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Rotation > EOR- GU/renal > Flashcards

EOR- GU/renal Flashcards

1
Q

what defines Acute kidney injury (AKI)?

A
  1. increase in serum Cr >50% OR 2. incr blood urea nitrogen (BUN) aka “azotemia”.
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2
Q

what is the RIFLE criteria?

A

stratum of progressive AKI injury: based on increasing % GFR decrease and decreased urine output:
Risk, Injury, Failure w/ outcomes - Loss, End stage kidney dz

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3
Q

3 types of AKI

A

pre-renal (MC), intrinsic, post-renal

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4
Q

define pre-renal AKI, what causes it?

A

decreased renal perfusion. Often leads to intrinsic if not corrected. Cause- hypovolemia or afferent constriction (Nsaids, IV contrast) w/ efferent dilation (ACEs,ARBs)

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5
Q

define intrinsic AKI, what are the 4 subtypes? which is most common

A

direct structural/fxn kidney damage - nephrotoxic, cytotoxic or prolonged ischemic = cellular cast formation. Includes… ATN (MC), AIN, acute glomerulonephritis, vascular

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6
Q

define ATN, what are the two types?

A

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.

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7
Q

define AIN, what is the MC cause?

A

inflammatory or allergic response in interstituim (spares glomeruli + vessels). Cause- drug hypersensitivity (MC), infection, autoimmune, idiopathic.

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8
Q

AKI: acute glomerulonephritis vs vascular

A

acute glomerulonephritis: immune mediated inflammation of glomeruli –> RBC + protein leakage
Vascular: TTP, DIC, aneurysm, etc.

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9
Q

UA: what does each result indicate?
RBCs
Muddy brown casts + epithelial cell casts
WBC casts

A

RBCs - glomerulonephritis (AGN)
Muddy brown casts + epithelial cell casts - ATN
WBC casts - AIN

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10
Q

BUN/Cr: pre-renal vs ATN

A

BUN/Cr: prerenal >20:1, ATN 10-15:1

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11
Q

txt pre-renal vs ATN

A

Prerenal: volume repletion - restore renal perfusion
ATN: remove offending agent, IV fluids, furosemide (if euvolemic + not urinating). Most return to baseline in 72hrs

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12
Q

txt AIN vs glomerulonephritis

A

AIN: remove offending agent

Glomerulonephritis (AGN): high-dose steroids, cytotoxic agents

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13
Q

pathophys of how nephrotic dz causes edema

A

glomerular damage → proteinuria → decrease plasma oncotic pressure → edema.

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14
Q

primary vs secondary causes of nephrotic syndrome

A

Primary - minimal change disease (MC nephrotic syndrome in kids), focal segmental glomerulosclerosis (HTN in african americans + IV heroin abuse, HIV)
Secondary - systemic dz - DM

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15
Q

S+S nephrotic syndrome

A

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).

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16
Q

Dx nephrotic syndrome - 2 ways

A

24hr urine collection = >3.5 g/day. UA dipstick = protein 3+, 4+ and oval fat bodies (“maltese cross shaped). Hypoalbuminemia, hyperlipidemia

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17
Q

txt for nephrotic syndrome: for minimal change dz, for edema, for proteinuria reduction

A

Minimal change = corticosteroids
Edema- diuretics
Proteinuria reduction - ACEIs, ARBs

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18
Q

hallmark signs of acute glomerulonephritis

A

Hallmark = HTN, hematuria (RBC casts), dependent edema, azotemia.

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19
Q

MC cause of acute glomerulonephritis worldwide? what is the typical presenting pt?

A

IgA nephropathy aka berger’s dz - young males w/in days after URI or GI infection.

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20
Q

young boy w/ facial edema after strep + cocacola urine.

A

post-infectious acute glomerulonephritis (MC GABHS)

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21
Q

goodpastures dz: what is the basic pathophys and resultant effects?

A

anti-GBM antibodies vs collagen of glomerular basement membrane in kidney and lung alveoli → kidney failure and hemoptysis. = linear IgG deposits.

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22
Q

what are 4 causes of acute glomerulonephritis?

A

IgA nephropathy (berger’s), post-infectious (i.e. GABHS), goodpastures dz (IgG), vasculitis

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23
Q

while UA is very useful for dx glomerulonephritis, what is the GOLD std?

A

renal Bx

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24
Q

prognosis of acute glomerulonephritis?

A

self-limited w/ good prognosis (except if rapidly progressive glomerulonephritis- MC in good pastures and vasculitis).

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25
Q

txt for bergers/proteinuria acute glom vs

txt for rapidly progressive/severe acute glomerulonephritis?

A

bergers/proteinuris: ACEIs +/- steroids.

severe: corticosteroids + cyclophosphamide (chemo drug)

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26
Q

define chronic kidney dz/failure, staging?

A

> 3 months progressive fxn decline.

Staging by GFR: I- normal (>90), II- 60-90, III- 30-60, IV - 15-30 V- <15.

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27
Q

Dx: Nephron destruction → hypertrophy of remaining nephrons → failure from increased workload = fibrosis, sclerosis, tubular dilation.

A

chronic kidney dz

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28
Q

3 MC causes of chronic kidney dz?

A

DM (MC), HTN, glomerulonephritis

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29
Q

Dx of chronic kidney dz: UA and imaging

A

proteinuria, UA- broad waxy casts (take shape of dilated tubules), incr BUN/Cr, kidney US - small kidneys.

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30
Q

txt of chronic kidney dz

A

prevent progression - HTN & proteinuria (ACEIs, ARBs), DM control
Stage V: end-stage renal dz requiring dialysis and/or transplant.

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31
Q

meds for BPH (4)

A

Meds- alpha1 agonists (zosins). Also can do PDE-5inhibitors (tadallafil), anticholinergics, 5-alpha reductase inhibitors (finasteride)

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32
Q

at what age can you dx cryptochordism?

A

if testical does not descend by 4months

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33
Q

txt for cryptochordism

A

Sx orchiopexy ASAP after 4months old.

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34
Q

define DM kidney dz vs DM nephropathy

A

“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.

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35
Q

Dx:persistently elevated albuminuria, DM/diabetic retinopathy, decreased GFR

A

DM nephropathy

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36
Q

when is DM nephropathy considered chronic?

A

> 3 months

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37
Q

txt for DM nephropathy

A

BP control - ACE or ARB w/ dihydropyridine CCB. Glycemic control - A1C <7%.

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38
Q

risk factors for erectile dysfxn

A

obese/sedentary, smoking, comorbidities, meds-SSRIs, CVD.

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39
Q

txt options for erectile dysfxn

A

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.

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40
Q

define hydrocele vs varicocele

A

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.

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41
Q

Dx hydrocele vs varicocele

A

Hydrocele: translumination
Varicocele: “bag of worms”, increases w/ valsalva, decreases w/ trendelenburg

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42
Q

Txt of hydrocele + varicocele

A

Hydrocele: none if asymptomatic, Sx removal of sac if symptomatic
Varicocele: none, maybe Sx ligation or percutaneous venous embolization if poor semen analysis.

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43
Q

meds for various types of incontinence (stress, urge, overflow)

A

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)

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44
Q

MC types of kidney stones

A

MC Ca+ oxalate stones. Also Ca+phosphate, uric acid, struvite, cystine.

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45
Q

txt options for kidney stones

A

pain meds, hydration. <5mm pass spontaneously = Meds- tamsulosin + nifedipine (4wks). >10mm + other complicating factors = uro consult for lithotripsy/Sx/stents.

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46
Q

txt options phimosis vs paraphimosis

A

Paraphimosis: timely reduction of foreskin (manually or dorsal slit), pain control
Phimosis: stretching exercise, topical steroids (betamethasone), circumcision

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47
Q

what is a horseshoe kidney?

A

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.

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48
Q

what does a horseshoe kidney incr your risk of ? (3)

A

Increased risk of infection from increased urine stasis, increased risk wilms tumor, vesicoureteral reflux.

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49
Q

Txt of horseshoe kidney

A

usually none, if VUR- prophylactic abx to prevent UTI

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50
Q

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.

A

polycystic kidney dz

51
Q

S+S polycystic kidney dz?

A

HTN, hematuria, proteinuria, kidney fxm impairment. Flank pain from renal hemorrhage, calculi or UTI

52
Q

Dx polycystic kidney dz

A

US- renal cyst + FH.

53
Q

mgmt polycystic kidney dz

A

HTN mgmt (ACE or ARB), Na restriction, increased fluids, tolvaptan - vasopressor.

54
Q

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

A

renal vascular dz

55
Q

txt options for renal vascular dz

A

HTN control + ASA, statins, smoking cessation, glycemic control (if DM), +/- revascularization (percutaneous transluminal renal angioplasty + stent)

56
Q

testicular torsion: after what amount of time is there irreversible damage? which direction does it MC torse?

A

Irreversible damage to teste after 8hrs. MC medial torsion

57
Q

Dx:? asymmetric high-riding teste, swelling, reactive hydrocele, +/- erythema, “knot” or blue dot superior to testes.

A

testicular torsion

58
Q

Txt of testicular torsion: if Sx not available in what timeframe do you manually detorse? what indicates a successful detorse?

A

two hours

Successful detorse = relief of pain, change in teste axis and position, normal pulses on doppler.

59
Q

MC pathogens to cause pyelo

A

MC - E coli. Also enterococci, pseudomonas, staph, candida.

60
Q

Txt options for pyelo

A

FQs, carbapenem + vancomycin, ceftriaxone or pip/tazo.

61
Q

MC causes of hypoCa+ (w/ low PTH, w/ high PTH), what results?

A

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.

62
Q

S+S hypoCa+

A

muscle cramp, finger/circumoral parasthesias, Tetany (Chvostek’s signs- facial spasm, Trousseau’s sign - carpal spasm), inc DTRs. diarrhea, abd pain, osteomalacia/dystrophy.

63
Q

what other electrolyte abnormalities come with low Ca+, what EKG changes ?

A

low ionized Ca +/- inc phos, low Mg. EKG = prolonged QT interval

64
Q

txt hypoCa+

A

oral Ca+ and Vit D (ergocalciferol, calcitriol). severe = IV Ca+ gluconate.

65
Q

what are the two most common causes of hyperCa+

A

MC hyperPTH: Triad incr Ca, incr intact PTH, low phos. 2. Malignancy: secretes increased PTH-related protein) w/ decreased intact PTH.

66
Q

what meds can cause hyperCa+

A

TZDs, lithium

67
Q

S+S hyperCa+

A

MC asymptomatic, kidney stones, painful bones, abd groans, pyschic moans (weak, AMS, decreased DTRs)

68
Q

txt for mild vs severe hyperCa+

A

mild (txt underlying cause). Severe: IV saline → furosemide, avoid HCTZ (increases Ca). severe: calcitonin, bisphosphonates IV, steroids.

69
Q

causes of hypoK+

A

GI/Renal loss (diuretic, V/D). increased intracellular shifts: metabolic alkalosis, beta2 agonists, insulin, vit B12 txt.

70
Q

EKG changes with hypoK+

A

EKG = Twave flattening → U wave.

71
Q

causes of hyperK+

A

decreased renal excretion (renal failure, low aldosterone, adrenal insufficiency), meds (spironolactone, ACE/ARB, digoxin, BBs, NSAIDs), cell lysis, metabolic acidosis (DKA), catabolic states

72
Q

symptoms of hyperK+

A

weakness, (progressive ascending), flaccid paralysis, cardiac (palpitations/arrhythmias), GI upset - diarrhea.

73
Q

EKG changes with hyperK+

A

EKG= peaked T waves, QR shortened, wide QRS → P wave flat → sine wave → arrhythmias.

74
Q

txt options for hyperK+

A

IV Ca gluconate, insulin w/glucose, kayexelate, B2agonists

75
Q

two major causes of hypoMagnesemia

A

GI (malabs, ETOHics) or renal loss (DM,diuretics, PPIs)

76
Q

s+s of hypomagnesemia

A

increased DTRs, Tetany (muscle cramps/contractions), AMS. hypocalcemia symptoms (Mg needed to make PTH), cardio- arrythmias, palpitations

77
Q

what other electrolyte abnormalities come with low Mg, what EKG changes?

A

blood (low Mg, Ca and K), EKG= prolonged PR & QT → torsades.

78
Q

causes for hyperNa+

A

HIGH Na+: hypovolemia (activates RAAS and ADH) or iatrogenic hyperKalemia (will prompt aldosterone to excrete K+ in exchange for Na+) → aldosterone = Na+ retention.

79
Q

causes of hypoNa+

A

LOW Na+: caused by incr ADH/incr water intake→ impaired kidney ability to excrete free water. Clinically significant/True is hypotonic hyponatremia.

80
Q

what is true hypoNa+ (hypertonic, isotonic, or hypotonic), what causes it - hypovolemic, hypervolemic, euvolemic?

A

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

81
Q

correction of hypo or hyper Na+, what is the rate of infusion and what is the reason?

A

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.

82
Q

metabolic acidosis w/ high anion gap: what causes it?

A

too much acid
“MUDPILERS” methanol, uremia, DKA/alcoholic KA, propylene glycol, isoniazid/infection, lactic acidosis, ethylene glycol, rhabdo/renal failure, salicylates.

83
Q

metabolic acidosis with normal anion gap: what causes it?

A

too little bicarbonate
“HARDUPS” hyperalimentation (artificial nutrient supply), acetazolamide, renal tubular acidosis, diarrhea, uretero-pelvic shunt, post-hypocapnia, spironolactone.

84
Q

what is a normal anion gap?

A

[Na-(Cl + HCO3)] = 8-18 (normal)

85
Q

causes of metabolic alkalosis

A

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.

86
Q

what causes respiratory acidosis or alkalosis?

A

acidosis: anything that causes hypoventilation
alkalosis: anything that causes hyperventilation

87
Q

MC cause of hypervolemia (fluid overload)

A

MC renal failure → Na retention → fluid retention.

88
Q

causes of dehydration from acute sequestration into “third space”?

A

intestinal obstruction, crush injury, Fx, acute pancreatitis).

89
Q

txt options for UTI/pyelo

A

keflex, TMP/SMX, macrobid. Also cipro

Pyelo - Inpt: 1g IV ceftriaxone.

90
Q

epididymitis/orchitis/urethritis MC pathogens and txt

A

MC GC, chlamydia. If not STI - pseudomonas, E.Coli.

Tx: ceftriaxone + doxycycline or azithromycin. Or levofloxacin

91
Q

prostatitis: MC pathogens + txt

A

MC E.Coli + gonorrhea, C trachomatis.

Txt: FQs, TMP/SMX or, for STD- ceftriaxone + doxycyline or azithromycin.

92
Q

horner’s syndrome: S+S,cause, Dx, txt

A

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.

93
Q

urethritis MC pathogens

A

Neisseria gonorrhoeae, Chlamydia trachomatis, and Mycoplasma genitalium are the most common organisms associated with urethritis. Trichomonas vaginalis and herpes simplex virus (HSV)

94
Q

urethritis S+S, txt

A

S+S: dysuria, urethral pruritus, and/or urethral discharge

Txt: ceftriaxone + azithromycin

95
Q

VERY itchy symmetric pattern of vesicles on palms and fingers, soles. Can be large bullae.Recurrent episodes over months/years.

A

dishydrotic eczema

96
Q

txt for nummular or dishydrotic eczema

A

general eczema guidelines + high potency topical steroids

97
Q

pruritic, polygonal, violaceous papules and/or plaques with an overlying white, lacelike pattern (Wickham’s striae)

A

lichen planus

98
Q

txt for lichen planus

A

resolves on its own over 1-2 yrs, high potency topical steroids.

99
Q

what kind of dermatitis is poison ivy?

A

allergic contact

100
Q

txt of perioral dermatitis

A

STOP steroids. topical erythromycin or metronidazole

101
Q

txt options for sebbhoreic dermatitis

A

topical antifungals, topical anti-inflammatories (calcineurin inhibitors - tacrolimus, pimecrolimus)

102
Q

txt options for psoriasis

A

topical steroids, emollients.

103
Q

txt for dermatophytes (tinea)

A

topical antifungals (terbinafine or azoles), oral if recurrent.

104
Q

bald patch + exclamation point hairs.

A

allopecia areata

105
Q

txt for onychomycosis (fingers vs toenails)

A

topical (for mild, <50% nail) or oral terbinafine. Fingernails - 6wks, toenails-12wks. (other options- azoles, griseofulvin)

106
Q

MC pathogens for paronychia (infected ingrown toenail)

A

MC - staph, strep. Chronic - pseudomonas.

107
Q

txt for paronychia

A

soak, I+D, abx staph coverage (augmentin, clindamycin, keflex)

108
Q

single or multiple, flat, dome-shaped, cauliflower-shaped, filiform, fungating, pedunculated, cerebriform, plaque-like, smooth (especially on the penile shaft), verrucous, or lobulated.

A

condyloma accuminata (anogenital warts)

109
Q

what strains HPV cause condyloma accuminata

A

HPV types 6,11

110
Q

Nonspecific prodrome then in two days slapped cheek then lacy rash. Dx and cause?

A

erythema infectiosum (5ths dz) parvovirus B19

111
Q

fever, malaise, cough, coryza, and conjunctivitis, followed by exanthem 2-4 days later. (starts on head and spreads down)

A

measles

112
Q

what is the contagious period before and after measles rash

A

Contagious 5 days before rash, 4 days after.

113
Q

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.

A

erythema multiform

114
Q

txt for erythema multiforme

A

Self limiting w/in weeks. Symptomatic topical steroids or antihistamines.

115
Q

MC causes of SJS and TEN

A

MC from drugs or mycoplasma PNA.

116
Q

Autoimmune blistering,1 to 3 cm tense bulla on an erythematous, urticarial, or noninflammatory base, and blisters may be numerous and widespread

A

pemphigoid

117
Q

Dx and Txt of bullous pemphigoid

A

Dx: clinical + detect circulating basement membrane zone antibodies by indirect immunofluorescence (IIF) and enzyme-linked immunoassay (ELISA)
Txt: topical steroid (e.g. clobetasol)

118
Q

txt for folliculitis

A

Mild staph resolves w.out txt. Topical mupirocin or topical clindamycin. More severe/chronic: dicloxacillin, keflex, tmp/smx, or clindamycin.

119
Q

txt for rosacea

A

avoidance of triggers of flushing, gentle skin care, and sun protection. metronidazole cream

120
Q

txt cellulitis and erysipelas

A

5 days abx - keflex, TMP/SMX. Systemic symp w/ erysipelas = ceftriaxone, cefazolin

121
Q

txt impetigo

A

Txt: mild - topical mupirocin, numerous/systemic - oral keflex, dicloxacillin

122
Q

scaly, erythematous macules or papules on sites of chronic sun exposure. May progress to squamous cell carcinoma. MC fair skin adults + sun exposure.

A

actinic keratosis

123
Q

which kind of spider bite do you txt with benzos or opiods for muscle spasm ?

A

black widow

Rotation (16 decks)

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