Internal Medicine Flashcards
Stage 1/2/3 AKI
Stage 1 –> Cr increase 1.5-1.9x baseline in 7 days, increase of 26 in 48h, or 0.5 urine output for 6-12h
Stage 2 –> Cr increase 2-2.9x baseline in 7 days, or under 0.5 urine output for over 12h
Stage 3 –> Cr increase 3x baseline in 7 days, over 354, initiation of renal replacement, or under 0.3 urine for over 24h or anuric for over 12h
Pre-Renal AKI Categories (i.e. causes)
True intravascular fluid loss –> blood loss, GI losses, decreased oral intake, fever, burns
Decreased ECV –> heart failure, shock, hypoalbuminemia (cirrhosis, malnutrition, nephrotic syndrome)
Impaired Renal Perfusion
–> Macro –> renal artery stenosis, dissection, thrombus
–> Micro –> NSAIDs (afferent constriction) and ACEis/ARBs (efferent dilation), cocaine, hypercalcemia
How to assess for Pre-renal AKI
- Labs?
- Management?
- volume status (JVP, blood pressure, edema, etc.)
- history (not eating/drinking, diarrhea, CHF non-compliance with meds, medications)
- bland urinalysis
- FeNa <1% (tubules are still absorbing Na)
- Urine Na <20 (RAAS is on)
- BUN:Cr high (urea 10x Cr)
- Give fluids if hypovolemic (careful w anuria), give diuretics if overloaded, stop offending meds
Post-Renal AKI Categories
- urethra (stricture, stenosis)
- prostate (BPH, prostatitis, prostate cancer)
- bladder (cancer, stone, clot, neurogenic)
- ureters (cancer, stone, clot, pregnancy, retroperitoneal fibrosis)
How to assess/manage post-renal AKI
- on hx - frequency, urgency, nocturia, hematuria, stones, B symptoms
- in/out foley catheter
- renal ultrasound
- if below bladder –> foley
- if above bladder –> nephrostomy
Renal AKI - Tubular
- Ischemic vs. Toxic
- Acute Tubular Necrosis (ATN) - most common cause of AKI along with pre-renal
- Ischemic –> due to prolonged pre-renal insult, most common, get MUDDY BROWN CASTS
- Toxic –> either exogenous (contrast, NSAIDs, chemo, aminoglycosides, acyclovir, amphotericin, MTX, etc.), or endogenous (Hgb, Mgb (muscle injury!), Ig light chains in multiple myeloma, oxalate crystals from ethylene glycol, urate crystals from tumor lysis/gout)
Labs you would expect for Renal (ATN) AKI
- Muddy brown casts
- FENa >1% (Na not being maximally absorbed)
- Urine Na >20 (RAAS turned off)
- BUN:Cr low (CR 20x urea)
Renal AKI - AIN
- 4 “I”s
- Acute Interstitial Nephritis
- Triad of fever, rash, and eosinophilia
- Infection –> viral i.e. HIV/CMV, TB, fungi, parasites
- Inflammation –> Sjogren’s, SLE, IgG4, TINU
- Infiltration –> sarcoidosis, lymphoma
- Ingestion –> NSAIDs, ABX, PPI, allopurinol (most common)
- Gold standard dx is biopsy
- Will see WBCs, WBC casts, RBCs, sometimes eosinophils
Renal AKI - Vascular
- damage to the microvasculature (larger vessels would be considered pre-renal)
- thrombocytic microangiopathy (TTP/HUS, malignant HTN)
- emboli (cholesterol, artheroembolic)
- scleroderma
- vasculitis
Renal AKI - Glomerular
- Nephrotic vs. Nephritic
- damage to endothelial/epithelial cells, basement membrane, podocytes, mesangium, bowman’s capsule
- may see purpura/active joints
- Nephrotic (mild) –> isolated injury to the filtration barrier leading to protein in the urine
- oncotic pressure in blood decreases leading to edema
- PALE (proteinuria over 3.5g, low albumin, hyperlipidemia, edema)
- Nephritic (severe) –> diffuse glomerular inflammation leading to urine sediment and decreased renal fucntion
- PHAROH (proteinuria, HTN, AKI, dysmorphic RBCs/casts, oliguria, hematuria)
Pathologies associated with nephrotic vs nephritic syndrome
Nephrotic –> membranous nephropathy, FSGS, minimal change disease, amyloid (can be secondary to cancer, HIV, NSAIDs, heroin, obesity, SLE, HBV/HCV, syphilis, solitary kidney)
Nephritic –> ANCA vasculitis/pauci-immune, anti-GBM Ab disease, cryoglobulinemic vasculitis, post-infectious GN
Inbetween –> IgA nephropathy, SLE nephritis, MPGN
Treatment for the different classes of Renal AKI
Tubular –> supportive
AIN –> withdraw culprits
Vascular –> treat underlying cause
GN –> call nephro
Acute indications for dialysis
Acidemia (refractory metabolic acidosis)
Electrolyte imbalance (refractory hyperkalemia)
Ingestion (methanol, ethylene glycol, ASA, Li)
Overload (refractory volume overload)
Uremia (pericarditis, encephalopathy - can both cause asterixis)
Urinalysis Findings
Leukocyte esterases –> pyelonphritis (AIN)
Calcium oxalate cyrstals –> ethylene glycol poisoning
Hyaline Casts –> non-specific but could indicate volume depletion
RBC Casts –> glomerulonephritis
WBC Casts –> AIN/pyelonphritis
Fatty Casts/ Frothy urine –> proteinuria (nephrotic syndrome)
Consequences of AKI
- dyspnea, orthopnea, PND
- edema
- oliguria
- uremic encephalopathy (confusion), nausea, malaise
- pleuritic chest pain (pericarditis)
- bleeding due to uremic platelets
ABC MOVIE
Airway, Breathing, Circulation
Monitors, Oxygen, qVitals, IVs, ECG
Signs suggestive of:
- ACS
- PE
- Pneumothorax
- Aortic Dissection
- Tamponade
- Esophageal Rupture
(Chest Pain Emergencies)
- ACS –> pressure pain in L shoulder/arm/jaw, cool periphery, worse with exertion and better with rest, known angina, associated with nausea/ diaphoresis/lightheadedness
- PE –> tachycardia, increased JVP, loud S2, DVT signs, risk factors (cancer, surgery, immobility, smoking)
-PTX –> emphysema, no breath sounds, trachea, not midline, increased JVP, hx of a thoracic procedure
- Aortic Dissection –> tearing pain to the back, neuro changes, asymmetric BP in both arms
- Tamponade –> increased JVP, quiet heart sounds, pulsus paradoxus (drop of BP more than 10 on inspiration), pericardial effusion
Esophageal Rupture –> emesis, hx of esophageal pathology or intervention
