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Step 1 USMLE Rx - Cardio > 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

3 MAIN ways to avoiding [Catheter Associated UTI]

A
  1. REMOVE CATHETER AS SOON AS IT IS NOT INDICATED ANYMORE (DURATION IS THE GREATEST RISK)
  2. Avoid Unnecessary catheterization
  3. Use Sterile technique during insert
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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 for 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

Describe the Differential Dx for Metabolic ALKalosis

A
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7
Q

A: How does Multiple Sclerosis affect the Bladder?

B: Describe the 3 Different etiologies of Urinary Incontinence and their sx

A

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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8
Q

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

B: Most common Risk Factor

C: Other Risk Factors (3)

D: Name 2 inhibitors of [Nephrolithiasis] (2)

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

D: Citrate vs. INC Water intake

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

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9
Q

ADPKD- Autosomal Dominant Polycystic Kidney Disease

A: Genetic MOD

B: Clinical MOD (2)

A
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10
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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11
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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12
Q

DKA- Diabetic KetoAcidosis

A: Tx (2)

B: MOD (2 pathways)

C: What type of Anion Gap Acidosis does this cause

D: What’s the pH of the Urine during DKA? Why (2)?

A

A: [IV Normal Saline + Insulin]

B: image

C: [INC Anion Gap Acidosis] (MUDPILES)

D: Urine is ACIDIC (HCO3 is completely reAbsorbed in acidotic states by PCT & INC production of NH4 & H2PO4)

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13
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. [Ballotable Flank Mass developing within weeks of pelvic surgery]
  3. [Normal Urine output & Serum creatinine (contralateral kidney compensates)]
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14
Q

[Post Strep Glomerulonephritis / Post infectious GN]

A: Clinical Presentation (5)

B: What part of the Kidney is affectred

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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15
Q

[Pauci Immune ANCA-associated RPGN]

A: Histology (3)

B: Clinical Presentation (2)

A

Is a type 2 Hypersensitivity

A:

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

B: [Renal Failure] + [Pulm (epistaxis vs. chronic sinusitis)

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16
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: ([Tubular Re-epithelization] + [Renal Function imprvmnt]) vs. [Foci of interstitial scaring associated w/permanent renal impairment (rare)]

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17
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
  • [RIGHT Varicocele]
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18
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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19
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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20
Q

A: Which substances INCREASE along the PCT (5)

B: Which substances DEC along the PCT (3)

A
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21
Q

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

A
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22
Q

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

A

Basically the same path as [Innulin & Mannitol]

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23
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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24
Q

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

A
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25
Q

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

A
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26
Q

Describe Tubular Solute Concentrations for [Na+ and Cl] along the renal tubule (PCT –> Loop–>DCT –> CD)

A
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27
Q

FORMULA for:

A: RPF: Renal plasma Flow

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

C: Filtration Fraction

A

A: rpf = PAH Clearance = [(urine PAH) x (urine flow rate)] ÷ (plasma PAH)

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

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

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28
Q

In the absence of ADH, what part of the Renal Tubule has the Highest Osmolarity?

A
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29
Q

Pheochromocytoma

A: Tumor arising from the _____

B: What does it secrete

C: Clinical Presentation (3)

A

A: Adrenal Medulla

B: Catecholamines –> High Epi levels –> [hypOkalemia via B2 receptor stimulation]

C:

  • HA
  • Tachycardia
  • Diaphoresis (Sweating)
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30
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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31
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 / aciditiy
  • Sodium
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32
Q

A: INHIBITORS of Nephrolithiasis (2)

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

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

B:

  • Tamsulosin
  • NSAIDs
  • [INC Fluid Intake to 2-3 L/day]
  • Proximal Ureter location –> Surgery
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33
Q

A: Describe Histology for [Multiple Myeloma Nephropathy]

B: Demographic

C: Other common sx with this presentation (3)

A

A: [Large PINK Eosinophilic light chain cast] made of [Bence Jones proteins] in tubular lumen –> [1º ATiN - Acute Tubular Interstitial Nephritis]

B: Elderly

C:

  1. [Azotemia COB - Creatinine INC / Oliguria / BUN INC]
  2. INC Serum Protein
  3. Constipation
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34
Q

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

B: What Drugs mostly cause this (3)

C: What Wt Loss Drug can cause this? How?

A

ERF me some DAN drugs !

A: [Edema & Eosinophilia], Rash, Fever

B: Diuretics / Abx / NSAIDs

C: [Chinese Herb Aristolochic Acid] –> RAPID ATiN!

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35
Q

A: Describe Histology (4)

B: Dz

A

A: image

B: [Drug induced ATiN - Acute Tubular Interstitial Nephritis] (can be chronic as well)

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36
Q

A: How does Transitional Cell Carcinoma of Bladder typically present

B: Risk Factors (2)

C: Describe Histology (2)

A

A: Gross Hematuria in an elderly Man

B:

  • Exposure to [RAP-Rubber / [Aromatic Amine Stuff] /Plastics]
  • Smoking

C: Malignant Epithelial Cells =

*Hyperchromatic nuclei

*INC nucleus to cytoplasm ratio

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37
Q

A: Most common causes of Acute Tubular Necrosis (4)

B:Which stage would these things lead to

A
  • Sepsis = MOST COMMON
  • Surgery
  • Hemorrhage
  • Acute MI

B: Initiation Stage (1st stage)

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38
Q

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

A
  • [Oliguria –> Volume Overload] from tubules not allowing any fluids through
  • INC Creatinine / BUN ratio
  • Hyperkalemia
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39
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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40
Q

A: Clinical Presentation of Papillary Necrosis (2)

B: Causes (9)

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

A

A:

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

B: POST CARDS for the Pappy!

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

C: Analgesics!

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41
Q

Classic Presentation for [Renal Cell Carcinoma] (4)

A

RCC looks like HAWF!

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

L RCC in image

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42
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: Pain + [LE Edema] + Palpable Kidneys

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43
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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44
Q

A: Describe image

B: Dz

C: What type of Hypersensitivitiy is this

D: Clinical Presentation (3)

A

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

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

C: Type 2

D: [ELK = ENT / Liver / Kidney] + [Destructive Sinusitis] + Hemoptysis

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45
Q

A: Clinical Presentation of [BrIAN-Berger’s IgA Nephropathy]

B: When does it onset

C: Demographic

D: Desribe the Histolgy

A

A-D: image

[Henoch Schoenlein Purpura]

Hinge problems = Joint Arthritis

Stomach problems = NV + bloody diarrhea + Stomach Pain

Palpable Purpura = mainly on Butt, Legs, Feet

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46
Q

What type of Renal Injury is associated with Infective Endocarditis

A

Glomerulonephritis 2° to [Circulating Immune Complex deposition]

47
Q

A: What Kidney Stone is in image?

B: What pH does it present in?

C: Demographic.

Causes.

Tx

A

A: [Calcium Oxalate / phosphate]

B: > 7 pH

C: image

48
Q

A: What Kidney Stone is in image?

B: What pH does it present in?

C: Demographic (2).

Causes (2).

Tx (2)

A

A: [MAPS- Mg+ Ammonium Phosphate Struvite]

B: > 7 pH

C: image

49
Q

A: What Kidney Stone is in image?

B: What pH does it present in?

C: Demographic

Causes (2)

Tx (3)

A

A: [Uric Acid]

B: less than 7 pH

C: image

50
Q

A: What Kidney Stone is in image?

B: What pH does it present in?

C: Demographic

Causes

Tx (3)

A

A: Cystine

B: less than 7 pH

C: image

51
Q

A: Dz in image

B: Composition (3)

A

A: Clear Cell Carcinoma (type of RCC)

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

52
Q

A: Identify in image (3)

B: Which portions of the Nephron are MOST affected by [ATN-Acute Tubular Necrosis] (2)

C: What Clinical Presenation is pathognomonic for ATN??

A

A: image

B: PCT & [thick aLOH]

C: Muddy Brown Cast!

53
Q

A: What is Conn’s Syndrome

B: Tx

A

A: [Primary Hyperaldosteronism] 2° to [aldosterone secreting adenoma] –> [hypOkalemia –>metabolic alkalosis] and HTN

B: Aldosterone Blockers (Spironolactone / Eplerenone)

54
Q

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

A

[ACEK2 inhibitors] vs. ARBS

55
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

56
Q

A: What is Foscarnet? Indication?

B: Foscarnet SE (3)

A

B: [Pyrophosphate Anti-viral analog] used for [Ganciclovir-resistant CMV]

  1. Chelates Ca+
  2. Promotes Nephrotoxic Mg+ Wasting!
  3. (1 and 2) –> Seizures
57
Q

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

A

“Fend Viruses with Agua”

  1. Acyclovir
  2. Valocyclovir
  3. Famciclovir
58
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
59
Q

Formula for :

A: Excretion Rate

B: [Excretion Rate when given [Plasma Concentration Substance A] and [Tubular Reabsorption Substance A]

A

A: [Urine Flow] x [Urine Concentration Substance A]

B: GFR x [Plasma Concentration Substance A] - [Tubular Reabsorption Substance A]

60
Q

A: Clinical Triad of DKA (3)

B: What type of Anion Gap 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
  4. Glasses foggy (Intermittent blurry vision)

B: High Anion Gap metabolic Acidosis

61
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
62
Q

List the Main Reabsorption rates for ions in the:

Late PCT

A
  • 60% of Ca+ ReAbsorption (mostly by PTH)
63
Q

List the Main Reabsorption rates for ions in the:

thin descending LOH

A
  • 15% of WATER ReAbsorption
64
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)
65
Q

List the Main Reabsorption rates for ions in the:

Early DCT

A
  • 5% of Na+ ReAbsorption
66
Q

List the Main Reabsorption rates for ions in the:

[Late DCT & Cortical CD]

A
  • 3% of Na+ ReAbsorption
67
Q

List the Main Reabsorption rates for ions in the:

Distal (Medullary) CD

A
  • 17% of WATER ReAbsorption
  • 3% of Na+ ReAbsorption
  • 110% of K+ SECRETION
68
Q

Describe the relationship between GFR and Serum Creatinine

A

Every time GFR halves…[Serum Creatinine] doubles

69
Q

Common Bacteria that cause Cystitis (6)

A
  • E.Coli (MOST COMMON!!!)
  • Klebsiella
  • Enterobacter
  • Staph
  • Saprophyticus (Young Women)
  • Proteus Mirabilis (Alkaline urine + Ammonia scent)
70
Q

Common Bacteria that cause Pyelonephritis (3)

A
  • E.Coli (MOST COMMON!!!)
  • Klebsiella
  • Enterococcus Faecalis
  • Pseudomonas Aeruginosa (indwelling bladder catheters)
71
Q

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

A

Pseudomonas

72
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

73
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. [Electron-dense Subepi HUMPS of BM] (shown in image)
74
Q

Chromosomal mutation associated with Renal Cell Carcinoma

A

[Chromo 3p VHL mutation/hypermethylation]

VHL = Tumor Suppressor Gene

75
Q

A: Clinical Manifestation of this Dz (4)

B: Which organ does this Dz spread to?

C: Where did this Dz originate from?

A

Clear Cell Carcinoma (type of RCC)

A: RCC was HAWF! = [Hematuria / Abd Mass / Wt loss / Flank pain] + [YELLOW MASS (Clear CC only)]

B: Lung

C: PCT of Kidney

76
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)

77
Q

A: Identify components of [Suprapubic Abd Wall]

B: Is the Bladder ExtraPeritoneal or IntraPeritoneal?

A

A: image

B: Bladder is ExtraPeritoneal (outside of the Peritoneum)

78
Q

A: What perfuses [Proximal Ureter]

B: What perfuses [Distal Ureter]

A

A: Renal A.

B: [SUP Vesical A.]

Middle Ureter is perfused variably

79
Q

From a Posterior view: where is the:

A: Kidney

B: Spleen

C: Pancreas

D: Liver

A

A: Deep to 12th rib

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

C: Partially retroperitoneal: Overlies 2nd lumbar Vertebra

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

80
Q

Crushing Abd trauma is most likely to injur which organ?

81
Q

Transplant Rejection: Hyperacute

A: Onset Time

B: Etiology

A

A: Minutes - Hours

B: Preformed Ab attack graft

82
Q

Transplant Rejection: Acute

A: Onset Time

B: Etiology

A

A:

B: Exposure to Donor Antigens –> Recepient Humoral & Cellular Naive immune cell Activation

83
Q

Transplant Rejection: Chronic

A: Onset Time

B: Etiology

A

A: Months - Years

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

84
Q

Transplant Rejection: Hyperacute

Histology (2)

A
  1. Gross mottling & Cyanosis
  2. [Arterial Fibrinoid Necrosis + Capillary occlusion]
85
Q

Transplant Rejection: Acute

Humoral Histology (3)

A
  • C4d deposition
  • Neutrophilic infiltrate
  • Necrotizing Vasculitis
86
Q

Transplant Rejection: Acute

Cellular Histology (2)

A
  • Lymphocytic interstitial infiltrate
  • Endotheliits
87
Q

Transplant Rejection: Chronic

Histology (4)

A
  1. Vascular Wall thickening
  2. Luminal narrowing
  3. Obliterative Intersitital Fibrosis
  4. Parenchyma Atrophy
88
Q

Identify

89
Q

Lithium SE (4)

A

LMNOP

Lithium SE:

Movement / Tremor

Nephrogenic Diabetes Insipidus (blocks ADH)

hypOthyroidism

Pregnancy problems (teratogenic)

90
Q

[Sirolimus Rapamycin] MOA

A

[Sirolimus Rapamycin]

Binds and forms complex with [FK506 Binding Protein] –> inhibits mTOR –> BLOCKS [IL2 signal transduction] –> Prevents lymphocyte growth/proliferation

91
Q

[Sirolimus Rapamycin] Indication (2)

A

[Sirolimus Rapamycin]

  1. Kidney transplant Rejection prophylaxis
  2. Helps Kidney Sirvive when [nephrotoxic cyclosporine] is given
92
Q

Mycophenolate MOA (2)

A

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

93
Q

Leflunomide MOA (2)

A

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

94
Q

A: Cyclosporine MOA

B: Which organ is harmful to?

A

Cyclosporine

A: Binds to and forms complex with Cyclophilin –> inhibits Calcineurin –> [inhibits IL2 transcription]

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

95
Q

Tacrolimus MOA

A

Binds to and forms complex with Cyclophilin –> inhibits Calcineurin –> [inhibits IL2 transcription]

96
Q

Cyclosporine Indications (3)

A
  1. Transplant Rejection Px
  2. Psoriasis
  3. Rheumatoid Arthritis
97
Q

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

B: This syndrome is mostly associated with _____

A

A: Antiphospholipid Abs –>

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

B: 30% of SLE pts have [Antiphospholipid Antibody Syndrome]

98
Q

A: Fabry Disease MOD

B: Mode of Inheritance

A

A: [lysosomal (a-galactosidase A) deficiency] –> [sphingolipid Gb3 accumulation] –> accumulates in multiple places

B: X-linked Recessive

99
Q

Fabry Disease Clinical manifestations (7)

B: When do they onset

A

“Fabry is [Never Too BRASH]”

  1. Sweating DEC (hypOhidrosis) - occurs early on
  2. Neuropathy - early on
  3. Angiokeratomas - late adolescence
  4. Telangiectasias - late adolescence
  5. Brain (TIA vs. stroke) - mid adult
  6. Heart (LVH) - mid adult
  7. [Renal Failure 2° to Glomerular & DCT accumulation]
100
Q

Acute Hemolytic Transfusion MOD

A

[Preformed Anti-ABO IgM Ab] bind to antigens on transfused donor RBC –> [Anaphylatoxin C3a and C5a activation] + [C5b-C9 membrane attack complex formation] –> [Complement-mediated cell lysis]

Type 2 Hypersensitivity

101
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

102
Q

A: Dz

B: Describe the Composition (3)

A

A: [Crescenteric RPGN]

B: FIBRIN / [Glomerular Parietal Cells] / [Macrophages & Monocytes] – all in Bowman’s Space

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

103
Q

[Crescenteric RPGN] MOD

A

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

104
Q

Name the 5 roles of IL2

105
Q

A: Which 2 CA can IL2 treat?

B: What’s the Mechanism (2)

A

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

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

106
Q

A: Potters Sequence MOD

B: Clinical Manifestation (3)

A

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

B:

  • Limb Deformities (low set ears)
  • Flattened Face
  • Lung hypOplasia (since lungs require fluid to inflate properly)
107
Q

A: ArPKD - [Autosomal recessive Polycystic Kidney Dz] MOD

B: Mode of inheritance

A

A: [Chromo 6 PKHD1 gene mutation] –> Defective Fibrocystin (present in kidney & liver)

B: Auto Recessive

108
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
109
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

110
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. [Electron-dense Subepi HUMPS of BM]
111
Q

Histology for nephrOtic syndrome (2)

A

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

112
Q

nephrOtic syndrome MOD

A

Immune Dysregulation (Cytokine Hyperproduction) Directly damages [Epithelial Podocyte foot processes] –> [Effacement and Fusion]

113
Q

Describe Histology for Acute Pyelonephritis (4)

A

MASSIVE Infiltration of Neutrophils in:

1) Tubular Lumen
2) Interstitium
3) Microabscesses
4) Tubulorrhexis

114
Q

Clinical Presentation for Acute Pyelonephritis (8)

A

[DUS FFLW]

[Cysitits Sx: Dysuria + (Urinary sx) + (Suprapubic pain)]

AND

[Pyelonephritis Sx: (Fever & Malaise) + (Flank pain) + (Leukocytosis AND {Pyruia- x>10 WBC on hpf in urine} ) + WBC CAST]

Step 1 USMLE Rx - Cardio (5 decks)

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