Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Step 1 USMLE Rx - Cardio > Renal and Urinary > Flashcards

Renal and Urinary Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Most common cause of nephrOtic syndrome in Children and its Tx

A

A: Minimal Change Dz

B: REVERSIBLE with Corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the Differential Dx for Metabolic ALKalosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ADPKD- Autosomal Dominant Polycystic Kidney Disease

A: Genetic MOD

B: Clinical MOD (2)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

A: Which substances INCREASE along the PCT (5)

B: Which substances DEC along the PCT (3)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

Basically the same path as [Innulin & Mannitol]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

Basically the same path as Creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

A: Describe Histology (4)

B: Dz

A

A: image

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

A

Pancreas

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

A
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

A

image

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions