Endocrinology Flashcards
what is secreted from hypothalamus?
GnRH
TRH
CRH
CHRH
where does GnRH act
anterior pituitary -> FSH/LH
where does TRH act
anterior pituitary -> TSH
where does CRH act
anterior pituitary -> ACTH
where does GHRH act
anterior pituitary -> GH
where does FSH/LH act
ovaries -> estrogen, progesterone, ovulation
where does TSH act
thyroid -> T3, T4, metabolism
where does ACTH act
adrenals -> cortisol, stress
where does GH act
liver -> IGF-1, growth
prolactinoma path
autonomously secreting prolactin
most common pituitary lesion
prolactinoma pt
women: galactorrhea, amenorrhea, micro adenoma, no vision change
men: decreased libido, gynecomastia, macro adenomas, vision changes
prolactinoma dx
1st: TSH/fT4
then: prolactin levels
best: MRI
prolactinoma tx
bromocriptine or cabergoline
surgery
prolactinoma f/u
surgery is NOT first line therapy for prolactinomas
- it is for all other secreting pituitary tumors and macroadenomas
acromegaly path
growth hormone = things that grow
child = long bones (gigantism)
adult = visceral organs
acromegaly pt
cardiomegaly -> DIA heart failure diabetes wide-spaced teeth hat/ring/shoe size increases coarse features, carpal tunnel big hands
acromegaly dx
IGF-I
glucose suppression test
MRI
acromegaly tx
surgery first
octreotide or cabergoline (adjunct)
acromegaly f/u
glucose suppression test = give glucose, test is positive (abnormal) if the GH does not change
acromegaly wait
carpal tunnel is more associated with RA than acromegaly, don’t be tricked
acute pan hypopituitarism path
infection, infarction, surgery, rads
acute pan hypopituitarism pt
TSH: lethargy, coma
ACTH: hypotension, tachycardia
GH/LH/FSH: irrelevant
acute pan hypopituitarism dx
clinical
hormone (cortisol and T4)
acute pan hypopituitarism tx
replace end hormones
acute pan hypopituitarism f/u
Sheehan’s: pregnancy, bloody delivery
Apoplexy: tumor outgrows blood supply and dies, necrosis
chronic pan hypopituitarism path
autoimmune, deposition, cancer
GH/FSH/LH sacrificed so that TSH and ACTH can persist
chronic pan hypopituitarism pt
decrease libido, changes in menstruation
decrease growth
chronic pan hypopituitarism dx
insulin stimulation test
- growth hormone fails to rise
MRI
chronic pan hypopituitarism tx
reverse underlying cause
replace hormones prn
empty sella syndrome path
normal variant
empty sella syndrome pt
asymptomatic
empty sella syndrome dx
MRI
empty sella syndrome tx
reassurance
SIADH path
too much ADH = too much water = patient becomes hypotonic
brain lesion = increase ADH
lung lesion = increase ADH (small cell, PNA)
SIADH pt
hyponatremia
SIADH dx
UNa increase
Uosm increase
Sosm decrease
SIADH tx
water restriction
demeclocycline
reverse underlying disease
central diabetes insipidus path
central: no ADH production
central diabetes insipidus pt
polydipsia
polyuria
normal blood glucose
central DI dx
water deprivation test
- corrects with ADH = central DI
central DI tx
intranasal desmopressin (DDAVP)
nephrogenic DI path
dysfunctional ADH receptor
nephrogenic DI pt
polydipsia
polyuria
normal blood glucose
nephrogenic DI dx
water deprivation test
-FAILS to correct
nephrogenic DI tx
gentle diuresis
psychogenic polydipsia path
excess free water intake causes medullary wash out
psychogenic polydipsia pt
polyuria
polydipsia
normal blood glucose
psychogenic polydipsia dx
water deprivation test
- corrects with water restriction
psychogenic polydipsia tx
stop drinking so much
when to use FNA for thyroid nodule
best test except excisions biopsy
if any doubt - get an FNA
when to use TSH for thyroid nodule
nodule suspected of being hot/active
when to use RAIU for thyroid nodule
if not sure, either before or after FNA to push one way or the other
when to use U/S for thyroid nodule
assess nodule before FNA, identify good sites for biopsy. confirm index of suspicion
papillary thyroid cancer need to knows
most common
associated with XRT
orphan-annie nuclei and psammoma bodies
papillary architecture (FNA), h/o head and neck cancer
positive prognosis (slow growing) -> resection
follicular thyroid cancer need to knows
tumor difficult to dx on bx, looks normal
spreads hematogenously
tx resection and I2 ablation
medullary thyroid cancer need to knows
C-cells producing calcitonin -> hypo-Ca
part of MEN2a and MEN2b genetics
anaplastic thyroid cancer need to knows
found in elderly patients
grows locally and quickly
dismal px correlates to degree of anaplasia
MEN1 path
autosomal dominant MEN1
MEN1 pt
pancreas -> gastrinoma, insulinoma
pituitary -> any pituitary
parathyroid -> hyper-Ca
MEN2A path
RET
MEN2A pt
pheochromocytoma
thyroid
parathyroid
MEN2B path
RET
MEN2B pt
pheochromocytoma
thyroid
neuronal
hyperthyroidism symptoms
tachycardia diarrhea increase DTR heat intolerance weight loss AFib
hypothyroidism symptoms
bradycardia constipation decrease DTR cold intolerance weight gain
grave’s disease path
autoimmune
thyroid stimulation antibodies bind to and activate thyroid
grave’s disease pt
exophthalmos
pre-tibial myxedema
hyperthyroidism
grave’s disease dx
TSH decrease
T4 increase
RAIU: diffuse uptake throughout
thyroglobulin: increase
grave’s disease tx
medications: PTU or methimazole
surgery: thyroidectomy
radiation: RAIU
thyroiditis path
release of preformed T4 with inflammation of the thyroid
thyroiditis pt
hyperthyroidism
thyroiditis dx
TSH decrease
T4 increase
RAIU: no uptake
thyroglobulin: increase
thyroiditis tx
ß-blockers for symptom control
thyroiditis f/u
Hashimoto’s: painless, then hypothyroidism
DeQuervain’s: painful, recovery
Lymphocytic: painless, recovery
multinodular goiter/toxic adenoma path
autonomous secretion of T4
multinodular goiter/toxic adenoma pt
hyperthyroidism
nodules
multinodular goiter/toxic adenoma dx
TSH decrease
T4 increase
RAIU: uptake in goiter/adenoma only
thyroglobulin: increase
multinodular goiter/toxic adenoma tx
resection
struma ovarii/factitious path
struma = ovarian production of T4 factitious = exogenous intake
struma ovarii/factitious pt
woman, healthcare field
struma ovarii/factitious dx
TSH decrease T4 increase RAIU: NO UPTAKE struma ovarii - thyroglobulin: increase factitious - thyroglobulin: decrease
struma ovarii/factitious tx
resection
confrontation
thyroid storm path
excess thyroid hormone to the point of shock and life-threatening emergency
thyroid storm pt
shock, fever, delirium
thyroid storm dx
T4 increase, TSH undetectable
thyroid storm tx
- propranolol (control rate)
- PTU/methimazole (decrease fT4)
- IV steroids (decrease fT4->fT3)
thyroid storm tx2
radioactive iodine
surgery
hypothyroidism path
iatrogenic (most common)
Hashimoto’s (most common non-iatrogenic)
hypothyroidism pt
hypothyroidism
hypothyroidism dx
TSH increase
T4 decrease
hypothyroidism tx
levothyroxine
hypothyroidism f/u
TSH in 3mo from start, track TSH
asx + TSH <10 = subclinical = no treat
myxedema coma path
too little T4
myxedema coma pt
shock, freezing, coma, pericardial effusion
myxedema coma dx
TSH very increased
fT4 decreased
myxedema coma tx
IVF (warmed)
blankets
T4 IV
Cushing’s syndrome path
cortisol excess ACTH dependent - pituitary tumor (Cushing's disease) - lung tumor ACTH independent - exogenous ingestion - adrenal tumor
Cushing’s syndrome pt
HTN, diabetes central/truncal obesity moon face purple striae buffalo hump
Cushing’s syndrome dx
- low dose dexa suppression test, then 24hr urinary cortisol
- ACTH
- high-dose dexa suppression test
- MRI brain OR CT chest/abd/pelvis
- inferior petrosal sinus sampling
Cushing’s syndrome tx
resection
Addison’s path
deficient cortisol = adrenal
- TB worldwide
- autoimmune US
deficient ACTH = pituitary
Addison’s pt
hypotension/orthostatics
decrease Na, increase K = adrenal deficiency
hyperpigmentation = adrenal deficiency
Addison’s dx
1st: AM cortisol
then: cosyntropin stim test
- if increase cortisol -> MRI
- if no change cortisol -> CT abdomen
Addison’s tx
adrenal gland = cortisol + fludrocortisone
pituitary = cortisone alone
pheochromocytoma path
catecholamine producing tumor
pheochromocytoma pt
paroxysm pain palpitations pressure perspiration
pheochromocytoma dx
24h urinary VMA, metanephrine
CT/MRI abd
adrenal vein sampling
pheochromocytoma tx
α-blockade
ß-blockade
resection
Conn’s syndrome
primary hyperaldosteronism
Conn’s syndrome path
primary adrenal tumor = primary hyperAldo
Conn’s syndrome pt
HTN + HypoK
Conn’s syndrome dx
1st: Aldo/Renin ratio >20
then: salt suppression test
then: CT/MRI
best: adrenal vein sampling
Conn’s syndrome tx
resection
secondary hyperaldosteronism path
young woman, fibromuscular dysplasia
old man, renal artery stenosis
secondary hyperaldosteronism pt
HTN + HypoK
secondary hyperaldosteronism dx
Aldo/Renin < 10
angiogram
secondary hyperaldosteronism tx
RAS: medically manage, no stent
FMD: stent
incidentaloma path
asx, non-active, ‘thing’ on the adrenal
incidentaloma pt
asx, incidentally found on a scan for something else
incidentaloma dx
r/o hyper-functioning adenoma
- Renin:Aldo (Conn’s)
- Low dose dexa (Cushing’s)
- Urine VMA, Meta (pheo)
incidentaloma tx
ignore it, once testing is negative
diagnosing diabetes by bG
random (needs 1)
>/= 200 = diabetes
< 200 = ???
Fasting (needs 2)
>/= 125 = diabetes
100-124 = glucose intolerance
< 100 = normal
2hr post-prandial glucose tolerance test
2hrs >/= 200 = diabetes
diagnosing diabetes by A1c
normal < 5.7
prediabetes 5.7-6.4
diabetes >/= 6.5
sulfonylureas
glyburide
glipizide
sulfonylureas mechanism
increase insulin secretion
biguanides
metformin
biguanides mechanism
decrease glucose made in liver
increase insulin sensitivity
thiazolidinediones
pioglitazone
rosiglitazone
thiazolidinediones mechanism
increase insulin sensitivity
DPP-4-i
(gliptins)
sitagliptin
saxagliptin
DPP-4-i mechanism
DPP-4-i increase GLP-1
GLP-1 analogs
eventide
liraglutide
GLP-1 analogs mechanism
increase GLP-1 -> increase incretin
Lantus, Levemir class
long acting insulin
Humalog, nova log class
rapid acting insulin combo
humulin, novolin class
medium acting insulin combo
NPH class
cheap version of ‘Lin’
regular class
cheap version of ‘log’
somogyi effect
too much insulin at night -> high AM bG
dawn phenomena
too little insulin at night -> high AM bG
how to tell difference of somogyi effect and dawn phenomena?
check early AM bG to tell the difference
T1DM path
autoimmune
no islet cells
no insulin
T1DM pt
DKA increase bG increase ketones increase acid polydipsia polyphagia polyuria, weight decrease onset childhood
T1DM dx
A1c, bG
anti-GAD ab
T1DM tx
insulin only
T2DM path
obesity
insulin insensitivity
pancreas burns out
T2DM pt
obese complications of - diabetes - neuropath - retinopathy - nephropathy HHS = HHNK
T2DM tx
2 oral anti-glycemics THEN insulin
primary care in diabetes: nephropathy
U/A -> microalbuminuria q1y
if retinopathy & CKD, presume diabetic nephropathy
primary care in diabetes: retinopathy
retina exam q1y
laser treatments
primary care in diabetes: neuropathy
monofilament wire to foot q1y
gabapentin, pregabalin
soft shoes, frequent foot checks
DKA path
Type 1, insulin dependent DM (IDDM)
DKA pt
+ diabetic coma
+ ketones
+ acidosis
DKA dx
bG 300-500
U/A: + ketones
ABG: + acidosis
BMP: + gap
DKA tx
replete K
IVF - bolus a lot
IV insulin
follow the gap
HHNKC/HHS path
Type II, non-insulin dependent DM (NIDDM)
HHNKC/HHS pt
+ diabetic coma
- ketones
- acidosis
HHNKC/HHS dx
bG 800-1000
U/A - no ketones
ABG - no acidosis
BMP - no gap
HHNKC/HHS tx
replete K
IVF - bolus a lot
IV insulin
follow the symptomatic improvement