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
Acute Pyelonephritis causes, MCC, sx, dx, tx
Infection of the upper GU tract (kidney parenchyma & renal pelvis)
PATHO: usually an ascending infection of the lower urinary tract
Etiologies: E. coli MC
sx
Upper tract sxs: fever, chills, back/flank pain; N/V
Lower tract sxs: dysuria, urgency, frequency
PE:
+ CVA tenderness
Fever, tachycardia
dx
UA:
*pyuria (>10WBCs/hpf)
*leukocyte esterase
*nitrites
*hematuria, cloudy urine
*WBC casts – HALLMARK
CBC: leukocytosis w/ left shift
Urine culture: definitive
tx
Outpatient: FQs first line (“floxacin”)
Inpatient: cephalosporins, FQs, aminoglycosides, penicillins
ADMIT: older age, signs of obstruction, comorbid conditions, inability to tolerate PO abx
Pregnancy: IV ceftriaxone
Epididymitis defintion, MCC, sx, dx, tx
Epididymal pain & swelling thought to be secondary to retrograde infection or reflux of urine – bacterial infection MC
Etiologies:
*males 14-35: chlamydia trachomatis (MC), Neisseria gonorrhea
*men >35: E. coli MC
S/SXS: gradual onset (hours to days) of unilateral testicular pain & swelling + groin, flank, or abdominal pain
+/- fever/chills, irritative sxs (urgency, frequency, dysuria)
PE:
▪︎scrotal swelling/tenderness
▪︎epididymal tenderness & induration
⊕Prehn sign: relief of pain w/ scrotal elevation
⊕cremasteric reflex: stroking of inner thigh causes elevation of ipsilateral testis
dx
Scrotal U/S – enlarged epididymis, increased testicular blood flow
UA: pyuria (↑ WBCs) or bacteriuria
NAAT for gonorrhea & chlamydia
tx
Scrotal elevation, NSAIDs, cool compresses
<35yrs: doxycycline (100mg BID x10d) + ceftriaxone (250mg IM x1)
>35yrs: FQs (ciprofloxacin, ofloxacin, levofloxacin)
Bacterial in children: cephalexin or amoxicillin
Orchitis defintion, MC, sx, dx, tx
Etiologies: viral MC (mumps, echovirus, coxsackie, rubella)
S/SXS: scrotal pain, swelling, tenderness
PE: scrotal erythema & tenderness
dx
UA: pyuria (↑ WBCs) or bacteriuria
NAAT for gonorrhea & chlamydia
tx
Symptomatic – NSAIDs, bed rest, scrotal support, cool packs
Prostatitis acute vs chronic: defintion, sx, dx, tx
Prostate gland inflammation secondary to an ascending infection
Acute:
*>35yrs: E. coli MC
*<35yrs: gonorrhea & chlamydia
Chronic:
*E. coli MC, proteus
sx
Irritative SXS ⇢ frequency, urgency, dysuria
Obstructive SXS ⇢ hesitancy, weak stream, incomplete emptying
Acute: exquisitely TENDER prostate
*fever, chills, perineal pain
Chronic: NONTENDER (or minimally tender) prostate
*usually presents as recurrent UTIs or intermittent dysfunction
PE: boggy prostate
dx
UA & urine culture:
*acute: pyuria & bacteriuria
*chronic: + after massage
tx
Acute:
>35: FQs or TMP-SMX x4-6wks
<35: ceftriaxone + doxycycline
Chronic: FQs or TMP-SMX x6-12wks
*tamsulosin can help w/ chronic pain
Hypovolemia defintion and causes
HYPOVOLEMIA:
*secondary to loss of sodium AND water from ECF
*results in compromised tissue perfusion
Etiology:
*GI losses: vomiting, diarrhea, bleeding
*Renal losses: diuretics, hypoaldosteronism, osmotic
diuresis via glucosuria, salt-wasting nephropathies
*Skin losses: sweat, burns
*Third-spacing sequestration: intestinal obstruction,
crush injury, ascites, pancreatitis/peritonitis
Compensatory Mechanisms:
*RAAS activation ⇢ Na & H2O reabsorption
*ADH release ⇢ H2O reabsorption
DEHYDRATION:
*H2O loss from ICF ⇢ ECF hypertonicity (⇡ Na)
*H2O net shift: ICF ⇢ ECF
Etiology: insensible losses, diabetes insipidus
S/SXS: secondary to hypernatremia (e.g., HA, confusion, dizziness)
Hypovolemia sx and PE
S/SXS related to VOLUME DEPLETION:
*lack of energy, easy fatigability, thirst, muscle cramps
*postural dizziness, oliguria
S/SXS related to FLUID LOSS ETIOLOGY:
*V/D, polyuria, severe skin burn
*pain caused by underlying third-spacing mechanism
S/SXS related to ELECTROLYTE ABNORMALITIES:
*hyponatremia ⇢ N/V, lethargy, confusion, seizures
*hyperkalemia ⇢ N/V/D, ileus, muscle weakness
*acidosis ⇢ tachypnea
*alkalosis ⇢ neuromuscular irritability (spasms)
Physical Exam:
*⇣ interstitial volume ⇢ skin/mucous membrane signs
▪︎ dry skin, ⇣ turgor, tenting, dry mucous membranes
*⇣ plasma (intravascular) volume ⇢ SBP & JVP reductions
▪︎ SBPΔ as severity of volume deficit increases
⤷ ~NML ⇢ orthostasis ⇢ posture-independent low SBP
▪︎ ⇣ intensity of Korotkoff sounds & radial pulse
▪︎ ⇣ JVP
*Hypovolemic Shock ⇢ tachycardia, cold/clammy extremities, cyanosis, low UO <15mL/h, agitation, confusion
Hypovolemia dx
LABS:
*low urine volume (oliguria)
*BUN/creatinine ratio >20:1
*d/t ⇡ Na reabsorption & resultant ⇣ urea excretion
▪︎ ⇡ BUN (ref. 5-20mg/dL) ⇢ prerenal azotemia
▪︎ creatinine ⇡ only if loss severe enough to ⇣ GFR
*hyponatremia (ref. 135-145mEq/L)
*hyperkalemia (ref. 3.5-5.0mEq/L)
*acid-base disturbances *depends on mechanism of loss
▪︎ vomiting, diuretics (H+ loss) ⇢ metabolic alkalosis
▪︎ diarrhea (HCO3 loss) ⇢ metabolic acidosis
*Hct & albumin *depletion of plasma volume
▪︎ ⇡ Hct (i.e., relative polycythemia)
▪︎ ⇡ albumin (ref. 3.5-5g/dL)
DX: clinical, confirmed by low urine Na concentration
*urine Na <20mEq/L
*FENA <1%
*urine osmolality concentration >450mOsm/kg
▪︎ specific gravity >1.015
*UA normal in hypovolemia since kidney is not diseased
▪︎ i.e., ⊖protein, ⊖cells/casts
Hypovolemia tx
Resuscitation: IV fluid boluses
*20mL/kg IV NS or LR
Maintenance:
*calculate maintenance rate
*D5½NS + 20mEq KCl preferred
Monitor: I&Os, electrolytes, weight
Hypervolemia causes
Isotonic Hypervolemia (salt gain = H2O gain):
*intravascular overload of IV fluids w/ electrolytes
*postop/trauma stress causing ⇣ Na/H2O excretion
*renal insufficiency, cirrhosis, CHF
Hypotonic Hypervolemia (salt gain < H2O gain):
*replacement of GI losses w/ NaCl-poor solutions
*third-spacing, ⇡ ADH w/ surgical stress, SIADH
Hypertonic Hypervolemia (salt gain > H2O gain):
*excessive Na load w/o adequate H2O intake
Hypervolemia sx, dx, tx
sx
*tachypnea, orthopnea, weight gain
*pulmonary edema, crackles, rales
*ascites, pleural effusions
*⇡ JVD, peripheral edema, oliguria
Hypertonic ⇢ symptoms of sodium excess
*HA, confusion, dizziness, etc.
DX: mainly clinical
*serum Na (ref. 135-145mEq/L)
Supportive labs/imaging:
*CXR, ECHO
*NT-proBNP
tx
*sodium & water restriction
*loop diuretics
*dialysis may be required if severe
Hyponatremia dx and tx
dx
Normal Serum Sodium: 135-145mEq/L
SEVERE HYPONATREMIA: <125mEq/L
*urine osmolality (mOsm/kg)
≤100 ⇢ ADH-independent
>100 ⇢ ADH-dependent ⇢ look at urine sodium
*urine sodium (ref. ~20mEq/L)
<25: extrarenal
25-40: give 1L IV NS ⇢ repeat urine Na
>40: renal ⇢ endo workup (e.g., TSH, cortisol)
▪︎⊖further workup⇢ SIADH
tx
Symptomatic (seizures, confusion):
*emergent tx required regardless of etiology
*IV 3% NaCl in 100mL bolus over 10min
▪︎can repeat up to 2x if needed
*4-5mEq/L ⇡ of Na usually sufficient to promptly
reverse neurological symptoms & ⇣ ICP
Hypovolemic: IV normal saline
Hypervolemic: fluid restriction +/- loop diuretics
Euvolemic: fluid restriction
Hypernatremia sx, dx, tx
sx
S/SXS (Na >160mEq/L): lethargy, weakness, & irritability
dx
DX: often from hx, MCC: water loss w/o replacement
*If Na >150 in alert patient w/ water access
⇢ suspect primary hypodipsia
*if etiology unclear ⇢ urine osmolality (mOsm/kg)
<300: diabetes insipidus ⇢ DDAVP challenge
▪︎Uosm ⇡ after DDAVP ⇢ central, if not ⇢ nephro
300-600: possible osmotic diuresis: ⊕glucosuria
>600: extrarenal ⇢ look at urine sodium
*urine sodium (mEq/L)
<20 ⇢ hypovolemia (e.g., vomiting, diarrhea, etc.)
>100 ⇢ sodium overload (i.e., iatrogenic)
tx
*requires induction of ⊕water balance
*calculate FWD
*hypotonic fluids ⇢ D5W most commonly used
If hypovolemic + hypernatremic
*FIRST: correct hypovolemia w/ ISOTONIC fluids
*then correction of sodium w/ hypotonic fluids
Hypokalemia sx, dx, tx
S/SXS: usually asymptomatic until K <3.0mEq/L
*magnesium regulates K: low Mg ⇡ renal K excretion *muscle weakness, cramps, ⇣ DTRs
dx
*normal K 3.6-5.0mEq/L
*24h-urinary K excretion >30mEq/d ⇢ renal wasting
*spot urine K/UCr ratio >13mEq/g ⇢ renal wasting
EKGΔ
*flat/inverted T waves ⇢ ST depression ⇢ U waves
*prolonged QT, PAC/PVCs, bradycardia, VT/VFIB
tx
*PO K replacement for mild/moderate
*IV KCl reserved for K <3.0mEq/L
▪︎avoid dextrose fluids ⇢ stimulates insulin
release which shifts K intracellularly
*give Mg w/ potassium replacement
Hyperkalemia sx, dx, tx
S/SXS: often asymptomatic until arrhythmias (K >7.0)
*CKD (uncommon until GFR <15) *arrythmias (e.g., AV blocks, VFIB, arrest), N/V/D
*hypoaldosteronism (Addison Disease)
*muscle weakness, flaccid paralysis
dx
LABS: glucose, electrolytes, CBC, transaminases, ABG
*chronic ⇡ K ⇢ workup for hypoaldosteronism
EKGΔ *NOTE ⇢ poor correlation between K & EKGΔ
*peaked T waves ⇢ ST depression ⇢ QRS widening
*QRS widening ⇢ sine waves ⇢ VFIB/asystole
tx
Cardiac toxicity, muscle weakness, K >6.5:
*IV calcium gluconate to stabilize myocardium
*Lower extracellular calcium: β-agonists, insulin w/ glucose (NaHCO3 reserved for severe cases)
*Magnesium sulfate if digitalis toxicity
*hemodialysis for refractory
Hypocalcemia sx, PE, dx, tx
SXS:
tetany**
*carpopedal spasm, cramps hyperphosphatemia, aminoglycoside abx, foscarnet
*perioral paresthesias
PE: maneuvers to elicit latent tetany
*Chvostek sign: tapping facial nerve (below/in front ear) causes twitching of facial muscles
*Trousseau sign: ipsilateral carpopedal spasm when upper arm compressed w/ BP cuff
dx
EKGΔ: prolonged QT
tx
Severe, Symptomatic (tetany, arrythmias):
*IV calcium gluconate + continuous Ca infusion
*usually added to D5W
*monitor calcium level q4-6h to maintain level
at 7-8.5mg/dL
Asymptomatic:
*PO calcium (calcium carbonate) & vitamin D
*Mg supplementation if also low
*low calcium associated w/ ⇣ albumin does not require replacement therapy
Hypercalcemia sx, dx, tx
S/SXS: <12mg/dL often asymptomatic ⇢ “stones, bones, abdominal groans, psychiatric moans”
*nephrolithiasis (Ca oxalate > Ca phosphate)
*bone pain, osteopenia/osteoporosis
*anorexia, N/V, constipation *anxiety, lethargy, cognitive changes
dx
Primary Hyperparathyroidism: ⇡ PTH, ⇡ Ca, ⇣ PO4
*if PTH normal/mildly ⇡ get 24h urine Ca excretion
tx
Symptomatic, >14mg/dL:
*IV NS until euvolemia achieved
*Cinacalcet: suppresses PTH secretion
Hypomagnesemia sx, dx, tx
S/SXS: tremors, cramps, confusion,
⇡ DTRs, Chvostek/Trousseau signs, weakness, HTN, tachycardia, torsades
dx
*normal Mg 1.8-3.0mg/dL
*associated ⇣ Ca & hypocalciuria, ⇣ PTH, ⇣ K
EKGΔ: wide QRS, prolonged PR, ventricular arrhythmias, torsades
tx
Symptomatic:
*IV magnesium sulfate in D5W or NS
Chronic: PO magnesium oxide
Hypermagnesemia sx dx tx
S/SXS: muscle weakness, ⇣ DTRs, confusion, flaccid paralysis, ileus, hypotension, respiratory muscle paralysis, complete heart block, cardiac arrest
dx
*normal Mg 1.8-3.0mg/dL
*CKD: ⇡ BUN, ⇡ Cr, ⇡ K, ⇡ PO4, ⇡ uric acid, calcium often ⇣
EKGΔ: wide QRS, prolonged PR, prolonged QT
tx
*DC exogenous sources of Mg
*calcium chloride (antagonizes Mg)
*hemodialysis may be necessary, especially in patients w/ severe CKD
Hypophosphatemia sx, dx, tx
S/SXS: rare until PO4 <1mg/dL
*weakness, paresthesias
*encephalopathy (irritability, confusion, seizures, dysarthria), ⇣ contractility, salicylate poison
*respiratory failure, bone pain
dx
*normal PO4 2.5-4.5mg/dL
*normal 24h urine PO4 <100mg/d, FEPO4 <5%
▪︎renal wasting MC in hyperparathyroidism & Fanconi
Fanconi: metabolic acidosis, glucosuria, aminoaciduria
XR (chronic): changes resembling osteomalacia
tx: PO phosphate
Hyperphosphatemia sx dx, tx
S/SXS: generally asymptomatic
*manifestations of underlying disorder
dx
labs and EKGΔ: QT prolongation
tx: IV calcium gluconate
Urge Incontinence sx, dx, tx
Involuntary urinary leakage preceded by or accompanied by sudden urge to urinate
sx
Involuntary urinary leakage preceded by or accompanied by sudden urge to urinate
tx
*bladder training (75% improvement) – timed frequent voiding, using a voiding diary to identify the shortest voiding intervals, decreased fluid intake
*diet: avoid spicy foods, citrus fruit, chocolate, alcohol, & caffeine
*lifestyle modifications & Kegel exercises
*antimuscarinics – first line medical therapy (tolterodine, oxybutynin)
Overflow Incontinence defintion, sx, dx, tx
Urinary retention & incomplete bladder emptying leads to involuntary urine leakage once the bladder is full (aka it overflows)
sx
*loss of urine w/ no warning (as in urge) or triggers (as in stress)
*leakage or dribbling in the setting of incomplete bladder emptying, weak or intermittent urinary stream, hesitancy, frequency, nocturia – leakage often occurs w/ changes in position
Diagnosis: clinical – post void residual >200mL
*Urodynamic testing to differentiate it from urethral obstruction in men
tx
Management of Bladder Atony:
*intermittent or indwelling catheterization first line
*cholinergics (Bethanechol) – increases detrusor muscle activity
Management of BPH: alpha-blockers for rapid symptom relief; 5-alpha-reductase inhibitors
Stress Incontinence causes, sx, dx, tx
Involuntary leakage of urine that occurs once ↑ abdominal pressure (e.g., exertion, coughing, laughing, sneezing) is greater than urethral pressure & resistance or urine flow
sx
urine leakage during times of increased intra-abdominal pressure (e.g., coughing, laughing, sneezing, lifting heavy objects) – there is NO urge to urinate prior to leakage
dx: clinical
UA with culture and sensitivity
*Cystoscopy and urodynamic testing to evaluate function
tx
*pelvic floor muscle (Kegel) exercises – initial treatment of choice
*lifestyle modifications – used in conjunction w/ pelvic floor exercises
*pessaries
*surgery
*alpha-agonists: midodrine & pseudoephedrine (only mildly efficacious)
Nephrolithiasis types, sx, dx, tx
Types:
*calcium oxalate (MC)
calcium phosphate
*uric acid: high protein foods, gout, chemo
*struvite: magnesium ammonium phosphate
*cystine: congenital defect in reabsorption
sx
Renal colic: sudden, constant upper lateral back or flank pain over the CVA radiating to the groin or anteriorly; difficult to find a comfortable position
N/V, frequency, urgency, hematuria
PE: CVA tenderness
dx
UA:
*hematuria
*pH <5.0: uric acid, cystine
*pH >7.2: struvite
Non-contrast CT abdomen/pelvis
KUB x-ray: calcium & struvite stones are radiopaque
tx
<5mm:
- 80% chance of spontaneous passage
- IV fluids, analgesics, antiemetics
- tamsulosin
5-10mm:
- 20% chance of spontaneous passage
- extracorporeal shock wave lithotripsy
- ureteroscopy w/ or w/o stent: immediate relief of obstruction
- percutaneous nephrolithotomy: stones >10mm
Urethritis sx, dx, tx
Non-gonococcal urethritis (NGU): chlamydia trachomatis
Gonococcal urethritis: abrupt onset of sxs
*opaque, yellow, white, or clear thick discharge
*pruritis
sx
Urethral discharge & penile or vaginal pruritis
Dysuria
Abdominal pain or abnormal vaginal bleeding
dx
NAAT
Gram stain:
*no organisms = NGU
*gram (-) diplococci: gonorrhea
tx
Gonorrhea: ceftriaxone 250mg IM x1 plus azithromycin 1g x1
Chlamydia: doxycycline 100mg BID x10d or azithromycin 1g PO
Balanitis sx, dx, tx
Inflammation of the glans penis
sx
Pain, tenderness, pruritis
PE: erythema
+/- purulent or curd-like exudate
+/- ulcerations
dx: clinical
Complications:
*phimosis: constricted foreskin cannot be retracted over the glans
*paraphimosis: constricted foreskin is retracted over the glans & cannot be reduced
tx
- improved hygiene
- saline solution bathing
Bacterial: topical metronidazole
Testicular Torsion sx, dx, tx
*spermatic cord twists & cuts off testicular blood supply due to congenital malformation
sx
ABRUPT ONSET: scrotal, inguinal, or lower abdominal pain
▪︎N/V
PE:
▪︎swollen, tender, retracted testicle (high-riding), may have horizontal lie
⊖Prehn sign: no pain relief w/ scrotal elevation
⊖cremasteric reflex: no elevation of testicle after stroking the inner thigh
dx
Clinical DX: in pts w/ H&P suggestive of torsion, imaging should NOT be performed **immediate surgical exploration
Emergency surgical exploration (definitive)
▪︎preferred over U/S if torsion is very likely
Testicular Doppler U/S
▪︎decreased or absent testicular blood flow
tx
*urgent detorsion & orchiopexy (ideally within 6hrs of pain onset)
*irreversible damage after 12hrs
*orchiectomy if not salvageable
