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[3] Step 1 USMLE > Renal and Urinary > Flashcards

Renal and Urinary Flashcards

1
Q

Laboratory Findings of [Post Strep GN] / [Post infectious GN] (4)

A
  • INC ASO (Anti-Streptolysin)
  • INC [Anti-DNase B]
  • [DEC C3 and total compliment]
    • Cryoglobulins
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2
Q

Name the greatest risk factor for [Catheter Associated UTI]

A

REMOVE CATHETER AS SOON AS IT IS NOT INDICATED ANYMORE

(DURATION IS THE GREATEST RISK)

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3
Q

Most common cause of nephrOtic syndrome in Children and its Tx

A

A: Minimal Change Dz

B: REVERSIBLE with Corticosteroids

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4
Q

What is almost always associated with Acute Pyelonephritis? (2)

A

[VUR -Vesicoureteral Reflux] (Anatomical vs. Functional) and [WBC Cast]

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5
Q

Diabetic Autonomic Neuropathy

A: Clinical Presentation (2)

B: Dx method

C: What’s the earliest sign/detection method for Diabetic Nephropathy

D: Diabetic Nephropathy is the leading cause of _____

A

A: [Overflow incontinence 2° to inability to sense full bladder] and [incomplete emptying when voiding]

B: [PVR-PostVoid Residual] testing with US vs. Catheter to confirm [incomplete emptying when voiding]

C: [INC Albuminuria ( urine will be)]

D: [ESRD Chronic Kidney Dz]

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6
Q

How does Multiple Sclerosis affect the Bladder?

A

[Loss of CNS inhibition on [Bladder Detrusor Contraction] allows bladder to always stay contracted –> Urge Incontinence–>eventually progresses [Bladder Atony and Dilation] –> Overflow Incontinence

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7
Q

A: Most common cause of [Nephrolithiasis/Kidney Stones]

B: Most common Risk Factor

C: Other Risk Factors (3)

A

A: Idiopathic Hypercalciuria = [Normocalcemia + Hypercalcuria]

B: Hypercalcuria

C:

  1. [Crohn Dz / Fat Malabsorption / Spinach]–> HyperOxaluria
  2. [Distal RTA Type 1] –> hypOcitraturia
  3. Gout –> Hyperuricosuria
    * Pts are Normocalcemic due to intact serum regulations by Vitamin D and PTH*
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8
Q

Benign Prostatic Hyperplasia

Clinical Manifestation (3)

A
  1. [Intermittent Bladder Outlet Obstruction]–>Urinary Retention –> Reflux Nephropathy
  2. Overflow Incontinence
  3. Later: Hydronephrosis–>[Renal Interstitial atrophy] –> Chronic Renal Failure
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9
Q

A: How do you Calculate Anion Gap

B: What is the normal Anion Gap

C: Name the Etiologies for [INC Anion Gap Acidosis] (9)

A

A: Never Carry Hotsauce: [Na+ - (Cl + HCO3)]

B: [10 - 12]

C: “The MUDPILES INC our Gap”

Methanol

Uremia

DKA (Tx= IV normal saline + Insulin)

Paraldehyde

[Isonizid vs. Iron]

Lactic Acid

Ethylene Glycol

Salicylates

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10
Q

DKA- Diabetic KetoAcidosis

A: Tx (3)

C: What type of Anion Gap Acidosis does this cause

D: Why is the pH of the Urine acidic during DKA

A

A: [IV Normal Saline + Insulin + K+]

C: [INC Anion Gap Acidosis] (MUDPILES)

D: INC production of NH4 & H2PO4

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11
Q

A: Which Renal Structure is subject to Injury from Pelvic Surgery and why?

B: Clinical manifestation (3)

A

A: Ureters can become unintentially ligated during [Pelvic surgery] –> Obstruction–> [Hydronephrosis w/Flank pain]

B:

  1. [Flank pain radiating to groin (from ureter and renal pelvis distension]
  2. [Flank Mass developing within weeks of pelvic surgery]
  3. [Normal Urine output & Serum creatinine (contralateral kidney compensates)]
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12
Q

[Post Strep Glomerulonephritis / Post infectious GN]

A: Clinical Presentation (5)

B: Which Kidney is most affectred from PSGN

A

A: [Older Child/Young Adult] with [Edema / Hematuria (Cola Colored Urine) / ProteinUria] few weeks after [Impetigo vs. pharyngeal infection]

B: Affects BOTH Kidneys (enlarged and swollen)

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13
Q

[Pauci Immune ANCA-associated RPGN]

Histology (3)

A

Is a type 2 Hypersensitivity

1) Absence of Ig and C3 deposit
2) Crescent formation
3) Focal Necrosis

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14
Q

Acute Tubular Necrosis

A: Clinical Course (3 Phases)

B: Outcomes (2)

A

A:

  1. Initiation phase =36 hour period = slight DEC in urine output from ischemic/toxic injury
  2. Maintenance Phase= 1-2 week period= Tubular damage is established –> [Oliguria/Fluid overload/Electrolyte abnormalitities]
  3. Recovery Phase= [Tubular Re-epithelization] which clears cast –> Transient polyuria and [loss of electrolytes from still impaired tube reabsorption]

B: ([[Renal Function imprvmnt]) vs. [Foci of interstitial scaring –> permanent renal impairment (rare)]

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15
Q

NephrOtic Syndrome

A: Classic Presentation (5)

B: COMMON Renal Complication from this. What are the sx (3)

A

A: CLag + [Proteinuria > 3.5 gm/day–>FOamy Urine] =

[INC Coagulability from loss of AT3]

[INC Lipidemia]

[DEC alubuminemia] –> Edema

[DEC gammaglobinemia]

B: Renal Vein Thrombosis –>

  • Acute Flank Pain
  • Hematuria
  • [LEFT Varicocele]
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16
Q

A: Describe Histology for Hyaline Arteriolosclerosis

B: Causes (2)

A

A: [Homogenous deposition of eosinophilic hyaline in intima and media of small vessels]

B:

1) Benign HTN
2) [Diabetic Autonomic NephrOpathy:–> will also have [Kimmelsteil Wilson Nodules from Mesangial Sclerosis]

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17
Q

Where in the Renal Tubule is PAH secreted into?

A

PCT (but also some PAH is freely filtered by Glomerulus)

so PAH concentration is lowest in Bowman’s Capsule

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18
Q

Describe Tubular Solute Concentrations for Creatinine along the renal tubule (PCT –> Loop–>DCT –> CD)

A

Basically the same path as [Inulin & Mannitol]

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19
Q

Describe Tubular Solute Concentrations for [Innulin & Mannitol] along the renal tubule (PCT –> Loop–>DCT –> CD)

A

Basically the same path as Creatinine

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20
Q

FORMULA for:

A: RPF: Renal plasma Flow

B: RBF: Renal Blood Flow. - Also Define RBF

C: Filtration Fraction

A

A: rpf = PAH Clearance =UV / P

B: RBloodF = [rpf ÷ (1 - Hct)] = volume of blood flowing thorugh kidneys per unit time

C: [Filtration Fraction] = [GFR ÷ rpf]

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21
Q

A: Demographic for Renal Artery Stenosis (2)

B: Manifestations (3)

A

A:

  1. Elderly
  2. [Pregnant Women 2º to fibromuscular Dysplasia]

B:

  • Unilateral Kidney Atrophy
  • HTN
  • Abd Bruit
  • R Kidney Atrophy from RAS in image*
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22
Q

Promoters of Nephrolithiasis (8)

A

IM COUGHS

  • Injury
  • [Mg+ –> Struvite Stones]
  • Calcinuria**
  • Oxalate INC**
  • [Uric Acid INC in urine (Tumor lysis syndrome vs. Gout)
  • Gravity
  • Hydrogen ions
  • Sodium
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23
Q

A: INHIBITORS of Nephrolithiasis (2)

B: Once a pt develops Nephrolithiasis, what are the tx (4)

A
  1. CITRATE (found in Fruits & Veggies) + Hydration
  2. INC Urine Flow

B:

  • Tamsulosin
  • NSAIDs
  • [INC Fluid Intake to 2-3 L/day]
  • Proximal Ureter location –> Surgery
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24
Q

A: Describe Histology for [Multiple Myeloma Nephropathy]

B: Demographic

C: Other common sx with this presentation (3)

A

A: [Large Eosinophilic light chain cast] made of [Bence Jones proteins] in tubular lumen –> [1º DTiN-DrugTubularInterstitialNephritis]

B: Elderly

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25
Q

A: Classic Presentation Triad for [Drug Induced -DTiN]

B: What Drugs mostly cause this (3)

C: What Wt Loss Drug can cause this?

A

ERF me some DAN drugs !

A: [Edema & Eosinophilia], Rash, Fever

B: Diuretics / Abx (PCN) / NSAIDs

C: [Chinese Herb AristoLochic Acid]

DTiN = Drug Tubular Interstitial nephritis

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26
Q

A: Describe Histology

B: Dz

A

A: image

B: [ATN - Acute Tubular Necrosis]

“ERF me some DAN drugs”

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27
Q

A: How does [Bladder Urothelial Transitional Carcinoma] clinically present

B: Risk Factors (5)

C: Describe Histology (2)

A

A: Gross Hematuria in an elderly Man

B: “aww, :-( your [Poor Pee SAC]”

Phenacetin/Plastics/Smoking/Aniline dyes/Cyclophosphamide]

C: Malignant Epithelial Cells =

*Papillary structures

*Nuclear atypica/pleomorphism

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28
Q

A: Most common causes of Acute Tubular Necrosis (7)

B:Which stage would these things lead to

A
  1. Ischemia (Sepsis = MOST COMMON/Hemorrhage/Surgery)
  2. Toxic (Aminoglycosides/Lead/Crush injury/Ethylene glycol antifreeze)

B: Initiation Stage (1st stage)

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29
Q

Describe the Maintenance Stage of [Acute Tubular Necrosis] (3)

A
  • [Oliguria –> Volume Overload] from tubules not allowing any fluids through
  • INC BUN/Creatinine ratio
  • Hyperkalemia
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30
Q

Describe the Recovery Stage of [Acute Tubular Necrosis] (3)

A
  • Polyuria –> Dilute Urine and [DEC Electrolyte]
  • Na+ is spared and actually –> Hypernatremia
  • hypOkalemia (too much K+ is kicked out)
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31
Q

Clinical Presentation of Renal Papillary Necrosis (2)

A
  1. Gross Hematuria (passage of small blood clots)
  2. Acute Flank pain
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32
Q

Classic Presentation for [Renal Cell Carcinoma] (4)

A

RCC looks like HAWF!

[Hematuria PAINLESS (most common)] / [Abd Yellow Mass] / [Wt loss] / [Flank Pain]

L RCC in image

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33
Q

A: What conditions can [Untreated Hydronephrosis] lead to (3)

B: Common cause

C: Clinical Presentation (3)

A

A: HTN, [DEC Renal Function] & Sepsis!

B: Lower Urinary Tract Obstruction

C: Palpable Kidneys + LE Edema + Pain

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34
Q

A: [Tumor Lysis Syndrome] MOD

B: What parts of the Nephron is involved (2)

C: Tx for [Uric Acid Nephrolithiasis] in general (4)

A

A: High cell turnover from tumors –> INC [K+ / Phosphorous / Uric Acid] in serum. [Uric Acid] precipitates in Kidneys 2° to [Acidity within normal urine]

B: DCT and CD (are where Uric Acid crystallizes)

C:

  • Urine Alkalinization (use NaHCO3 vs. [K+ citrate])
  • Hydration
  • Allopurinol (if gout)
  • [low purine diet (EtOH vs. seafood)]
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35
Q

A: c-ANCA Hypersensitivity targets what antigen

B: Dz

C: What type of Hypersensitivitiy is this

D: Clinical Presentation (3)

A

A: [Positive c-ANCA in vasculature] = Ab against [Lysosomal PR3 of neutrophil/monocytes]

B: [Wegener’s Granulomatosis + Polyangiitis] (Type 3 Crescenteric RPGN)

C: Type 2

D: [ELK = ENT (Destructive Sinusitis & Hemoptysis) / Liver / Kidney(Type 3 Crescenteric RPGN)]

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36
Q

Clinical Presentation of [BrIAN-Berger’s IgA Nephropathy] (4)

A

[Henoch Schoenlein Purpura]

Hinge problems = Joint Arthritis

Stomach problems = NV + bloody diarrhea

Palpable Purpura (Butt, Legs, Feet) + [Pee with blood]

Mesangial IgA-C3 immune complex deposition

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37
Q

How can Infective Endocarditis affect Kidneys

A

[Immune Complex deposition] in kidneys –> Glomerulonephritis]

Think [SubEpithelial humps from IC deposition in PSGN]

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38
Q

A: What Kidney Stone is in image?

B: What urine pH does it precipitate in?

C: Causes (4)

A

A: [Calcium Oxalate / Phosphate]

B: [Oxalate < 7] but [Phosphate >7]

C: [Ethylene Glycol (Antifreeze)] / Excess VitC / Crohn Disease / poor hydration

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39
Q

A: What Kidney Stone is in image?

B: What urine pH does it precipitate in?

C: Causes

A

A: [MAPS- Mg+ Ammonium Phosphate Struvite]

B: MORE THAN 7 pH

C: Urease + Organisms

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40
Q

A: What Kidney Stone is in image?

B: What urine pH does it precipitate in?

C: Causes

A

A: [Uric Acid] is RadioLUcent

B: [less than 7 pH] “Uric Acid likes Acid”

C: High Cell turnover (Leukemia)

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41
Q

A: What Kidney Stone is in image?

B: What urine pH does it precipitate in?

C:Cause

A

A: Cystine

B: less than 7 pH

C: auto recessive [Cysteine ReAbsorb transporter defect] in PCT–>Staghorn Calculi

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42
Q

A: Dz in image

B: Composition (3)

A

A: Clear Cell Carcinoma (type of RCC)

B: [Clear Cytoplasm] / Large cells that are [Round vs. Polygonal cells]

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43
Q

A: What parts of the nephron are most affected by [ATN-Acute Tubular Necrosis] (2)

B: Lab finding for ATN??

A

A:PCT & [thick aLOH]

B: Muddy Brown Cast!

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44
Q

A: What is Conn’s Syndrome

B: Tx

A

A: [Primary Hyperaldosteronism] 2° to Adenoma

B: Aldosterone Blockers (Spironolactone / Eplerenone)

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45
Q

Which BP medication is used in pts with [Diabetic Nephropathy]? (2)

A

[ACEK2 inhibitors] vs. ARBS

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46
Q

A: In pts with Renal Artery Stenosis, what renal factor do they become Dependent on for appropriate GFR

B: What drugs are Contraindicated in these pts (2)

A

A: [Angiotensin 2 efferent vasoconstriction]

B: [ACEk2 inhibitors] vs. ARBS

Same rule applies for CHF vs. hypOvolemic vs. [Chronic Renal Dz] pts

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47
Q

Which Anti-Virals cause [crystalline neprhopathy] if adequate hydration is not given? (3)

A

“Fend Viruses with Agua”

  1. Famciclovir
  2. Valocyclovir
  3. Acyclovir
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48
Q

A: What 3 things does ADH do? What receptors are used for this?

B: How does this affect medullary osmotic gradient??

A

USES [Distal Collecting Duct V2 Receptor] to..

  1. INC Water Reabsorption
  2. INC Urea Reabsorption –> INC [medullary osmotic gradient] –> production of maximally concentrated urine!
  3. Use V1 Receptors to Vasoconstrict
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49
Q

Excretion Rate formula

A

UV (Urine concentration x Urine flow)

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50
Q

A: Symptoms of DKA (3)

B: What type of metabolic acidosis would this cause

A

“Too Many FUDGE bars –> DKA!”

  1. PolyUria –>POTENTIAL WT LOSS from urinating out water weight
  2. PolyDipsia
  3. [Fruity odor in breath vs. urine from acetone]
  4. Glasses foggy (Intermittent blurry vision)
  5. Eats a lot (polyphagia)

B: Anion Gap metabolic Acidosis

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51
Q

List the Main Reabsorption rates for ions in the:

Early PCT (6)

A
  • MOST OF WATER REABSORPTION (done passively with solute ReAbsorption)
  • 98% of Glucose ReAbsorption
  • 85% of HCO3 ReAbsorption
  • 70% of Phosphate ReAbsorption
  • 67% of Na+ ReAbsorption
  • 67% of K+ ReAbsorption
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52
Q

List the Main Reabsorption rates for ions in the:

Late PCT

A
  • 60% of Ca+ ReAbsorption (mostly by PTH)
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53
Q

List the Main Reabsorption rates for ions in the:

thin descending LOH

A
  • 15% of WATER ReAbsorption
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54
Q

List the Main Reabsorption rates for ions in the:

THICK aLOH (4)

A
  • 25% of Na+ ReAbsorption
  • 20% of K+ ReAbsorption
  • Trace Mg+ (driven by positive lumen potential)
  • Trace Ca+ (driven by positive lumen potential AND PTH)
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55
Q

List the Main Reabsorption rates for ions in the:

Early DCT

A
  • 5% of Na+ ReAbsorption
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56
Q

List the Main Reabsorption rates for ions in the:

[Late DCT & Cortical CD]

A
  • 3% of Na+ ReAbsorption
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57
Q

List the Main Reabsorption rates for ions in the:

Distal (Medullary) CD (3)

A
  • 17% of WATER ReAbsorption
  • 3% of Na+ ReAbsorption
  • 110% of K+ SECRETION
58
Q

Describe the relationship between GFR and Serum Creatinine

A

Every time GFR halves…[Serum Creatinine] doubles

59
Q

Common Bacteria that cause Cystitis (6)

A
  • E.Coli (MOST COMMON!!!)
  • Klebsiella
  • Enterobacter
  • Staph
  • Saprophyticus (Young Women)
  • Proteus Mirabilis (Alkaline urine + Ammonia scent)
60
Q

Common Bacteria that cause Pyelonephritis (4)

A
  • E.Coli (MOST COMMON!!!)
  • Klebsiella
  • Enterococcus Faecalis
  • Pseudomonas Aeruginosa (indwelling bladder catheters)
61
Q

Which Bacteria causes Pyelonephritis in pts with [Indwelling Bladder Catheters]?

A

Pseudomonas

62
Q

A: SE of Amphotericin B (2)

B: Mechanism of SE

A

A:

  • hypOkalemia –> weakness and arrhythmias (T wave flattening)
  • hypOmagnesemia

B: INC DCT permeability (from damage) allows K+ and Mg+ to escape into urine

63
Q

Describe Histology for [Post Strep GN] / [Post infectious GN] (3)

A
  1. Hypercellular Inflammed Glomerulus w/RBC Cast
  2. [Lumpy Bumpy IgG and C3 granular deposits on IF]
  3. [Subepithelial HUMPS on EM]
64
Q

Renal Clearcell Carcinoma MOD (3)

A

RCC (3 letters) =

  1. [Chromo 3 VHL hypermethylation]–>[INC IGF1 & HIF tx factor] –> [INC VEGF & PDGF]
    * VHL = Tumor Suppressor Gene*
  2. Sporadic = upper pole = smokers
  3. Hereditary = Bilateral = AUTO DOM
65
Q

A: Clinical Manifestation of this [Renal Clearcell Carcinoma] (4)

B: Where does RCC spread to? (3)

C: Where did this Dz originate from?

A

Clear Cell Carcinoma (type of RCC)

A: RCC was HAWF! = [Hematuria / Abd Yellow Mass / Wt loss / Flank pain]

B: Lung, Bone, [Retroperitoneal lymph nodes]

C: PCT of Kidney

66
Q

A: Most common cause of [Unilateral Fetal Hydronephrosis]

B: What typically causes NON-Obstructive Fetal Hydronephrosis

A

A: Inadequate canalization of Ureteropelvic Junction

B: Vesicoureteral Reflux (incomplete closure of vesicoureteral junction during detrusor contraction)

67
Q

Is the Bladder ExtraPeritoneal or IntraPeritoneal?

A

Bladder is ExtraPeritoneal (outside of the Peritoneum)

68
Q

A: What perfuses [Proximal Ureter]

B: What perfuses [Distal Ureter]

A

A: Renal A.

B: [SUP Vesical A.]

Middle Ureter is perfused variably

69
Q

From a Posterior view: where is the:

A: Kidney

B: Spleen

C: Liver

D: Pancreas

A

A: Deep to 12th rib

B: [L abd cavity - in front of (L 9th - 11th ribs)]

C: [RUQ - in front of (R 8th-11th) ribs]

D: Mostly retroperitoneal: Overlies 2nd lumbar Vertebra

70
Q

Crushing Abd trauma is most likely to injur which organ?

71
Q

Transplant Rejection: Hyperacute

A: Onset Time

B: Etiology

A

A: Minutes - Hours

B: Preformed Ab attack graft

72
Q

Transplant Rejection: Acute

A: Onset Time

B: Etiology

A

A: Days

B: Exposure to Donor Antigens –> Naive Recepient Humoral & Cell-mediated attack

73
Q

Transplant Rejection: Chronic

A: Onset Time

B: Etiology

A

A: Months - Years

B: continued low-grade immune response, refractory to immunosuppressants :-(

74
Q

Transplant Rejection: Hyperacute

Histology (3)

A
  1. Gross mottling
  2. Cyanosis
  3. [Arterial Fibrinoid Necrosis + Capillary occlusion]
75
Q

Transplant Rejection: Acute

Humoral Histology (3)

A
  • C4d deposition
  • Neutrophilic infiltrate
  • Necrotizing Vasculitis
76
Q

Transplant Rejection: Acute

Cellular Histology (2)

A
  • Lymphocytic interstitial infiltrate
  • Endotheliits
77
Q

Transplant Rejection: Chronic

Histology (4)

A
  1. Vascular Wall thickening
  2. Luminal narrowing
  3. Obliterative Intersitital Fibrosis
  4. Parenchyma Atrophy
78
Q

Lithium SE (4)

A

LMNOP

Lithium SE:

Movement / Tremor

Nephrogenic Diabetes Insipidus (blocks ADH)

hypOthyroidism

[Pregnancy teratogenic - Epstein anomaly]

79
Q

[Sirolimus Rapamycin] MOA

A

[Sirolimus Rapamycin]

Forms complex with [FK506 Binding Protein] –> inhibits mTOR –> BLOCKS [IL2 signal] –> Prevents lymphocyte growth/proliferation

80
Q

[Sirolimus Rapamycin] Indication (2)

A

[Sirolimus Rapamycin]

  1. Sirvival of Kidney when [nephrotoxic cyclospoRine] is given
  2. Renal transplant px
81
Q

Mycophenolate MOA

A

[Reversibly inhibits nucleotide synthesis], required for lymphocyte proliferation –> [promotes T-cell apoptosis]

82
Q

Leflunomide MOA

A

[Reversibly inhibits nucleotide synthesis], required for lymphocyte proliferation –> [promotes T-cell apoptosis]

83
Q

A: CyclospoRine MOA

B: Which organ is harmful to?

A

CyclospoRine

A: Forms complex with Cyclophilin –> inhibits Calcineurin –> [inhibits IL2 transcription]

B: Renal toxic (give with [Sirolimus Rapamycin] to lessen nephrotoxicity)

84
Q

CyclospoRine Indications (3)

A

Prevents Transplant Rejection

  1. Psoriasis
  2. Transplant Px
  3. Rheumatoid Arthritis
85
Q

A: What 2 things are pts with [Antiphospholipid Ab Syndrome] at risk for

B: This syndrome is mostly associated with _____

A

A: Antiphospholipid Abs –>

  1. [Thromboembolism]
  2. [Unexplained AND Recurrent Miscarriages] (placental insufficiency vs. preeclampsia)

B: some SLE pts have [Antiphospholipid Ab Syndrome]

86
Q

A: Fabry Disease MOD

B: Mode of Inheritance

A

A: [lysosomal (a-galactosidase A) deficiency] –> [sphingolipid accumulation]

B: X-linked Recessive

87
Q

Fabry Disease Clinical manifestations (7) - also list onset time

A

“Fabry is [Never Too BRASH]”

  1. Sweating DEC (hypOhidrosis) - early on
  2. Neuropathy - early on
  3. Angiokeratomas - late adolescence
  4. Telangiectasias - late adolescence
  5. Brain (TIA vs. stroke) - mid adult
  6. Hypertrophied LV - mid adult
  7. [Renal Failure 2° to Glomerular & DCT accumulation]
88
Q

Acute Hemolytic Transfusion MOD

A

[Preformed Anti-ABO IgM] bind to donor RBC –> [Anaphylatoxin C3a and C5a activation] + [C5b-C9 membrane attack complex] –> Cy-2-toxicity

Type 2 Hypersensitivity

89
Q

Acute Hemolytic Transfusion

A: Manifestations (6)

B: What type of Hypersensitivity is this

A

A: Transfusions Left Harry & Berry Cold & Fuckd!

Tachycardia

Lumbar Pain

Hemoglobinuria (Red/Brown urine)

Bleeding w/hypOtension

Chest Constriction

Flu-like Sx

B: Type 2 Hypersensitivity

90
Q

Describe the Composition of Crest in [Cresenteric RPGN] (3)

A

FIBRIN / [Glomerular Parietal Cells] / [Macrophages] – all in Bowman’s Space

Macrophages pass through gaps into Bowman’s Space–> Macrophages secrete factors that INC fibrin deposition and fibrin deposition–>[Glomerular Parietal cell proliferation]

91
Q

[Crescenteric RPGN] MOD for Crest formation

A

Macrophages pass through gaps(from destruction) into Bowman’s Space–> Macrophages secrete factors that INC fibrin deposition and fibrin deposition–>[Glomerular Parietal cell proliferation]

92
Q

A: Which 2 CA can IL2 treat?

B: What’s the Mechanism (2)

A

A: [Renal Clearcell Carcinoma] & [Metastatic Melanoma]

B: Activation of [NK cells] and [T-cell Growth]

93
Q

A: Potters Sequence etx

B: Clinical Presentation - 6

A

A: [Fetal Renal Agenesis / Dysfunction] –> Oligohydraminos (No Amniotic Fluid)

B: POTTER

Pulm hypOplasia

Oligohydraminos

Twisted Face

Twisted Limbs

[Ears set low & Extremities shortened]

Renal agenesis = cause

94
Q

ArPKD - [Autosomal recessive Polycystic Kidney Dz] MOD

A

[Chromo 6 PKD1 gene mutation] –> Defective Fibrocystin (present in kidney & liver)

95
Q

ArPKD - [Autosomal recessive Polycystic Kidney Dz]

Manifestations (4)

A
  • Bilaterally Enlarged Kidneys with Reniform shape
  • [Sponge-like Cross Section]
  • Liver Fibrosis
  • Saccular Dilitation of CD
96
Q

ADPKD - [Autosomal Dominant Polycystic Kidney Dz]

Describe the Dz (8)

A

ADPKD

Aneurysm (Berry) and [Adults affected]

Doomed [HTN and MVP]

[PrOteinuria AND Hematuria]

Kidney Failure (Early vs. Late onset)

Differentation problem = etiology

97
Q

Histology for nephrOtic syndrome (2)

A

[Diffuse [Epithelial Podocyte foot process] effacement ONLY SEEN ON ELECTRON MICROSCOPY] All other imaging is normal!

98
Q

nephrOtic syndrome MOD

A

Cytokine Hyperproduction Directly damages [Epithelial Podocyte foot processes] –> [Effacement and Fusion]

99
Q

Describe Histology for Acute Pyelonephritis (3)

A

1) Tubular Lumen neutrophils
2) Interstitial neutrophils
3) Microabscesses

100
Q

Clinical Presentation for Acute Pyelonephritis (8)

A

[DUCS FFLW]

[Cysitits Sx: Dysuria + (Urinary sx) + (Culture>100K colonies/Pyruia/+LE&Nitrites) + (Suprapubic pain)]

AND

[Pyelonephritis Sx: (Fever & Malaise) + (Flank pain) + Leukocytosis + WBC CAST]

[Pyruia- x>10 WBC on hpf in urine} & [Positive Leukocyte Esterase & Nitrites] are seen in BOTH

101
Q

Where does the majority of water ReAbsorption occur in the nephron?

A

PCT!

occurs passively with ReAbsorption of Solutes

102
Q

Which artery perfuses Proximal ureter

103
Q

Which artery perfuses Distal ureter

A

SUP Vesical A.

104
Q

What is the Urachus and how is it related to Dz

A

Remnant of Allantois that connects bladder with yolk sac during fetal development

Failure of Urachus to obliterate –> Urine discharge from the Umbilicus

Normally: Allantois –> Urachus –> MediaN umbilical ligament

105
Q

Which main vessels lie in front and behind the Ureter within the pelvic inlet

A

In Front of Ureter = Water Under Bridge = Uterine a. vs. Vas Deferens

Behind Ureter (in the pelvis) = Internal iliac A.

106
Q

In addition to Water permeability, what other substance does ADH INC permeability to and what part of the nephron?

A

Urea

Medullary DCPC(Distal CD Principal Cell)

Aquaporin channels = Cortical Collecting Duct

107
Q

In Metabolic acidosis, Urine pH DEC because of INC excretion of what 3 compounds?

A
  1. H+
  2. NH4+
  3. H2PO4
108
Q

[Stress Incontinence] MOD (2)

A

Loss of pelvic floor support & incompetence of urethral sphincter; Exacerbated w/coughing

109
Q

Name 2 inhibitors of [Nephrolithiasis] (2)

A

Citrate vs. INC Water intake

Pts are Normocalcemic due to intact serum regulations by Vitamin D and PTH

110
Q

What 2 chromosomes are associated with ADPKD

A
  • [PKD1 Chromo 16 mutation = most common]
  • [PKD1 Chromo 4 mutation]
111
Q

A: Causes of Renal Papillary Necrosis (9)

B: Out of these, which is the MOST COMMON CAUSE

A

POST CARDS for the Pappy!

[Pyelonephritis/Obstruction/Sickle Cell/TB / Cirrhosis/ [Analgesics vs. Alcohol] / [Renal Vein Thrombosis] / DM / Systemic Vasculitis

: Analgesics most common!

112
Q

Tx for this Kidney Stone (3)

A

[Calcium Oxalate / Phosphate]

Citrate vs. Thiazides vs. Hydrate

113
Q

Tx for this Kidney stone (2)

A

[Uric Acid] is RadioLUcent

Alkalinize urine vs. Allopurinol

114
Q

Tx for this Kidney Stone (2)

A

[MAPS- Mg+ Ammonium Phosphate Struvite]

Treat infection AND Surgical removal

115
Q

Tx for this Kidney Stone

A

Cystine

Alkalinize Urine

116
Q

Classic Presentation for Nephritic Syndrome (3)

A
  1. [Hematuriiia w/some proteinuria]
  2. [Periorbital Edema & HTN from Na+ retention]
  3. RBC Cast

Caused by Hypercellular finlammed Glomeruli

117
Q

Nephritic Syndrome MOD

A

Immune complex deposition activates C5a –> recruits neutrophils–> Hypercellular inflammed Glomeruli

118
Q

Immunofluorescence pattern for [GoodPasture Type 1 Crescenteric RPGN] (2)

and clinical presentation (2)

A

Linear (anti-Basement membrane Ab) + Sieve effect;

GoodPasture

Glomerulus damage–>Hematuria

Pulmonary damage–> Hemoptysis

119
Q

Immunofluorescence pattern for [PSGN-PiG] and [Diffuse Proliferative GN]

[Type 2 Crescenteric RPGN]

A

Granular (Immune complex deposition)

120
Q

What’s the most common renal dz in SLE

A

[Diffuse Proliferative GN] - Type 2 Crescenteric RPGN

SLE pts may also have membranous nephropathy

121
Q

Which type of [Crescenteric RPGN] has NO immunofluorescence pattern?

A

Pauci-immune (microscopic polyangiitis vs. Wegener vs. ChurgStrauss)

122
Q

A: Clinical Presentation for [Microscopic Polyangiitis Type 3 Crescenteric RPGN] (2)

B: MOD

A

A: Hemoptysis + [Vasculitis with NO granulomas or asthma]

B: p-ANCA attacks [Neutrophil MPO]

123
Q

A: Clinical Presentation for [Churg Strauss Type 3 Crescenteric RPGN] (3)

B: MOD

A

“PAGE Churg Strauss! “

A: p-ANCA / Asthma / Granulomas / Eosinophilia

B: p-ANCA attacks [Neutrophil MPO]

124
Q

Tx for [Type 3 Crescenteric RPGN] (2)

A

Cyclophosphamide vs. Steroids

125
Q

What’s the most common nephropathy worldwide?

A

[BrIAN - Berger IgA Nephropathy]

126
Q

A: Clinical Presentation for [AXS- Alport X-linked Syndrome] (3)

B: MOD

A

A:

  1. Hearing Loss
  2. Hazy view (ocular disturbances)
  3. Hematuria

B: [Type 4 Collagen thinning & splitting of Basement membrane]

127
Q

How can you differentiate Cystitis vs. Urethritis

A

Urethritis does NOT have [Culture >100K] = Sterile Pyuria

128
Q

Which Kidney cells produce EPO

A

[Peritubular interstitial cells]

129
Q

Why are ESRD pts closely monitored during Dialysis

A

Cyst develop within shrunken ESRD Kidneys during dialysis –> [Renal Cell Carcinoma]!

130
Q

Scarring of the kidney upper and lower poles usually describes _____

A

VUR - Vesicoureteral Reflux

131
Q

Histology for Chronic Pyelonephritis (3)

A
  1. Atrophic tubules containing eosinophilic proteinaceous thyroidization (shown in image)
  2. Waxy Cast
  3. Cortical scarring with blunted calyces (if at upper and lower poles only = VUR etiology)
132
Q

What type of Paraneoplastic characteristics does [Renal Clearcell carcinoma] have? (2)

A

can secrete PTHrP or ACTH!

133
Q

Clinical Presentation of a Malignant kidney tumor made of Blastema. What’s the cause

A

Wilms Tumor = WAGR

Wilms tumor (unilateral flank mass w/hematuria & HTN from renin)

Aniridia

Genital abnormalities

Retardation

Caused by [Chromo 11 WT1 tumor suppressor gene deletion]

134
Q

Describe [Denys Drash Syndrome] (3)

A

Wilms tumor + [progressive glomerular dz] + [male pseudohermaphroditism]

135
Q

What are the 2 pathways for [BUTC - Bladder Urothelial Transitional Carcinoma] and which is associated with early p53 mutation

A
  1. Flat = early p53 mutation –> Immediately High grade
  2. Papillary= starts as low grade –>progresses to High grade
136
Q

Which Bladder CA arises from Urachal remnant and develops at the ___ of the bladder?

A

[Bladder ADC] arises from Urachal remnant –> develops at DOME of bladder

Also can come from exstrophy

137
Q

Which Bladder CA is associated with Middle Eastern man, Schistosoma Haemotobium and Chronic Cysitis?

A

Bladder SQC

Urothelial cells undergo metaplasia –> Squamous due to Chronic cystitis–>dysplasia –> SQC

138
Q

Common characteristics for Nephriiitic Syndrome (4)

A

HARP

[Hypercellular inflammed Glomeruli w/Hematuria]

Azotemia COB

RBC Cast

[Periorbital Edema + HTN]

139
Q

Classic signs of Uremia-4

A
  • Pericardial Rub
  • Lethargy
  • Pruritus
  • Nausea
140
Q

What is normal Creatinine Clearance for Men vs Women

A

Men = 97-137

Women = 88-128

[3] Step 1 USMLE (8 decks)

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