity) 2' = hypovolemia
desmolase: other name, job, regulated by
= side chain cleavage enzyme
Turns cholesterol to pregnenolone
Increased by ACTH
Inhibited by Ketoconazole
renin levels in CAHs
21 = high 17 = low 11 = low
Hormone in 11-CAH that causes HTN
11-deoxycorticosterone
17-CAH presentation wrt sexes
XX = lack secondary sex characteristics XY = pseudohermaphroditism, cryptorchidism
Rx CAH
Exogenous cortisol to inhibit ACTH release
Other supplements i.e. aldosterone
Functions of cortisol:
BP: upregulates a1-Rs, acts as aldosterone at high conc
Insulin resistance
Gluconeo, lipolysis, proteolysis
Decrease fibroblast activity (striae)
Decrease immune system (incl. IL-2 production –> candidiasis and reactivation of TB). Neutrophilia
Decreased OBL activity
Ca and pH
40% Ca bound by albumin (45% ionized = free)
Increase pH = less H+ = albumin binds more Ca++ = hypocalcemia (tetany, cramps, spasms, paresthesias)
Vit D2 vs D3
D2 = plant foods D3 = skin
Vit D regulation
Increased by: low Ca, low PO4, high PTH
Decreased by: high Vit D (inhibits itself and PTH)
Ca++ regulation cells
Chief = parathyroid (bone, kidney, vitD) C-cell = calcitonin (bone)
PTH in kidney
PO4 - decrease resorption in PCT
Ca - increase resorption in DCT
Vit D - increase a-1-OHase in PCT
PTH in bone
increase Macrophage-CSF and OBL to secrete RANK-L
PTH secretion and Mg levels
Low Mg = increased PTH release
VERY low Mg = decreased PTH release
*get low Mg via diarrhea, loops, aminoglycosides, alcohol abuse
Increase SHBG via:
pregnancy and OCPs
.: more T bound up .: feminizing
5’deiodinase: role and inhibitors
converts T4 to T3 peripherally
Inhibited by: Propylthiouracil Glucocorticoids Amiodarone Iopanoic acid (contrast agent) Non-selective b-blockers
Wolf-Chaikoff
High Iodine temporarily inhibits TPO
Competitive inhibitors of NIS
Perchlorate
Pertechnetate
Thiocyanate
S/S of adrenal insufficiency:
Electrolytes: low Na+, high K+, metabolic acidosis (NON-ion gap), high Cl-
weak, fatigue, N/V/D, muscle aches, ORTHOSTATIC HYPOTENSION, weight LOSS, salt/sugar cravings
Dx of adrenal insufficiency:
ACTH stimulation test
OR
Metyrapone stimulation test (blocks 11-deoxycortisol to cortisol)
Normal = high 11-deoxy an high ACTH
1’ = no 11-deoxy but high ACTH
2’ = now 11-deoxy or ACTH
Addison underlying disease
Autoimmune, TB, mets
When do you see skin pigmentation and when do you see hyperkalemia in adrenal insufficiency
1’ = skin and hyperkalemia
2’ and 3’ = NO skin (no ACTH) and NO hyperkalemia (aldosterone synthesis preserved)
Na+ levels in hyperaldosteronism
NORMAL!
Aldosterone increases Na+ and H2O, so increased GFR causes Na+ loss; so HTN with normal Na+ and no edema = “aldosterone escape”
Opsoclonus myoclonus: underlying disease and characteristics
NEUROblastoma irregular abdominal mass, can cross midline HVA, VMA, bombesin, neuron-spec enolase N-myc HOMER-WRIGHT ROSETTES
Homer-Wright Rosettes
Neuroblastoma
Medulloblastoma
Theo associated with what syndromes:
NF-1
VHL
MEN2A
MEN2B
Signs and level sin hyperaldosteronism
NORMAL Na+
Low K+ [muscle weakness and parenthesias]
Metabolic alkalosis (high HCO3-)
low Cl- (for electroneutrality of bicarb)
hypertension (no edema or hyperNa+)
low renin (if primary)
Most sensitive measure for hypothyroidism
High TSH
Cholesterol levels in hypo and hyper thyroidism
Hypothyroid = hyper cholesterolemia (via decreased LDL-R expression)
hyperthyroid = hypocholesterol
[also hyperglycaemia and hypercalcemia (bone resorption)]
Myoedema
Hit muscle, stays bulged for longer because of slow Ca uptake into SR. Seen in hypothyroidism
hashimotos ABs
anti-TPO
anti-TG
anti-microsomal
Immune gene of hashimotos
HLA-DR5
umbilical hernia, tongue sticking out
cretinism
DeQuervains
post flu-like
Hyper then hypo
granulomatous inflammation with mixed cell infiltrate and giant cells
High ESR, jaw pain, tender thyroid
Reidel Thyroiditis
Fibrosis extending i.e. airway (ddx = anaplastic but thats old ppl) = rock/wood-like
young woman
IgG4 related - autoimmune pancreatitis, retroperitoneal fibrosis, non-infectious aortitis
Ab for Graves
IgG
Mutation in TSH-R causes:
toxic multinodular goiter - hot nodule, rarely malignant
Thyroid storm s/s and rx
Stress-induced
Agitation, delerium, fever, diarrhea, vomiting, coma
COD = tachyarrythmia
Rx = b-blocker, PTU, corticosteroids
Jod-Basedow phenomenon
Iodine deficient person made iodine replete presenting with thyrotoxicosis
Thyroid artery matched with nerve that can be damaged:
Superior thyroid artery = superior laryngeal nerve
- external = cricothyroid (low-pitched monotone)
- internal = sensation above vocal cords (aspiration)
Inferior thyroid artery = recurrent laryngeal nerve = all laryndeal muscles (less cricothyroid)
- hoarseness and sensation below vocal cords
Papillary thyroid cancer:
Orphan annie RET or BRAF Psammoma Nuclear grooves childhood iradiation
Follicular thyroid cancer
Hematogenous mets
RAS
Invasion of thyroid capsule
Medullary CA thyroid
Calcitonin
C-cells
Amyloid background
RET
Undifferentiated/anaplastic Thyroid CA
old person
Invades local structures (ddx = riedel’s thyroiditis)
p53
Hematogenous CA mets
Follicular CA thyroid
ChorioCA
HCC
RCC
Pseudohypoparathyroidism =
Albright hereditary osteodystrophy
- kidneys unresponsive to PTH so low Ca and high PO4
- short 4th and 5th digits, short, AD
Albright hereditary osteodystrophy
Pseudohypoparathyroidism =
- kidneys unresponsive to PTH so low Ca and high PO4
- short 4th and 5th digits, short, AD
Familial hypocalciuric hypercalcemia
Defective Ca-sensory on parathyroid
Keep resorbing it from bone = hypercalcemia
Dont excrete it in kidneys = hypocalciuria
Kidneys unresponsive to PTH vs. defective Ca-sensor on parathyroid
unresponsive kidneys = pseudohypoparathyroidism/albrights
defective sensor = familial hypocalciuric hypercalcemia
increased cAMP in urine
hyperparathyroidism (signalling molecule)
2’ hyperPTH levels via kidney failure
Low Ca
High PO4
Acromegaly s/s, complication, test, rx
Large tongue with deep furrows, insulin resistance
Increased risk of colorectal polyps and cancer
Test = GH not suppressed with OGTT
Rx:
- Octerotide (somatostatin analog)
- Pegvisomant (GH-R antagonist)
Causes, urine spec. gravity, and rx of central vs nephrogenic DI
Central:
- pituitary tumour, hypothalamus problem, trauma, surgery, ischemic encephalopathy, idiopathic
-
SIADH: complication, causes, rx
Cerebral edema
- fix too quick, get osmotic demyelination syndrome
Via small cell, head trauma, PULMONARY DISEASE, cyclophosphamide, carbamazepine
Rx = IV hypertonic saline (slowly), conivaptan, tolivaptan, demeclocycline
Empty sella pt
obese woman
pregnancy and pituitary problems
Sheehans = ischemic infarct post-blood loss
Autoimmune hypophysitis = acute HA, visual field changes, cortisol deficiency in late pregnancy or early post-delivery
DM: lipolysis and proteolysis
present in TIDM
NOT usually in T2 because some basal insulin to prevent it
Both have increased protein catabolism
MCCD DM
MI
Osmotic damage: what enzymes
Have aldose reductase
NO or LOW sorbitol dehydrogenase
Gestatoinal DM: hormone and s/s in fetus
hPL
Caudal regression syndrome, VSD, transposition of great vessels, neural tube defects, rectal atresia, renal agenesis
T1DM HLA link
DR-3 and DR-4
DKA complications
life-threatening mucor, cerebral deem, arrythmias, heart failure
Glucagonoma s/s
Dermatitis - necrolytic migratory erythema Depression Diabetes DVT Diarrhea Normo normo anemia
whipples triad
insulinoma
carcinoid markers
Neuroendocrine (chromogrannin) 5-HIAA Niacin deficiency (pellagra)
MEN genes
MEN1 = MEN1 = menin tumour supressor MEN2 = RET = tyrosine kinase
