Flashcards in DIT Endocrine Deck (64):
What hormones use cAMP? mnemonic plus more
FLAT ChAMP and glucagon (basophiles use cAMP. think BASE CAMP)
So basophilic anterior pituitary:
FSH (alpha subunit)
LH (alpha subunit)
TSH (alpha subunit)
hCG (alpha subunit)
calcitonin, GHRH, glucagon
Inositol triphosphate messenger for? (IP3 from Gq pathway)
GnRH, Oxytocin, ADH (V1), TRH, Histamine, Angiotensin II, Gastrin
Tyrosine kinase receptors are used by what? Mnemonic?
Growth factors and insulin
And acidophiles and cytokines
PIG: prolactin, IL_, GH
What hormones use steroid receptors?
Steroids, VITAMIN D, T3 and T4
What hormones have common alpha subunit? What type of receptor do they work on?
It is the FLAT without the A + hCG. all work with cAMP (Gs)
What is cabergoline?
Dopamine agonist (prolactinoma tx), similar to bromocriptine
What enzyme does cholesterol to pregnenolone?
What activates it?
What inhibits it?
ACTH activates it
Ketaconazole blocks it
What is Cushing Disease?
Pituitary Adenoma secreting ACTH (causes secondary hypercortisol)
Dexamethasone test. What type of tumor responds?
High dexamethasone suppresses ACTH secreting pituitary hormone.
Ectopic ACTH (Small cell lung) won't respond to dexamethasone b/c its abnormal anyway)
Adrenal tumor just doesn't need ACTH, so it laughs at dexamethasone test
What causes secondary hyperaldosterone? Lab finding?
Low perfusion to kidney causes kidney to perceive low blood volume
Renal artery stenosis
Low protein state (low oncotic pressure so intravascular volume, so renin response)
Patient has DIC and after septicemia, what is risk for endocrine?
Neisseria can case this. It can cause weterhouse friderichsen syndrome and adrenals are just filled with blood and they die.
What findings are different in secondary adrenal insufficiency than primary?
No ACTH is made, but renin pathway is fine.
So: normotensive, not hyperkalemic. No hyperpigmentation b/c no POMC action.
but still fatigued, malaised, and feeling like garbage
What happens if you take off glucocorticoids without taper?
tertiary adrenal insufficiency b/c negative feedback of cortisol had shut down the hypothal
What are the 3 main causes of Addison's?
Primary adrenal insufficiency:
Autoimmune is most common
What tumors secrete epo?
Medicaiton to give to pheo patient on their way to OR to have it removed?
ALPHA BLOCKER: phenoxybenzamine. (nonselective and irreversible. Phentoalamine is nonselective and reversible and sued for MAO people who eat tyramine)
Then you can give a beta blocker but don't want unaposed alpha activity
What is the adrenal tumor in children?
Adrenal neuroblastoma. Can be anywhere on symp chain and presents as abdominal distension with firm mass.
HVA is present in urine as a dopamine breakdown product.
Less likely to have HTN.
over expression of n-myc
n-myc (transcription factor)
Neurofilament stain (makes sense)
Homer right pseudorosette
MEN 1, 2A, 2B
Where does thyroid come from?
What can happen with problems in migration?
From pharynx. ENDODERMAL (gut tissue)
Most common ectopic site is tongue and thyroglossal duct connotes it to tongue
Thyroglossal duct cyst is in middle of the neck and moves with swallowing
Difference in mechanism for propylthiouracil and methimazole?
Difference in toxicity?
Propylthiouracil blocks peripheral T4 to T3 and peroxidase (methimazole is just the latter)
PPT is liver toxicity
Methimazole is very teratogenic in first trimester
BOTH can cause agranulocytosis
Patient is having weight loss and anxiety. You do iodine scan and patches of thyroid take up iodine. Dx? pathophys?
Toxic multinodular goiter
Mutation in TSH receptor causes parts of thyroid to be acting without signaling. (why nodules are working, and toxic b/c it is functioning)
Tx of thyroid storm?
3 P's Propranalol, propylthiouracil, Prednisolone (corticosteroids)
Hypothyroid with painless goiter?
Hashimotos! if autoimmune.
Hashimotos MHC info?
HLA D5 and B5
Hashimotos on histo?
Looks like lymph node b/c shrunken follicles and germinal ceneters
Rapidly growing thyroid mass in hashimotos, consider what?
B cell lymphoma
Difference in histology of hashimoto and de Quervain?
De Quervain is painful and is granulomatous inflammation (after viral infection or even during)
Hashimotos is lymphocytic inflammation and painless.
Histo of Riedel's? Presentation?
Rock hard mass and hypo thyroid and painless
Histo is fibrosis with macrophage and eosinophils
What is a big med to think about for causes of hypothyroidism?
Tyrosine kinase inhib, lithium are ohters
Histo of papillary carcinoma of thyroid?
RET and BRAF mutations. (Zach BRAF would be all over annie eye nuclei) Radiation or tobacco can cause it too
Orphan Annie Eye nuclei (empty nucleus)
and psammoma bodies b/c annie's horse was sandy and thats what psammoma means
Follicular carcinoma appearance?
Looks like follicular adenoma but invades capsule.
Spreads in blood but still good prognosis
Histo of medullary carcinoma?
Genes of it?
What do you check before you remove this tumor?
Medullary thyroid is C cells and you see amyloid (congo red)
associated MEN2A and 2B so might have pheo, check this before going into surgery
Hard thyroid mass in an old patient?
Anaplastic/undifferentiated carcinoma. Invasive. Bad.
What thyroid cancers have tyrosine kinase receptor activation?
Papillary and medullary (tyrosine kinase)
What can cause restrictive cardiomyopathy? mnemonic
Loffler (Endomyocardial fibrosis with eosinophilic)
How does glucose cause insulin release?
Through GLUT 2
ATP is made from glycolysis
ATP sensitive K+ channels close
Ca++ comes in
Exocytosed vesicles with insulin
Where are GLUT 2 cells?
Beta cells, liver, kidney, small intestine
DMI HLA stuff?
HLA DR3-DQ2 and DR4-DQ2
What are some small vessel issues with diabetes?
Thicken of basement membrane causes retinopathy (and eventual vessel proliferation), and
nephropathy: proteinuria. ACE INHIBITORS HELP
Can also cause vascular disease
What does osmotic damage hurt in diabetes?
Cells with no sorbitol dehydrogenase
Lens, retina, kidney, SCHWANN CELLS
What does diabetic neuropathy feel like?
Can be like pins and needles (its like when your foot falls asleep)
Gabapentin and amytriptylin and all sorts of shit for tx
What causes DKA? Put it simply
Stress. IE. Things that increase corticosteroids, glucagon, or catecholamine.
Cells think they are starving b/c no insulin. Ketones are made while urine is lost and dehydration plus acidosis is bad
Major complications of DKA for:
Low magnesium and potassium can cause V tach or Torsades
K+ serum levels are high b/c acidosis and potassium put into blood, but a lot is peed out so total body potassium is LOWWW need to give potassium as you treat
Mucormycosis and rhizopus
Who gets hyperosmolar hyperglycemic state? How is it different than DKA?
There is some insulin in DMII, so there is not the ketoacidosis. Instead there is extreme hyperglycemia (>800)
Pateints are confused, delierus and severe dehydration. maybe coma
Tx: potassium and IV insulin
Tx of DKA?
Treat acidosis. Keep giving insulin anion gap normalizes (may need to add glucose)
Potassium for intracellular stores
Less gluconeogenesis in liver, lower LDL and triglycerides.
GI upset: diarrhea (limiting use early on)
LACTIC ACIDOSIS: can't give it in renal failure. (CAREFUL with IV contrast)
Sulfonylureas suffix? Mechanism?
Prefix: glyburide, glimepiride, glipizide. Secretagogues
Close K+ channel in Beta cells so cells depolarize and trigger insulin release by Ca++ influx
Hypoglycemia and weight gain, can be long lasting effects.
Thiazolidinediones are what drugs?
Increase sensitivity to insulin in peripheral tissue. PPAR-gamma receptor.
Hepatotoxic. Inclease fluid retension: Worsen CHF
What are DPP-4 inhibitors?
Mechanism: Inhibit DPP-IV which would break down GLP-1 which is released as you eat which increases insulin release and blocks glucagon. Prolongs incretin actions
Increase insulin release, less glucagon release
What are the GLP-1 analogues?
Exenatide, and Liraglutide
they are incretin analogues so more insulin release and less glucagon release
N/V and also pancreatitis
Exeneatide is an analog of exendin, a hormone in the Gila monster which allows them to eat once a week! neat!
What is the amylin analog action?
Satiety and decreased emptying and less glucagon
What are the alpha glucosidase inhibitors?
Acarbose and miglitol
Inhibit intestina alpha glucosidase so less sugar absorption.
Leptin is from what? What does it signal?
Inhib Lateral hypothal (stop being hungry)
Stim ventromedial hypothal (signal youa re satisfied)
2 main causes of lipodystrophy?
HIV medications (protease inhibitors)
Cushing can cause it too
Without knowing numbers, what are the criteria for metabolic syndrome? 3 star
3 of the 5
Fasting serum glucose
Weight loss meds?
Orlistat (pancreatic lipase inhib)
PTH affect on bone?
Hits osteoblasts which make more RANK-L which hit RANK of osteoclast so more bone turnover
More reabsorption of Ca in DCT of kidney
Less reabsorption of phosphate in PCT
Moare 1,25 OH production by stimulating kidney 1 alpha hydroxylase
Other than low calcium, what signals affect PTH release?
Low magnesium increases PTH release. VERY LOW or prolonged decreases PTH, weird.
Low magnesium caused by: diarrhea (duh, not absorbed), too much pee (diuretics and booze), amino glycosides)
3 functions of Vit d?
dietary absorption of Ca++
Dietary absorption of phosphate
More bone resoprtion so more Ca and phosphate
What malignancies can cause hypercalcemia?
SQUAMOUS CELL (especially lung)
Renal cell (makes sense b/c vit D)
Multiple myeloma b/c osteolytic factors
Parathyroid adenoma (duh)
What are labs for secondary hyperparathyroidism?
High alkaline phosphatase (duh)
(b/c renal can't make 1-25 OH Vit D so high PTH. Also renal failure means can't excrete phosphate so high phosphate)
Mnemonic for hypercalcemia?
• MD PIMPS ME
• Malignancy (MM and squamous)
• Parathyroid (hyperparathyroidism)
• Megadose of vitamin D
• Paget disease
• Milk-alkali syndrome
• Endocrine (thyrotoxicosis)