Endocrine/Metabolic Flashcards
Elderly w/ nervousness , insomnia, hyperactivity and weight loss?
hyperthyroidism
Graves disease?
people seen?
Autoimmune IgG binding to TSH receptors -> synthesis -> hyperthyroidism
young women w/ other immune disorders
diffuse uptake on scan
Plummer disease
mulinodular toxic goiter - hyperthyroidism
high T4 and T3 levels -> low TSH and atrophy of thyroid
patchy uptake on thyroid scan
Transient hyperthyroidism
hashimotos and subacute thyroiditis
post partum thyroiditis (rare)
Graves uniques signs (3)
exothalamos
periorbital myxedema
thyroid bruit
Factors that increase TBG and as a result T4(4)
pregnancy*, liver disease, OCP and ASA
increase in bound T4 and not necessarly free T4
Pharmacologic for hyperthyroid (4)
Monitor?
methimazole and propylthiouracil - inhibit synthesis (PTU inhibits conversion)
- Monito agranulocytosis
beta blockers for symotms
Sodium ipodate lowers serum levels
Radio iodide 121-> destruction of thyroid follicular cells
hypocalcemia peri neck surgery
took out parathyroids or have inflammation temporrarily
Hyperthyroid and pregnant
propylthiuracil
Thyroid storm
Rare and life threatening complication of thyrotoxicosis
Precipitant (infeciton, DKA, surgery. etc)
20% die.coma
FEVER, tachy, agitation, psychosis and GI
IV fluids, cooling, PTU q2hrs, w/ iodine, beta blockers
Causes of hypothyroidism (3)
primary
- Hashimotis - common
itaragenic - prior tx for hyperthyroidism
secondary (pituitary disease, low TSH)
tertiary(hypothalamic, low TRH)
LOW free T4 and TSH think of
seondary and tertiary hypothyroidsm
Sublclinical hypothyrpoidism
thyroid inadequate -> increased TSH to maintain normal T4
elv TSH — normal T4
nonspecific signs, Tx w. thyroxine if goiter develops, hypercholerolemia, or symotms
HIGH TSH should 1st think of
Also order?
hypothyroidism
not true in seconday and tertiary
Lipids and CBC
Increase antimicrosomal antibodies
Hashimotos thyroiditis
Subacute (viral) thyroiditis
features
Dx
TX
prodromal period, transient hyperthyroidism -> decrease
PAINFUL, tender thyrod
Radioiodine uptake is low, damaged follicles
NSAIDs, ASA, steriods
Subacute lymphocytyc thyroiditis
PAINLESS (vs subacute viral)
transient thyrotoxic-> hypothyroid
low uptake (vs graves)
Chonic lymphocytic thyroiditis - hashimotos ot lymphocytic
See?
most common
antithyroid and antiperoxidase antibodies, goiter common,
Fibrous/Riedels thyroditis
fiberous tissue replaces -> thyroid firm
Surger
maybe hypothyroid
Detectable thyroid nodules by exam are ?
Malignancy suggested by?(7(
> 1cm
nodule fixed/no movement w/swallow; firm consistency; solitary; Hx of neck radiation; rapid development; vocal cord paralysis; cervical adenopathy
Cold thyroid nodules get what?
surgery
hot observe
FNA is reliable for all CA exceot?
Follicular
good for: papillary, medullary, anapestic
Hurthle cell tumor
Variant of follicular CA but more aggressive
spread by lymphatics and does not take up iodine
Tx: total thyroidectomy
Papillary CA
70-80% of Ca
least aggressive
risk w/ neck radiation
spreads via lymphatics; + iodine uptake
only one you may get away w/ a partial thyroidectomy, >3cm all comes out
Follicular carcinoma
15% CA
Absords iodine
Spreads hematogenously and early (brain, lung, bone, liver)
Extension through tumor capsule differentiates from benign
NEED a biopsy
Medullary carcinoma
2%
1/3 sporadic, 1/3 familal, 1/3 MEN II (pheo)
Parafollicular cells -> calcitonin
malignant w/ 10 yr survival
Anaplastic carcinoma
5% and seen in elderly
highly malignant
arise from follicular/papillary thyroid carcinoma
months prognosis
Calctonin levels if concerned w/ what thyroid CA
medullary
Thyroid CA Tx
thyrodectomy (partial in papillary if <3cm)
radioiodine therapy
(unsuccesful in medullary)
Chemo and radiation in anaplastic
pituitary adenoma
usually benign but may have hormonal effects
Either hyper secretion: Prolactin -> GH ->acromegaly ACTCh -> cushings TSH -> hyperthyroidism
hypo w/crushed**
HA and vision defects - tunnel vision
Get what test ?
Parasellar signs->
bitemporal hemianopsia in pituitary adenoma
MRI and pituitary hromone levels
hypogonadism, decreased labido infertility, galactorrhea/gynecomastia in men think of
hyperprolactinemia 2/2 prolactinoma
can also be MEDs, pregnancy, renal failure, hypothyroidism
parasellar signs more common
High prolactin levels inhibit what hormone
GnRHH -> decreased LH and FSH and low estrogen and testosterone
Premenopausal (oligomenorrhagia irregular) decreased labido, dyspareunia, vaginal dryness, glactorrhea in women be concerned of?
hyperprolactinemia 2/2 prolactinoma
can also be MEDs, pregnancy, renal failure, hypothyroidism
Tests for prolcatinoma? (4)
elv serum prolactin
pregnancy and TSH for r/o
CT/MRI
Prolactinoma Tx
bromocriptine (dopamine agonist) ddecreases production
Tx for 2 yrs before stopping
Cabergoline (dopamine agonist) maybe better tolerated
Surgery if persist
Prolactinoma Tx
bromocriptine (dopamine agonist) ddecreases production
Tx for 2 yrs before stopping
Cabergoline (dopamine agonist) maybe better tolerated
Surgery if persist
Common cause of death w/ acromegaly
CV disease
Acromegaly vs gigantism
excess pituitary GH after epiphyseal closure
10% of pituitary adenomas
Features of acromegaly
- 3 classes
Growth - soft tissue skeletal/ coarse face/ hands + feet/ organomegaly/arthralgia w/ joint tissue, hypertrophy cardiomyopathy, macrgnathia
Metabolically
-glucose intolerance and hyperhidrosis
Parasellula manifestations
-HA, vision change, HTN, sleep apnea
IGF 1 - somatomedin C elvated in?
Confirm w?
Acromegaly
Oral glucose suppression- failure confirms
MRI pf pituitary
Tx of acromegaly -
Surgery - transphenoidal ressection
Radiation if elv after
Octreotide to suppress?
Calcification of suprasellar region seen in the brain imaging is?
origin?
craniopharyngioma
remnants of Rathke’s pouch
usually visual field defects, maybe hyperprolacinemia, DI, panhypopituitarism
Panhypopituitarism casues
hypothalamic or pituitary tumor most common
Also - radiation, sheehans, infiltrative, head trauma, cavernous sis thrombosis
LH, FSH and GH lost first
Then TSH and ACTH
Central DI vs Nephrogenic DI
Risk factors
Central - more common 2/2 low ADH production from posterior pituitary
- trauma/surgery, idiopathuc*, other destructive processes
Nephrogenic is lack of response to ADH
- Lithium use**, hypercalcemia, pyelonephritis,
5-15L of urine daily that is colorless - think of?(4)
DI, DM, poly dypsia, Diuretics
hyponatreamia mild unless impaired thirst drive
Low specific gravity and low osmolarity
Normally Mosm 250-290
Test for Central DI vs Nephrogenic
water deprivation and measure urine Osm every Hr, when stable add 2g desmopressin subQ,
+ for central if concentrates in presence of desmopressin. no Change is normal(max adh response as is) or nephrogenic
Tx pf nephrogenic vs Central DI
Central gets desmopressin
Nephrogenic gets Na restriction and thiazide diuretics (depletes body of Na and leads to reabsorption of Na and pater in proximal tubule, less water reaches distal -> decrease urination)
Despite volume expansion what is not seen in SIADH
edema
due to naturesis, excretion of excess Na despite hyponatremia
SIADH pathophys and cuases (6)
excess ADH from ectopic source of posterior pituitary -> hyponatremia and volume expansion
Neoplasms(lung, pancreas, prostate, bladder), lymphoma, leukemia
CNS (stoke, trauma, infection)
Pulm (pneumonia, TB)
Ventilators (+ pressure)
Medication (vincristine, SSRIs, chlopropromide)
Post op
Hypovolemic hyponatremia
hypervolemic hyponatremia
SIADH
volume contracted
volume expanded w/ edema
volume expanded w/out edema
SIADN -> hyponatremaia
acutely causes?
Chronicially
Acute - lethargy, somnolence, weakness
-Seizures**, coma death
Chronic- asymptomatic, anorexia, N/V, CNS symptoms less common, brain edema decreased