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120 Cards in this Set

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pituitary adenomas
<1cm --> microadenoma

>1cm macroadenoma and associated with panhypopituitarism and visual symptoms

prolactin 50-60%; GH 15-20%; ACTH 10-15%; LH/FSH 10-15%
hyperprolactinemia definition
excess prolactin release results in galactorrhea-amenorrhea syndrome

prolactin inhibits the LH surge that causes ovulation by inhibition of hypothalamus (LHRH) which results in the amenorrhea

possible but rare in males
hyperprolactinemia etiology
physiologic --> pregnancy, early nursing, hypoglycemia, seizure, exercise, stress, sleep, nipple stimulation

prolactinoma

block of pituitary stalk and dopamine by tumors, cranippharyngioma, meningioma, dysgerminoma, empty sella, trauma

pharmacologic --> dopamine synthesis blockers (phenothiazines, metoclopramide), dopamine-depleting agents (methyldopa, reserpine), tricyclics, narcotics, cocaine, SSRIs, risperidone

also high TRH due to primary hypothyroidism stimulates prolactin (always check TSH)
hyperprolactinemia clinical presentation
women: galactorrhea, menstrual abnormalities, osteoposoris, osteopenia, infertility, gynecomastia

men: hypogonadism, erectile dysfunction, decreased libido, gynecomastia, infertility
hyperprolactinemia diagnosis
exclude pregnancy, lactation, hypothyroidism and medications
prolactinomas may co-secrete GH

normal basal fasting PRL level is <20mg/L
>100ng/mL in nonpregnant --> probable pituitary adenoma --> MRI of pituitary
hyperprolactinemia management
1st line: cabergolide or bromocriptine (reduces prolactin to <10% of pre-treatment levels)

if no response or compressive neurologic symptoms --> surgery

only 30% of macroadenomas can be resected and >50% recurr
acromegaly etiology
GH-secreting pituitary adenomas (75% are macroadenomas); rarely ectopic GH or GHRH-secreting tumors
acromegaly clinical presentation
enlargement of hands and feet, coarse facial features, thick skin folds; shoe, hat, glove, ring size increase; prognathism and separation of teeth; deeper voice; increased sweating; obstructive sleep apnea; visceromegaly, osteoarthritis, entrapment neuropathy; menstrual problems (prolactin is co-secreted); 30% get cardiac pathologies (cardiomyopathy, hypertension, arrythmia, hypertrophy, diastolic dysfunction, premature atherosclerosis); impaired glucose tolerance (80%), diabetes (13-20%), hypertension (33%), joint disease (articular cartilage proliferation)
acromegaly diagnosis
Initial test: IGF-1 levels
confirmation: GH level >5ng/mL after glucose load (should supress GH)
if GH excess is confirmed --> MRI (detects tumor in 90%) or CT to localize tumor
acromegaly management
1st line --> surgery

2nd line --> octeotride (↓GH in 66%)
bromocriptine/carbegolide (↓GH in 25%)
pegvisomant (GH analog receptor antagonist)

3rd line --> radiotherapy

surgery and radiotherapy can result in hypopituitarism (10-20%)
acromegaly complications
tumor pressure or rupture into brain or sinuses
cardiac failure (MCCOD)
diabetes mellitus
cord compression
visual defects
hypopituitarism etiology
Tumors:
pituitary adenomas, cysts, hypothalamic tumors (craniopharyngioma, meningioma, glioma);

Inflammatory:
sarcoidosis, TB, syphilis, eosinophilic granuloma, autoimmune lymphocytic hypophysitis

Vascular:
Sheehan postpartum necrosis, pituitary apoplexy, hemochromatosis, amyloidosis, CVA/stroke

Other: trauma, radiation, surgery, infections, hypoxia
hypopituitarism presentation
defficiencies in order

gonadotropin deficiency (amenorrhea, genital atrophy/impotence, infertility, decreased libido, loss of axillary and pubic hair)

GH deficiency (maybe assymptomatic, hypersensitivity to insulin, hyperlipidemia, short stature in children)

TSH deficiency ( hypothyroidism, fatigue, weakness, hyperlipidemia, cold intolerance, dry skin, no goiter)

ACTH deficiency (secondary adrenal insuficiency, hypocortisolism, fever, hypotension, hyponatremia [minimal], decreased response to stress, weightloss)
hypopituitarism diagnosis
measure hormones:

GH --> insulin-induced hypoglycemia ↓ glucose to <40mg/dL which ↑ GH > 10mg/L - if <10mg/L there is deficiency; or arginine infusion;

ACTH --> insulin tolerance test should increase plasma cortisol to > 19mg/dL or metyrapone test should suppress cortisol and increase serum ACTH, failure indicates deficiency;

measure LH, FSH, estrogen/testosterone

TSH --> low T4/T3 levels with normal to low TSH
hypopituitarism management
treat underlying cause; hormone replacement therapy specially cortisol
Empty sella syndrome (ESS)
herniation of suprasellar subarachnoid space through diaphragm; no pituitary seen on MRI or CT; can be idiopathic or secondary to trauma or radiotherapy; presentation: obesity, multiparoous women, headeache and 30% will have hypertension; therapy is reassurance.
diabetes insipidus definition
disorder of the neurohypophyseal system (hypothalamus or neurohypophisis) results in ADH deficiency (central DI); or renal resistance to the action of ADH (nephrogenic DI)
central diabetes insipidus etiology
neoplastic/infiltrative lessions in hypothalamus or pituitary (60% have adenohypophisis deficiency):

Craniopharyngiomas
Encephalitis
Meningitis
Trauma
Tuberculosis
Radiotherapy
Adenomas
Anoxia
Leukemia
Histocytosis
Hypertension
Idiopathic
syphillis
surgery

"CEMTTRAAL HHIgh"
nephrogenic diabetes insipidus etiology
Demeclocycline
Idiopathic
Sickle cell
Sarcoidosis
Sjogren
Colchicine
Lithium
Amyloidosis
Myeloma
Pyelonephritis
or secondary to hypercalcemia, hypokalemia

"DIureSSSis CLAMP"
diabetes insipidus presentation
polyuria
polydipsia
hypernatremia
urine specific gravity <1,010
severe dehydration
weakness
fever
altered mental state
prostration
nocturia
diabetes insipidus diagnosis
plasma/urine osmolarity ratio falls to the right of shaded area
then if vasopressin response is normal --> central diabetes insipidus, else nephrogenic
diabetes insipidus differential
primary polydipsia
drug-induced polydipsia from chlorpromazine, anticholinergics, thioridazine
hypothalamic disease
diabetes insipidus management
CDI: ADH hormone replacement or ADH secretion stimulators (chlorpropamide, clofibrate, carbamazepine)

NDI: HCTZ or amiloride or chlortalidone as well as correction of calcium balance
SIADH etiology
cancer: small cell lung CA, pancreas CA, ectopic ADH secretion

infections: TB, lung abscess

CNS: head injury, CVA, encephalitis

drugs:
chlorpropamide, clofibrate, vincristine, vinblastine, cyclophosphamide, carbamazepine

"inappropriate CCCCCancer VVIBE"
Cancer, 4 C drugs, 2 V drugs, Infections, Brain, Ectopic
SIADH presentation
water retention
ECF expansion without edema or hypertension (natriuresis)
hyponatremia
concentrated urine
signs of cerebral edema when hyponatremia is severe (irritability, confusion, seizures, coma)
SIADH diagnosis
high ADH is most accurate test

hyponatremia <130mEq/L
urine sodium > 20mEq/L; maintained hypervolemia
↓RAA
low electrolytes in blood (BUN, creatinine, uric acid)
low albumin
SIADH management
treat underlying cause
fluid restriction to 800-1000mL/d
demeclocycline (AVP inhibitor)
in case of cerebral edema: hypertonic 3% saline 200-300mL IV in 3-4h
hyperthyroidism etiology
Graves (toxic diffuse goiter)(most common)
hyperfunctioning adenoma,
Plummer disease (toxic multinodular goiter)
amiodarone
excess TSH (rare)

transient hyperthyroidism due to
subacute thyroiditis (painful)
lymphocytic thyroiditis (painless)

thyrotoxicosis factitia
ectopic thyroid tissue (struma ovarii, functioning follicular CA)
hyperthyroidism presentation
Cardiac:
atrial fibrillation, dyspnea, palpitations, angina, heart failure

Adrenergic:
nervousness, insomnia, irritability, tremors, frequent bowel movements, excessive sweating, heat intolerance, warm moist skin

Metabolic:
weight loss, weakness, palmar erythema, oligomenorrhea, osteoporosis/hypercalcemia

Eye:
staring, infrequent blinking, lid lag

Graves has diffuse goiter + exopthalmus + dermopathy-pretibial myxedema and may be associated with PA, MG or DM

"CAME"
hyperthyroidism diagnosis
history and PE plus lab confirmation:
TSH (↓ in primary, ↑ in secondary)
↑ free T4/T3
↑RAIU
TSI in Graves
↑ anti-thyroglobulin and antimicrosomal Ab in Graves and Hashimoto's
hyperthyroidism differential
Pheochromocytoma
Acromegaly
Cardiac (A fib)
Mania
Myasthenia
Anxiety
Neurosis

MG and orbital tumors can cause opthalmoplegia and exopthalmus
if primary, need to specify Graves or thyroiditis

"hyperthyroid PACMMAN"
hyperthyroidism management
immediate: propranolol, PTU, methimazole (can cause agranulocytosis)

later: radioactive iodine ablative therapy or thyroidectomy if 2nd trimester pregnancy, children or compressive symptoms

levothyroxine hormone replacement may be needed to avoid hypothyroidism
thyroid storm presentation
endocrine emergency precipitated by stress, infection, surgery, trauma; presents with:

Tachychardia
Hypotension
Hot (fever
Vomiting
Restlessness
Irritability
Icteric
Coma
Diarrhea
Dehydration
Delirium

"Thyroid HHVRIICaneD"
thyroid storm management
saline/glucose hydration, oxygen, cooling blanket;

1. PTU, 100mg every 2h
2. iodine (inhibits hormone release)
3. propranolol
4. dexamethasone (inhibits hormone release, impairs peripheral generation of T3 and adrenal support)

PTU blocks uptake of RAI and should be stopped 1-2 weeks before and after RAIU treatment
hypothyroidism etiology
95% primary:
Congenital defects
Lithium
Aspirin
Amiodarone
Surgery (postablative)
Sulfonamides
Iodine (radioactive and deficiency)
Interferon
Hashimoto (MCC)

also secondary (pituitary) and tertiary (hypothalamus)

"hypothyroidism due to CLAASSIIc Hashimoto"
hypothyroidism presentation in newborn
Cretinism
Cry hoarsely
Coarse features
Constipation
Retardation (mental and skeletal)
Eating problems
Eyes widely set
Tongue protruding
Teeth problems
Nose broad and flat
Sommnolence
Sparse hair
Skin is dry
Jaundice
Abdomen protrudes with umbilical hernia
Milestones delayed
Migit (dwarfism)

"CCCCREETTiNSS JAM"
hypothyroidism presentation in adult
lethargy, constipation, cold intolerance, mental dullness, anorexia with weight increase, dry skin and hair, deep hoarse voice, myxedema, slow tendon reflexes with prolonged relaxation, pale cool dry skin

hypercholesterolemia, expressionless face, sparse hair, periorbital puffiness, macroglosia, hypokinesis, deafness, hyponatremia, anemia, stiffness, muscle cramps, carpal tunnel syndrome, menorrhagia,
hypothyroidism diagnosis
history and PE plus lab confirmation:

↑ TSH (primary) or normal/↓ TSH (secondary)
↓T4 and FT4
↓ T3
also may have hypercholesterolemia
↑ CPK
↑ AST
hyponatremia
↑ LDH
and 12% have PA
hypothyroidism management
gradual metabolic restoration with levothyroxine (monitor TSH/T3)
if suspicion of 2dary or 3ary give hydrocortisone first then hormone replacement
if myxedema coma signs (respiratory depression and ↑CO2 retention) use very high doses of T4 and T3
subacute thyroiditis
also called granulomatous or De Quervain; viral etiology

presents with upper respiratory symptoms plus painful enlarged and firm thyroid

lab confirmation is made by ↑ ESR, ↓ RAIU and initial ↑ of T3/T4 then ↓

symptomatic management: aspirin, prednisone, propanolol

differential: Graves (there's ↑ RAIU);

subsides to normal function
Hashimoto etiology
chronic autoimmune lymphocytic infiltration of the thyroid with antimicrosomal and antithyroglobulin antibodies
Hashimoto presentation
painless asymmetrical nontoxic goiter of firm/rubbery consistency with signs and symptoms of hypothyroidism
Hashimoto diagnosis
history and PE
confirmation with needle biopsy
labs: normal or ↑ TSH
normal or ↓ T4/T3
antimicrosomal
antithyroglobulin
antiperoxidase antibodies
Hashimoto management
levothyroxin hormone replacement
Lymphocytic thyroiditis
self-limiting episode of thyrotoxicosis associated with chronic lymphocytic thyroiditis

thyroid is nontender, firm, symemetrical and slightly enlarged

normal ESR, ↑T4/T3, ↓RAIU
antithyroid antibodies may be present but in low titer; its recurrent

symptomatic treatment with propranolol
Reidel thyroiditis
intense fibrosis and enlargement of the thyroid
surgery is needed
associated with mediastinal and retroperitoneal fibrosis
thyroid adenomas
may be nonfunctioning or hyperfunctioning
slow growth
types are follicular (most common), papillary and Hurthle
treat with ablation surgery or RAI
papillary thyroid carcinoma
most common and differentiated
more common in women, bimodal frequency
slow growing; lymphatic spread
psamomma bodies seen in X-rays
treat with surgery alone (small) or surgery + radiotherapy
and also TSH suppression with levothyroxine
follicular thyroid carcinoma
2nd most common
more frequent in elderly women
hematogenous spread with metastasis to lung and bone
total thyroidectomy with postoperative ablative radiation
anaplastic thyroid carcinoma
3rd most common; more frequent in elderly women; highly malignant with rapid and painful enlargement; 80% die in 1 year of diagnosis; direct spread
medullary thyroid carcinoma
least common
arises from parafollicular cells and produces calcitonin
associated with MEN IIa and MEN IIb

thyroidectomy is indicated
differentiate paraneoplastic calcitonin production in lung, breast, pancreas and colon cancer
thyroid cancer diagnosis
recent growth of thyroid mass with nontenderness or hoarseness

solitary nodule, ↑ calcitonin, x-ray calcifications or increased density suggest malignancy

first test is TSH
if normal TSH --> FNA procedure (preferred) or scintillation scanning

functioning nodules are most likely adenomas while nonfunctioning nodules are malignant in 20% of cases; ultrasound is usefull to distinguish cyst from solid nodule
metabolism of calcium
regulated by PTH via osteoclast activation, vitamin D activation and distal tubule reabsorption; 80% of ingested calcium is excreted, 20% absorbed; 2% of total calcium is in blood 50% free, 40% protein-bound and 10% bound to citrate or phosphate buffers
hyperparathyroidism etiology
most common is primary hyperPTH
malignancies (lung) produce PTH-like peptide
granulomatous diseases (sarcoidosis, TB, berylliosis, histoplasmosis)
vitamin D intoxication
thiazides
lithium
Paget disease
acidosis
hyperparathyroidism presentation
CONfusion
CONstipation
Nephrolithiasis
Anorexia
Nausea
Pancreatitis
Polyuria
Polydipsia
Hypertension (30-50%)
short QT wave, ulcers, lethargy

"CONstANt PPPtH"
hyperparathyroidism management
Fluid replacement, furosemide (loop diuretics), biphosphonates (alendronate)
calcitonin if can't wait 2 days for biphosphonates to make effect
primary hyperparathyroidism etiology
one gland adenoma (80%), gland hyperplasia (20%), MEN I or II
primary hyperparathyroidism presentation
Pancreatitis
Peptic ulcer
Polyuria
Polydipsia
Psychiatric disorders
Nephrocalcinosis
Stones
Osteitis fibrosa cystica
Fatigability
Constipation
hypertension
short QT arrhythmia

"PaNS OF Calcium"

osteitis fibrosa cystica: bone pain, fractures, deformities, localized demineralization, bone cysts, brown tumors
primary hyperparathyroidism management
parathyroidectomy if symptoms of hypercalcemia, bone disease, renal disease, pregnancy

medical RX if calcium <11.5mg/dL: biphosphonates, restriction of dietary calcium, oral hydration, phosphate supplements

emergency RX: IV normal saline, furosemide, IV biphosphonates and calcitonin if rapid effect is necessary
secondary hyperparathyroidism management
cinacalcet: calcimimetic agent shuts off parathyroids; used in secondary hyperPTH caused by hemodialisis and parathyroid OA
hypocalcemia etiology
hypoparathyroidism
renal failure
hyperphosphatemia
hypomagnasemia
alkalosis
low albumin levels (pseudo hypocalcemia)
massive blood transfusion
hypocalcemia presentation and RX
neural hyperexcitability (seizures, tetany, numbness, tingling), prolonged QT arrhythmia; treat with calcium and vitamin D supplementation
hypoparathyroidism etiology
most common is surgical removal of parathyroids
hypomagnesemia, hereditary

note: chronic renal failure and low vitamin D produce high levels of PTH but signs and symptoms of hypocalcemia.
hypoparathyroidism presentation
neuromuscular irritability
tetany
laryngospasm
cramps
seizures
Chevostek
Trousseau
QT prolongation arrhythmia
refractory CHF
hyperventilation worsens hypoPTH due to alkalosis
hypoparathyroidism diagnosis
signs and symptoms
low serum calcium or albumin suggests hypoPTH
preferable to measure ionized calcium
PTH may be high or low
hypoparathyroidism management
acute: calcium gluconate IV
maintenance: oral calcium, vitamin D and phosphate binders if hyperphosphatemia
diabetes etiology
type I: genetically susceptible autoimmune destruction of beta cells following viral infection
type II: unknown but theres abnormal insulin secretion and resistance to insulin
diabetes presentation
polyuria
polydipsia
polyphagia
hyperglycemia
ketoacidosis or hyperosmolar coma
signs and symptoms of complications may exist
diabetes diagnosis
random plasma glucose >200mg/dL plus symptoms or 2 fasting plasma glucose >126mg/dL; glucose tolerance test may be required to show >200mg/dL at 2h and at least one earlier sample; HgA1c >7% suggests diabetic patient has been noncompliant with treatment for the previous 8-12 weeks
type II diabetes management
patient education, weight reduction, low fat diet and physical activity
if this fails to keep HgA1c below 7% then drugs;

1st line: sulfonylurea (thin patients) or metformin (obeese patients);
2nd line: add sulfonylurea or metformin;
3rd line: add glitazone or switch to insulin 0.5U/kg;
diabetes complications
acute: DKA or HONK
chronic: myocardial infarction (#1 cause of death in diabetics)
hyperlipidemia
diabetic nephropathy (#1 cause of chronic renal failure)
diabetic retinopathy
gastroparesis
erectile dysfunction
diabetic foot
neuropathy
diabetic ketoacidosis presentation
Kussmaul respiration
Acidosis
Anorexia
Abdominal pain
Consciousness altered
Dehydration
Vinegar breath
Vomiting
and hyperkalemia

"Keto AAACiD & Vinegar"
diabetic ketoacidosis diagnosis
signs and symptoms plus elevated plasma glucose, elevated levels of acetoacetate and hydroxybutirate, metabolic acidosis and increased anion gap
diabetic ketoacidosis management
insulin bolus with 5-10 units; potassium if plasma levels <4 mEq/L; fluid and electrolyte replacement
hyperosmolar nonketotic coma presentation
Water (profound dehydration)
Weakness
Polyuria
Polydipsia
Confusion
Coma
SEizures
lethargy

"dehydrated CCOMAtoSE"
hyperosmolar nonketotic coma diagnosis
elevated plasma glucose (1000 mg/dL)
extremely high serum osmolality
high BUN
mild metabolic acidosis (bicarbonate around 20 mEq/L) without ketosis
hyperosmolar nonketotic coma management
high-volume fluid and electrolyte replacement + insulin
myocardial infarction risk in diabetes
#1 cause of death in diabetics (75%); for every 1% reduction in HgA1c there's 14% risk reduction; for every 10 point decrease in blood pressure there's additional 12% risk reduction
lipid management in diabetics
target LDL is <100mg/dL

if 100-130mg/dL: recommend diet, exercise and consider statin

if >130mg/dL statin is recommended
diabetic nephropathy
affects 30-40% of type I and 20-30% of type II diabetics
diffuse membrane and mesangial thickening is most common
nodular glomerulosclerosis is also common (Kimmelstiel-Wilson syndrome)
screen for proteinuria annually
proteinuria is >300mg of albumin in 24 hour urine
microalbuminuria is first stage and between 30-300mg
all diabetics with proteinuria should be given ACE inhibitor or ARB
diabetic retinopathy
screen type II diabetics at diagnosis and annually thereafter
screen type I diabetics 5 years after diagnosis and annually thereafter

proliferative retinopathy shows vitreous hemorrhages and/or neovascularization and is treated with laser photocoagulation
diabetic gastroparesis and erectile dysfunction
treat gastroparesis with metoclopramide or erythromycin

50% of diabetics have erectile dysfunction after 10 years, treat with sildenafil
diabetic foot
due to trauma and infection in presence of diabetic neuropathy
podiatric examination annually
responsible for 50% of nontraumatic amputations
diabetic neuropathy
peripheral neuropathy: most common, symmetrical, numbness, paresthesia, pain, absent reflexes, loss of vibratory sense (treat with gabapentin (best), pregabalin (best), analgesics, amitriptyline, carbamazepine)

mononeuropathy: sudden foot drop, wrist drop or paralysis of III, IV or VI nerves

autonomic neuropathy: orthostatic hypotension, syncope, gastroparesis and constipation or diarrhea, bladder dysfunction and urinary retention, impotence and retrograde ejaculation
hypoglycemia presentation
excessive secretion of epinephrine -->
sweating, tremor, tachychardia, anxiety, hunger

CNS -->
dizziness, headache, clouded vision, loss of fine motor skills, confusion, seizures, coma
posprandial hypoglycemia
due to alimentary hyperinsulinism after gastrectomy, vagotomy, etc…; idiopathic or galactosemia
fasting hypoglycemia
underproduction of glucose due to hormone deficiencies (panhypopituitarism, adrenal insufficiency), enzyme defects, malnutrition, late pregnancy, acquired liver disease, alcohol, propanolol, salicylates, hyperinsulinism (insulinoma, exogenous insulin, sulfonylureas, quinine, endoteoxic shock, autoimmune insulin receptor antibodies)
insulinoma
subacute or chronic hypoglycemia causes blurred vision, headache, slurred speech, weakness

diagnosis: serum insulin level > 8mg/mL with blood glucose <40mg.dL

CT, ultrasound or arteriography to localize tumor

surgical, diet and medical treatment
factitious hyperinsulinism
due to self-administration of insulin, Equal or sulfonylureas
hypoglycemia, high immunoreactivity, high insulin and low C peptide
ethanol-induced hypoglycemia
glycogen is depleted in 18-24 hours and gluconeogenesis is blocked by ethanol concentration of 45mg/dL in blood
classification of hypoglycemia
posprandial, fasting, insulinoma, factitious, ethanol-induced
Cushing syndrome etiology
MCC is prolonged use of glucocorticoids; adrenal hyperplasia secondary to pituitary adenomas (40%), nonendocrine ACTH-producing tumors; adrenal neoplasia (30%)
Cushing syndrome presentation
Buffalo hump
Weakness
Wound healing
Fat deposition
Amenorrhea
Leukocytosis
Osteoporosis
Hypertension
Hirsutism
Potassium
Psychiatric disorders
Striae
Stones
Glucose intolerance
Immune depression

"BWWFALO HHumPPSS & DIabetes"
Cushing syndrome diagnosis
Initial test: 1mg overnight dexamethasone suppression test;
if abnormal or false+ --> 24-hour urine free cortisol;
if normal, exclude Cushing,
if abnormal Cushing syndrome diagnosis;

determine etiology:
high dose dexamethasone suppression
if supression to <50% of control --> pituitary adenoma;
if no response then ACTH-producing tumor or adrenal hyperplasia

measure ACTH level
if high, then it's ACTH-producing tumor (do chest CT)
if low it's adrenal hyperplasia -->
urinary 17KS, DHEA-S, abdominal CT: if high and >4cm mass then its adrenal CA
if normal or <4cm mass then adrenal adenoma
hyperaldosteronism etiology
primary hyperaldosteronism (low renin) due to unilateral adrenal adenoma (70%)
or bilateral hyperplasia (25-30%)
secondary hyperaldosteronism (high renin) due to
primary hyperaldosteronism presentation
diastolic hypertension
muscle weakness
polyuria
polydipsia
hypokalemia
hypernatremia
metabolic alkalosis
no edema
secondary hyperaldosteronism presentation
hypokalemia
metabolic alkalosis
may or may not have muscle weakness
polyuria
polydipsia
edema
no diastolic hypertension
no hypernatremia
primary hyperaldosteronism diagnosis
high urine aldosterone levels and low plasma renin levels (give high-salt diet before lab tests); confirm with CT scan of adrenals
primary hyperaldosteronism management
adrenal adenomas are removed surgically
bilateral hyperplasia --> spironolactone
Bartter syndrome
defect in Na-K-2CL transporter of loops of Henle, acts as furosemide-secreting tumor loosing NaCl which stimulates renin and aldosterone secretion

presentation: secondary hyperaldosteronism with no hypertension, no edema and severe hypokalemic alkalosis
syndrome of adrenal androgen excess
excess DHEA and androstenidione which are then converted to testosterone due to congenital adrenal hyperplasia or adrenal neoplasia

presentation: hirsutism, oligomenorrhea, acne, virilization;
congenital adrenal hyperplasia etiology
enzyme deficiencies: 21-beta hydroxylase, 17-hydroxylase, 11-hydroxylase
congenital adrenal hyperplasia presentation
21-beta hydroxylase deficiency (95%): low aldosterone in 1/3 (salt-loss, hyponatremia, hyperkalemia, dehydration, hypotension), female pseudohermaphroditism or precocious puberty in males

11-hydroxylase deficiency: virilization and hypertension/hyperkalemia due to 11-deoxycorticosterone;

17-hydroxylase deficiency: hypogonadism (17KS are blocked), hypokalemia, hypertension (11-deoxycorticosterone)
congenital adrenal hyperplasia diagnosis
suspect infants with failure to thrive, adrenal insufficiency, salt-wasting and/or hypertension

lab studies: serum testosterone, androstenidione, dehydroepiandrostenidione, 17-hydroxyprogesterone, urinary 17KS and pregnanetriol
congenital adrenal hyperplasia management
hydrocortisone
Adisson disease etiology
autoimmune destruction of the adrenals (80%), idiopathic destruction of the adrenals; surgical removal of the glands, destruction due to infection (TB, fungal, CMV, mycobacterium avium); hemorrhage, trauma, metastatic invasion
Adisson disease presentation
Acidosis
Weakness
Weight loss
Pressure is low (in primary)
Pigmentation (in primary)
Paresthesia
Potassium is high
Intolerance to stress
Cramping
Sparse axillary hair
Sodium is low

"Addison WWith PPPPICmentSS"
Addison disease diagnosis
initial test: plasma cortisol after 250um of consyntropin -->
subnormal increase in cortisol -->
measure ACTH -->
if high it's primary adrenal insufficiency;
if low its secondary adrenal insufficiency

also hemogram (neutropenia, lymphocytosis, eosinophiliaa); elevated potassium and BUN; low sodium; low glucose; low plasma cortisol and low urinary 17-hydroxycorticosteroid
Addison disease management
glucocorticoid, mineralocorticoid (fludrocortisone) and NaCl replacement; patient education
Adrenal crisis
due to major stress in previously undiagnosed patient, bilateral adrenal infarction or hemorrhage, abrupt glucocorticoid withdrawal

presentation: FEver, Vomit, Abdominal pain, Altered mental status, Hypotension

"glucocorticoid withdrawal causes FeVAAH"

Rx: fluid replacement + hydrocortisone
pheochromocytoma epidemiology
10% Malignant
10% Children
10% no Hypertension
10% Bilateral
10% Extraadrenal

"10% MuCH BEtter adrenaline"

5%
autosomal dominnant alone
MEN II
MEN III
von Recklinghousen
neurofibromatosis
von Hippel-Lindau
retinal cerebellar hemangioblastomatosis

affects 0.1% of hypertensives
pheochromocytoma presentation
paroxystic crisis of sudden onset
headache
profuse sweating
palpitations
chest or abdomen pain
nausea/vomit
hypertensive crisis and tachychardia
anxiety
tremor
weight loss
pheochromocytoma diagnosis
screening:
plasma metanephrine (no smoking 4 hours before test)
urinary free catecholamines
urinary metanephrines
urinary vanillylmandelic acid
plasma catecholamines

if screening equivocal --> clonidine suppression test
if screening is positive --> CT or MRI
if not shown --> MIBG scan

serum chromogranin levels correlate with tumor size
pheochromocytoma differential
essential hypertension
anxiety attacks
factitious crisis
intracranial lesions
autonomic epilepsy
pheochromocytoma management
if crisis: phentolamine or phenoxybenzamine
after stabilization may use other antihypertensives and surgery
primary (hypergonadotropic) hypogonadism etiology
Klinefelter
anorchia
surgical or accidental castration
radio therapy
chemotherapy
mumps
TB
leprosy
secondary (hypogonadotropic) hypogonadism etiology
hypopituitarism
Kallman syndrome (hypogonadism and decreased sense of smell)
hypogonadism presentation
undeveloped external genitalia, no seondary sexual characteristics, low libido and potency, retarded bone age;
hypogonadism diagnosis and Rx
low-normal urinary 17KS
low serum testosterone
low LH/FSH in pituitary origin
high LH/FSH in primary testicular failure

Rx: testosterone
Klinefelter syndrome
47XXY
hypogonadism
gynecomastia
sterility
small testes
high LH/FSH
low-normal serum testosterone
low urinary 17KS
high serum estradiol