Endocrine, Metabolism Flashcards
osteomalacia
vitamin D deficiency - normally, vitamin D promotes Ca and phos absorption
- secondary hyperparathyroidism - increased PTH to increase blood Ca (and excrete phos)
causes - malabsorption, intestinal bypass surgery, celiac sprue, chronic liver disease, CKD
sxs - asx or bone pain and muscle weakness
- muscle cramps
- difficulty walking, waddling gait
dx - elevated alkP, PTH
- decreased Ca, phos, urinary Ca, and 25-OH-D
- reduced bone density and pseudofractures (Looser zones) on xray
compared to:
osteoporosis - normal PTH, Ca, phos
Paget’s disease - elevated alk phos
- px - most pts are asx; sxs include skull (headache, hearing loss), spine (spinal stenosis, radiculopathy), and long bone involvement (bowing, fracture, arthritis of adjacent joints); giant cell tumor, osteosarcoma
- pathophys - due to osteoclast dysfunction –> increased bone turnover and elevated alk P (Ca and phos are normal)
- imaging - XR will show osteolytic/sclerotic lesions, radionuclide bone scan for staging
- tx - bisphosphonates
hyperthyroidism
sxs - tachy, systolic HTN (due to increased inotropic and chronotropic effects), increased PP, afib/flutter
- b1 receptors - increased cardiac contractility (increased myocardial O2 demand, angina)
- can have high-output cardiac failure, valvular abnormalities
- bone disease - thyroid hormone –> increases bone resorption, hypercalcemia –> decreases PTH secretion –> decreased renal Ca absorption and conversion to active vitamin D –> net Ca wasting (decreased Ca absorption in gut and reabsorption in kidney)
Primary
Graves? - if no - get radioactive iodine uptake
–> high - diffuse (Graves), nodular (toxic adenoma, multinodular goiter)
–> low - measure serum thyroglobulin (protein precursor of thyroid hormone) - high thyroglobulin (thyroiditis, iodine exposure), low (exogenous hormone)
Graves (primary hyperthyroidism - problem is with thyroid) - can cause fetal hyperthyroidism
- antithyroid drugs - agranulocytosis
- methimazole - 1st trimester teratogen, cholestasis
- PTU - hepatic failure, ANCA-associated vasculitis
- radioiodine ablation (RAI) - causes cell necrosis, permanent hypothyroidism in 90% of pts, within mo), worsening of ophthalmopathy (because titers of antibody increase after radioiodine therapy, so give glucocorticoids with RAI)
- surgery - permanent hypothyroidism, risk of recurrent laryngeal damage and hypoparathyroidism (may need to give antithyroid drug prior to surgery in older pts)
toxic adenoma (hot nodule), toxic multinodular goiter - activating mutation in TSH receptor –> TSH independent thyroid hormone secretion
- b-blocker - for sx relief
- methimazole, PTU to decrease thyroid hormone secretion
- RAI is only taken up by nodules - normal tissue is unaffected
(- hot nodules are rarely malignant)
Secondary hyperthyroidism - get MRI of pituitary - excess a-subunit
Thryoid storm - occurs in Graves pts (due to an increase in circulating catecholamines)
- tachy, hyperthermic, risk of fatal arrhythmias
diabetes medications
metformin (biguanide) - first line - weight neutral, low risk of hypoglycemia
- lactic acidosis (contraindication is renal insufficiency), loose stools
sulfonylureas - second med that you would add - weight GAIN and hypoglycemia
pioglitazone (TZD) - used if pt cant tolerate metformin or sulfonylurea
- weight GAIN, edema, CHF, bone fracture, bladder cancer
- can be used in renal insufficiency
DDP-V inhibitors (-gliptin) - weight neutral - can be used in renal insufficiency
GLP-1 receptor agonist (exenatide, liraglutide) - second med if pt desires *weight loss*
- associated with pancreatitis
insulin - when A1c > 8.5 - weight gain, hypoglycemia
- long-acting - NPH, glargine
reduction in A1C: metformin, sulfonylureas > pioglitazone > DDP4 inhibitors, GLP receptor agonists
statin for all pts 40-75 with diabetes (regardless of lipid levels)
milk-alkali syndrome
pathophys: excessive intake of Ca and alkali - hypercalcemia –> renal vasoconstriction and decreased GFR - hypercalcemia inhibits Na-K-2Cl in ascending loop, impaired ADH activity - renal loss of Na, water
- hypovolemia - contraction alkalosis, reabsorption of bicarb
sxs - N&V, constipation
- polyuria, polydipsia - neuropsych sxs
lab findings - hyperCa, metabolic alkalosis, AKI, suppressed PTH
meds that increase risk of milk-alkali syndrome - thiazides (but would not cause symptomatic hypercalcemia on its own), ACEi/ARBs, NSAIDs d/c causative agent - give NS + lasix
DKA and HHS
DKA: may be initial manifestation of DM
- initial - polydipsia/polyuria, blurred vision, weight loss
- later - AMS, hyperventilation, abd pain
- mental status changes when plasma osm > 330
1) fingerstick glucose - 250-500 mg/dL - other labs will show - bicarb <18, elevated AG, pos serum ketone
- urine - glucose, ketones
- ketones accumulate because of absolute insulin deficiency
tx - high flow IV fluids (NS) and IV insulin
- follow and replace K
- best index to monitor response = AG (nl 10-14) (or direct b-hydroxybutyrate assay)
HHS: type 2 DM, older age
- due to relative deficiency of glucose
- precipitated by illness
px - *gradual* hyperglycemic symptoms (polyuria, polydipsia), AMS
glucose > 1000 - normal pH, bicarb, AG
- negative or small serum ketones
- serum osm > 320
- note: effective plasma osmolality = 2*plasma sodium + plasma glucose/18
tx - NS (initially) and IV insulin
- careful monitoring of K - add K when serum K is between 3.3-5.3
- fluid replacement is the most important initial step because hyperglycemia can cause osmotic diuresis
General management
- high flow NS, 5% dextrose when serum glucose < 200 (continue insulin throughout)
- insulin: IV initially, SQ when pt can eat (and electrolytes are more normal), overlap SQ and IV insulin by 1-2 hrs -
K - add IV K if <5.2, hold insulin if K < 3.3
- bicarb - consider for pts with pH < 6.9
- phosphate - for pts with phosphate < 1.0 mg, cardiac dysfunction, respiratory depression, monitor serum Ca frequently
hyperaldosteronism
HTN + hypokalemia - think hyperaldosteronism
- get early morning renin-aldosterone level
Primary:
px - HTN, metabolic alkalosis, hypoK, hyperNa
- no significant peripheral edema due to aldosterone escape dx - plasma aldosterone/renin >20 and aldosterone > 15 (elevated aldosterone will lead to decreased renin, feedback inhibition)
- adrenal suppression after oral saline load = confirms dx
- CT abd and adrenal venous sampling - will distinguish between adrenal adenoma and bilateral adrenal hyperplasia
tx - unilateral adrenal adenoma
- *surgery*, aldosterone antagonists (eplerenone is more selective than spironolactone)
- bilateral - aldosterone antagonists - can add more agents for persistent HTN
if PAC/PRA ~ 10 (means both are high) = secondary hyperaldosteronism
- diuretic use, cirrhosis, CHF, renovascular HTN, renin-secreting tumor, malignant HTN, coarctation
low renin, low aldosterone –> look for other causes of HTN and hypokalemia
- CAH, glucocorticoid resistance, exogenous mineralocorticoid, Cushing’s, altered aldosterone metabolism
diabetic nephropathy
1) hyperfiltration and microalbuminuria
2) macroproteinuria (>300mg/24hr) and DECLINE in GFR
tx - intensive BP control (140/90)
- ACEI (reduce blood pressure and intraglomerular pressure) - but start these carefully because they can cause and acute decline in GFR and hyperkalemia
- in inds with diabetic nephropathy A1c < 7 has been shown to reduce the progression to microalbuminuria…
thyroid cancer
for ALL thyroid nodules:
1) TSH, US, risk factors –> no RFs/suspicious findings (hypoechoic, microcalcifications, internal vascularity)
- normal/elevated TSH –> FNA
- low TSH –> scintigraphy –> hot (hyperfunctioning)/cold (FNA) nodule
- RFs/suspicious findings –> FNA
A > F > P (autopsy, f-ed, pissed)
anaplastic
follicular - firm (cold) nodule
- FNA findings will be same in follicular carcinoma (will invade tumor capsule) and adenoma
- partial thyroidectomy, complete thyroidectomy
- invasion of capsule - propensity to hematogenously spread
papillary
- pale nuclei with inclusion bodies and central grooving, psammoma bodies
- more likely to spread to LNs
- tx - surgery (partial or total) - then radioiodine ablation for patients with increased risk of tumor recurrence
- pts at increased risk should also receive thyroid replacement to suppress TSH levels - TSH can stimulate growth of residual or metastatic tissue
medullary - calcitonin
hypothyroidism
Hashimoto - TPO antibodies painless thyroiditis - variant of chronic autoimmune thyroiditis (so will have positive TPO antibodies)
subacute thyroiditis (de Quervains) - fever, neck pain, thyroid tenderness, elevated ESR
- preceded by viral illness - hyperthyroid for 2 mo –> then hypothyroid for few mo –> euthyroid
Riedel’s fibrous thyroiditis - fibrosclerosis of thyroid and surrounding tissues (retroperitoneum)
hypothyroidism - increases SVR (hyperthyroidism decreases SVR) –> high BP
hypothyroidism can cause additional lab abnormalities - HLD, hyponatremia (due to decreased free water clearance), asx elevations of CK and LFTs
- statin can increase risk of myopathy in pts with hypothyroidism (use with caution)
DI
primary polydipsia - antipsychotics, anxious middle-aged women
- low serum Na –> central DI - idiopathic, trauma, pituitary surgery, ischemic encephalopathy
- high serum Na - due to renal losses and impaired thirst mechanism - tx - intranasal desmopressin
nephrogenic DI - ADH resistance in kidney - chronic Li use, hypercalcemia, hereditary
- normal serum Na - renal losses but intact thirst mechanism
- tx - thiazides water deprivation test and continuous measurement
- urine osm > 600 = primary polydipsia
- no change in urine osm, plasma osm > 295, plasma Na > 145 –> give desmopressin
- central DI - urine osm will increase by 50-100% with desmopressin
- nephrogenic DI - no change in urine osm
other causes of increased urination - BPH - osmotic diuresis - glucose, mannitol, urea
diuretics and electrolyte changes
HCTZ - hypoK, hyperglycemia, hyperuricemia
diuretic use - stimulates ADH –> concentrated urine
adrenal insufficiency
primary adrenal insufficiency aka Addisons disease
- high ACTH levels, low serum cortisol…
- most commonly due to autoimmune adrenalitis - autoimmune adrenal destruction
- less common causes - CMV/fungal/Tb infection, malignant infiltration (small cell), hemorrhage in the setting of warfarin use and sepsis, adrenoleukodystrophy (congenital)
- adrenoleukodystrophy - young males, accumulation of long chain fatty acids central (secondary - pit, tertiary - hypothalamic)
- chronic glucocorticoid therapy - cortisol and ACTH will be low, aldosterone will be normal (because aldosterone is controlled by the RAAS system and not the pituitary)
pheochromocytoma
catecholamine surge can occur due to anesthesia - can look like thyroid storm
- but thyroid storm will have fever
b-blockers - can cause unopposed a-adrenergic stimulation –> vasoconstriction, paradoxical HTN
paraganglionoma - similar, originates from extra-adrenal paraganglia
hyperparathyroidism
*parathyroid adenoma*, hyperplasia, carcinoma - increased risk in MEN 1 and 2A
- multiglandular hyperparathyroidism, additional endocrine tumors
sxs - asx or bones, groans, moans, psych overtones
indications for parathyroidectomy - age < 50, symptomatic, for pts with complications
complications - osteoporosis (T score < 2.5), nephrolithiasis/calcinosis, CKD
- pts with elevated risk of complications - Ca > 1 above nl, urinary Ca excretion > 400 mg/day
- osteitis fibrosa cystica - occurs due to hyperparathyroidism from parathyroid carcinoma
- osteoclastic resorption –> replacement of boen with fibrous tissue (brown tumors), salt and pepper appearance of the skull
euthyroid sick syndrome
fall in total and free T3, nl T4 and TSH
- occurs during acute, severe illness
if illness continues - serum T4 and TSH levels can decrease as well
note - thyroid function testing is not recommended in acute ill pts
