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1399 Cards in this Set

  • Front
  • Back
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 causes: 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 causes: 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
pituitary adenomas, cysts, hypothalamic tumors (craniopharyngioma, meningioma, glioma);

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

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):


nephrogenic diabetes insipidus etiology
Sickle cell
or secondary to hypercalcemia, hypokalemia

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)
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
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)
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
atrial fibrillation, dyspnea, palpitations, angina, heart failure

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

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

Staring, infrequent blinking, lid lag

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

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

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:

Hot (fever)

"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
Surgery (postablative)
Iodine (radioactive and deficiency)
Hashimoto (MCC)
also secondary (pituitary) and tertiary (hypothalamus)

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

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

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
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
Paget disease
hyperparathyroidism presentation
Hypertension (30-50%)
short QT wave, ulcers, lethargy

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
Peptic ulcer
Psychiatric disorders
Osteitis fibrosa cystica
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
renal failure
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
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
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)
diabetic nephropathy (#1 cause of chronic renal failure)
diabetic retinopathy
erectile dysfunction
diabetic foot
diabetic ketoacidosis presentation
Kussmaul respiration
Abdominal pain
Consciousness altered
Vinegar breath
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)

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); dysfunction of 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)
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
Wound healing
Fat deposition
Psychiatric disorders
Glucose intolerance
Immune depression

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
metabolic alkalosis
no edema
secondary hyperaldosteronism presentation
metabolic alkalosis
may or may not have muscle weakness
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
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
Weight loss
Pressure is low (in primary)
Pigmentation (in primary)
Potassium is high
Intolerance to stress
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"

autosomal dominnant alone
von Recklinghousen
von Hippel-Lindau
retinal cerebellar hemangioblastomatosis

affects 0.1% of hypertensives
pheochromocytoma presentation
paroxystic crisis of sudden onset
profuse sweating
chest or abdomen pain
hypertensive crisis and tachychardia
weight loss
pheochromocytoma diagnosis
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
surgical or accidental castration
radio therapy
secondary (hypogonadotropic) hypogonadism etiology
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
small testes
high LH/FSH
low-normal serum testosterone
low urinary 17KS
high serum estradiol
diseases that present with prominent dysphagia/odynophagia
esophageal cancer (SCC, adenocarcinoma)
diffuse esophageal spasm
Schatzcki's rings
Zenker diverticulum
Mallory-Weiss syndrome
achalasia presentation
progressive dysphagia to solids and liquids
weight loss
due to loss of inhibitory neurons of LES
achalasia diagnosis
most accurate test is manometry
also barium esophagography (bird beak sign)
if alarm symptoms (>60, heme-positive stools, >6 months, weight loss) esophagogastroduodenoscopy
achalasia management
pneumatic dilation or botulinum toxin injections; if fails then surgical myotomy
esophageal cancer etiology
SCC is in upper two thirds and due to alcohol and tobacco
adenocarcinoma in lower third and is associated with reflux disease or Barret's
esophageal cancer presentation
progressive dysphagia to solids then to liquids
weight loss
can have halitosis
esophageal cancer diagnosis
barium swallow
endoscopy with biopsy is mandatory
CT to detect local spread
bronchoscopy to detect spread to bronchi
endoscopic ultrasound for staging
esophageal cancer management
if metastasis --> 5-fluoracil and radiotherapy
esophageal scleroderma
dysphagia or reflux in scleroderma patient
diagnose with manometry
treat with omeprazole and metoclopramide (promotility)
diffuse esophageal spasm/ nutcracker esophagus
intermittent chest pain simulates myocardial infarction with dysphagia
no relation with exertion or swallowing
precipitated by cold liquids
screen with barium swallow (corkscrew pattern)
most accurate test is manometry (disorganized contractions)
treat with nifedipine and nitrates
Schatzcki's ring
painless intermittent dysphagia located distally at squamous-columnar junction of LES
barium esophagram and pneumatic dilation
Plummer-Vinson syndrome
intermittent dysphagia without pain located in hydropharynx (proximal)
associated with iron defficiency anemia and predisposes to SCC
diagnose wih barium esophagram
treat iron defficiency and pneumatic dilation
due mostly to candida in HIV patients; also CMV, HSV or diabetes
also drugs such as alendronate, quinine, risedronate, vitamin C, pottasium, doxycycline, NSAIDs
presents with progressive odynophagia only when swallowing (not intermittent)
fluconazole or endoscopy
Zenker diverticulum
outpouching of posterior pharyngeal muscles; halitosis, difficulty initiating swallow, undigested regurgitated food; barium studies; surgery (endoscopy or tube is contraindicated)
Mallory-Weiss syndrome
painless upper GI bleeding without dysphagia or odynopahgia
melena or hematemesis
diagnose with upper endoscopy
resolves spontaneously or epinephrine injections or cauterization
etilogy of epigastric pain
ulcer disease
gastric cancer (rare)
most common etiology is nonulcer dyspepsia (all tests are normal)
diagnosis of diseases causing epigastric pain
if >45
and/or alarm symptoms (weight loss, dysphagia, odynophagia, bleeding)
and/or nonrespondant to PPIs or H2 blockers -->
endoscopy for cancer, lower esophagus dysplasia

biopsy ulcer, serology, breath tests and stool antigen detection can be used for H. pylori diagnosis
diseases that manifest with epigastric pain
peptic ulcer disease
dumping syndrome
gastric cancer
nonulcer dyspepsia
GERD etiology
GERD presentation
epigastric pain, sore-throat, metal taste, hoarseness, cough, wheezing
GERD diagnosis
if symptoms are clear, clinical diagnosis
if equivocal, 24h pH monitoring
GERD management
PPIs (omeprazole); if nonrespondant then surgery
Barret esophagus
complication of GERD
if patient has GERD > 5 year --> endoscopy
if Barret --> endoscopy every 2-3 years to check for dysplasia or cancer
if low-grade dysplasia --> endoscopy in 3-6 months to check progression
if high-grade dysplasia --> distal esophagectomy
all should be given PPIs
peptic ulcer disease etiology
90% of duodenal ulcers and 70-80% of gastric ulcers are due to H. pylori
NSAIDs is second cause
also Zollinger Ellison
gastric cancer
Crohn disease
head trauma
prolonged intubation
mechanical ventilation
peptic ulcer disease presentation
midepigastric pain after eating (gastric) or relieved by eating (duodenal)
could have nausea or vomit
there's rarely abdominal tenderness
peptic ulcer disease diagnosis
most sensitive and specific is upper endoscopy with biopsy and it's performed routinely on those over 45 or with alarm symptoms (weight loss anemia, heme+ stools, dysphagia)

it's the only test to exclude gastric cancer

serum antibody against H. pylori is sensitive and cheap; stool antigen and breath tests are also sensitive and can diffferentiate between new and old disease as well as determine if it's cured after treatment
peptic ulcer disease management
if H. pylori --> PPI+clarithromycin+amoxicillin or tetracycline+metronidazole+-bismuth

ordinary ulcers w/o H. pylori --> PPI alone, misoprostol (rarely), celecoxib

indications for surgery --> UGI bleeding or perforation, refractory ulcers, gastric outlet obstruction
type A gastritis etiology
alcohol, NSAIDs, H. pylori, head trauma, burns, mechanical ventilation
type B gastritis etiology
gastric atrophy due to autoimmune destruction of parietal cells with pernicious anemia
gastritis presentation
epigastric pain, nausea/vomitting, hematemesis, melena
it can also manifest as asymptomatic bleeding
gastritis diagnosis and treatment
if H. pylori, dignose and treat as peptic ulcer disease

type B gastritis diagnose with low B12 levels and high methylmalonic acid levels and also antiparietal cell antibodies, anti-intrinsic factor antibodies
treat with B12 replacement
Zollinger-Ellison presentation
95% present with ulcer disease that is recurrent after therapy
multiple ulcers at distal duodenum or resistant to therapy
watery diarrhea or steatorrhea due to inhibition of lipase by acid
can also present metastatic disease or hypercalcemia in MEN I
Zollinger-Ellison diagnosis
after clinical suspicion --> elevated gastrin levels while off antisecretory medication
can also measure elevated gastric acid output
positive secretin stimulation test (rise in gastrin after secretin injection, abnormal)

CT/MRI/ultrasound to localize is 60-80% sensitive for metastasis and can include but not exclude
somatostatin receptor scintigraphy is 90% sensitive for metastatic disease
endoscopic ultrasound is most sensitive for metastatic disease
early satiety, posprandial nausea, sense of abdominal fullness
clinical diagnosis --> abdominal pain and bloating in patient with long history of diabetes
treat ith promotility agents such as metoclopramide or erythromycin
dumping syndrome
rapid release of hypertonic chyme into duodenum with osmotic effects and sudden glucose/insulin peak with hypoglycemia; presents with sweating, shaking, palpitations, lightheadedness shortly after a meal; treat by eating multiple small meals
nonulcer dyspepsia
of unknown etiology and diagnosed when all causes of epigastric pain have been excluded and there is still pain
Crohn disease presentation
discontinuous transmural granulomas in small or large intestines result in
fever, diarrhea, weight loss
abdominal pain and bleeding
episcleritis, scleritis, iritis
pyoderma gangrenosum
erythema nodosum
calcium/cholesterol stones
painful abdominal masses can be palpated
can cause fistulas and predisposes to colon cancer if lessions are located in colon
ulcerative colitis presentation
continuous ulcerations limited to the mucosa and submucosa of large intestines result in
fever, bloody diarrhea, abdominal pain, weight loss
episcleritis, scleritis, iritis
pyoderma gangrenosum
erythema nodosum
no fistulas, no masses
predisposes to colon cancer
inflammatory bowel disease diagnosis
gold standard is endoscopy

CD has vitamin and iron deficiencies; anti-Saccharomyces cerevisiae antibodies (ASCA); increased PT due to vit K deficiency; calcium kidney stones in CD

ANCA antibodies in UC
inflammatory bowel disease management
mesalamine derivatives: pentasa for CD, asacol for UC, rowasa for rectal disease
acute episodes treated with budesonide
azathiorprine and 6MP used for long term
infliximab for CD in case of fistulas
surgery will be required in 60% UC cases and is effective
general considerations about diarrhea
can be infectious, antibiotic-associated, lactose-intolerance, irritable bowel or carcinoid syndrome

if patient is hypotensive, has orthostasis, fever, abdominal pain or bloody stools is more important to hospitalize and treat than to determine etiology
bacillus cereus diarrhea
ingestion of spores in refried chinese food
1-6 hour onset
vomitting is prominent and no fecal blood
campylobacter diarrhea
most common cause of infectious diarrhea
can be bloody or not
associated with reactive arthritis and Guillain-Barre
cryptosporidia, isospora diarrhea
found in AIDS < 100 CD4
E. coli O157:H7 diarrhea
bloody stools
associated with contaminated hamburger meat and shiga-like toxin
antibiotics are contraindicated because dead organism causes HUS
platelet transfusions are contraindicated in HUS
giardia diarrhea
ingestion of unfiltered river or lake water
no bloody stools
fullness, bloating and gas
can simulate celiac disease
salmonella diarrhea
most commonly due to ingestion of chicken and eggs or dairy products
shigella diarrhea
no clues in diarrhea are strong enough to point to this etiology; only stool culture
yersinia diarrhea
no clues in diarrhea are strong enough to point to this etiology, only stool culture
can mimic appendicitis
common in people with iron overload/hemochromatosis
vibrio diarrhea
ingestion of raw shellfish
viral diarrhea
associated with children in day-cares; there's absence of red or white cells in stools
staph diarrhea
ingestion of dairies, eggs, salads, custards
1-6 hour onset
nausea and vomitting predominate
ciguatera toxin diarrhea
2-6 hours after ingestion of large reef fish (grouper, red snapper, barracuda)
paresthesias, weakness, reversal of heat and cold
diagnosis of diarrhea
invasive organisms produce fecal leukocytes within 24-36 hours
salmonella, shigella, e. coli, campylobacter, yersinia, vibrio

definitive diagnosis of diarrhea is stool culture and fecal analysis for ova

for giardia can use ELISA stool antigen detection
for cryptosporidia need modified acid-fast test
diarrhea management
empiric antibiotics until stool culture and if there's abdominal pain, bloody stools and fever;
high-volume stools and dehydration don't justify antibiotics;

empirical treatment is ciprofloxacin or fluoroquinolone+metronidazole

scombroid is treated with antihistamines
giardia with metronidazole
isospora with TMP/SMX
doxycycline for vibrio
antibiotic-associated diarrhea
caused mostly by C. difficile and by any antibiotic but mostly associated with clindamycin; history of antibiotics + diarrhea makes diagnosis and patient should have stool C. difficile toxin test; treat with metronidazole or oral vancomycin if resistance
lactose intolerance
high prevalence; diarrhea associated with bloating and gas but no blood or leukocytes in stools; empirical diagnosis and treatment is to remove milk, cheese and dairies (except yogurt) with resolution of symptoms in 24-36 hours; precise diagnosis is increased stool osmolality and increased stool osmolar gap
irritable bowel syndrome presentation and diagnosis
abdominal pain plus constipation alone (20%) or diarrhea alone or both
diagnosis of exclusion: lactose intolerance, IBD, celiac, carcinoid, giardia, anatomic defects
diagnostic criteria: pain relieved by bowel movement, fewer symptoms at night, diarrhea alternating with constipation
irritable bowel syndrome management
high-fiber diet
antidiarrheals (loperamide, diphenoxylate)
antispasmodics (hyoscyamine, dicyclomine, alkaloids)
tricyclics for resistant cases
intestinal serotonin agents: tegaserod (constipation-predominant) or alosetron (diarrhea-predominant)
carcinoid syndrome
most located in appendix or ileum but could be bronchial
implies metastatic disease

presents with diarrhea, flushing, tachychardia, hypotension, niacin deficiency rash (depletion of tryptophan), endocardial fibrosis (right heart)

diagnose with high urinary 5-HIAA
treat with octeotride or surgery if tumor is localized
malabsorption/steatorrhea syndromes
celiac disease, chronic pancreatitis, tropical sprue, Whipple's
malabsorption syndromes general presentation
steatorrhea, weight loss, ADEK deficiency, hypocalcemia, easy-bruising/increased PT, iron deficiency (duodenum), folate deficiency megaloblastic anemia), B12 deficiency (megaloblastic anemia, terminal ileum)
malabsorption syndromes specific presentation
celiac --> iron deficiency anemia and dermatitis herpetiformis
chronic pancreatitis --> recurrent episodes from alcohol or gallstones
tropical sprue --> history of tropical country travel
Whipple --> dementia, arthralgias, opthalmoplegia
celiac disease diagnosis
screen with antigliadin, antiendomysial and antiglutaminase antibodies
endoscopic biopsy is required to exclude small bowel lymphoma and confirm diagnosis
chronic pancreatitis diagnosis
history of repeated pancreatitis episodes with pancreatic calcifications on x-rays or CT
secretin stimulation test (gold standard but rarely performed) or low trypsin levels
tropical sprue and Whipple diagnosis
biopsy showing organisms
for Whipple, most sensitive test is PCR of biopsy showing PAS+ macrophages
how to differentiate between malabsorption diseases
d-xylose, iron, folate and carotene malabsorption point to mucosal problems (celiac, sprue, Whipple)
vitamin B12 malabsortion can also indicate pancreatic enzyme deficiency
vitamin K and calcium deficiencies are due to fat malabsorption
malabsorption syndromes treatment
celiac --> gluten-free diet
chronic pancreatitis --> pancreatic enzyme pills
tropical sprue --> TMP-SMX or doxycycline for 6 months
Whipple --> TMP-SMX or doxycycline or ceftriaxone for 1 year
50% prevalent over 50
asymptomatic or left lower quadrant colicky pain +- painless bleeding
diagnose with colonoscopy
treat with increased dietary fiber and bulking agents
infected diverticula
fever, tenderness, pain, leukocytosis
diagnose with CT
barium and endoscopy are contraindicated
treat with ciprofloxacin/metronidazole, ampicillin/sulbactam, piperazillin/tazobactam, cefotetan/gentamycin
can be due to lack of dietary fiber, insuficient fluid intake, CCBs, oral ferrous sulfate, hypothyroidism, opiates, anticholinergics; painful defecation can be dark due to bismuth or iron; treat by stopping medications, hydration, bulking agents, milk of magenesia, docusate
colon cancer
heme-positive brown stool and chronic anemia for right side
obstruction and decreased stool caliber for left side
can present with strep bovis or C. septicum endocarditis

diagnose with colonoscopy or sigmoidoscopy if located 60cm of distal colon

if localized to mucosa or submucosa then surgery, else 5FU chemotherapy
hereditary nonpolyposis syndrome
no polyps
three family members in at least two generations with colon cancer
increased incidence of ovarian and endometrial cancer
start screening at age 25 and then every 1-2 years
hereditary polyposis syndromes
FAP has APC gene which confers 100% penetrance for adenomas by 35 and colon cancer by 50
screen with flexible sigmoidoscopy at age 12 and 1-2 years thereafter
perform colectomy when first polyp is found

juvenile polyposis syndromes has 10% risk of colon cancer and produces hamartomas, not adenomas

Cowden syndrome is colon hamartomas with slight risk of colon cancer

all can present with rectal bleeding as a child
Gardner syndrome
colon cancer with multiple, soft tissue tumors such as osteoma, lipoma, cysts, fibrosarcomas
if casual osteoma found in x-ray --> colonoscopy
Peutz-Jeghers syndrome
hamartomatous polyps in colon with hyperpigmented melanotic spots on lips and skin
abdominal pain due to intussusception/bowel obstruction
Turcot syndrome
colon cancer with CNS malignancies
GI bleeding etiology
upper GI bleed: ulcer, gastritis, Mallory-Weis, esophagitis, gastric cancer, esophageal varices from portal hypertension

lower GI bleed: diverticulosis, angiodysplasia, hemorrhoids, cancer, inflammatory bowel disease;
GI bleeding management
first fluid resucitation with saline or Ringer
hemogram, PT, type and crossmatch

if elevated PT --> fresh frozen plasma
if platelets <50,000 transfuse platelets
if concomitant cirrhosis --> octeotride to decrease portal hypertension
if severe bleed or coagulopathy --> fluids, blood, platelets and plasma
if esophageal varices --> octeotride or place bands by endoscopy or perform TIPS

elderly --> maintain hematocrit >30% with fluids and/or transfusion
younger --> transfuse if hematocrit <20%

after these measures --> endoscopy to determine etiology
GI bleeding presentation
red blood in stools if lower GI bleed
ocult blood with >5-10ml or melena with >100ml of upper GI blood

orthostasis: >10 point rise in pulse or >20 point drop in systolic pressure from supine to sitting or standing after 1 minute between measurements indicates 15-20% blood loss

pulse above 100 or systolic pressure below 100 indicates 30% blood loss
GI bleeding diagnosis
nuclear bleeding scan (technetium tagged red blood cells from the patient)
angiography usefull in high-volume bleeding
also capsule endoscopy
acute pancreatitis etiology
alcoholism, gallstones, hypercalcemia, hypertriglyceridemia, medications (pentamidine, didanosine, azathiorpine, sulfas), ERCP, trauma, mumps virus
acute pancreatitis presentation
midepigastric pain radiates to the back, nausea, vomitting
severe disease can have fever, hypotension, ARDS, leukocytosis
Cullen sign (blue umbilical discoloration)
Turner's sign (bluish discoloration of flanks)
acute pancreatitis diagnosis
screening with amylase and lipase levels
Ranson criteria for severity
(leukocytosis, hypoxia, hyperglycemia, high LDH and AST)
hypocalcemia, high BUN

CT scan is more accurate than Ranson criteria for severity
gold standard is ERCP
acute pancreatitis management
supportive with fluids, bowel rest and analgesics
necrosis on CT is indicative of imipenem or cefuroxime to diminish infection risk
severe necrosis is indication for percutaneous needle biopsy of pancreas
if there's necrosis and infection surgical debridement is indicated
drain pseudocyst if >5cm, pain, fistula or rupture
acute pancreatitis complications
ascites high in amylase
pleural effusion is transudate high in amylase
splenic vein thrombosis
cirrhosis etiology
alcohol (#1 cause)
primary billiary cirrhosis
sclerosing cholangitis
alpha-1 antitrypsin deficiency
Wilson disease
general presentation of cirrhosis
low albumin level
portal hypertension
esophageal varices
ascites (do paracenthesis to exclude infection)
peripheral edema
increased PT
spider angiomata
palmar erythema
low clotting factors except factor VIII and vonWillebrand
spontaneou bacterial peritonitis (WBC count >500/mm3 or >250/mm3 neutrophils, treat with ceftriaxone)
serum-ascites albumin gradient
serum albumin is always higher than ascitic fluid
when SAAG >1.1 then portal hypertension
when SAAG <1.1 (high ascitic albumin) then cancer and infections
cirrhosis management
edema --> diuretics (spironolactone because of high aldosterone levels)
portal hypertension and varices --> propanolol (prevents bleeding)
encephalopathy --> neomycin or lactulose (metabolized by bacteria in colon which increases acidity and converts NH3 into amonium which is not absorbed well and eliminated
vitamin K is not effective because there are no clotting factors
primary billiary cirrhosis
fatigue and pruritus
osteoporosis in 20-30% and cirrhosis signs
associated with Sjogren, RA, scleroderma

diagnose with normal transaminases, high alkaline phosphatase and GGTP, high IgM and antimitochondrial antibodies (specific)
biopsy is gold standard

treat with orsodeoxycholic acid and cholestyramine
UV light for pruritus and liver transplant in late stages
primary sclerosing cholangitis
fatigue and pruritus, elevated alkaline phosphatase, osteoporosis in 20-30% and cirrhosis signs
associated with inflammatory bowel disease (specially UC)
can predispose to cancer of billiary system (15%)
diagnose with normal transaminases, high alkaline phosphatase and GGTP, high IgM
no antimitochondrial antibodies
biopsy is not gold standard, it's ERCP or cholangiogram
treat with orsodeoxycholic acid and cholestyramine
UV light for pruritus and liver transplant in late stages
genetically predisposed overabsorption of iron in duodenum with accumulation
cirrhosis is most common finding
hepatocellular CA (15-20%)
restrictive cardiomyopathy (15%)
arthralgias, skin hyperpigmentation, diabetes, hypogonadism, vibrio vulfinicus and yersinia infections

screen with elevated iron levels, low iron binding capacity and high ferritin
biopsy is gold standard

treat with phlebotomy or deferoxamine
Wilson disease
underexcretion and overabsorption of copper with deposition in brain, liver and cornea
coreathetoid movements with psychosis --> slit lamp exam --> Kayser-Fleischer corneal rings
also cirrhosis

lab tests: low ceruloplasmin and high urinary copper
gold standard is biopsy

treat with copper chelator penicillamine or liver transplant;
alpha-1 antitrypsin deficiency
antiprotease is not produced enough by liver
leads to cirrhosis and emphysema at young age in nonsmoker
confirm diagnosis with enzyme levels
enzyme replacement therapy and smoke cessation
chronic hepatitis B/C
virus transmitted by blood transfusions, needle sticks and sex
mostly asymptomatic until advanced disease then cirrhosis
HbSAg >6 months makes chronic hep B diagnosis
hep C antibody and high viral load on PCR is diagnosis for chronic hep C
treat hep B with interferon, lamiduvine or adefovir monotherapy
treat hep C with pegylated interferon and ribavirin multitherapy
characteristics of pain
duration, quality, location, radiation, frequency, alleviating or precipitating factors, associated symptoms
chest pain in acute coronary syndrome
substernal opressive quality described as tightness, heaviness or pressure; in MI pain lasts >20-30min; constant in frequency, precipitated by exercise, radiates to left shoulder

inferoposterior MI can present with upper abdominal pain, nausea, hypotension and dizziness or fainting (due vagal reflexes)

transient ischemia is releived with nitroglycerin
associated symptoms are diaphoresis, tachypnea and anxiety
musculoskeletal or pulmonary chest pain
described as sharp or knife-like and reproduced by changes in position or palpation
nonspecific but seen in MI or pulmonary embolism
blood pressure in evaluation of chest pain
difference of >20mmHg between two arms suggests aortic dissection (70%); hypotension is seen in massive pulmonary embolism or cardiac shock and it could also be seen in inferoposterior MI
fever in evaluation of chest pain
suggests pneumonia or mediastinitis
signs of atherosclerosis
corneal lipid rings
narrowed retinal arteries
pigment and hair changes in legs
may be seen in acute coronary syndrome
chest wall exam in chest pain evaluation
check for tender areas, respiratory motion, respiratory retractions or accessory muscle use; if palpation reproduces the pain consider musculoskeletal etiology
heart sounds in chest pain evaluation
wide physiologic splitting of S2 (inspiration) --> right bundle branch block or right ventricular infarction

paradoxical splitting (expiration) --> LBBB or anterior/lateral infarction

S3 --> heart failure

S4 --> angina or infarction;

aortic regurgitation --> aortic dissection

mitral regurgitation --> angina or infarction due to papillary muscle dysfunction
lung auscultation in chest pain evaluation
assymetry of breath sounds in spontaneous pneumothorax; absent lung sounds in spontaneous pneumothorax or pleural effussion
work-up of chest pain
all patients should have 12-lead ECG (MI diagnostic findings are ST elevation or Q waves in 50%, ischemia findings are ST depression or T wave inversion in 35%)

CK-MB, troponins T I C

chest x-ray
differential diagnosis of chest pain
noncardiovascular: costochondritis, hiatal hernia, GERD, peptic ulcer, gallbladder disease

cardiovascular: MI, aortic stenosis, myocarditis, pericarditis, dissecting aortic aneurysm, mitral valve prolapse

pulmonary: embolism, pulmonary hypertension, pneumothorax
costochondritis differentiating features
pain exacerbated with inspiration; reproduced with chest wall palpation
hiatal hernia differentiating features
reflux of food, relief with antacids
GERD differentiating features
acid reflux, relief with antacids
peptic ulcer differentiating features
epigastric pain worse 3h after eating
gallbladder disease differentiating features
right upper quadrant pain and tenderness
myocardial infarction differentiating features
severe pain > 20 minutes
aortic stenosis differentiating features
systolic ejection murmur
myocarditis differentiating features
vague mild pain
pericarditis differentiating features
sharp pain, worse with lying down, relieved by sitting up
diffuse ST elevation
responds to analgesics
dissecting aortic aneurysm differentiating features
sharp, tearing pain also felt in the back
loss of pulses, wide mediastinum on x-ray
diagnosis confirmed by CT, MRI, transesophageal ultrasound or aortography
mitral valve prolapse differentiating features
transient pain, midsystolic click, young females
pulmonary embolism differentiating features
tachypnea, dyspnea, cough, pleuritic pain, hemoptysis
diagnosis confirmed by CT, lung scan or pulmonary angiogram
pulmonary hypertension differentiating features
signs of right ventricle failure
pneumothorax differentiating features
sudden onset of pain and dyspnea
major modifiable IHD risk factors
high cholesterol, tobacco, hypertension, physical inactivity, obesity, diabetes
uncontrollable IHD risk factors
age, sex, heredity
minor IHD risk factos
sex hormones and stress
cholesterol levels in ischemic heart disease
the higher the level, the more risk for IHD; LDL is most important to consider (>100mg/dL)
low HDL (<40mg/dL)
hypertriglyceridemia (>150mg/dL)
high HDL/cholesterol ratio
high lipoprotein A
stable angina presentation
cardiac chest pain episodes on exertion relieved by rest that last 5-15min; ST depression in seen during attack
stable angina diagnosis
perform baseline ECG then exercise stress test which is positive when there is >2mm ST depression and/or drop of >10mmHg in systolic pressure

this test is diagnostic (67% sens, 70% spec), determines severity, effectiveness of treatment and functional capacity; contraindicated in most other cardiac diseases

can also use thallium nuclear stress test (82% sens, 95% spec), dobutamine or adenosine stress test, stress echocardiogram

patients with stable angina need evaluation of severity
stable angina management
acute episodes --> sublingual nitroglycerin
long-term --> long-acting nitrates (isosorbide), beta-blockers, aspirin, statins, modification of risk factors
after evaluating severity decide on revascularization (stent or bypass)
differentiate NSTEMI and unstable angina diagnosis
if there are ECG signs + elevated cardiac markers --> NSTEMI
if normal cardiac markers 6-24 hours after presentation --> unstable angina
unstable angina presentation
cardiac chest pain episodes occuring at rest or of increasing severity, frequency and duration resistant to nitrates
thrombolytic therapy
beneficial in STEMI but not NSTEMI; in NSTEMI ischemia is mostly due to thrombus-related embolization and platelet-rich instead of fibrin-rich thus thrombolytics are not effective
ECG diagnosis in NSTEMI
ST segment deviation (>0.5mm) or new T-wave inversion (>2mm)
but normal ECG or minor changes in up to 50%
high-risk features of UA/NSTEMI
repetitive or prolonged chest pain (>10min)

elevated biomarkers
persistent ECG changes
hemodynamic instability (SBP<90)
sustained ventricular tachycardia
LV EF <40%
chronic kidney disease
prior PTCA or CABG
UA/NSTEMI management
antiplatelet: aspirin and clopidogrel (300mg loading, 75mg/day)
anticoagulant; unfractionated heparin or enoxaparin for 48-72 hours or until angiography
glycoprotein IIb/IIIa inhibitors: abciximab, tirofiban (diabetics), eptifibatide
invasive: early coronary angiography (48 hours) and revascularization recommended in NSTEMI or high-risk patients
STEMI diagnosis
clinical symptoms plus ECG:
persistent ST elevation of >1mm in two contiguous limb leads
ST elevation of >2mm in two contiguous chest leads
new LBBB pattern
cardiac biomarkers are not needed for initial diagnosis
STEMI atypical presentation
elderly or diabetics can present with nausea or dyspnea as sole symptom
as many as 20% are silent (symptoms not severe enough for patient)
STEMI general management
cardiac monitor
oxygen therapy
IV line
localizations of STEMI
inferior, anteroseptal, anterior, lateral, posterior
inferior STEMI ECG localization
leads II, III and aVF; artery is right coronary
anteroseptal STEMI ECG localization
leads V1-V3; LAD artery
anterior STEMI ECG localization
leads V2-V4; LAD artery
lateral STEMI ECG localization
leads I, aVL, V4-V6; artery is LAD or circumflex
posterior STEMI ECG localization
leads V1-V2 --> tall broad initial R wave, ST depression, tall upright T wave
usually in association of inferior or lateral STEMI
artery is posterior descending
abnormal Q wave
>25% the height of partner R wave
greater than 0.04sec and 2mm deep
Q waves are normal in lead III
ECG evolution of STEMI
hyperacute T waves (immediately to 6-24 hours)
ST elevation (immediately to 1-6 weeks)
Q waves (1/several days to years/never)
T wave inversion (6-24 hours to months-years)
reperfusion therapy
PCI (angioplasty/stents) are preferred if <12 hours and <90 minutes from first medical encounter; if PCI is unavailable or too late then thrombolytic therapy
thrombolytic therapy
appropiate in place of PCI if >12 hours of onset of STEMI
streptokinase and alteplase by IV infusion
reteplase and tecneplase by rapid bolus
tPA is most common in US
due to antibody formation streptokinase is contraindicated if had been given within 1 year to same patient
absolute contraindications to thrombolytic therapy
active bleeding
significant closed head or facial trauma within 3 months
suspected aortic dissection
prior intracranial hemorrhage
ischemic stroke within 3 months
relative contraindications to thrombolytic therapy
recent major surgery (<3 weeks)
traumatic/prolonged cardiopulmonary rescucitation
recent internal bleeding
active peptic ulcer
severe poorly controlled hypertension
ischemic stroke <3 months
antiplatelet therapy in STEMI
aspirin (to all patients) and clopidogrel (300mg) to patients undergoing PCI or fibrinolysis; with long-term maintanance of 75mg (up to 1 month after fibrinolysis or 1 year after stent)
anticoagulant therapy in STEMI
unfractionated heparin (or perhaps enoxaparin) an GP IIb/IIIa inhibitors should be used in conjunction with PCI; only heparin in case of fibrinolytic therapy
heparin dosages in STEMI
in PCI it depends on concomitant use of GP Iib/IIIa inhibitors; in fibrinolysis: unfractionated heparin in initial bolus of 60 units/kg, followed by initial infusion of 12 units/kg (max 1,000/h); adjusted to attain activated PTT to 1.5-2 times control; enoxaparin may be used in patients <75 but dose adjustment in renal patients
CABG indications
should be considered in patients who failed PCI or persistent ischemia resistant to drugs; patient should have suitable anatomy
discharge medications after acute coronary syndrome
aspirin (75mg indefinitely)
clopidogrel (75mg upto 1 year after PCI or 1 month or if aspirin contraindicated)
beta-blocker (if heart failure carvedilol or metoprolol)
ACE inhibitors (if heart failure)
statins to all patients should be initiated in hospital
short-acting nitrates or isosorbide if continuous frequent pain
warfarin in those at risk for systemic thromboembolism

drug treatments shown to reduce mortality in IHD
CABG in triple vessel or left main disease
dysrhythmias as ACS complication
bradycardia (treat with atropine)
premature beats
supraventricular tachycardias (atrial tachycardia, fibrillation, flutter)
ventricular tachyarrhythmias (ventricular tachycardia, accelerated idioventricular rhythm, fibrillation)
conduction abnormalities as ACS complication
1st, 2nd and 3rd degree heart blocks, hemiblocks, branch blocks
mechanical dysfunction as ACS complication
heart failure (left/right or biventricular)
true or pseudoventricular aneurysm
acute mitral regurgitation
ventricular septal rupture
free wall rupture

mechanical problems are treated with emergency surgery
ischemia as ACS complication
recurrent infarction or extension
post-infarction angina after thrombolytics or PCI requires bypass surgery
sudden cardiac death
is a complication of ACS; most commonly ventricular fibrillation or tachycardia
thromboembolic complications of ACS
mural thrombus
deep vein thrombosis due to prolonged immobilization
ischemic stroke
right ventricular infarction
often a complication of inferior MI (30%); diagnosed with ECG and treated with fluids (if its complication)
hypercoagulable states as nonatherosclerotic cause of MI
polycythemia vera
factor V Leyden
protein C deficiency
antiphospholipid antibodies
vasculitis as nonatherosclerotic cause of MI
SLE, PAN, takayasu, Kawasaki
coronary spasm
due to prinzmetal or cocaine abuse which are nonatherosclerotic causes of MI
Prinzmetal angina
episodes of severe angina due to coronary vasospasm
occurs at rest (night or morning hours)
ST elevation and can be associated with MI, ventricular arrhythmias or sudden death, migraines
exercise stress tests and angiography are normal
diagnose with ergonovine
coronary embolus as nonatherosclerotic cause of MI
atrial myxoma, atrial or ventricular thrombus
compensatory mechanisms in heart failure
cardiac: Frank-Starling, tachycardia, ventricular dilation;
neuronal: increased sympathetic adrenergic, reduced vagal activity;
hormonal: vasopressin, catecholamines and BNP, renin-angiotensin-aldosterone system
systolic heart failure
decreased ventricle contraction, dilation and EF<45% due to ischemic cardiomyopathy, dilated cardiomyopathy
dyastolic heart failure
filling of one or both ventrciles is impaired with normal EF; can be due to amyloidosis
congestive heart failure
syndrome of dyspnea, fatigue, peripheral edema, high JVP and pulmonary edema with crackles
causes of heart failure
70% are due to ischemic heart disease
hypertensive, alcoholic and other cardiomyopathies
valvular disease
congenital heart disease
precipitating factors in heart failure
important to exclude in diagnosis

excessive dietary Salt
uncontrolled Hypertension
cardiac Ischemia
myocardial Infarction

"SHIIIT precipitates A failure"
heart failure presentation
paroxysmal nocturnal dyspnea
pulmonary rales
peripheral edema
jugular venous distention
displaced apical impulse
cardiac Vs. pulmonary dyspnea
cardiac is more sudden, not associated with sputum production, without history of pulmonary disease, no lung disease evidence on x-ray, cardiomegaly seen on x-ray

pulmonary dyspnea is the contrary
classification of heart failure severity
Class I: no limitation of daily activities
Class II: mild limitation, can perform mild exertion
Class III: marked limitation, only comfortable at rest
Class IV: confined to bed or chair; physical activity or rest brings discomfort
heart failure diagnosis
check cardiac enzymes to exclude ischemia or MI
x-ray to exclude infection
test of choice is echocardiography for diagnosis and classification (ejection fraction)
chest x-ray to exclude infection shows cardiomegaly, vascular redistribution, Kerley B-lines, interstitial edema
ECG indentifies hypertrophy, ischemia or precipitating arrhythmias
BNP is 97% sensitive for decompensated HF
heart failure management
first line: ACEi + loop diuretic then add carvedilol/metoprolol +- digitalis

ACE inhibitors improve survival and reduce hypertrophy and symptoms; loop diuretics decrease congestive symptoms; betablocker decrease mortality, reduce hospitalizations and improve ejection fraction; other vasodilators: nitrates/hydralazine used if ACEi or ARB are contraindicated; digitalis does not improve survival but reduces severe symptoms; if dyastolic HF use less diuretics and vasodilators and give CCBs (verapamil) to slow heart rate and allow filling
pulmonary edema
medical emergency
tachypnea, expectoration, cyanosis, nocturnal dyspnea, rales, ronchi, wheezing;
x-rays: prominent pulmonary vessels, enlarged cardiac silhouette, Kerley B lines, pleural effusions
ECG: to determine if arrhythmia
treatment: morphine, furosemide, sitting patient upright, oxygen, nitroglycerin (reduce preload), digoxin (if atrial fibrillation), IV ACEi
mitral stenosis etiology
abnormal mitral leaflets are affected due to rheumatic fever autoimmune deposits
reduced left ventricular filling, increased left atrial and pulmonary pressure, forward and right heart failure ensues
mitral stenosis presentation
paroxysmal nocturnal dyspnea
systemic embolism
right heart failure
atrial fibrillation
pulmonary rales
decreased pulse pressure
loud S1 with opening snap following S2
diastolic rumble
sternal lift
mitral stenosis auscultation
pulmonary rales, loud S1 with opening snap following S2, diastolic rumble, sternal lift
mitral stenosis diagnosis
chest x-ray: large left atrium (double-density right heart border, posterior displacement of esophagus and elevated left mainstem bronchus), Kerley B lines, large pulmonary arteries
ECG: signs of ventricular hypertrophy, left/right atrial abnormalities, atrial fibrillation
echocardiography: thickening of mitral valve leaflets, left atrial enlargement
mitral stenosis management
diuretics, salt restriction, digitalis and anticoagulants if atrial fibrillation
if drugs fail --> surgical valve replacement or commissurotomy
acute etiology of mitral regurgitation
rupture of chordae tendinae
papillary muscle rupture
endocarditis (valvular destruction)
chronic etiology of mitral regurgitation
Hypertrohpic cardiomyopathy
Endocardial cushion defect
Papillary muscle dysfunction
Rheumatic fever
mitral Prolapse
severe left ventricular dilation

"regurgitation by CHEF PReP"
mitral regurgitation pathogenesis
retrograde left ventricle flow into left atrium increases atrial pressure and decreases forward output which results in volume overload, decreased afterload (flow is eased into left atrium) which allow compensated increased ejection fraction which eventually leads to left ventricular dysfunction
mitral regurgitation presentation
dyspnea, orthopnea, paroxysmal nocturnal dyspnea; if severe, right sided failure;
mitral regurgitation auscultation
hyperdynamic and displaced (downward left) left ventricular impulse
carotid upstroke diminished
holosystolic apical murmur
S3 with widely split S2
distended neck veins
mitral regurgitation diagnosis
x-ray: cardiac enlargement and possble pulmonary congestion
ECG: left ventricular hypertrophy and left atrial enlargement
echocardiography: mitral valve can prolapse; distended neck veins
mitral regurgitation management
therapy: digitalis, diuretics, ACEIs, warfarin; if symptoms persist or are severe: surgery
mitral prolapse presentation
most are asymptomatic; can have lightheadedness, palpitations, syncope, chest pain
mitral prolapse auscultation
mid-systolic click and late systolic murmur at apex, worsens with Valsalva, improves with squatting
mitral prolapse complications
sudden death
bacterial endocarditis
valve calcifications
transient cerebral ischemic attacks
mitral prolapse diagnosis
clinical + doppler echocardiography which shows systolic displacement of mitral leaflets into left atrium
mitral prolapse management
endocarditis prophylaxis (in severe cases)
betablocker for chest pain or arrhythmias
surgery rarely necessary
aortic stenosis etiology
due to age-related calcification of the valve or calcification and fibrosis of congenitally bicuspid valve; also rheumatic fever
aortic stenosis pathogenesis
stiff aortic valve increases afterload and left ventricular pressure which results in concentric hypertrophy
noncompliant ventricle and S4 gallop with increased LVEP
the heart has increased oxygen demands with decreased coronary flow due to thickness
aortic stenosis presentation and auscultation
pulsus pardus et tardus
carotid thrill
systolic ejection murmur in aortic area
S4 gallop
mitral stenosis diagnosis
ECG: right ventricular hypertrophy, atrial fib
chest x-ray: large left atrium and pulmonary artery with increased lung vascularity
echocardiography: thickening of mitral valve leaflets, left atrial enlargement
mitral stenosis management
endocarditis prophylaxis no longer recommended
if symptomatic: surgical valve replacement or balloon valvuloplasty
aortic stenosis Vs. aortic valve sclerosis
both have systolic murmur but in aortic valve sclerosis carotids don’t have delayed upstroke
no hypertrohpy in ECG
no excursion of valve leaflets in ecochardiography
no hemodynamically significant aortic valve gradient
aortic stenosis Vs. hypertrophic obstructive cardiomyopathy
both have systolic murmur but in HOC there's characteristic change in murmur with maneuvers; large septal Q waves; characteristic echocardiographic features (asymmetrical hypertrohpy)
aortic stenosis Vs mitral regurgitation
both have systolic murmurs but in MR is holosystolic and radiates to axilla, not carotids
carotid upstroke normal
dilated ventricle
aortic valve normal in eco
aortic stenosis Vs. pulmonic stenosis
both have systolic murmurs but in pulmonic stenosis it does not radiate to neck; it's loudest on left sternal border and increases with inspiration; chest x-ray and EKG reveal enlarged right heart and valve stenosis
aortic regurgitation etiology
hypertension (most common)
infectious endocarditis
ankylosing spondylitis
rheumatic fever
aortic dissection
aortic trauma
aortic regurgitation pathogenesis
valve insufficiency leads to volume overload of left ventricle with compensating Frank-Starling; dilation, overstretching and decreased contraction force; if acute, can have large LEVEDP because ventricle is not adapted; acute pulmonary edema can occur; lower systolic blood pressure is due to regurgitation of blood out of aorta and decreased SVR; there's increased systolic pressure and widened pulse
aortic regurgitation presentation
diastolic decrescendo, systolic flow and Austin-Flint (presystolic low-pitched apical) murmurs
Duroziez sign (murmur over femoral)
S3 when decompensated
aortic regurgitation diagnosis
chest x-ray: LV and aortic dilation
EKG: LV hypertrophy with volume overload (narrow deep Q waves in left precordial leads)
echocardiogram: dilated LV and aorta, LV volume overload, fluttering of anterior mitral valve leaflet
aortic regurgitation management
endocarditis prophylaxis not recommended; salt restriction, ACEIs, aortic valve replacement
dilated cardiomyopathy etiology
most common is idiopathic
drugs --> Doxorubicin, Cyclophosphamide, Vincristine, Alcohol
infections --> Tuberculosis, Coxsackie
metabolic --> Uremia, chronic Hypophosphatemia, Hypokalemia, Hypocalcemia
toxins --> arsenic, cobalt, lead
dilated cardiomyopathy presentation
signs of left and right systolic heart failure
dilated cardiomyopathy diagnosis
x-ray: cardiomegaly/pulmonary congestion
EKG: sinus tachycardia, arrhythmias, conduction abnormalities
echo: gold standard, dilated left ventricle, decreased wall motion, mitral regurgitation
dilated cardiomyopathy differential
valvular heart disease
coronary artery disease
hypertensive heart disease
dilated cardiomyopathy management
treated as those with systolic heart failure
hypertrophic cardiomyopathy etiology
autsomal dominant in 60% or sporadically
aortic stenosis
hypertrophic cardiomyopathy pathogenesis
unexplained myocardial asymmetrical hypertrophy results in reduced compliance of left ventricle and hypercontractility; increased ejection fraction to 80-90%; obstruction of blood flow
contractility in obstruction of hypertrophic cardiomyopathy
increased contractility increases obstruction: digitalis, beta stimulats (isoproterenol, epinephrine), tachycardia, premature beats

decreased contractility decreases obstruction: betablockers, heavy sedation/anesthesia, CCBs
preload in obstruction of hypertrophic cardiomyopathy
reduced preload increases obstruction: valsalva, low volemia, standing, nitroglycerin, vasodilators, tachycardia

increased preload decreases obstruction: increased volemia, squatting, bradycardia, betablockers
afterload in obstruction of hypertrophic cardiomyopathy
reduced afterload increases obstruction: hypovolemia, nitroglycerin, vasodilators
increased afterload decreases obstruction: hypervolemia, squatting, alfa stimulation, handgrip exercise
hypertrophic cardiomyopathy presentation
large jugular A wave
systolic murmur
mitral regurgitation murmur
hypertrophic cardiomyopathy diagnosis
EKG: LV hypertrophy, pseudo Q waves, ventricular arrhythmias
echo: gold standard, asymmetrical hypertrophy, systolic anterior motion of mitral valve, midsystolic closure of aortic valve
hypertrophic cardiomyopathy treatment
betablockers, CCBs, surgery in severe cases
restrictive cardiomyopathy etiology

"restrictive Neo-HeARtSS"
restrictive cardiomyopathy pathogenesis
myocardium is rigid and noncompliant, impeding ventricular filling and altering diastolic function similar to constrictive pericarditis
restrictive cardiomyopathy manifestations
exercise intolerance
elevated jugular venous pressure
S3, S4
Kussmaul sign
restrictive cardiomyopathy diagnosis
x-ray: mild cardiomegaly, pulmonary congestion
EKG: low voltage, conduction disturbances, Q waves
echo: characteristic texture with thickening of all cardiac structures
restrictive cardiomyopahty treatment
no good therapy; eventually die from CHF; consider heart transplant
acute pericarditis etiology
viral infections
metabolism disorders
drug reactions
acute pericarditis presentation
substernal or left-sided chest pain worsened by lying down, coughing and deep inspiration, relieved by sitting up and leaning forward

pericardial friction rub best heard with stethoscope diaphragm as patient sits forward and forced expiration
acute pericarditis diagnosis and treatment
EKG may be diagnostic with diffuse ST elevation and upright T waves at onset of pain
treat etiology and anti-inflammatories

"acute pericarditiST"
pericardial effusion etiology
can be transudate (CHF, overhydration, hypoproteinemia) or exudate (TB, neoplasia) or hemopericardium (aortic aneurysm, aortic dissection, penetrating trauma, free wall rupture, bleeding due to coagulation defects)
pericardial effusion diagnosis and treatment
echo is gold standard showing echo-free space between posterior pericardium and posterior left ventricular epicardium; or heart swinging freely in pericardial sac; x-ray shows water-bottle configuration of cardiac silhouette; treat with pericardiocentesis and etiology cure
cardiac tamponade etiology
TB or suppurative pericarditis
intrapericardial hemorrhage
mediastinal radiotherapy
cardiac tamponade manifestations
neck vein distention
decreased heart sounds
pulsus paradoxus (dissapearance during inspiration)
cardiac tamponade diagnosis and treatment
clinical + echo + catheterization to confirm left and right atrial pressures
pericardiocentesis, subxiphoid surgical drainage
Kussmaul sign
jugular venous distention that increases with inspiration
constrictive pericarditis etiology
thickening of pericardium due to idiopathic
open-heart surgery
thoracic radiation
postviral infection
constrictive pericarditis manifestations
dyspnea on exertion
orthopnea (50%)
right congestion signs
Kussmaul sign
distant heart sounds
early diastolic apical pericardial knock confused with S3
constrictive pericarditis diagnosis
CT is gold standard and shows pericardial thickening and calcifications
x-ray: normal heart
EKG: low-voltage T waves
first-degree heart block
progressive prolongation of PR interval until P wave is blocked and ventricular beat is dropped
block is usually at AV node
normal QRS
PR interval shortens after dropped beat; RR interval narrows progressively; RR interval is narrower after dropped beat
second-degree heart block
blocked ventricular beat not preceded by PR changes
site of block is usually infranodal
wide or narrow QRS
if PR is prolonged, the duration is constant
third-degree heart block
all atrial beats are blocked; complete dissaciation between PR and QRS

due to fibrous degenerative changes in elderly, inferior or posterior infarction, infiltrative or granulomatous diseases, digitalis, ankylosing spondylitis

Adam-Stoke (sudden asystole or ventricular tachyarrhythmias) are common

associated with bradycardia and congestion
treat with pacemaker
paroxysmal supraventricular tachycardia presentation
ectopic tachyarrhythmias with sudden onset and termination
regular rhythm between 130-220 beats
initiated by supraventricular premature beat
80% are by re-entry;
paroxysmal supraventricular tachycardia treatment
right carotid massage is first line
IV verapamil or adenosine is preferred second line
or IV propanolol, esmolol or digitalis

cardioversion if unstable
multifocal atrial tachycardia
irregular supraventricular rhythm between 100-200 beats
QRS preceded by P but P waves vary in morphology
atrial flutter
regular rhythm with ventricular rate of 125-150 and atrial rate of 250-300; treat with cardioversion if unstable OR digitalis, verapamil, betablockers
atrial fibrillation etiology
associated with heart disease (rheumatic fever, coronary artery disease, CHF, hypertension)
noncardiac (hyperthyroidism, hypoxemia, alcohol intoxication)
lone AF (~30%, no structural disease)
atrial fibrillation presentation
supraventricular tachyarrhythmia with disorganized fribrillatory waves that replace P waves that vary in morphology and are irregular along with rapid ventricular response (iregularly irregular); shortness of breath, dizziness, palpitations
EKG in flutter Vs. atrial fibrillation
flutter waves that replace P waves (atrial contractions) are more regular than fibrillatory waves which are irregularly irregular
atrial fibrillation diagnosis
exam: severity, clinical type (paroxysmal, persistent, first episode), frequency, duration, precipitating factors and associated disease

x-ray: lung disease
EKG: verifies rhythm, LVH, pre-excitation, prior MI
echo: LVH, valve disease, atrial size
thyroid function: exclude hyperthyroidism
atrial fibrillation management
if hemodynamically unstable --> sedation and cardioversion

else --> control rate with diltiazem, verapamil, B-blocker or digoxin

if no spontaneous conversion to sinus rhythm and AF > 48 hours --> immediate cardioversion

else --> anticoagulation and elective cardioversion in 3 weeks

if AF persists --> long-term anticoagulation (warfarin) and rate control; catheter ablation is also common
cardioversion drugs
amiodarone, defetilide, felicanide, ibutilide, propafenone, quinidine

"PROPer cardioversion DEFEcates amiodarone"

drugs to maintain sinus rhythm:
amiodarone, disopyramide, defetilide, flecainide, propafenone, sotalol

"PROPer rhythm DEFEcates Amiodarone and DISses Sotalol"
complications of cardioversion
thromboembolism --> both electrical and pharmacologic; use anticoagulants if elective cardioversion
torsade de pointes --> drug cardioversion
Wolf-Parkinson-White syndrome diagnosis
ventricle is pre-excited by accesory pathway (Kent bundle); associated with paroxysmal supraventricular arrhythmia, atrial fibrillation and flutter

EKG shows short PR interval, wide QRS wave and delta waves

"delta PRwIDE"
Wolf-Parkinson-White syndrome management
if hemodynamically unstable --> immediate electrical cardioversion
else --> procainamide (digoxin, CCBs and BBs can inhibit normal pathway and are not indicated)
definitive treatment is ablation
ventricular tachycardia etiology
3 or more consecutive ventricular beats at rate >120b/min with wide and bizarre QRS
due to
mitral prolapse
metabolic imbalances
digoxin toxicity
ventricular tachycardia presentation
hypotension, CHF, syncope, cardiac arrest
variation in systolic pressure and intesity of heart sounds, intermittent canon waves in jugular venous pulse, extra heart sounds
wide split between S1 and S2 due to asynchronous ventricular beats
ventricular tachycardia management
if pulse is not present --> treat as ventricular fibrillation
else if stable pulse --> O2, IV access, lidocaine/amiodarone or procainamide
or if hemodynamically unstable, cardioversion
if unstable pulse --> O2, IV access, sedation, electrical cardioversion (100, 200, 300, 360J)
differential diagnosis of arrhythmias by QRS complex
wide and regular: VT, SVT aberration, WPW
wide and irregular: AF rarely
narrow and regular: ST, PSVT, AFL
narrow and irregular: AF, MAT
torsades de pointes etiology
undulating QRS on EKG baseline initiated by long-QT arrhythmias; drugs:
subarachnoid or intracerebral hemorrhage
torsades de pointes diagnosis and treatment
undulating QRS
recurrent dizziness

treat underlying disorder
replace antiarrhythmic with lidocaine or phenytoin
cardiac pacing
isoproterenol (shortens QT)
if hemodynamically unstable then electrical cardioversion
ventricular fibrillation presentation
significant activity on EKG with completely disorganized pattern
dead person (no pulse, no breathing, etc…) with VF EKG
ventricular fibrillation treatment
CPR, electrical cardioversion, epinephrine, amiodarone (follow ACLS pulseless arrest algorhythm)
definition of hypertension
multiple readings with systolic >140mmHg or diastolic >90mmHg in the absence of specific identifiable underlying cause
hypertension in those with diabetes or renal disease
defined as pressure > 130/80
hypertension stages
preHTN --> systolic 120-129, diastolic 80-89
stage I --> systolic 140-159, diastolic 90-99
stage II --> systolic >160, diastolic > 100
long term cardiac complications of hypertension
myocardial ischemia or infarction
left ventricular hypertrophy
aortic aneurysm
long term cerebrovascular complications of hypertension
transient ischemic atack or stroke
long term renal complications of hypertension
microscopic hematuria, elevation of BUN/creatinine which may need dialysis
long term eye complications of hypertension
arteriolar narrowing
results in blurred vision, scotomata, sometimes blindness
hypertension diagnosis
allow patient to sit quietly for 5 minutes before pressure is measured
repeat reading 3-6 times over several months before labeling as hypertensive and giving treatment
hypertension routine laboratory analysis
urinalysis for protein, glucose or red blood cells
glucose and lipids (for athersoclerosis risk)
serum potassium (exclude hyperaldosteronism)
who to treat
diastolic >90 after 3-6 months of nonpharmacologic therapy
what to use for hypertension
best initial treatment is diuretic such as hydroclorothiazide; stage III add ACEI, ARB, CCB or beta blocker; if not enough add another drug
specific antihypertensives for diabetics
goal is <130/80 (as in renal insufficiency, CHF, retinopathy or stroke)
specific antihypertensives for post MI
beta blockers
specific antihypertensives for CHF or left ventricle dysfunction post MI
ACEIs and/or betablocker
specific antihypertensives for pregnant
alpha methyldopa, labetalol, hydralazine or CCB
ACEIs and ARB are absolutely contraindicated
diuretics relatively contraindicated
hypertensive emergency definition
diastolic >120 with end-organ damage
malignant hypertension definition
has encephalopathy or nephropathy with accompanying papilledema
hypertensive emergency neurologic presentation
subarachnoid or intracerebral hemorrhage
hypertensive emergency cardiac presentation
chest pain
pulmonary edema
jugular venous distention
hypertensive emergency nephropathy presentation
acutely progressive hematuria, proteinuria, renal dysfunction
hypertensive emergency retinopathy presentation
papilledema, hemorrhages, blurred vision
hypertensive emergency diagnosis
no concern for white coat artifact; EKG is first initial test to exclude MI; head CT to exclude hemorrhage
hypertensive emergency treatment
IV nitroprusside and labetalol
if MI, nitroglycerin is preferred
IV enalaprilat is also being used
do not reduce pressure more than 25% in 1-2 hours to not compromise cerebral or myocardial perfusion (keep it above 95-100 diastolic)
causes of secondary hypertension
renal artery stenosis
also oral contraceptives, acromegaly, glomerulonephritis
renal artery stenosis
2dary hypertension
presents with upper abdominal bruit radiating laterally
best initial screen is abdominal ultrasound
captopril renogram is noninvasive to confirm
best confirmation is arteriogram
treat with percutaneous transluminal angioplasty or surgical resection
secondary hypertension due to Conn syndrome
presents with hypertension + hypokalemia
muscular weakness
nephrogenic diabetes insipidus
diagnosis --> high aldosterone levels in blood and urine
surgical resection of adenoma or spironolactone if hyperplasia
secondary hypertension in pheochromocytoma
episodic hypertension with headaches, sweating, palpitations and tachycardia
best initial test is VMA, metanephrines and free urine catecholamines
then do CT or MRI to locate tumor
treat with alpha adrenergics blockers followed by surgery
secondary hypertension in Cushing
present with hypertension, truncal obesity, buffalo hump, menstrual abnormalities, striae, etc… best initial tests are dexamethasone suppression test and 24-hour urine cortisol; treat with surgery
thiazide drugs
hydrochlorothiazide, chlortalidone, metolazone, indapamide
loop diuretic drugs
furosemide, bumetanide, torsemide
potassium sparing diuretics
spironolactone, amiloride, triamterene
specific indications of diuretics
CHF, edematous states, african-american patients, least expensive
side effects of diuretics
↓ magnesium
↑uric acid
relative contraindications of diuretics
diabetes, gout, hyperlipidemia
specific indications of beta blockers
myocardial infarction or ischemic heart disease
supraventricular arrhythmias
diastolic heart failure
side effects of beta blockers
heart block, bradycardia, conduction defects
↓HDL, ↑triglycerides
masking of hypoglycemia
relative contraindications of beta blockers
asthma or COPD
conduction defects
systolic heart failure
specific indications of ACEIs
diabetics (prevents neuropathy)
CHF (decreases afterload)
postmyocardial infarction with systolic failure
side effects of ACEIs
cough, angioedema, neutropenia, hyperkalemia, taste disturbance, anaphylactoid reaction
relative contraindications of ACEIs
less effective in african americans
absolute contraindications of ACEIs
bilateral renal artery stenosis, pregnancy
specific indications of calcium channel blockers
supraventricular arrhythmia
esophageal spasm
side effects of calcium channel blockers
peripheral edema
heart block
reflex tachycardia
relative contraindications of calcium channel blockers
AV conduction defects, CHF from systolic dysfunction
angiotensin receptor blocker specific indications
those intolerant to ACEIs (specially due to cough)
angiotensin receptor blockers side effects
fewer than ACEIs
angiotensin receptor blockers absolute contraindications
first-line drugs for hypertension
diuretics, betablockers, ACEIs, ARBs
second-line drugs for hypertension
central acting sympatholytics
direct vasodilators
alpha adrenergic blockers
central-acting sympatholytics drugs
clonidine, guanabenz, guanfacine, methyldopa
specific indications of central-acting sympatholytics
clonidine in opiate detox
central-acting sympatholytics side effects
dry mouth
heart block
memory loss
methyldopa specific side effects
hepatitis, Coombs+ hemolytic anemia
relative contraindications of central-acting sympatholytics
elderly or depressed patients
direct vasodilator drugs
hydralazine, minoxidil
specific indications of direct vasodilators
hydralazine in eclampsia; minoxidil in baldness
minoxidil specific side effects
fluid retention, pericardial effussion, hirsutism
hydralazine specific side effects
lupus-like syndrome
direct vasodilator relative contraindications
alpha adrenergic blocker drugs
doxazosin, prazosin, terazosin
specific indications of alpha adrenergic blockers
lipid disorders (they ↓LDL and ↑HDL)
prostatic hypertrophy
side effects of alpha adrenergic blockers
first-dose syncope, dizziness, headache
prerenal azotemia etiology
acute renal failure due to
hypovolemia (dehydration, burns, diuretic, vomitting, diarrhea, sweating, hemorrhage)
hypotension (shock, anaphylaxis)
third-spacing of fluids (peritonitis)
osmotic diuresis
low aldosterone (Addison)
low cardiac output (CHF)
low albumin (nephrotic syndrome)
renal artery stenosis
hepatorenal syndrome (hepatic failure, vasoconstriction of afferent)
ACEi-induced (in susceptible patients, vasodilation of efferent)
prerenal azotemia diagnosis
BUN/creatinine ratio 20:1
low urine sodium (<20)
high urine osmolality (>500)
low fractional Na (<1%)
specific gravity >1.010 (RAA system retains water and concentrates urine)
postrenal azotemia etiology
renal failure due to bilateral obstruction to urine flow
bladder stone or clot
bladder cancer
prostate hypertrophy or cancer
bilateral ureteral disease (retroperitoneal fibrosis)
neurogenic bladder
postrenal azotemia pathogenesis
bilateral obstruction to urine outflow leads to postrenal azotemia
if obstruction takes a long time it can lead to tubular necrosis
postrenal azotemia diagnosis
BUN/creatinine ratio can go as high as 20:1 but then starts to decrease
there's also concentrated urine and low fractional Na
need to find distended bladder on physical
OR bilateral hydronephrosis on renal sonogram or CT
OR large volume of urine after Foley catheter
acute tubular necrosis etiology
any cause of hypoperfusion or hypodrainage (pre or postrenal azotemia) can lead to tubular necrosis if prolonged;
acute tubular necrosis phases
prodromal (between injury and acute renal failure)
oliguric or anuric
post oliguric (polyuria due to tubular death and lack of urine concentration function)
acute tubular necrosis diagnosis
BUN/creatinine ration close to 10:1
low urine osmolarity (<350)
high urine sodium (>40)
high fractional Na (>1%)
brown pigmented granular casts and epithelial casts
acute tubular necrosis management
no effective medical therapy, just hydration and if life-threatening, dyalisis
dopamine or diuretics cannot reverse it
allergic interstitial nephritis etiology
accounts for 10-15% of intrinsic renal failure
due to drug allergy in 70%
penicillins, cephalosporins, sulfas, NSAIDs, allopurinol, rifampin, quinolones, CCBs, PPIs
also caused by leptospira, legionella, CMV, ricketsia and strep
allergic interstitial nephritis presentation
fever (90%)
rash (25-50%)
hemolysis (95%, nonspecific)
eosinophilia, eosinophiluria, proteinuria, increased IgE
allergic interstitial nephritis diagnosis
initial test is urinalysis looking for WBCs then Hansel or Wright stain for eosinophils
also eosinophilia, eosinophiluria, proteinuria (<2g/24h), increased IgE
allergic interstitial nephritis management
remove offending agent; if persistent failure then short course of steroids
renal failure from pigments etiology
hemoglobin and myoglobin are toxic to tubules and also precipitate
rhabdomyolisis can be caused by crush injury, seizures, severe exertion, statins, hypokalemia, hypophosphatemia, ABO incompatibility
renal failure from pigments diagnosis
best intitial test --> urinalysis looking for positive blood dipstick but absence of red cells
confirm by extremenly high CPK levels
also rapidly rising creatinine
most important test is EKG or potassium level looking for peaked T waves which can lead to arrhythmia death
renal failure from pigments management
if EKG abnormalities --> calcium chloride or gluconate is best initial therapy
hydration, manitol and urine alkalinization
acute renal failure from oxalate
most commonly by ethylene glycol overdose in suicide attempt
intoxicated patient with anion gap metabolic acidosis and renal insuficiency
confirm with oxalate crystals in urinalysis
treat with ethanol or fomepizole, dyalisis and bicarbonate
acute renal failure from urate
seen in tumor lysis syndrome of leukemia/lymphoma patients
treat with allopurinol and alkalinization of urine before chemo
confirm with uric acid crystals in urinalysis
renal failure from calcium
hypercalcemia is most common in hyperparathyroidism
surgical resection of parathyroids indicated if renal impairment
aminoglycoside renal toxicity
10-20% of drug-induced nephrotoxocity and usually reversible; due to high trough levels, not peak levels therefore give once a day to allow same bactericidal effect (peak level) and low trough levels (less toxicity)
amphotericin B renal toxicity
leads to renal insufficiency and distal tubular acidosis after several days from cumulative dosing; find high creatinine; stop medication
atheroembolic renal failure
usually angioplasty patient after several days
presents with eosinophilia, low complement, bluish discoloration of fingers and toes, livedo reticularis
contrast agent renal failure
onset is faster than other toxics (12-24 hours)
rise in creatinine in 3-5 days
BUN/creatinine ratio may be as high as 20:1
diabetics, hypertensives and myeloma patients are predisposed
nephrotoxic drugs
contrast agents
NSAID nephropathy
mechanisms: interstitial nephritis, direct toxic, papillary necrosis, membranous GN, inhibition of vasodilatory prostaglandins

risk factors are elderly, hypertension, diabetes or other renal impairment

diagnose with history of NSAIDs + rise in BUN/creatinine and sterile pyuria
papillary necrosis
risk factors are sickle cell, diabetes, urinary obstruction, chronic pyelonephritis and acutely precipitated by NSAIDs

flank pain, hematuria, pyuria, fever and necrotic cells in urinalysis
most accurate diagnosis is bumpy countours of renal pelvis on CT
prevention of contrast-induced renal failure
most importantly is hydration; then bicarbonate and N-acetyl cysteine have been shown to decrease it
glomerulonephritis general presentation
hematuria with dysmorphic red cells, edema, hypertension, proteinuria <2gm/24h
biopsy is extremely important for specific Rx
glomerulonephritis from vascular causes
glomerulonephritis from glomerular disease
postinfectious GN
IgA nephropathy
diabetes (nodular or diffuse glomerulosclerosis)
Wegener glomerulonephritis presentation
glomerulonephritis associated with rhinitis, sinusitis, nasal ulcers, cough and hemoptysis
it's systemic and also affects skin, joints, eyes
nonspecific: ↑ESR, anemia, leukocytosis

best initial test: c-ANCA (anti-proteinase-3)
most accurate: biopsy of kidney or lung looking for granulomas

treat with cyclophosphamide + steroids
Churg-Strauss glomerulonephritis
glomerulonephritis with respiratory symptoms similar to Wegener
eosinophilia and adult-onset asthma are characteristic
best initial tests are ↑eosinophils and p-ANCA (antimyeloperoxidase)
definitive is lung biopsy showing granulomas
treat with cyclo + steroids
Goodpasture syndrome
glomerulonephritis + hemoptysis, cough and shortness of breath
no other organs are affected
best intial test: anti-basement membrane Abs to type IV colagen
confirm with biopsy showing hemosiderin-ladden macrophages (in lungs) and linear Ig deposits (kidneys)
treat with plasmapheresis and steroids
polyartheritis nodosa
involves every organ except lungs
kidney involvement presents as GN and renal insufficiency
there are systemic nonspecific signs
abdominal and joint pain are prominent
best initial tet is p-ANCA (present only in minority)
biopsy is confirmatory (usually sural nerve)
treat with cyclo + steroids
Henoch-Schonlein purpura
palpable purpura, arthralgias, abdominal pain and GN/renal insufficiency due to systemic IgA deposition

biopsy is confirmatory but not performed in majority of patients because it's self-limited

treatment is supportive, steroids if severe
IgA nephropathy (Berger)
most common glomerulopathy worldwide
IgA deposition that affects only kidney causing GN
presents as hematuria 1-2 days following viral illness or pharyngeal infection
40-50% progress to end-stage renal disease
initial test --> IgA (↑ in 50%)
confirm with kidney biopsy showing IgA deposits
no proven effective therapy
postinfectious glomerulpnephritis
due to any organism but mostly from throat or skin infection with group A strep
hematuria, red cell casts, proteinuria, edema, hypertension
initial test: ASO and anti-hyaluronic acid test
biopsy --> humps on electron micro and granular IgG/C3 deposits on IF
treat hypertension and proteinuria with ACEi or ARBs and penicillin for infection
thrombotic thrombocytopenic purpura
pentad for clinical diagnosis
hemolytic anemia, uremia, thrombocytopenia, fever, neurologic findings
intravascular hemolysis with schistocytes and fragmented RBCs, ↑LDH, ↑reticulocytes, ↓haptoglobin

mild disease resolves, if severe --> plasmapheresis
don't transfuse platelets or give antibiotics
hemolytic uremic syndrome
E. coli 0157:H7
triad for clinical diagnosis --> hemolytic anemia, uremia, thrombocytopenia
intravascular hemolysis with schistocytes and fragmented RBCs, ↑LDH, ↑reticulocytes, ↓haptoglobin
mild disease resolves, if severe --> plasmapheresis
don't transfuse platelets or give antibiotics
renal diasease associated with hep B or C, joint pain, neuropathy and purpura; no GI involvement (different from HSP); ↑ESR, ↓complement and confirmation with cryoglobulins; treat underlying hepatitis with interferon and ribavirin; if severe --> pulse steroids and plasmapheresis
diabetic nephropathy
directly proportional to duration of diabetes
nodular (Kimmelstein-Wilson) or diffuse glomerulosclerosis
screen for microalbuminuria and creatinine level
treat with ACEi or ARB
lupus nephritis
asymptomatic proteinuria or hematuria or severe renal disease requiring dialysis
initial test is dsDNA
confirm and determine treatment with kidney biopsy
if sclerosis --> no therapy needed
if proliferative --> steroids with mycophenolate
Alport syndrome
glomerular disease + congenital eye problems and sensorineural hearing loss
rapidly progressive glomerulonephritis
can be due to other glomerular diseases or idiopathic in which there's crescent formation
amyloidosis etiology
AL type is from Ig light chains in multiple myeloma
AA is from rheumatoid arthritis, IBD, myeloma
amyloidosis presentation
restrictive cardiomyopathy, arrhythmias, heart blocks
carpal tunnel syndrome
amyloidosis diagnosis
biopsy of involved organ such as kidney shows green birefringence in Congo red stain
amyloidosis treatment
control underlying disease; melphalan and prednisone can control protein production
nephrotic syndrome etiology
primary: membranous GN, Nil, membranoproliferative, focal-segmental GN
1/3 associated with diabetes, hypertension or myeloma
any glomerulonephritis can convert to nephrotic syndrome if severe enough
nephrotic syndrome presentation
proteinuria >3.5g/24h, edema, hyperlipidemia, hypoalbuminemia
can have hyperlipiduria (maltese cross) and hypercoagulable states (arterial or venous thrombosis from loss of antithrombin, proteins C and S)
nephrotic syndrome diagnosis
initial test is proteinuria >3.5g/24h or albumin/creatinine ratio >3.5 on urinalysis
renal biopsy is most accurate
nephrotic syndrome management
treat underlying disease
if primary --> steroids
if unresponsive --> cyclo or mycophenolate
ACEIs for all with proteinuria
membranous glomerulonephritis
most common nephrotic syndrome in adults
associated with lymphoma, breast cancer, endocarditis, chronic hepatitis, lupus
treat with steroids
Nil lesion
minimal change disease most common in children, 15% adults
electron micro shows fusion of foot processes
responds to steroids
membranoproliferative glomerulonephritis
nephrotic syndrome associated with chronic hepatitis and hypocomplement
immunofluorescensce detects mesangial IgM deposits
steroid-resistant, dipyridamole and aspirin are useful
focal segmental glomerulonephritis
nephrotic syndrome associated with heroin use and HIV; limited response to steroids; ESRD over 5-10 years
things to check for in urinalysis
proteinuria, hematuria, nitrites, bacteriuria, casts
urine dipstick detects only albumin not Ig light chains
found in glomerular or tubular disease, glomerulonephritis, diabetes, fever, CHF, severe exercise, orthostatic
microalbuminuria is 30-300g/24h in diabetic nephropathy
found in diseases of bladder or kidney; stones, cancer, bleeding disorders, trauma, cyclo, glomerulonephritis, cystitis, prostatitis
gram negative bacteria reduce nitrate to nitrite and is marker for infection
if isolated, has limited significance unless pregnant since they can develop pyelonephritis; >100,000 colonies indicates urinary infection
hyaline casts
dehydration; not necessarily disease
red cell casts
broad, waxy casts
chronic renal failure
granular/muddy casts
acute tubular necrosis
white cells in urinalysis
pyelonephritis, interstitial nephritis
indications for dyalisis
life-threatening abnormalities such as refractory fluid overload, acidosis, pericarditis, encephalopathy, other neuropathies, hyperkalemia, uremia (nausea, vomitting, bleeding diathesis)
end-stage renal disease etiology
diabetic nephropathy
glomerulonephritis (15%)
cystic disease (5%)
interstitial nephritis (5%)
requires dialysis
anemia as ESRD complication
normo normo anemia from decreased production of erythropoietin; replace EPO
hypocalcemia as ESRD complication
from decreased production of 1,25 dihydroxy vitamin D (1-hydroxylase); vitamin D replacement
hyperphosphatemia as ESRD complication
from decreased ability to excrete
treat with calcium carbonate or calcium acetate
cinacalcet in refractory cases
aluminum-containing binders should not be used due to dementia and bone abnormalities risk
osteodystrophy as ESRD complication
osteitis fibrosa cystica
bone cysts due to ↓vitamin D --> secondary hyperparathyroidism
manage by improving calcium and treating hyperPTH
hypertension and atherosclerosis as ESRD complication
acceleratd atherosclerosis not known why
most common COD for dialysis patients
hypertension goal is 130/80
infection as ESRD complication
second most common COD
white cells don't function well under uremia
staph is most common due to catheters
bleeding as ESRD complication
uremia-induced platelet dysfunction increases bleeding time
treated with desmopressin to increase vWB and factor VIII
minor signs present in ESRD
decreased libido
glucose intolerance
not indications for dialysis
dietary treatment in ESRD
restricted Na, K, protein, magnesium, phosphate
renal transplant
live related donor 95%/1 year, 72%/5years
cadaver donor 88%/1 year, 58%/5 years
dialysis alone 30-40%/5 years
average wait for transplant is 2-4 years
graft rejection prevention with cyclosporine, tacrolimus, mycophenolate
renal tubular acidosis type I etiology
problem in distal tubules
usually sporadic or secondary to autoimmune disease, ampB, lithium, NSAIDs, nephrocalcinosis, sickle cell, familial, chronic hepatitis
renal tubular acidosis type I presentation
inability to develop ↑[H+] in urine
urine pH >5.4
secondary hyperaldosteronism
renal tubular acidosis type I diagnosis
Acid load test: give amonium chloride which should lower urine pH, with disease urine pH remains high; serum bicarbonate ~10; hypokalemia
differentiate RTA from diarrhea acidos
urine anion gap = (Na + K) - Cl
both have normal serum anion gap metabolic acidosis but diarrhea has negative urine anion gap (↑ urine Cl-) and RTA type I cannot excrete H+ so Cl- will be low and urine anion gap is positive
renal tubular acidosis type I treatment
oral bicarbonate because proximal tubule reabsoprtion is intact and potassium replacement
renal tubular acidosis type II etiology
inability to absorb bicarbonate in proximal tubules
Fanconi, Wilson, amyloidosis, myeloma, acetazolamide, vitD deficiency, secondary hyperPTH, chronic hypocalcemia
renal tubular acidosis type II presentation
initial urine pH is basic but then becomes <5.4
serum bicarbonate 18-20
malabsorption of glucose, amino acids, urate, phosphate
renal tubular acidosis type II diagnosis
sodium bicarbonate IV is not reabsorbed; basic urine in presence of acidemia; bicarbonate in urine
renal tubular acidosis type II treatment
potassium, thiazides and large amounts of HCO3
difference between type I and type II RTA
type I is inability to excrete H+ and has nephrolithiasis
type II inability to reabsorb HCO3 and has osteomalacia/rickets
renal tubular acidosis type IV etiology
aldosterone deficiency or adrenal insensitivity to angiotensin II
diabetes (50%)
sickle cell
renal failure
renal tubular acidosis type IV presentation
asymptomatic hyperkalemia
mild to moderate renal failure
hyperchloremic (nonanion gap) metabolic acidosis
renal tubular acidosis type IV diagnosis
high urine sodium with oral salt restriction is diagnostic
renal tubular acidosis type IV treatment
fludrocortisone has mineralocorticoid effect
types of kidney stones
calcium oxalate (70%)
calcium phosphate (10%)
Mg/aluminum/phosphate (struvite)
uric acid
causes of hypercalciuria
increased absorption: vitamin D intoxication, ↑vitamin D from sarcoidosis or granulomatous diseases; familial, idiopathic; resorptive: hyperPTH, multiple myeloma
causes of hyperoxaluria
primary familial, enteric; fat malabsorption binds calcium and leaves oxalate to be reabsorbed
causes of uric acid stones
acid tubules and high uric acid from gout, hematologic malignancies, Crohn
radiolucent on x-rays
causes of struvite stones
infections with urease-producing proteus, pseudomonas, klebsiella; highly alkaline urine
nephrolithiasis presentation
constant flank pain, hematuria, pain radiating to groin
stones < 5mm should pass spontaneously
nephrolithiasis diagnosis
plain x-ray is rarely used
ultrasound, spiral CT
strain the urine
check serum and urine calcium
never do intravenous pyelogram
nephrolithiasis treatment
analgesia, hydration, bed rest
shockwave lithotripsy for stones <2cm but fragments may obstruct
percutaneous removal (anesthesia and hospital stay)
adult polycystic kidney disease presentation
flank pain, hematuria, palpable mass, UTIs, calculi
hepatic cysts (40%)
colonic diverticula
intracraneal aneurysm
mitral valve prolapse
adult polycystic kidney disease diagnosis and treatment
ultrasound and CT; treatment is nonspecific with management of hypertension, UTIs and calculi
simple cysts
cysts with irregular walls or debris should be aspirated to exclude malignancy
dialysis can cause cysts
serum osmolality formula
(2 x sodiun) + (BUN / 2.8) + (glucose / 18); if glucose and BUN are normal then ~ 2 x Na + 10
hyponatremia specific etiologies
pseudohyponatremia, hypervolemic state, hypovolemic state, euvolemic states, SIADH
hypovolemic hyponatremia causes
dehydration (with free water replacement)
sweating (with free water replacement)
renal salt waste
cerebral sodium waste
hypervolemic hyponatremia causes
CHF, nephrotic syndrome, cirrhosis, renal insufficiency
hyponatremia general presentation
Na < 135mEq; symptoms depend on how fast it drops
neurologic in nature
forgetfulness --> disorientation --> obtundation --> seizure --> coma
hyponatremia management
if asymptomatic --> fluid restriction
mild symptoms --> normal saline + furosemide
seizure or coma --> 3% hypertonic saline
avoid central pontine myelinolysis by correcting Na at 0.5-1mEq/hour or 2mEq if seizure or coma
total Na is normal, serum Na is low
for every 100mg/dL of hyperglycemia there's 1.6mEq/L decrease in Na
hyperlipidemia causes Na lab artifact
euvolemic hyponatremia
psychogenic polydipsisa, hypothyroidism, diuretics, ACEIs, endurance exercise, SIADH
SIADH etiology
small cell lung CA, pancreas CA, ectopic ADH secretion
TB, lung abscess
head injury, CVA, encephalitis
chlorpropamide, clofibrate, vincristine, vinblastine, cyclophosphamide, carbamazepine
SIADH presentation
water retention
ECF expansion without edema or hypertension (natriuresis)
concentrated urine
signs of cerebral edema when hyponatremia is severe (irritability, confusion, seizures, coma)
SIADH diagnosis
hyponatremia <130mEq/L
urine sodium > 20mEq/L
maintained hypervolemia
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
insensible water losses and hypernatremia
↑skin loss (sweating, burns, fever, exercise), respiratory infections
gastrointestinal water losses and hypernatremia
osmotic diarrhea from gluten or lactose intolerance, some infectious diarrhea
transcellular water shift and hypernatremia
rhabdomyolysis or seizures cause muscle to take up lots of water
renal disease and hypernatremia
diabetes insipidus or osmotic diuresis (diabetic KA, nonketotic hyperosmolar coma, mannitol, diuretics
central diabetes insipidus etiology
neoplastic/infiltrative lessions in hypothalamus or pituitary adenomas, craniopharyngiomas, leukemia, sarcoid histocytosis

surgery, radiotherapy, trauma, anoxia, hypertension, meningitis, encephalitis, TB, syphillis

could also be idiopathic
nephrogenic diabetes insipidus etiology
idiopathic or secondary to
sickle cell
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
hypokalemia from GI losses
vomitting, diarrhea, tube drainage
hypokalemia from transcellular shift
alkalosis, ↑insulin, B12 replacement, ↑beta-adrenergeic activity (trauma)
hypokalemia from urinary losses
diuretics, ↑aldosterone states (Conn, licorice, Barter, Cushing, renal artery stenosis), ↓magnesium, type I and II RTA
hypokalemia presentation
muscular weakness to paralysis; arrhythmias; rhabdomyolisis
hypokalemia diagnosis
normal levels is 3.7-5.2mEq/L; in emergencies do EKG looking for T-wave flattening and U-waves
hypokalemia treatment
treat underlying cause
give 4-5mEq/Kg/point; IV max 10-20mEq/h
don't use dextrose containning fluids
complication is fatal arrhythmia
hyperkalemia from transcellular shift
pseudohyperkalemia (secondary hemolysis, mechanical trauma from venipuncture, platelets >1,000,000, WBCs >100,000)
insulin deficiency
tissue breakdown (rhabdomyolisis, tumor lysis, seizures)
hyperkalemia in acidosis
for every 0.1 in pH potassium increases 0.7 points
hyperkalemia from renal causes
renal failure, hypoaldosteronism (ACEIs, type IV RTA, adrenal enzyme deficiency, heparin), Addison, amiloride, spironolactone
hyperkalemia presentation
muscular weakness when K > 6.5
abnormal cardiac conduction
hyperkalemia diagnosis
normal levels 3.7-5.2mEq/L; ECG: peaked T waves, wide QRS, short QT or prolonged PR
hyperkalemia management
if ECG abnormalities -->
calcium chloride (membrane stabilizer)
sodium bicarbonate (alkalosis, not in same IV line as calcium)
glucose/insulin (30-60 minutes to work)
cation exchange resin (absorbs 1mEq og K/gram)
anion gap formula
(Na + K) - (HCO + Cl); normal = 8-14
low anion gap metabolic acidosis
myeloma (myeloma proteins are cations, HCO and Cl go up)
↓albumin (for every 1 point, 2 point decrease in anion gap)
lithium (decreases Na level) "MAL"
normal anion gap metabolic acidosis
diarrhea, renal tubular acidosis, uretero sigmoidoscopy "DiREct (ureter sigmo)"
increased anion gap metabolic acidosis
diabetic ketoacidosis
propylene glycol
ethylene glycol
respiratory acidosis
hypoventilation of any cause
sleep apnea
metabolic alkalosis from H+ loss
GI loss (vomitting, nasgastric suction)
renal loss (Conn, Cushing, ↑ACTH, licorice)
↓Cl intake, diuretics
metabolic alkalosis from HCO3 retention
bicarbonate administration, contraction alkalosis, milk-alkali syndrome
metabolic alkalosis from transcellular shift
respiratory alkalosis
hyperventilation of any cause
pulmonary embolus
gram+ catalase+ cocci
coagulase+: stah aureus
caogulase-: staph epidirmidis (novobiocin sens), staph saprophyticus (novobiocin res)
gram+ catalase- cocci
alpha hemolytic -->
pneumococcus (optochin sens)
viridans (optochin res)

beta hemolytic -->
group A strep pyogenes (bacitracin sens)
group B stret agalactiae (bacitracin res)
gram+ rods
bacillus, clostridium, corynebacterium, listeria
gram- cocci
meningococcus (maltose fementer), neisseria gonorrheae (maltose non fermenter)
gram- cocobacillus
gram- rods
lactose fermenters --> e. coli, klebsiella
lactose nonfermenter oxidase- --> salmonella, shigella, proteus
lactose nonfermenter oxidase+ --> campylobacter, pseudomonas, vibrio, H. pylori
DNA viruses
HHAPPPPy: herpes, hepadna, adeno, parvo, papilloma polyoma, pox
RNA+ viruses
Calici (Norwalk), PEeCoRnA, Flavi (hepC, dengue, yellow fever, WNV), Toga (rubella), Corona, Retro. "Call Pico and Flava To Come Rap"
RNA- viruses
PaRaMyxo, Rhabdo, Arena, Filo, Orthomyxo (influenza), Bunya, Delta
"Para Rabiar in the Arena, Fill OR Buny"
Togavirus, flavivirus, bunyavirus
meningitis etiology
bacterial: pneumococcus (adults), mningococcus (children/adolescents), agalactiae (neonates)
listeria is more common in immunosupressed
staph aureus (neurosurgery)
cryptococcus (HIV)
RMSP (geographic)
Lyme (borrelia, geographic)
TB, syphilis
viral: coxackie, HIV, herpes simplex
meningitis presentation
photophobia, headache, nuchal rigidity
fever, nausea, vomitting
altered mental status, seizures, neurological deficits (specially CN VIII)

petechial rash (meningococcus)
writs/ankle centripetal rash (RMSF)
facial nerve palsy (Lyme)
abnormal chest x-ray (TB)
meningitis diagnosis
lumbar puncture is initial procedure
if papilledema, focal motor deficits, seizures, mental status changes, or HIV --> do CT of head first

CSF analysis:
↑WBCs (neutrophils) --> bacterial;
↑WBCs (lymphocytes) --> viral, ricketsia, Lyme, TB, syphilis;
↑proteins (mostly in bacterial, but any)
↓glucose (mostly bacterial)

Lyme and RMSF have specific serology
cryptococcus detect with India ink test and serum/CSF cryptococcal antigen
syphilis with VDRL or FTA-ABS
TB with culture or PCR
meningitis treatment
empirical: vancomycin + ceftriaxone +- ampicillin (HIV, steroids, pregnancy or malignancies)

listeria is resistant to all cephalosporins
vancomycin if resistant pneumococcus
Lyme --> ceftriaxone
cryptococcus --> amphotericin + fluconazole
neurosyphilis --> high-dose penicillin

dexamethasone as adjuvant in bacterial meningitis
encephalitis etiology
most commonly by HSV-1
also by VZV, CMV, coxackie and encephalitis viruses
HSV-1 has predilection for temporal lobes
encephalitis presentation
altered mental status with fever and headache are main clues; can also have stiff neck
encephalitis diagnosis and treatment
due lumbar puncture first
PCR of CSF is sensitive and specific for HSV-1
CT or MRI to exclude other diseases and may see temporal lobe involvement
IV acyclovir or gancyclovir/foscarnet for CMV
brain abscess etiology
organisms spread to brain from
otitis media, sinusitis, mastoiditis, dental infections, endocarditis, pneumonia, HIV

most common -->
strep pneumonia (60-70%)
bacteroides (20-40%)
enterobacteriacea (25-35%)
staph (10%)
toxoplasmosis in AIDS
can often by polymicrobial
brain abscess presentation
headache is most common symptom
focal neurologic deficits (60%)
brain abscess diagnosis
initial test is contrast CT
MRI is more accurrate
precise etiology is with examination of abscess fluid
90% of HIV brain abscess is from toxoplasma or lymphoma and diagnosis is made if it responds to 10-14 days with pyrimethadine or sulfadiazine
brain abscess treatment
stereotactic aspiration (preferred) or surgical excision

antibiotics are also given in combination depending on etiology
if toxoplasmosis --> pyrimethadine and sulfadiazine
else give combo; example: penicillin for strep, metronidazole for anaerobes and third-gen ceph for gram-
otitis media etiology
preceeded by viral upper respiratory infection with edema of eustachian tube
strep pneumo (35-40%)
H. influenzae (25-30%)
moraxella (15-20%)
rest is viral etiology
same breakdown as sinusitis and bronchitis
otitis media presentation
ear pain
decreased hearing
red bulging tympanic membrane on physical
otitis media diagnosis
physical exam of ear
otitis media treatment
amoxicillin is DOC
can also use second-gen ceph
penicillin allergies --> azi/clarithromycin
quinolones have broader spectrum than required
sinusitis etiology
strep pneumo (35-40%)
H. influenzae (25-30%)
moraxella (15-20%)
rest is viral etiology
same breakdown as otitis media and bronchitis
sinusitis presentation
facial pain, headache, postnasal, purulent drainage; fever in 50%
sinusitis diagnosis
clinical diagnosis
routine imaging is not recommended
if in doubt or no response to treatment --> CT
sinus puncture may be necessary
sinusitis treatment
if mild or uncomplicated --> oral pseudoephedrine, oxymetazoline
if severe --> amoxicillin is DOC
can also use second-gen ceph
penicillin allergies --> azi/clarithromycin
viral sinusitis resolves within 10 days with symptomatic treatment (antihistamines, NSAIDs, decongestants)
pharyngitis etiology
majority are viral
S. pyogenes is only 15-20% but is most important due to complications
pharyngitis presentation
sore throat
cervical adenopathy
pharynx inflammation and exudate are suggestive of S. pyogenes (or EBV)
horaseness and cough are not suggestive of pharyngitis
pharyngitis diagnosis
rapid strep antigen test are unsensitive but specific and diagnostic but absence doesn't exclude
pharyngitis treatment
penicillin; macrolides if allergic
influenza A or B virus leads to coryza, nonproductive cough, sore throat, conjunctival injection and systemic symptoms as fever, myalgia, headache and fatigue

diagnosis confirmation is with rapid antigen detection

treat symptoms with acetaminophen and antitussives
specific treatment is oseltamivir and zanamivir
vaccination is recommended in older than 50, lung or cardiac diasease, immunosupressed, diabetics
bronchitis etiology
vast majority are caused by viruses
then strep pneumo, nontypable Haemophilus, moraxella, mycoplasma
cigarette smoke is predisposing factor
bronchitis presentation and diagnosis
cough and sputum production with normal x-ray confirms diagnosis
lungs are clear to auscultation
fever may occur
bacterial etiology is suggested by discolored sputum
bronchitis treatment
mild cases require no treatment
acute exacerbations of chronic bronchitis are treated with amoxicillin, doxycycline or TMP-SMX
repeated infections: amoxicillin/clavulanate, clarithromycin, azithromycin, 2nd or 3rd-gen cephs or quinolones
lung abscess etiology
90% have oral anaerobes peptostrep, prevotella and fusobacterium
45% only anaerobic, 45% mixed, 10% aerobes
aerobics found are staph, e. coli, klebsiella, pseudomonas
associated oral periodontal disease or predisposition to aspiration
lung abscess presentation
fever, cough, sputum, chest pain, putrid odor, chronic course with weight loss, anemia, fatigue
lung abscess diagnosis
sputum Gram stain will not show anaerobes
chest x-ray may show cavitary lesion most commonly in lower lobes or posterior segmenet of right upper lobe
aspiration and analysis of abscess fluid confirms
lung abscess treatment
empiric drug is clindamycin; drainage is not required
pneumonia etiology
in children <5 viruses are most common
older than 5, pneumococcus is leading cause
typical agents (40-60%) S. pneumoniae, Haemophilus, moraxella
atypicals: legionella, mycoplasma, chlamydia
pneumonia predisposing factors
cigarette smoking, diabetes, alcoholism, malnutrition, obstruction from tumors, immunosupression
pneumonia associations: haemophilus
smokers and COPD patients
pneumonia associations: mycoplasma
atypical presentation in young otherwise healthy patients
pneumonia associations: legionella
epidemic; older smokers
associated with infected water sources and air conditioning systems
pneumonia associations: pneumocystis jiroveci
HIV+ <200 CD4
pneumonia associations: coxiella
Q fever; exposure to animals specially specially when they are giving birth
pneumonia associations: klebsiella
pneumonia associations: staph aureus
following viruses or viral bronchitis, specially influenza
pneumonia associations: coccidioidomycosis
southwestern deserts
pneumonia associations: chlamydia psittaci
pneumonia associations: histoplasma
bird droppings and spelunking
pneumonia associations: bordetella
cough with inspiratory whoop and post-tusive vomitting
pneumonia associations: francisella
hunters or exposure to rabbits
pneumonia associations: SARS/avian flu
travel to south east asia
pneumonia associations: anthrax, yersinia, francisella
pneumonia presentation
cough, fever, sputum production, pleuritic chest pain, tachypnea
viral and atypicals produce a non-productive dry cough

on physical: rales, ronchi, dullness to percusion, bronchial breath sounds, increased fremitus, egophony

bacterial sputum is purulent and can be mixed with blood (rusty, pneumococcus) or blood and mucous (currant-jelly, klebsiella)
pneumonia diagnosis
chest x-ray is first --> localized or diffuse infiltrates and alveolar or interstitial pattern
next --> sputum Gram stain and culture (most specific for lobar pneumonia)
atypicals don't show in Gram stain or culture

mycoplasma --> cold agglutinins
legionella --> antigen tests and charcoal yeast culture
pneumocystis --> increased LDH in bronchoalveolar lavage
chlamydia pneumonia, coxiella, coccidiodes all have specific antibody titers
pneumonia major severity signs
hypoxia (PO2<60mmHg)
O2 saturation <94%
respiratory rate >30/min
confusion, uremia, hypotension
pneumonia minor severity signs
high fever
pulse >125/min
dehydration determined by high BUN
empiric treatment for pneumonia outpatients
azithromycin or clarithromycin are DOC
alternative are levofloxacin, moxifloxacin, gatifloxacin
empiric treatment for pneumonia inpatients
new quinolones OR 2nd/3rd gen ceph with macrolide or doxyclycline
empiric treatment for hospital-acquired pneumonia
3rd gen ceph with antipseudomonal activity OR imipenem OR piperacillin/tazobactam
should also cover MRSA with vancomycin or linezolid
haemophilus pneumonia specific treatment
2nd or 3rd gen ceph
mycoplasma pneumonia specific treatment
macrolides, doxycycline or new quinolone
legionella pneumonia specific treatment
macrolides, doxycyline or new quinolone
pneumocystis pneumonia specific treatment
add steroids if PO2<70mmHg or A-a >35mmHg
if allergic to sulfa use IV pentamidine or atovoquone
prophylaxis with dapsone or atovoquone
coxiella pneumonia specific treatment
staph pneumonia specific therapy
oxacillin, nafcillin, etc… if MRSA --> vacomycin or linezolid
coccidioides pneumonia specific therapy
only need treatment if diseminated disease
mild diseasse --> fluconazole or itraconazole
severe disease --> ampB
pneumococcal vaccine indications
older than 65
serious lung, cardiac, liver or renal disease
steroid patients
splenectomized patients
leukemia/lymphoma patients
tuberculosis etiology
25% of world population is exposed; higher risk of exposure in alcoholics, healthcare workers, prisoners, homeless shelters, nursing homes, HIV, steroids, organ transplant, leukemia, lymphoma
tuberculosis presenation
cough, sputum, fever, weight loss, night sweats and abnormal lung exam
may also involve any organ specially lymph nodes, meninges, GI and GU
tuberculosis diagnosis
chest x-ray is best initial test in symptomatic patients, PPD in asymptomatic
x-ray shows apical infiltrates and sometimes cavitations, adenopathy and calcifications (Ghon complex)

acid-fast stain of sputum (3 smears >90% sensitive)
culture is specific and needed for bug sensitivity testing

if acid-fast is unrevealing can do thoracentesis, gastric aspirate in children, biopsy or needle aspiration of organ involved or lumbar puncture in meningitis

pleural biopsy is most sensitive
look for casseating granulomas
tuberculosis treatment
empiric treatment is combo of INH/pyridoxine, rifampin, pyrazinamide, ethambutol for first 2 months or until sensitivty testing; then INH + rifampin for another 4 months

if sensitivity is not known give also ethambutol
TB meningitis add steroids + 12 months
TB in pregnancy 9 months
tuberculosis drugs side effects
all cause liver toxicty except streptomycin
INH --> peripheral neuropathy (give pyridoxine)
ethambutol --> optic neuritis
rifampin --> red/orange metabolites
pyrazinemide --> benign hyperuricemia
PPD test generalities
used to screen asymptomatic populations at risk of TB to see if they have been exposed; consits of intradermal injection of the PPD with induration of the skin 48-72 hours after

if test is <10mm, do a second test to rule out false negative
if positive do chest x-ray and acid-fast stain

positive PPD with no evidence of active disease receive prophylaxis with INH+pyridoxine for 9 months
PPD test > 5mm induration
considered positive if
close contacts of active TB cases
abnormal chest x-ray
steroids or organ transplant
PPD test > 10mm induration
considered positive if
children < 4
leukemia or lymphoma
injection drug users
healthcare worker
immigrants (recent)
nursing home residents

CLIP HINDuration
PPD test > 15mm induration
considered positive for people with no risk factors for TB
food poisoning/infectious diarrhea etiology
campylobacter is most common
salmonella (raw eggs and poultry)
e. coli (traveler's diarrhea, undercooked hamburger meat)
B. cereus (reheated fried rice)
giardia, cryptosporidia (contaminated water)
V. parahemolyticus (contaminated shellfish)
V. fulnificus (raw shellfish)
rotavirus, Norwalk agent (children)
C. difficile (antibiotics)
C. botulinum (canned food)
C. perfringes (unrefrigerated meats)
food poisoning/infectious diarrhea presentation
most importantly is presence of blood and specific symptoms
bloody diarrhea --> salmonella, shigela, yersinia, invasive e. coli, campylobacter
watery diarrhea --> protozoans except entamoeba, clostridium, vibrio, viruses, B. cereus, staph
predominantly nausea/vomitting --> B. cereus, staph
food poisoning/infectious diarrhea diagnosis
if there's no blood in stool then check for leukocytes in stools with methylene blue test
then do culture for specific etiology
for protozoans direct stool examination for parasites or ova
food poisoning/infectious diarrhea treatment
empiric antibiotics until stool culture and if there's abdominal pain, bloody stools and fever or hypotension; high-volume stools and dehydration don't justify antibiotics

empirical treatment is ciprofloxacin or fluoroquinolone+metronidazole

scombroid is treated with antihistamines
giardia with metronidazole
isospora with TMP/SMX
doxycycline for vibrio
acute viral hepatitis presentation
jaundice, dark urine, light-colored stools, fatigue, malaise, weight loss, tender liver, hepatomegaly
indistiguishable from drug-induced hepatitis; hep b and C can also have serum sickness, arthritis, rash; PAN is associated with hep B
acute viral hepatitis diagnosis
all hepatitis gives ↑total and ↑direct bilirubin
ALT > AST in viral
AST>ALT in drug-induced
alkaline phosphatase and GGTP may not be elevated unless canalicular damage
viral hepatitis serology
IgM indicates acute infection with A, C, D or E viruses
IgG antibody to A, C, D or E indicates old, resolved disease
hep C activity is followed with PCR viral load

hep B acute diagnosis: ↑HbsAg, ↑IgM-HbcAb and HbeAg (infectivity)
resolution is indicated by ↓HbsAg, ↑HbsAb, ↑HbcAb-IgG (only marker in window-period), ↑HbeAb-IgG
acute viral hepatitis treatment
ne effective treatment for acute viral hepatitis
chronic hep B --> either interferon, entecavir, adefovir, lamiduvine
chronic hep C --> combo of interferon and ribavirin
treatment for cirrhosis is transplant
after needlestick with hep B and if no adequate levels from vaccine --> HBIg + hep B vaccine;
no post-exposure prophylaxis for hep C
by gonococcus or chlamydia, ureaplasma, mycoplasma, trichomona or HSV
purulent urethral disharge, dysuria, urgency, frequency

diagnose with gram stain showing coffee bean-shaped diplococci or fluorescent antibodies for chlamydia (on urethral swab or urine)

treat with single-dose ceftriaxone IM and single-dose azithromycin orally
pelvic inflammatory disease
gonococcus, chlamydia, mycoplasma, enterobacteria
lower abdominal pain on palpation of cervix, uterus or adnexa
cervical motion tenderness is key
fever, leukocytosis and discharge also

do gram stain of discharge and culture on Thayer-Martin
do pregnancy test
diagnosis is clinical; laparoscopy is definitive
may do culdocentesis or sonography

treat with doxycycline and cefoxitin (inpatient) or single-dose ceftriaxone and doxycyline for two weeks for outpatient
syphilis presentation
primary --> chancre (1-3 weeks) and regional nontender lymphadenopathy

secondary --> cutaneous rashes (6-12 weeks) on flexor areas, lympahdenopathy and condylomata lata (papules at mucocutaneous junctions)

latent stage --> may persist for life

tertiary --> 1/3 of patients, gummas lead to tabes dorsalis and Argyll-Robertson pupil
syphilis diagnosis
screening: VDRL, RPR
specific: FTA-ABS, MHA-TP, darkfield exam
false positive VDRL in EBV, collagen vascular disease, TB, subacute bacterial endocarditis
syphilis treatment
2.4 million units if IM benzathine penicilline given once for primary and secondary and once a week 2 weeks for latent (VDRL >1:8 without symptoms); tertiary is treated with 10-20 million units/day IV for 10 days; if allergic give doxycycline but desensitize for tertiary and pregnancy
caused by Haemophilus ducreyi
small, soft, painful papules that coalesce and become ulcers with ragged edges
tender and enlarged inguinal nodes
diagnosis is clinical
Gram stain and culture to confirm
treat with single-dose azithromycin or ceftriaxone OR erythromycin for 7 days OR cipro for 3 days
lymphogranuloma venereum presentation
small, transient, nonindurated lesion that ulcerates and heals quickly producing unilateral inguinal node enlargement, multiple drainning sinuses that persist or recur; also fever, malaise, joint pains, headaches
lymphogranuloma venereum diagnosis and treatment
clinical diagnosis
high or rising titer of complement fixing antibodies
isolate chlamydia trachomatis from pus in buboes
treat with doxycycline
granuloma inguinale
painless red nodule that turns into elevated granulomatous mass by donovantia granulomatis
looks like conylomata lata or carcinoma
diagnose with Giemsa or Wright stain, punch biopsy
treat with doxycyline or ceftriaxone
gential herpes
vesicles on genital area or mucous membranes that become eroded ulcers with red areola; itching and soreness; can have inguinal lymphadenopathy; diagnose with Tzanck test and culture; treat with acyclovir, famcyclovir, valacyclovir or foscarnet; explain relapsing nature
genital warts
papilloma virus causes condylomata acuminata which are warm, moist, pink pedunculated swellings with cauliflower appearance

clinical diagnosis

treatment: destruction (curettage, sclerotherapy, trichloroacetic acid), cryotherapy, podophyllin, imiquimod, laser removal
painless papules and pustules that ulcerate near genital areas
condylomata lata; syphilis
painful small soft papules that become ulcers with ragged edges and coalesce
chancroid; H. ducreyi
painless small transient nonindurated lesion that ulcerates and heals quickly leaving scar
lymphogranuloma venereum; C. trachomatis
painless red nodule develops into elevated granulomatous mass
granuloma inguinale; donovania granulomatis, calymmatobacterium granulomatis
painful vesicles on skin or mucous membranes that become ulcers with red areola
genital herpes; HSV
painless soft moist redish swellings that grow rapidly into pedunculated masses with califlower appearance
genital warts
condylomata acuminata
papilloma virus
painful genital lesions
genital herpes
painless genital lessions
condylomata lata
lymphogranuloma venereum
granuloma inguinale
condylomata acuminata
cystitis etiology
infection of bladder by E. coli, proteus, klebsiella
predisposed by urinary stasis, tumors, stones, strictures, prostatic hypertrophy, neurogenic bladder, sexual intercourse
cystitis presentation
dysuria, frequency, urgency and suprapubic (but not flank) tenderness
may also have hematuria, low fever
cystitis diagnosis and treatment
screening test is urinalysis looking for WBCs, RBCs, protein or bacteria
nitrites indicate gram- bacteria
urine culture with >100,000 colonies per mL of urine is confirmation
treat with 3 days of TMP/SMX or any quinolone (not pregnancy)
7 days for diabetics
acute bacterial pyelonephritis etiology
ascension of E. coli, klebsiella, proteus
predisposed by female sex, obstruction due to strictures, tumors, calculi, prostatic hypertrophy, neurogenic bladder, vesicouretheral reflux, catheter; catherterized immunocompromised patients are predisposed to candida
acute bacterial pyelonephritis presentation
fever, chills
frequeny, dysuria
flank pain, costovertebral angle tenderness
acute bacterial pyelonephritis diagnosis
clinical diagnosis with confirmation by clean-catch urinalysis and culture >100,000 bacteria/mL
if patient does not improve in 3 days or complications are suspected --> ultrasound or CT is indicated
acute bacterial pyelonephritis treatment
10-14 days with fluoroquinolone OR
ampicillin + gentamycin OR
third-gen ceph
if can't tolerate medication --> hospitalization
perinephric abscess etiology
abscess from kidney cortex to surrounding areas due to E. coli, klebsiella, proteus
predisposed by kidney stones (20-60%)
prostatic hypertrophy
neurogenic bladder
perinephric abscess presentation
insidious onset (2-3 weeks) of fever, flank pain, palpable flank mass, abdominal pain, and persistence of symptoms after pyelonephritis treatment
perinephric abscess diagnosis and treatment
urinalysis and culture of urine
then ultrasound and aspiration of abscess for definitive etiology and sensitivity
quinolone, ampicillin/gentamycin, third-gen ceph
drainage is necessary
impetigo etiology
superficial pustular infection with due mainly to staph aureus and group A strep
impetigo presentation
maculopapules that progress to vesicles, pustules and bullae with golden crusts
can lead to lymphangitis, furunculosis or cellulitis
more common on limbs and face, may follow trauma to skin
impetigo diagnosis and treatment
clinical diagnosis
treat with first-gen ceph OR oxacillin, cloxacillin, dicloxacillin
can also use topical mupirocin or bacitracin in mild cases
if allergic use macrolides
superficial cellulitis due to group A strep
tender, demarcated, shiny red, indurated, edematous lesions on limbs or face
treat with semisynthetic penicillin or first-gen ceph if undistinguishable with cellulits, else penicillin for Group A strep
tinea etiology
dermatophytes: microsporum, trichophyton, epidermophyton
tinea presentation
corporis: papulosquamous lesions with riased border in the body; pedis: macerated and scaling borders; unguium: thickened nails; capitis: small scaly semibold graysish patched on head; cruris: ringed lesions on crural folds and inner thighs; barbae: on face
tinea diagnosis and treatment
potassium hydroxide preparation; culture as definitive test; treat with terbinafine or itraconazole orally for capitis, corporis and unguium; topical clotrimazole/ketoconazole for cruris, pedis and mild corporis
candidiasis etiology
candida infection more frequently in:
systemic antibacterial therapy
corticosteroid or antimetabolites
blood dyscrasias
intertriginous candidiasis presentation
intertriginous: well-demarcated, erythematous, itchy, exudative patches rimmed with red small pustules; in groin, gluteal folds (diper rash), axilla, umbillicus, inframmary areas
vulvovaginitis presentation
candidiasis with white or yelloish discharge with inflammation of the vaginal wall and vulva; common in pregnancy and diabetes
oral candidiasis
also known as thrush; white patches of exudates on tongue or bucal mucosa
candidal paronychia
painful red swelling around the nail
candidiasis diagnosis and treatment
potassium chloride on slide, culture is definitive
treat with topical nystatin or azoles
if serious infection or paronychia use amphotericin and fluconazole
tinea versicolor
pityrosporum orbiculare (malassezia furfur) leads to tan/brownish scaling macules that coalesce on neck, face and abdomen; diagnose with KOH showing spaghetti and meatballs; treat with topical selenium sulfide or azoles
due to itch mite or sarcoptes scabiei; pruritus, burrows and papules on skin folds; immunocompromised and Down patients can have malodorous discharge; diagnose by showing parasites in scrapings with mienral oil; treat with permethrin, lindane or ivermectin
due to pediculus humanus capitis, pediculus humanus corporis, phthirus pubis; itching, excoriations, erythematous macules and papules may have secondary bacterial infection; diagnose with direct analysis of hair-bearing surfaces; treat with permethrin, lindane
molluscum contagiosum
small waxy papules with central umbilication due to poxvirus
specially in children and HIV
clinical diagnosis
treat by cryotherapy, curettage, electrocautery
osteomyelitis etiology
most common organism is staph

acute hematogenous: in children occurs mostly in metaphysis of tibia and femur, in adults in the vertebral bodies

secondary to contiguous infection: recent trauma or prosthetic (could be polymicrobial)

vascular insufficiency: diabetics over 50, small bones of lower limb and majority are polymicrobial
osteomyelitis presentation
pain, erythema, swelling and tenderness over affected bone; in vascular insuf. May have ulcer; sometimes also drainning tract
osteomyelitis diagnosis
plain x-ray is usually first test but takes at least 2 weeks to show periosteal elevation
technetium scan and MRI detect it much earlier
a normal ESR strongly excludes osteomyelitis
bone biopsy and culture is best diagnostic test and its needed
osteomyelitis treatment
empiric: semisynthetic penicillin or vancomycin + aminoglycoside or third-gen ceph
then specific treatment
total is 6-12 weeks
adults also need drainage and debridment
septic arthritis etiology
joint infection mostly by gonococcus but also by gram+ (85%, staph 60%)
other gram- (10-15%) or polymicrobial (5%)
main risk factor for gonococcal is sexual activity
nongonococcal is mostly hematogenous spread by bites, direct inoculation by surgery or trauma, RA, OA, prothesis, gout, sickle cell, IV drug use, diabetes, HIV
septic arthritis presentation
gonococcal: polyarticular (50%) swollen, tender, erythematous joint with decreased range of motion also with tenosynovitis, migratory polyarthralgia, and petechiae or purpura

non-gonococcal is mostly monoarticular and doesn't have systemic involvement
septic arthritis management
joint aspiration along with empiric nafcillin combined with aminoglycoside or third-gen ceph
for gonococcal: ceftriaxone
gas gangrene etiology
80% C. perfringens associated with trauma, war and motor vehicle accidents; the wound must be deep, necrotic and without exit to surface
gas gangrene presentation
pain, swelling and edema 1-4 days after incubation
later hypotension, tachycardia, fever, crepitation and renal failure
gas gangrene diagnosis
gram+ rods on stain without white cells, culture and gas bubble on x-ray are suggestive
direct visualization of pale, dead muscle with sweet-smelling discharge is definitive diagnosis
gas gangrene management
24 million units of penicillin/day or clindamycin if allergic + debridment or amputation
hyperbaric oxygen might be of benefit
infective endocarditis predisposing factors
dental procedures
oral and upper respiratory surgery
some GI procedures
GU surgery
prosthetic heart valves
valvular heart disease
catheters to heart
IV drug abuse
top 5 organisms of endocarditis in native valves
strep viridans (50-60%)
staph aureus (20-30%)
other strep (15-20%
enterococci (5-15%)
staph epidermidis (1-3%)
top 3 organisms of endocarditis in narcotic addicts
staph aureus (60-95%), streptococci (10-20%), staph epidermidis (5-10%)
top 3 organisms of endocarditis in prosthetic valves
staph epidermidis (40-50%, 10-20 days later)
staph aureus (15-20%, 40-60 days later)
strep viridans (5-20%, 20-30 days later)
acute endocarditis etiology
bactermia with staph aureus seeds previously healthy valves and produces large vegetations, fever, spesis, splenomegaly
subacute endocarditis etiology
strep viridans is most common
low virulence seeding of abnormal valves with small vegetations made of fibrin, platelets, debris and bacteria
infective endocarditis presentation
fever + new heart murmur + anemia
chills, sweats, weakness, dyspnea, anorexia, cough, embolic events (petechiae, splinter hemorrhages, Janeway lesions), skin manifestation, splenomegaly, FROM JANE
infective endocarditis major diagnostic criteria
positive blood culture and abnormal echo; need both or 1 major/3minor for diagnosis
infective endocarditis minor criteria
cardiac lesion from IV drug use
vascular events (arterial emboli, septic lung infarcts, Janeway)
immunologic events (Osler, Roth, GN, rheumatoid factor)
microbiologic evidence (active infection consistent with endocarditis)
need 3 minor and 1 major or 2 major for diagnosis
infective endocarditis empiric treatment
antistaph (nafcillin) + antistrep (penicillin/ampicillin) + gentamicin
change as soon as specific agent is known by blood culture
infective endocarditis specific treatment for strep viridans
4 weeks penicillin OR if allergic, 4 weeks of ceftriaxone or vancomycin OR 2 weeks of penicillin or ceftriaxone + gentamicin
infective endocarditis specific treatment for native valve/staph aureus
if methicillin sensitive:
4-6 weeks of nafcillin + 5 days gentamicin
OR cefazolin or vancomycin + 5 days of gentamicin if allergic

for methicillin resistant:
4-6 weeks of vancomycin
infective endocarditis specific treatment for enterococcus
4-6 weeks of penicillin/ampicillin + gentamicin OR vacomycin + gentamicin
major criteria for infective endocarditis surgery
progressive or unresponsive CHF
recurrent systemic emboli
persistent bacteremia despite antibiotics
fungal etiology
extravalvular infection
prosthetic valve dehiscence or obstruction
recurrence despite therapy
minor criteria for infective endocarditis surgery
resolved CHF with therapy
single systemic embolic event
large aortic or mitral vegetations on echo
prosthetic valve infection other than penicillin sensitive strep
gram- tricuspid endocarditis
persistent fever
new regurgitation
indications of prophylaxis for infective endocarditis
when there's serious cardiac defect and procedure causing bacteremia; for dental procedures give amoxicillin or clindamycin/macrolide if allergic
cardiac conditions that indicate infective endocarditis prophylaxis
prosthetic heart valves
previous bacterial endocarditis
most congenital cardiac malformations
conditions that don’t require infective endocarditis prophylaxis
surgically corrected systemic pulmonary shunts, rheumatic valve dysfunction, hypertrophy cardiomyopathy, mitral valve prolapse with regurgitation, surgical repaired intracardiac defects
acute pericarditis etiology
any infectious agent
coxsackie and ECHO viruses are most common viruses
vascular --> SLE, RA, scleroderma
1/3 of uremic patients
neoplasia adjacent to heart
mediastinal irradiation
rheumatic fever
injury to heart
acute pericarditis presentation
sharp pleuritic chest pain improved by leaning forward; friction rub heard at apex; low fever
pericardial tamponade presentation
signs and symptoms of perdicarditis plus pulsus paradoxus, distended neck veins, tachycardia, hypotension
acute pericarditis diagnosis
diffuse ST elevation and maybe PR depression
echo normal in viral but used to detect effusion
pericardiocentesis for microbiology
acute pericarditis therapy
treat underlying cause; if viral give indomethacin or ibuprofen or prednisone if no response or if TB; pericardiocentesis for large effusions
myocarditis etiology
any infectious agent but coxackie B is very common
also radiotherapy, drugs, vascular disease, hyperthyroidism
myocarditis presentation
asymptomatic or any presentation
signs of myocardial dysfunction (dyspnea, fatigue) or rapid progression to chest pain and arrhythmia
may have S3 and murmurs
myocarditis diagnosis
any EKG alteration like ST-T wave changes, heart blocks
elevated cardiac enzymes may be found
may have left ventricular systolic dysfunction on echo
viruses may be isolated from body fluids or titers of serum antibodies are found
myocarditis treatment
supportive for viral (resolves spontaneously); steroids can be damaging
Lyme disease presentation
80% develop erythema migrans rash 3-30 days after bite
flulike illness occurs in 50%
neurologic symptoms develop weeks later in 10-20%
(facial paralysis, meningitis, encephalitis or headaches)
heart block, arrhythmia, myocarditis or pericarditis in <10%
migratory polyarthritis develops months to years later in 60%;
Lyme disease diagnosis
diagnostic criteria are presence of rash with at least one late manifestation + ELISA and western blot looking for anti borrelia antibodies (serum studies may not false negative early when rash is still present)
Lyme disease treatment
rash, facial palsy and joint pain with doxycyline
if serious neurologic or cardiac --> IV ceftriaxone
AIDS etiology
decrease in CD4 count by HIV; in US transmitted mostly by men who have sex with men or in heterosexuals; in developing world is transmitted mostly by heterosexuals; takes 5-10 years to drop CD4 from 700 to 200
principal opportunistic infections in AIDS
pneumocystis jirovecii, cytomegalovirus, mycobacterium avium, toxoplasma, cryotococcus
pneumocystis jirovecii pneumonia presentation
pneumonia, dyspnea on exertion, dry cough, fever, chest pain when CD4>200/uL
pneumocystis jirovecii pneumonia diagnosis
bronchoscopy with bronchoalveolar lavage for direct indentification; chest x-ray may be normal or bilateral interstitial infiltrates; elevated serum LDH
pneumocystis jirovecii pneumonia management
TMP-SMX (first-line, may cause rash) OR dapsone/trimethoprim OR primaquine/clindamycin; pentamidine (may cause pancreatitis); steroids if severe pneumonia (PaO2<70mmHg or A-a >35mmHg
pneumocystis jirovecii pneumonia prophylaxis