Uro/Renal Flashcards
Metabolic Acidosis: high anion gap (MUDPILES)
M: methanol
U: uremia (AKI/CKD, rhabdomyolysis)
D: DKA
P: propylene glycol
I: iron/isoniazid
L: lactic acidosis
E: ethylene glycol
S: salicylates
Metabolic acidosis disturbance and compensation
Primary Disturbance: ⇣ pH (<7.4), ⇣ HCO3 (<24)
*loss of bicarb or gain of H+
Calculate anion gap: [Na] – [Cl + HCO3]
*high-anion gap (>12mEq/L) ⇢ “MUDPILES” ⇢
*normal (6-12mEq/L) ⇢ calculate UAG
UAG: [urine Na] + [urine K] – [urine Cl]
*⊖UAG ⇢ GI HCO3 loss (diarrhea)
*⊕UAG ⇢ RTA (⇣ renal acid excretion)
Respiratory Compensation: ⇡ RR ⇢ hyperventilation = ⇣ PCO2 (<40)
Expected PCO2: ⇣ [PCO2] 1.3mmHg per 1mEq/L ⇣ [HCO3]
*full compensation expected within 12-24h
DX: ketones, lactate, BUN/creatinine +/- tox screen
TX: directed at underlying cause
TX: Na, K, & HCO3 repletion PRN
TX: correct metabolic abnormalities to prevent nephrocalcinosis/CKD
*Distal: NaHCO3, often requires K supplementation
*Proximal: NaHCO3 or KHCO3 (more needed), thiazide diuretic
*⇡⇡ K: fludrocortisone, restrict dietary K, furosemide, NaHCO3
Metabolic Alkalosis primary disturbance and respiratory compensation
Primary Disturbance: ⇡ pH (>7.4), ⇡ HCO3 (>24)
*loss of H+ or gain of bicarb
Urinary Cl <20mEq/L ⇢ chloride responsive ⇢
Urinary Cl >20mEq/L ⇢ chloride unresponsive ⇢
*Urinary K <30mEq/L ⇢ laxative abuse, severe ⇣ K
*Urinary K >30mEq/L ⇢ look at BP
⊘HTN: Bartter, Gitelman
⊕HTN: consider mineralocorticoid excess
Respiratory Compensation: ⇣ RR ⇢ hypoventilation = ⇡ PCO2 (>40)
Expected PCO2: ⇡ [PCO2] 0.7mmHg per 1mEq/L ⇡ [HCO3]
*full compensation expected within 12-24h
TX: IV 0.9% NaCl (NS), treat underlying cause
TX: patients w/ severe alkalosis (pH >7.6) sometimes require more urgent correct of blood pH
*hemodialysis an option if volume overloaded + renal dysfunction
*Acetazolamide 250-375mg ⇡ HCO3 excretion but may also
accelerate urinary losses of potassium & phosphate
Respiratory Acidosis (hypercapnia) acute vs chronic
ACUTE:
*acute lung disease (e.g., pneumonia, pulmonary edema), acute COPD/asthma exacerbation
*CNS depression d/t head trauma, postictal state, drugs (e.g., opiates, BDZs), OSA
S/SXS: HA, confusion, anxiety, drowsiness, tremor, blunted DTRs, myoclonic jerks, asterixis +/- papilledema
CHRONIC:
*airway obstruction (e.g., COPD/asthma)
*respiratory muscle weakness (e.g., Myasthenia gravis, ALS, Guillain-Barre, Multiple Sclerosis)
S/SXS: may be well tolerated, but may have memory loss, sleep disturbances, excessive daytime sleepiness, personality changes
Respiratory Acidosis primary disturbance and metabolic compensation
Primary Disturbance: ⇣ pH (<7.4), ⇡ PCO2 (>40)
*hypoventilation (retain CO2)
ACUTE TX:
*noninvasive ventilation (BiPAP) to blow off CO2
*invasive ventilation (trach) sometimes needed
*Naloxone for opioid OD
Metabolic Compensation: ⇡ HCO3 reabsorption (>24)
Expected HCO3, Acute: ⇡ [HCO3] 1mEq/L per 10mmHg ⇡ [PCO2]
Expected HCO3, Chronic: ⇡ [HCO3] 3.5mEq/L per 10mmHg ⇡ [PCO2]
*full compensation expected within 3-5d
CHRONIC TX:
*directed at underlying cause
*chronic hypercapnia must be corrected slowly (i.e., over hours to minutes) because lowering PCO2 too rapidly can cause post-
hypercapnic “overshoot” alkalosis ⇢ seizures, death
Respiratory Alkalosis acute vs chronic
ACUTE: **think ⇢ pain, anxiety, or hypoxemia (e.g., high altitude, pneumonia, PE, ARDS)
*fever, sepsis, stroke, seizures (postictal)
*mechanical overventilation, drugs (e.g., salicylates, theophylline, progesterone)
S/SXS: lightheadedness, confusion, peripheral/circumoral paresthesias, cramps, syncope
*hypocalcemia ⇢ carpopedal spasms
CHRONIC: PE during pregnancy, liver failure, hyperthyroidism, brainstem tumor
S/SXS: asymptomatic, no specific signs
Respiratory Alkalosis primary disturbance and metabolic compensation
Primary Disturbance: ⇡ pH (>7.4), ⇣ PCO2 (<40)
*hyperventilation (blow off CO2)
expected within 3-5d
TX: directed at underlying cause
*not life-threatening, pH lowering interventions not needed
Metabolic Compensation: ⇣ HCO3 reabsorption (<24)
Expected HCO3, Acute: ⇣ [HCO3] 2mEq/L per 10mmHg ⇣
full compensation
AKI defintion and sx
AKI: sudden loss of renal function w/ subsequent BUN/Cr ⇡
➀ SCr ⇡ ≥0.3mg/dL within 48h ➁ SCr ⇡ ≥1.5x baseline within 7d ➂ Urine output <0.5mL/kg/h for ≥6h
S/SXS: symptoms of uremia may develop later as nitrogenous
products accumulate ⇢ anorexia, N/V, weakness, confusion,
myoclonic jerks, seizures, coma
PE: +/- asterixis & hyperreflexia
» Uremic pericarditis: pleuritic CP worse when supine, improves w/ leaning forward
▪︎⊕pericardial friction rub
Prerenal AKI: MCC of AKI
causes, dx, tx
PATHO: any condition that leads to decreased renal perfusion (MCC, ~60%)
» Hypovolemia: GI loss (e.g., V/D, bleeding), renal losses (e.g., diuretics), sweat/burns, 3rd-spacing
» Hypotension: shock (e.g., hypovolemic, myocardial, septic)
» Edematous states: heart failure (⇣ CO), cirrhosis
» Afferent (preglomerular) arteriolar dilation (e.g., NSAIDs, calcineurin inhibitors)
» Efferent (postglomerular) arteriolar constriction (e.g., ACEI/ARBs)
dx
▪︎BUN/Cr ratio >20:1
▪︎FENA <1%
▪︎UNa <20mEq/L
▪︎urine osmolality >500mOsm/kg
▪︎urinary sediment ⇢ hyaline casts
tx
▪︎IV fluid resuscitation for hypovolemia
▪︎DC offending drugs
▪︎hemodynamic support as indicated (e.g., shock)
Postrenal AKI (~5%) causes, dx, tx
PATHO: bilateral obstruction of urinary flow from renal pelvis to urethra
» Acquired obstructions (e.g., BPH, catheter injuries, tumors, stones, bleeding w/ clot formation)
» Neurogenic bladder (e.g., multiple sclerosis, spinal cord lesions, peripheral neuropathy)
» Congenital malformations (e.g., posterior urethral valves)
dx
▪︎⇡ creatinine in bilateral obstruction
▪︎urine osmolality <350mOsm/kg
▪︎postvoid residual volume >200mL suggests BOO
▪︎urinary sediment ⇢ normal, red cells, white cells, or crystals
*BUN/Cr ratio, FENA, & UNa vary
Renal U/S ⇢ hydroureter/hydronephrosis
Bladder outlet obstruction (BOO):
▪︎urethral catheterization to relieve obstruction
Ureteral or renal pelvic obstruction:
▪︎ureteral stenting, percutaneous nephrostomy
Intrinsic AKI: Acute Tubular Necrosis (ATN), MC intrinsic AKI
causes, dx, tx
ATN: caused by either ischemic damage or toxins; tubules necrose, die, & slough off
» Ischemic: renal hypoperfusion most often caused by hypotension or sepsis
» Nephrotoxins: IV contrast, aminoglycosides, amphotericin B, NSAIDs, cyclosporine, vancomycin
▪︎Heme pigments: myoglobinuria (rhabdomyolysis), hemoglobinuria (hemolysis)
▪︎Endogenous toxins: uric acid (tumor lysis syndrome), Bence-Jones proteins (multiple myeloma)
dx
▪︎BUN/Cr ratio <20:1 ▪︎FENA >1%
▪︎urine osmolality <350mOsm/kg ▪︎UNa >20mEq/L
▪︎urinary sediment ⇢ muddy brown granular casts, renal tubular epithelial cells
tx
▪︎DC any potential nephrotoxins
▪︎supportive therapy w/ IV fluids
» Oliguric: strict fluid balance monitoring
» Polyuric: replace fluid/electrolyte losses
Intrinsic AKI: Acute Interstitial Nephritis (AIN) causes, dx, tx
AIN: inflammatory infiltrate & edema affecting the renal interstitium; develops over days to months
▪︎inflammatory infiltrates ⇢ tissue edema & tubular cell damage ⇢ compromised tubular flow
▪︎allergic: drugs act as haptens ⇢ type IV hypersensitivity reaction
» Medications (MCC)
» Bacterial infections
» Viral infections
» Autoimmune
S/SXS: AKI +/- morbilliform rash, fever, arthralgias, flank pain
dx
▪︎BUN/Cr ratio <20:1
▪︎urinary sediment ⇢ white cells, white cell casts +/- eosinophils
tx
▪︎DC causative agents, treat underlying disease
▪︎AKI supportive therapy x3-5d
Glucocorticoids
Intrinsic AKI: Acute Glomerulonephritis (AGN) causes
Poststreptococcal GN: usually affects children 3-12yo, self-limiting
▪︎occurs after group A strep infections ⇢ 1-2wks after pharyngitis (MC), 3-4wks after skin infection (impetigo)
▪DX: ⊕ASO, ⊕ADB, ⇣ C3
» IgA Nephropathy (Berger disease): MCC of AGN; young males within days (24-48h) after URI/GI infection
▪︎S/SXS: gross hematuria & flank pain + acute URI ▪︎BX: mesangial IgA immune complex deposits
» Membranoproliferative GN (MPGN): associated w/ SLE, HCV, & cryoglobulinemia
▪︎glomerular injury d/t immune complex deposition &/or a complement-mediated mechanism
▪︎DX: ⇣ C3/C4
» Alport syndrome (hereditary nephritis): genetic defect in type IV collagen; most often X-linked, ♂︎ > ♀︎
▪︎S/SXS: isolated persistent hematuria, sensorineural hearing loss, anterior lenticonus
▪︎BX: variable thickening/thinning of GBM (basket-weave appearance)
» Rapidly progressive GN (RPGN): severe manifestations of glomerulonephritis
▪︎renal function declines rapidly over days to weeks; poor prognosis (ESRD within weeks to months)
▪︎BX: crescent formation made of plasma proteins & fibrin
Goodpasture syndrome (anti-GBM antibody disease): antibodies against type IV collage of the GBM
▪︎DX: ⊕anti-GBM antibodies, normal C3
▪︎BX: linear IgG deposits along GBM
Intrinsic AKI: lupus nephritis causes, sx, dx, tx
PATHO: mesangial/subendothelial immune complex deposition (e.g., anti-dsDNA/anti-Sm Ab), expansion/thickening of mesangium, capillary walls, &/or GBM
▪︎S/SXS: hematuria, edema, foaming urine, HTN
▪︎DX: UA + creatinine, confirm w/ renal BX
▪︎TX: cyclophosphamide + prednisone
Intrinsic AKI: Acute Glomerulonephritis sx, dx, tx
S/SXS: hematuria (i.e., cola-colored urine), HTN
▪︎AKI symptoms, edema (less than nephrotic)
dx
LABS: proteinuria <3.5g/d, often ⇣ C3
AKI ⇢ ▪︎BUN/Cr ratio >20:1
▪︎UNa <20mEq/L
▪︎FENA <1%
▪︎urinary sediment ⇢ RBC casts*
TX: supportive AKI therapy plus
▪︎sodium/water restriction
▪︎symptomatic azotemia: dialysis
Protein &/or HTN: ACEI/ARBs
Severe HTN &/or edema: diuretics
Poststreptococcal GN ⇢ ABX
▪︎PCN (throat), topical mupirocin (skin)
kidney transplant only definitive
Nephritic vs nephrotic syndrome: patho, hallmarks, sx, UA, bx
NEPHROTIC
patho: glomerular damage (increase urinary protein loss)
Hallmarks: proteinuria, edema, hypoalbuminemia, hyperlipidemia
sx: edema (peripheral and periorbital) frothy urine
UA: proteinuria, fatty casts, maltese cross
bx: hypocellular
NEPHRITIC
patho: immune mediated glomerular inflammation, increased urinary protein and RBC loss
Hallmarks: hematuria, HTN, proteinuria, azotemia
Sx: Hematuria, HTN, azotemia, oliguria, fever, abdominal pain
UA: hematuria, proteinuria
bx: hypercellular
Priapism ischemic vs nonischemic
dx, tx
Prolonged, painful erections w/o sexual stimulation
Ischemic (Low-Flow): decreased venous outflow may lead to a compartment syndrome, increasing acidosis, & hypoxia in the cavernous tissue; painful & rigid erection – MC type
*EMERGENCY
Nonischemic (High-Flow): increased arterial inflow due to a fistula between the cavernosal artery & corpus cavernosum
*commonly related to perineal or penile trauma
*less painful, not fully rigid compared to ischemic
dx
Cavernosal blood gas:
*high-flow: results similar to ABG; normal glucose
*low-flow: hypoglycemia, hypoxemia, hypercarbia, acidemia
Doppler U/S:
*high-flow: normal or high blood flow
*low-flow: minimal or absent blood flow
tx
Ischemic (Low-Flow):
*phenylephrine intracavernosal injection (1st line)
-MOA: alpha-agonist 🡪 contracts cavernous
smooth muscle 🡪 increased venous outflow
-CI: cardiac or cerebrovascular hx
*needle aspiration *can be added to phenylephrine
Nonischemic (High-Flow):
*observation – most resolve within hrs-days
*refractory: nonpermanent arterial embolization or surgical ligation may be used if refractory
Acute Cystitis defintion, sx, dx, tx
PATHO: usually an ascending infection of the lower urinary tract from the urethra
Etiologies:
*E. coli MC
sx
Irritative sxs: dysuria (burning), frequency, urgency
*hematuria, suprapubic pain & tenderness
dx
UA: pyuria (>10WBCs/hpf), hematuria, leukocytes esterase, nitrites, cloudy urine, bacteriuria
Urine culture: definitive
*epithelial (squamous cells) = contamination
tx
- nitrofurantoin or TMP-SMX
- FQs second line (“floxacin”)
- phenazopyridine (analgesic)
*turns urine orange
