Endocrine (U.W.) Flashcards
what nerve runs with the superior thyroid A? What does it supply
External Br of Superior Laryngeal N
Cricothyroid
list the cells that originate from NCC
MOTEL PASS melanocytes Odontoblasts tracheal cartilage enterochromaffin cells laryngeal cartilage parafollicular cells of thyoid adrenal medulla and all ganglia schwann spiral membrane
central ADH is most likely due to damage of which stucture?
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)
how does estrogen affect thyroid levels
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
anosmia + hypogonadism
Kallman’s
how does insulin allow for glycogen synthesis?
through the tyrosin kinase pathway, through PIP3 which activates PROTEIN PHOSPHATASE and this activates GLYCOGEN SYNTHASE
whats needed for the cell to shift to gluconeogenesis
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
Sheehan Syndrome
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
thyroid imbalance following viral infection with painful thyroid to palpation
deQuervain’s aka subacute granulomatous
note while this is hypothyroid, there can be transient hyperthyroid
electrolyte results of primary adrenal insufficiency
hyponatremia
hyperkalemia
hyperchloremia
non-anion gap metabolic acidosis
what diabetes medication has high risk of hypoglycemia? why?
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
how do glucocorticoids,glucagon, tnfalpha, etc cause insulin resistance
they phosphorylate the intracellular ser or threonine of membrane tyrosine receptor (insulin receptor) blocking insulin’s downstream effects
HAART can cause which undesired side effect physically?
lipdystrophy
thinning of arms and legs
fat on central
in a normal metyrapone test what is likely to be seen?
increase in ACTH
increase in 11 OHcortisol
increase in urinary 17 hydroxycorticosteroid levels
what enzyme is necessary to use glycerol to make glucose
glycerol kinase
why would a pituitary resection affect epineprhine levels???
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
what reaction makes DOPA
Tyrosine Hydroxylase with THB as cofactor
which thyroid cancer: nest/sheet of polygonal cells derviced from parafollicular C cells? Stains for Congo Red
Medullary Thyroid Ca
Kleinfelter’s, what going on with LH/FSH?
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
mononuclear infiltrate, dense with lymphocytes making follicular centers, Hurthle cells might be seen
Hashimoto’s
what amino acids are best for a pt with PDH def?
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
corticosteroid reduce levels of all types of WBC except one type? which one and why?
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
how does the sympathetic nervous system affect insulin release?
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
vol status of SAIDH pt? why
EUvolemic
even though Na+ levels are low, compensatory increase in natureitic peptides and decrease in RAAS keeps euvolemia
Conn’s syndrome electrolytes?
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)
which GI drug leads to hypertriglyceridemia?
Bile Acid binding resins (chloestyramine)
which enzyme is needed to make glycerol go to gluconeogenesis after fat breakdown
glycerol kinase
Familial Hypocalcuric Hypercalcemia
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
impaired beta oxidation what might be responsible?
defect in Acyl CoA dehydrogenase
defect in carnitine transport
thiamine is needed for?
pyruvate dehydrogenase
alpha ketoglutarate dehydrogenase
transketolase
pyruvate –> OAA what is the cofactor?
biotin
Leuprolide
GnRH analog
which thyroid cancer: large cells, overlapping nuclei, fine and sparse chromatin, ground glass appearance, grooves in nucleus
Papillary Carcinoma (thyroid)
how do adipocytes respond to insulin resistance?
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
symptoms of Niacin deficiency+ neutral AA in urine?
Hartnup Disease
what does PPP do?
(1) make bases
(2) generate NADPH which is needed for
(a) glutathione- RBC stability
(b) bioSYNTHESIS of fats and cholesterols
maturity onset diabetes in the young (ex: gestational) is caused by?
mutations in glucokinase
which is to do glycolysis in the pancreatic B cells producing insulin
what happens to a fetus that has a hyperglycemic mom
B cells hypertrophy (note insulin does not cross the placenta)
in alcoholism and DKA how are ketone ratios different than normal
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
Hashimoto’s has what unexplained clinical abnormality
amenorrhea
