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Boards DIT > DIT Endocrine > Flashcards

DIT Endocrine Flashcards

1
Q

What hormones use cAMP? mnemonic plus more

A

FLAT ChAMP and glucagon (basophiles use cAMP. think BASE CAMP)

So basophilic anterior pituitary:
FSH (alpha subunit)
LH (alpha subunit)
ACTH
TSH (alpha subunit)
hCG (alpha subunit)
CRH
hCG
ADH (V2)
MSH
PTH

calcitonin, GHRH, glucagon

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2
Q

Inositol triphosphate messenger for? (IP3 from Gq pathway)

A

GOAT HAG

GnRH, Oxytocin, ADH (V1), TRH, Histamine, Angiotensin II, Gastrin

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3
Q

Tyrosine kinase receptors are used by what? Mnemonic?

A

Growth factors and insulin

And acidophiles and cytokines

PIG: prolactin, IL_, GH

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4
Q

What hormones use steroid receptors?

A

Steroids, VITAMIN D, T3 and T4

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5
Q

What hormones have common alpha subunit? What type of receptor do they work on?

A

It is the FLAT without the A + hCG. all work with cAMP (Gs)

LH
FSH
TSH
hCG

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6
Q

What is cabergoline?

A

Dopamine agonist (prolactinoma tx), similar to bromocriptine

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7
Q

What enzyme does cholesterol to pregnenolone?

What activates it?
What inhibits it?

A

Desmolase

ACTH activates it
Ketaconazole blocks it

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8
Q

What is Cushing Disease?

A

Pituitary Adenoma secreting ACTH (causes secondary hypercortisol)

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9
Q

Dexamethasone test. What type of tumor responds?

A

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

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10
Q

What causes secondary hyperaldosterone? Lab finding?

A

Low perfusion to kidney causes kidney to perceive low blood volume

HIGH RENIN!!!

Renal artery stenosis
CHF
Low protein state (low oncotic pressure so intravascular volume, so renin response)

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11
Q

Patient has DIC and after septicemia, what is risk for endocrine?

A

Neisseria can case this. It can cause weterhouse friderichsen syndrome and adrenals are just filled with blood and they die.

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12
Q

What findings are different in secondary adrenal insufficiency than primary?

A

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

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13
Q

What happens if you take off glucocorticoids without taper?

A

tertiary adrenal insufficiency b/c negative feedback of cortisol had shut down the hypothal

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14
Q

What are the 3 main causes of Addison’s?

A

Primary adrenal insufficiency:

Autoimmune is most common
Then metastasis
Then tb

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15
Q

What tumors secrete epo?

A

Pheo
RCC
Hemangioblastoma
HCC

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16
Q

Medicaiton to give to pheo patient on their way to OR to have it removed?

A

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

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17
Q

What is the adrenal tumor in children?

A

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

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18
Q

Adrenal neuroblastoma

Oncogene?

Tumor marker

Stain?

Histo?

A

n-myc (transcription factor)

bombesin (NeuroBOMBESInoma)

Neurofilament stain (makes sense)

Homer right pseudorosette

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19
Q

MEN 1, 2A, 2B

A

PPP (diamond)
Pituitary
Pancreas
Parathyroid

PPM (Square)
Parathyroid
Pheo
Medullary thyroid

PMM (triangle)
Pheo
Mucosal neuroma
Medullary thyroid

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20
Q

Where does thyroid come from?

What can happen with problems in migration?

A

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

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21
Q

Difference in mechanism for propylthiouracil and methimazole?

Difference in toxicity?

A

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

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22
Q

Patient is having weight loss and anxiety. You do iodine scan and patches of thyroid take up iodine. Dx? pathophys?

A

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)

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23
Q

Tx of thyroid storm?

A

3 P’s Propranalol, propylthiouracil, Prednisolone (corticosteroids)

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24
Q

Hypothyroid with painless goiter?

A

Hashimotos! if autoimmune.

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25
Q

Hashimotos MHC info?

A

HLA D5 and B5

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26
Q

Hashimotos on histo?

A

Looks like lymph node b/c shrunken follicles and germinal ceneters

27
Q

Rapidly growing thyroid mass in hashimotos, consider what?

A

B cell lymphoma

28
Q

Difference in histology of hashimoto and de Quervain?

A

De Quervain is painful and is granulomatous inflammation (after viral infection or even during)

Hashimotos is lymphocytic inflammation and painless.

29
Q

Histo of Riedel’s? Presentation?

A

Rock hard mass and hypo thyroid and painless

Histo is fibrosis with macrophage and eosinophils

30
Q

What is a big med to think about for causes of hypothyroidism?

A

Amiodarone

Tyrosine kinase inhib, lithium are ohters

31
Q

Histo of papillary carcinoma of thyroid?

Risks:

A

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

Good prognosis

32
Q

Follicular carcinoma appearance?

A

Looks like follicular adenoma but invades capsule.

Spreads in blood but still good prognosis

33
Q

Histo of medullary carcinoma?

Genes of it?

What do you check before you remove this tumor?

A

Medullary thyroid is C cells and you see amyloid (congo red)

RET mutation

associated MEN2A and 2B so might have pheo, check this before going into surgery

34
Q

Hard thyroid mass in an old patient?

A

Anaplastic/undifferentiated carcinoma. Invasive. Bad.

35
Q

What thyroid cancers have tyrosine kinase receptor activation?

A

Papillary and medullary (tyrosine kinase)

36
Q

What can cause restrictive cardiomyopathy? mnemonic

A

LEASH

Loffler (Endomyocardial fibrosis with eosinophilic)
Endocardial fibroealstosis
Amyloidosis
Sarcoidosis
Hemochromatosis

Radiation

37
Q

How does glucose cause insulin release?

A 
Through GLUT 2
ATP is made from glycolysis
ATP sensitive K+ channels close
Cell depolarizes
Ca++ comes in
Exocytosed vesicles with insulin
38
Q

Where are GLUT 2 cells?

A

Beta cells, liver, kidney, small intestine

39
Q

DMI HLA stuff?

A

HLA DR3-DQ2 and DR4-DQ2

40
Q

What are some small vessel issues with diabetes?

A

Thicken of basement membrane causes retinopathy (and eventual vessel proliferation), and

nephropathy: proteinuria. ACE INHIBITORS HELP

Can also cause vascular disease

41
Q

What does osmotic damage hurt in diabetes?

A

Cells with no sorbitol dehydrogenase

Lens, retina, kidney, SCHWANN CELLS

Retinopathy
Nephropathy
VASCULAR disease
Motor NEUROPATHY
Sensory NEUROPATHY
Autonomic NEUROPATHY
42
Q

What does diabetic neuropathy feel like?

A

Can be like pins and needles (its like when your foot falls asleep)

Gabapentin and amytriptylin and all sorts of shit for tx

43
Q

What causes DKA? Put it simply

A

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

44
Q

Major complications of DKA for:

Arrythmia

K+ levels

Infection

A

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

45
Q

Who gets hyperosmolar hyperglycemic state? How is it different than DKA?

A

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

46
Q

Tx of DKA?

A

Treat acidosis. Keep giving insulin anion gap normalizes (may need to add glucose)

Potassium for intracellular stores

IV fluid

47
Q

Biguanides mechanism:

Tox?

A

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)

48
Q

Sulfonylureas suffix? Mechanism?

Tox?

A

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.

49
Q

Thiazolidinediones are what drugs?

Mehanims?

Tox?

A

glitazones

Increase sensitivity to insulin in peripheral tissue. PPAR-gamma receptor.

Hepatotoxic. Inclease fluid retension: Worsen CHF

50
Q

What are DPP-4 inhibitors?

A

Gliptins.

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

51
Q

What are the GLP-1 analogues?

A

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!

52
Q

What is the amylin analog action?

A

Satiety and decreased emptying and less glucagon

53
Q

What are the alpha glucosidase inhibitors?

A

Acarbose and miglitol

Inhibit intestina alpha glucosidase so less sugar absorption.

GI issues

54
Q

Leptin is from what? What does it signal?

A

From adipocytes

Inhib Lateral hypothal (stop being hungry)
Stim ventromedial hypothal (signal youa re satisfied)

55
Q

2 main causes of lipodystrophy?

A 
Leptin deficiency
HIV medications (protease inhibitors)

Cushing can cause it too

56
Q

Without knowing numbers, what are the criteria for metabolic syndrome? 3 star

A

3 of the 5

Waist circumference
triglycerides
HDL
BP
Fasting serum glucose
57
Q

Weight loss meds?

A

Orlistat (pancreatic lipase inhib)

Phentermine

58
Q

PTH affect on bone?

Kidney?

A

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

59
Q

Other than low calcium, what signals affect PTH release?

A

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)

60
Q

3 functions of Vit d?

A

dietary absorption of Ca++
Dietary absorption of phosphate
More bone resoprtion so more Ca and phosphate

61
Q

What malignancies can cause hypercalcemia?

A 
SQUAMOUS CELL (especially lung)
Renal cell (makes sense b/c vit D)
Breast mets
Multiple myeloma b/c osteolytic factors
Parathyroid adenoma (duh)
62
Q

What are labs for secondary hyperparathyroidism?

A

Low calcium
high phosphate
high parathyroid
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)

63
Q

Mnemonic for hypercalcemia?

A

• MD PIMPS ME

  • Malignancy (MM and squamous)
  • Diuretics
  • Parathyroid (hyperparathyroidism)
  • Idiopathic
  • Megadose of vitamin D
  • Paget disease
  • Sarcoidosis
  • Milk-alkali syndrome
  • Endocrine (thyrotoxicosis)
64
Q

What is pseudohypoparathyroidism?

What are findings?

A

Low calcium b/c AUTOSOMAL DOMINANT unresponsiveness of kidney to PTH so hypocalcemia and shorteend 4th/5th digits. Short stature. OSTEOITIS FIBROSIS CYSTICA b/c PTH causes RANKL to be made by osteoblasts and bones are destroyed by osteoclasts

Albrithgt hereditary osteodystropghy

Boards DIT (43 decks)

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