Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
80 Cards in this Set
- Front
- Back
what is the difference between pheo and neuroblastoma?
|
neroblastoma does ot cause episodic hypertension
|
|
what is common to TSH, LH, FSH, hCG?
|
alpha subunit
|
|
what are the acidophils? basophils?
|
acidophils = GH, prolactin (maybe a chromophobe?)
basophils - FSH, LH, ACTH, TSH |
|
what effect does insulin have on sodium?
|
increase sodium reteniton in the kidneys
|
|
name 6 organs that do not need isulin for glucose uptake
|
BRICKL
brain, RBCs, intestine, cornea, kidney, liver |
|
GLUT-1? GLUT-2
|
Glut1 - RBC, brain. GLUT-2 = beta cells, liver, kidney
|
|
what is the most common cell in pituitary gland?
|
somatotrophs
|
|
What 2 hormones regulate prolactin?
|
dopamine and TRH (hypothyroidism causes hyperprolactinemia)
|
|
what 2 hormones does somatostatin inhibit?
|
GH, TSH
|
|
prolactin regulates its own secretion via what?
|
increasing dopamine syntehsis from hypothalamus
|
|
what enzyme converts prenenolone to progesterone?
|
3betahydroxysteroid dehydrogenase
Fetal adrenal gland lacks this enzyme, only makes DHEA (can't make androstenedione |
|
what metabolites build up in 11betahydroxylase deficiency
|
11-deoxycorticosterone, 11-deoxycortisol. no corticosterone, cortisol are made
|
|
17-hydroxylase defciiecny causes what sex charateristics in men and women?
|
men = pseudohermaphroditism (no internal structures cause of MIF, externally female)
women - externally phenotypic female with normal internal sex organs, but lacking secondary sexual characteristics |
|
how does cortisol cause hypertension?
|
upregulates alpha receptors on arterioles
|
|
what effect does magnesium have on PTH, and are causes of low magnesium
|
decrease free magnesium decreases PTH (due to diarrhea, aminoglycosides, diuretics, alcohol abuse)
|
|
effect of PTH on osteoblasts/clasts?
|
directly stimulates osteoblasts, indirectly osteoclasts
|
|
what is PTH also known as
|
1-84 (84 amino acids)
|
|
in hyperPTH, what are the finger findings? skull findings?
|
subperiosteal thinning on radial side of 2,3 fingers. skull has salt and pepper appearance
|
|
D3 source? D2 source?
|
D3 = sun, D2 = plants
|
|
what effect does calcitriol have on bones?
|
increases bone resorption of calcium and phosphate to increase it in blood and for new bone remodelling
|
|
hormones of cAMP?
hint: FLAT CHAMP CG |
FSH, LH, ACTH, TSH, CRH, hCG, ADH, MSH, PTH, Glucagon, Calcitonin
|
|
IP3 pathway?
|
GnRH, GHRH, oxytocin, ADH V1, TRH
|
|
tyrosine kinase?
|
insulin, IGF-1, growth factors, cytokines, prolactin, GH (GH, prolactin, HPL are chemical homologues)
|
|
Which use JAK STAT
|
prolactin, GH, cytokines
|
|
Which have intrinsic TK activity?
|
insulin, growth factors FGF/PDGF
|
|
which pathways use GTP?
|
MapKinase/RAS and GPCR (which have intrinsic GTPase)
|
|
which hormone has it's receptor in nucleus
|
thyroxine and T3
|
|
effects of Thyroid hormone?
|
bone growth (permissive for GH), CNS maturation, increase B1 receptors in heart, increase basal metabolic rate via Na/K atpase, glycogenolysis, gluconeognesis, lypolysis
|
|
which hormone feedsback back, T3 or T4
|
T3
|
|
what is the dexamethasone suppression test measuring?
|
cortisol levels, not ACTH
|
|
causes of secondary hyperaldosteronism?
|
renal artery stenosis, CRF, CHF, cirrhosis, nephrotic syndrome
|
|
causes of Addison's disease?
|
CHRONIC insufficiency via autoimmune (most common in US), TB, metastasis
|
|
what is a big difference between primary and secondary addisons?
|
no pigmentation and no hyperkalemia (aldosterone works normally)
|
|
what is waterhouse friderichsen syndrome associated with?
|
DIC, endotoxic shock, Neisseria septicemia (no meningitis)
|
|
Pheos?
malignant, calcify, kids? |
nope, benign, don't calcify, occur in adults
|
|
paraneoplastic syndrome of neuroblastoma?
|
opsoclonus-myoclonus (nonrhythmic eye movmeent with myoclonus). N-myc copies most prognosticotr. pseudorosettes on histo
|
|
hypothyroidism - describe the skin. what about muscle. what about T3resin uptake?
|
skin is dry an dcool
muscle - CPK increased due to myopathy T3 resin uptake - decreased (cause the resin will bind radiolabelled T3 that doesn't bind TBG) |
|
Hashimotors - what is it like at begining?
|
hashitoxicosis
|
|
histo of hashimoto's? antibodies?
|
histo: germinal center, lympohcytic infiltrate. hurthle cells (enlarged epithelial cells with abundant eosinophilic granular cytoplasm as a result of altered mitochondria)
antibodies: antimicrosomal, antithyrogobulin. |
|
difference of sporadic and endemic cretinism?
|
sporadic - defec tin T4 formation or development failure in thyroid formation, not lack of dietary iodine
|
|
in thyroiditis, is there increased iodine uptake or decreased?
|
decreased
|
|
what is lympohcytic subacute thyroiditis? Painful or not?
|
Subacute painless lymphocytic thyroiditis – known as silent thyroiditis.
features a small goiter without tenderness. This condition tends to have a phase of hyperthyroidism followed by a return to a euthyroid state, and then a phase of hypothyroidism, followed again by a return to the euthyroid state. The time span of each phase can vary; however, each phase usually lasts 2-3 months. heavy lymphocytic infiltrate, germinal centers |
|
when does Graves present? what is the cause of death?
|
presents during stress (pregnancy). catecholamine stress induced surrge leads ot death by arrhthmia. the dermopath of graves = pretibial myxedema, diffuse lower skin thickening
|
|
what is a toxic multinodular goiter?
|
focal patches of hyperfuncitoning follicular cells independently working due to mutation in TSH receptor, nodules not malignant
|
|
what is Jod-Basedow phenomenon
|
JodBasedow effect - iodine overload may stimulate autonomous nodules. This can cause THYROTOXICOSIS in patient with toxic multinodular goiter following administration nof iodine rich radiographic contrast media and iodinated drugs (amiodarone)
|
|
What cancer occurs with Hashimoto's?
|
lymphoma
|
|
what thyroid cancer has best prognosis? what is the mutation in both familial and sporadic medullary carcinoma?
|
papillary has best prognosis. follicular is second best.
medullary carcinoma has RET protooncogene in both forms |
|
some causes of hypercalcemia?
|
hyperthyroid (breaking odwn of bone), addison's disease, zollinger-ellison syndrome, excess vitamin D or A, paget's disease if patient is immobilized
|
|
most common cause of hyperPTH primary?
|
adenoma
|
|
what is the calcium level in urine of primary hyperPTH
|
hypercalciuria (renal stones)
|
|
what is trousseua's sign
|
occlusion of brachial artery with BP cuff gives a carpal spasm
|
|
what is Albright's hereditary osteodystrophy?
|
pseudohypoparathyrodism
AD, short stature, retardation, short 4/5 digits. Gs subunit not responsive |
|
what is pituitary apoplexy?
|
a bleed into the adenoma
|
|
what is the cause of laron dwarfism?
|
defective GH receptor at liver
|
|
treatment of acromegaly? diagnosis of it?
|
pituitary adenoma resection followed by octreotide
diagnosis - serum IGF1 levels and failure to suppress serum GH following GTT |
|
what factors increase GH?
|
stress, exercise, hypoglycemia
|
|
what are some causes of central DI?
|
histiocystotis X, pituitary tumor, trauma
|
|
treatment of central DI? nephrogenic DI?
|
central - intranasal desmopressin
nephorgenic - HCTZ, indomethacin, or amiloride |
|
in SIADH, what is the total body volume?
|
normal
|
|
causes of SIADH?
|
ectopic ADH, CNS disorders, pulmonary disease, cyclophosphamide, oral hypoglycemic agent chlorpropamide, carbamazepine, oxcarbazepine (a derivative of carbamazepine),
|
|
what fat does your waist represent? what about hip?
|
waist = visceral fat
hip = subcutaneous |
|
what are the osmotic injuries in DM?
|
neuropathy (schwann cells), cataracts
|
|
what is more genetic, DMI or II
|
DMII
|
|
what is the cause of ketoacidosis? which ketoacid is made in the highest quantity?
|
increased free fatty acids
beta-hydroxybutyrate is made most |
|
what is the rule of 1/3 with carcinoids? treatment?
|
1/3 metastasize
1/3 present with 2nd malignancy 1/3 are multiple tx - octreotide |
|
what is the newest addition to MEN2A = sipple's syndrome?
|
lichen amyloidosis
pruritic, scaly, papular, and pigmented, and located in the interscapular region or on the extensor surfaces of the extremities |
|
what is MEN 2b?
|
medullary thyroid, pheo, oral and intestinal ganglioneuromatosis with marfanoid habitus
|
|
what are the short acting insulin? intermediate? longa cting?
|
short acting = lispro, regular, aspart
intermeidat e= NPH (2 shorts/day) long acting = glargine, determir lispro, aspart as the fastest acting |
|
what are the first generation sulfonylureas and side effects?
|
tobutamide
chlorpropamide (note: chlorpromazine = antipsychotic) disulfiram reaction |
|
how does metformin work?
contraindications? |
decreases hepatic gluconeogenesis and increases glycolysis. overall acts as insulin sensitizer
contraindications - renal failure or heart failure |
|
what are 3 side effects of thiazolidinediones/glitazones?
|
edema, hepatoxicity, CV toicity (contraindicated in CHF)
check LFTs |
|
pramlintide MOA?
|
amylin analogue cosecreted by beta cells that causes decreased glucagon
reduces postprandial glucose increases via the following mechanisms: 1) prolongation of gastric emptying time, 2) reduction of postprandial glucagon secretion, and 3) reduction of caloric intake through centrally-mediated appetite suppression |
|
exenatide MOA? side effect?
|
GLP-1 mimetic that increases isulin release
may cause pancreatitis |
|
sitagliptin MOA?
|
DPP-4 inhibitor that increases insulin. DPP IV degrades incretin (GLP-1)
|
|
how does orlistat work?
|
alters fat metabolism by inhibitng pancreatic lipases
|
|
what is Sibutramine?
|
SNRI and MAOi for obesity management
|
|
treatment of thionamide induced agranulocytosis?
|
G-CSF (filgrastim)
|
|
what is octreotide used for?
|
acromegaly, carcinoid, gastinoma, glucagonoma, esophageal bleeding
|
|
oxytocin uses?
|
stimulate labor, uterine contractions, milk let down, and control uterine hemorrhage
|
|
names of glucocorticoids? mechanism?
|
hydrocortisone, triamcinolone, budesonide, beclomethasone
mechanism - decrease PLA2 and COX2 expression |