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Renal 2 > Robbins Ch. 20 - Tubulointerstitial Disease > Flashcards

Robbins Ch. 20 - Tubulointerstitial Disease Flashcards

1
Q

6 types of tubulointerstitial injury

A
  • Tubular injury (ischemic or toxic)
  • Tubulointerstitial nephritis (inflammation)
  • Acute Pyelonephritis
  • Chronic pyelonephritis
  • Papillary necrosis
  • Nephrolithiasis
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2
Q

Acute tubular injury

2 types?

A

Tubular necrosis –> decreased renal function

  1. Ischemic
  2. Toxic
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3
Q

Ischemic causes of tubular necrosis

A
  • Decreased blood volume (shock, hypotension)

- Renal BV compromise (HTN, microangiopathy, HUS, TTP, DIC)

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4
Q

Tubular necrosis generally occurs where?

A

Proximal convoluted tubule

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5
Q

Tubular necrotic cell cast formation/blockage generally occurs where?

A

DCT and CD

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6
Q

Phases of acute tubular injury

A
  1. Initiation (36 hours, oliguria)
  2. Maintenance (oliguria, uremia, hyperkalemia)
  3. Recovery (polyuria, hypokalemia, infection)
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7
Q

How to tell if patient is in maintenance or recovery phase of acute tubular injury?

A 
Maintenance = hyperkalemia, oliguria
Recovery = hypokalemia, polyuria
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8
Q

Tubulointerstitial nephritis:

Patient presentation

A

Azotemia + polyuria + metabolic imbalances

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9
Q

Acute vs. chronic tubulointerstitial nephritis

A 
Acute = edema, neutrophils, eosinophils
Chronic = lymphocytes, fibrosis, tubular atrophy
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10
Q

Causes of tubulointerstitial nephritis

A
  • Infection (UTI, cystitis, pyelonephritis)
  • Toxins
  • Metabolic disease
  • Obstruction
  • Neoplasm
  • Immuno reaction
  • Vascular disease
  • Other
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11
Q

Infection categories causing tubulointerstitial nephritis

A
  • Acute pyelonephritis (via UTI or hematogenous spread)
  • Chronic pyelonephritis (via VUR or obstruction)
  • UTI (anywhere along the tract)
  • Cystitis (bladder)
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12
Q

Predisposing conditions for acute pyelonephritis

A
  • Vesicoureteral reflux / intrarenal reflux
  • Diabetes
  • Pregnancy
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13
Q

Vast majority of acute pyelonephritis infections arrive how?

A

Via ascension from bladder infection

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14
Q

Vast majority of pyelonephritis infections are from what group of organisms?

A

Own fecal flora (enteric bacteria)

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15
Q

Vast majority of acute pyelonephritis requires the combo of what two things to occur?

A
  1. Ascending cystitis

2. Anatomic defect

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16
Q

Pathology of acute pyelonephritis

A
  • Tubular inflammatory cell infiltration

- Yellow-gray (pus) areas and abscesses on cortical surface

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17
Q

3 complications of acute pyelonephritis

A
  • Papillary necrosis
  • Pyonephrosis (pus in pelvis, calyces, ureter)
  • Perinephric abscess
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18
Q

See acute pyelonephritis + papillary necrosis…

Think ______

A
  • Diabetic
  • Sickle cell
  • Obstruction
19
Q

See acute pyelonephritis + pyonephrosis…

Think ______

A

Obstruction (higher in urinary tract)

20
Q

See damaged renal calyces…

Think ______

A
  • Chronic pyelonephritis

- Analgesic nephropathy

21
Q

Corticomedullary scars in pyelonephritis seen on gross exam of kidneys are due to what?

A

Destruction of papillae and calyces that receives the filtration from that area

22
Q

Foamy macrophages, immune cells, giant cells

Accumulation in the tubulointerstitium

A

Xanthogranulomatous pyelonephritis

- Via PROTEUS infection

23
Q

Initially diagnosed as renal cell carcinoma, then later determined to be pyelonephritis

A

Xanthogranulomatous pyelonephritis via PROTEUS infection

24
Q

Acute drug-induced interstitial nephritis

Other name?

A

Analgesic drug –> IgE-mediated hypersensitivity –> inflammation of papillae –> tubulointerstitial infiltrates/eosinophilia + fever

Analgesic nephropathy

25
Q

Those with analgesic nephropathy may develop what?

A

Urothelial carcinoma of the renal pelvis

26
Q

Top 2 causes of acute kidney injury

A
  1. Pyelonephritis

2. Drug-induced tubulointerstitial nephritis

27
Q

Acute uric acid nephropathy (cause)

A

Leukemia/lymphoma patient + chemotherapy –> nucleic acids released from killed cells –> uric acid build-up

28
Q

Chronic uric acid nephropathy (cause)

A

Urate deposits (GOUT) –> mononuclear response –> tubular obstruction –> cortical atrophy and scarring

29
Q

Myeloma kidney

A

Bence-Jones (Ig light chain) proteinuria

30
Q

Benign nephrosclerosis

Causes?

A
  • Small vessel hyaline sclerosis –> multifocal ischemia

- Aging, HTN, Diabetes –> intimal thickening due to hemodynamic changes

31
Q

Malignant hypertension - pathophysiology

A

Renal vascular damage (hemodynamic) –> endothelial injury –> vascular cell death (–> hemorrhage) –> platelet deposition (–> thrombosis) –> fibrinoid necrosis of arterioles –> renal failure

32
Q

What starts the malignant hypertension cycle?

A

Ischemic damaged kidney –> RENIN –> HTN

33
Q

Gross pathology of malignant hypertension

A

“Flea-bitten” appearance (via tiny hemorrhages)

34
Q

Pathophysiology of renal artery stenosis

Causes?

A

Decreased perfusion of kidney –> renin –> water retention –> increased blood volume –> HTN exacerbated

Atherosclerosis (elderly/obese), fibromuscular dysplasia (young women)

35
Q

Cause of thrombotic microangiopathies

3 types?

A

Diverse insults –> excess platelet activation –> thrombi in renal capillary beds

Typical HUS, Atypical HUS, TTP

36
Q

Triggers for endothelial cell injury that starts the process of thrombotic microangiopathies

A

Bacterial toxins, cytokines, viruses, medications, anti-endothelial Ab’s

37
Q

Typical HUS

A

Diarrhea due to consuming food w/ Shiga-like toxin

  • E. coli O157:H7
  • CHILDREN
38
Q

Atypical HUS

A
  • NON-diarrheal, inherited mutations in complement regulation
  • ADULTS
  • Caused by a variety of endothelial injury (chemo, immunosuppressive drugs, PREGNANCY, etc.)
39
Q

TTP

A

Mutations in ADAMTS13, dysregulation of vWF

- ADULTS
- NEUROLOGIC INVOLVEMENT is prominent
- Caused by platelet activation/aggregation
40
Q

How to diagnose atypical HUS?

A

Genetic testing for abnormalities in complement regulators

41
Q

Clinical pentad of TTP (NEED ALL 5)

A

Fever, neurologic symptoms, microangiopathic hemolytic anemia, decreased platelets, renal failure

42
Q

Most common embolism to reach the kidney and cause necrosis

A

Mural thrombosis from L heart

43
Q

Sickle cell nephropathy

Can also progress to what?

A

Hematuria + polyuria + patchy papillary necrosis

Progressive glomerulosclerosis –> PROTEINURIA/nephrotic syndrome

44
Q

Diffuse cortical necrosis

A

Obstetric emergency, septic shock, surgery –> microthrombi –> diffuse coagulative CORTICAL necrosis (glomeruli AND tubules)

Renal 2 (11 decks)

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