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CPR Exam 3 > Tubular and Interstitial Diseases > Flashcards

Tubular and Interstitial Diseases Flashcards

1
Q

What two major processes lead to clinical manifestations in acute kidney injury?

A
  • Ischemic or toxic tubular injury

- Inflammation of the tubules and interstitium

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2
Q

What is ischemic ATI due to?

A
  • Due to decreased or interrupted blood flow
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3
Q

What is nephrotoxic ATI due to?

A
  • May be caused by endogenous agents
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4
Q

What are present and considered pathognomonic of ATI? What is the association?

A
  • Abundance of the “extreme” coarsely granular casts

- Associated with a greater likelihood of dialysis requiring acute kidney injury

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5
Q

What is responsible for the color of the casts seen in ATI?

A
  • Mitochondrial pigments or lipofuscin
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6
Q

When is the initiation phase of AKI?

A
  • Lasts 36 hours
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7
Q

What is seen in the initiation phase of AKI?

A
  • Dominated by the inciting medical, surgical, or obstetric event
  • Only renal involvement sign is a slight decline in urine output with a rise in BUN
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8
Q

What is the maintenance phase characterized by?

A
  • Sustained decreases in urine output to between 40 and 400 mL/day
  • Salt and water overload
  • Rising BUN concentrations
  • Hyperkalemia
  • Metabolic acidosis
  • Other manifestations of uremia
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9
Q

What is seen in the recovery phase of AKI?

A
  • Steady increase in urine volume that may reach up to 3L /day
  • Tubules are still damaged, so large amounts of water, sodium, and potassium are lost in the flood of urine
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10
Q

What is a big clinical problem in the recovery phase of AKI?

A
  • Hypokalemia due to potassium loss
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11
Q

How are tubulointerstitial disorders distinguished from glomerular diseases?

A
  • Absence of nephritic or nephrotic syndrome
  • Presence of defects in tubular function such as impaired ability to concentrate urine, evidenced clinically by:
    1. Polyuria or nocturia
    2. Salt wasting
    3. Diminished ability to excrete acids
    4. Isolated defects in tubular reabsorption or secretion
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12
Q

What is acute pyelonephritis?

A
  • Generally caused by bacterial infection and is associated with UTI
  • Suppurative inflammatory process involving the kidney that is the result of bacterial and sometimes viral infection
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13
Q

What is chronic pyelonephritis?

A
  • More complex disorder

- Bacterial infection plays a dominant role, but other factors predispose to repeat episodes of acute pyelonephritis

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14
Q

What are some associations with acute pyelonephritis?

A
  • Urinary tract obstruction
  • Instrumentation
  • VUR
  • Pregnancy
  • Gender and age
  • Pre Existing renal lesions
  • Diabetes
  • Immunosuppression and immunodeficiency
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15
Q

How does acute pyelonephritis present?

A
  • CVA tenderness
  • Systemic features (fever, elevated WBC)
  • Dysuria, frequency, urgency
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16
Q

How can uncomplicated E. coli cystitis be treated?

A
  • With a single dose of antibiotics or a 3 day course of TMP/SMZ or nitrofurantion
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17
Q

What is a viral pathogen that causes pyelonephritis in kidney allografts?

A
  • Polyomavirus
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18
Q

What is polyomavirus infection characterized by?

A
  • Nuclear enlargement and intranuclear inclusions visible by light microscopy in tubular epithelial cells
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19
Q

What are some complications of pyelonephritis?

A
  • Papillary necrosis
  • Pyonephrosis
  • Perinephric abscess
20
Q

Who is most likely affected with papillary necrosis?

A
  • Diabetics
  • Sickle cell disease
  • In those with urinary tract obstruction
21
Q

What is papillary necrosis?

A
  • One or all of the pyramids of the affected kidney may be involved
  • On cut section, tips or distal two thirds of the pyramids have areas of gray-white to yellow necrosis
22
Q

What is seen on microscopic examination in papillary necrosis?

A
  • The necrotic tissue shows characteristic ischemic coagulative necrosis, with preservation of outlines of tubules
23
Q

What is pyonpehrosis?

A
  • Is seen when there is total or almost complete obstruction, particularly when it is high in the urinary tract
  • Suppurative exudate is unable to drain and fills the renal pelvis, calyces, and ureter with pus
24
Q

What is a perinephric abscess?

A
  • An extension of suppurative inflammation through the renal capsule into the perinephric tissue
25
Q

What is a staghorn calculus?

A
  • Dilated calyces
  • Cystic cavities
  • Yellow tissue
26
Q

What is seen on histology in a staghorn calculus?

A
  • Fibrosis and chronic granulomatous inflammatory infiltrate with lipid laden foamy macrophages and necrotic debris
27
Q

What types of agars are used for pus and urine samples?

A
  • Blood agar

- MacConkey agar

28
Q

What can grow on blood agar?

A
  • Proteus grows in successive waves to form a thin filmy layer of concentric circles
29
Q

What is the treatment for an uncomplicated UTI due to P. mirabilis?

A
  • 3 day course of TMP/SMZ or an oral fluoroquinolone
30
Q

What is the treatment for a complicated UTI due to P. mirabilis?

A
  • Outpatient setting with oral antibiotics for 10 to 21 days as long as they receive adequate follow up
31
Q

What is the second most common cause of AKI?

A
  • Drug- and toxin-induced tubulointerstitial nephritis
32
Q

What are some causes of drug- and toxin-induced tubulointerstitial nephritis?

A
  • Sulfonamides
  • Synthetic penicillins
  • Other synthetic antibiotics
  • Diuretics
  • NSAIDs
33
Q

How can toxins and drugs injure kidneys?

A
  1. Trigger an interstitial immunologic reaction, exemplified by the acute hypersensitivity nephritis induced by drugs
  2. Cause ATI
  3. Cause subclinical but cumulative injury to tubules that takes years to result in chronic kidney disease
34
Q

What is drug induced acute interstitial nephritis characterized by?

A
  • Fever
  • Eosinophilia
  • Rash
  • Renal abnormalities (hematuria, mild proteinuria, and leukocyturia)
  • Rising serum creatinine or AKI with oliguria
35
Q

What are the three types of nephropathy with hyperuricemia?

A
  • Acute uric acid nephropathy
  • Chronic urate nephropathy
  • Nephrolithiasis
36
Q

What does tumor lysis syndrome result from?

A
  • Release of intracellular electrolytes and nucleic acids from malignant cells that were lysed by anticancer therapies
37
Q

What is tumor lysis syndrome characterized by?

A
  • Increases in serum levels of uric acid, potassium, and phosphorus
  • Accompanied by hypocalcemia
38
Q

What can disorders associated with hypercalcemia lead to?

A
  • Kidney stones
  • Chronic tubulointerstitial disease
  • Renal insufficiency
39
Q

What distinctive genetic mutations are seen in autosomal dominant tubulointerstitial kidney disease (ADTKD)?

A
  • MUC1 encodes mucin-1
  • UMOD encodes uromodulin
  • REN encodes preprorenin
  • HNF1B encodes hepatocyte nuclear factor 1B
40
Q

What are some contributing factors to kidney damage in multiple myeloma?

A
  1. Bence Jones proteinuria and nephropathy
  2. Amyloidosis of AL type
  3. Light chain deposition disease
  4. Hypercalcemia and hyperuricemia
41
Q

What does uromodulin do?

A
  • Tamm-Horsfall protein

- Guardian of urinary and systemic homeostasis

42
Q

What do mutations in THP (uromodulin) cause?

A
  • Increased risks of UTI, kidney stone, hypertension, hyperuricemia, and acute and chronic kidney diseases
43
Q

What is hepatorenal syndrome?

A
  • Form of renal failure occurring in individuals with liver failure in whom there is no intrinsic morphologic or functional cause for kidney dysfunction
44
Q

What marks the onset of hepatorenal syndrome?

A
  • Drop in urine output and increasing levels of urea and creatinine in the blood
45
Q

What is seen in patients with hepatorenal syndrome?

A
  • Portal hypertension due to cirrhosis
  • Severe alcoholic hepatitis
  • Metastatic tumors

CPR Exam 3 (16 decks)

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