EOR- GU/renal Flashcards
what defines Acute kidney injury (AKI)?
- increase in serum Cr >50% OR 2. incr blood urea nitrogen (BUN) aka “azotemia”.
what is the RIFLE criteria?
stratum of progressive AKI injury: based on increasing % GFR decrease and decreased urine output:
Risk, Injury, Failure w/ outcomes - Loss, End stage kidney dz
3 types of AKI
pre-renal (MC), intrinsic, post-renal
define pre-renal AKI, what causes it?
decreased renal perfusion. Often leads to intrinsic if not corrected. Cause- hypovolemia or afferent constriction (Nsaids, IV contrast) w/ efferent dilation (ACEs,ARBs)
define intrinsic AKI, what are the 4 subtypes? which is most common
direct structural/fxn kidney damage - nephrotoxic, cytotoxic or prolonged ischemic = cellular cast formation. Includes… ATN (MC), AIN, acute glomerulonephritis, vascular
define ATN, what are the two types?
acute destruction tubules of nephron
Ischemic: cause- prolonged prerenal, hypotension, hypovolemia, post-operative
Nephrotoxic: exogenous (i.e. aminoglycosides), endogenous (gout, myoglobinuria from rhabdo, lymphoma/leukemia.
define AIN, what is the MC cause?
inflammatory or allergic response in interstituim (spares glomeruli + vessels). Cause- drug hypersensitivity (MC), infection, autoimmune, idiopathic.
AKI: acute glomerulonephritis vs vascular
acute glomerulonephritis: immune mediated inflammation of glomeruli –> RBC + protein leakage
Vascular: TTP, DIC, aneurysm, etc.
UA: what does each result indicate?
RBCs
Muddy brown casts + epithelial cell casts
WBC casts
RBCs - glomerulonephritis (AGN)
Muddy brown casts + epithelial cell casts - ATN
WBC casts - AIN
BUN/Cr: pre-renal vs ATN
BUN/Cr: prerenal >20:1, ATN 10-15:1
txt pre-renal vs ATN
Prerenal: volume repletion - restore renal perfusion
ATN: remove offending agent, IV fluids, furosemide (if euvolemic + not urinating). Most return to baseline in 72hrs
txt AIN vs glomerulonephritis
AIN: remove offending agent
Glomerulonephritis (AGN): high-dose steroids, cytotoxic agents
pathophys of how nephrotic dz causes edema
glomerular damage → proteinuria → decrease plasma oncotic pressure → edema.
primary vs secondary causes of nephrotic syndrome
Primary - minimal change disease (MC nephrotic syndrome in kids), focal segmental glomerulosclerosis (HTN in african americans + IV heroin abuse, HIV)
Secondary - systemic dz - DM
S+S nephrotic syndrome
edema (peripheral, periorbital - kids) - from low albumin in blood = low oncotic pressure. → ascites, anscara. DVT (liver tries to make more clotting factors to incr. Oncotic pressure).
Dx nephrotic syndrome - 2 ways
24hr urine collection = >3.5 g/day. UA dipstick = protein 3+, 4+ and oval fat bodies (“maltese cross shaped). Hypoalbuminemia, hyperlipidemia
txt for nephrotic syndrome: for minimal change dz, for edema, for proteinuria reduction
Minimal change = corticosteroids
Edema- diuretics
Proteinuria reduction - ACEIs, ARBs
hallmark signs of acute glomerulonephritis
Hallmark = HTN, hematuria (RBC casts), dependent edema, azotemia.
MC cause of acute glomerulonephritis worldwide? what is the typical presenting pt?
IgA nephropathy aka berger’s dz - young males w/in days after URI or GI infection.
young boy w/ facial edema after strep + cocacola urine.
post-infectious acute glomerulonephritis (MC GABHS)
goodpastures dz: what is the basic pathophys and resultant effects?
anti-GBM antibodies vs collagen of glomerular basement membrane in kidney and lung alveoli → kidney failure and hemoptysis. = linear IgG deposits.
what are 4 causes of acute glomerulonephritis?
IgA nephropathy (berger’s), post-infectious (i.e. GABHS), goodpastures dz (IgG), vasculitis
while UA is very useful for dx glomerulonephritis, what is the GOLD std?
renal Bx
prognosis of acute glomerulonephritis?
self-limited w/ good prognosis (except if rapidly progressive glomerulonephritis- MC in good pastures and vasculitis).
txt for bergers/proteinuria acute glom vs
txt for rapidly progressive/severe acute glomerulonephritis?
bergers/proteinuris: ACEIs +/- steroids.
severe: corticosteroids + cyclophosphamide (chemo drug)
define chronic kidney dz/failure, staging?
> 3 months progressive fxn decline.
Staging by GFR: I- normal (>90), II- 60-90, III- 30-60, IV - 15-30 V- <15.
Dx: Nephron destruction → hypertrophy of remaining nephrons → failure from increased workload = fibrosis, sclerosis, tubular dilation.
chronic kidney dz
3 MC causes of chronic kidney dz?
DM (MC), HTN, glomerulonephritis
Dx of chronic kidney dz: UA and imaging
proteinuria, UA- broad waxy casts (take shape of dilated tubules), incr BUN/Cr, kidney US - small kidneys.
txt of chronic kidney dz
prevent progression - HTN & proteinuria (ACEIs, ARBs), DM control
Stage V: end-stage renal dz requiring dialysis and/or transplant.
meds for BPH (4)
Meds- alpha1 agonists (zosins). Also can do PDE-5inhibitors (tadallafil), anticholinergics, 5-alpha reductase inhibitors (finasteride)
at what age can you dx cryptochordism?
if testical does not descend by 4months
txt for cryptochordism
Sx orchiopexy ASAP after 4months old.
define DM kidney dz vs DM nephropathy
“diabetic kidney dz” is an umbrella term, not a specific pathology - indicates albuminuria, decreased GFR or both. DM nephropathy = glomerular basement membrane thickening, endothelial damage, mesangial expansion and nodules, and podocyte loss.
Dx:persistently elevated albuminuria, DM/diabetic retinopathy, decreased GFR
DM nephropathy
when is DM nephropathy considered chronic?
> 3 months
txt for DM nephropathy
BP control - ACE or ARB w/ dihydropyridine CCB. Glycemic control - A1C <7%.
risk factors for erectile dysfxn
obese/sedentary, smoking, comorbidities, meds-SSRIs, CVD.
txt options for erectile dysfxn
lifestyle changes/reduce risk factors, meds- PDE-5 inhibitors (-afils) but NOT if taking nitrates, injections, vacuum device, implant. Testosterone replacement only if documented hypogonadism.
define hydrocele vs varicocele
Hydrocele: peritoneal fluid between parietal and visceral layers of tunica vaginalis. Caused from imbalance of production and abs of fluid from tunica vag. MC idiopathic. also inflammatory (i.e. epididymitis).
Varicocele: dilation of pampiniform plexus of spermatic veins. MC left sided (nutcracker effect of aorta + SMA on renal vein) , appears at puberty and grows over time.
Dx hydrocele vs varicocele
Hydrocele: translumination
Varicocele: “bag of worms”, increases w/ valsalva, decreases w/ trendelenburg
Txt of hydrocele + varicocele
Hydrocele: none if asymptomatic, Sx removal of sac if symptomatic
Varicocele: none, maybe Sx ligation or percutaneous venous embolization if poor semen analysis.
meds for various types of incontinence (stress, urge, overflow)
stress- alpha agonists (psuedophed, midodrine) [ not used clinically]
Urge - anticholinergics (oxybutinin, tolterodine), beta-3 agonists (mirabegron), Tricyclic antidepressants (TCAs) (amipramine - for nighttime symptoms)
Overflow: cholinergics or alpha blockers (tamsulosin)
MC types of kidney stones
MC Ca+ oxalate stones. Also Ca+phosphate, uric acid, struvite, cystine.
txt options for kidney stones
pain meds, hydration. <5mm pass spontaneously = Meds- tamsulosin + nifedipine (4wks). >10mm + other complicating factors = uro consult for lithotripsy/Sx/stents.
txt options phimosis vs paraphimosis
Paraphimosis: timely reduction of foreskin (manually or dorsal slit), pain control
Phimosis: stretching exercise, topical steroids (betamethasone), circumcision
what is a horseshoe kidney?
Horseshoe is the MC type of fusion - abnormal migration of both kidneys (ectopy) → fusion of one pole of each kidney. Congenital abnormality, MC lower poles.
what does a horseshoe kidney incr your risk of ? (3)
Increased risk of infection from increased urine stasis, increased risk wilms tumor, vesicoureteral reflux.
Txt of horseshoe kidney
usually none, if VUR- prophylactic abx to prevent UTI
Dx?: common d/o, often clinically silent, abnormality on chromosome 16 - PKD1 and PKD2 gene mutations. Can cause HTN and kidney fxn impairment. Can lead to end stage renal dz.
polycystic kidney dz
S+S polycystic kidney dz?
HTN, hematuria, proteinuria, kidney fxm impairment. Flank pain from renal hemorrhage, calculi or UTI
Dx polycystic kidney dz
US- renal cyst + FH.
mgmt polycystic kidney dz
HTN mgmt (ACE or ARB), Na restriction, increased fluids, tolvaptan - vasopressor.
Dx:? persistent reduction in GFR, txt resistant HTN, rise in serum creatinine (following ACE or ARB), recurrent flash pulm edema or CHF, deterioration of kidney fxn after aortic stent
renal vascular dz
txt options for renal vascular dz
HTN control + ASA, statins, smoking cessation, glycemic control (if DM), +/- revascularization (percutaneous transluminal renal angioplasty + stent)
testicular torsion: after what amount of time is there irreversible damage? which direction does it MC torse?
Irreversible damage to teste after 8hrs. MC medial torsion
Dx:? asymmetric high-riding teste, swelling, reactive hydrocele, +/- erythema, “knot” or blue dot superior to testes.
testicular torsion
Txt of testicular torsion: if Sx not available in what timeframe do you manually detorse? what indicates a successful detorse?
two hours
Successful detorse = relief of pain, change in teste axis and position, normal pulses on doppler.
MC pathogens to cause pyelo
MC - E coli. Also enterococci, pseudomonas, staph, candida.
Txt options for pyelo
FQs, carbapenem + vancomycin, ceftriaxone or pip/tazo.
MC causes of hypoCa+ (w/ low PTH, w/ high PTH), what results?
MC: w/ low PTH = postsurgical hypoPTH or autoimmune hypoPTH. With high PTH = chronic renal failure, Vit D deficiency, hypoMg.
Decreases excitation threshold for heart, nerves, muscles = less stimulus needed for contraction.
S+S hypoCa+
muscle cramp, finger/circumoral parasthesias, Tetany (Chvostek’s signs- facial spasm, Trousseau’s sign - carpal spasm), inc DTRs. diarrhea, abd pain, osteomalacia/dystrophy.
what other electrolyte abnormalities come with low Ca+, what EKG changes ?
low ionized Ca +/- inc phos, low Mg. EKG = prolonged QT interval
txt hypoCa+
oral Ca+ and Vit D (ergocalciferol, calcitriol). severe = IV Ca+ gluconate.
what are the two most common causes of hyperCa+
MC hyperPTH: Triad incr Ca, incr intact PTH, low phos. 2. Malignancy: secretes increased PTH-related protein) w/ decreased intact PTH.
what meds can cause hyperCa+
TZDs, lithium
S+S hyperCa+
MC asymptomatic, kidney stones, painful bones, abd groans, pyschic moans (weak, AMS, decreased DTRs)
txt for mild vs severe hyperCa+
mild (txt underlying cause). Severe: IV saline → furosemide, avoid HCTZ (increases Ca). severe: calcitonin, bisphosphonates IV, steroids.
causes of hypoK+
GI/Renal loss (diuretic, V/D). increased intracellular shifts: metabolic alkalosis, beta2 agonists, insulin, vit B12 txt.
EKG changes with hypoK+
EKG = Twave flattening → U wave.
causes of hyperK+
decreased renal excretion (renal failure, low aldosterone, adrenal insufficiency), meds (spironolactone, ACE/ARB, digoxin, BBs, NSAIDs), cell lysis, metabolic acidosis (DKA), catabolic states
symptoms of hyperK+
weakness, (progressive ascending), flaccid paralysis, cardiac (palpitations/arrhythmias), GI upset - diarrhea.
EKG changes with hyperK+
EKG= peaked T waves, QR shortened, wide QRS → P wave flat → sine wave → arrhythmias.
txt options for hyperK+
IV Ca gluconate, insulin w/glucose, kayexelate, B2agonists
two major causes of hypoMagnesemia
GI (malabs, ETOHics) or renal loss (DM,diuretics, PPIs)
s+s of hypomagnesemia
increased DTRs, Tetany (muscle cramps/contractions), AMS. hypocalcemia symptoms (Mg needed to make PTH), cardio- arrythmias, palpitations
what other electrolyte abnormalities come with low Mg, what EKG changes?
blood (low Mg, Ca and K), EKG= prolonged PR & QT → torsades.
causes for hyperNa+
HIGH Na+: hypovolemia (activates RAAS and ADH) or iatrogenic hyperKalemia (will prompt aldosterone to excrete K+ in exchange for Na+) → aldosterone = Na+ retention.
causes of hypoNa+
LOW Na+: caused by incr ADH/incr water intake→ impaired kidney ability to excrete free water. Clinically significant/True is hypotonic hyponatremia.
what is true hypoNa+ (hypertonic, isotonic, or hypotonic), what causes it - hypovolemic, hypervolemic, euvolemic?
hypotonic hyponat+ : increased free water. cause based on volume status…
hypovolemic: diarretics or diarrhea/vomitting
euvolemic: SIADH, hypothyroid, adrenal insufficiency, water intoxication
hypervolemic: edema (decr flow to kidney), nephrotic syndrome, cirrhosis
correction of hypo or hyper Na+, what is the rate of infusion and what is the reason?
LOW: correct level with water restriction +/- Na restriction, normal saline or ½ normal saline, hypertonic saline + furosemide.
Correct <0.5 mEq/L/h to prevent demyelination
HIGH: hypotonic fluids
Correct <0.5 mEq/L/h to prevent cerebral edema.
metabolic acidosis w/ high anion gap: what causes it?
too much acid
“MUDPILERS” methanol, uremia, DKA/alcoholic KA, propylene glycol, isoniazid/infection, lactic acidosis, ethylene glycol, rhabdo/renal failure, salicylates.
metabolic acidosis with normal anion gap: what causes it?
too little bicarbonate
“HARDUPS” hyperalimentation (artificial nutrient supply), acetazolamide, renal tubular acidosis, diarrhea, uretero-pelvic shunt, post-hypocapnia, spironolactone.
what is a normal anion gap?
[Na-(Cl + HCO3)] = 8-18 (normal)
causes of metabolic alkalosis
little acid or too much bicarb - seen with incr PCO2, hypovolemia, hypoK.
Causes: “CLEVER PD” contraction, licorice, endo (i.e. cushings), vomiting, excess alkali, refeeding alkalosis, post-hypercapnia, diuretics.
what causes respiratory acidosis or alkalosis?
acidosis: anything that causes hypoventilation
alkalosis: anything that causes hyperventilation
MC cause of hypervolemia (fluid overload)
MC renal failure → Na retention → fluid retention.
causes of dehydration from acute sequestration into “third space”?
intestinal obstruction, crush injury, Fx, acute pancreatitis).
txt options for UTI/pyelo
keflex, TMP/SMX, macrobid. Also cipro
Pyelo - Inpt: 1g IV ceftriaxone.
epididymitis/orchitis/urethritis MC pathogens and txt
MC GC, chlamydia. If not STI - pseudomonas, E.Coli.
Tx: ceftriaxone + doxycycline or azithromycin. Or levofloxacin
prostatitis: MC pathogens + txt
MC E.Coli + gonorrhea, C trachomatis.
Txt: FQs, TMP/SMX or, for STD- ceftriaxone + doxycyline or azithromycin.
horner’s syndrome: S+S,cause, Dx, txt
miosis, ptosis, anhidrosis. Caused by lesion in the sympathetic pathway (stroke, tumor, spinal cord injury) Dx: confirm with cocaine or apraclonidine eye drops (positive = no dilation). Txt underlying cause.
urethritis MC pathogens
Neisseria gonorrhoeae, Chlamydia trachomatis, and Mycoplasma genitalium are the most common organisms associated with urethritis. Trichomonas vaginalis and herpes simplex virus (HSV)
urethritis S+S, txt
S+S: dysuria, urethral pruritus, and/or urethral discharge
Txt: ceftriaxone + azithromycin
VERY itchy symmetric pattern of vesicles on palms and fingers, soles. Can be large bullae.Recurrent episodes over months/years.
dishydrotic eczema
txt for nummular or dishydrotic eczema
general eczema guidelines + high potency topical steroids
pruritic, polygonal, violaceous papules and/or plaques with an overlying white, lacelike pattern (Wickham’s striae)
lichen planus
txt for lichen planus
resolves on its own over 1-2 yrs, high potency topical steroids.
what kind of dermatitis is poison ivy?
allergic contact
txt of perioral dermatitis
STOP steroids. topical erythromycin or metronidazole
txt options for sebbhoreic dermatitis
topical antifungals, topical anti-inflammatories (calcineurin inhibitors - tacrolimus, pimecrolimus)
txt options for psoriasis
topical steroids, emollients.
txt for dermatophytes (tinea)
topical antifungals (terbinafine or azoles), oral if recurrent.
bald patch + exclamation point hairs.
allopecia areata
txt for onychomycosis (fingers vs toenails)
topical (for mild, <50% nail) or oral terbinafine. Fingernails - 6wks, toenails-12wks. (other options- azoles, griseofulvin)
MC pathogens for paronychia (infected ingrown toenail)
MC - staph, strep. Chronic - pseudomonas.
txt for paronychia
soak, I+D, abx staph coverage (augmentin, clindamycin, keflex)
single or multiple, flat, dome-shaped, cauliflower-shaped, filiform, fungating, pedunculated, cerebriform, plaque-like, smooth (especially on the penile shaft), verrucous, or lobulated.
condyloma accuminata (anogenital warts)
what strains HPV cause condyloma accuminata
HPV types 6,11
Nonspecific prodrome then in two days slapped cheek then lacy rash. Dx and cause?
erythema infectiosum (5ths dz) parvovirus B19
fever, malaise, cough, coryza, and conjunctivitis, followed by exanthem 2-4 days later. (starts on head and spreads down)
measles
what is the contagious period before and after measles rash
Contagious 5 days before rash, 4 days after.
acute, immune-mediated. target like lesions, often accompanied by erosions or bullae involving the oral, genital, and/or ocular mucosae. Common cause by HSV or other infections.
erythema multiform
txt for erythema multiforme
Self limiting w/in weeks. Symptomatic topical steroids or antihistamines.
MC causes of SJS and TEN
MC from drugs or mycoplasma PNA.
Autoimmune blistering,1 to 3 cm tense bulla on an erythematous, urticarial, or noninflammatory base, and blisters may be numerous and widespread
pemphigoid
Dx and Txt of bullous pemphigoid
Dx: clinical + detect circulating basement membrane zone antibodies by indirect immunofluorescence (IIF) and enzyme-linked immunoassay (ELISA)
Txt: topical steroid (e.g. clobetasol)
txt for folliculitis
Mild staph resolves w.out txt. Topical mupirocin or topical clindamycin. More severe/chronic: dicloxacillin, keflex, tmp/smx, or clindamycin.
txt for rosacea
avoidance of triggers of flushing, gentle skin care, and sun protection. metronidazole cream
txt cellulitis and erysipelas
5 days abx - keflex, TMP/SMX. Systemic symp w/ erysipelas = ceftriaxone, cefazolin
txt impetigo
Txt: mild - topical mupirocin, numerous/systemic - oral keflex, dicloxacillin
scaly, erythematous macules or papules on sites of chronic sun exposure. May progress to squamous cell carcinoma. MC fair skin adults + sun exposure.
actinic keratosis
which kind of spider bite do you txt with benzos or opiods for muscle spasm ?
black widow
