Renal Disorders Flashcards

1
Q

What is Glomerulonephritis and its causes

A
  • Inflammatory process of the kidneys
  • 2nd leading cause of kidney failure

Causes

  • Hereditary
  • Other disease process (DM, HPTN, toxins)
  • Immunologic (usual process)
    1. Injury from antibodies reacting with antigens in glomeruli
    2. Injury from circulating antibody/antigen complexes lodging in glomeruli
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2
Q

How is Glomerulonephritis categorized?

A
Categorized by appearance
Proliferative
- Infiltration of WBC & proliferation of glomerular cells
Membranous
- Thickening of glomerular capillary wall
Sclerotic
- Increased extracellular matrix
Diffuse/focal/segmental
e.g. mesangial
- Involves only mesangial cells
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3
Q

What are Different Types of Glomerular Disease?

A
  1. Acute Nephritic syndrome
  2. Rapidly progressive glomerulonephritis
  3. Nephrotic syndrome
  4. Asymptomatic hematuria or proteinuria
  5. Chronic glomerulonephritis
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4
Q

Acute Nephritic Syndrome

A

Inflammatory response damaging glomerular capillary wall
Manifestations
- Hematuria
- Decreased GFR
- Azotemia (nitrogenous based waste)
- Oliguria (poor to no urine output)
- Fluid retention (d/t decreased urine output)
Fluid retention causes edema and hypertension!

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5
Q

Treatment of Nephritic syndrome

A

Symptomatic
Possible permanent kidney damage
Children often have spontaneous recovery

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6
Q

Rapidly Progressive Glomerulonephritis

A
  • Signs of severe glomerular injury without specific cause
  • Rapid (over a few months)
  • Proliferation of glomerular cells, with monocytes & macrophages destroy Bowman space

Goodpasture’s Syndrome
- rare, autoimmune

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7
Q

Nephrotic Syndrome Causes & Signs & Symptoms

A

> Integrity of glomerular membrane is affected

  • Medication
  • Neoplasms
  • Inflammation
  • Increased GFR
  • Massive proteinuria
  • Hypoalbuminemia
  • Edema (anasarca)
  • Lipidurea/hyperlipidemia
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8
Q

Asymptomatic Hematuria or Proteinuria

A
  1. IgA nephropathy (Berger disease)
    - IgA complex deposits d/t inflammation
  2. Alport syndrome (hereditary)
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9
Q

Chronic Glomerulonephritis

A
  1. Acute forms either resolve or progress

2. Small kidneys, sclerosed glomeruli, etc.

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10
Q

Acute Pyelonephritis Cause and Contributing factors

A

Cause
- Bacterial infection of upper UT with intrarenal reflux (UTI infection moves up to the kidney)

> Contributing factors

  • Outflow obstruction
  • Catheterization/urinary instrumentation
  • Vesicoureteral reflux (urine backtracking up ureter and to the kidney)
  • pregnancy (large body pushing/creating increased pressure)
  • Neurogenic bladder (disfunction nerve supply to bladder)
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11
Q

Acute Pyelonephritis Manifestations & Treatment

A

Manifestations

  • Usually rapid progressing
  • Chills, fever
  • Aches/pain unilateral or bilateral
  • Dysuria, frequency, urgency
  • Nausea, vomiting, abd. pain radiating to the back

Treatment

  • Symptomatic pain relief
  • Fluids to aid dysuria
  • Antibiotics
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12
Q

Chronic Pyelonephritis

A
  • Scarring and deformation of renal calyces and pelvis, with atrophy and thinning of cortex
  • Primarily affects proximal and distal tubules

Causes:

  • Recurrent or persistent infection
  • Intrarenal reflux
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13
Q

Toxin-Related Nephropathies: Effect dependent on…

A
  • Action of drugs/toxins
  • Number of toxins involved
  • Existence of pre-renal issues that decrease blood flow to kidney
  • Formation of crystals
  • Hypersensitivity response
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14
Q

Polycystic Kidney Disease

A
  • Inherited autosomal dominant
  • Generally older population; progresses slowly
  • Fluid-filled cysts in kidney and liver
    (Less so the spleen or pancreas)

> Deformity of epithelial cell interfere with fluid absorption/cellular maturation resulting in cyst formation

  • Inflammatory mediators accumulate, and renal tubular cells are destroyed
  • Kidneys enlarge
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15
Q

Polycystic Kidney Disease (PKD) Manifestations & Complications

A

Manifestations

  • Pain
  • Hematuria
  • Infested cysts- UTI
  • Hypertension

Complications
- Nephrolithiasis (15-20% of PKD) (kidney stones)
- Valvular deformities (d/t other infection)
- Cerebral artery aneurysm (10-30% of PKD patients)
Subarachnoid hemorrhage occurs d/t cerebral aneurysm

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16
Q

Obstructive Disorders of the Kidneys

A
  • Sudden, or develop slowly
  • One or both kidneys
  • Partial or complete
  • If acute obstruction is caught early, effects are reversible
    If not, damage/atrophy/chronic
17
Q

Obstructive Disorders – Where & Why

A
  1. Renal Pelvis
    - Calculi (lumps of calcium), necrosis
  2. Ureter
    - Calculi, pregnancy, tumors, stricture, congenital origins
  3. Bladder & ureter
    - Calculi, neurogenic bladder, cancer, BPH, & strictures
18
Q

Damage from Obstructive Disorders

A
  1. Stasis of urine
    - Causes UTI (common), stone formation
    Progressive dilation of renal collecting ducts & tubular structures
    - Causes destruction & atrophy of renal tissue
  2. Hydronephrosis
    - Urine-filled dilation of renal pelvis and calyces d/t obstruction of outflow, leading to atrophy of kidney
19
Q

Manifestations of Urinary Obstructions

A

Recurrent UTIs

Minimal to severe pain
- Dependent of level & degree of obstruction

Complete obstruction

  • Oliguria/anuria
  • Renal failure
20
Q

Renal Calculi (nephrolithiasis)

A
>  Most common cause of upper UT obstruction
> Usually develop in kidney
- May travel down without damage
- May stay in kidney or lodge elsewhere
> “Supersaturation” + crystal aggregation
- theories
> Contributing factors
- Type of stone dependent on cause
See pg. 633
21
Q

Types of Renal Calculi (Kidney stones)

A
  1. Calcium (oxalate or phosphate)
    - d/t immobilization, hyperparathyroidism, diffuse bone disease
  2. Magnesium ammonium phosphate
    - Struvite/staghorn; d/t UTIs
  3. Uric acid
    - d/t gout, high purine diet
  4. Cystine (rarer/children)
    - inherited
22
Q

Manifestations of Nephrolithiasis

A
  1. Pain
    - Ureter stone: severe flank & upper abd. quadrant, with radiation
    - Renal pelvis stone: less severe
  2. Nausea & vomiting
  3. Pallor & diaphoresis
  4. Frequency & burning
  5. Fever & chills
  6. Hematuria
23
Q

Renal Malignancy: Wilms Tumor

A

Wilms Tumor (nephroblastoma)

  • Most common malignant abdominal tumor in children (ages 3-5 years)
  • Usually encapsulated
  • Associated with other congenital anomalies

Symptoms: abdominal mass, hypertension, abdominal pain, vomiting

24
Q

Renal Malignancy: Renal Cell Carcinoma (symptoms, risk, treatment)

A

Symptoms:

  • Hematuria, flank pain, mass
  • Silent disorder in early stages

High risk factor: smoking

Treatment: surgery, chemotherapy, radiation
good survival rate

25
Q

Describe two types of immune mechanism involved in glomerular disorders

A
  1. Injury from antibodies reacting with antigens in glomeruli
  2. Injury from circulating antibody/antigen complexes lodging in glomeruli
26
Q

Use the terms proliferation, sclerosis, membranous, and mesangial to explain changes in glomerular structure that occur with glomerulonephritis

A

Proliferative
- Infiltration of WBC & proliferation of glomerular cells
Membranous
- Thickening of glomerular capillary wall
Sclerotic
- Increased extracellular matrix
Diffuse/focal/segmental

27
Q

Compare the five classifications of glomerular syndromes

A
  1. Acute Nephritic syndrome - inflammatory process that occludes the glomerular capillary lumen and damages the capillary wall.
  2. Nephrotic syndrome - massive proteinuria and lipiduria.
  3. Rapidly progressive glomerulonephritis - signs of severe glomerular injury without specific cause.
  4. Hereditary Nephritis (Alport syndrome) - defect of the glomerular basement membrane resulting in hematuria.
  5. Chronic glomerulonephritis - 1. Acute forms either resolve or progress
  6. Small kidneys, sclerosed glomeruli, etc.
28
Q

Differentiate the pathology and manifestations of the nephrotic syndrome from those of the nephritic syndrome.

A
  1. Nephritic syndrome - Inflammatory response damaging glomerular capillary wall
    Manifestations
    - Hematuria
    - Decreased GFR
    - Azotemia (nitrogenous based waste)
    - Oliguria (poor to no urine output)
    - Fluid retention (d/t decreased urine output)
    Fluid retention causes edema and hypertension!
  2. Nephrotic syndrome - Integrity of glomerular membrane is affected
    - Medication
    - Neoplasms
    - Inflammation
  • Increased GFR
  • Massive proteinuria
  • Hypoalbuminemia
  • Edema (anasarca)
  • Lipidurea/hyperlipidemia
29
Q

Explain how diseases such as systemic lupus erythematosus result in glomerular injury.

A
  1. systemic lupus erythematosus glomerulonephritis:
    - most glomerular injury is triggered by the deposition of immune complexes within the glomerular wall.
    - subendothelial immune complexes have greater exposure to inflammatory cells and mediators, therefore, produce inflammation.
    - immune complexes may also localize in the renal interstitium, walls of interstitial vessels, and basement membranes, causing intertubulointerstitial inflammation.
30
Q

Explain how diseases such as Diabetes mellitus result in glomerular injury.

A
  1. diabetes mellitus:
    - lesions of diabetic nephropathy involve the glomeruli.
    - widespread thickening of the glomerular capillary basement membrane is followed by increase in mesangial matrix, with mild proliferation of mesangial cells.
    - as the disease progresses, the mesangial cells impinge on the capillary lumen, reducing the surface area for glomerular filtration.
31
Q

Explain how diseases such as hypertension result in glomerular injury.

A
  1. hypertension:
    - High blood pressure can damage blood vessels in the kidneys, reducing their ability to work properly. When the force of blood flow is high, blood vessels stretch so blood flows more easily. Eventually, this stretching scars and weakens blood vessels throughout the body, including those in the kidneys.
  • If the kidneys’ blood vessels are damaged, they may stop removing wastes and extra fluid from the body. Extra fluid in the blood vessels may then raise blood pressure even more, creating a dangerous cycle.
32
Q

List common causes of urinary tract obstruction.

A
  • calculi
  • necrosis
  • strictures
  • tumours
  • pregnancy
  • BPH
  • neurogenic bladder
33
Q

Describe the effects of urinary tract obstruction on renal structure and function.

A
  1. Stasis of urine
    - Causes UTI (common), stone formation
    Progressive dilation of renal collecting ducts & tubular structures
    - Causes destruction & atrophy of renal tissue
  2. Hydronephrosis
    - Urine-filled dilation of renal pelvis and calyces d/t obstruction of outflow, leading to atrophy of kidney
34
Q

Cite three theories that are used to explain the formation of kidney stones

A
  1. supersaturation of urine
  2. environment that allows stone to grow
  3. nucleus that facilitates crystal aggregation
35
Q

Explain the mechanisms of pain and infection that occur with kidney stones.

A

Pain

  • Ureter stone: severe flank & upper abd. quadrant, with radiation d/t stretching of the ureter.
  • Renal pelvis stone: less severe
    2. Nausea & vomiting
    3. Pallor & diaphoresis
    4. Frequency & burning
    5. Fever & chills
    6. Hematuria