Systems - Nephro - Urology

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Systems - Nephro - Urology
2014-11-26 12:18:03
Systems Nephro Urology
Systems - Nephro - Urology
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  1. What are two drugs you should never combine WRT the kidney? Why?
    • -Anything that blocks ANG II (e.g. ACE i) and an NSAID
    • -NSAID blocks prostaglandins, the effect of this is constriction of the afferent arteriole
    • -blocking ANG II wil cause vasodilation of the efferent arteriole
    • -result is decreased blood flow to the kidney and death
  2. What are the EKG changes you see in hyperkalemia? (9)
    • -peaked T waves
    • -increased PR
    • -flat or no p wave
    • -shortened QT
    • -AV blocks
    • -wide QRS
    • -sine wave
    • -V fib
    • -asystole
  3. A patient presents with hyponatremia, low serum osmoles, and hypo-osmolar urine (<100 mosm/L). What is on your DDx? (3)
    polydipsia (drank lots of water), poor solute intake, or a reset osmostat
  4. What are the 6 D's of HYPERnatremia?
    • Diuresis
    • Dehydration
    • Diabetes insipidus
    • Docs (iatrogenic)
    • Diarrhea
    • Disease
  5. What is the maximum rate you should correct sodium imbalance at? What are the big concerns for a) hypernatremia and b) hyponatremia
    12mmol/L per day

    a) cerebral edema

    b) central pontine myelinolysis
  6. What are the normal physiological ranges for Na, K, Cl, HCO3
    • Na: 135-145 mmol/L
    • K: 3.5-5 mmol/L
    • Cl: 95-105 mmol/L
    • Bicarb: 18-23 mmol/L
  7. How do you treat hyperkalema?
    • C BIG K Drop
    • Calcium: stabalize cardiac myocyte membrane
    • Beta agonist: reuptake K; Bicarb: correct the metabolic acidosis, reuptake K
    • Insulin: shifts K into the cell
    • Glucose: to compensate for the insulin administration
    • Kayexalate: binds K in the GIT and you then excrete in your feces
    • Dialysis/diuresis
  8. What is azotemia?
    abnormally high levels of nitrogenous wastes in the  (elevated BUN)
  9. In what two cases would you correct hyponatremia with hypertonic saline? What is usually the best replacement fluid?
    • 1) neurological sx due to hypoNa
    • 2) serum Na is <120

    otherwise, normal saline is usually the best choice.
  10. What are the ECG findings in hyperkalemia (4)? what can it progress to?
    • -peaked T waves, QRS prolongation, PR prolongation, low P waves
    • - can progress to sine waves and then death
  11. What is the DDx of metabolic acidosis? treatments for some
    • Methanol: fomepiloz
    • Uremia: dialysis
    • Diabetic ketoacidosis (also eTOH and starvation: insulin and fluids
    • Paraldehyde
    • Iron/isoniazide: GI lavage, charcoal
    • Lactic acidosis
    • Ethylene glycol: fomepizole
    • Salicylates: alkanize urine
  12. Describe the appropriate compensation you expect to see in metabolic/respiratory acidosis/alkalosis
    • met acidosis: 1 decreased HCO3 = 1 dec pCO2
    • met alkalosis: 1 inc. HCO3 = 1 inc pCO2
    • acute resp acidosis: 10 inc pCO2 = 1 inc HCO3
    • chron resp acidosis: 10 inc pCO2 = 3 inc HCO3
    • acute resp alk: 10 dec pCO2 = 2 dec HCO3
    • chron resp alk: 10 dec pCO2 = 4 dec HCO3
  13. DDx for normal anion gap acidosis (2). describe two of the subtypes of the second one
    • -Diarrhea
    • -Renal tubular acidosis
    •   -Type I (distal): problem with low H+ secretion, low serum K, pH > 5.3
    •  - Type IV (distal): aldosterone deficiency/resistance, high serum K, pH < 5.3
  14. Describe the three anatomical categories of Acute Kidney Injury.
    • Prerenal: hypovolemia
    • Renal: Glomerular, tubulointerstitial, small/large BV
    • postrenal: obstruction
  15. What are the indications for dialysis?
    • KAPPEL! as in Dr. Kappel
    • -hyperKalemia
    • -acidosis
    • -Pulmonary Edema (fluid overload)
    • -Pericarditis
    • -Encephalopathy
    • -"Looped" out on drugs
  16. With regards to the FENa, UNa, Uosm; how do pre-renal azotemia and acute tubular necrosis differ?
    • PRA vs ATN
    • FENa: <1%, >1%
    • Urine sodium: <20, >20
    • Urine osm: >500, <300 
    •   -high in pre-renal azotemia because low volume status of patient
  17. What does aldosterone do? How does a deficiency cause hyperK
    secretes K into the lumen, reabsorbs Na, both Via the ENAC channels.

    Also antiports 3Na/2K on the basal membrane

    Also secretes H+ into the lumen via the Na/H antiporter
  18. In a hyponatremia case where the ADH is working, but patient is euvolemic what is on your DDx?
    • rule out thyroid
    • rule out adrenal insufficiency
    • if not these: SIADH
  19. What is always the treatment in hypernatremia?
    give water
  20. How do you calculate water deficit in hypernatremia?
  21. What is the threshold for acuve vs chronic kidney injuries
    3 weeks
  22. What are the 4 general renal (intrinsic) causes of AKI? some prototypical disorders of each.
    • vessels: HTN crisis (scleroderma), TTP-HUS
    • glomerulus: nephritic and nephrotic syndromes
    • tubules: ATN
    • interstitium: Acute interstitial nephritis
  23. Classical 4 findings in nephrotic syndrome (which three are NEEDED!). How does this compare to nephritic syndrome?
    • >3g/day proteinuria (albuminuria)
    • low serum albumin (duh!)
    • generalized edema
    • hyperlipidemia

    Nephritic syndrome: proteinuria <1.5g/day, HTN, hematuria, rising Cr, mild edema
  24. what is the MOST COMMON cause of secondary nephrotic syndrome?
    diabetes, diabetes, diabetes
  25. what are the three categories of nephritic syndrome? Examples of each
    • Type I - Anti-GBM disease: Goodpasture's syndrome, Alport's syndrome
    • Type II - Immune Complex: post-infectious GN (GAS usually), IgA nephropathy (Berger's disease)
    • Type III - Pauci immune: Wegener's gran.,
  26. Primary and secondary causes of nephrotic syndrome
    Primary: Minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy (IVDU's), membranoproliferative GN

    Secondary: Diabetes, lupus, amyloidosis, multiple myeloma
  27. three causes of ATN
    Ischemic, nephrotoxic, septic
  28. What is the triad of acute interstitial nephritis?
    fever, rash, eosinophilia
  29. What is the definition of CKD?
    • kidney damage > 3 months and one of the following
    • -GFR<60 ml/min
    • -structural or functional (urinary) abnormalities of the kindey
  30. what are 4 conditions that can give decreased GFR, but no structural or functional kidney abnormalities
    • -congestive heart failure
    • -liver cirrhosis
    • -hypothyroidism
    • -history of being a kidney donor
  31. Classification of CKD (3 categories)
    • Cause: GN, tubulointerstitial, vascular, congenital (these are pretty much the same as AKI)
    • GFR category: stage increases as GFR decreases
    • albuminuria level: can combine with GFR to get a prognostic score
  32. three congenital causes of AKI
    • ADPKD
    • Fabry's disease
    • Alport;s syndrom
  33. When someone has a vascular disease, what do you need to be concerned about?
  34. What happens generally to kidney size in AKI and CKD. 5 exceptions
    generally normal in AKI and small in CKD

    exceptions (big kidneys in chronic): DM, MM, lymphoma, hydronephrosis, PKD
  35. what is RBC cast's and dysmorphic RBC's pathognomonic for?
  36. What are the indications for renal biopsy (5)
    • -unexplained glomerular hematuria
    • -unexplained glomerular proteinuria
    • -nephrotic syndrome
    • -acute nephritic syndrome (RBC casts and dysmorphic RBC's)
    • -unexplained acute kidney failure
  37. When should you refer CKD patients to a nephrologist?
    • -eGFR < 30
    • -progressive decline in eGFR
    • -persistent significant proteinuria
    • -failure to reach treatment goals
  38. top two causes of ESRD in kids
    • aplasia (no/small kidney)
    • hypoplasia (not enough)
  39. What is the definition of hematuria?
    >5 RBCs/microL in uncentrifuged midstream urine

    3+ RBCs/HPF in HPF
  40. How can you differentiate glomerular and non-glomerular hematuria
    • glom: brown, RBC casts, dysmorphic RBCs
    • non-glom: pink/red
  41. What usually causes postinfectious GN? treatment/prognosis
    • Preceeding GAS infection
    • supportive tmt with diuretic to prevent fluid overload, usually a complete recovery
  42. Three steps when approaching hematuria
    • Is it blood?
    • What is the clinical story?
    • Where is the blood from?
  43. Proteinuria and hematuria...which is worse?
  44. What are the 4 mechanisms of proteinuria?
    • Increased glom permeability (glomerular)
    • Decreased tubular reabsorption (tubular)
    • Increased renal protein secretion (secretory)
    • Overproduction of plasma proteins (overflow)
  45. When measuring protein (24 hr void) in kids, what is:
    1) normal
    2) abnormal
    3) nephrotic

    What is a more humane way to measure this in a kid?
    • 1) <4 mg/m^2/hr
    • 2) >4
    • 3) >40

    Do a Pr:Cr ratio
  46. First line tmt for nephrotic syndrome
  47. If you use a BP cuff that is too small, will the BP be too high or low?
    too high. you will need to pump it up way more in order to occlude the artery
  48. Describe how to define prehypertension and hypertension in peds patients?
    pHTN: 90%tile<SBP or DBP<95%tile, OR any adolescent 12+ yo with BP >120/80

    HTN: SBP or DBP>95th %tile for

    both need to be measured at least 3 times and averaged
  49. What are the 3 categories of peds HTN?
    • stage1: 95-99th percentile plus 5 mmHg
    • Stage 2: >99th percentile plus 5 mmHg
    • Emergency: Stage 2 plus Sx
  50. How do you treat peds HTN?
    treat underlying cause

    if it is not known what the cause is, treat like adult HTN
  51. What is the #1 cause of ESRD?
    diabetic nephropathy
  52. What is the hallmark of glomerular disease?
  53. What is are the thresholds for proteinuria and albuminuria (micro and macro) in diabetics?
    • proteinuria: 150+ mg/day
    • albuminuria: 30+ mg/day
    •   -microalb. 30-300 mg/day
    •   -macroalb. 300+ mg/day
  54. Describe the progression of diabetic nephropathy
    • hyperfiltration (elevated GFR)
    • microalb
    • macroalb
    • progressive nephropathy (decreased GFR)
    • ESRD (GFR<15)
  55. Remember that proteinuria in a diabetic is NOT always what?
    diabetic nephropathy
  56. What are the targets for controlling diabetes?
    fasting glucose
    2hrs post prandial
    • HbA1c: < 7
    • fasting glucose: 4-7 mmol/L
    • 2hrs post prandial: 5-10 mmol/L
    • BP: 130/80
  57. What is the single most effective measure to prevent the progression to diabetic nephropathy? How?
    BP control. Usually requires 3+ medications.

    • -RAAS blockade
    • -CV protection (happy heart = happy kidneys)
    • -lifestyle
  58. What is the pathophysiological char's of diabetic nephropathy? (3)
    • Mesangial expansion
    • GBM thickening
    • Glomerulosclerosis
  59. Why do ACEi's cause increased serum Cr?
    They impair alpha2-mediated efferent arteriole vasoconstriction (less GFR)
  60. What is malignant hypertension (hypertensive emergency)?
    BP>= 180/120 WITH end organ damage

    end organs are: brain, heart, kidneys, eyes
  61. How do you treat a hypertensive emergency?
    IV meds to decrease DBP to about 100 mg over 6 hours. Any more may cause ischemic events

    then use oral meds to decrease BP over several weeks
  62. What is hypertensive urgency? What to do?

    asymptomatic (no acute end organ damage)

    oral meds to decrease BP slowly
  63. Describe the long-term complications of HTN (4 categories)
    • Brain: ischemic stroke, hemorrhage
    • Heart: CHF, LVH
    • Kidneys:
    • -hypertensive nephhroslerosis -> CKD-> ESRD
    • -accelerate other renal diseases -> ESRD
    • Eyes: retinopathy
  64. How many cases are primary (essential) HTN? secondary? 4 categories of secondary. When should you screen for secondary?
    95% are essential HTN and don't need further investigation

    Secondary: renal, endocrine, drugs, other

    no need to screen for secondary unless there are clues
  65. What are the 4 major drugs used to treat HTN?
    • -thiazide diuretics
    • -ACE inhibitors/ARB's
    • -CCB's
    • -beta blockers (last line)
  66. What are the indications (1) and contraindications (5) to renal transplant?
    • indications: ESRD (CKD stage 5)
    • contraindications: cancer, infection, systemic disease, psychiatric disease, obesity
  67. How do you take a history for obstructive and irritative LUTS.
    • FUN(irritative, filling) WISE (obstructive, voiding)
    • Frequency increased (>8 times in 24 hours)
    • Urgency (need to go immediately)
    • Nocturia (2+ times per night)
    • Weak stream
    • Intermittent flow
    • Straining to empty
    • Emptying is incomplete
  68. Describe the typical presentation of prostate cancer
    non-specific. May have elevated PSA +/- nodules on DRE +/- BPH symptoms
  69. Do you want to screen with PSA levels or DRE? When is PSA the most informative? When should you stop routine screening?
    • both! higher sens and spec if you do both tests. When you have previous PSA tests to compare to, you can see if the PSA is elevated in that patient.
    • Stop when they are 75, unless there is a clinical indication to test
  70. Describe how to assess risk in prostate cancer using the PSA, Gleason, and clinical staging
  71. Describe the tmts for prostate cancer (4)
    • Radical prostatectomy (laproscopic removal)
    • Radiotherapy (external beam or brachytherapy)
    • androgen deprivation (only for metastatic disease, it is palliative)
    • Palliative radiotherapy
  72. What is normal urinary frequency and amount?
    5-8 times (300-400 mls per time)
  73. What is the normal prostate size?
    walnut size (25-30 mm)
  74. In BPH, size does not correlate to what?
    symptoms or degree of obstruction
  75. What zone of the prostate do you usually see cancer? BPH?
    • cancer: peripheral zone
    • BPH: central
  76. Describe the tmt progression in BPH.
    • -alpha blockers (terazosin, relax SM)
    • -5-alpha reductase inhib (inhibit the production of DHT)
    • -transurethral resection of the prostate (TURP, basically hollowing it out from the inside out)
  77. Complications of BPH (6)
    • -overflow incontinence
    • -renal insufficiency
    • -bladder stones
    • -bladder distension
    • -recurrent UTI
    • -hematuria
  78. What is the cornerstone of medical tmt in OAB? optical contraindication
    antimuscanarics such as oxybutynin. narrow angle glaucoma
  79. What can cause an elevated PSA (5)?
    • -Ca
    • -BPH
    • -UTI
    • -prostatic trauma
    • -prostatitis
  80. What is the pain that you classically see in renal colic (acute UUT obstruction). What is the main etiology?
    flank/abdomen pain, radiates to groin, labia, testicles, the patient CANT get comfortable!

    main cause is stones.
  81. What is the most common cause of chronic UUT obstruction
    UPJ obstruction
  82. 3 most common locations for UUT obstruction
    • uretopelvic junction (UPJ)
    • pelvic brim (iliac vessels)
    • uretovesicle junction (UVJ)
  83. two most common causes of urethral strictures
    • trauma
    • iatrogenic (operations, catheters)
  84. Most common cause of bladder stones. most common make-up of stones
    infection stones. Usually made up of CaOx (usually due to hypercalcemia)
  85. What is the best diagnostic technique in urolithiasis?
    CT is the gold standard
  86. What medical treatments are used for stones? (3)
    • -Hydration DOES NOT facilitate expulsion and may increase renal capsular distension.
    • -analgesics (NSAIDS -> narcotics)
    • -relax smooth muscles (alpha-blockers, CCB's)
  87. When should you urgently and emergently refer stones to urology
    -Urgent: intractable pain and/or intractable N/V

    -Emergent: fever (urosepsis) is most urgent, solitary kidney, or bilateral obstructing stones
  88. Urological (surgical) tmts for stones (3)
    • -extracorporeal lithotripsy
    • -uretorenoscopy laser lithotripsy
    • -percutaneous nephrolithotomy (definitive tmt for the biggest stones)
  89. What ANS components are responsible for ejaculation and eretion?
    • Point and Shoot
    • Para is erection
    • Symp is ejaculation
  90. Describe reflex and psychogenic erections
    • reflex: somatic sensation vi pudendal nerve increases parasymp outflow via cavernosal nerves
    • psychogenic: erotic stimuli increases BOTH symp and parasymp outflow
  91. Describe the 4 steps in the physiology of an erection
    • 1) dilation of arteries
    • 2) enlargement of sinusoidal spaces
    • 3) compression of subtunical veins
    • 4) increase in cavernosal pressure
  92. What drugs are an absolute contraindication to PDE5 inhibitors (e.g. sildenafil, aka viagra)? why?
    nitroglycerine, because the combined effects lead to a severe HYPOtension.
  93. how many men suffer from ED by age 50?
    50% by age 50
  94. describe the functional classification of ED
    • 1) arterial: same RF's in CAD
    • 2) cavernosal: Peyronie's disease (ED, painful plaque, curvature)
    • 3) hormonal: libido is the first thing to go in testosterone deficiency
    • 4) neurological: CNS, PNS, demyelinating, surg
    • 5, but is involved in all) psychological
  95. Big things to ask in and ED Hx and look for in an ED PE?
    • Hx: nocturnal erections, masturbation erections mean pshycogenic etiology
    • PE: groin pulses, neuro (including anal tone), scrotal and penile exam
  96. Why is tadalifil (cialis) better than viagra and levitra?
    • -longer half life (17 hours as opposed to 2 hours)
    • -no interaction with alcohol
  97. What is the DDx for PainFUL scrotal masses? (6)
    • -testicular torsion
    • -torsion of appendix epididymis
    • -Epididymitis
    • -testicular abscess
    • -hematocele (usually from trauma)
    • -testicular tumor with hemorrhage
  98. What is the DDx for painLESS scrotal masses (5)
    • -hydrocele
    • -spermatocele
    • -variocele
    • -hernia
    • -testicular or paratesticular tumor
  99. If you see a sexually active young man in your office with scrotal pain what should you think?
    chlamydia and gonorrhea
  100. If you clinically suspect testicular torsion what should you do? how long do you have?
    urgently refer to a urologist for an emergent right detorsion and bilateral orchidopexy (fixation of testes to scrotum). salvage rates are 100% if you get at it in the first 6 hours
  101. What are the 4 key clinical findings for testicular torsion?
    • -ipsilateral loss of kremasteric reflex
    • -high riding testicle
    • -pain
    • -erythema
  102. What is the most important RF for testicular cancer. Etiology of 95% of testicular cancers. route of metastatic spread
    • cryptorchidism (undescended testicle)
    • 95% are primary germ cell tumors (not mets).  
    • retroperitoneal LNs->lungs->liver->brain
  103. What are the 2 types of primary testicular tumors. What are the tumor markers for testicular cancer?
    • hCG
    • Alpha feto protein
    • LDH

    • seminoma is hCG only
    • non-seminoma is AFP +/- hCG
  104. painless scrotal masses are what until proven otherwise
    testicular cancer
  105. So you have someone coming in with a NAGMA, what are the 2 common etiologies? how do you differentiate?
    either renal tubular acidosis or diarrhea

    • RTA has a positive urine anion gap
    • diarrhea has a strongly NeGUTive urine anion gap.
  106. If you see a patient come in with ADPKD and a headache, what is the first thing that you MUST rule out? most common cause of death in ADPKD?
    • an aneurysm in the circle of willis
    • renal failure is the most common cause of death
  107. What is the most common congenital urethral obstruction? Classic findings?
    • -posterior urethral valves
    • -male infant with distended, palpable bladder with low urine output.
  108. DDx of hematuria
    • I PEE RBCS
    • Infection (UTI)
    • PKD
    • Exercise
    • External Trauma
    • Renal glomerular disease
    • BPH
    • Cancer
    • Stones
  109. If someone has a dipstick test positive for blood, what should you do?
    Urinalysis. hematuria is defined as >2-3 RBC's per HPF
  110. When should you refer hematuria to urology? (4)
    • -anyone with gross hematuria (unless UTI)
    • -anyone over 40
    • -anyone who smokes (high risk of bladder cancer)
    • -abnormal cytology/ultrasound
  111. 2 key concepts for family docs evaluation hematuria
    • -don't investigate +ve dipstick, confirm with microscopic analysis first
    • -rule out serious disease, not always necessary to make a diagnosis (we usually dont)
  112. What is the most common cause of dysuria? who gets it most often? why?
    infection, 3F:1M, they have a short urethra
  113. describe the history and initial investigations with someone coming in with dysuria? PE?
    • Hx: sexually active?, vaginal/urethral discharge?, fever?
    • urinalysis
    • urine culture
    • PE: not in women with classic signs, always in men because it is less common
  114. When can you give an appropriate empirical abx in suspected UTI? (3) when to refer?
    • abx if:
    • -classic symptoms in young women
    • -abnormal urinalysis
    • -vaginal urethral discahrge

    refer if it not clearly an infection
  115. When should you do an intravenous urogram?
    NEVER! Just refer them on for CT
  116. How do you manage renal trauma?
    Usually just watch and wait. The renal capsule will hold the kidney together and the tamponade pressure will limit bleeding. If you surgically incise the parenchyma you will lose this pressure. You save more renal tissue this way
  117. If there is suspected urethral trauma what should you NEVER do? Why? What should you do instead?
    DONT INSERT A FOLEY CATHETER!! you can turn a partial urethral injury into a full injury and then they need surgery! use a suprapubic catheter
  118. How do you investigate suspected urethral injury?
    retrograde urethrogram (xray contrast up the urethra)
  119. Describe 5 things you typically see in primary nocturnal enuresis histories
    • bedwetting since toilet training
    • no daytime Sx
    • no bowel Sx
    • developmental stages are normal
  120. 80% of children achieve night time control of urination by what age?
  121. What is the definition of a UTI?
    >10^5 microbes/ml
  122. When should you do a voiding cystourethrogram? what is it looking for?
    • -recurrent febrile UTI
    • -U/S or nuclear renal scan (which you would do first) is abnormal. 

    looking for vesicouretral reflux
  123. If you have UTI and a high fever what does this suggest?
  124. What is the most common cause of hematuria in children?
    glomerulonephritis (think especially if they are post GAS-infection) and there are RBC casts and proteinuria
  125. If testicles dont come down by this age, they are NOT going to come down on their own
    6 months
  126. In crytptorchidism. Why should you do orchidopexy by year one?
    because of worry about infertility (starts decreasing at this point). Cancer risk does not change with surgery
  127. If you see a child with hypospadius (large urethral opening on the underside of the penis) what should you never do? why?
    circumcise him, because you will need the skin later on for reconstruction.
  128. Prostate cancer is a dietary disease. three dietary things for reducing prostate cancer?
    green tea, soy products, cooked tomato products
  129. According to dee dee what drink should you suggest for preventing UTI?
    cranberry juice
  130. What are reasonable hippie choices for treating nonbacterial prostatitis (2)
    quercetin, cernilton
  131. If a patient has elevated kidney function tests what should you not forget to ask about?
    supplements and botanical therapies
  132. Describe the clinical classification of urinary incontinency (5)
    -urgency: strong desire to pee, but can't wait long enough for the toilet

    -stress urinary: caused by increased intraabdominal pressure (e.g. cough)

    -mixed urinary: combo of stress and urge

    -overflow: retention, void small amounts with large residual volume

    -total: complete loss of control
  133. Describe the common lesions than can cause neurogenic bladder
    brain (4)
    spinal cord (2)
    peripheral (2)
    • Brain: stroke, concussion, tumor, parkinson's
    • SC: MS, acute lesions
    • peripheral: sensory (diabetes), motor (polio, herpes, etc)
  134. Describe what the following measure:
    • -cystometrogram: intrabladder pressure changes in response to gradual filling. 
    •   -persistent flatline: atonic bladder
    •   -early spike: overactive bladder
    • -uroflowmetry: pattern of urination
  135. Absolute indications for catheter drainage/urinary diversion (3)
    • -UUT deterioration or persistently poor emptying despite optimal treatment
    • -Unmanageable vesicouretral reflux with infection causing UUTI
    • -temp diversion for an abscess or fistula makes LUT unusable as a reservoir or conduit
  136. DDx of Pre renal causes of AKI (5)
    • -hypovol
    • -renal artery stenosis
    • -CHF
    • -cirrhosis
    • -sepsis
  137. Vascular causes of AKI (2)
    • TTP-HUS
    • scleroderma
  138. Key urine findings in these AKI types
    -pre renal
    • -pre-renal: empty (hyaline) casts
    • -glom: RBC casts
    • -tubular: granular "muddy brown" casts
    • -interstitial: WBC casts
    • -vascular: "bland" urine
  139. compare and contrast pre-renal AKI and ATN
    • They are both different end of the same spectrum:
    • pre-renal: hyaline casts, reversible, Urine Na is low
    • ATN: granular casts, irreversible, urine Na is not low
  140. What are the non-glomerular renal causes of hematuria (4+)
    • pyelonephritis
    • stones
    • PKD
    • trauma
    • others
  141. definition of proteinuria and albuminuria
    • >150 mg/day protein
    • >30 mg/day albuminuria
  142. Describe the 5 causes of proteinuria
    • Transient (benign: exercise, illness, etc)
    • glomerular (nephrotic, nephritic)
    • tubular (tubes secreting)
    • overflow (too much monoclonal protein, e.g. MM)
    • Orthostatic (benign, young people, split urine test)
  143. What are the top 5 causes of nephrotic syndrome?
    • 1) minimal change disease
    • 2) focal segmental glomerular sclerosis
    • 3) membranous
    • 4) amyloidosis
    • 5) DM
  144. What is the clinical triad of nephritic syndrome?
    • -elevated BP
    • -dysmorphic RBC's/casts
    • -AKI - subacute increase in Cr
  145. list some examples of the three types (based on path stain) of nephritic syndrome
    • pauci: ANCA
    • linear: anti-GBM (goodpasture's)
    • granular (low C3, C4): IgA nephropathy, lupus nephritis, membranoproliferative GN, post infectious GN
  146. What is a Normal Anion Gap Metabolic Acidosis (NAGMA)? How do you differentiate the causes
    Basically if the ion gap is normal OR if the change in bicarb is greater than the change in anion gap (which basically means that there is something else causing the bicarb to dip) then there is NAGMA as well. Either RTA or Diarrhea

    • Urine ion gap = Na+K-Cl
    • -If it is neGUTive, bicarb is being made (and putting lots of Cl in the urine) and this is due to diarrhea
    • -If it is positive, there is low Cl meaning that bicarb is not being made because of some problem in the tubules (RTA)
  147. Describe the 3 types of RTA
    • Type I (distal) - decreased acid secretion into DT
    • Type II (proximal) - decreased bicarb reabsorption in proximal tubule
    • Type IV (aldosterone) - not enough aldo production, decreases acid secretion in distal tubule and cause hyperkalemia