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;
88 Cards in this Set
- Front
- Back
- 3rd side (hint)
Which adrenal vein is longer?
|
Left
goes via the left renal vein before draining to the IVC, whereas the right goes directly to IVC |
same as left vs. right gonadal veins
|
|
What is the distribution of islet cells within a pancreatic bud?
|
inner = beta cells
outer = alpha cells interspersed = delta |
|
|
physio of insulin release:
|
glucose comes in via the GLUT-2 transporter ==> inc. ATP ==> closing of K+ channels ==> opening of Ca2+ channels ==> depol ==> exocytosis of insulin
|
|
|
what does insulin to to K+ uptake?
|
increases it
|
|
|
where are the GLUT-4 receptors found?
|
in the insulin dependent glucose uptake cells: adipocytes and skeletal muscle
|
|
|
Where are the GLUT-1 receptors found?
|
RBC's and brain (insulin-independt uptake of glucose)
|
|
|
Where are the GLUT-2 receptors found?
|
pancreas
liver kidney SI |
|
|
What does somatostatin do to HPA hormone regulation?
|
inhibits both GH and TSH release
|
|
|
What does TRH do to HPA hormone regulation?
|
stimulates release of both TSH and prolactin
|
|
|
17-alpha-hydroxylase deficiency pathophys
|
you can't convert pregnenolone or progesterone into gluccocorticoid or DHEA precursors so:
inc. mineralocorticoids dec. cortisol dec. sex hormones |
|
|
17-alpha-hydroxylase deficiency symptoms
|
HTN
HypOkalemia XY: pseudohermaphroditism (you look female but you don't have repro organs inside) XX: you are a woman inside but you don't develop 2ndary sex characteristics |
|
|
21-hydroxylase deficiency pathophys
|
inc. sex hormones
dec. mineralocorticoids dec. cortisol |
|
|
21-hydroxylase deficiency sx
|
HypOtension
hyperkalemia inc. renin ==> volume depletion/salt-wasting ==> hypovolemic shock in newborn XY: masculinization XX: female pseudohermaphitidism |
????
|
|
11-beta-hydroxylase deficiency pathophys
|
dec. cortisol
dec. aldosterone/corticosterone inc. sex hormones there is a back-up in the aldosterone syn pathway at the level of 11-deoxycorticosterone which builds up and has some cross-reactivity with aldosterone receptors in kidneys |
|
|
11-beta-hydroxylase deficiency sx
|
HTN
masculinization |
|
|
What are the functions of cortisol?
|
BBIIG:
Blood pressure (up-regulates alpha-1) Bone formation (dec.) Anti-inflammatory Immune function (dec.) Gluconeogensis (inc.) + lypolysis, proteolysis) - opposed the effects of insulin |
|
|
what does magnesium do to PTH secretion?
|
dec. MG = dec. PTH secretion
(as in aninoglycosides, diuretics and etoh abuse) |
|
|
Which hormones use cAMP signaling?
|
FLAT CHAMP
FSH, LH, ACTH, TSH, CRH, hCG, ADH(V2), MSH, PTH plus: calcitonin, GHRH, glucagon |
|
|
Which hormones use cGMP signaling?
|
ANP
NO (EDRF) |
|
|
Which hormones use IP3 signaling?
|
GOAT:
GnRH Oxytocin ADH(V1) TRH |
|
|
Which hormones use tyrosine kinase (MAP kinase pathway) signaling?
|
growth factors:
Insulin IGH-1 FGF PDGF |
|
|
Which hormones use tyrosine kinase (JAK/STAT pathway) signaling?
|
GH
prolactin (cytokine IL-2) |
|
|
Thyroid hormone functions
|
Brain maturation
Bone growth Beta-adrenergic effects (upregulates beta-1 receptors in heart) Basal metabolic rate inc. |
|
|
How does thyroid hormone increase BMR?
|
1) inc. Na+/K+-ATPase activity = inc. O2 consumption, RR, body temp
2) inc. glycogenolysis, gluconeogenesis, lipolysis |
|
|
What inhibits iodine uptake from blood into follicular cells?
|
anions like perchlorate and pertechnetate
|
|
|
What enzyme is responsible for thyroid hormone production
|
peroxidase:
oxidizes iodine and couples thyroglobulin to I2 to form MIT and DIT |
|
|
Dexamethasone suppression test interpretation
|
If it is due to over production of ACTH (pit. tuomr) then it will suppress cortisol but only if given at higher than normal doses
If it is due to ectopic ACTH (eg small cell lung cancer) it will not suppress If it is due to overproduction of cortisol with low ACTH (eg from an adrenal adenoma) it will not suppress If it is |
|
|
Primary hyperaldosteronism finding:
|
decreased renin
HYPERtension HYPOkalemia metabolic alkalosis |
|
|
What is Conn's syndrome?
|
primary hyperaldosteronism
|
|
|
Conn's syndrome tx
|
surgery to remove adrenal tumor and/or spironolactone (aldosterone antagonist, K+ sparing)
|
|
|
What is Addison's disease?
|
chronic primary adrenal insufficiency due to adrenal atrophy or destruction
low aldo and cortisol |
|
|
Addison's disease sx?
|
Adrenal insufficiency so:
HYPOtension (due to hyponatremia) HYPERkalemia Metabolic acidosis skin hyperpigmentation |
|
|
Causes and findings in secondary adrenal insufficiency:
|
dec. ACTH from pituitary
hypotension/hyponatremia (no hyperkalemia or skin hyperpigmentation as with primary) |
|
|
Waterhouse-Friderichsen syndrome
|
acute primary adrenal insufficiency due to adrenal hemorrhage associated with N. meningitidis septicemia, DIC and endotoxic shock
|
|
|
From what cells/embryonic origin to adrenal medulla cells arise?
|
chromaffin cells
neural crest |
|
|
What conditions are pheochromocytomas associated with?
|
MEN 2A and 2B
neurofibromatosis |
|
|
Pheochromocytoma tx
|
non-selective alpha-antagonist like phenoxytbenzamine (irreversible)
surgery |
|
|
Pheochromocytoma dx test
|
elevated VMA in urine
(breakdown product of NE) |
|
|
What is neuroblastoma?
|
most common tumor of the adrenal medulla in kids - can occur anywhre along the sympathetic chain - usually does not cause HTN
|
|
|
neuroblastoma dx test?
|
elevated levels of HVA (breakdown product of dopamine) in urine)
|
|
|
Hashimoto's thyroiditis lab/histo/genetic findings
|
antimicrosomal, antithyroglobulin antibodies
HLA-DR5 Hurthle cells (lymphocytic infiltrate with germinal centers) in thyroid |
|
|
Cretinism causes and symptoms
|
fetal hypothyroidism - mom has goiter, no Iodine in diet
mental retardation dec. bone formation pot-bellied, protuberant umbilicus pale puffy-faced protuberant tongue |
|
|
Subacute (de Quervain's) thyroiditis
|
self-limited hypothyroidism following viral infection
jaw pain, very tender thyroid, may be hyper very early in its course |
|
|
Riedel's thyroiditis
|
thyroid replaced by fibrous tissue ==> hypothyroidsm
hard, painless goiter |
|
|
Jod-Basedown phenomenon
|
thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete
|
|
|
Papillary thyroid cancer findings
|
most common
excellent prognosis "ground-glass nuclei" (orphan annie) psammoma bodies nuclear grooves inc. risk if childhoo irradiation |
|
|
Follicular thyroid carcinoma findings
|
good prognosis
uniform follicles |
|
|
Medullary thyroid carcinoma findings
|
from parafollicular "C cells"
produces calcitonin sheets of amyloid stroma assoc. with MEN 2A/B |
|
|
Undifferentiate/anaplast thyroid carcinoma
|
older patients
very poor prognosis |
|
|
Primary hyperparathyroidism findings
|
hypercalcemia/hypophosphatemia ==> renal stones
weakness constipation inc. AlkPhos (from inc. bone resportion) ==> osteitis fibrosa cystica ==> bone pain (usually do to an adenoma) |
"bones, stones, groans"
|
|
Secondary hyperparathyroidism findings
|
due to chronic renal disease so secondary to Vit. D deficiency:
hypocalcemia hyperphophatemia?? |
|
|
Tertiary hyperparathyroidism findings
|
refractory phyperparathyroidism from chronic renal disease. Overshoot with PTH compensation and end up making yourself hypercalcemic
OR due to autonomous production from a PTH secreting tumor |
|
|
Albright's hereditary ostodystrophy finding/causes
|
causes pseudohypoparathyroidism because the kidneys are unresponsive to PTH
hypocalcemia shortened 4th/5th digits short stature |
|
|
Hypoparathyroid findings
|
hypocalcemia ==> tetancy
chvostek's sign (CNVII) Trousseau's sign (brachial artery) |
|
|
Acromegaly dx tests
|
inc. serum IFG-1
failure to suppress serum GH following oral glucose tolerance test |
|
|
Acromegaly tx
|
remove pit. adenoma
octreotide (somatostatin analog) |
|
|
Causes of nephrogenic DI include:
|
secondary to hypercalcemia
lithium demeclocycline (ADH antagonist) |
|
|
How do you distinguish between central and nephrogenic DI?
|
desmopressin (ADH analog) test:
central is responsive, nephrogenic is not |
|
|
What causes diabetes insipidus?
|
lack of ADH (central)
OR unresponsiveness to ADH in kidneys (nephrogenic) |
|
|
Diabetes insipidus findings
|
can't concentrate your urine (even when water deprived)
urine specific gravity <1.006 serum osmolality >290 |
|
|
Diabetes insipidus tx
|
central - intranasal desmopressin (ADH analog)
nephrogenic - HCTZ, indomethacin or amiloride |
???
|
|
SIADH sx/findings:
|
excessive water retention
hyponatremia (if sever ==> seizures) urine osmolality > serum osmolality Inc. aldosterone (compensatory) |
|
|
SIADH causes
|
ectopic ADH (small cell lung cancer)
CNS disorders/head trauma pulmonary disease drugs (cyclophosphamide) |
|
|
SIADH tx
|
demeclocycline (ADH antagonist)
H20 restriction |
|
|
Carcinoid syndrome tx
|
octreotide
|
|
|
MEN I includes:
|
Pancreatic tumors
Parathyroid tumors Pituitary tumors (commonly presents with kidney stones and stomach ulcers) |
AD
|
|
MEN 2A includes:
|
medullary thyroid carcinoma
pheochromocytoma parathyroid tumor |
AD
|
|
MEN 2B
|
medullary thyroid carcinoma
pheochromocytoma oral/intestinal ganlioneruomatosis |
AD
assoc. with ret gene |
|
Which are the rapid-acting insulin?
|
Lispro
Aspart Regular |
|
|
Which are the intermediate-acting insulin?
|
NPH
|
|
|
Which are the long-acting insulin?
|
Glargine
Detemir |
|
|
Sulfonylureas include:
|
1st gen:
tolbutamide chlorpropamide 2nd gen: Glyburide Glimepiride Glipizide |
|
|
Sulfonylureas MOA
|
close K+ channel in beta-cell so that the cell depolarizes and releases insulin via inc. Ca2+ influx
|
|
|
Sulfonylureas toxicity
|
1st gen: disulfiram-like effects
2nd gen: hypoglycemia |
|
|
Biguanides include:
|
metformin
|
|
|
Biguanides MOA
|
unknown:
dec. gluconeogenesis inc. glycolysis inc. peripheral insulin sensitivity (inc. glucose uptake) |
|
|
Biguanides toxicity
|
metformin - lactic acidosis '
*contraindicated in renal failure |
|
|
Glitazones/thazolidinediones include:
|
Pioglitazone
Rosiglitazone |
|
|
Glitazones MOA
|
bind PPAR-gamma nuclear transcription regulator ==> inc. insulin sensitivity in peripheral tissue
|
|
|
alpha-glucosidase inhibitors include:
|
acarbose
miglitol |
|
|
alpha-glucosidase inhibitors MOA
|
inhibit intestinal bursh-border alpha-glucosidases ==> delayed sugar hydroplysis and glucose absorption ==> dec. postprandial hyperglycemia
|
|
|
Glitazones MOA
|
weight gain
edema hepatotoxicity CV toxicity |
|
|
Pramlintide MOA
|
it is an amylin agonist so it:
dec. glucagon delays gastric emptying inc. satiety |
|
|
Pramlintide toxicity
|
hypoglycemia
nausea diarrhea |
|
|
Exenatide MOA
|
GLP-1 analog:
inc. insulin release dec. glucagon release |
|
|
Exenatide toxicity
|
nausea
vomiting pancreatitis |
|
|
Propylthiouracil (PTU) MOA
|
inhibit organification of iodide
inhibit coupling of thyroid hormone dec. peripheral T4==>T3 conversion |
|
|
Propylthiouracil (PTU) toxicity
|
skin rash
agranulocytosis aplastic anemia |
|