Endocrine Flashcards

1
Q

why can gigantism therapy lead to hypothyroidism?

A

somatostatin inhibits both GH and TSH (watch out for hypothyroidism when treating gigantism)

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2
Q

cutting stalk of pituitary stalk causes increase in which hormone levels? not prolactin or oxytocin because?

A

prolactin and oxytocin will be secreted by hypothalamus at normal levels not increased levels

however, prolactin release is under negative control by dopamine which is produces in hypothalamus and transported to pituitary lactrotroph cells-cutting the stalk removes this inhibition and prolactin levels increase

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3
Q

describe Kimmelstiel-Wilson nodule-structure, location, disease

A

ovoid, PAS-positive, hyaline masses. found in mesangial core at edge of glomerulus
seen in diabetes glomerulosclerosis

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4
Q

effect of glucagon, Epi, and glucocorticoids on glycogen synthesis?

A

glucagon and Epi (catabolic) both increase glycogen phosphorylase activity, increasing glycogenolysis
glucagon also inhbits glycogen synthase, promoting glycogenolysis
glucagon works in liver and epi works on muscle and adipose tissue and liver
glucocorticoids (anabolic) act in liver to increase glycogen synthesis and accumulation

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5
Q

Grave’s disease-def, clinical symptoms, levels of rT3, T4 and TSH, and radioactive iodine uptake

A

thyroid-stimulating immunoglobins results in excessive movement of thyroglobin from colloid into plasma.

  • thyroglobin bind iodine and produces thyroxine (T3)
  • rT3 and T4 and radioactive iodine uptake are increased
  • TSH is decreased
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6
Q

hypothyroidism-clinical features

A

dry skins, brittle hari, hair loss, weight gain, fatigue, and cold intolerance

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7
Q

Hashimoto disease-def, thyroid gland description, TSH, T4 levels

A
  • autoimmune disorder that leads to hypothyroidism, elevated levels of anti-thyroid peroxidase (TPO) and antithyroglobulin antibodies
  • gland is enlarged and uniformly firm (from chronic inflammation)
  • elevated TSH and reduced T4 levels
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8
Q

name 2 examples of ketoacids

A

3-hydroxybutyrate, acetoacetate

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9
Q

acetoacetate:3-hydroxybutyrate ratio

A

decreases in diabetes and alcoholism because 3-hydrox increases

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10
Q

suspect pseudohypoparathyroidism when? levels of serum ca2+ phosphate, PTH. defined as

A

mentally retarded child with shorten metacarpals

  • low CA2+, high phosphate, high PTH
  • due to end-organ insensitivity to PTH, can be caused by decreased expression of Gs in RBCs-leads to decreased cAMP expression
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11
Q

why is Acetly-Coa carboxylase activated by hepatocytes response to insulin? why not increased activity of hexokinase?

A

Acetyl-CoA carboxylase catalyzes the rate-limiting step in fatty biosynthesis and is activated by insulin
hexokinase is not found in liver cells (glucokinase is) nor is it regulated by insulin. instead glucokinase gene expression is increased with hyperinsulinemia

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12
Q

role of glucokinase when a pt has high insulin serum levels and low glucose levels

A

mutated glucokinase has a higher affinity for glucose and coverts glucose to glucose-6-phosphate trapping it in the hepatocytes. other cells are unable to utilize glucose (i.e.) pancreas and insulin is up regulated in order to increase uptake of more glucose in blood.

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13
Q

urinary sodium levels in SIADH? why?

A

serum sodium levels are low b/c of increase water reabsorption. also increase volume inhibits release of renin from kidneys, decreasing action of aldosterone and increase urine sodium

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14
Q

name the hormones released in a cyclic manner- which one depends on suprachiasmatic nucleus

A

TSH, GH, prolactin (rely on sleep patterns more than light and darkness) and LH (linked to pulsatile manner of GnRH which does not rely on suprchiasmatic nucleus)
ACTH relies on circadian clock

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15
Q

describe three different types of hypothyroidism and effect of TRH injection test on TSH levels

A

hypothalamic hypothyroidism- slightly increase TSH response, but slower and
pituitary-no response
primary-exaggerated response, TSH levels are already high b/c of low thyroid hormone

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16
Q

diffuse nontoxic goiter has similar histology

A

multinodular goiter, just not as nodular

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17
Q

thyroid adenoma aka

A

thyroid (follicular) adenoma
histo-similar to normal thyroid gland, benign colloid follicles
resected b/c could become cancerous

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18
Q

best initial test to perform in order to evaluate thyroid function

A

TSH levels

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19
Q

if pt has hyperpigmented skin and mucous membranes then which level of adrenocortical insufficiency is it?

A

hyperpigmentation indicates high levels of ACTH to it’s most likely primary (ie. Addison’s disease) b/c the pit is responding to low levels of cortisol

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20
Q

medullary carcinoma produces what hormone this can be converted to what? what neuroendocrine disorders are they associated with?

A

calcitonin, can be converted to amyloid

-associated with MEN 2a and MEN 2b

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21
Q

most common type of pituitary adenoma

A

prolactin, produces galactorrhea

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22
Q

thyroid surgery can cause risk of what other endocrine gland? describe down stream effects of it’s hormone

A
  • parathyroid hormone
  • PTh activates 1-hydroxlyase in the kideny which converts 25-hydroxyvitamin D3 to 1,25 dihydroxyvitamin D3.
  • 1,25dihydroxyvitamin D3 promotes insteastinal absorption of Ca2+ and phosphate by controlling the expression fo the calcium transporters in the intestines
23
Q

type I hypersensitivity- mediated by? mech? result?

A

IgE-mediated. immediate or allergy. caused by crosslinking of IgE bound to mast cells resulting in their degranulation and tissue damage. immediate response to allergen

24
Q

type II cytotoxic-mediated by what molecule? activates? result?

A

autoantibodies bind to specific tissues or cells, activate complement and cause destruction of underlying tissue

25
Q

type II noncytotoxic hypersen- mediated by, mech, result. give example

A

autotantibodies bind to receptor stimulate function and cause eventual exhaustion of organ function (i.e Grave’s disease-hyperthyrodism to hypothyroidism)

26
Q

type III hypersensitivity-aka, mediators activate what? system or organ damage?

A

aka immune complex hypersens. caused by deposition of complexes of antigen and antibody, causing complement activation in small vasculature. system wide vs organ specific

27
Q

type IV hypersen-aka, mediators (2), timing, example

A

aka, T-cell mediated, or delayed type. mediated by TH1 cells and macrophages. occurs 48-72hrs after exposure to protein antigens. (i.e Hashimoto thyroiditis)

28
Q
pancreas releases what from:  
ancinar cells
alpha
beta
delta
G cell
name diseases associated with each one
A
  • main exocrine gland, digestive enzymes (amylase and lipase)
  • glucagon (hyperglycemia)
  • insulin (hypoglycemia)
  • somatostatin (Diabetes, steatorrhea)
  • gastrin (Zollinger-Ellison Syndrome)
29
Q

effect of TSH on GH release

A

stimulates it’s release from anterior pituitary

30
Q

how does 11beta hydroslyase effects mineralocorticoid vs glucocorticoid levels.

A

increases 11-deoxycortcosterone (is a mineralocorticoid that acts like aldosterone not a glucocorticoid that acts like cortisol). glucocorticoid levels are always low.

31
Q

calcium sensing receptor- produced from which gene, role, found where, disease if sensitivity is decreased (characterized by- 3 things)

A
  • CaSR gene on chromosome 3q
  • mediates feedback inhibition of secretion of parathyroid by blood CA2+ concentration
  • also found in kidney, mediated ca-stimulated feedback inhibition of PTH hormone-independent ca2+ reabsorption
  • familial hypocalcuric hypercalcemia-hypercalcemia, relative hypocalciuria, and normal/high levels of PTH
32
Q

gene mutation and relation to PTH endocrine disorders:

  • Cyclin D gene inversion
  • AIRE mutation
  • GCM2 mutation
  • tyrosine receptor RET
A
  • sporadic parathyroid adenomas
  • autoimmune hypoparathyroidism
  • autosomal recessive form of familial isolate hypoPTH
  • MEN type II
33
Q

presence of Psammoma bodies in an endocrine disorder

A

papillary carcinoma of thyroid

34
Q

name 3 major contraindications of acetalozamide

A

pts with

  • electrolyte imbalances (hypokalemia, hyponatremia, or hypercalemia)
  • acid/base distrubances (metabolic acidosis or DKA)
  • adrenal insuffiencey
35
Q

how are pheochromocytomas diagnosed

A

24-hr urine for vanillylmandelic acid and metanephrines- both metabolites of NE

36
Q

bence-jones protein-def, associated with which disease

A
  • myeloma light chains detected in urine

- marker for multiple myelomas

37
Q

octerotide is an analog for

A

somatostatin- used to manage acromegaly

38
Q

role of endorphins and enkephalins on GH

A

both stimulate GH

39
Q

hormone that has orexigenic activity

A

orexigenic- appetite stimulating-ghrelin

40
Q

methimazole-similar to, treats, mech, serious side effect and early signs, therapy to treat side effect

A
  • anti-thryoid drug similar to proplthiouracil; treat hyperthyroidism
  • interferes with incorporation of iodine into tyrosyl residues of thyroglobulin and inhibits coupling of iodotyrosyl residues to form iodothyrglobulin
  • agranulocytosis, early signs- fever, and sore throat
  • discontinue drug and give granulocyte-stimulating factor
41
Q

Nelson Syndrome

A

-excessive hyperpigmentation from excessive ACTH from pituitary adenoma

42
Q

symptoms of excessive aldosterone vs adrenal insufficiency-name diseaeses

A
  • Conn syndrome (hyperALDO)- hypertension, hypernatremia, and hypokalemia
  • Addison ( adrenal insufficiency) hypotension and weakness, increased skin pigmentation, and hyperkalemia
43
Q

antibodies present in type 1 diabetes

A

antibodies against glutamic acid decarboxylase (enzyme present in beta cells)

44
Q

breast mass size required for fine-needle aspiration

A

greater than 4cm in post-pubertal pt

45
Q

cinacalet-def, mech, uses (2)

A

calcimimetic agent that increases sensitivity of parathyroid calcium-sensing receptor to Ca2+ leading to a reduction in PTH
-used to manage sencondary hyperPTH in pt wih chronic renal dz and treat hyperCa2+ in pt with parathyroid cancer

46
Q

relationship b/t phosphate and Ca2+

A

they tend to precipate together. too much phosphate can lead to hypoCa2+

47
Q

cretinism-develops from, symps, can’t produce, role of mother

A

infantile hypothyroidism,
appears normal at first and then develops feeding problems, somnolence, constipation, and failure to thrive.
-maternal-fetal transfer of T4 initially mask the condition

48
Q
complications of diabetes dugs:
glucagon
metformin
glyburide
miglitol
repaglinide
A
  • pain at site of injection and hyperglycemia
  • lactic acidosis (increased anion gap acidosis)
  • hypoglycemia
  • abdominal discomfort and flatulence
  • hypoglycemian, nausea and vomiting
49
Q

calculate anion gap

A

Na+ - (Cl- +HCO3-)

normal 10-12

50
Q

pentagrin-stimulate calcitonin secretion is a maker for vs serum gastrin

A

medullary carcinoma of thyroid a component of MEN IIa

-marker for pancreatic and duodenal endocrine tumors send in MEN I, they also secrete insulin or glucagon

51
Q

MEN I vs MEN II

A

both have parathyroid hyperplasia
big clue is mutliple angiofibromas and or lipomas seen in MEN I pts

MEN I- pituitary, parathyroid, and pancreas
MEN IIa-parathyroid, pheo, and medullary thyroid carcinoma

52
Q

triiodothyronine aka

A

T3

53
Q

if coritsol is increased but MRI brain scan is normal-pt has, levels of CRH and ACTH

A

then pt has primary hypercortisolism of adrenal orgrin

ACTH and CRH are decreased due to feedback mechanism