Endocrine Flashcards
prolcatinoma basics
benign
men - decreased libido, macroadenoma, bitemporal hemaniopsia
women - amenorrhea + galactorrhea - microadenoma
dx of prolactinoma
check meds –> check TSH –> normal –> check prolactin level –> if elevated –> MRI
tx of prolactinoma
dopamine agonist - carbergoline > bromocriptine
sx only if tumor unresponsive to meds or >3cm
Acromegaly basics
benign GH secreting tumor, increased risk for cancer
kids - gigantism
adults - big hands, feet, face, visceral organs (diastolic HF), diabetes
dx of acromegaly
increased ILGF-1 –> glucose suppression test –> (+) –> MRI
glucose suppression test explained
give pt glucose you expect: insulin to go down epi to go up cortisol to go up growth hormone to go up - but here it doesnt change
Acute or sudden hypopituitarism
path - infection, infarction, iatrogenic
(Sheehans, apoplexy (big tumor))
hypotensive, tachy - lack of cortisol
lethargy, coma - lack of T4
dx and tx of acute hypopituitarism
dx - cortisol levels, T4 levels
tx - replace hormones
chronic hypopituitarism
path - autoimmune, deposition dz ( sarcoidosis, etc), tumor
prioritize ACTH and TSH so stop making FSH/LH –> decreased libido, fatigability, menstrual issues
dx and tx of chronic hypopituiraism
dx - insulin stim test - similiar to glucose stim test - no Change in GH –> MRI
tx- replace hormones and fix underyling dz
empty stella
pituitary gland out of place
pt asymptomatic
dx - MRI
tx - nothing
SIADH
path - brain lesion, small cell lung cancer - exogenous ADH production
dx of SIADH
increase Urine Osm and increased Urine Na
decreased serum Osm - due to continuous absorption of water
tx of SIADH
water restriction -> doesnt work –> democlocycline (which basically induces DI)
causes of nephrogenic DI
democlocycline or lithium ADR
leads to decreased ADH
presentation of DI
polydipsia
polyphagia
nml blood glucose
no glucose in urine
dx of DI
water deprivation test
- deprive them of water
- > pts urine osm goes up = psychogenic
- > no change –> give ADH
- –> urine osm goes up = central DI
- –> no change in urine osm = nephrogenic Di
tx of central DI
DDAVP - vasopressin
tx of nephrogenic DI
gentle diuresis with HCTZ +/- amilioride
basic hyperthyroidism symptoms
tachycardia
heat intolerance
increased DTR
weight loss
diarrhea
afib
dx of hyperthryoidism
TSH decreased
T4 increased
TSH decreased
T4 decreased
central thyroid issue TRH issue
Graves dz
thyroid stimulating abs –> increased growth and activity
diffuse increased RAIU
exopthalmus, tibial myxedema
Thyroiditis Painless
painless
due to preformed T4 –> gets released due to inflammation –> spills T4 –> initial transient Hyperthyroidism state –> goes normal or hypothyroidism (Hashimotos)
Painless Thyroiditis RAIU
cold nothing
Mutlinodular goiter
toxic adenoma
RAIU - active in multiple nodules or toxic adenoma
Both of these make T4 –> –> T4 increased –> decreased TSH
Other causes of hyperthyroidism
facticious
stroma ovarii
radioactive ablation can treat which types of hyperthyrodism
multinodular goiter
toxic adenoma
facticious
stroma ovaria
tx of graves
thionomides - PTU or methimazole
thyroid storm presentation
severe hyperthyroidism
medical emergency
afib, shock severe fever, toxic, hypotensive, AMS
tx of thyroid storm
1 - cool IVF and cool blankets
2 - propranolol
3 - PTU or methimazole
4 - steroids
Hypothyroidism
decreased T4
Increased TSH
MCC - Iatrogenic
Hashimoto (TPO - Ab = Dx)
Subclinical hypothyroidism
T4 down
TSH Up
no symptoms
tx - if TSH >9 or if symptoms start
tx - same leveothyroxine
tx of hypothyroidism
levothyroxine
hypothyroidism symptoms
bradycardia
constipation
weight gain
cold intolerance
decreased DTR
heavy periods
carpal tunnel syndrome
Myxedema Coma
coma, hypothermic, hypotension
tx - warm IVF, warm blankets –> IV T4 –> doesnt work IV T3
Subquevervains thyroiditis
painful
risk factors for thyroid cancer
pts who have received head and neck radiation
history of cancer - HL, family hx
hoarseness
Age <20 with nodule
Age >60 with nodule
Physical exam findings suspicous of thyroid cancer
fixed
firm
hard nodule
nontender Lymphadenopathy
U/S findings suspicious of thyroid cancer
solid mass
hyperechogenic
size >2cm
microcalcified
irregular borders
thyroid nodule workup
check TSH
- > low -> RAIU - > hot -> tx
- > low > RAIU -> cold -> U/S -> FNA
-> high or nml –> U/S –>
> 1cm - FNA
< 1cm - U/S - repeat U/S in 6-12mo
Papillary Thyroid cancer
MCC
orphan annie nuclei
tx - resect
Follicular Thyroid Cancer
looks like thyroid tissue on biopsy
spreads hematogenously
tx - radioactive iodine ablation
medullary thyroid cancer
c-cells (parafollicular cells)
produces calcitonin
MEN2A, MEN2B - Ret oncogene - pheochromocytoma
Anaplastic Thyroid Cancer
elderly
locally invasive
rapidly fatal
layers of the adrenal gland outside in
glomerulata - aldosterone
fasculata - cortisol
reticularis - testosterone
medulla - catecholamines
Cushing syndrome
path
cortisol excess
ACTH dependent
ACTH independent
pt presentation of Cushing syndrome
HTN, Obese, DM
bad acne - (moon facies)
truncal obesity (buffalo hump)
stretch marks (purple striae)
workup of cushing syndrome
low - dose dexa suppression test –> fails to suppress –> cushing syndrome –>
ACTH –>
- > nml -> adrenal tumor –> CT/MRI –> resect
- > elevated -> High dose dexa suppress
- —-> suppressed –> cushing dz -> pit tumor -> resect
- —-> fails to suppress - >ectopic -> pan CT
Cushing Syndrome - dx criteria
1 - low dose dexa suppression
2- 24 hr urine
3 - late night salivary cortisol
need 2/3
causes of cushing syndrome
small cell lung cancer
ingestion steroids - cortisol excess
primary pituitary tumor producing cortisol
Addisons Dz
path - autoimmune dz (mcc in US) or TB (mcc worldwide)
pt - acute - hypotensive, N/V Coma - hemorrhage
- chronic - orthrostatic hypotension, hyperpigmentation increased K, decreased Na
addisons workup
cortisol AM –> low cortisol –> cosyntrpin stim test
- –> no change –> adrenal gland –> CT/MRI adrenals -> replace both cortisol and fludrocortisone
- –> rises –> Ant pituitary issue –> MRI –> replace cortisol
tx of adrenal gland tumors causing addisons
cortisol and fludrocortison
basics on renin system
renin (system in TAL) –> ang II –> makes adosterone –> inserts channels in collecting ducts –> reabsorb Na and expels K and reabsorbs H20
path of conn syndrome
Primary Tumor
renovascular
- fibromuscular dysplasia (young women)
- atherosclerosis dz (old man)
pt presentation of conn syndrome
HTN - secondary - refractory to medications
hypokalemia
workup of conn syndrome
check aldo : renin
- -> (-) aldo and (-) renin –> mimicker -> CAH or licorice
- -> (+) aldo and (+) renin <10 –> renovascular HTN –> FMD (stent) or AS (no stent)
–> (+) aldo and (-)Renin, >30 –> Conn syndrome –> salt suppression –> fails –> MRI –> adrenal venous sampling —> resect
pheochromocytoma
catecholamine secreting tumor of medulla p - paroxysmal p - pain (HA) p - pressure (HTN) p - palpitations (tachy) p - perspiration
dx of pheochromocytoma
plasma free catecholamines (faster)
or
24hr urine metenephrines, VMA (more sensitive)
then –> CT/MRI abd –> adrenal vein sampling
tx of pheochromocytoma
pre op management
1st - alpha blockade
2nd - beta blockade
3rd - resect
incidentiloma
path - unknown
asymptomatic
r/o - conn, cushing, pheo – 24hr urine
tx - <4cm - obs
>4cm - resect
functioning - resect
who needs to be screened for DM
> 45 y/o
BMI >25
HTN pts
types of screeing
Random BGx1 + symptoms
Fasting BG x2
2hr Oral glucose tolerance test x1
HgbA1c
random BG screen + symptoms
> 200 = DM
fasting BG x2
> 125 = DM
100 - 125 = pre diabetes
<100 = nml
2hr oral GTT
>200 = DM 140-200 = pre diabets <140 = nml
HgbA1c
> 6.5 = DM
5.7 - 6.4 = pre diabetes
<5.7 = nml
contraindications to metformin
CKD
CHF
Liver Disease
Type I DM
polydipsia
polyuria
increased BG
dx - GAD (best) or IA-2 antibodies
tx - insulin
pre diabetes tx
lifestyle and metformin
diabets tx breakdown
1) life style + metfomin
2) add 2nd agent
3) add insulin
- If HgbA1C > 9% go straight to step 3
Hgb A1C goal for DM
< 7 %
affects of HgbA1c on:
- oral meds
- insulin
oral meds - decreased it 3%
insulin - decrease 7%
complications of DM
eye - retinopathy - annual eye exams - laser ablation
kidney - nephropathy - U/A - microalbumin:Cr - ACE-I
feet - neuropathy - monofilament - gabapentin
biguande
meformin - example
adr - diarrhea
c/i - chf, ckd, lactic acidosis
sulfonylurea
glypizide
adr - hypoglycemia
c/i - ckd
tzd group
glitazones
adr - chf
c/i - weight gain
DDP4-I
gliptins
weight neutral
Alphaglucosidase I
acarbose
adr - diarrhea/flatulence
GLP-1
tides
promote weight loss
SGLT-1 Inhibitors
glifozines
adr - euglycemic DKA
Long Acting Insulin
Glargine
Determir
QHS
Basal
NPH
Regular Insulin
timeline
NPH - intermediate
Regular - Rapid acting - given IV
Rapid Acting Insulin
Lispro
Aspart
Glusine
QAC
(ex; humlog)
Starting an insulin regiment in type 2 DM
start with long acting insulin (0.1units/kg) –> check sugar in am -> keep titrating until AM glucose is controlled
If goal is not reached –> add short acting insulin with big meal
Best way to manage insulin in the hospital
basal bolus + sliding scale insulin
Total Daily Insulin
- 5units/kg
- 50% basal
- 50% bolus - 1/3 breakfast, 1/3 lunch, 1/3 dinner - 3units/kg
- >1.5
- age >65
- BG < 130
causes of diabetic hypoglycemia
sepsis
not eating enough
iatrogenic
exercise
symptoms of diabetic hypoglycemia
palpitations
diaphoresis
pre syncope
awake -> po glucose
coma - > IV - D50
dx - <70
causes of non diabetic hypoglycemia
insulinoma
facticous
work up of non diabetic hypoglycemia
check BG, c-peptide, pro insulin, secretogogue screen
hypoglycemia
decreased c-peptide
increased insulin
factious - exogenous insulin administration
hypoglycemia
increased c-peptide
increased insulin
next step check sulfonlyurea screen
- –> (+) –> faking it
- —> (-) —> perform 72hr fast –> CT/MRI abdomen –> insulinoma
DKA
basics and presentation
type I DM DM coma - AMS ketones acidosis n/v
dx of DKA
BG 300-500
urine (+) ketones
ABG - acidosis
BMP - anion gap metabolic acidosis
tx of DKA
first fluids
check K if >4.0
insuline 10 units –> insulin drip
—> BG falls –> 5% dextrose fluids –> gap falls –> sub q insulin
HHS basics
type II DM
DM coma
no ketones
no acidosis
dx and tx of HHS
BG 800-1000
no ketones
no acidosis
no gap
tx IVF and IV insulin
MEN1
pituitary parathyroidism - primary - increased Ca pancreatic - zollinger ellison - ulcers or - insuinoma - hypogycemia
MEN 2A
P- pheochromocytoma
M- medullary thyroid cancer
P- parathyroidism
RET oncogene
MEN2B
pheochromocytoma
medullary thyroid cancer
neuronal tumors or marfanoid habitus
RET oncogene
multinodular toxic goiter RAIU
patchy uptake
ADR of thionamides and MOA
agranulocytosis
MOA - inhibit hormone synthesis - PTU also inhibits peripheral conversion of T4–> T3
subacute viral thyroiditis RAIU
decreased RAIU
subacute lymphocytic thyroditis
painful thyroiditis
silient thyroiditis
decreased RAIU
FNA is not reliable in what thyroid cancer
follicular
cold nodules vs hot nodules
cold nodules - malignant
hot nodules - functioning - not malignant
MCC of death in pts with acromegaly
cardiomyopathy
dx labs of acromegaly
increased IGF-1
increased BG
increased TGLs
increased PO4
if after surgery GH tumor is still causing issues tx =
octreotide or somatostatin
both suppress GH secretion
craniopharyngioma
remnant of rathkes pouch
calcification of supresellar region in brain imaging
causes of central DI
idiopathic (50%)
trauma - surgery or head trauma
tumors, syphillis , TB, sarcoidosis
causes of nephrogenic DI
MCC - chronic lithium use hypercalcemia pyelonephritis demeclocycline even congenital
ADH level in central DI
low
causes of SIADH
neoplasms (small cell Lung ca) CNS disorders - stroke, head trauma, infection pulm disorders ventilators with (+) pressure post op
meds that causes SIADH
vincristine
SSRIs
oxytocin
desmopressin
major characteristics of SIADH
hyponatremia
volume expansion without edema
natriuresis
hypouricemia and low back pain
central pontine myelinolysis
occurs when you increase Na too rapidly
pseudohyoparathyroidism
end organ resistance to PTH
low calcium
high PO4
increased PTH
chvostek sign
low Ca
taping of facial N elicits contraction of facial muscles
trousseaus signs
low Ca
inflating BP cuff greater then systolic pressure for greater than 3min leading to carpal spasms
other signs of hypocalcemia
increased QT interval
basal ganglia calcifications
grand mal seizures
QT interval in hypercalcemia
shortened QT interval
mcc of hypercalcemia in an outpatient setting
primary hyperparathyroidism
surgical indications for primary hyperaparathyroidism
<50 y/o marked decrease in bone mass nephrolithiasis renal insufficiency urine Ca >400 for 24hrs
mcc of cushing syndrome
iatrogenic - due to prescrubed prednisone or other steroids
2nd MCC = ACTH secreting adenoma of pituitary
effects of cortisol
impaired collagen production
enhanced protein catabolism
anti insulin effects (leads to glucose intolerance)
impaired immunity
enhances catecholamine activity (leading to HTN)
other causes of cushing syndrome
small cell carcinomas
bronchial carcinoid
thymomas
only pts with Cushing dz not cushing syndrome will have
hyperpigmentation
cushing dz
dx labs
increased cortisol
increased ACTH
no suppression at low dose dex methasone
YES suppression at high dose dexa methasone
adrenal tumor causing cushing syndrome
dx labs
increased cortisol
low ACTH
no suppression at low dose dexa
no suppression at high dose dexa
primary hyperaldosteronism
excessive aldosterone production by the adrenal glands - independent of the renin angio system
excessive mineralcorticoids increase the activity of Na/K pumps in CT
HYPOKALEMIA and HTN
excess aldoserone –> secretion of hydrogen ions –> metabolic alkalsosis
infusion of saline in nml pts leads to what affect on aldosterone
decreased aldosterone BUT in primary hyperaldosteronism –> after saline infusion aldosterone is increased
adrenal crisis
severe hypotension
cardiovascular collapse
acute abdomen appearance
tx - IV hydrocortisone and IVF
most common clinical findings of Addisons dz
weight loss weakness abd pain nausea postural hypotension hypoglycemia
CAH
90% due to 21 hydroxylase def
decreased cortisol, decreased aldosterone
Low Na
high K
increased ACTH –> build up of cortisol and aldosterone precursors –> synthesis of androgens –> DHEA and testosterone production –> virilization in females
dx of CAH
increased levels of 17 hydroxprogesterone
largest risk factor for DM
obesity –> increased FFAs –> make muscles more insulin resistant –> reducing glucose uptake
obesity exacerbates insulin resistance through this
characteristic lipid profile of a pt with insulin resistance
High TGLs
Low HDL
somogyi effect
rebounds response to nocturnal hypoglycemia leading to AM hyperglycemia
Goals in treating DM pts
HgbA1c <7% BP goal <130/85 LDL <100 HDL >40 Fasting BG <130 posprandrial BG <180
pathophys of peripheal neuropathy in DM
microscopic vasculitis leading to axonal ischemia
metformin MOA
blocks gluconeogenesis
diabetic nephropathy
mcc of ESRD
nodular glomerular sclerosis (kimmelstiel Wilson)
hyaline deposition in one area of glomeruli
definition of microalbumin
30 to 300mg/day
albumin: creatine ration (0.02 -0.20)
DM pts are more susceptible to
radiocontrast induced ARF
hydrate well beforehand
fundoscopic exam in DM
hemorrhages
exudates
microaneurysms
and venous dilations
leading cause of vision loss in DM pts
edema of the macula which is exacerbated by HTN
in DKA when do you stop IV insulin
continue IV insulin until anion gapcloses and metabolic acidosis is corrected –> then begin to decrease insuline –> then give subcu insuline + add 5% dextrose so pt doesnt become hypoglycemic
serum sodium decreased 1.6 per every
100 increase in BG
complications of DKA
cerebral edema - occurs if glucose levels drop too fast
hypercholermic nonanion gap metabolic acidosis - too much fluids too fast
insulinoma
tumor of beta cells MEN I benign increased insulin increased c-peptide
tx of zollinger ellison
high dose PPI and surgery
glucagonaoma
glucagon producing tumor in pancreas
necrotizing migratory erythema
somatostatinoma
malignant pancreatic tumor
triad
1 gallstones
2 diabetes
3 steatorrhea
