Brainscape's Knowledge GenomeTM

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


See full index

USMLE Preparation > Renal Pathology > Flashcards

Renal Pathology Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

Metabolic acidosis
pH
pCO2
[HCO3-]

Compensation:

A

pH: low
pCO2: low
[HCO3-]: low

Compensation: hyperventilation

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

Metabolic alkalosis
pH
pCO2
[HCO3-]

Compensation:

A

pH: high
pCO2: high
[HCO3-]: high

Compensation: hypoventilation

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

Respiratory acidosis
pH
pCO2
[HCO3-]

Compensation:

A

pH: low
pCO2: high
[HCO3-]: high

Compensation: increased renal [HCO3-] reabsorption

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

Respiratory alkalosis
pH
pCO2
[HCO3-]

Compensation:

A

pH: high
pCO2: low
[HCO3-]: low

Compensation: decreased renal [HCO3-] reabsorption

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

Distal RTA (type 1)

Defect

Urine pH

Serum K+

Causes

A

Defect: inability of a-intercalated cells to secrete H+, thus no new HCO3- is generated.

Urine pH: >5.5

Serum K+: low

Causes: amphotericin B, analgesics, congenital anomalies, SLE.

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

Proximal RTA (type 2)

Defect

Urine pH

Serum K+

Causes

A

Defect: impaired PCT reabsorption of HCO3-.

Urine pH: <5.5

Serum K+: low

Causes: Fanconi syndrome (increased risk for Rickets), Multiple Myeloma, CA inhibitors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hyperkalemic RTA (type 4)

Defect

Urine pH

Serum K+

Causes

A

Defect: hypoaldosteronism/aldosterone-resistance causing hyperkalemia and decreased NH4+ excretion.

Urine pH: <5.5

Serum K+: high

Causes: decreased aldosterone production or aldosterone-resistance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

RBC casts in urine suggests…

A

GN

HTN emergency

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

WBC casts in urine suggests…

A

Tubulointerstitial inflammation

Acute pyelonephritis

Transplant rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Fatty casts in urine suggests…

A

Nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Granular casts in urine suggests…

A

Acute tubular necrosis (“muddy brown” in appearance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Waxy casts suggests…

A

ESRD/CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the nephrotic syndromes? (5)

A

Minimal change disease

Focal segmental glomerulosclerosis (FSGS)

Membranous nephropathy

Amyloidosis

Diabetic glomerulonephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Minimal change disease

Light microscopy finding(s)
Electron microscope finding(s)

A

Light microscopy finding(s) - normal appearing glomeruli; possible lipid deposition in PCT cells.

Electron microscope finding(s) - effacement of podocyte foot processes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Underlying disorders associated with FSGS (5)

A

HIV infection

Sickle cell disease

Heroin use

Morbid obesity

Interferon treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

FSGS

Light microscopy finding(s)
Immunofluorescence finding(s)
Electron microscope finding(s)

A

Light microscopy finding(s) - segmental sclerosis and hyalinosis.

Immunofluorescence finding(s) - possibly non-specific focal deposits of IgM, C3 and C1.

Electron microscope finding(s) - effacement of podocyte foot processes (similar to MCD).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Membranous nephropathy can occur secondary to…

Drugs

Infections

Autoimmune disease

A

Drugs: NSAIDs, penicillamine, gold.

Infections: HBV, HCV, syphilis.

Autoimmune disease: SLE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Membranous nephropathy

Light microscopy finding(s)
Immunofluorescence finding(s)
Electron microscope finding(s)

A

Light microscopy finding(s): diffuse capillary and GBM thickening.

Immunofluorescence finding(s): granular immune complex deposition.

Electron microscope finding(s): “spike and dome” appearance of subEPIthelial deposits.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the pathogenesis of diabetic glomerulonephropathy?

A

Hyperglycemia causes non-enzymatic glycation of tissue proteins. This leads to mesangial expansion, GBM thickening and increased permeability.

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

Diabetic glomerulonephropathy

Light microscopy finding(s)

A

Light microscopy finding(s) - mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis.

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

On light microscopy Kimmelstiel-Wilson lesions are noted. What is the diagnosis?

A

Diabetic glomerulonephropathy

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

What are the nephritic syndromes? (6)

A

Acute post-streptococcal glomerulonephritis

Rapidly progressing (crescentic) glomerulonephritis (RPGN)

Diffuse proliferative glomerulonephritis

IgA nephropathy (Buerger disease)

Alport syndrome

Membranoproliferative glomerulonephritis

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

What type of hypersensitivity is associated with acute post-streptococcal glomerulonephritis?

A

Type 3

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

What symptoms are apparent with acute post-streptococcal glomerulonephritis?

A

Peripheral and periorbital edema

Tea-colored urine

HTN

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

What lab finding is noted in acute post-streptococcal glomerulonephritis?

A

Decreased complement (C3) levels due to consumption.

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

Acute post-streptococcal glomerulonephritis

Light microscopy finding(s)
Immunofluorescence finding(s)
Electron microscope finding(s)

A

Light microscopy finding(s) - enlarged, hypercellular glomeruli.

Immunofluorescence finding(s) - “starry sky” granular appearance (“lumpy bumpy”) due to IgM and C3 deposition along the GBM and mesangium.

Electron microscope finding(s): subEPIthelial humps.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Rapidly progressing (crescentic) glomerulonephritis (RPGN)

Light microscopy finding(s)

A

Light microscopy finding(s) - crescents containing fibrin and plasma proteins with glomerular parietal cells, monocytes and macrophages.

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

What most often causes diffuse proliferative glomerulonephritis?

A

SLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Diffuse proliferative glomerulonephritis

Light microscopy finding(s)
Electron microscopy finding(s)

A

Light microscopy finding(s) - “wire looping” of capillaries.

Electron microscopy finding(s) - subENDOthelial immune complexes with C3 deposition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is IgA nephropathy (Buerger disease) associated with?

A

Episodic hematuria that occurs at the same time as respiratory or GI infections; it is the renal pathology of IgA vasculitis (Henoch-Schonlein purpura).

31
Q

IgA nephropathy (Buerger disease)

Light microscopy finding(s)
Immunofluorescence finding(s)
Electron microscopy finding(s)

A

Light microscopy finding(s) - mesangial proliferation.

Immunofluorescence finding(s) - IgA-based immune complex deposition in the mesangium.

Electron microscopy finding(s) - mesangial immune complex deposition.

32
Q

What is the pathogenesis of Alport syndrome?

What are other associated problems?

What is the inheritance?

What is the major finding on electron microscopy?

A

Mutation in type IV collagen leading to thinning/splitting of the GBM.

Eye problems (retinopathy, lens dislocation), GN and sensorineural hearing loss (“can’t see, can’t pee, can’t hear a bee”).

XLD

“Basket-weave” appearance.

33
Q

What 2 processes often exhibit both nephritc and nephritic symtoms?

A

Diffuse proliferative glomerulonephritis

Membranoproliferative glomerulonephritis

34
Q

What may cause secondary type 1 membranoproliferative glomerulonephritis?

A

HBV and HCV

35
Q

Type 1 membranoproliferative glomerulonephritis

Electron microscopy finding(s)
Immunofluorescence finding(s)
A

Electron microscopy finding(s) - subENDOthelial immune complex deposition with

Immunofluorescence finding(s) - granular immunofluorescence.

36
Q

What is type 2 membranoproliferative glomerulonephritis associated with?

A

C3 nephritic factor (an IgG auto-antibody that stabilizes C3 convertase leading to constant complement activation and low [C3]).

37
Q

Why is type 2 membranoproliferative glomerulonephritis also known as “dense deposit disease”?

A

Because there are significant intramembranous deposits.

38
Q

GBM splitting and a “tram-track” appearance is noted on H/E and PAS stains. What is the likely diagnosis?

A

Either type 1 or type 2 membranoproliferative glomerulonephritis

39
Q

Envelope or dumbbell-shaped urine crystals suggest…

A

Calcium oxalate stone

40
Q

What is given to someone with calcium stones?

A

Thiazides, citrate, low-sodium diet

41
Q

Wedge-shaped prism urine crystals suggest…

A

Calcium phosphate stone

42
Q

Coffin lid urine crystals suggest…

A

Ammonium magnesium phosphate stone

43
Q

Rhomboid or rosette urine crystals suggest…

A

Uric acid stone

44
Q

Hexagonal urine crystals suggest…

A

Cystine stone

45
Q

Which renal stones occur in settings of high pH?

Which renal stones occur in settings of low pH?

A

High pH: calcium phosphate and ammonium magnesium phosphate.

Low pH: uric acid and cystine stones.

46
Q

What causes ammonium magnesium phosphate stones?

A

Infection by urease positive bugs: P. mirabilis, Staph saprophyticus and Klebiella.

47
Q

What causes cystine stones?

A

A hereditary (AR) condition in which cystine-reabsorbing PCT transporter loses function and leads to cystinuria.

This defect also results in poor absorption of ornithine, lysine and arginine (COLA).

48
Q

Staghorn calculi are seen on microscopy. What is the likely diagnosis?

A

Ammonium magnesium phosphate crystals

49
Q

What is the presentation of a patient with renal cell carcinoma?

How does it metastasize?

What do they malignant cells look like on microscopy?

A

Hematuria, palpable masses, secondary polycythemia, flank pain, fever and weight loss are all common.

Hematogenous spread via the renal vein to the lungs and bone.

Polygonal clear cells filled with lipids and carbohydrates. They often look yellow due to the lipid accumulation.

50
Q

What are the major risk factors for renal cell carcinoma?

What are some associated paraneoplastic syndromes?

A

Smoking and obesity (most common in men 50-70 y/o).

PEAR - PTHrP, Ectopic EPO, ACTH, Renin.

51
Q

What is the most common primary renal malignancy?

What is its most common subtype?

What chromosome is involved?

A

Renal cell carcinoma

Clear cell carcinoma

Chr. 3

52
Q

What is the presentation of a renal oncocytoma?

What cells are neoplastic?

What is seen on microscopy?

A

Painless hematuria, flank pain and abdominal mass.

Benign collecting ducts.

A well-circumscribed mass with a central scar; large eosinophilic cells with many mitochondria.

53
Q

What is a unique presentation of a patient with renal cell carcinoma if it invades the left renal v.?

A

Varicocele, because the gonadal v. joins the left renal v.

54
Q

What chromosome and mutations are associated with Wilms tumor?

A

Loss of function mutations of tumor-suppressor genes WT1 or WT2 on chr. 11.

55
Q

What exists in the following syndromes associated with Wilms tumor? What gene is mutated?

WAGR complex

Denys-Drash syndrome

Beckwith-Wiedemann syndrome

A

WAGR complex: Wilms tumor, Aniridia, Genitourinary malformations, Retardation (WT1).

Denys-Drash syndrome: diffuse mesangial sclerosis dysgenesis of gonads (WT1).

Beckwith-Wiedemann syndrome: macroglossia, organomegaly, hemihyperplasia (WT2).

56
Q

What is the presentation of transitional cell carcinoma?

What may increase one’s risk? (4)

A

Painless hematuria without casts.

Phenacetin, smoking, aniline dyes and cyclophosphamide (problems in you “Pee SAC”).

57
Q

What are risk factors for squamous cell carcinoma of the bladder? (4)

A

Schistosoma infection (Middle East), chronic cystitis, smoking and chronic nephrolithiasis

58
Q

What causes the following types of urinary incontinence?

Stress incontinence

Urgency incontinence

Overflow incontinence

A

Stress incontinence: outlet incompetence (urethral hypermobility or sphincteric deficiency) that allows for leakage with increase intra-abdominal pressure. + bladder stress test.

Urgency incontinence: overactive bladder leading to uncontrollable leakage. Associated with UTI.

Overflow incontinence: incomplete emptying of the bladder. Associated with polyuria (DM), outlet obstruction and neurogenic bladder (MS).

59
Q

CT scan shows striated parenchymal enhancement. What is the likely diagnosis?

A

Acute pyelonephritis

60
Q

What may cause chronic pyelonephritis?

What may be seen on microscopy?

A

Recurrent/inadequately treated episodes of acute pyelonephritis. Often required predisposition to infection, like VUR or obstructing stones.

Coarse, asymmetric corticomedullary scarring with blunted calcyes. Tubules can be eosinophilic and resemble thyroid tissue.

61
Q

What is xanthogranulomatous pyelonephritis?

What does it look like on microscopy?

What infection is associated with it?

A

Widespread kidney damage due to granulomatous tissue containing foamy macrophages.

Grossly orange nodules that may mimic tumor nodules.

Proteus infections.

62
Q

What lab values are seen with pre-renal azotemia?

Urine Osm.
Urine Na+
BUN/creatinine

A

Urine Osm.: >500
Urine Na+: <20
BUN/creatinine: >20

63
Q

What lab values are seen with intrinsic-renal azotemia (i.e. acute tubular necrosis)?

Urine Osm.
Urine Na+
BUN/creatinine

A

Urine Osm.: <350
Urine Na+: >40
BUN/creatinine: <15

64
Q

What is the pathogenesis of acute tubular nephritis?

What can cause secondary acute tubular nephritis?

A

Drugs, acting as haptens, induce hypersensitivity reactions leading to pyuria (eosinophils) and azotemia.

Infections - Mycoplasma
Autoimmune disease - Sjogren syndrome, SLE, sarcoidosis.

65
Q

What is the presentation of acute tubular nephritis?

What drugs is it associated with? (5)

A

Fever, rash, hematuria, pyuria and CVA tenderness, but may also be asymptomatic.

5 P’s:

  • Pee (diuretics)
  • Pain-free (NSAIDs)
  • Penicillins and cephalosporins
  • PPIs
  • RifamPin
66
Q

What occurs in the following 3 phases of acute tubular necrosis?

  1. Inciting phase
  2. Maintenance phase
  3. Recovery phase
A
  1. Inciting phase
  2. Maintenance phase: oliguria; lasts 1-3 weeks risk of hyperK+, metabolic acidosis, uremia.
  3. Recovery phase: polyuria; BUN and creatinine fall; risk of hyperK+ and renal wasting.
67
Q

What 2 processes can cause acute tubular necrosis?

A

Ischemic injury: secondary to low RBF (hypotension, shock, sepsis, hemorrhage, etc.) results in death of tubular cells that may slough into tubular lumen (PCT and TAL are most susceptible to injury).

Nephrotoxic injury: secondary totoxic substances, crush injury and hemoglobinuria (PCT most susceptible).

68
Q

Diffuse cortical necrosis is associated with what?

What is it?

A

Obstetric complications and septic shock.

Acute generalized cortical infarction of both kidneys, likely due to a combination of vasospasm and DIC.

69
Q

What causes the hematuria and proteinuria seen in renal papillary necrosis?

What is renal papillary necrosis associated with? (4)

A

Sloughing of necrotic renal papillae due to recent infection or immune stimulus.

  • Sickle cell disease or trait
  • Acute pyelonephritis
  • Analgesics (NSAIDs)
  • DM

“SAAD papa with papillary necrosis”

70
Q

What is the presentation of a patient with AD polycystic kidney disease?

What mutations and which chromosomes are involved?

How is it treated?

A

Flank pain, HTN, urinary infection, progressive renal failure in 50%.

PKD1 on chr. 16 (85%) or PKD2 on chr. 4 (15%).

If HTN or proteinuria develop, treat with ACE inhibitors or ARBs.

71
Q

What is the appearance of a kidney with ADPKD?

What is the appearance of a kidney with ARPKD?

A

ADPKD: numerous cysts in cortex and medulla causing BL enlarged kidneys that destroy the parenchymal tissue.

ARPKD: cystic dilation of collecting ducts.

72
Q

What is the presentation of AR polycystic kidney disease?

What is it associated with?

A

Presents in infancy with congenital hepatic fibrosis. It may lead to systemic HTN, progressive renal insufficiency and portal HTN (due to congenital hepatic fibrosis).

Potter sequence.

73
Q

AD tubulointerstitial kidney disease (medullary cystic kidney disease) leads to what?

What is seen on ultrasound?

A

Tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine.

Small kidneys - poor prognosis.

74
Q

What do complex renal cysts look like?

How are they approached clinically?

A

They may be septated, enhanced or have solid components (as opposed to simple cysts filled with ultrafiltrate).

They must be followed or removed due to risk of RCC.

USMLE Preparation (7 decks)

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