CHAPTER 8: RENAL DISEASE Flashcards

(108 cards)

1
Q

Deposition of immune complexes, in conjunction with streptococcal Infection, on the glomerular membrane

A

Acute or Post-streptococcal
Glomerulonephritis

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2
Q

Deposition of immune complexes from systemic immune disorders on the glomerular membrane

A

Rapidly Progressive Glomerulonephritis

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3
Q

Attachment of a cytotoxic antibody formed during viral respiratory infections to glomerular and alveolar
basement membranes

A

Goodpasture’s Syndrome

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4
Q

Binding of antineutrophilic cytoplasmic antibody to neutrophils in vessel walls

A

Wegener’s Granulomatosis

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5
Q

Disruption of vascular integrity
following viral respiratory infections

A

Henoch-Schonlein Purpura

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6
Q

Deposition of IgA on the glomerular membrane resulting from increased levels of serum IgA

A

IgA Nephropathy

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7
Q

Thickening of the glomerular membrane following IgG immune complex deposition associated with systemic disorders

A

Membranous Glomerulonephritis (MGN)

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8
Q

Type of MPGN that displays increased cellularity in the subendothelial cells of the mesangium (interstitial area of Bowman capsule), causing thickening of the capillary walls

A

Type 1 Membranoproliferative glomerulonephritis (MPGN)

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9
Q

Type of MPGN that displays extremely dense deposits in the glomerular basement membrane, tubules, and Bowman capsule

A

Type 2 Membranoproliferative glomerulonephritis (MPGN)

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10
Q

Type of MPGN that is characterized by both subepithelial and subendothelial deposits

A

Type 3 Membranoproliferative glomerulonephritis (MPGN)

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11
Q

Refers to a sterile, inflammatory process that affects the glomerulus and is associated with the finding of blood, protein, and casts in the urine

A

Glomerulonephritis

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12
Q

Marked by the sudden onset of symptoms consistent with damage to the glomerular membrane

A

Acute glomerulonephritis (AGN)

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13
Q

Symptoms usually occur in children and young adults after respiratory infections caused by certain strains of group A β-hemolytic streptococci that contain M protein in the cell wall

A

Acute glomerulonephritis (AGN)

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14
Q

Primary urinalysis findings include marked hematuria, proteinuria, and oliguria, accompanied by red blood cell (RBC) casts, dysmorphic RBCs, hyaline and granular casts, and white blood cells (WBCs)

A

Acute glomerulonephritis (AGN)

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15
Q

These are a hallmark characteristic of acute glomerulonephritis

A

RBC casts

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16
Q

Formerly called Wegener granulomatosis

A

Granulomatosis with polyangiitis (GPA)

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16
Q

This autoantibody can be detected in a patient’s serum

A

Antiglomerular basement membrane antibody

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17
Q

Initial laboratory results are similar to AGN but become
more abnormal as the disease progresses, including protein levels that are markedly elevated and glomerular filtration rates
that are very low

A

Rapidly Progressive (or crescentic) Glomerulonephritis (RPGN)

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18
Q

Key to the diagnosis of GPA is the
demonstration of?

A

Antineutrophilic cytoplasmic antibody (ANCA) in the patient’s serum

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19
Q

If the neutrophils are fixed in ethanol, the antibodies form a perinuclear pattern which is called?

A

p-ANCA

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19
Q

This includes incubating the patient’s serum with either ethanol or formalin/formaldehyde-fixed neutrophils and examining the preparation using indirect immunofixation to detect the serum antibodies attached to the neutrophils

A

ANCA for GPA

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20
Q

This disease occurs primarily in children after upper respiratory infections.

A

Henoch-Schönlein Purpura

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20
Q

When the neutrophils are fixed with formalin/formaldehyde, the pattern is granular
throughout the cytoplasm
and is referred to as

A

c-ANCA

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21
Q

Cellular proliferation affecting the capillary walls or the glomerular basement membrane

A

Membranoproliferative Glomerulonephritis

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22
A **marked decrease in renal function** resulting from ***glomerular damage*** precipitated by other renal disorders
Chronic Glomerulonephritis
23
Disruption of the **electrical charges** that produce the tightly fitting podocyte barrier resulting in a massive loss of protein and lipids
Nephrotic Syndrome
24
Disruption of podocytes in certain areas of glomeruli associated with heroin and analgesic abuse and with HIV and hepatitis viruses
Focal Segmental Glomerulosclerosis
25
Disruption of the podocytes that occurs primarily in children after allergic reactions and immunizations; dysfunction of T-cell immunity
Minimal Change Disease (MCD)
26
Ascending bacterial infection of the bladder
Cystitis
27
Complete recovery with normal renal function is seen in more than 50% of patients. In other patients, progression to a more serious form of glomerulonephritis and renal failure may occur
Henoch-Schönlein Purpura
28
Its predominant characteristic is a pronounced thickening of the glomerular basement membrane resulting from the deposition of immunoglobulin G immune complexes
Membranous Glomerulonephritis
29
Their presence is often seen in chronic glomerulonephritis that progresses to ESRD
Broad casts
30
Also known as Berger disease
IgA nephropathy
31
The most common cause of glomerulonephritis.
IgA nephropathy
32
Marked by massive proteinuria (greater than 3.5 g/day), low levels of serum albumin, high levels of serum lipids, and pronounced edema
Nephrotic syndrome
33
Genetic disorder showing lamellated and thinning glomerular basement membrane
Alport syndrome
33
Acute onset after systemic shock Gradual progression from other glomerular disorders and then to renal failure
Nephrotic syndrome (NS)
33
Frequent complete remission after **corticosteroid treatment**
Minimal change disease (MCD)
33
It may resemble nephrotic syndrome (NS) or minimal change disease (MCD)
Focal segmental glomerulosclerosis (FSGS)
33
**Slow progression** to nephrotic syndrome (NS) and end-stage renal disease
Alport syndrome
33
Hemoptysis and dyspnea followed by hematuria
Goodpasture syndrome
33
Their presence in the urine sediment is characteristic for ATN
RTE cell casts and RTE cells
33
Demonstration of positive results of these tests provides evidence that the disease is of streptococcal origin (2pts)
Anti–group A streptococcal enzyme tests (antistreptolysin O [ASO] and Antideoxyribonuclease-B antibody [anti-DNase B]) *These are under the Acute Poststreptococcal Glomerulonephritis*
33
This may be elevated during the acute stages of AGN, but, like the urinalysis, returns to normal
Blood Urea Nitrogen (BUN)
33
Since the development of this, which can be performed in a physician’s office, urgent care facility, or emergency department, the incidence of acute poststreptococcal glomerulonephritis has declined.
rapid anti–group A streptococcal enzyme tests
33
Secondary complications of AGN
Hypertension and Electrolyte imbalance
33
Morphological changes to the glomeruli resembling those in rapidly progressive glomerular nephritis are seen in conjunction with?
the autoimmune disorder termed **Goodpasture syndrome**
34
Initial pulmonary complaints are **hemoptysis and dyspnea**, followed by the development of hematuria
Goodpasture syndrome
34
Urinalysis results include proteinuria, hematuria, and the presence of RBC casts. Progression to chronic glomerulonephritis and end-stage renal failure is common
Goodpasture syndrome
34
Initial symptoms include the appearance of **raised, red patches on the skin**
Henoch-Schönlein purpura
34
Causes a granuloma-producing inflammation of the small blood vessels, primarily of the kidney and respiratory system
Granulomatosis with polyangiitis (GPA)
34
**Renal involvement** is the most serious complication of this disorder and may range from mild to heavy proteinuria and hematuria with RBC casts
Henoch-Schönlein Purpura
34
Respiratory and gastrointestinal symptoms, including blood in the sputum and stools, may be present
Henoch-Schönlein Purpura
35
Disorders associated with the development of this disease include SLE, Sjögren syndrome, secondary syphilis, hepatitis B, gold and mercury treatments, and malignancy.
Membranous Glomerulonephritis (MGN)
36
In MGN, about 75% of cases, the etiology is?
Unknown
37
This disease has a tendency toward thrombosis.
Membranous Glomerulonephritis (MGN)
38
Laboratory findings include microscopic hematuria and elevated urine protein excretion that may reach concentrations similar to those in nephrotic syndrome. **RBC casts are rare**, but microscopic hematuria is common
Membranous Glomerulonephritis (MGN)
39
In MPGN, Type 1 patients progress to? While Type 2 patients experience symptoms of?
Type 1: Nephrotic syndrome Type 2: Chronic glomerulonephritis
40
Progression of glomerulonephritis from one form to another:
Rapidly progressive glomerulonephritis > chronic glomerulonephritis > nephrotic syndrome > renal failure
41
There is a high incidence of recurrence of this disease after renal transplant
Membranoproliferative glomerulonephritis (MPGN)
41
Its laboratory findings vary, but hematuria, proteinuria, and decreased serum complement levels are usual findings. There appears to be an association with autoimmune disorders, infections, and malignancies.
Membranoproliferative glomerulonephritis (MPGN)
42
Except for periodic episodes of macroscopic hematuria, a patient with this disorder may remain essentially asymptomatic for 20 years or more; however, there is a gradual progression to chronic glomerulonephritis and ESRD
IgA nephropathy
43
A glomerular filtration rate that is markedly decreased is present in conjunction with increased BUN and creatinine levels and electrolyte imbalance
Chronic Glomerulonephritis (CGN)
43
Primary urinary results in the early stages of IgA nephropathy
Macroscopic or microscopic hematuria
44
Primary urinary results in the late stages of IgA nephropathy
Chronic glomerulonephritis (CGN)
44
Damage to renal tubular cells caused by ischemia or toxic age
Acute tubular necrosis (ATN)
45
**Acute onset of renal dysfunction** usually resolved when underlying cause is corrected
Acute tubular necrosis (ATN)
46
Inherited in association with cystinosis and Hartnup disease or acquired through exposure to toxic agents
Fanconi syndrome
47
Generalized defect in **renal tubular reabsorption** requiring supportive therapy
Fanconi syndrome
48
Inherited defect in the production of normal uromodulin by the renal tubules and increased uric acid causing gout
Uromodulin-associated kidney disease
49
Continual monitoring of renal function for progression to renal failure and possible kidney transplantation
Uromodulin-associated kidney disease
50
Inherited defect of tubular response to ADH or acquired from medications
Nephrogenic diabetes insipidus (DI)
50
Requires supportive therapy to prevent dehydration
Nephrogenic diabetes insipidus (DI)
51
Benign disorder
Renal glucosuria
51
Inherited **autosomal recessive trait**
Renal glucosuria
52
Acute onset of urinary frequency and burning; resolved with antibiotics
Cystitis
53
Infection of the renal tubules and interstitium related to interference of urine flow to the bladder, reflux of urine from the bladder, and **untreated cystitis**
Acute pyelonephritis
54
**Recurrent infection** of the renal tubules and interstitium caused by structural abnormalities affecting the flow of urine
Chronic pyelonephritis
55
Acute onset of urinary frequency, burning, and **lower back pain**; resolved with antibiotics
Acute pyelonephritis
56
Frequently diagnosed in children; requires correction of the underlying structural defect Possible progression to renal failure
Chronic pyelonephritis
57
Allergic inflammation of the renal interstitium in response to certain medications
Acute interstitial nephritis (AIN)
58
**Acute onset of renal dysfunction** often accompanied by a ***skin rash*** Resolves after discontinuation of medication and treatment with corticosteroids
Acute interstitial nephritis (AIN)
59
Renal calculi (kidney stones) may form in the:
- calyces and pelvis of the kidney - ureters - bladder
60
In this condition, the calculi vary in size from barely visible to large, staghorn calculi resembling the shape of the renal pelvis and smooth, round bladder stones with diameters of 2 or more inches.
Renal Lithiasis
61
Conditions favoring the formation of renal calculi are similar to those favoring the formation of urinary crystals, including:
- pH - chemical concentration - urinary casts
62
Broad casts are often referred to as?
Renal failure casts
63
A procedure using high-energy shock waves, can be used to break stones located in the upper urinary tract into pieces that then can be passed in the urine.
Lithotripsy
64
This has little importance in predicting calculi formation
crystals
64
This has been noted during the summer months in people known to form renal calculi
Increased crystalluria
65
Approximately 75% of the renal calculi are composed of?
calcium oxalate or calcium phosphate
66
These are the other primary calculi constituent
- Ammonium magnesium phosphate (struvite/ triple phosphate) - Uric acid - cystine
67
Frequently this is associated with **metabolic calcium and phosphate disorders** and, occasionally, diet
calcium calculi
68
May be associated with an increased intake of foods with high purine content and uromodulin-associated kidney disease.
Uric acid
69
Identify if pre, renal, or postrenal causes of ARF: - Acute glomerulonephritis (AGN) - Acute tubular necrosis (ATN) - Acute pyelonephritis - Acute interstitial nephritis (AIN)
Renal
70
Identify if pre, renal, or postrenal causes of ARF: - Renal calculi - Tumors
Postrenal
71
Identify if pre, renal, or postrenal causes of ARF: - Decreased blood pressure/cardiac output - Hemorrhage - Burns - Surgery - Septicemia
Prerenal
72
It exists in both acute and chronic forms.
Renal failure
72
In contrast to chronic renal failure, this exhibits a sudden loss of renal function and frequently is reversible
Acute Renal Failure (ARF)
73
Renal calculi is also known as?
Kidney stones
74
Its urinalysis findings include glycosuria with normal blood glucose and possible mild proteinuria. Urinary pH can be very low due to the failure to reabsorb bicarbonate
Fanconi syndrome
75
The disorder associated with **tubular dysfunction** most frequently is?
Fanconi syndrome
76
The syndrome can be inherited as a sex-linked or autosomal genetic disorder. Males inheriting the X-linked gene are affected more severely than females inheriting the autosomal gene.
Alport Syndrome
77
Can be inherited as a sex-linked recessive gene or acquired from medications, including lithium and amphotericin B. It also may be seen as a complication of polycystic kidney disease and sickle cell anemia.
Nephrogenic DI
78
This affects only the reabsorption of glucose
Renal Glycosuria
79
This is significant for differentiating between cystitis and pyelonephritis.
WBC casts
80
Their presence in the urine sediment is characteristic for AIN
Eosinophil casts and eosinophils
81
General characteristics of ARF:
decreased glomerular filtration rate, oliguria, edema, and azotemia.
82
Provides a more comprehensive analysis of Renal Lithiasis
X-ray crystallography