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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
Tumors:
pituitary adenomas, cysts, hypothalamic tumors (craniopharyngioma, meningioma, glioma);

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

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


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

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

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

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

ACTH deficiency (secondary adrenal insuficiency, hypocortisolism, fever, hypotension, hyponatremia [minimal], decreased response to stress, weightloss)
hypopituitarism diagnosis
measure hormones:
GH --> insulin-induced hypoglycemia ↓ glucose to <40mg/dL which ↑ GH > 10mg/L - if <10mg/L there is deficiency; or arginine infusion;

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

measure LH, FSH, estrogen/testosterone

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

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

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

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

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

infections: TB, lung abscess

CNS: head injury, CVA, encephalitis

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

"inappropriate CCCCCancer VVIBE"

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

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

transient hyperthyroidism due to
subacute thyroiditis (painful)
lymphocytic thyroiditis (painless)
thyrotoxicosis factitia
ectopic thyroid tissue (struma ovarii, functioning follicular CA)
hyperthyroidism presentation
Cardiac:
atrial fibrillation, dyspnea, palpitations, angina, heart failure

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

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

Eye:
Staring, infrequent blinking, lid lag

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

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

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

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

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

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

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

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

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

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

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

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

hypercholesterolemia, expressionless face, sparse hair, periorbital puffiness, macroglosia, hypokinesis, deafness, hyponatremia, anemia, stiffness, muscle cramps, carpal tunnel syndrome, menorrhagia,
hypothyroidism diagnosis
history and PE plus lab confirmation:
↑ TSH (primary) or normal/↓ TSH (secondary)
↓T4 and FT4
↓ T3
also may have hypercholesterolemia
↑ CPK
↑ AST
hyponatremia
↑ LDH

and 12% have PA
hypothyroidism management
gradual metabolic restoration with levothyroxine (monitor TSH/T3); if suspicion of 2dary or 3ary give hydrocortisone first then hormone replacement; if myxedema coma signs (respiratory depression and ↑CO2 retention) use very high doses of T4 and T3
subacute thyroiditis
also called granulomatous or De Quervain; viral etiology
presents with upper respiratory symptoms plus painful enlarged and firm thyroid
lab confirmation is made by ↑ ESR, ↓ RAIU and initial ↑ of T3/T4 then ↓
symptomatic management: aspirin, prednisone, propanolol
differential: Graves (there's ↑ RAIU);

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

thyroid is nontender, firm, symemetrical and slightly enlarged

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

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

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

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

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

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

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

"PaNS OF Calcium"

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

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

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

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

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

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

"WWeePPing CCOMAtoSE"
hyperosmolar nonketotic coma diagnosis
elevated plasma glucose (1000 mg/dL)
extremely high serum osmolality
high BUN
mild metabolic acidosis (bicarbonate around 20 mEq/L) without ketosis
hyperosmolar nonketotic coma management
high-volume fluid and electrolyte replacement + insulin
myocardial infarction risk in diabetes
#1 cause of death in diabetics (75%); for every 1% reduction in HgA1c there's 14% risk reduction; for every 10 point decrease in blood pressure there's additional 12% risk reduction
lipid management in diabetics
target LDL is <100mg/dL
if 100-130mg/dL: recommend diet, exercise and consider statin
if >130mg/dL statin is recommended
diabetic nephropathy
affects 30-40% of type I and 20-30% of type II diabetics
diffuse membrane and mesangial thickening is most common
nodular glomerulosclerosis is also common (Kimmelstiel-Wilson syndrome)
screen for proteinuria annually
proteinuria is >300mg of albumin in 24 hour urine
microalbuminuria is first stage and between 30-300mg
all diabetics with proteinuria should be given ACE inhibitor or ARB
diabetic retinopathy
screen type II diabetics at diagnosis and annually thereafter

screen type I diabetics 5 years after diagnosis and annually thereafter
proliferative retinopathy shows vitreous hemorrhages and/or neovascularization and is treated with laser photocoagulation
diabetic gastroparesis and erectile dysfunction
treat gastroparesis with metoclopramide or erythromycin

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

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

autonomic neuropathy: orthostatic hypotension, syncope, gastroparesis and constipation or diarrhea, bladder dysfunction and urinary retention, impotence and retrograde ejaculation
hypoglycemia presentation
excessive secretion of epinephrine (sweating, tremor, tachychardia, anxiety, hunger); 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)
insulinoma
subacute or chronic hypoglycemia causes blurred vision, headache, slurred speech, weakness

diagnosis: serum insulin level > 8mg/mL with blood glucose <40mg.dL
CT, ultrasound or arteriography to localize tumor

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

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



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

measure ACTH level
if high, then it's ACTH-producing tumor (do chest CT)
if low it's adrenal hyperplasia -->

urinary 17KS, DHEA-S, abdominal CT: if high and >4cm mass then its adrenal CA

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

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

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

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

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

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

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

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

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

"glucocorticoid withdrawal causes FeVAAH"

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

"10% MuCH BEtter adrenaline"

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

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

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

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

Rx: testosterone
Klinefelter syndrome
47XXY
hypogonadism
gynecomastia
sterility
small testes
high LH/FSH
low-normal serum testosterone
low urinary 17KS
high serum estradiol
diseases that present with prominent dysphagia/odynophagia
achalasia
esophageal cancer (SCC, adenocarcinoma)
scleroderma
diffuse esophageal spasm
Plummer-Vinson
Schatzcki's rings
esophagitis
Zenker diverticulum
Mallory-Weiss syndrome
achalasia presentation
progressive dysphagia to solids and liquids
regurgitation
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
regurgitation
hoarseness
hypercalcemia
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
surgery
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
esophagitis
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
pancreatitis
GERD
gastritis
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
GERD
Barret
peptic ulcer disease
gastritis
Zollinger-Ellison
gastroparesis
dumping syndrome
pancreatitis
gastric cancer
nonulcer dyspepsia
GERD etiology
idiopathic
nicotine
alcohol
caffeine
peppermint
chocolate
anticholinergics
CCBs
nitrates
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
burns
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
gastroparesis
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
cholangitis
arthritis
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
cholangitis
arthritis
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
diverticulosis
50% prevalent over 50
asymptomatic or left lower quadrant colicky pain +- painless bleeding
diagnose with colonoscopy
treat with increased dietary fiber and bulking agents
diverticulitis
infected diverticula
fever, tenderness, pain, leukocytosis
diagnose with CT
barium and endoscopy are contraindicated
treat with ciprofloxacin/metronidazole, ampicillin/sulbactam, piperazillin/tazobactam, cefotetan/gentamycin
constipation
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
endoscopy
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
hemochromatosis
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
asterixis
encephalopathy
jaundice
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
hemochromatosis
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
tachycardia/tachypnea
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
syncope
LV EF <40%
diabetes
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
beta-blocker
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
aspirin
nitroglycerin
morphine
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

ABCDE
drug treatments shown to reduce mortality in IHD
statins
aspirin
beta-blockers
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
thrombocytosis
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
Infections
Thyrotoxicosis
Arrhythmias
Anemia

"SHIIIT precipitates A failure"
heart failure presentation
dyspnea
orthopnea
paroxysmal nocturnal dyspnea
fatigue
pulmonary rales
peripheral edema
ascites
hepatomegaly
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
dyspnea
orthopnea
hemoptysis
hoarseness
paroxysmal nocturnal dyspnea
fatigue
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)
trauma
chronic etiology of mitral regurgitation
Calcifications
Hypertrohpic cardiomyopathy
Endocardial cushion defect
Endocarditis
Fibroelastosis
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
arrhythmias
sudden death
CHF
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
antiarrhythmics
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
angina
syncope
dyspnea
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
syphillis
ankylosing spondylitis
Marfan
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
dyspnea
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
peripartum
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
hypertension
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
dyspnea
angina
presyncope
syncope
palpitations
large jugular A wave
S4
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
Neoplasia
Hemochromatosis
Amyloidosis
Radiation
Sarcoidosis
Scleroderma

"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
dyspnea
exercise intolerance
weakness
elevated jugular venous pressure
edema
hepatomegaly
ascites
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
idiopathic
viral infections
vasculitis
metabolism disorders
neoplasms
trauma
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
neoplasia
viral
TB or suppurative pericarditis
intrapericardial hemorrhage
wounds
postpericardiotomy
uremia
mediastinal radiotherapy
vasculitis
cardiac tamponade manifestations
dyspnea
fatigue
orthopnea
neck vein distention
hypotension
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)
idiopathic
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
IHD
MI
cardiomyopathies
mitral prolapse
metabolic imbalances
digoxin toxicity
thioridazines
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:
quinidine
procainamide
disopyramide
phenothiazines
thioridazine
tricyclics
lithium
hypokalemia
hypomagnesemia
subarachnoid or intracerebral hemorrhage
torsades de pointes diagnosis and treatment
undulating QRS
recurrent dizziness
syncope

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
CHF
left ventricular hypertrophy
aortic aneurysm
dissection
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
retinopathy
hemorrhages
exudates
arteriolar narrowing
papilledema
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
cretinine/BUN
hematocrit
glucose and lipids (for athersoclerosis risk)
serum potassium (exclude hyperaldosteronism)
ECG for LVH
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
ACEIs
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
encephalopathy
headache
confusion
seizures
subarachnoid or intracerebral hemorrhage
hypertensive emergency cardiac presentation
chest pain
MI
palpitations
dyspnea
pulmonary edema
jugular venous distention
gallops
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
Conn
pheochromocytoma
Cushing
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
↓potassium
↓ magnesium
↑calcium
↑uric acid
hyperglycemia
↑LDL
gynecomasia
relative contraindications of diuretics
diabetes, gout, hyperlipidemia
specific indications of beta blockers
myocardial infarction or ischemic heart disease
supraventricular arrhythmias
migraines
glaucoma
anxiety
diastolic heart failure
side effects of beta blockers
bronchospasm
heart block, bradycardia, conduction defects
depression
impotence
fatigue
↓HDL, ↑triglycerides
masking of hypoglycemia
relative contraindications of beta blockers
asthma or COPD
conduction defects
systolic heart failure
diabetes
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
angina
supraventricular arrhythmia
migraines
Raynaud
esophageal spasm
side effects of calcium channel blockers
peripheral edema
constipation
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
pregnancy
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
depression
fatigue
dry mouth
impotence
bradycardia
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
angina
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
aminoglycosides
contrast agents
pentamidine
vancomycin
cyclosporine
lithium
indinavir
ampB
NSAIDs
cysplatine
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
Wegener
Churg-Strauss
Henoch-Schonlein
PAN
TTP
HUS
cryoglobulinemia
glomerulonephritis from glomerular disease
Goodpasture
postinfectious GN
IgA nephropathy
RPGN
Alport
SLE
hypertension
amyloid
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
cryoglobulinemia
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
glomerulonephritis
restrictive cardiomyopathy, arrhythmias, heart blocks
macroglosia
carpal tunnel syndrome
malabsorption
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
proteinuria
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
hematuria
found in diseases of bladder or kidney; stones, cancer, bleeding disorders, trauma, cyclo, glomerulonephritis, cystitis, prostatitis
nitrites
gram negative bacteria reduce nitrate to nitrite and is marker for infection
bacteriuria
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
glomerulonephritis
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
hypertension
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
pruritus
hyperuricemia
decreased libido
weakness
fatigue
glucose intolerance
not indications for dialysis
dietary treatment in ESRD
restricted Na, K, protein, magnesium, phosphate
renal transplant
survival
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
nephrocalcinosis
nephrolithiasis
hypokalemia
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
hypokalemia
serum bicarbonate 18-20
malabsorption of glucose, amino acids, urate, phosphate
osteomalacia/rickets
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%)
Addison
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
cysteine
indinavir
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
ureteroscopy
percutaneous removal (anesthesia and hospital stay)
adult polycystic kidney disease presentation
flank pain, hematuria, palpable mass, UTIs, calculi
hypertension
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)
vomitting
diarrhea
sweating (with free water replacement)
diuretics
ACEIs
renal salt waste
Addison
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
pseudohyponatremia
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)
hyponatremia
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
↓RAA
low electrolytes in blood (BUN, creatinine, uric acid)
low albumin
SIADH management
treat underlying cause
fluid restriction to 800-1000mL/d
demeclocycline (AVP inhibitor)
in case of cerebral edema: hypertonic 3% saline 200-300mL IV in 3-4h
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
hypercalcemia
hypokalemia
sickle cell
amyloidosis
myeloma
pyelonephritis
sarcoidosis
Sjogren
lithium
demeclocycline
colchicine
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)
acidosis
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
hypoventilation
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)
dialysis
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
lactate
aspirin
methanol
uremia
diabetic ketoacidosis
paraldehyde
propylene glycol
ethylene glycol
respiratory acidosis
hypoventilation of any cause
COPD
pickwickian
obesity
suffocation
opiates
sleep apnea
kyphoscoliosis
myopathies
neuropathy
effusion
aspiration
metabolic alkalosis from H+ loss
steroids
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
hypokalemia
respiratory alkalosis
hyperventilation of any cause
anemia
pulmonary embolus
sarcoid
anxiety
pain
"SAAPP"
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
Haemophilus
brucella
pastereulla
bordetella
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"
arbovirus
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
fever
focal neurologic deficits (60%)
seizures
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
fever
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
fever
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
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
alcoholics
pneumonia associations: staph aureus
following viruses or viral bronchitis, specially influenza
pneumonia associations: coccidioidomycosis
southwestern deserts
pneumonia associations: chlamydia psittaci
birds
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
bioterrorism
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
hypothermia
leukopenia
pulse >125/min
hyponatremia
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
TMP-SMX
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
doxycycline
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
HIV+
splenectomized patients
diabetics
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
HIV+
abnormal chest x-ray
steroids or organ transplant
PPD test > 10mm induration
considered positive if
children < 4
leukemia or lymphoma
injection drug users
prisoners
homeless
healthcare worker
immigrants (recent)
nursing home residents
diabetics
dialysis

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
urethritis
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
chancroid
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
chancroid
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
nausea/vomitting
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%)
strictures
prostatic hypertrophy
neurogenic bladder
trauma
diabetes
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
erysipelas
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
obesity
diabetes
corticosteroid or antimetabolites
pregnancy
malignancies
blood dyscrasias
HIV
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
scabies
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
pediculosis
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
hypothyroidism
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
used if CD4>200/mm3; TMPSMZ (most effective) OR dapsone OR atovaquone
CMV retinitis
blurry vision, double vision, any visual disturbance in patients with CD4<50/uL; treat with oral valganciclovir and intravitreal ganciclovir
CMV colitis
diarrhea in patients with CD4<50/uL; treat with oral valganciclovir
CMV esophagitis
odynophagia, fever, retrosternal pain; shallow ulcers in distal esophagus seen with upper GI endoscopy; do biopsy; treat with oral valganciclovir
CMV encephalitis
altered mental status and cranial nerve deficits with CD4 <50/uL; treat with IV ganciclovir
CMV prophylaxis in AIDS
oral valganciclovir for maintenance
CMV therapy side effects
ganciclovir: neutropenia; foscarnet: renal toxicity; cidofovir: renal toxicity
mycobacterium avium complex presentation
fevers, night sweats, bacteremia, wasting, anemia, diarrhea in patients with CD4<50/uL
mycobacterium avium complex diagnosis and therapy
blood culture or culture of bone marrow, liver or other tissue or fluid; treat with clarithromycin + ethambutol +- rifabutin; prophylaxis if CD<100/uL with weekly azithromycin or clarithromycin twice daily
toxoplasmosis presentation
brain mass lesion, headache, confusion, seizures, focal neurologic deficits in patient with <100 CD4/uL
toxoplasmosis diagnosis
ring enhancing lesion on CT or MRI with edema and mass effect; shrinkage after 2 weeks of therapy is diagnostic; also toxoplasma serology an CSF PCR; brain biopsy may be necessary if no shrinkage
toxoplasmosis treatment
pyrimethamine + sulfadiazine; if sulfa allergy substitute with clindamycin; prophylaxis with TMP/SMX OR dapsone/pyrimethamine
cryptococcosis presentation
mainly meningitis, fever, headache, malaise in patient with CD4<100/uL
crytocococcal meningitis diagnosis
india ink of CSF and specific cryptococcal antigen testing in CSF and serum
cryptococcal meningitis therapy
IV ampB 10-14 days followed by oral fluconazole for maintenance; fluconazole is not recommended for general use prophylaxis
vaccinations in HIV+
all should receive pneumococcus, influenza and hepatitis B vaccines
diseases with CD4 200-500/uL
oral thrush, Kaposi sarcoma, TB, zoster, lymphoma
diseases with CD4 100-200/uL
pneumocystis pneumonia, dementia, PML, disseminated histoplasmosis, coccidiomycosis
diseases with CD4 <100/uL
toxoplasmosis, cryptococcal meningitis, cryptosporidiosis, disseminated herpes
diseases with CD4 <50/uL
CMV, mycobacterium avium complex, CNS lymphoma
HIV viral load monitoring
to monitor response to antiretrovirals, determine risk of complications and prognosis; higher load indicates CD4 will drop more rapidly
nucleoside reverse transcriptase inhibitors
zidovudine (AZT, ZDV), didanosie, stavudine, lamivudine, emtricitabine, tenofovir, abacavir, zalcitabine
zidovudine
NRTI; leukopenia, anemia, gastrointestinal
didanosine
NRTI; pancreatitis, peripheral neuropahty
stavudine
NRTI; peripheral neuropathy
lamivudine
NRTI; nothing additional to placebo
emtricitabine
NRTI; nothing additional to placebo
tenofovir
NRTI; nucleotide instead of nucleoside
abacavir
NRTI; hypersensitivity reaction; discontinue immediately and don't restart
zalcitabine
NRTI; pancreatitis, peripheral neuropathy, lactic acidosis
protease inhibitors
nelfinavir, indinavirm ritonavir, saquinavir, amprenavir, lopinavir, atazanavir; all cause hyperlipidemia, hyperglycemia and elevated liver enzymes plus specific effects
nelfinavir
PI; GI side effects
indinavir
PI; nephrolithiasis, hyperbilirubinemia
ritonavir
PI; severe GI disturbance
saquinavir
PI; GI effects
lopinavir
PI; diarrhea
atazanavir
PI; diarrhea, asymptomatic hyperbilirubinemia
non-nucleoside reverse transcriptase inhibitors
noncompetitive inhibitors; efavirenz, nevirapine, delavirdine
efavirenz
NNRTI; neurologic effects, somnolence, confusion, psychiatric
nevirapine
NNRTI; rash, hepatotoxicity
delavirdine
NNRTI; rash
when to start antiretroviral therapy
CD4 <350/uL or viral load by PCR-RNA >55,000 by RNA
which antiretrovirals to start with
2 NRTI + PI or NNRTI OR 2 NRTI + efavirenz OR 2 nrti + 2 PI
antiretroviral contraindicated in pregnancy
efavirenz
what is considered adequate therapy
any combo that decreases viral load near or to undetectable amounts and increases CD4; in the first month viral load should drop at least 50%
HIV management in pregnant women
25-30% of children will be truly HIV+ if no treatment is given; recommended is AZT + NRTI + PI; C-section indicated if viral load >1,000 at time of delivery; should not breastfeed
HIV post-exposure prophylaxis
recommended AT + lamiduvine + nelfinavir OR any fully suppressive combo for 4 weeks
Q fever
coxiella by inhalation and found in placenta of cattle, sheep and goats; can cause febrile illness, atypical pneumonia, hepatitis, hepatomegaly, endocarditis; diagnose with specific serology; treat with doxycyline
Rocky Mountain spotted fever
ricketsia transmitted by wood tick in south, upper south and midwest; abrupt onset fever, headache, erythematous maculopapules with centripetal spread and neurological deficits; differential with syphilis; serology and biopsy; treat with doxycyline
tetanus etiology and presentation
neurotoxin by C. tetani in 1-7 days; tonic spasms, respiratory arrest, dysphagia, stiff body, lockjaw, arm flexion and leg extension
tetanus diagnosis and treatment
clinical diagnosis; tetanus toxoid (10-year boosters), surgical debridment; tetanus immunoglobulin antitoxin, 10-14 days of penicillin
aspergillosis etiology
most common is aspergilus fumigatus causes pulmonary disease in immunocompromised; risk factors are neutropenia <500, steroids and cytotoxics
aspergillosis presentation
allergic asthma-like signs, mycetoma with hemoptysis
aspergillosis diagnosis
abnormal chest x-ray and aspergillus in sputum; eosinophilia and elevated IgE; positive skin testing; if invasive, biopsy necessary
aspergillosis treatment
allergic: steroids and asthma medications, not antifungals; mycetoma: surgical removal; if invasive: voriconazole and caspofungin
drawbacks of screening
iatrogenia, expensive, unpleasant, inconvenient, harmful, stigma

"screening-HESIItant"
valid screening test
shown to decrease overall mortality in screened population in randomized double-blind trial
malignancies to regularly screen for
colon, breast and cervix cancers
screening for colon cancer, no significant family history
after age 50: annual fecal occult blood, sigmoidoscopy every 5 years and barium enema. Preferred modality: colonoscopy every 10 years
screening for colon cancer, high-risk patients
colonoscopy every 5 years starting at age 40 or 10 years younger than at the age at which youngest affected relative was diagnosed
screening for breast cancer
mammography every 1-2 years from age 40
breast exam by physician every 3 years from ages 20-30
self breast exam is no longer recommended
patients with strong family history should receive prophylactic tamoxifen
screening for cervix cancer
Pap smear annually starting 3 years after becoming sexually active or at age 21

patients <30 screen annually if conventional methods or every 2 years if using liquid-based

patients >30 screen every 2 years if >3 normal annual Pap smears
vaccinations for travelers
Hep A
Hep B
malaria
rabies
yellow fever
typhoid fever
polio
meningococcal meningitis
depending on case
Hep A vaccination
if traveler is leaving within 2 weeks of being seen give Hep A vaccine plus immune serum globuline; booster after 6 months confers immunity for 10 years; also recommended for day-care employees, homosexual men and chronic liver disease
Hep B vaccination
for travelers who will work closely with indigenous population or will engage in sexual intercourse, receive medical or dental care and those who plan to remain abroad for over 6 months; also IV drug users, male homosexuals, contact with carriers, frequent exposure to blood or chronic liver disease
prophylaxis for malaria
for patients traveling to Mexico, Central America or Caribbean: chloroquine

for areas with chloroquine resistance: mefloquine or doxycyline (2nd line)

for pregnant: atovaquone plus proguanil
prophylaxis for rabies
patients travelling to Mexico, India, Asia
intradermal vaccine or intramuscular in case patient is also receiving malaria prophylaxis
not routine for most
yellow fever vaccine
for patients travelling to sub-saharan Africa and some south American countries
typhoid vaccination
travelers to developing countries; live atenuated vaccine is contraindicated in HIV patients; intramuscular polysacchride vaccine is preferred
polio vaccination
given to unvaccinated travelers to developing countries
three doses of inactivated vaccine or one-time booster if previously immunized
meningococcal meningitis vaccine
travelers to endemic or epidemic areas (Nepal, sub-Saharan Africa, northern India); required for pilgrims to Mecca; patients with functional asplenia or terminal complement deficiencies
11-12 years
tetanus and diptheria immunization
unvaccinated adults should receive three doses
first 2 are 1-2 months apart and third dose 6-12months later
booster every 10 years
2, 4, 6 months; 15-18 months; booster 10 years
influenza vaccination
recommended annually for all healthy adults after age 50
patients with history of cardiopulmonary disease
diabetes
hemoglobinopathy
pregnant women will be in 2nd or 3rd trimester during influenza season
pneumococcal vaccination
Revaccination recommended for all over 65

or at any age in case of: sickle-cell patients, splenectomy, cardiopulmonary disease, alcoholism, cirrohsis, immunocompromised (hematologic malignancies, chronic renal failure, HIV, etc.)

Patients with high risk of fatal infections should be revaccinated every 5 years

"enCCApSSIlated over 65"
varicella vaccine
live attenuated recomemded for all adults who lack childhood history of varicela except immunocompromised or pregnant
MMR vaccine
live attenuated vaccine given to children or unvaccinated adults born after 1956; except HIV or pregnant;

given at 12-15 months with pre-school booster 4-6 years
smoking cessation
responsible for 1/5 of deaths in US

Ask
Advise
Attempt
Assist
Arrange follow-up
osteoporosis prevention
women older than 65 should receive DEXA scan
if low body weight or fracture risk start screening at 60
abdominal aortic aneurysm screening
ultrasound to male smokers older than 65
no screening necessary for male non-smokers and women regardless of smoking history
hypertension screening
patients older than 18, at every visit, at least every 2 years
cholesterol screening
start screening at age 35 in men and 45 in women without risk factors

patients with risk factors for atherosclerosis screen routinely after 20 years of age
diabetes screening
if risk factors are present (obesity, impaired fasting glucose, high-risk ethnicity, positive family history, hypertension, hyperlipidemia)

two fasting glucose above 126mg/dL or random measure greater than 200 w/symptoms are diagnostic
alcohol abuse screening
two "yes" answers to CAGE questionare
Cut down
Annoyed
Guilty
Eye opener
important considerations in evaluating arthritis
1. distribution and number of joints involved
2. acute or chronic
3. systemic symptoms
4. signs of inflammation
important tests in rheumatologic disease
joint aspiration (cell count, crystals, cultures, Gram)
antinuclear antibodies
rheumatoid factor
antineutrophil cystoplasmic antibodies
antiphospholipid antibodies
joint aspiration test
arthrocentesis; synovial fluid tests to run:
cell count
crystals
cultures
Gram stain
hemogram (anemia)
ESR

if <2,000 WB consider OA or trauma
if 5,000-50,000 WBCs probable inflammatory etiology but also consider septic
if > 50,000 WBCs consider septic etiology;
ANAs
seen in 5% of normal people
95% of SLE as well as Sjogren, CREST, systemic sclerosis, MCTD

ANA subsets:
anti-ds-DNA (60% of SLE, indicates diseae activity and nephritis)
anti-Smith (SLE 25-30%)
anti-histone (drug-induced lupus, 95%)
anti-Ro/SSA (neonatal lupus, Sjogren, ANA-negative lupus)
anti-LA/SSB (Sjogren)
anti-centromere (CREST)
anti-RNP (MCTD, 100%)
rheumatoid factor
IgM against Fc portion of IgG found in 70% of patients of RA and 5% of healthy adults
neither sensitive nor specific for RA but has prognostic significance
ANCAs
cANCA are diffuse antibodies against neutrophils seen in 90% of Wegner cases
pANCA are localized in around the neutrophil nucleus and atacks myeloperoxidase and it's seen in PAN and Churg-Strauss
antiphospholipid antibodies
also called lupus anticoagulant or anticardiolipin antibodies

associated with hypercoagulable state of antiphospholipid syndrome
high PTT
false-positive VDRL
spontaneous abortions
thromboembolism
rheumatoid arthritis etiology
unknown (most cases) or due to mycoplasma or parvovirus infection
rheumatoid arthritis presentation
need four of the following criteria:
morning stiffness > 1h
swelling of wrists, MCPs and PIPs
swelling of three joints
symmetric involvement
joint erosions on x-rays
RF positive
rheumatoid nodules
constitutional symptoms: fatigue, anorexia, weight loss, generalized wekness
DIPs and lower back joints are not involved

signs: radial deviation of wrist with ulnar deviations of digits
Boutonniere and Swan-neck deformities
nodules are usually on olecranon, occiput or Achilles tendon

Felty syndrome (RA, splenomegaly, neutropenia)
Caplan syndrome (RA, pneumoconiosis)
rheumatoid arthritis management
aspirin
celecoxib (other COX-2 recalled due to increased risk of cardiac ischemia and stroke)

glucocorticoids

disease modifying agents:
hydroxychloroquine
gold salts
methotrexate
TNF inhibitors (infliximab, adalimumab, ethanercept)
rheumatoid arthritis complications
alantoaxial subluxation
pannus formation at C1-C2 with neurologic symptoms
(paraplegia, paresthesias of hands and feet, myelopathy)

cervical x-ray is initial screening test

rupture of Baker cyst manifests with swollen painful calf
systemic lupus erythematosus presentation and diagnosis
four diagnostic criteria are needed:
malar rash
discoid rash
photosensitivity
oral ulcers
arthritis
serositis
renal involvement
neurologic disorder
hematologic disorder (hemolytic anemia, leukopenia, thrombocytopenia)
immunologic disorder (anti-ds DNA, anti-SM)

best screening test: ANAs

anti-ds-DNA and anti-SM are specific for SLE
systemic lupus erythematosus management
symptomatic
NSAIDs for arthritis
corticosteroids for rashes
cytotoxics (azathiorpine, cyclophosphamide) for severe synptoms (nephritis, endocarditis, pleuritis, hemolytic anemia, CNS)

also wear sunglasses and sunscreen
drug-induced lupus
reactions to hydralazine, isoniazid, procainamide and quinidine
presents with fever, arthritis, fatigue and rarely plurisy
severe symptoms of lupus are not seen including skin disease and photosensitivity
anti-histone antibodies are present
in hydralazine-induced lupus only 1/3 have anti-histone antibodies present
manage by withdrawing causing drug which confirms diagnosis when symptoms subside within 2 weeks
diffuse scleroderma presentation
raynaud phenomenon
skin thickening throughout the body
esophageal dysmotility
achalasia
intestinal hypomotility
malabsorption
large intestine diverticula
lung fibrosis
malignant hypertension
acute renal failure
Scl-70 antibodies are present
limited scleroderma presentation
CREST syndrome: calcinosis, raynaud, esophageal dysmotility, sclerodactily, telangiectasia

skin involvment is in distal extremities
pulmonary artery hypertension in 25-50%
interstitial lung disease in 10%
anticentromere antibodies are present
scleroderma management
d-penicillamine for skin; CCB for raynaud; ACEIs for hypertension

"sCleroDermA"
Calcium, D-penicilamine, ACEIs
Sjogren syndrome
lymphocytic infiltration of exocrine glands seen alone or in association with RA, PBC, SLE

presents with itchy eyes with sandy feeling (keratoconjunctivitis sicca) and difficulty swallowing food, parotid enlargement and dental caries

advanced stages affects lungs and kidneys and predisposes to malignant lymphoma

screen with anti-Ro/La antibodies
confirm with biopsy of salivary glands
diseases associated with symmetrical polyarthritis
RA (involves mostly the joints), SLE, scleroderma, Sjogren
also parvoB19 and hepB
seropositive arthropathies
RA, SLE, scleroderma, Sjogren
seronegative arthropathies
associated with HLA-B27 allele; ankylosing spondylitis, reactive arthritis, psoriatic arthritis, enteropathic arthropathy; PAIR
ankylosing spondylitis
3-4 times more common in men; 90% HLA-B27+

presentation --> chronic back pain and morning stiffness lasting >1h improves with exercise, decreased spine mobility, no lumbar lordosis
anterior uveitis, aortic insufficiency and 3rd degree heart block

X-rays show fusing of sacroiliac joint, sacroilitis, bamboo spine
diagnose with clinical and x-ray, no HLA-B27

treat with NSAIDs, physical therapy, exercise and possibly TNF inhibitors

"BEHNkylosing spondylitis needs x-ray"
reactive arthritis
Reiter: nongonococcal urethritis (chlamydia, ureaplasma) with mucocutaneous manifestations (keratoderma blenorrhagica, circinate balanitis, genital ulcers, conjunctivits, arthritis)

ReA: after infectious diarrhea from campylobacter, shigella, salmonella

diagnosis is clinical with x-ray findings of seronegative arthropathy
osteoarthritis etiology
idiopathic (most common)
or secondary due to:
gout, diabetes, acromegaly, hemochromatosis, mechanical factors
osteoarthritis presentation
affects elderly with chronic asymetrical pain of weight bearing joints or PIPs, DIPs, which increases with excersise and decreases with rest

morning stiffness <30m

crepitation

no systemic nor inflammatory symptoms
osteoarthritis diagnosis
clinical presentation + x-ray findings:

osteophytes and unequeal joint space
osteophytes in PIPs are Bouchard nodules

in DIPs are Heberden's nodules
osteoarthritis management
reduce joint load, physiotherapy
NSAIDs specially acetaminophen (4,000mg/d, 1st line)
ibuprofen (1,200mg/d)
celecoxib used for patients with gastric side effects

capsaicin cream depletes local nerves of substance P

intraarticular hyaluronic acid injections are used also
if no improvement or decreased quality of life then joint arthroplasty
gout presentation
acute monoarthritis afecting first MTP (podagra) or other joints
signs of inflammation over joint
precipitated by alcohol, trauma, surgery, steroid withdrawal and drugs (HCTZ, furosemide, pyrazinamide, ethambutol)
chronic gout may involve monosodium urate deposition in connective tissue and kidneys
gout diagnosis
clinical signs
erosive calcifications on x-ray
negatively birefringent needle-shaped monosodium urate crystal in synovial fluid
5,000-50,0000 WBCs

first step in diagnosis: joint aspiration
acute gout management
indomethacin 50mg/8h
colchicine 0.6mg until symptoms resolve or GI upset
if elderly with low NSAID toleration or renal impairment give steroids without NSAIDs or colchicine
if previously using allopurinol, do not withdraw
chronic gout management
low purine diet, limitation of alcohol and diuretics

if recurrent attacks: probenecid in undersecretors or allopurinol in undersecretors or overproducers or renal failure

goal is to lower uric acid levels so monitor plasma uric acid
pseudogout
same presentation as gout
diagnose with synovial fluid showing positively birefringent romboid calcium pyrophsphate crystals and condrocalcinosis in x-rays

pseudogout raises suspicion of hyperparathyroidism, hemochromatosis, hypophsphatemia, hypomagnesemia

management same as gout
septic arthritis
due to gonococcus (young people) or staph (elderly) infection

presents with sudden onset monoarticular arthritis and signs of inflammation

diagnose with arthrocentesis (gram stain, negative culture, no crystals and > 50,000 WBCs)

treat with ceftriaxone (gonorrhea) or nafcillin/vancomycin (staph)
Wegener granulomatosis
small vessel vasculitis
presents with rhinitis, sinusitis, nasal ulcers, hemoptysis, dyspnea, kidney involvement and arthritis

cANCA+
diagnosis is made with biopsy of affected area

treat with prednisone + cyclophosphamide
polyarteritis nodosa
medium vessel vasculitis; presents with
nonspecific signs fever, malaise, anorexia, weight loss, abdominal pain
does not affect lungs
peripheral neuropathy (tingling, numbness, pain, mononeuritis)
GI bleeds, 30% hepB
kidney involvement

diagnose with biopsy; can do angiogram
Churg-Strauss syndrome
affects medium vessels

adult-onset asthma, eosinophilia, neuropathy and non-specific symptoms

diagnose with biopsy
treat with prednisone + cyclophosphamide
temporal arteritis
affects large vessels of head and neck

headache, jaw claudication, visual disturbances
25% polymyalgia rheumatica

first test is ESR, if high give prednisone then biopsy of temporal arteries looking for giant cells
polymyositis/dermatomyositis
proximal muscle weakness without eye muscle compromise (different than myasthenia and EDS)

dermatomyositis has heliotrope rash over face and eyelids

screening: aldolase and CPK; anti-Jo-1
diagnose with electromyography (short-duration, low amplitude potentials)
confirm with muscle biopsy

treat with steroids
spinal cord compression etiology
acute --> trauma, hematoma
subacute --> cancer (lymphoma, multiple myeloma, prostate, lung, breast, kidney, colon), epidural abscess
chronic --> herniated disk
spinal cord compression presentation
back pain (96%)
history of cancer, fever
bowel or bladder dysfunction
insidious onset of mild sensory disturbance
lower limb weakness or rigidity
spinal cord compression diagnosis
plain x-rays are 84-94% sensitive
gold standard is MRI
if MRI is contraindicated --> CT myelogram
spinal cord compression management
high-dose dexamethasone immediately upon suspicion
surgical decompression in trauma, herniated disk or epidural abscess
radiotherapy in case on cancer
syringomyelia etiology
central cavitation of spinal cord
communicating is associated with Arnold-Chiari
non-communicating is associated with trauma or spinal cord tumors
syringomyelia presentation
cervical and upper limb pain and temperature loss
may have lower motor neuron deficits in upper limbs and upper motor neuron deficits in lower limbs
syringomyelia diagnosis and treatment
MRI is gold standard; surgery is unsatisfactory
subacute combined degeneration
B12 deficiency results in
corticospinal --> upper motor neuron signs, flaccid/spastic paralysis
dorsal columns --> ataxia, vibration and propioception deficits, distal paresthesia
diagnosis --> low serum B12 and high methylmalonic acid
treatment --> B12 replacement
anterior spinal artery occlusion
bilateral paralysis
pain, temperature and autonomic loss below lession
conserved vibration and propioception
Brown-Sequard syndrome
ipsilateral upper motor neuron signs below lesion
ipsilateral vibration and propioception loss below lesion
contralateral pain/temerature loss 1-2 levels below lesion
bilateral flaccid paralysis and anesthesia at level of lesion
ipsilateral Horner syndrome if above T1
anterior cerebral artery irrigation
medial surface of frontal and parietal lobes
1 inch of supero-lateral surface of frontal and parietal lobes
anterior limb of internal capsule
caudate nucleus
anterior 4/5 of corpus callosum
anterior cerebral artery stroke presentation
contralateral lower limb paralysis
contralateral lower limb sensory loss
urinary incontinece, behavioral disturbances
middle cerebral artery irrigation
lateral surfaces of frontal, parietal and temporal lobes except superior inch
genu and posterior limb of internal capsule
globus pallidus
putamen
middle cerebral artery stroke presentation
contralateral hemiplegia, contralateral anesthesia
contralateral homonymous hemianopia with eye deviation toward lesion
contralateral central facial paralysis
aphasia if left, apraxia and spacial disturbance if right
posterior cerebral artery irrigation
cerebellum, brain stem, pons, occipital lobe
posterior brain circulation arteries
posterior cerebral artery
basilar artery
cerebellar arteries
paramedian branches
vertebral artery
posterior cerebral artery stroke
contralateral homonymous hemianopia
visual hallucinations
agnosia
associated Weber or Benedikt syndromes
Weber syndrome
results from occlusion of penetrating branches of PCA
contralateral hemiplegia and CNIII palsy
Benedikt syndrome
results from occlusion of penetrating branches of PCA
CNIII palsy with contralateral ataxia or athetosis
paramedian branches of basilar artery stroke
quadriparesis with intact vertical eye movement
PICA stroke
Wallenberg / lateral medullary syndrome -->
lateral spinothalamic --> contralateral pain/temperature loss
trigeminal nucleus --> ipsilateral facial sensory loss
vesticular nucleus --> vertigo, nystagmus, nausea
ambigus nucleus --> dysarthria, dysphagia, gag reflex
inferior cerebellar peduncle --> ataxia
descending sympathetics --> Horner syndrome
Wallenberg syndrome
results from posterior cerebellar artery occlusion
lateral spinothalamic --> contralateral pain/temperature loss
trigeminal nucleus --> ipsilateral facial sensory loss
vesticular nucleus --> vertigo, nystagmus, nausea
ambigus nucleus --> dysarthria, dysphagia, gag reflex
inferior cerebellar peduncle --> ataxia
descending sympathetics --> Horner syndrome
cerebellar artery stroke
vertigo
vomitting
nystagmus
ipsilateral limb ataxia
stroke diagnosis
initial test is noncontrast CT to diffeentiate between ischemic or hemorrhagic
CT will be normal in ischemic stroke in first 48 hours
if ischemic --> check for embolic sources with echocardiogram, carotid duplex, 24-hour Holter and check for hypercoagulability
if hemorrhagic --> do EKG for inverted T-waves
tPA use in ischemic stroke
use if onset <3 hours in ischemic stroke

contraindications -->
history of intracranial hemorrhage
stroke or head trauma within 3 months
hemorrhage within 3 weeks
surgery within 2 weeks
arterial puncture within 1 week
lumbar puncture within 1 week
BP > 185/110
anticoagulants
thrombocytopenia
PT > 15s
stroke treatment
ischemic --> tPA if onset <3h; then aspirin +- dypiridamole OR clopidogrel +- endarterectomy
hemorrhagic --> nimodipine +- craniotomy or coiling or shunt
seizures/epilepsy etiology
"VITAMINS" -->
Vascular (stroke, bleed, AVM)
Infections (meningitis, encephalitis)
Trauma
Autoimmune
Metabolic (hyponatremia, hypocalcemia, hypoglycemia, hypoxia, drug overdose)
Idiopathic
Neoplasm
pSychiatric
seizures/epilepsy general presentation
sudden onset of convulsions with or without aura
postictal symptoms --> disorientation, sleepiness, aching muscles
associated signs --> incontinence, tongue biting, headache
patients with syncope don’t have postictal symptoms or signs
partial simple seizure
focal deficits without loss of consciousness
partial complex seizure
focal deficits with loss of consciousness
partial seizure with secondary generalization
begins as partial and converts to generalized
generalized tonic-clonic seizure
tonic contractions followed by clonic relaxation of muscles
first line --> valproic
second line --> phenytoin, carbamazepine, lamotrigine
absence seizures
sudden brief loss of consiousness without loss of postural tone
treat with ethusuximide or valproic
atonic seizures
sudden loss of postural tone for 1-2 seconds
myoclonic seizures
sudden brief muscle contraction
status epilepticus
recurrent continuous seizures lasting at least 5-30min
epilepsy diagnosis
EEG is test of choice
abnormal EEG alone is not diagnostic (2-18% of population has abnormal EEG)

first rule out reversible causes of seizures checking electrolytes, glucose, toxicology, arterial blood gases and structural lesions with CT or MRI
acute management of seizures
1) secure ABCs
2) evaluate precipitating causes
3) medications in order: lorazepam/diazepam, phenytoin, phenobarbital, midazolam/propofol
maintenance treatment of epilepsy
tonic-clonic --> valproic acid is first OR lamotrigine, carbamazepine, phenytoin
partial --> carbamazepine, phenytoin first OR lamotrigine, valproic second
absence --> ethosuximide or valproic
myoclonic and atonic --> valproic
pregnant --> carbamazepine
vertigo etiology
Meniere
labyrinthitis
positional vertigo
traumatic vertigo
perilymphatic fistula
cervical vertigo
vertigo presentation
patient feels room is spinning without any real movement, nausea and vomitting
differentiate from presyncope which is described as lightheadedness and feeling of blackout
vertigo is neurologic presyncope is cardiologic
central vertigo Vs. peripheral vertigo
central --> gradual onset, absent tinnitus and hearing loss, diplopia, cortical blindness, dysarthria, weakness, vertical nystagmus

peripheral is contrary
Meniere disease
endolymphatic pressure changes
peripheral episodic vertigo 1-8 hours
common causes are syphillis and head trauma
labyrinthitis
follows respiratory tract infection
peripheral vertigo lasts for several days
benign paroxysmal positional vertigo
peripheral vertigo exacerbated by head movements lasts 10-60 seconds
central vertigo
due to cerebellar or brain tumor, bleed, bleed, drug toxicity or multiple sclerosis
vertigo treatment
peripheral --> symptomatic with meclizine or diazepam
Meniere --> low-salt diet and diuretics
benign paroxysmal --> head maneuvers
headache etiology
primary --> migraine (15% of population), cluster, tension
secondary --> hemorrhage, brain tumor, meningitis, temporal arteritis, glaucoma
meningitis headache
accompanied with fever and nuchal rigidity
intracranial hemorrhage headache
associated with nuchal rigidity, sudden onset, severe and without fever
brain tumor headache
deep, dull, aching pain disturbs sleep
posterior brain fossa tumor headache
history of vomitting weeks before, or induced by coughing, lifting or bending
temporal arteritis headache
unilateral pounding, dull headache associated with visual disturbances, jaw claudication, weight loss, arthritis, increased ESR
migraine presentation
pain described as pulsatile, throbbing, unilateral, aggravated by movement
nausea and vomitting
photophobia, phonophobia
may have aura or not
aura --> scintillating scotoma, flashes of light, motor, sensory or visual symptoms
tension headahces presentation
tight, band-like, bilateral headaches
builds slowly, may persist for days and is not exacerbated by movement
may have tightness of posterior neck muscles
cluster headache presentation
excrutiating, unilateral, pulsatile, periorbital headache that begins without warning and peaks in intensity within 5 minutes; lasts 30 minutes to 3 hours, 1-3 times/day for a 4-8 week period; associated with rhinorrhea, reddening of the eye, lacrimation and nasal stuffness
headache diagnosis
clinical history and tests to exclude secondary causes
if severe, sudden onset of first time headache --> head CT
acute management of migraines
mild --> NSAIDs
severe, first line --> triptans (contraindicated in heart disease)
severe, 2nd line --> ergotamine + caffeine
prophylaxis of migraines
first line --> propranolol, timolol, valproic acid, topiramate
second line --> verapamil, tricyclics, SSRIs
treatment of tension headaches
relaxation + acetaminophen/NSAIDs +- muscle relaxant
treatment of cluster headaches
100% O2, prednisone and lithium
may use sumatriptan, ergotamine, verapamil
pseudotumor cerebri etiology
8-10x more common in women
associated with obesity, COPD, Addison, oral contraceptives, tetracyclines, vit A toxicity
pseudotumor cerebri presentation
headache, diplopia, abducens palsy, papilledema
CT/MRI are normal
CSF is normal beyond increase in pressure
pseudotumor cerebri treatment
weight loss
removing offending agent
diuretics (acetazolamide, furosemide)
prednisone may be useful as well as repeated lumbar punctures
trigeminal neuralgia presentation
sudden, severe, sharp pain starts near mouth and progresses towards ear, eye or nostril and lasts few seconds; can be a manifestation of multiple sclerosis or posterior fossa tumors
trigeminal neuralgia treatment
carbamazepine
may also try phenytoin, baclofen or gabapentin
Guillain-Barre syndrome presentation
progressive paralysis
arreflexia
pain or tingling
autonomic instability
history of recent infection (campylobacter, herpes, CMV, EBV)
lack of constitutional symptoms
Guillain-Barre syndrome diagnosis
history + lumbar puncture looking for ↑proteins and normal cell count
(best initial test, 48 hours after onset)
electromyography is most specific
Guillain-Barre syndrome treatment
IV immunoglobulin or plasmapheresis are equally effective
glucocorticoids are not effective
early respiratory support to prevent death
What are the basic molecules used in serological classification of streptococcie?
(serological classification = using serum antibodies to identify similar and different types of bacteria)
pg 281
presence of POLYSACCHARIDE antigens associated with the gram POSITIVE peptidoglycan layer
myasthenia gravis diagnosis
best initial test --> acetylcholine receptor antibodies
most specific test --> electromyography (decrease in contraction on repetitive stimulation)
edrophonium test is sensitive but not specific
should do x-ray or CT to exclude thymoma
Eaton-Lambert or botulism difference with myasthenia
Eaton-Lambert and botulism improve weakness with repetitive stimulation
myasthenia gets worse
myasthenia gravis treatment
symptomatic relief --> pyridostigmine, neostigmine + plasmapheresis
thymectomy indicated in postbubertal and <60 with generalized myasthenia
if thymectomy fails then steroids +- azathioprine
mycophenolate is newer immunosuppressive
avoid aminoglycosides
amyotrophic lateral sclerosis presentation
upper motor neuron and lower motor neuron signs concomitantly is unique presentation
fasciculations, tongue atrophy, renervation after denervation on biopsy
also nerve palsies (dysphagia, difficulty chewing, decreased gag reflex, etc)
respiratory involvement with intact cognitive, sensory and autonomic function
amyotrophic lateral sclerosis diagnosis
physical exam + electromyogram
CSF and MRI are normal
amyotrophic lateral sclerosis management
riluzole slows progression
multiple sclerosis presentation
young female with relapsing remitting episodes of
weakness
numbness
tingling
urinary urgency or retention
blurry/double vision
episodes resolve spontaneously
multiple sclerosis diagnosis
clinical diagnosis + MRI of brain and spine
evoked potentials are rarely used
CSF shows mild pleocytosis and mildly elevated proteins
CSF for oligoclonal IgG banding is recommended when clinical suspicion remains after unconfirmatory MRI
multiple sclerosis treatment
remitting relapsing disease --> interferon-B1a, interferon-B1b, glatiramer
secondary progressive disease --> interferon-B1b and mitoxanthrone (2nd-line)
primary progressive disease --> no effective therapy
acute exacerbations --> IV glucocorticoids
spasticity --> baclofen
trigeminal neuralgia --> carbamazepine
bladder hyperactivity --> oxybutynin
urinary retention --> bethanecol
reversible causes of dementia
hypothyroidism
B12 deficiency
hepatic encephalopathy
CNS vasculitis
syphilis
brian abscess
brain tumor
anticholinergics
apnea
trauma
subdural hematoma
normal pressure hydrocephalus
depression
irreversible causes of dementia
Alzheimer (most common)
multifocal leukoencephalopathy
Lewy bodies
frontotemporal degeneration (Pick)
vascular dementia
Creutzfeld-Jakob
dementia definition
memory loss along with impairment of other cognitive functions that interferes with social functioning
Alzheimer
memory loss + aphasia or apraxia or agnosia; inability to make plans and execute them
Pick disease
personality changes precede memory loss; patient lacks insight into condition
dementia with Lewy bodies
fluctuating cognitive impairment
Creutzfeld-Jakob
short, aggressive progression of dementia, myoclonus, ataxia and 14-3-3 protein in CSF
multi-infarct dementia
stepwise progression associated with discrete cerebrovascular events
Binswanger
slowly progressive vascular dementia that affects subcortical white matter
normal pressure hydrocephalus dementia
associated with gait abnormalities early in the course and urinary incontinence
dementia diagnosis
assesment of cognitive impairment with mini mental exam

CBC, electrolytes, calcium, creatinine, liver function tests, glucose, TSH, B12, RPR, HIV

brain imaging in cases of focal deficits, seizures, gait abnormalities
Alzheimer treatment
anticholinestrase inhibitors donepezil, rivastigmine, galantamine improve cognitive function
memantine is disease modifying used in advanced disease alone or in combo
Huntington
chorea + behavioral disturbances (irritability, anger, paranoia, depression)
diagnosed with genetic testing for CAG triplet repeat expansion
cerebral atrophy (cortex, basal ganglia) can be seen in brain imaging
Parkinson etiology
structural lesions in basal ganglia
survivors of encephalitis
neuroleptics (haloperidol, chlorpromazine)
metoclopramide
methyldopa
reserpine
Parkinson presentation
Bradykinesia
cogwheel Rigidity
postural Instability
resting Tremor
"BRITish"
Parkinson+ syndromes
parkinsonism + vertical gaze palsy --> supranuclear palsy
parkinsonism + ataxia --> olivopontocerebellar atrophy
parkinsonism + orthostatic hypotension --> Shy-Drager syndrome
diseases that mimic parkinsonism
severe depression
essential tremor
normal pressure hydrocephalus
Huntington
Parkinson diagnosis
clinical diagnosis
Parkinson treatment with intact functional status
anticholinergics --> amantadine are first-line, then the rest
Parkinson treatment with compromised functional status
initial therapy is carbidopa/levodopa
if dyskinesia, akathisia or on-off --> add pramipexole, selegiline or COMT inhibitor (tolcapone)
essential tremor
improves with alcohol; treat with propranolol
pemphigus vulgaris etiology
antibodies against desmosomes of epidermal cells; mostly idiopathic but also ACEIs and penicillamine
pemphigus vulgaris presentation
young patient with skin erosions and thin bullae that are painful
mouth erosions are prominent
Nikolsky sign
pemphigus vulgaris diagnosis
skin biopsy with immunofluorescence shows deposits of IgG and C3 in the epidermis
pemphigus vulgaris treatment
systemic glucocorticoids
if not effective --> azathioprine, mycophenolate or clyclophosphamide, rituximab, IVIG
Nikolsky sign
removal of skin like a sheet with slight pressure
seen in pemphigus vulgaris, staph scalded syndrome, toxic epidermal necrolysis
blistering diseases
pemphigus vulgaris
bullous pemphigoid
pemphigus foliaceous
porphyria cutanea tarda
pemphigus foliaceous
more superficial than vulgaris with no oral lesions or intact bullae; same diagnosis and treatment as vulgaris
bullous pemphigoid presentation
autoantibodies against hemidesmosome at dermo-epidermal junction/basement membrane result in tense bullae that don't rupture easily in elderly; oral lesions are rare
bullous pemphigoid diagnosis and treatment
lesion biopsy with immunofluorescence shows depostis at basemanet membrane
systemic steroids
alternative --> tetracycline or erythromycin combined with nicotinamide
porphyria cutanea tarda etiology
deficiency of uroporphyrinogen decarboxulase results in accumulation of porphyrins and photosensitive reaction; there may be history of HIV, alcoholism, liver disease, chronic hepatitis C or oral contraceptives
porphyria cutanea tarda presentation
fragile, nonhealing blisters on sun-exposed areas with hyperpigmentation and hypertrichosis
porphyria cutanea tarda diagnosis
urinary uroporphyrins are elevated
porphyria cutanea tarda treatment
initial management is to stop alcohol and discontinue estrogens
barrier sun protection (not sunscreen)
if insufficient --> phlebotomy, deferoxamine, chloroquine
urticaria etiology
local skin anaphylaxis (IgE/mast cell mediated) without hypotension due to
drugs --> aspirin, NSAIDs, penicillins, morphine, codeine, quinolones
foods --> peanuts, shellfish, tomatoes, strawberries
insect bites and contact with latex
urticaria presentation
acute --> wheals and hives and itching within 30 minutes last for <24h
chronic --> skin reactions last >6 weeks associated with pressure on skin, cold or vibration
urticaria treatment
acute --> H1 antihistamines (diphenhydramine, cyproheptadine)
if life-threatening --> add H2 antihistamines + steroids
chronic --> nonsedating antihistamines loratadine, desloratadine, fexofenadine, cetirizine
most dangerous/avoid --> terfenadine, astemizole
desensitization --> when trigger can't be avoided, beta blockers must be stopped before
morbilliform rash
generalized maculo-papular rash that blanches with pressure (resembles measles), secondary to drug allergy; can appear days after exposure and after medication has been stopped; lymphocyt-mediated; treat antihistamines, steroids rarely necessary
hypersensitivity rashes
urticaria
morbilliform
erythema nodosum
erythema multiforme
Stevens-Johnson
toxic epidermal necrolysis
fixed drug reaction
erythema multiforme
most commonly due to herpes or mycoplasma infections
target-like lesions on palms and soles
don't involve mucous membranes
treat with antihistamines and underlying infection
Stevens-Johnson
<10-15% of body surface area with mucous membrane involvement in 90% of cases
treat with early admission to burn unit and if needed, mechanical ventilation
toxic epidermal necrolysis
involves 30-100% of body surface area; Nikolsky sign is present; clinical diagnosis; spesis is common cause of death but antibiotics are not used prophylactically; steroids not effective
fixed drug reaction
localized allergy to drugs; round, shaprly demarcated lesions that leave hyperpigmented spot after they resolve; treat with topical steroids
erythema nodosum etiology
localized skin reaction secondary to infections or inflammation
strep, coccidioides, histoplasma, syphilis, hepatitis
Crohn, UC, sarcoidosis
erythema nodosum presentation, diagnosis and treatment
multiple painful red raised nodules on anterior surface of lower limbs that do not ulcerate
ASO titers in case of strep
treat underlying disease and give NSAIDs and analgesics
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
capitis, corporis, unguium --> treat with oral terbinafine or itraconazole
cruris, pedis, mild corporis --> topical clotrimazole/ketoconazole
oral and IV anti-staph drugs
oral --> dicloxacillin, cefadroxil (preferred); IV --> cefazolin (preferred), oxacillin, nafcillin
impetigo
most commonly by staph or also by strep; affects only epidermis; lesions have purulent drainning material; treat with topical antibiotics (muciprocin, retapamulin) or oral if not effective (dicloxacillin, cephalexin)
erysipelas
most commonly by group A strep
involves dermis and epidermis with bright red swollen lesion, fever, chills and bacteremia
treat with oral or IV penicillins or cephalosporins
cellulitis
affects dermis and subcutaneous tissue; redness, swelling, warmth, tenderness without drainning lesions; treat with dicloxacillin or cefadroxil or if hypotension/sepsis --> IV oxacillin, nafcillin or cefazolin
folliculitis, furuncles, carbuncles
different stages of severity; carbucles are several confluent furuncles
furuncles and carbuncles are extremely tender
treat with systemic antistaph drugs and surgical drainage of carbuncles
necrotizing fascitis
by strep and clostridium
very high fever, portal of entry into skin, pain out of proportion, bullae and palpable crepitus
diagnose with elevated CPK and image that shows air in the tissue and necrosis
best initial step is surgery, then antistaph drugs
toxic shock syndrome presentation and diagnosis
3 or more:
fever >102
systolic pressure <90
desquamative rash
vomitting
involvement of mucous membranes
hyperbilirubinemia
theombocytopenia
there can also be increased CPK and liver enzymes, confusion and hypocalcemia
toxic shock syndrome treatment
fluid resuscitation + dopamine
empiric --> clindamycin + vancomycin
specific depending on methicillin resistance
staph scalded skin syndrome
from staph toxin; Nikolsky sign is present; normal blood pressure and no involvement of viscera; treat with antistaph IV drugs
anthrax
woolsorters and bioterrorism
papule that becomes inflamed and develops central necrosis
confirm with Gram and culture
treat with penicillin V or doxycycline
if terrorism treat with criprofloxacin
seborrheic keratosis
hyperpigmented lesions with stuck-on appearance on face, shoulders, chest and back of elderly; no malignant potential; removed for cosmetic issues with liquid nitrogen or curettage
actinic keratosis
asymptomatic lesions on sun-exposed areas of elderly can progress to SCC
treat with sunscreen and remove with cryotherapy, 5FU, imiquimod, topical retinoic acid, curettage
melanoma
malignant lesions grow in size, have irregular borders, uneven shape and incosistent coloring; full-thickness sample for biopsy; treat with excision
squamous cell carcinoma of skin
develops on sun-exposed areas of elderly
ulceration is common
metastases rare
diagnose with biopsy
treat with surgery
basal cell carcinoma
most common skin cancer
shiny or pearly lesion
rare metastases
diagnosis --> excisional biopsy
treatment --> surgery
kaposi sarcoma
purplish lesions on skin of HIV patients caused by HHV-8; treat with antiretrovirals; if CD4 doesn’t raise --> doxorubicin or vinblastine
psoriasis presentation
silvery scales on extensor surfaces, local or extensive, nail pitting, lesions with epidermal injury
psoriasis treatment
salicylic acid to remove scaly material
if localized --> topical steroids
severe diseases --> add coal
long-term --> calcipotriene (vitD) and tazarotene (vit A)
if large area --> UV light
if extensive and severe --> methotrexate
new agents --> alefacept, efalizumab, etanercept, infliximab
all patients should use emollients
atopic dermatitis presentation
allergy with high levels of IgE result in extremely pruritic, red, plaques on flexor surfaces
children may have it on cheeks and scalp
adults may have lichenification
atopic dermatitis treatment
preventive --> moist skin, emollients, avoid drying sopas, cotton clothes
active diseae --> topical steroids, antihistamines, coal and phototherapy
tacrolimus and pimecrolimus to decrease steroid use
itching --> doxepin
seborrheic dermatitis
scaly, greasy, flaky skin on scalp and face due to sebaceous secretion and pytirosporum ovale; treat with topical hydrocortisone or shampoos (ketoconazole, zinc pyrithione)
stasis dermatitis
hemosiderin hyperpigmentation from lower limb venous incompetence
prevent progression with elevation of legs
contact dermatitis
hypersensitivity to soap, detergents, latex, sunscreen, jewelry, nickel
linear streaked vesicles
confirm diagnosis with patch testing
treat with topical steroids and antihistamines
pityriasis rosea
pruritic, erythematous, salmon colored lesions spare palms and soles
clinical diagnosis, VDRL is negative
treat with topical steroids
scaling diseases
psoriasis, atopic dermatitis, seborrheic dermatitis, stasis dermatitis, contact dermatitis, pityriasis rosea
decubitus pressure ulcers
chronic sores where bone is close to skin in immobilized patients; stage I --> nonblanchable lesion; stage II --> superficial epidermis, partial dermis; stage III --> full skin thickness ecept fascia; stage IV --> all the way to bone; never culture or drain unless in surgery room for debridement; relieve pressure and if truly infected use antibiotics
alopecia areata
autoimmune destruction of hair follicles; treat with localized steroid injections
telogen effluvium
hair loss in response to big stress such as cancer or malnutrition
acne presentation
propionibacterium acne causes closed comedones, open comedones, pustules and cysts
acne treatment
mild --> topical clyndamycin, erythromycin, benzoyl peroxide, topical retinoids
moderate --> benzoyl peroxide with retinoids (tazarotene, tretinoin, adapalene)
severe --> systemic tetracyclines and isotretinoin
normal PA chest x-ray quality
1) centralized --> trachea and spinous apophysis are midway between clavicles 2) fully inhaled --> at least 10 ribs 3) exposure --> can see verterbra behind heart
x-ray for pneumothorax
should be expiratory looking for small lung fields and air in pleural space
anterior mediastinal masses on x-ray
seen on lateral view
thymus, thyroid, lymph nodes, teratoma
posterior mediastinal masses on x-ray
seen on lateral view; more likely a neurally derived tumor
detection of small pleural effusions on x-ray
blunting of costophrenic angle can start to show with 50mL on lateral chest x-ray; need 100mL for PA view
lateral chest x-ray hemidiaphragm
right hemidiaphragm crosses the heart
decubitus x-ray
with patient laying on his side; taken after PA or lateral film shows blunting of costophrenic angles; effusions will move with gravity, alveolar infiltrates do not
interstitial lung syndromes seen on x-ray
"SHIT FACED": Sarcoidosis, Histiocitosis, IPF, Tumor, Failure, Asbestosis, Collagen disorders, Environmental, Dust, Drugs; also pneumocystis, mycoplasma, viruses and chlamydia
emphysema x-ray
hyperinflation of lung fields, flattening of diaphragm, elongated heart, increased antero-posterior diameter (barrel chest)
pneumonia on x-ray
alveolar infiltrate makes lobes look whiter
silhouette sign --> border between affected lobe and denser surrounding area is obscured
lower lobe --> silhouette over hemidiaphragms
right-middle lobe --> obscures right heart border
upper lobe --> will not pass major fissure
interstitial pneumonia --> fine, lacy appearance in most lobes
chronic lung fibrosis --> reticulo-nodular pattern and honeycombing due to membrane thickening
congestive heart failure x-ray
cephalization --> apical blood vessels become prominent due to excess fluid; cardiomegaly, effusions and Kerley B-Lines
endotracheal tube chest x-ray
should be 1-2cm above carina
central venous line on chest x-ray
tip of catheter should be at junction of SVC and right atrium, where right mainstem bronchus is seen; not inside atrium
air under the diaphragm on x-ray
hyperlucidity seen over liver and spleen and under diaphragm in upright position
chest x-ray is initial test in perforation
high res CT indications
to detect lung parenchymal changes
1) symptomatic patients with normal x-ray
2) detecting metastatis, solitary nodules, bullae, bronchiectasis, diffuse parenchymal disease
3) guide for biopsy type and site
abodminal x-ray
used to detect obstruction such as voluvulus or Hirchsprung
uses of ultrasound
colelithiasis, nephrolithiasis (except retroperitoneal ureters), abdominal and pelvic masses, ascites, pregnancy, patients with contraindication of IV contrast agents, endoscopic ultrasound for pancreatic pathology
endoscopic retrograde cholangiopancreatography
catheter through sphicter of Oddi injects contrast materal
excellent for pancreatic strictures, stones and neoplastic masses
can perform removal of stones, dilate strictures and perform biopsy
barium studies
used for esophageal strictures, webs, Zenker
not as accurate as endoscopy for esophageal cancer (needs biopsy)
not as accurate as manometry for achalasia or muscular disorders
not as accurate as colonoscopy for colon
capsule endoscopy
used specially to visualize jejunum and ileum; if upper or lower endoscopy don't reveal source of bleeding then capsule endoscopy
HIDA
nuclear scan to visualize gallbladder for chocystitis; abnormal/positive --> no viasualization of gallbladder; normal/negative --> visualizes gallbladder
pet scanning
detects malignant versus benign thoracic cancers (after CT) by absorption of fluorodeoxyglucose; to asses cancer resection (if benign lung mass, more likely to be successful resection)
MRI
superior than CT for detection of stroke, cancer, multiple sclerosis, infection and visualize brainstem and cerebellum; stroke is visible in first 24 hours on MRI
CT scan
superior than MRI for detenction of blood so indicated for head trauma; to exclude hemorrhagic stroke if patient presents within 3 hours (to asses use of thrombolytics); detection of subarachnoid hemorrhage
contrast CT
used to detect abscess and infection which shows ring-enhancing lesion due to extravasation of blood through blood-brain barrier
bone scans
x-ray is first test for trauma and fracture; if suspicion of esteomyelitis then do x-ray first looking for elevation of periosteum; if its negative and still suspicious then do MRI
nonproliferative diabetic retinopathy
dilation of veins, microaneurysms, retinal edema, retinal hemorrhages due to glycolyzation of endothelial lining
proliferative diabetic retinopahty
neovascularization and vitreous hemorrhages
diabetic retinopathy diagnosis
yearly screening eye exam by opthalmologist for diabetics; fluorescein stain identifies vessels that should undergo laser photocoagulation
diabetic retinopathy treatment
tight control of glucose, blood pressure and lipids
aspirin, clopidogrel and antiplatelet therapy doesn’t work
retinal detachment etiology
spontaneous or trauma; predisposing factors: myopia, surgical extraction of cataracts, proliferative retinopathy, retinal vein occlusion, age-related macular degeneration
retinal detachment presentation
unilateral blurry vision without pain or redness, floaters and flashes in periphery vision
retinal detahcment diagnosis
opthalmologic exam
retinal detahcment treatment
lean head back
mechanical reatachment by photocoagulation, cryotherapy or injection of expansile gas into vitreal cavity
if all fails then remove vitreous humor and surgically reatach to sclera
age-related macular degeneration presentation
dry form --> slow progressive visual loss in elderly with presence of drunsen; wet --> rapid visual abnormalities due to abnormal growth of choroid vessels with subretinal exudative retinal detachment
age-related macular degeneration treatment
dry type --> no clear treatment; zinc and antioxidants may help
wet type --> laser photocoagulation and photodynamic therapy
photodynamic therapy
verteporfin is injected IV which is a photosensitive agent then photoactivating laser is applied
central retinal artery occlusion presentation
sudden, painless unilateral loss of vision without redness
opthalmoscopy shows pale retina and cherry-red spot at fovea
central retinal artery occlusion diagnosis
opthalmoscopic exam + carotid artery imaging
echocardiogram and evaluation of thrombophilia
central retinal artery occlusion etiology
carotid artery embolic disease
temporal arteritis
cardiac thrombi from myxoma
diseases of thrombophilia
central retinal artery occlusion treatment
similar to stroke or TIA
give O2 and occular masage
acetazolamide and thrombolytics may be used
central retinal vein occlusion
sudden, painless unilateral loss of vision without redness
funduscopy shows disk swelling, venous dilation, tortuosity and importantly retinal hemorrhages (difference with central retinal artery occlusion)
no specific treatment
glaucoma etiology
precipitated by anticholinergics such as ipratropium and tricyclics
open-angle glaucoma presentation and diagnosis
accounts for 90% of glaucoma
mostly asymptomatic
cup-to-disk ratio >0.3 confirmed by elevation of intraocular pressure by tonometry
open-angle glaucoma treatment
↓aqueous humor -->
betablockers (timolol, betaxolol, levobunolol)
alpha agonists (apraclonidine, brimonidine)
carbonic ahydrase inhibitors (dorzolamide, brinzolamide)

↑outflow -->
prostaglandins (latanoprost, travoprost) and pilocarpine

if medical treatment doesnt work --> laser trabeculoplasty, surgical trabeculectomy
closed-angle glaucoma presentation
eye is red
painful
hard to palpation
fixed midpoint pupil
clouded cornea
diminished visual acuity
closed-angle glaucoma treatment
opthalmologic emergency
IV azetazolamide, urea, osmotic diuretics
pilocarpine to open canal of Schelmm
betablockers to decrease production of aqueous humor
if all fails --> laser trabeculoplasty
cataracts
opacification of lens results in slow progressive blurry vision; diagnose with physical exam and slit lamp; treatment is surgical removal of lens with intraocular lens placement
conjunctivitis
bacterial --> unilateral red eye with discharge and little itching
treat with topical erythromycin, sulfacetamide, fluoroquinolones

viral --> more often bilateral, red eyes with severe itching
symptomatic treatment
subconjunctival hemorrahge
most commonly due to trauma
hematoma stops at limbus without intraocular or intravitreal damage
no impairment of vision
no specific therapy
herpes simplex keratitis
severe pain in the eye
dendritic pattern over cornea on fluorescein stain
therapy is oral acyclovir, famicyclovir, valacyclovir and topical trifluridin 1%
periorbital cellulitis
by staph or strep invading dermis surrounding the eye
treat with antistaph penicillins or first-gen ceph if allergy
uveitis etiology
psoriasis, sarcoidosis, syphilis, Reiter, inflammatory bowel disease
uveitis presentation
unilateral painful red eye with marked photophobia
uveitis diagnosis and treatment
inflammation of iris, cilliary body and choroid is visible by slit lamp
keratic precipitates may be visible in cornea
treat with topical or systemic steroids
anemia generalities
presentation --> fatigue, tiredness, exercise intolerance, dyspnea, tachycardia, angina, palpitations, lightheadedness, confusion

Hct < 41% in men or 36% in women
hemoglobin <13.5mg/dL in men or 12mg/dL in women
MCV < 80 --> microcytic; MCV >100 --> macrocytic
anemia general etiology
microcytic --> iron deficiency, thalassemia, sideroblastosis, lead poisoning

macrocytic --> folate or B12 deficiency, alcohol, liver disease, methotrexate, AZT, phenytoin

normocytic --> sickle cell, paroxysmal nocturnal hemoglobinuria, hereditary spherocytosis, G6PDH deficiency, drug-induced

AOCD can be micro or normocytic
anemia general diagnosis
determine hematocrit and hemoglobin
if anemia --> MCV
then iron levels, reticulocyte count, peripheral smear, RDW, Coombs, B12/folate levels or marrow biopsy depending on on the case
anemia general treatment
packed red blood cells to maintain hematocrit > 25-30%
hematocrit rises 3 points for every unit of red blood cells
iron deficiency anemia
general anemia symptoms plus brittle spoon-shaped nails, glossitis, pica
ferrtin<10ng/mL is highly specific but low sensitivity
↓serum iron, ↑TIBC, ↓MCV, ↓reticulocytes
ferrous sulfate tablets or parenteral iron in some cases
anemia of chronic disease
can't use storage iron of reticuloendothelial system with consequent excess
due to neoplasia, systemic inflammation or infection
general symptoms of anemia
normal or ↑ferritin, ↓serum iron and TIBC
treat underlying disease
iron or erythropoietin will not help except in renal failure or chemotherapy
sideroblastic anemia
defect in Hb synthesis with trapped iron in mitochondria of RBCs
genetic --> ALA deficiency or defect in B6 metabolism
acquired --> chloramphenicol, isoniazid, alcohol, lead poisoning
can be associated with myelodysplastic syndromes and can progress to AML
initial tests --> ↑ferritin, ↑serum iron, ↓TIBC
confirmation --> marrow smear shows ringed sideroblasts in Prussian blue stain
treatment --> remove causing agent, lead and iron chelators, B6 in some cases
alpha thalassemia presentation
1 gene deletion is asymptomiaic
2-gene deletion presents with mild anemia (Hct 30-40%) and profound microcytosis
3-gene deletion presents with severe anemia (Hct 20-30%) and profound microcytosis
4-gene deletion patients die in utero
alpha thalassemia diagnosis and treatment
anemia with profound microcytosis and target cells are clues
normal iron studies with microcytosis make diagnosis
Hb electrophoresis determines type and has normal HbF and HbA2 with HbH in 3 or 4 gene deletion
no specific treatment required
beta thalassemia presentation
beta thalassemia minor --> mild anemia and profound microcytosis

beta thalassemia major --> profound anemia and microcytosis, symptoms start when HbF decreases 6 months after birth; growth failure, bone deformities, hepatosplenomegaly, jaundice

beta thalassemia major requires monthly transfusions which lead to iron overload (managed with deferasirox), hemochromatosis, cirrhosis, CHF
beta thalassemia diagnosis and treatment
anemia + microcytosis
electrophoresis shows increased HbA2 and HbF
beta thalassemia major requires monthly transfusions and deferasirox for iron overload
may do splenectomy or marrow transplant
B12 deficiency etiology
atrophic gastritis, gastrectomy, Crohn, sprue, pancreatic insuficiency, D. latum
B12 deficiency presentation
anemia of varying severity and neurologic symptoms of any kind alone or in combination
may have glositis, diarrhea or abdominal pain
B12 deficiency diagnosis and treatment
made by showing anemia and macrocytosis
anti-intrinsic factor antibodies in pernicious anemia
hypersegmented neutrophils, macro-ovalocytes
hypercellular marrow, pancytopenia
↑LDH, ↑billirubin, ↑iron
may do Schilling test
treat --> intramuscular B12
Folic acid deficiency
due to ↓intake (diet, alcoholics)
↑requirements (pregnancy)
↑loss (eczema, dialysis, phenytoin)
general anemia presentation depending on severity
diagnosis --> ↓Hb and ↓folic acid levels
may show macro-ovalocytes, hypersegmented neutrophils
sickle cell disease etiology
autosomal recessive substitution of valine for glutamic acid at sixth amino acid of beta globin chain; painful crisis can be spontaneous or precipitated by fever, acidosis, dehydration, infection and fever
sickle cell disease presentation
symptoms of anemia
chronic manifestations --> isothenuria, ulcerations of the skin of the legs, bilirubin gallstones, asceptic necrosis of femoral head, osteomyelitis, retinopathy, recurrent pneumococcus or Haemophilus infections, growth retardation, splenomegaly/splenectomy

acute painful crisis --> back, rib, chest and leg pain
acute chest syndrome --> indistiguishable from pneumonia, severe chest pain, fever leukocytosis, hypoxia, x-ray lung infiltrates, pripapism, blindness, MI, abortions
sickle cell disease diagnosis
mild to moderate anemia plus normal MCV
sickle cells on peripheral smear
high reticulocyte count
↑bilrubin, ↑LDH
microhematuria
leukocytosis
electrophoresis is the most specific test
also sickle cell prep test
sickle cell disease management
acute pain crisis --> fluids, analgesics, oxygen
if fever/leukocytosis --> ceftriaxone or cefotaxime
severe manifestations such as priapism and cardiac --> packed RBCs if hematocrit is low or exchange transfusion if high

chronic management --> folic acid, pneumococcus and influenza vaccinations and hydroxyurea to decrease frequency of vaso-oclusive/pain crisis
autoimmune/drug-induced hemolytic anemia etiology
IgG antibodies against RBC membrane with destruction mostly in spleen by macrophages
idiopathic or secondary to
leukemias (CLL), lymphoma, viral infections
collagen vascular diseases, lupus
penicillins, cephs, sulfas, quinidine, methyldopa, procainamide, rifampin, thiazides
autoimmune/drug-induced hemolytic anemia presentation
symptoms related to severity
sudden onset may have fever, syncope, CHF, hemoglobinuria, weakness, pallor, jaundice, dark urine
autoimmune/drug-induced hemolytic anemia diagnosis and treatment
normocytic anemia, reticulocytosis, ↑LDH, ↓haptoglobin, ↑indirect bilirubin
Coombs test is specific
mild disease does not require specific treatment
steroids in more severe disease
splenectomy if unresponsive
cold agglutinin anemia etiology
IgM against RBC membrane in response to lymphoma, Waldenstrom, mycoplasma or mononucleosis, ulcerative colitis
RBCs destroyed in liver
cold agglutinin anemia presentation
symptoms related to severity
cyanosis in nose, ears, fingers and toes
weakness, pallor
jaundice, dark urine
cold agglutinin anemia diagnosis and treatment
normocytic anemia, reticulocytosis, ↑LDH, ↓haptoglobin, ↑indirect bilirubin, often spherocytes
Coombs test is specific
mild disease does not require specific treatment
steroids or splenectomy won't work
managed by avoiding cold weather or with azathiorpine, cyclosporine, cyclophosphamide, rituximab (anti-CD20 Ab)
hereditary spherocytosis etiology
autosomal dominant defect in spectrin of RBC membrane;
hereditary spherocytosis presentation
mild to moderate symptoms of anemia, spherocytes
splenomegaly and jaundice
sometimes cholecystitis
hereditary spherocytosis diagnosis and treatment
anemia, normal MCV, ↑LDH, ↑reticulocytes, ↑indirect bilirubin
spherocytes and negative Coombs test
positive osmotic fragility test
treat with folate or splenectomy
paroxysmal nocturnal hemoglobinuria etiology
red cell membrane defect in phosphatidyl inositol glycan A leads to increased complement lysis and intravascular hemolysis
paroxysmal nocturnal hemoglobinuria presentation
symptoms of anemia acording to severity
hemoglobinuria (specially in morning urine)
thrombosis (specially hepatic vein, Budd-Chiari)
paroxysmal nocturnal hemoglobinuria diagnosis and treatment
↓DAF, hematuria
normal MCV, ↑LDH, ↑reticulocytes, ↑indirect bilirubin, ↓haptoglobin
specific tests are sugar-water test and acidified hemolysis test
treat with folate, corticosteroids and anticoagulation for thrombosis
G6PDH deficiency
enzyme deficiency leads to ↓NADPH, ↓gluthathione peroxidase activity and ↑unmetabolized H2O2 which precipitates Hb (Heinz bodies)

precitpitated by infections, sulfa drugs, primiquine, quinidine, dapsone, nitrofurantoin

presentation --> sudden-onset anemia symptoms, jaundice, dark urine
normal MCV, ↑indirect bilirubin, ↑LDH, ↑reticulocytes, ↓haptoglobin, hemoglobinuria, Heinz bodies, bite cells

definitive test is ↓G6PDH

treat with hydrration
aplastic anemia etiology
most common is idiopathic; radiation, benzene, NSAIDs, chloranphenicol, alcohol, alkylating agents; infections: hepatitis, HIV, CMV, EBV, ParvoB19;
aplastic anemia presentation
bleeding from thrombocytopenia
fatigue, anemia and may have infections from neutropenia
may have history of using precipitating drugs
aplastic anemia diagnosis and treatment
screening --> pancytopenia
confirm --> bone marrow biopsy showing absence of marrow cells, fat and no signs of cancer, infection or fibrosis in marrow

treat --> bone marrow transplant; if not, antithymocyte globulin, cyclosporine and prednisone
acute leukemia etiology
most have no apparent cause; associated with radiation, benzene, melphalan, etoposide, retroviruses, Down and Klinefelter, myelodysplasia and sideroblastic anemia
acute leukemia presentation
fatigue, anemia and bleeding from thrombocytopenia +- leukopenia or leukocytosis
ALL --> in children, hepatosplenomegaly, lymphadenopathy, bone pain
AML --> DIC (promyelocytic M3), CNS meningitis-like (monocytic M4, M5)
acute leukemia diagnosis
pancytopenia although leukocytes can be up, down or normal
leukemic blasts in peripheral blood
bone marrow biopsy showing >20% blasts confirms diagnosis

to differentiate -->
AML --> Auer rods (specially M3), myeloperoxidase and esterase
ALL --> CALLA and TdT
specific types of leukemia are diagnosed with monoclonal antibodies
acute leukemia treatment
AML --> AraC with danourubicin or idarubicin
ALL --> daunorubicin, vincristine and prednisone
add all-trans-retinoic acid in promyelocytic leukemia
remission is removal of 99.9% of leukemic cells and elimination of blasts in peripheral blood
differential diagnosis for pancytopenia
marrow --> aplastic anemia, metastatic cancer to marrow, myelofibrosis
infectious --> parvirus, retrovirus
auto-immune --> B12 deficiency, SLE, hypersplenism
drugs --> chloramphenicol
acute leukemia is only one that shows blasts in peripheral blood
chronic myelogenous leukemia etiology
clonal disorder of myelocytes associated in 95%with translocation t(9,22) (Philadelphia chromosome) which produces an enzyme with tyrosine kinase activity
chronic myelogenous leukemia presentation
leukocytosis and sometimes thrombocytosis lead to
fatigue, night sweats, low-grade fever
abdominal pain, splenomegaly, bone pain
rare --> lymphadenopathy, infection or bleeding
leukostasis has dyspnea, blurry vision, priapism, thrombosis, stroke
chronic myelogenous leukemia diagnosis
leukocytosis (mostly neutrophils)
↓LAP (difference with leukemoid reaction)
absent or very low blast count
if leukocytosis and ↓LAP --> check for Philadelphia chromosome
chronic myelogenous leukemia treatment
imatinib is an inhibitor of the tyrosine kinase produced by disease
90% hematologic response and 60-70% loose Philadephia chromosome
if imatinib doesn’t work --> bone marrow transplant
chronic lymphocytic leukemia presentation
older patients can be asymptomatic
0 --> lymphocytosis alone
1 --> lymphadenopathy
2 --> splenomegaly
3 --> anemia
4 --> thrombocytopenia
infection and bleeding are unusual
survival of stage 0-1 is 10-12 years
survival of 3-4 is 1-2 years
chronic lymphocytic leukemia diagnosis
suspected in older patient with leukocytosis (80-98% lymphocytes)
bone marrow biopsy confirms leukemic lymphocytes
smudge cells on peripheral smear
chronic lymphocytic leukemia treatment
stages 0-1, no specific treatment
symptomatic patients are given fludarabine (DOC) or chlorambucil
prednisone for autoimmune hemolysis and thrombocytopenia
pentostatin for relapses
multiple myeloma presentation
bone pain (specially back, ribs), lytic lessions, osteoporoosis, pathologic fractures
hypercalcemia (polyuria, polydipsia, altered mental status)
renal failure (Bence Jones light chains)
infection with encapsulated bugs
anemia
multiple myeloma diagnosis
normo normo anemia, hypercalcemia, ↑BUN, ↑creatinine
lytic bone lessions on x-rays
Bence Jones protein
↑serum microglobulin B2 (75%)
electrophoresis with monoclonal IgG spikes
cofirmation --> bone marrow biopsy showing >10%plasma cells confirms
multiple myeloma treatment
younger patients --> transplant (pre-treat with thalidomide, dexamethasone)
older patients --> melphalon, prednisone, thalidomide
treat hypercalcemia with loop diuretics
monoclonal gammopathy of uncertain origin
overproduction of clonal immunoglobulin by plasma cells without systemic manifestations
patient is asymptomatic
clue to diagnosis is elevated serum protein
monoclonal Ig spike on protein electrophoresis
no bone lessions, no anemia, no renal failure, no hypercalcemia
no treatment necessary
Hodgkin disease presentation
nontender lynmphadenopathy
cervical, supraclavicular or axillary nodes are most common
B symptoms are drenching night sweats, 10% weight loss, fever
Hodgkin disease diagnosis
first step --> excisional lymph node biopsy showing Reed-Sternberg cells
second step --> determine staging with CT
if CT is unrevealing and radiotherapy is contemplated then do laparotomy
also anemia, leukocytosis, eosinophillia, ↑LDH, ↑ESR (adverse prognosis) may be seen
Hodgkin disease adverse prognostic factors
large mediastinal lymphadenopathy
age older than 40
B symptoms
↑ESR
Hodgkin disease treatment
stage I and II --> radiotherapy
B symptoms or stage III or IV --> ABVD chemo (adriamycin, bleomycin, vinblastine, dacarbazine) has less side effects than MOPP chemo (meclorethamine, oncovin/vincristine, prednisone, procarbazine)

potential side effects --> permanent sterility, cancer, leukemia, aplastic anemia, peripheral neuropathy
non-Hodgkin lymphoma etiology
HIV, hepatitis C, EPV, HTLV-1, H. pylori
HIV and EPV are associated with Burkitt and high-grade high-stage lymphomas
non-Hodgkin lymphoma presentation
nontender lymphadenopathy with rubbery consistency
B symptoms --> drenching night sweats, 10% weight loss, fever
cervical/supraclavicular --> 10-20%
more likley to involve extra-lymphatic sites
non-Hodgkin lymphoma diagnosis
first test --> excisional lymph node biopsy which excludes Reed-Sternberg cells
staging --> CT; laparotomy is not needed
may do marrow biopsy
also anemia, leukocytosis, eosinophillia, ↑LDH, ↑ESR may be seen
non-Hodgkin lymphoma treatment
stages I and II --> radiotherapy
B symptoms or stages II or III --> CHOP chemo (cyclophosphamide, hydroxy-adriamycin, oncovin/vincristine, prednisone)
if CNS lymphoma give radiotherapy with CHOP
treat relapse with bone marrow transplant
Hodgkin and non-Hodgkin staging
stage I --> one lymphatic group or extra-lymphatic tissue
stage II --> two lymphatic groups or extra-lymphatic tissue on same side of diaphragm
stage III --> lymph nodes on both side of diaphragm or extralymphatic involvement contiguous to primary site
stage IV --> widespread lymph involvement or diffuse extra lymphatic sites
idiopathic thrombocytopenic purpura
antibodies against platelets leads to destruction and bleeding

epistaxis, bruising, petechiae, echymoses
hematuria, dysfunctional uterine bleeding, GI bleeding

thrombocytopenia is found and splenomegaly is absent

exclude HUS, TTP, DIC --> peripheral smear without schistocytes and normal creatinine
exclude marrow thrombocytopenia --> marrow biopsy with normal megakaryocytes

treat with prednisone or splenectomy if unresponsive
von Willebrand disease etiology
autosomal dominant defect in factor VIII production results in inability of platelets to adhere to vascular endothelium; aggregation is normal
von Willedrand disease presentation
petechiae, echymoses, epistaxis, bruising
hematuria, dysfunctional uterine bleeding, GI bleeding
increased with aspirin
von Willebrand disease diagnosis
platelet count is normal, ↑PTT, ↑BT
↓factor VIII antigen (vWB factor)
abormal ristocetin test
von Willebrand disease treatment
desmopressin used in mild bleeding and before minor surgery
if moderate to severe symptoms give factor VIII
avoid aspirin
causes of prolonged PT only
inherited --> factor VII deficiency
acquired --> vitamin K deficiency, liver disease, warfarin
causes of prolonged PTT only
inherited --> vWF, factors VIII, IX, XI or XII deficiencies
acquired --> heparin, antiphospholipid antibody
causes of prolonged PT and PTT
inherited --> prothrombin, fibrinogen, factors V or X deficiencies
acquired --> liver disease, vitamin K deficiency, DIC, supratherapeutic heparin or warfarin, inhibitors (thrombin, prothrombin, fibrinogen, factor V or factor X)
hemophilia etiology
x-linked recessive; manifests in males; females are carriers
hemophilia presentation
obvious by age 2, apparent at time of circumcision
mild deficiencies --> asymptomatic
severe deficiencies (<5-10% activity) --> factor-type bleeding, hemarthrosis, hematoma, GI or urinary bleeding, bruising or CNS bleeding
hemophilia diagnosis
prolonged PTT, normal PT

mixing study indicates deficiency when PTT corrects to normal in 50:50 mixture patient and control blood

if it doesn't correct, factor inhibitor is cause, not deficiency

specific factor VIII or IX levels are necessary for precise diagnosis
hemophilia treatment
mild hemophilia A is treated with desmopressin
severe deficiencies treated with specific factor replacement
desmopressin doesn't work in hemophilia B
vitamin K deficiency
decreased factors 2, 7, 9, 10 due to dietary deficiency of vitamin K, malabsorption or antibiotics

presentation --> hemarthrosis, hematoma, GI or urinary bleeding
evident as oozing at venapuncture sites
PT and PTT are elevated

diagnosis --> confirmed after vitamin K injection and PT/PTT correction

treat severe bleeding with fresh frozen plasma and vitamin K infusion
liver disease coagulopathy
decreased clotting factors except 8 and vWB
due to severe liver disease or cirrhosis
presents with bleeding, elevation of PT and PTT
clinically indistinguishable from vitamin K deficiency except that it doesn’t correct with infusion
low platelets due to acompanying hypersplenism
treat with fresh frozen plasma and management of liver condition
disseminated intravascular coagulation etiology
idiopathic
sepsis
pancreatitis
promyelocytic leukemia
rhabdomyoloysis
adenocarcinomas
heatstroke
transfusion reactions
burns
trauma
abruptio placenta
amniotic fluid embolism
snakebites
disseminated intravascular coagulation presentation
factor-type and platelet-type bleeding at any site
hemolysis can lead to acute renal failure, jaundice, confusion
disseminated intravascular coagulation diagnosis
↑PT/PTT
↓platelets
↓fibrinogen
↑fibrinogen split products and d-dimers
schistocytes present in peripheral smear
disseminated intravascular coagulation treatment
fresh frozen plasma and maybe platelet transfusions; correct underlying disorder
pulmonary function tests
spirometry (mechanical ventilation)
Dlco (gas exchange)
methacholine challenge test (bronchial hyperreactivity)
TLC
restrictive pattern
FEV1/FVC > 80%
obstructive pattern
FEV1/FVC < 80%
seen in emphysema, chronic bronchitis, asthma, bronchiectasis
↓DLco
if FEV1/FVC < 80% suggests emphysema
if FEV1/FVC > 80% suggests interstitial lung disease or mild left heart failure
↑DLco
suggests hemorrhage such as in Goodpasture
methacholine test
bronchoprovocation in patients with cough or wheezing who have normal pulmonary function tests, for possible asthma
do basal and postprovocation spirometry
postitive test if baseline FEV1 decreased >20%
A-a gradient formula
150 - (1.25 x PaCO2) - PaO2 normal: 5-15mmHg; increases with age and all forms of hypoxemia except hypoventilation and high altitude
solitary pulmonary nodule
1/3 are malignant
first step in management is looking for previous image study
if none available then consider if patient is high or low risk for cancer
low risk nonsmoker <35 --> x-ray every 3 months for 2 years, if no growth stop follow-up
high risk smoker >50 --> open-lung biopsy and removal due to cancer risk
transudative pleural effusion
↓hydrostatic pressure or ↓oncotic pressure; usually bilateral and equal
low LDH and proteins in fluid and serum (200, 0.6, 0.5)
need all three values for diagnosis, else exudate
exudative pleural effusion
due to local process; usually unilateral; need further investigation; high LDH and proteins in fluid and serum (200, 0.6, 0.5); don't need all three values high to make diagnosis
transudative causes of pleural effusion
heart failure
nephrotic syndrome
liver disease
pulmonary embolism
atelectasis
exudative causes of pleural effusion
pneumonia
cancer (lung, breast or lymphoma)
pulmonary embolism
drug-induced
pancreatitis
TB
RA
SLE
transudative pleural effusion with no apparent cause
consider pulmonary embolism which can be either transudative or exudative
indications of thoracocentesis
any new and unexplained pleural effusion --> rule out empyema
decubitus x-ray --> <1cm free-flowing fluid --> minimal risk
if non-free fluid need ultrasound guidance
malignant pleural effusions
due mostly to breast cancer, lung cancer and lymphoma
send thoracocentesis fluid for cytologic exam also
hemorrhagic pleural effusion
seen in mesothelioma, metastatic lung or breast cancer, pulmonary embolism with infarction and trauma
lymphocytic-predominant pleural effusions
suggests TB due to tuberculin hypersensitivity
check ↑adenosine deaminase and postivie PCR for TB
acid-fast and culture of fluid are only positive in 30%
respiratory compromise and distress
presents with shortness of breath, dyspnea, tachypnea (>30) and associated symptoms such as agitation, confusion or ↓consciousness
evaluation of respiratory distress
ensure patent airway
focus on quickness of onset and associated symptoms
most important lab test is arterial blood gases then B-natriuretic peptide and chest x-ray
acute respiratory distress with fever, cough or sputum
suggests infectious etiology
acute respiratory distress without systemic symptoms
suggests airway obstruction, cardiac disease or thromboembolism
chronic respiratory distress
suggests interstitial lung disease or COPD
common lung physical exam findings
diffuse wheezing --> asthma
localized wheezing --> foreign object
rales --> pneumonia, interstitial disease, heart failure
dull percusion --> pneumonia or atelectasis
normal exam --> pneumocystis jirovecci, central respiratory problems
B-natriuretic peptide in acute dyspnea
elevation is sensitive for heart failure but can also be elevated in cor pulmonale and acute right ventricular failure (thromboembolism)
chest x-ray without parenchymal infiltrates in acute dyspnea
suggests thromboembolism
central respiratory depression
neuromuscular disease
upper airway obstruction
chest x-ray hyperinflation in acute dyspnea
suggests asthma and COPD
chest x-ray with focal infiltrates in acute dyspnea
suggests bacterial, viral or fungal pneumonia, aspiration or pulmonary hemorrhage
chest x-ray with diffuse edema in acute dyspnea
suggests heart failure or ARDS
ICU indications in respiratory failure
persistent hypoxemia --> hospitalization

ICU indications -->
need for mechanical ventilation
close monitoring
increasing oxygen demand
continuous nursing
indications for intubation and/or mechanical ventilation
respiratory acidosis and hypercapnia in asthmatic patient
upper airway injury (burns, laryngeal edema, trauma)
neurologic airway depression (often with loss of gag and cough reflexes)
respiratory distress in hospitalized patients
inpatient who develops dyspnea, tachypnea and/or hypoxemia should raise possiblity of pulmonary embolism or aspiration
types of asthma
intrinsic (50%) is secondary to nonimmunologic stimuli (infections, irritating inhalants, cold air and emotional); extrinsic (20%) due to allergens
asthma stimuli
infections (RSV, rhinovirus), drugs (aspirin/NSAIDs, coloring agents, betablockers), allergens, cold air, emotions
asthma presentation
tachypnea, tachycardia, diffuse wheezing, use of accesory muscles, diminished breath sounds, hyperresonance, intercostal retractions
asthma poor prognosis factors
fatigue
diaphoresis
pulsus paradoxus
inaudible breath sounds
decreased wheezing
cyanosis
bradycardia
asthma diagnosis
initial tests for acute attacks --> ↓PaCO2, ↑pH, normal or ↓PaO2
severe attack -->↓PaO2, ↑PaCO2, ↓pH
chest x-ray to rule out infection as cause
spirometry --> obstructive pattern that reverses with beta agonist (FEV1 reverses by 12%)
methacholine test --> ↓FEV1/FVC of 20%
acute asthma management
O2
metered inhaled beta agonists --> albuterol/salbutamol, terbutaline
salmeterol is long-lasting for nocturnal variant
catecholamines may be used but not routinely
aminophylline and theophyline have modest potency and are not routine
anticholinergics (ipratropium) if heart disease (slow onset, medium potency)
chronic asthma management
acute exacerbations: systemic prednisone 10-14 days along with inhaled albuterol; inhaled corticosteroids are first line maintenance; cromolyn is first line maintenance in children and prophylaxis in adults; zileuton, zafirlukast, mmonteleukast for severe asthma resistant to maximum doses of inhaled steroids
mild asthma definition and treatment
symptoms ~2 days/week and rare night symptoms
FEV1 is normal
no long-term control needed only inhaled beta agonists for attacks
moderate asthma definition and treatment
symptoms on most days and at least 5 nights/month with FEV1 60-80%
treat with daily inhaled steroids (also cromolyn specially in children)
maybe also salmeterol
severe asthma definition and treatment
daily symptoms, frequent night symptoms and hospital emergencies with FEV1 <60%; daily inhaled steroids, daily inhaled salmeterol along with antileukotriene drug and possibly low-dose oral steroid
physical exam in emphysema
distant breath sounds
pink skin
thin
barrel chest
accesory muscles
symptoms of right heart failure and clubbing
physical exam in chronic bronchitis
rhonchi and wheezes
signs of cyanosis
weight gain
symptoms of right heart failure and clubbing
chest x-ray findings in COPD
chronic bronchitis --> increased pulmonary markings
emphysema --> bilateral hyperinflantion, diaphragm flattening, small heart size, increase in retrosternal space
COPD diagnosis
↓FEV1/FVC
FEF 25-75
↑RV and TLC
emphysema has ↓DLco and chronic bronchitis has normal DLco
FEV1/FVC after bronchodilation will stay the same
COPD complications
hypoxemia with nocturnal desaturation
secondary erythrocytosis
cor pulmonale
chronic ventilatory failure
CO2 retention
maintenance treatment for COPD
first-line --> ipratropium via metered inhaler; inhaled beta agonists can be used concomitantly; inhaled corticosteroids are not used in COPD; if above fails --> theophylline (watch for cytochrome inhibitors and inducers)
only treatment that reduces mortality in COPD
home O2 supplementation and smoking cessation
home oxygen for hypoxemia (PaO2<55mmHg or saturation <88%)
pneumococcal vaccine every 5 years, influenza vaccine yearly and haemophilus vaccine if unvaccinated
COPD exacerbation general management
1) measure O2 saturation (pulse oximetry)
2) arterial blood gases
3) chest x-ray
4) check theophylline levels
5) CBC and ECG
6) hospital admission if significant hypercapnia or hypoxemia
7) consider intubation and mechanical ventilation
8) specific treament
spirometry is NOT done or useful in exacerbation
COPD exacerbation specific treatment
1) O2 supplementation
2) inhaled bronchodilators and anticholinergics concomitantly
3) IV or oral prednisone for 2 weeks
4) antibiotics despite normal x-ray
5) council on smoking cessation
6) teach optimal use of MDI
no benefit in IV theophylline and avoid opiates and sedatives
bronchiectasis etiology
secondary to recurrent pneumonias, TB, fungal or abscess
cystic fibrosis, immotile cilia syndrome (50% Kartagener)
bronchiectasis presentation
suspect in anyone with
chronic cough
foul-smelling sputum
hemoptysis
recurrent pulmonary infections
sinusitis
immune deficiencies

presents with purulent copious sputum, wheezes, crackles and history of recurrent pneumonias (specially gram- and pseudomonas)
bronchiectasis diagnosis
early chest x-ray may be normal or severe cases show 1-2cm cysts and crowding of bronchi; chest CT is best noninvasive test
bronchiectasis treatment
bronchodilators, chest physical therapy, postural drainage, rotating gram- antibiotics
surgery in cases of localized bronchiectasis or massive hemoptysis
yearly influenza vaccine and pneumococcal vaccine with booster at 5 years
bronchiectasis complications
massive hemoptysis, amyloidosis, cor pulmonale, visceral abscesses
interstitial lung disease general presentation
exertional dyspnea
nonproductive cough
crackles
pulmonary hypertension
clubbing
restrictive pattern
interstitial lung diseases
idiopathic pulmonary fibrosis
sarcoidosis
pneumoconiosis --> asbestosis, silicosis, coal pneumoconiosis
idiopathic pulmonary fibrosis presentation
exercise intolerance, dyspnea, coarse crackles
idiopathic pulmonary fibrosis diagnosis
reticular or reticulonodular pattern on chest x-ray
restrictive pattern on PFTs
increased macrophages on bronchoalveolar lavage (nonspecific)
idiopathic pulmonary fibrosis treatment
steroids with or without azathioprine works in 20%; the rest develop fatal lung disease
idiopathic pulmonary fibrosis prognosis
20-40% 5-year survival; best prognostic factor is response to steroids as evidenced in PFTs
sarcoidosis presentation
"GRAIN"
gammaglubilinemia
rheumatoid arthritis
ACE increase
interstitial fibrosis
non-casseating granuloma
hilar and left paratracheal adenopathy
hypercalcemia due to vitamin activation by macrophages
uveitis/conjunctivitis in >25%
chest x-ray findings
restrictive or normal PFTs
chest x-ray findings in sarcoidosis
four stages found (not progressive)
bilateral hilar adenopathy
hilar adenopathy with reticulonodular parenchyma
reticulonodular parenchyma alone
honeycombing of bilateral lung fields with fibrosis
sarcoidosis diagnosis
biopsy of affected tissue showing noncasseating granulomas; all patients should have ophthalmologic exam
sarcoidosis prognosis
80% remain stable or spontaseoulsy resolves; 20% progress to organ compromise
sarcoidosis treatment
no treatment is effective
if organ compromise may use trial of high-dose steroids
if uveitis, CNS involvement or hypercalcemia --> steroids are mandatory
pneumoconiosis general presentation
dyspnea, shortness of breath, cough, sputum, cor pulmonale, clubbing, restrictive pattern, ↓DLco, hypoxemia with ↑A-a
ocupations associated with asbestosis
mining, milling, foundry work, shipyards, pipes, break linings, insulation, boilers; history of exposure necessary for Dx
asbestosis x-ray findings
diffuse or local pleural thickening, pleural plaques, calcifications near diaphragm, pleural effusions, lower lobe interstitial infiltrate
asbestosis associated cancers
lung adenocarcinoma or SCC
pleural mesothelioma is less common
asbestosis diagnosis
history of exposure + lung biopsy showing barbell-shaped asbestos fibers
asbestosis treatment
no effective treatment; must stop smoking due 75x increased risk of cancer
ocupations associated with silicosis
mining, quarrying, tunneling, glass and pottery making, sandblasting
silicosis x-ray findings
1-10mm nodules throughout the lungs, most prominent in upper lobes
in progressive massive fibrosis nodules are >10mm and coalesce
silicosis diagnosis
history of exposure + lung biopsy showing silica particles
pathologic lesion is the hyaline nodule
silicosis treatment
no effective treatment; should have yearly PPD test and if >10mm --> INH prophylaxis for 9 months
Lofgren syndrome
acute sarcoidosis presentation with erythema nodosum, arthritis, hilar adenopathy
Heefordt-Waldenstrom syndrome
acute sarcoidosis presentation with fever, parotid enlargement, uveitis and facial palsy
Caplan syndrome
rheumatoid nodules in periphery of lung, rheumatoid arthritis and coesxisting pneumoconiosis (usually CWP)
coal worker's pneumoconiosis x-ray findings
small round parenchymal densities
usually in upper half of lungs
progressive massive fibrosis has 1cm densities in whole lung
coal worker's pneumoconiosis immunologic findings
↑IgA, ↑IgG, ↑C3, ANA and rheumatoid factor
pulmonary embolus site of origin
most are from above-the-knee deep veins which result from distal deep vein thrombosis; in patients with catheters it can originate from upper limb, subclavian and internal jugular veins
criteria for high-risk pulmonary embolism patients
recent surgery (specially orthopedic, knee replacement has 70% risk); cancer history (prostate, breast, pelvic, abdominal); immobilized patients; acquired thrombophilia (lupus anticoagulant, nephrotic syndrome); oral contraceptives; inherited thrombophilia (factor V Leiden, protein C/S deficiency, antithrombin III deficiency); pregnancy; need 1 risk factor and consistent signs and symptoms for high-risk label
signs and symptoms consistent with pulmonary embolism
sudden onset of dyspnea, tachypnea, thigh/calf swelling, pleuritic chest pain, hemoptysis, tachycardia, ↑P2
when to consider pulmonary embolism
all patients with dyspnea and normal chest x-ray
nonspecific routine tests for dyspnea; may suggest PE
arterial blood gases show hypoxemia with ↑A-a
chest x-ray (normal in PE)
ECG (to exclude others) shows S1, Q3, T3, tachycardia
specific tests for pulmonary embolism
best initial test is spiral CT scan; V/Q scan (if normal excludes PE); angiogram is gold standard
deep venous thrombosis specific tests
best intial test is compression or duplex ultrasound; venogram is rarely done; MRI
tests for DVT and PE
D-dimer is most sensitive; can only exclude thromboembolism if normal levels
may also be high in surgery, infection, trauma, pregnancy and DIC
normal D-dimer and CT scan rule out thromboembolism in 98% of low-risk patients
tests results that exclude pulmonary embolism
normal CT + normal D-dimer in low-risk patients
normal CT + normal doppler in low-risk patients
V/Q scan is completely normal
generalities of pulmonary embolism diagnosis
all patients should be on heparin during diagnosis and imaging; if PE is suspected start CT scan right after chest x-ray; if all tests are negative but it's high-risk patient --> angiogram; normal CT + normal D-dimer or doppler excludes PE in low-risk patients
pulmonary embolism treatment
1) O2
2) start heparin before confirmation and during work-up
3) concomitant warfarin
4) if hemodynamically unstable or massive PE --> thrombolytics (tPa, streptokinase)
heparin considerations in pulmonary embolism
if LMWH then no need to follow PTT and less chance of heparin-induced thrombocytopenia
HIT is associated with more thrombotic events, not bleeding diathesis, and is treated with new anticoagulants (argatroban, lepirudin)
start heparin immediately
warfarin considerations in pulmonary embolism
monitor PT
titrate to INR of 2-3
skin necrosis can occur if protein C deficiency already present
contraindicated in pregnancy (use LMWH 6 months instead)
contraindications of anticoagulation therapy in PE
contraindicated in patients with recent neurosurgery or eye surgery; use inferior vena cava filter instead
post thrombotic syndrome
pain
edema
hyperpigmentation
skin ulceration in 2/3 of PE patients
compression stockings can prevent it
fat embolism
acute dyspnea, petechiae in neck or axilla, confusion, 3 days after long bone fracture or after CPR; no anticoagulation necessary
ARDS etiology
sepsis
trauma
DIC
Goodpasture
SLE
drug overdose
toxin inhalation
drowning
ARDS presentation
dyspnea, tachypnea, diffuse rales and ronchi
ARDS diagnosis
chest x-ray --> diffuse interstitial or alveolar infiltrates
ABGs --> ↓PaO2, ↑PaCO2
Swan-Ganz --> normal cardiac output and capillary wedge pressure but ↑pulmonary artery pressure
ARDS treatment
treat underlying cause; mechanical ventialtion with positive end-expiratory pressure
ARDS prognosis
70% mortality
sleep apnea
cessation of airflow >10s at least 10-15/hour of sleep + daytime somnolence
confirm with polysomnography
treat obstructive with weight loss and nasal continuous positive airway pressure (CPAP)
treat central with acetazolamide, progesterone and O2
lung cancer etiology
90% of cases are directly related to cigarette smoke; nonsmokers develop adenocarcinoma; all lung cancers are associated with smoking; active smokers have 10x greater risk; 40 pack-year history increases risk 60-70x; asbestos increases risk 75x
types of lung cancer
most common is adenocarcinoma (40%); squamous cell carcinoma, small cell and large cell
centrally located lung cancers
squamous cell and small cell
peripheral located lung cancers
adenocarcinoma and large cell
lung cancer paraneoplastic syndromes
SCC --> hypercalcemia (PTH-like peptide)
small cell --> SIADH and Eaton-Lambert
lung cancer metastasis
SCC --> direct extension to hilar node and mediastinum
small cell and adenocarcinoma --> liver, adrenals, brain, bones
lung cancer presentation
cough
weight loss
dyspnea
hemoptysis
chest pain
recurrent pneumonic processes
hoarseness
lung cancer diagnosis
sputum cytology (specially SCC)
bronchoscopy for centrally located lessions
needle aspiration biopsy if highly suspicious and nonspecific bronchoscopy findings or peripheral lession
symptoms of unresectable lung cancer
weight loss >10%
bone pain
extrathoracic metastasis
CNS symptoms
SVC syndrome
hoarseness
contralateral mediastinal adenopathy
lung cancer treatment
resectable small cell --> VP16 (etoposide, platinum); resectable non-small --> CAP (cyclo, adriamycin, platinum) and radio
lung cancer prognosis
5-8% 5-year survival
after resection of SCC --> 30-35%
after resection of large-cell and adeno --> 25%
atelectasis etiology
most common is postsurgery; also mucuous plug, foreign body or tumor
atelectasis presentation
tachycardia, dyspnea, fever, hypoxemia
atelectasis diagnosis
ipsilateral trachea deviation --> upper lobe
mediastinal deviation --> massive atelectasis
elevation of hemidiaphragm --> lower lobe
atelectatic lobe looks denser, consolidated and smaller than normal contralateral lobe
basic life support measures
1) assess responsiveness
2) call for help
3) postiion face up on flat surface
4) open the airway
5) assess breathing (if no breathing, perform 2 rescue breaths)
6) check carotid pulse 5-10 seconds (if no pulse, give 30 compressions and two ventilations until help arrives)
asystole and dysrhythmia etiology
"Hi 5, T5": hypoxia, hypo/hyperkalemia, hypothermia, hypoglycemia, hypoveolemia, trauma, toxins, tamponade, tension pneumothorax, thrombosis
advanced cardiac support
if pulseless + shockable --> shock + 5 cycles of CPR + 1mg epi every 3-5min until pulse present
if pulseless + not shockable --> 5 cycles of CPR + 1mg epi + 1mg atropine until electrical activity then check pulse;
shockable rhythms
ventricular fibrillation and ventricular tachycardia
unshockable rhythms
asystole, pulseless electrical activity
signs of hemodynamic instability
hypotension, chest pain, altered mental status, CHF
general measures of tachycardia with pulses
ABC, O2, identify rhythm on ECG, identify reversible causes
hemodynamically unstable patient with pulse and tachycardia
perform immediate cardioversion
IV access and sedation
until stable
hemodynamically stable patient with pulse and tachycardia, narrow QRS, regular rhythm
vagal maneuvers or adenosine
if converts --> probable SVT, treat recurrence with adenosine
if doesn’t convert --> probable atrial flutter, ectopic atrial tachycardia
control rate with diltiazem or betablockers
hemodynamically stable patient with pulse and tachycardia, narrow QRS, irregular rhythm
probable A-fib or MAT; control rate with diltiazem or betablockers
hemodynamically stable patient with pulse and tachycardia, wide QRS, regular rhythm
if VT --> amiodarone 150mg IV over 10min, repeat as needed
if SVT --> adenosine and check for rhythm conversion
hemodynamically stable patient with pulse and tachycardia, wide QRS, irregular rhythm
if WPW --> avoid nodal blocking agents adenosine, digoxin, CCB
consider amiodarone 150mg over 10min
basic algorhythm for tachycardia with pulses
general measures --> check if stable --> check QRS --> check rhtyhm regularity
miosis as sign of toxicity
sugests clonidine, barbiturates, opiates, cholinergics, pontine stroke
mydriasis as sign of toxicity
sugests sympathomimetics, anticholinergics
dry skin as sign of toxicity
sugests anticholinergics
wet skin as sign of toxicity
cholinergics, sympathomimetics
blisters as sign of toxicity
barbiturates, carbon monoxide
common signs of toxicity
miosis, mydriasis, dry skin, wet skin, blisters
measures for toxic ingestion management
induced vomiting
lavage
charcoal
whole bowel irrigation
dialysis
cathartics
forced diuresis
naloxone/dextrose/thiamine
induced vomitting
ipecac can only be used 1-2 hours after toxic ingestion (limited use)
not indicated in children or for caustic substances
lavage
indicated in those with mental status
preceded by intubation
used 1 hour after ingestion (limited use)
contraindicated for caustic substances
charcoal
used if patient arrives more than 1-2 hours after ingestion; decreases absorption and increases removal of absorbed substance
whole bowel irrigation
used when many pills are seen on x-ray; 1-2 liters/hour of GoLytely via gastric tube
dialysis for toxicity management
used for ehtylene glycol, lithium overdose, methanol poisoning, aspirin overdose, theophyline overdose and there is coma, hypotension or apnea
cathartics
useful only when charcoal is used; generally wrong answer
forced diuresis
alkaline diuresis is only useful for salicylates and phenobarbital
naloxone/dextrose/thiamine administration
given to any patient who ingested substance and has altered mental status
acetaminophen toxicity stages
gastritis, nausea, vomitting 12-24 hours after ingestion; 24-48 hours: asymptomatic period with subclinical elevation of transaminases and bilirubin; 48-72 hours: jaundice, abdominal pain, hepatic encephalopathy, renal failure and death
acetaminophen toxicity treatment
N-acetyl-cysteine preferably within first 8 hours
activated charcoal
no gastric emptying
after 24 hours of ingestion no treatment can prevent or reverse toxicity
methanol ingestion sources
paint thinner, sterno, photocopier fluid, solvents, windshield washer solution
ethylene glycol ingestion sources
car antifreeze
methanol and ethylene glycol metabolism
methanol + alcohol dehydrogenase --> formaldehyde + formic acid
ethylene glycol + alcohol dehydrogenase --> oxallic acid/oxalate
general signs of alcohol intoxication
confusion, ataxia, lethargy, drowsiness, slurred speech
isopropyl alcohol intoxication
ketonuria, ketonemia, without acidosis and no increased anion gap
methanol intoxication specific signs
visual disturbances, blindness
ehtylene glycol intoxication specific signs
renal failure and oxalate crystals/stones in urine
alcohol intoxication diagnosis
determine specific alcohol levels in blood
oxalate crystals in urine and ↑BUN/creatinine are characteristic of ethylene glycol
ethylene glycol and methanol produce increased anion gap metabolic aciosis different from isopropyl alcohol which is normal
alcohol intoxication treatment
fomepizole is alcohol dehydrogenase inhibitor which decreases toxic metabolites
carbon monoxide poisoning presentation
dyspnea, tachypnea, shortness of breath, headache, nausea, dizziness, confusion, syncope, chest pain, arrhythmia, hypotension
carbon monoxide poisoning diagnosis
carboxyhemoglobin levels
arterial blood gases (metabolic acidosis with normal PO2)
↑CPK
pulse oximetry not helpful
CO poisoning might present similar to hypoglycemia, if glucose is normal, raise suspicion of CO
carbon monoxide poisoning treatment
removal from source of exposure, 100% O2, hyperbaric O2 if CNS or chest pain
caustic substance intoxication presentation
oral pain, drooling, odynophagia, abdominal pain
esophageal injury and gastric perforation may occur
caustic substance intoxication diagnosis
by history of exposure and upper endoscopy if ingested
caustic substance intoxication management
wash out mouth, eyes or skin with large volumes of cold water
follow eye wash out with fluorescein corneal exam
don't induce emesis or neutralize substance
charcoal and steroids are not effective
digoxin toxicity etiology
from suicide attempt or accidental overdose; hypokalemia predisposes to toxicity
digoxin toxicity presentation
nausea, vomitting, diarrhea, anorexia
blurred vision, color abnormalities
hallucinations
confusion
arrhythmia
digoxin toxicity diagnosis
history + ECG looking for any arrhythmia
check for hyperkalemia
digoxin toxicity management
repeated doses of charcoal, digoxin antibodies, potassium correction
pacemaker might be necessary for refractory bradycardia or 3rd degree heart block
opiate intoxication
respiratory depression
respiratory acidosis
miosis
constipation
bradycardia
hypothermia
hypotension
treat with naloxone
cocaine intoxication
hypertension, hemorrhagic stroke, MI, arrhythmia, seizures
pulmonary edema is specific to crack
treat with benzodiazepines for acute agitation
combined alpha/beta blockers such as labetalol or alpha blockers such as phentolamine
avoid beta blockers
benzodiazepine intoxication
somnolence, dysarthria, ataxia, stupor
death is not from respiratory depression but concomitant ethanol or barbiturates
flumazenil antidote is not always used due to seizures from withdrawal
barbiturate intoxication
hypothermia, loss of deep tendon reflexes
loss of corneal reflexes, coma and death from respiratory depression
no EEG activity can be seen
no specific antidote but increase urinary excretion with bicarbonate
hallucinogens
marijuana, LSD, mescaline, peyote, psilocybin, PCP (angel dust)
hallucinogen toxicity
delirium and bizarre behavior
anticholinergic effects (flushed skin, dry mouth, dilated pupils, urinary retention)
PCP may cause seizures
treat severe intoxication with benzodiazepines
lead sources
ingested paint, soil, dust, drinking water
lead metabolism
absorbed from GI tract, skin or inhalation
5-10% in blood (mostly in RBC)
80-90% in bones, remainder in brain and kidneys
lead poisoning presentation
adults: abdominal pain, anemia, renal disease, neurologic manifestations
children: abdominal pain, anemia, lethargy, seizures, coma, irreversible mental retardation and cognitive damage
lead poisoning diagnosis
best test is blood lead levels (<10ug/dL is normal)
lead lines at metaphyseal plate of long bones in children
anemia
azotemia
lead poisoning treatment
removal of source
chelators (EDTA, dimercaprol, penicillamine or succimer)
acute poisoning: charcoal + urination
mercury poisoning
interstitial pneumonitis from inhalation
irreversible neurologic symptoms (tremors, excitability, memory loss, delirium, insomnia)
GI symptoms from ingestion
treat with succimer or dimercarprol
salicylates intoxication presentation
tinnitus
nausea, vomitting, gastritis
hyperventilation, noncardiogenic pulmonary edema
hyperthermia, CNS toxicity
lactic metabolic acidosis with increased anion gap
salicylates intoxication diagnosis
most specific test is aspirin level
suggestive is elevated anion gap metabolic acidosis but blood may have ↑pH, ↓pH or normal
chest x-ray may be normal or pulmonary edema
salicylates intoxication management
if within 1 hour of ingestion, gastric decontamination + charcoal
mainstay of therapy is alkalinization of urine with aggressive fluid resuscitation
dialysis is sometimes used
tricyclic antidepressant intoxication presentation
anticholinergic (dry mouth, tachycardia, dilated pupils, flushed skin)
cardiac (wide QRS, ventricular tachycardia)
CNS (altered mental status, seizures)
tricyclic antidepressant intoxication diagnosis
serum drug levels is most specific but EKG is more important to do first
tricyclic antidepressant intoxication management
within hours --> charcoal
bicarbonate if cardiac toxicity
don't use flumazenil to reverse concomitant benzodiazepine overdose because it leads to seizures
head trauma presentation
headache, amnesia, loss of consciousness
focal findings are most common with epidural hematomas, then subdural hematomas and contusion
head trauma diagnosis
CT scan always
hemorrahge is visible immediately
subdural hematoma is crescent-shaped
epidural hematoma is lens-shaped
if focal findings consistent with radiculopathy or spinal tenderness --> cervical spine x-ray
concussion diagnosis is loss of consiousness + normal head CT
head trauma treatment
if intracrannial hemorrhage --> hyperventilation to a PCO2 of 30-35
osmotic diuretics and elevation of head of the bed
maintain cerebral perfusion by keeping blood pressure 110-160mmHg
subarachnoid hemorrhage presentation
acute --> sudden headache, loss of consiousness (50%), focal neurologic symptoms (30%)
long-term --> focal deficits, seizures, rebleeding, hydrocephalus, stroke
subarachnoid hemorrhage diagnosis
intial best test is CT scan which has 90-95% sensitivity within first 24 hours
if CT is normal and SAH is still suspect --> lumbar puncture for absence of red cells
angiography to determine site for surgery
inverted or enlarged T-waves on ECG are not alarming
subarachnoid hemorrhage management
maintain blood pressur at 110-160mmHg
nimodipine to prevent spasm and stroke
angiography to determine site of bleeding for surgical correction
shunt if hydrocephalus is present
skin burns classification
first-degree --> skin is intact
second-degree --> blister formation
third-degree --> destruction of skin appendages and pain receptors which result in relative lack of pain
burn presentation
altered mental status, dyspnea, headache and chest pain suggest carbon monoxide poisoning
stridor, hoarseness and dyspnea suggest laryngeal edema
soot in nose and mouth suggests impending airway compromise
rule of nines for burns
arms and head are 9% each
chest, back and legs are 18% each
patchy burns estimated with width of hand which is 1%
watch out for circumferential burns which compromise circulation
diagnosis work-up of burns
aside from actual burn, determine carboxyhemoglobin levels in severe burns
chest x-ray and/or bronchoscopy to determine respiratory injury extent
definition of severe burns
combined second and third-degree burns >20% in adults or >10% in old or young
OR third-degree burns >5% of body surface
burn injury management
if signs of respiratory injury --> intubation is initial step
if carboxyhemoglobin is elevated --> 100% O2
Ringer lactate fluid rescucitation using Parkland formula
H2 blocker prophylaxis, topical silver sulfadiazine to prevent infections
grafts as needed
Parkland formula
4ml of ringer lactate for each % BSA burned per Kg; give 1/2 in first 8 hours, 1/4 in second 8 hours, 1/4 in third
heat stroke
lost ability to romeve heat from body
excessive body temperature elevation
confusion, disorientation, nausea, blurred vision, seizures
hemoconcentration, ↑BUN/creatinine, rhabdomyolysis, anuria, DIC, lactic acidosis
place body in cool temperature, water and fan + IV fluid replacement
malignant hyperthermia
idiopathic reaction to any anesthetic specially halothane and succinylcholine
rhabdomyolysis and hyperthermia
treat with dantrolene
neuroleptic malignant syndrome
reaction to phenothiazines, chlorpromazine, haloperidol
muscular rigidity, hyperthermia, ↑CPK, encephalopathy, rhabdomyolysis
treat by removing agent + bromocriptine or dantrolene
hypothermia
core body temperature <35C
lethargy, confusion, weakness, arrhythmias with J-wave elevation (may mimic ST elevation)
treat with warm bed, bath or blankets
rescucitation efforts from pulselessness can go on beyond 10 minutes until temperature >35C
nonionizing radiation
infrared, ultraviolet and microwave; present primarily as burns
ionizing radiation
bone marrow depression with infections and bleeding
permanent sterility in males around 4-5Gy
nausea and vomitting 100% at 3Gy
supportive therapy with antiemetics, transfusions, colony-stimulating factors, antibiotics as needed
electrocution presentation
local 1st, 2nd and 3rd degree burns
ventricular fibrillation (AC current)
aystole (DC current, lightning)
respiratory arrest (injury to medulla or respiratory muscle paralysis)
neurologic damage
loss of consiousness and amnesia in 75% of lightning cases
renal failure from dehydration and rhabdomyolysis
cataracts in 5-30%
electrocution treatment
cardiopulmonary resuscitation, fluid replacement, local wound care
types of drowinig
dry drowning from laryngospasm, fresh water drowning, sea water drowning
fresh water drowning
hypotonic water alters surfactanct and causes collapse
water is absorbed and results in hypervolemia, hemodilution and hemolysis
lungs have little water
sea water drowning
hypertonic water draws fluid into lungs resulting in pulmonary edema, systemic hypovolemia, hemoconcentration
near drowning presentation
coma
agitation
cyanosis
coughing
sings of pulmonary edema (tachypnea, tachycardia, rales)
near drowning lab exams
arterial blood gases show hypoxia and hypercabia and metabolic acidosis
drowning management
removal from water
ABCs (first step)
endotracheal intubation
O2
positive pressure mechanical ventilation (most effective)
drowning ineffective treatments
abdominal thrusts, antibiotics, steroids
anaphylaxis presentation
hives rash (urticaria), angioedema and swelling, dyspnea, stridor, tachycardia, hypotension, hemodynamic collapse
anaphylaxis management
antihistamine diphenhydramine
if hemodynamic instability --> epinephrine, IV fluids, antihistamines and steroids
cat and dog bites
treat with exploration, debridement, irrigation, proper wound care
prohylactic antibiotic of choice is amoxicillin/clavulanate