Class 4 chapter 25 Flashcards

1
Q

Glomerulonephritis

A

Inflammatory process
2nd leading cause of kidney failure
Categorized by appearance
1. Proliferative (Infiltration of WBC and proliferation of glomerular cells)
2. Membranous (Thickening of glomerular capillary wall)
3. Sclerotic (Increased extracellular matrix)
4. Diffuse/focal/segmental (Ex mesangial (involves only mesangial cells)

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

Glomerulonephritis causes

A

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

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

Types of Glomerular Disease

A
Acute Nephritic syndrome
Rapidly progressive glomerulonephritis
Nephrotic syndrome
Asymptomatic hematuria or proteinuria
Chronic glomerulonephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Acute Nephritic Syndrome

A

Inflammatory response damaging glomerular capillary wall

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

Treatment of Nephritic syndrome

A

Symptomatic
Possible permanent kidney damage
Children often have spontaneous recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Goodpastures Syndrome (rare, autoimmune)

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

Nephrotic syndrome

A
Integrity of glomerular membrane is affected
1. Medication
2. Neoplasms
3. Inflammation 
Increased GFR
Massive proteinuria
Hypoalbuminemia
Edema (anasarca - massive edema)
Lipidurea/hyperlipidemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Asymptomatic Hematuria or Proteinuria

A
IgA nephropathy (Berger disease)
IgA complex deposits d/t inflammation
Alport syndrome (hereditary)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Chronic Glomerulonephritis

A

Acute forms either resolve or progress

Small kidneys, sclerosed glomeruli etc

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

Acute Pyelonephritis cause

A

Bacterial infection of upper UT with intrarenal reflux

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

Acute Pyelonephritis contributing factors

A
Outflow obstruction (enlarged prostate)
Catheterization/urinary instrumentation
Vesicoureteral reflux (urine going in opposite direction as it should)
Pregnancy
Neurogenic bladder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Acute Pyelonephritis manifestations

A

Usually rapid progression
Chills, fever
Aches/pain unilateral or bilateral (costovertebral angle)
Dysuria, frequency, urgency
Nausea, abdominal pain radiating to the back

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

Acute Pyelonephritis treatment

A

Symptomatic pain relief
Fluids to aid dysuria
Antibiotics

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

Acute Nephritic Syndrome manifestations

A
Hematuria
Decreased GFR
Azotemia (nitrogenous waste in the blood)
Oliguria
Fluid retention (edema and htn)
SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chronic Pyelonephritis

A

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

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

Chronic Pyelonephritis causes

A

Recurrent or persistent infection

Intrarenal reflux

17
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
18
Q

Polycystic Kidney Disease

A

Inherited autosomal dominant
Generally older population; progresses slowly
Fluid-filled cysts in kidney and liver (less so spleen, 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)

19
Q

Polycystic Kidney Disease manifestations

A

Pain
Hematuria
Infected cysts – UTI
Htn

20
Q

Polycystic Kidney Disease complications

A

Nephrolithiasis (15-20% of PKD)
Valvular deformities
Cerebral artery aneurysm (10-30% of PKD pts) - subarachnoid hemorrhage

21
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

22
Q

Obstructive Disorders Where and Why?

A
  1. Renal pelvis
    Calculi, necrosis
  2. Ureter
    Calculi, pregnancy, tumours, stricture, congenital origins
  3. Bladder and ureter
    Calculi, neurogenic bladder, cancer, BPH and strictures
23
Q

Damage from Obstructive Disorders

A
  1. Stasis of urine
    Causes UTI (common), stone formation
  2. Progressive dilation of renal collecting ducts & tubular structures
    Causes destruction and atrophy of renal tissue
  3. Hydronephrosis
    Urine-filled dilation of renal pelvis and calyces d/t obstruction of outflow, leading to atrophy of kidney
24
Q

Manifestations of Urinary Obstructions

A
  1. Recurrent UTIs
  2. Minimal to severe pain
    Dependent on level and degree of obstruction
  3. Complete obstruction
    Oliguria/anuria
    Renal failure
25
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
Contributing factors (Type of stone dependant on cause, see chart pg 633)
26
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
27
Q

Manifestations of Nephrolithiasis

A
1. Pain
Ureter stone - severe flank and upper abdominal quadrant with radiation
Renal pelvis stone - less severe
2. NV
3. Pallor and diaphoresis
4. Frequency and burning
5. Fever and chills (with infection)
6. Hematuria
28
Q

Treatment of kidney stones

A
Analgesics, Anti-spasmotics
Allopurinol (changes pH to decrease acidity)
Increased fluids to produce 2 liter/day
Strain urine 
Diet modification
Extracorporeal shockwave lithotripsy (ESWL)
Ureteroscopic removal
Percutaneous nephrolithotomy
29
Q

Renal Malignancy

A
  1. Wilms Tumor (nephroblastoma)
    Most common malignant abdominal tumor in children (usually 3 to 5 years)
    Usually encapsulated
    Associated with other congenital anomalies
    Symptoms - abdominal mass, htn, abdominal pain, vomiting
  2. Renal cell carcinoma
    Symptoms - Hematuria, flank pain, mass, silent disorder in early stages
    High risk factor - smoking
    Treatment - surgery, chemotherapy, radiation (good survival rate)