Medicine Part 2 Flashcards
Most common causes of ESRD
Diabetes
HTN
How is ESRD defined?
Not by BUN or Cr
Loss of kidney function leading to clinical and lab findings of uremia
Calciphylaxis
Hyperphosphatemia –> calcium adn PO4 precipitate –> vascular calcifications –> skin lesions/necrosis!
Absolute indications for dialysis
AEIOU
Acidosis
Electrolytes - HYPERkalemia
Intoxications - methanol, eth glycol, lithium, aspirin
Overload - hypervolemia that can’t be solved
Uremia - based on clinical presentation, like pericarditis
Microscopic hematuria usually
glomerular in origin
Gross painless hematuria usually
Bladder or kidney cancer
Hematuria
> 3 erythrocytes / HPF on UA
Order to evaluate proteinuria
Urine dipstick - specific for albumin
UA
Dipstick + blood
UA no RBC
What is it?
Hemoglobinuria
Myoglobinuria
Proteinuria
> 150 mg protein/days
Glomerular d/o vs tubular d/o
In glomerular but not in tubular:
- need biopsy usually
- steroids and immunosuppressive meds for tx
In tubular but not in glomerular:
- acute presentation,
- caused by toxins
- does not cause nephrotic syndrome
Acute Interstitial Nephritis
- features
- seen on labs
- causes
Polyruia and sterile pyruria (maybe some WBC casts) are early manifestations
acute interstitial renal inflammation + pyuria + eosinophils (hypersensitivity) + azotemia
happens after drugs METHICILLIN #1 NSADs captopril penicillins sulfonamides rifampin TMP cephalosporins
AIN treatment
Remove offending agent
Steroids if still getting worse
Acute tubular necrosis
- causes
- stages
Toxic (#1 aminoglycosides) or Ischemic (more serious, prerenal azotemia usually (shock, sepsis) or crush injury w/ myoglobinuria) → granular casts (muddy brown)
o This is medullary necrosis and ATN is limited to outer medullar segments b/c renal medulla is susceptible to ischemic injury b/c low medullary blood flow → glomeruli look normal
o Stages: (1) inciting event → (2) Maintenance (oliguric, risk of hyperkalemia & met acidosis) → (3) Recovery (polyuric, risk of hypoK)
Nephrotic syndrome
- features
o Hyperlipidemia b/c increased hepatic lipoprotein synth – but only LDL; HDL will decrease!
o Hypoagammaglobinemia = increased risk infection
o Hypoalbuminemia = edema
o Hypercoagulable = loss antithrombin 3
Minimal change disease
-only lose albumin, not all globulins
Diffuse cortical necrosis
usually due to hypOperfusion of kidney (vasospasm, DIC, abruption placentae, septic shock), medulla spared
Renal papillary necrosis
- what is it
- causes
- dx
necrosis of renal papillae (supplied by vasa recta) = hematuria, proteinuria
o “POSTCARDS” = Pyelonephritis, Obstruction, Sickle Cell, TB, Cirrhosis, Analgesic abuse (phenacetin, acetaminophen, aspirin), Renal transplant rejection, Diabetes (#1), Systemic vasculitis
o DACS = Diabetes Mellitus (#1), Acute pyelonephritis, Chronic phenacetin use (acetaminophen), Sickle Cell
Dx w/ ecretory urogram - note change in papilla or medulla
Acute renal failure
↓ renal function → ↓GFR → INCREASE BUN and Creatinine (azotemia)
will also have met acidosis!
Chronic renal failure
Hyper K (#1 COD b/c arrhythmia) Metabolic ACIDosis (increase H+, ↓ bicarb) Uremia Anemia renal osteodystrophy dyslipidemia Na/H2O retention growth retardation in children;
FREE Ca will be decreased b/c increase in PO4 will bind up the free Ca in blood
Renal tubular acidosis
D/o of renal tubules –> nonanion gap HYPER Cl metabolic acidosis
Glomerular function OK
decrease in acid excreted in urine
Type 1 RTA
- what is it?
Distal
Can’t secrete H+ at distal tubule –> new bicarb cannot be made
Urine pH does not go below 6
Type 1 RTA
- effects of it
Decrease ECF
Hypo K, HYPER Cl, met acidosis
Renal stones
Type 1 RTA
- causes
MM
Nephorcalcinosis
Amphotericin B
Lupus, Sjorgen’s
Medullary sponge kidney
Analgesics