Genitourinary Flashcards
acute kidney injury (AKI) - definition, risk factors
note: good summary table on side 14 of PPT
sudden dec. in renal fx (GFR) which causes build up of nitrogenous waste (uric acid)
- over hrs to days
- severity based on inc. in BUN and Cr and reduction of urine output (oliguria)
- can be pre-renal, intrinsic, or post-renal
risk factors:
- age, heart and liver dz
- exposure to nephrotoxins
- surgery, sepsis, vol. depletion
important nephrotoxins
IV contrast dye ACE-I and ARBs Loop and thiazide diuretics lithium NSAIDs statins some ABX
acute kidney injury (AKI) - sxs, dx
sxs: vary depending on cause
- +/- oliguria
- change in urine color
- N/V, malaise, abd pain, itching
dx:
- BUN/Cr ratio rises
- image/biopsy may be done
acute kidney injury (AKI) - pre-renal causes and tx
Pre-renal (most common):
- vol. depletion: dehydration, blood loss
- dec. effective circulating vol: CHF, ascites, nephrotic syndrome
- impaired renal blood flow: ACEIs, NSIADS, renal artery stenosis
- systemic vasodilation: sepsis
Tx: treat cause, maintain euvolumia, check K+
acute kidney injury (AKI) - intrinsic causes (3)
- acute tubular necrosis
- ischemia
- endogenous nephrotoxins: rhabdomyolysis, hemolysis
- exogenous nephrotoxins: amphotericin B, contrast dye
- sepsis/infection - interstitial nephritis
- drugs: Penicillin, cephalosporins, sulfa, NSAIDs - glomerularnephritis
- IgA nephropathy
- post strep (antibody against strep antigen that settled in kidney)
- Good pastures (antibody against basement membranes of kidney and lung
- HUS: hemolytic uremic syndrome (E. Coli)
acute kidney injury (AKI) - post-renal causes and tx
Post-renal (think obstruction; least common):
- BPH
- nephrolithiasis (bilateral)
- bladder outlet syndrome
tx: catheterization or stent
acute tubular necrosis - causes, dx, tx
most common intrinsic cause of AKI
causes:
- ischemia
- endogenous nephrotoxins: rhabdomyolysis, hemolysis
- exogenous nephrotoxins: amphotericin B, contrast dye
- sepsis/infection
dx:
- U/A: “muddy brown sediment” and granular casts
- Labs: hyperkalemia, high phase, FeNa>1, BUN:Cr<20:1
tx:
- remove toxin or tx cause to prevent further kidney injury!
- loop diuretic, correct electrolytes
- dialysis if needed
- low protein diet
interstitial nephritis - causes (drugs), sxs, dx, tx
inflammation of renal tubules and interstitial
- intrinsic cause of AKI
causes:
- DRUGS: Penicillin, cephalosporins, sulfa, NSAIDs
- infection: strep, CMV
- immune d/c: sarcoid, SLE (Lupus)
sxs: fever, maculopapular rash
dx:
- U/A: WBC casts, eosinophils
- CBC: peripheral blood eosinophils
Note: this is a hypersensitivity reaction to drug… why we see eosinophils
tx:
- address underlying cause
- urgent dialysis
glomerulonephritis - causes (many)
Note: only intrinsic cause list out on blueprint!
inflammatory lesions of glomerulus from immune complex deposition or development of antibodies against glomerulus
- intrinsic cause of AKI
causes:
- IgA nephropathy (aka Berger dz): assoc. w/ URI sxs, gastroenteritis; hematuria
- Post strep (immune complex deposition): occurs 2-6 wks post-impetigo and 1-3 wks post-strep pharyngitis; +ASO, inc. C3; steroids NOT helpful
- Good pastures: autoantibodies against basement membrane; tx is plasma exchange
- HUS (hemolytic uremic syndrome): uremia, low platelets, hemolytic anemia
glomerulonephritis - sxs, dx, tx
Note: only intrinsic cause list out on blueprint!
sxs:
- related to underlying cause
- hematuria, HTN and edema (periorbital and scrotal edema), flank pain
dx:
- U/A: tea or coca-cola colored urine w/ red cell casts
tx:
- treat underlying cause
- high dose corticosteroids (except if post-strep)
AKI - what medical calculation can help you determine cause?
FeNa
FeUrea - can be used on patients on diuretics
chronic renal failure - definition, sxs
destruction of nephrons leading to progressive decline in kidney fx
- common (1 in 9 adults)
- often with other chronic diseases
- most people die of other cause (CVD) and not ESRD
sxs:
- HTN (#1 sx)
- uremic syndrome
uremic syndrome
build-up of metabolic wastes w/ advanced chronic kidney dz
sxs:
- urinary changes
- fatigue, dec. appetite, pruritus, edema, SOB
chronic renal failure - dx, tx, prevention
Dx:
- renal fx: inc. BUN/Cr, inc. Cr, dec. GFR (< 60 for 3+ mo)
- hyper K, metabolic acidosis, proteinuria, etc.
tx:
- diet: protein restriction, also salt, water, potassium, and phosphate restriction
- dialysis or transplant
Prevent:
- treat HTN: ACE-I or ARB
chronic renal failure - stages
based on GFR
1: normal, but evidence of kidney dz; GFR 90+
2: mild; GFR 60-89
3: moderate: GFR 30-59
4: severe; GFR 15-29
5: failure (ESRD); GFR<15 (on hemodyalysis)
hydronephrosis - definition and cuases
distention of renal calyces and pelvis of kidney(s) by urine
- is the result of urinary blockage anywhere along urinary tract
- will see dec. GFR if bilateral
causes:
- BPH
- VUR
- nephrolithiasis (esp. at ureteropelvic jx)
- pregnancy
- large fibroids
- neurogenic bladder
hydronephrosis - sxs, dx, tx
sxs:
- pain, sxs related to cause
dx: U/S
- can also use IV urogram or CT
tx: treat cause!
- catheter for BPH
- anticholinergics for neurogenic bladder
- emergent stenting or nephrostomy for infection
nephrotic syndrome - definition, causes, sxs
increased permeability of glomerular capillary walls that allows passage of large amounts of protein into urine
- proteinuria + hypoalbuminemia + edema
Primary causes:
- minimal change dz
- focal glomerulosclerosis
- membranous nephropathy
- menbranous proliferative nephropathy (MPGN)
Secondary causes:
- DM
- amyloidosis
sxs:
- edema: periorbital and scrotal (also feet and ankles)
- pleural effusion: SOB
nephrotic syndrome - dx, management
Dx:
- proteinuria > 3g/day
- oval fat bodies: lipid passed into urine, as well (maltese crosses are signs of oval fat bodies under microscope)
Manage:
- diet: low protein, salt restriction
- tx hyperlipidemia and hypercoaguability
- diuretics (thiazide, loop) and ACE-I
polycystic kidney disease - definition, sxs, dx
genetic, cystic d/o of the kidneys often resulting in massive enlargement
- MOST common hereditary dz in US
sxs:
- present in 30-40’s; ESRD by age 60
- hematuria + abd/flank pain + 2ndary HTN
- large, palpable kidneys
- frequent UTIs and nephrolithiasis
dx:
- U/S for screening
- CT or MRI give anatomic details
polycystic kidney disease - complications, management
complications:
- pain from cyst and rupture
- renal infection
- nephrolithiasis
- HTN: must tx aggressively!
- cerebral aneurysms
- MVP (mitral valve prolapse)
- cysts in other locations
Management:
- treat complications
- aspirate cysts
- treat HTN aggressively
- VASOPRESSIN receptor antagonist delays ESRD
- renal transplant
renal artery stenosis
narrowing of 1 or both renal arteries
sxs:
- HTN onset <20 or >50 y/o
- HTN resistant to meds
- renal bruits
dx:
- U/S: screening
- renal arteriography: gold standard
tx:
- renal artery angioplasty +/- stent
- antihypertensives
renal vein thrombosis - definition, causes, sxs, dx, tx
acute or chronic thrombosis of renal vein
causes:
- Kids: severe dehydration
- Adults: infection, ascending thrombosis of vena cava, clotting d/o
sxs:
- flank pain
- palpable kidney
- nephrotic syndrome if bilateral
dx:
- renal U/S
- renal venography
tx:
- eliminate cause
- anticoagulation or thrombolytic therapy
Acid-Base Basics
acid-base balance is coordinated by lungs and kidneys to keep optimal pH
- goal pH: 7.35-7.45
- lungs regulate pCO2
- kidneys regulate HCO3-
Note: when one system fails, the other tries to compensate to bring back balance
acidosis
results when pH is too low (<7.35)
- pCO2 is HIGH (>40)
- HCO3 is LOW (<24)
Note: think of CO2 as Hydrogen
alkalosis
results when pH is too high (>7.45)
- HCO3- is HIGH (>24)
- pCO2 is LOW (<40)
acid-base question: approach
- identify if you have an acidic or basic state
- acidic: pH<7.35
- basic: pH>7.35 - identify if it is metabolic (HCO3-) or respiratory (pCO2) underlying the cause
- Consider underlying cause and correct
metabolic acidosis (w/ elevated anion gap) - causes
low pH, low HCO3-
anion gap > 16
causes: MUDPILERS
M: methanol U: uremia D: DKA P: propylene glycol, acetaminophen, I: iron, isoniazid (due to seizures), inborn errors of metabolism L: lactic acidosis E: ethanol (due to lactic acidosis), ethylene glycol R: rhabdomyolysis S: salicylates/ASA/Aspirin
anion gap
positive ions minus negative ions
anion gap = Na+ - (HCO3- + Cl-)
normal: 8-16 mEqu
metabolic acidosis (w/ normal anion gap) - causes
low pH, low HCO3-
anion gap b/t 8-16
causes:
- dec. bicarb with diarrhea
metabolic acidosis - what is compensation
increased ventilation to blow off CO2
- can get Kussmaul breathing
metabolic alkalosis - causes, compensation, other s/sx, tx
high pH, high HCO3-
causes: loss of H+ or excess HCO3-
- vomiting, suction gastric contents
- diuretics
- overcorrect metabolic acidosis
compensation: decreased ventilation (inc. pCO2)
other s/sx:
- hypocalcemia: paresthesias, confusion, coma
- hypokalemia: polyuria, polydipsia, weakness
tx: fix underlying cause, IV fluids
respiratory acidosis - causes, compensation, tx
low pH, high CO2
causes: anything that dec. respirations (COPD, narcotics OD)
compensation: inc. reabsorption of HCO3- by kidneys
tx:
- fix underlying cause, assist ventilation, naloxone (if all else fails)
respiratory alkalosis - causes, s/sx, compensation, tx
high pH, low CO2
causes: anything that inc. respirations and blows off too much CO2
- hysterical hyperventilation
- salicylate intoxication
- pulmonary embolism
s/sx: rapid breathing, lightheadedness
compensation: inc. elimination of HCO3- by kidneys
tx: underlying cause