Endocrine (U.W.) Flashcards

1
Q

what nerve runs with the superior thyroid A? What does it supply

A

External Br of Superior Laryngeal N

Cricothyroid

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2
Q

list the cells that originate from NCC

A
MOTEL PASS
melanocytes
Odontoblasts
tracheal cartilage
enterochromaffin cells 
laryngeal cartilage 
parafollicular cells of thyoid 
adrenal medulla and all ganglia 
schwann 
spiral membrane
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3
Q

central ADH is most likely due to damage of which stucture?

A

HYPOTHALAMUS (SVN, PVN)
(note post pit injury may cause transeint Central DI but not permanent bc its just a storage and release spot, the hypothalamus can undergo wallerian regen and get its ADH out there again)

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4
Q

how does estrogen affect thyroid levels

A

it increases TBG levels.. less free thyroid hormone will feed back to pituitary and increase TSH which will increase thyroid hormone production. All in all, TOTAL thyroid hormone will increase but FREE thyroid hormone will stay normal

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5
Q

anosmia + hypogonadism

A

Kallman’s

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6
Q

how does insulin allow for glycogen synthesis?

A

through the tyrosin kinase pathway, through PIP3 which activates PROTEIN PHOSPHATASE and this activates GLYCOGEN SYNTHASE

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7
Q

whats needed for the cell to shift to gluconeogenesis

A

It must get Pyruvate (usually from Alanine) and this Pyruvate must undergo Pyruvate Carboxylase to go towards Gluconeogenesis ( not pyruvate dehydrogenase which is in glycolysis) for pyruvate carboxylase to happen, there needs to be INCREASED acetyl COa

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8
Q

Sheehan Syndrome

A

Panhypopituitarism (low prolactin, low TSH etc) post delivery of baby.Cause: ischemia
during pregnancy pituitary undergoes hypertrophy. During birthing if there is hemorrhage, the blood supply may not be enough for pituitary

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9
Q

thyroid imbalance following viral infection with painful thyroid to palpation

A

deQuervain’s aka subacute granulomatous

note while this is hypothyroid, there can be transient hyperthyroid

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10
Q

electrolyte results of primary adrenal insufficiency

A

hyponatremia
hyperkalemia
hyperchloremia
non-anion gap metabolic acidosis

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11
Q

what diabetes medication has high risk of hypoglycemia? why?

A

Sulfyureas (espcially long acting ones like Glyburide) because of their ability to close K+ channels independent to glucose concentration, causing insulin release from B cell independent of glucose level

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12
Q

how do glucocorticoids,glucagon, tnfalpha, etc cause insulin resistance

A

they phosphorylate the intracellular ser or threonine of membrane tyrosine receptor (insulin receptor) blocking insulin’s downstream effects

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13
Q

HAART can cause which undesired side effect physically?

A

lipdystrophy
thinning of arms and legs
fat on central

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14
Q

in a normal metyrapone test what is likely to be seen?

A

increase in ACTH
increase in 11 OHcortisol
increase in urinary 17 hydroxycorticosteroid levels

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15
Q

what enzyme is necessary to use glycerol to make glucose

A

glycerol kinase

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16
Q

why would a pituitary resection affect epineprhine levels???

A

The final step of Epinephrine synthesis is NE–> Epi via PNMT in adrenal medulla. PNMT requires cortisol to be active. If pituitary is resected, ACTH is low and thus cortisol is low

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17
Q

what reaction makes DOPA

A

Tyrosine Hydroxylase with THB as cofactor

18
Q

which thyroid cancer: nest/sheet of polygonal cells derviced from parafollicular C cells? Stains for Congo Red

A

Medullary Thyroid Ca

19
Q

Kleinfelter’s, what going on with LH/FSH?

A

Kleinfelters XXY, cause of long extremeties, gynecomastia and small testes. Problem is destruction of the Leydig and Sertoli Cells. These cells are no longer able to make T and sperm respectively. Lack of neg feedback leads to elevated LH and FSH

20
Q

mononuclear infiltrate, dense with lymphocytes making follicular centers, Hurthle cells might be seen

A

Hashimoto’s

21
Q

what amino acids are best for a pt with PDH def?

A

Lysine and Leucine. They are both AA that are only ketogenic, not glucogenic. So there is no chance they will go down the glycolysis pathway and encounter the defective PDH

22
Q

corticosteroid reduce levels of all types of WBC except one type? which one and why?

A

corticosteroid actually INCREASE neutrophil count in the blood. This is because it causes the neutrophils to detatch from blood vessel walls reducing its ability to fight an infection

23
Q

how does the sympathetic nervous system affect insulin release?

A

alpha 2- inhibits insulin release
beta 2- stimulates insulin release
note that alpha 2 predominates, so when epinephrine binds although it binds to both, inhibition overrides

24
Q

vol status of SAIDH pt? why

A

EUvolemic

even though Na+ levels are low, compensatory increase in natureitic peptides and decrease in RAAS keeps euvolemia

25
Q

Conn’s syndrome electrolytes?

A

Na+ - normal, would expect to be high but ALDOSTERONE escape
K+ - low
HCO3- - increased b/c H+ is being excreted more, HCO3- is being reabsorbed more due to exchanger (H+/HCO3- exchanger)
H+- low, aldosterone increase H+ excretion (met alk)

26
Q

which GI drug leads to hypertriglyceridemia?

A

Bile Acid binding resins (chloestyramine)

27
Q

which enzyme is needed to make glycerol go to gluconeogenesis after fat breakdown

A

glycerol kinase

28
Q

Familial Hypocalcuric Hypercalcemia

A

AD disorder of Ca sensing receptors in parathyroid. This increases the setpoint, HIGHER Ca2+ levels are required to stop PTH production. So even at moderately high Ca2+ levels, PTH will be increased. Note the CaSR is a transmembrane G-coupled metabotropic

29
Q

impaired beta oxidation what might be responsible?

A

defect in Acyl CoA dehydrogenase

defect in carnitine transport

30
Q

thiamine is needed for?

A

pyruvate dehydrogenase
alpha ketoglutarate dehydrogenase
transketolase

31
Q

pyruvate –> OAA what is the cofactor?

A

biotin

32
Q

Leuprolide

A

GnRH analog

33
Q

which thyroid cancer: large cells, overlapping nuclei, fine and sparse chromatin, ground glass appearance, grooves in nucleus

A

Papillary Carcinoma (thyroid)

34
Q

how do adipocytes respond to insulin resistance?

A

with insulin resistance, lipolysis occurs more (remember, insulin inhibited lipolysis). this causes an increase in FFA, which WORSENS insulin resistance by increasing hepatic gluconeogenesis (even high blood sugars) and impairing glucose transport into cells

35
Q

symptoms of Niacin deficiency+ neutral AA in urine?

A

Hartnup Disease

36
Q

what does PPP do?

A

(1) make bases
(2) generate NADPH which is needed for
(a) glutathione- RBC stability
(b) bioSYNTHESIS of fats and cholesterols

37
Q

maturity onset diabetes in the young (ex: gestational) is caused by?

A

mutations in glucokinase

which is to do glycolysis in the pancreatic B cells producing insulin

38
Q

what happens to a fetus that has a hyperglycemic mom

A

B cells hypertrophy (note insulin does not cross the placenta)

39
Q

in alcoholism and DKA how are ketone ratios different than normal

A

normally- acetoacetate and 3-hydroxybutyrate are somewhat equal. In DKA and alcoholism, there is way more 3-hydroxybutyrate than acetoacetate due to high NADH levels

40
Q

Hashimoto’s has what unexplained clinical abnormality

A

amenorrhea