Endocrinology Flashcards
sx associated w. gigantism
HA
visual defects
wt gain
enlarged forehead/hands/feet/tongue
diaphoresis
acromegaly and gigantism are caused by
1. mc - pituitary adenoma that secretes GH
2. non pituitary tumors secreting GnRH
gigantism is GH secretion in:
acromegaly is GH secretio in:
gigantism: childhood (before epiphyseal closure)
acromegaly: adulthood
dx for gigantism/acromegaly
-GH test 2 hr after glucose load
-increased IGF-1
-MRI/CT
tx for gigantism/acromegaly
pituitary tumor removal
primary adrenal insufficiency is aka
addison’s dz
25 yo M w. fatigue, wt loss, recurrent n/v, and weakness - PE shows darkened skin - BP 90/70
addison’s dz
hallmark labs of addison’s
hyponatremia
hyperkalemia
pathophys of addison’s
AI destruction of adrenal cortex -> loss of cortisol
6 nonspecific sx of addison’s
hyperpigmentation
hypotn
fatigue
myalgias
GI
wt loss
dx for addison’s
high dose cosyntropin stimulation test - cortisol measured after cosyntropin injxn
what is cosyntropin
synthetic ACTH
normal response to cosyntropin test
rise in blood and urine cortisol after injxn
addison’s dz findings of consyntropin test
little to no increase (<20 mcg) in cortisol levels after cosyntropin injxn
tx for addison’s: maintenance vs crisis
maintenance: hydrocortisone/prednisone daily
crisis: IV saline, glucose, steroids
collection of s/sx due to prolonged exposure to cortisol
cushing’s syndrome
ACTH secreting pituitary microadenoma
cushing’s dz
cushing’d dz is aka
secondary cushing’s
hallmark features of cushing’s dz
obesity
buffalo hump
moon facies
supraclavicular fat pads
htn
excessive thirst
polyuria
pigmented striae
sx of cushing’s dz
backache
HA
oligomenorrhea/amenorrhea
ED
emotional lability
psychosis
gs dx for cushing’s dz
1. 24 hr urine free cortisol - gs/initial
2. ACTH level to confirm cortisol source
alt: low dose dexamethasone suppression test
what do high and low ACTH levels indicate when working up cushing dz
high: ACTH dependent cause (pituitary adenoma) -> order a brain MRI
low: ACTH independent cause (adrenal mass) -> order adrenal CT
how does the low dose dexamethasone suppression test work
- give low dose dexamethasone
- failure of steroid to decrease cortisol -> dx of cushing’s ->
- order high dose dexamethasone suppression test -> 4. no cortisol suppression = cushing’s syndrome
- suppression of cortisol -> exclude cushing’s
tx for cushing’s dz
transsphenoidal selective resection of pituitary tumor
diabetes insipidus is caused by
deficiency/resistance to vasopressin (ADH) -> decreases kidney reabsorption of water -> massive polyuria
2 types of diabetes insipidus
central - mc
nephrogenic
deficiency of ADH from posterior pituitary/hypothalamus -> no ADH production
central diabetes insipidus
cause of central diabetes insipidus
AI destruction of posterior pituitary:
head trauma
brain tumor
infxn
sarcoidosis
lack of reaction to ADH -> partial vs complete insensitivity to ADH
neprogenic diabetes insipidus
4 causes of nephrogenic diabetes insipidus
drugs
hypercalcemia
hypokalemia
ATN
2 drugs mc associated w. nephrogenic diabetes insipidus
lithium
ampho b
dx for diabetes insipidus
-high serum osmolality: unable to stop secretion of water into kidneys
-water deprivation test: continued production of dilute urine despite water deprivation
-desmopressin stimulation test
most reliable test for diabetes insipidus
water deprivation
desmopressin stimulation test of central vs nephrogenic diabetes insipidus
central: reduction in urine output due to response to ADH
nephrogenic: continued production of dilute urine (no response to ADH)
tx for diabetes insipidus: central vs nephrogenic
central: desmopressin/DDAVP
nephrogenic: Na and pro restriction, HCTZ, indomethacin
what abs are associated w. T1DM
HLA-DR3/4/O
islet cell
GAD65
IA-2
what is the dawn phenomenon
decreased insulin sensitivity/nightly surge of counter-regulatory hormones during nighttime fasting -> elevated BG from 2-8 AM
management of dawn phenomenon
bedtime injxn of NPH insulin
avoid late night CHO
what is the somogyi effect
surge in nocturnal growth hormone -> nocturnal hypoglycemia followed by rebound hyperglycemia
management of somogyi effect
decreased nighttime NPH dose
bedtime snack
what is the insulin warning
progressive rise in BG from bedtime to morning
sx of DKA
fruity breath
wt loss
rapid respirations
hypotn
management of DKA
-admit
-large volume IVF NS
-electrolyte replacement
-insulin
dx for DM
one of the following:
-random BG > 200 x 2
-fasting BG BG > 126 x 2
-BG > 200 following 3 hr OGTT
-A1C > 6.5
gs dx for GDM
3 hr OGTT
high fasting C-peptide is associated with which type of DM
type 2
low or inappropriately normal fasting C-peptide levels suggest which type of DM
type 1
BG goals for DM
fasting: <130
postprandial: <180
moa for metformin
decreases:
hepatic glucose production
peripheral glucose utilization
intestinal glucose absorption
2 main s.e of metformin
lactic acidosis
GI
contraindications for metformin
GFR <30
Cr >1.5
not recommended for GFR 30-45
name 3 sulfonylureas
glyburide
glipizide
glimepiride
moa for sulfonylureas
insulin secretagogue
main s.e of sulfonylureas
hypoglycemia
name 2 thiazolidinediones
pioglitazone
rosiglitazone
moa for thiazolidinediones
increase peripheral insulin sensitivity
contraindications for thiazolidinediones
CHF
liver dz
2 s.e of thiazolidinediones
fluid retention
wt gain
name 2 alpha-glucosidase inhibitors
acarbose
miglitol
moa for alpha glucosidase inhibitors
delay intestinal glucose absorption
s.e of alpha glucosidase inhibitors to know
GI
name 2 meglitinides
repaglinide
nateglinide
moa for meglitinides
insulin secretagogue
s.e to know of meglitinides
hypoglycemia
name the GLP-1 agonists
exenatide
dulaglutide
semaglutide
liraglutide
moa for GLP-1 agonists
incretin mimetic -> insulin secretagogue
decrease glucagon -> delay gastric emptying
s.e of GLP-1 agonists
GI
caution using GLP-1 agonists in pt’s w. what condition
gastroparesis
2 benefits of GLP-1 agonists
wt loss
reduced CV mortality
name 2 DPP-4 inhibitors
sitagliptin
saxagliptin
moa for DPP-4 inhibitors
dipetpidylpetase inhibition -> inhibit degradation of GLP-1 -> increase insulin secretion and delay gastric emptying
s.e of DPP-4 inhibitors
increased risk of heart failure