Acute vs. Chronic Renal Failure

Acute renal failure (ARF): caused by dehydration, blood loss from major surgery or injury, or the use of medications, such as contrast agents used in X-ray tests, antibiotics such as gentamicin, or nonsteroidal anti-inflammatory drugs (NSAIDS) such as aspirin or ibuprofen.
Chronic kidney disease (CKD): caused by a long-term disease, such as high blood pressure or diabetes, that slowly damages the kidneys and reduces their function over time.

ARF usually presents with decrease urine output and electrolyte abnormalities and sudden elevation of BUN and Cr (BUN more)

CRF usually presents with mild elevation of Cr over a long time and sx's don't present until only 10%-20% kidney function is left. On U/S CRF shows more atrophic kidney

Correcting anion gap for albumin

observed anion gap =
= ((sodium in mEq/L) + (potassium in mEq/L)) - ((chloride in mEq/L) + (HCO3 in mEq/L))
corrected anion gap =
= (observed anion gap) + (0.25 * ((normal serum albumin in g/L) - (observed albumin in g/L)) =
= (observed anion gap) + (0.25 * (44 - (observed albumin in g/L))

Abnormal LFTs

Hepatocellular injury: increase in ALT and AST (AST more in alcoholic liver disease, ALT more in viral hepatitis), (+/-) ALP and Tbili
Cholestasis: increase in ALP and Tbili, (+/-) ALT and AST
Isolated hyperbilirubinemia: increase in Tbili, normal transaminases and ALP

Liver Disease

Acute: First presentation is transaminitis (AST, ALT), ALP (if any obstruction presents)
Chronic: ALT and AST elevated for more than 6 months-> increase bilirubin-> decrease in albumin-> decrease in platelet count-> coagulation factors

Isolated Hyperbilirubinemia

1) Unconjugated:
a) Over production: hemolytic anemia
b) Defective conjugation: Gilbert's syndrome (jaundice when hungry), Crigler-Najjar
2) Conjugated
Defective excretion: Dubin-Johnson, Rotor's syndrome (black liver)

Acute vs. Chronic Renal Failure

DDx for Muscle Weakness

1) Muscle:
a) Congenital myopathies and mitochondrial myopathies: Sx. bilateral, proximal to distal wasting. Dx: elevated CK and LDH, abnormal EMG, normal nerve conduction. definite diagnosis with genetic testing.
b) Polymyositis: Abnormal CK and LDH, Dx with muscle biopsy
c) Dermatomyositis: Abnormal CK and LDH, Dx made with muscle biopsy
d) CREST syndrome: Anti-centromere ab
2) NMJ
a) Myesthenia gravis: Dx with EMG. Contractile force reduced with repetition
b) Lambart-Eaton: Dx with EMG. Contractile force increased with repetition
3) PNS
a) Diabetic Neuropathy: loss of sensation first. abnormal NC labs
b) Peripheral nerve degeneration/demyelination. Abnormal NC studies. Weakness in isolated motor neauron units
c) Radiculopathy: weaknes in motor neuron unit bundles. Abnormal NC studies
4) CNS
a) Gullian-Barre: ascending progression. increased ab levels in CSF
b) MS: lesions on CNS on MRI
c) B12 deficiency: depleted B12 levels
d) Polio
e) ALS: intact sensation, both upper neuron and lower neuron signs

Meld's Score

Fever of unknown origin

Petersdorf and Beeson criteria:
1) Fever higher than 38.3°C (101°F) on several occasions
2) Persisting without diagnosis for at least 3 weeks
3) At least 1 week's investigation in hospital
Work up:
1) comprehensive histpry with repeated PE
2) laboratory tests: serological, blood culture, immunological
3) studies: U/S to r/o cholelithiasis, echo to r/o endocarditis, CT-scan to r/o infection, abscess, malilgnency. Gallium-67 scanning which seems to visualize chronic infections more effectively.
4) invasive techniques : biopsy and laparotomy for pathological and bacteriological examination
5) PET scan: has been reported to have sensitivity of 84% and a specificity of 86% for localizing the source of fever of unknown origin.
6) systematic discontinuation of medications to r/o drug fever

CHADS2 criteria

Calculating CHADS score:
C : Congestive heart failure, 1
H: Hypertension (or treated hypertension), 1
A: Age more than 75 years, 1
D: Diabetes, 1
S2: Prior Stroke or TIA, 2
Recommendations for anticoagulation:
0: Low risk: daily ASA 81-325 mg
1: Moderate risk: ASA daily or raise INR to 2-3
2 or higher: Moderate to high risk: Warfarin with targer INR 2-3

Tumor lysis syndrome

Cairo-Bishop Definition
1) Laboratory tumor lysis syndrome: abnormalitiy in two or more of the following and occurs within 3 days before or 7 days after chemotherapy.
a) uric acid > 8 mg/dL or 25% increase
b) potassium > 6 meq/L or 25% increase
c) phosphate > 4.5 mg/dL or 25% increase
d) calcium < 7 mg/dL or 25% decrease
2) Clinical tumor lysis syndrome: laboratory tumor lysis syndrome plus one or more of the following:
a) increase serum creatinine (1.5 times upper limit of normal)
b) cardiac arrhythmia or sudden death
c) seizure
(A grading scale (0-5) is used depending on the presence of lab TLS, serum creatinine, arrhythmias, or seizures.)

UA findings in ARF

1) Prerenal: benign sediments or few hyaline casts, (-) protein, (-) blood
2) Intrarenal:
a) ATN: "muddy brown" casts, granular casts, trace protein, (-) blood
b) Acute glomerulonephritis: RBC casts, WBC casts, fatty casts, 3+-4+ protein, 3+ blood
c) Acute interestitial nephritis: WBC casts, eosinophils, 1+ protein, 2+ blood
3) Postrenal: No sediments, (-) protein, (-) blood

Renal Tubular Necrosis

Type I: distal; inability to secrete H+; hpokalemia; Rx: correct acidosis with sodium bicarbonate
Type II: proximal; inability to reabsorb bicarbonate; hypokalemia; Rx: Na restriction
Type IV: distal; hypoaldosteronism or aldosterone resistance; hyperkalemia, H+ in urine

ATN vs. AIN

ATN: Acute tubular necrosis leads to ARF. Causes: 1) ischemic: globar ischemia, shock, hemorrhage, sepsis, DIC 2) nephrotoxic: aminoglycosides, radiocontrast, NSAIDs (especially in the setting of CHF), poisons, myoglobinuria, hemoglubinuria, cisplastin, multiple myeloma (kappa and gamma light chains). Dx: elevation of BUN and Cr and decrease in UOP consistant with ARF

AIN: Acute interestitial nephritis inflammation of the glomerular and tubular interestitium. 10% risk of ARF. Causes: acute allergic reaction to medications (e.g. penicillins, NSAIDs, anticoagulants, thiazides, furosemide, phenytoin, sulfa drugs), infection (streptococcus and legionella pneumophilia), CVD (e.g. sarcoidosis). Dx: increased BUN, Cr, eosinophiluria

ESR

Elevated ESR: severe infection, multiple myeloma, Waldenstrom macroglobulinemia, temporal arthritis, polymyalgia rheumatica

Depressed ESR: polycythemia, extreme leukocytosis, sickle cell anemia

Pseudogout

Risk factors: age, osteoarthiritis, hemochromatosis, hyperparathyroidism, hypothyroidism, Bartter's syndrome

Gout Meds

CHRONIC GOUT:
Xanthine oxidase inhibitors (decrease production): allopurinol, oxypurinol, tisopurine, febuxostat, and inositols

Uricosurics (increase secretion): probenecid, benzbromarone and sulfinpyrazone, EDTA

Urate oxidase (breaks down uric acid deposits): pegloticase
ACUTE GOUT:
NSAIDs (antiinflammatory):diclofenac, etoricoxib, indomethacin, ketoprofen, naproxen
Corticosteroids (antiinflammatory): prednisone
Cholchicine (inhibits neutrophils and uric acid deposition)

Acid Base Problems:

pH=bicarb/PCO2
Metabolic Acidosis: Low bicarb, Low pCO2 (compensation)
Metabolic Alkalosis: High bicarb, High pCO2 (compensation)
Respiratory Acidosis: High pCO2, High bicarb (compensation)
Respiratory Alkalosis: Low pCO2, Low bicarb

Cancers with Bone Metastasis:

BLT w/ Kosher Pickle, Mustard, Myo: Breast, Lung, Thyroid, Kidney (renal), Prostate, Multiple Myeloma

Causes of Hyponatremia

Urine Na >10: Diuretics, ACEI, Renal Salt Wasting, Cerebral Salt Wasting, Addison's
Urine Na <10:>Dehydration, Vomiting, Sweating, Diarrhea