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MS3 > Chapter 50: Glomerulonephritis > Flashcards

Chapter 50: Glomerulonephritis Flashcards

1
Q

Which of the following is the primary site of inflammation in glomerulonephritis?

A. Renal pelvis
B. Glomerulus
C. Renal tubules
D. Renal cortex

A

B. Glomerulus

Rationale: In glomerulonephritis, the primary site of inflammation is the glomerulus, although other parts of the kidney, such as the tubules and interstitial tissue, may also be affected.

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2
Q

Which of the following is a major risk factor for the development of glomerulonephritis?

A. Recent upper respiratory tract infection
B. Hyperkalemia
C. Elevated cholesterol levels
D. Renal artery stenosis

A

A. Recent upper respiratory tract infection

Rationale: A recent upper respiratory tract infection, such as a sore throat, is a significant risk factor for developing acute glomerulonephritis, such as acute poststreptococcal glomerulonephritis (APSGN).

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3
Q

What is the most likely outcome if chronic glomerulonephritis is left untreated?

A. Reversible renal function with no long-term damage
B. Rapid resolution of symptoms
C. Progression to irreversible renal failure
D. Development of acute kidney injury

A

C. Progression to irreversible renal failure

Rationale: Chronic glomerulonephritis typically progresses slowly and can lead to irreversible renal failure if left untreated or inadequately managed.

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4
Q

Which of the following conditions is associated with glomerulonephritis?

A. Urinary tract infections
B. Systemic diseases
C. Renal colic
D. Hypercalcemia

A

B. Systemic diseases

Rationale: Glomerulonephritis is associated with various systemic diseases, including autoimmune disorders and infections, which can contribute to kidney inflammation and damage.

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5
Q

A patient with acute glomerulonephritis reports a recent sore throat. Which diagnostic study is most helpful in confirming the diagnosis of acute poststreptococcal glomerulonephritis (APSGN)?

A. Urinalysis with protein and red blood cells
B. Kidney biopsy
C. Urine culture for bacterial pathogens
D. Throat culture for streptococcus

A

D. Throat culture for streptococcus

Rationale: A throat culture for streptococcus is helpful in confirming a diagnosis of acute poststreptococcal glomerulonephritis (APSGN), which is often triggered by a recent streptococcal infection, such as a sore throat.

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6
Q

Which of the following is the primary cause of end-stage renal disease (ESRD) in the United States?

A. Focal segmental glomerulosclerosis
B. Diabetic nephropathy
C. Hypertension
D. Poststreptococcal glomerulonephritis

A

B. Diabetic nephropathy

Rationale: Diabetic nephropathy is the primary cause of end-stage renal disease (ESRD) in the United States due to the microvascular changes that occur in the kidneys as a result of chronic diabetes.

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7
Q

What is the most common cause of focal segmental glomerulosclerosis (FSGS)?

A. Immune-mediated injury
B. Infection-related inflammation
C. Hypertension
D. Unknown cause

A

D. Unknown cause

Rationale: Focal segmental glomerulosclerosis (FSGS) is characterized by scattered scarring of the glomeruli, and the cause can be either a result of another disease or occur for unknown reasons.

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8
Q

Which of the following conditions is most commonly associated with the development of nephrosclerosis?

A. Hypertension
B. Diabetic nephropathy
C. Poststreptococcal glomerulonephritis
D. Granulomatosis with polyangiitis

A

A. Hypertension

Rationale: Nephrosclerosis, which involves scarring of the kidney tissue, is a complication of hypertension and can contribute to glomerulonephritis (GN).

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9
Q

Which autoimmune disorder is associated with glomerulonephritis and often has a poor prognosis?

A. Systemic lupus erythematosus (SLE)
B. Scleroderma
C. Granulomatosis with polyangiitis
D. IgA nephropathy

A

A. Systemic lupus erythematosus (SLE)

Rationale: Systemic lupus erythematosus (SLE) is an autoimmune disorder that frequently involves the kidneys, causing glomerulonephritis (GN), and it often has a poor prognosis.

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10
Q

Which condition is most commonly associated with the development of glomerulonephritis after a streptococcal throat infection?

A. Amyloidosis
B. Poststreptococcal glomerulonephritis
C. IgA nephropathy
D. Infective endocarditis

A

B. Poststreptococcal glomerulonephritis

Rationale: Poststreptococcal glomerulonephritis (PSGN) can develop 1-3 weeks after a streptococcal throat infection due to immune complexes depositing in the glomeruli, leading to inflammation.

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11
Q

Which viral infections are most likely to trigger glomerulonephritis (GN)?

A. HIV, hepatitis B, hepatitis C
B. Herpes simplex virus, Epstein-Barr virus
C. Cytomegalovirus, varicella zoster virus
D. Influenza virus, rhinovirus

A

A. HIV, hepatitis B, hepatitis C

Rationale: Viral infections such as HIV, hepatitis B, and hepatitis C can trigger glomerulonephritis (GN) by affecting the kidneys directly.

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12
Q

Which of the following diseases is characterized by glomerulonephritis as a result of small and medium blood vessel inflammation?

A. Polyarteritis nodosa
B. Amyloidosis
C. Granulomatosis with polyangiitis
D. Scleroderma

A

A. Polyarteritis nodosa

Rationale: Polyarteritis nodosa is a rare autoimmune disease that affects small and medium blood vessels, potentially leading to glomerulonephritis as a result of renal involvement.

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13
Q

In amyloidosis, what is often the first clinical manifestation of kidney involvement?

A. Hematuria
B. Proteinuria
C. Decreased urine output
D. Hypertension

A

B. Proteinuria

Rationale: Proteinuria is often the first clinical manifestation of kidney involvement in amyloidosis, where abnormal amyloid deposits infiltrate kidney tissues.

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14
Q

Which of the following is a risk factor for glomerulonephritis associated with illegal drug use?

A. Direct kidney toxicity from substances
B. Chronic hypertension
C. Autoimmune response triggered by drugs
D. Increased infection risk due to drug use

A

A. Direct kidney toxicity from substances

Rationale: Illegal drug use can increase the risk of glomerulonephritis due to direct kidney toxicity caused by certain drugs, including heroin and other substances.

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15
Q

Which of the following conditions is characterized by vascular lesions and fibrosis in the kidneys due to systemic inflammation of connective tissue?

A. Scleroderma
B. Lupus nephritis
C. Granulomatosis with polyangiitis
D. Hypertensive nephrosclerosis

A

A. Scleroderma

Rationale: Scleroderma involves systemic inflammation that can lead to vascular lesions and fibrosis in the kidneys, contributing to glomerulonephritis.

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16
Q

Which condition is caused by the infiltration of tissues with amyloid, potentially leading to kidney involvement and glomerulonephritis?

A. Scleroderma
B. Granulomatosis with polyangiitis
C. Amyloidosis
D. Systemic lupus erythematosus

A

C. Amyloidosis

Rationale: Amyloidosis is a condition where amyloid deposits infiltrate tissues, including the kidneys, potentially leading to glomerulonephritis and other renal complications.

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17
Q

Which of the following systemic diseases can contribute to glomerulonephritis through immune complex deposition in the kidneys?

A. Systemic lupus erythematosus
B. Diabetic nephropathy
C. Hypertension
D. Amyloidosis

A

A. Systemic lupus erythematosus

Rationale: Systemic lupus erythematosus (SLE) can lead to glomerulonephritis through the deposition of immune complexes in the kidneys, causing inflammation and damage.

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18
Q

What is the common pathophysiological mechanism for glomerulonephritis caused by poststreptococcal infections?

A. Direct bacterial invasion of the glomeruli
B. Immune complex deposition from antibody-antigen interactions
C. Inflammation of renal tubules
D. Vascular constriction and ischemia

A

B. Immune complex deposition from antibody-antigen interactions

Rationale: Poststreptococcal glomerulonephritis is caused by immune complex deposition from antibody-antigen interactions, leading to inflammation and injury of the glomeruli.

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19
Q

Which of the following describes the nature of IgA nephropathy?

A. Infection-induced inflammation
B. Autoimmune-mediated damage with IgA deposits
C. Genetic mutation leading to glomerular damage
D. Endothelial cell injury from hypertension

A

B. Autoimmune-mediated damage with IgA deposits

Rationale: IgA nephropathy is an autoimmune-mediated condition characterized by the deposition of immunoglobulin A (IgA) in the glomeruli, which causes recurrent episodes of hematuria.

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20
Q

Which of the following is a common complication of diabetic nephropathy that can contribute to glomerulonephritis?

A. Glomerular basement membrane thickening
B. Hyperkalemia
C. Urinary tract infections
D. Hypertensive crisis

A

A. Glomerular basement membrane thickening

Rationale: Diabetic nephropathy is associated with glomerulosclerosis and thickening of the glomerular basement membrane, which can lead to glomerulonephritis and eventually kidney failure.

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21
Q

Which of the following findings would most likely indicate the severity of renal impairment in a patient with acute poststreptococcal glomerulonephritis?

A. Elevated serum creatinine and blood urea nitrogen (BUN) levels
B. Normal urine output with clear urine
C. Low white blood cell count with negative urine culture
D. Decreased blood pressure and elevated albumin

A

A. Elevated serum creatinine and blood urea nitrogen (BUN) levels

Rationale: Elevated serum creatinine and BUN levels are indicative of renal impairment and the extent of damage to the kidneys in APSGN.

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22
Q

Which of the following is a potential complication of acute poststreptococcal glomerulonephritis (APSGN)?

A. Chronic renal failure
B. Nephrotic syndrome
C. Hypertensive crisis
D. Rapidly progressive glomerulonephritis

A

C. Hypertensive crisis

Rationale: Hypertension is a common complication of APSGN, primarily due to increased extracellular fluid volume caused by fluid retention.

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23
Q

Which of the following is the most common type of acute glomerulonephritis worldwide?

A. Chronic glomerulonephritis
B. Acute poststreptococcal glomerulonephritis
C. Focal segmental glomerulosclerosis
D. Diabetic nephropathy

A

B. Acute poststreptococcal glomerulonephritis

Rationale: Acute poststreptococcal glomerulonephritis (APSGN) is the most common type of acute glomerulonephritis worldwide, particularly in children aged 5 to 7 years and adults older than 60.

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24
Q

What is the primary cause of acute poststreptococcal glomerulonephritis (APSGN)?

A. Inflammation from systemic lupus erythematosus
B. Direct kidney infection from Escherichia coli
C. Chronic hypertension leading to glomerular injury
D. Immune response to group A β-hemolytic streptococcus

A

D. Immune response to group A β-hemolytic streptococcus

Rationale: APSGN occurs after infection with nephrotoxic strains of group A β-hemolytic streptococci, triggering an immune response and deposition of antigen-antibody complexes in the glomeruli.

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25
Q

Which of the following is a common manifestation of acute poststreptococcal glomerulonephritis (APSGN)?

A. Hypotension and weight loss
B. Generalized edema and hematuria
C. Polyuria and low serum creatinine
D. Hyperkalemia and jaundice

A

B. Generalized edema and hematuria

Rationale: Common manifestations of APSGN include generalized edema, hypertension, oliguria, hematuria, and proteinuria, with edema often starting around the eyes (periorbital edema).

26
Q

Which diagnostic test is commonly used to confirm an immune response to streptococcal infection in acute poststreptococcal glomerulonephritis?

A. Streptozyme test
B. Urinary pH measurement
C. Serum albumin level
D. Chest X-ray

A

A. Streptozyme test

Rationale: The streptozyme test measures antibodies to streptococcal antigens and is used to confirm an immune response in APSGN. This includes antistreptolysin-O (ASO) antibodies.

27
Q

What is the role of complement activation in the pathophysiology of acute poststreptococcal glomerulonephritis (APSGN)?

A. It causes increased blood pressure in the glomeruli.
B. It leads to deposition of antigen-antibody complexes in the glomeruli.
C. It increases glomerular filtration rate.
D. It causes destruction of the glomerular basement membrane.

A

B. It leads to deposition of antigen-antibody complexes in the glomeruli.

Rationale: In APSGN, complement activation occurs after the deposition of antigen-antibody complexes in the glomeruli, which leads to inflammation and tissue injury.

28
Q

Which of the following urine findings is commonly seen in patients with acute poststreptococcal glomerulonephritis?

A. Leukocyturia without red blood cells
B. Decreased protein levels and no red blood cells
C. Large number of red blood cells with or without casts
D. Positive for bacteria but negative for red blood cells

A

C. Large number of red blood cells with or without casts

Rationale: Dipstick urinalysis and urine microscopy often reveal significant numbers of red blood cells (RBCs), with or without casts, and proteinuria that ranges from mild to severe.

29
Q

What is the typical time frame for the development of acute poststreptococcal glomerulonephritis following a streptococcal infection?

A. 1–3 days
B. 1–6 weeks
C. 3–12 months
D. 6–12 months

A

B. 1–6 weeks

Rationale: APSGN typically develops 1 to 6 weeks after an infection of the tonsils, pharynx, or skin with nephrotoxic strains of group A β-hemolytic streptococci.

30
Q

Which laboratory test finding would most likely indicate an immune-mediated response in a patient with acute poststreptococcal glomerulonephritis (APSGN)?

A. Elevated C3 and CH50 levels
B. Elevated blood urea nitrogen (BUN)
C. Decreased antistreptolysin-O (ASO) antibodies
D. Decreased C3 and CH50 levels

A

D. Decreased C3 and CH50 levels

Rationale: Decreased complement components, especially C3 and CH50, are commonly seen in APSGN, indicating an immune-mediated response.

31
Q

What is the primary goal of nursing management in acute poststreptococcal glomerulonephritis (APSGN)?

A. To manage symptoms and provide supportive care
B. To promote complete renal failure prevention
C. To increase protein intake to aid kidney function
D. To eliminate the need for diuretic therapy

A

A. To manage symptoms and provide supportive care

Rationale: The management of APSGN primarily focuses on symptomatic relief and supportive care, including managing fluid balance, hypertension, and proteinuria.

32
Q

Which intervention is recommended to reduce edema in a patient with acute poststreptococcal glomerulonephritis (APSGN)?

A. Restricting protein intake
B. Administering antihypertensive medications
C. Increasing sodium intake
D. Restricting sodium and fluid intake while administering diuretics

A

D. Restricting sodium and fluid intake while administering diuretics

Rationale: Restricting sodium and fluid intake while administering diuretics helps manage edema in patients with APSGN by promoting fluid excretion.

33
Q

Which of the following is a critical intervention to prevent acute poststreptococcal glomerulonephritis (APSGN)?

A. Early diagnosis and treatment of sore throats and skin lesions
B. Encouraging low-protein diets for all patients
C. Prescribing antibiotics only for symptomatic streptococcal infections
D. Regular renal biopsies to monitor kidney function

A

A. Early diagnosis and treatment of sore throats and skin lesions

Rationale: Early diagnosis and treatment of streptococcal infections, such as sore throats and skin lesions, are essential in preventing APSGN.

34
Q

What is the role of antibiotics in the management of acute poststreptococcal glomerulonephritis (APSGN)?

A. To treat any ongoing streptococcal infection
B. To prevent hypertension from occurring
C. To promote renal function recovery
D. To reduce proteinuria and hematuria

A

A. To treat any ongoing streptococcal infection

Rationale: Antibiotics are prescribed if a streptococcal infection is still present, to prevent further complications and resolve the infection.

35
Q

Which dietary modification is often recommended for patients with acute poststreptococcal glomerulonephritis (APSGN)?

A. High-protein, high-sodium diet
B. Low-protein, low-sodium, and fluid-restricted diet
C. High-carbohydrate, low-sodium diet
D. Low-fat, high-calorie diet

A

B. Low-protein, low-sodium, and fluid-restricted diet

Rationale: A low-protein, low-sodium, and fluid-restricted diet is recommended for patients with APSGN to help manage edema, reduce nitrogenous wastes, and support kidney function.

36
Q

What is the reason for restricting protein intake in patients with acute post-streptococcal glomerulonephritis (APSGN)?

A. To decrease proteinuria
B. To reduce the risk of nephrotoxic side effects
C. To manage elevated blood urea nitrogen (BUN) levels
D. To support tissue regeneration

A

C. To manage elevated blood urea nitrogen (BUN) levels

Rationale: Protein intake may be restricted if there is evidence of increased nitrogenous wastes, such as elevated BUN levels, to reduce the burden on the kidneys.

37
Q

Which of the following is a potential complication if acute poststreptococcal glomerulonephritis (APSGN) is not treated appropriately?

A. Nephrotic syndrome
B. Urolithiasis
C. Polycystic kidney disease
D. Chronic glomerulonephritis

A

D. Chronic glomerulonephritis

Rationale: If acute poststreptococcal glomerulonephritis is not treated properly, it can progress to chronic glomerulonephritis, which can lead to permanent kidney damage.

38
Q

Which of the following is most commonly associated with the development of chronic glomerulonephritis?

A. Nephrotic syndrome and other forms of glomerulonephritis
B. Acute kidney infections
C. Single episodes of proteinuria
D. High urinary tract infections

A

A. Nephrotic syndrome and other forms of glomerulonephritis

Rationale: Chronic glomerulonephritis often develops as a progression from nephrotic syndrome or other types of glomerulonephritis, leading to progressive renal fibrosis and eventual ESRD.

39
Q

What is a common clinical finding in patients with chronic glomerulonephritis?

A. Sudden onset of hematuria and proteinuria
B. Severe acute renal failure with no prior symptoms
C. Gradual development of uremia and progressive kidney impairment
D. Immediate onset of flank pain and edema

A

C. Gradual development of uremia and progressive kidney impairment

Rationale: Chronic glomerulonephritis progresses slowly, with kidney impairment developing over time. Patients may not be aware of the damage until advanced stages.

40
Q

Which diagnostic test is most useful in detecting chronic glomerulonephritis?

A. MRI of the brain
B. Renal biopsy
C. Urinalysis, ultrasound, or CT scan
D. Chest X-ray

A

C. Urinalysis, ultrasound, or CT scan

Rationale: Urinalysis, ultrasound, and CT scans are commonly used to detect abnormalities in the kidneys, and a renal biopsy may be performed to determine the cause of the glomerulonephritis.

41
Q

Which of the following conditions is a potential cause of chronic glomerulonephritis?

A. Acute streptococcal throat infection
B. Autoimmune disorders, such as systemic lupus erythematosus (SLE)
C. Viral infections, such as HIV
D. High blood pressure from a sudden onset

A

B. Autoimmune disorders, such as systemic lupus erythematosus (SLE)

Rationale: Autoimmune disorders, like SLE, are potential causes of chronic glomerulonephritis, along with other conditions such as inherited disorders (e.g., Alport syndrome).

42
Q

What symptom is commonly seen in patients with chronic glomerulonephritis as kidney function declines?

A. Sudden sharp abdominal pain
B. Progressive uremia
C. Intermittent episodes of fever
D. Seizures due to electrolyte imbalance

A

B. Progressive uremia

Rationale: As kidney function declines, uremia (the buildup of waste products in the blood) develops slowly, contributing to various symptoms in chronic glomerulonephritis.

43
Q

What is the primary method for assessing the extent of kidney damage in chronic glomerulonephritis?

A. Serum potassium levels
B. Urinary specific gravity
C. BUN and serum creatinine levels
D. Urine pH levels

A

C. BUN and serum creatinine levels

Rationale: BUN (blood urea nitrogen) and serum creatinine levels are important indicators of renal function and are commonly elevated in chronic glomerulonephritis as kidney function declines.

44
Q

What is a common finding in the urine of a patient with chronic glomerulonephritis?

A. Presence of WBCs only
B. Gross hematuria and proteinuria
C. No abnormalities in urine composition
D. Increased glucose and ketones

A

B. Gross hematuria and proteinuria

Rationale: Patients with chronic glomerulonephritis often have proteinuria and hematuria, with RBCs, WBCs, and casts present in the urine.

45
Q

Which of the following factors should be assessed in the history of a patient with suspected chronic glomerulonephritis?

A. History of recent trauma to the kidneys
B. Family history of kidney stones
C. Previous history of benign prostatic hyperplasia (BPH)
D. Exposure to drugs such as NSAIDs and infections like hepatitis

A

D. Exposure to drugs such as NSAIDs and infections like hepatitis

Rationale: Assessing for drug exposure (e.g., NSAIDs) and infections (e.g., hepatitis) is important, as these can contribute to the development of chronic glomerulonephritis.

46
Q

What is the long-term consequence of untreated chronic glomerulonephritis?

A. Complete renal recovery with treatment
B. Spontaneous resolution of proteinuria
C. Development of nephrotic syndrome
D. Progression to end-stage renal disease (ESRD)

A

D. Progression to end-stage renal disease (ESRD)

Rationale: Chronic glomerulonephritis can slowly progress to end-stage renal disease (ESRD) if not managed properly, requiring dialysis or kidney transplantation.

47
Q

Which of the following is the primary cause of kidney and lung damage in anti-glomerular basement membrane (GBM) disease?

A. Direct bacterial infection
B. Antibodies attacking the glomerular and alveolar basement membranes
C. Excessive fluid retention in the lungs and kidneys
D. Genetic mutations affecting the kidney filtration barrier

A

B. Antibodies attacking the glomerular and alveolar basement membranes

Rationale: In anti-GBM disease, the immune system produces antibodies that attack the glomerular and alveolar basement membranes, leading to inflammation and damage in the kidneys and lungs.

48
Q

Which of the following is a common pulmonary symptom associated with anti-glomerular basement membrane (GBM) disease?

A. Wheezing and dry cough
B. Hemoptysis
C. Pleuritic chest pain
D. Chest tightness with exertion

A

B. Hemoptysis

Rationale: Hemoptysis (coughing up blood) is a common pulmonary manifestation of anti-GBM disease, along with mild shortness of breath and crackles.

49
Q

Which of the following laboratory findings is likely in a patient with anti-glomerular basement membrane (GBM) disease?

A. Elevated bilirubin levels
B. Decreased serum creatinine
C. Hematuria and proteinuria
D. Elevated white blood cell count

A

C. Hematuria and proteinuria

Rationale: Hematuria (blood in urine) and proteinuria (protein in urine) are common findings in anti-GBM disease, as kidney damage occurs due to antibody attack.

50
Q

What is the primary treatment used to remove circulating anti-glomerular basement membrane (GBM) antibodies in patients with anti-GBM disease?

A. Plasmapheresis
B. Dialysis
C. Diuretics
D. Corticosteroids

A

A. Plasmapheresis

Rationale: Plasmapheresis is used to remove the circulating anti-GBM antibodies from the patient’s blood, which is a key part of managing this autoimmune disease.

51
Q

Which of the following is a common complication in patients with advanced anti-glomerular basement membrane (GBM) disease?

A. Spontaneous recovery of renal function
B. Sudden onset of congestive heart failure
C. Gastrointestinal bleeding
D. Pulmonary hemorrhage leading to respiratory failure

A

D. Pulmonary hemorrhage leading to respiratory failure

Rationale: Pulmonary hemorrhage (bleeding in the lungs) is a common and life-threatening complication of anti-GBM disease, often leading to respiratory failure.

52
Q

What is the role of glucocorticoids in the treatment of anti-glomerular basement membrane (GBM) disease?

A. To increase urine output
B. To reduce antibody production and inflammation
C. To prevent kidney transplant rejection
D. To manage electrolyte imbalances

A

B. To reduce antibody production and inflammation

Rationale: Glucocorticoids are used to reduce inflammation and inhibit the production of anti-GBM antibodies, which helps to control the autoimmune response in the disease.

53
Q

Which of the following is a potential complication after a kidney transplant in a patient with rapidly progressive glomerulonephritis (RPGN)?

A. Recurrence of RPGN in the transplanted kidney
B. Development of insulin-dependent diabetes
C. Chronic hypertension
D. Development of tuberculosis

A

A. Recurrence of RPGN in the transplanted kidney

Rationale: RPGN may recur in the transplanted kidney after a kidney transplant, as the underlying autoimmune or inflammatory process may continue to affect the new organ.

54
Q

In patients with rapidly progressive glomerulonephritis (RPGN) who progress to end-stage renal disease (ESRD), which of the following treatment options may be required?

A. Liver transplant
B. Kidney dialysis or kidney transplant
C. Pancreatic enzyme therapy
D. Blood transfusions for anemia

A

B. Kidney dialysis or kidney transplant

Rationale: For patients with RPGN who progress to ESRD, kidney dialysis or a kidney transplant may be necessary to manage the loss of renal function.

55
Q

Which of the following treatments is commonly used to manage rapidly progressive glomerulonephritis (RPGN)?

A. Antibiotics and antipyretics
B. Diuretics and ACE inhibitors
C. Corticosteroids and cyclophosphamide
D. Angiotensin receptor blockers and calcium channel blockers

A

C. Corticosteroids and cyclophosphamide

Rationale: Corticosteroids and cyclophosphamide are often used in the treatment of RPGN to reduce inflammation and immune response, helping to prevent further kidney damage.

56
Q

What is the primary treatment aim in managing rapidly progressive glomerulonephritis (RPGN)?

A. Decreasing blood sugar levels
B. Promoting the growth of new kidney cells
C. Increasing protein intake to support renal function
D. Correcting fluid overload, hypertension, and uremia

A

D. Correcting fluid overload, hypertension, and uremia

Rationale: The primary goals in treating RPGN include correcting fluid overload, controlling hypertension, managing uremia, and reducing the inflammatory injury to the kidneys.

57
Q

Which of the following is a characteristic feature of rapidly progressive glomerulonephritis (RPGN)?

A. Gradual onset of renal failure over several years
B. Glomerular crescent formations
C. Only mild proteinuria and hematuria
D. Chronic edema without renal involvement

A

B. Glomerular crescent formations

Rationale: Rapidly progressive glomerulonephritis is characterized by glomerular crescent formations, which are a hallmark of the disease and distinguish it from chronic glomerulonephritis.

58
Q

Which of the following types of rapidly progressive glomerulonephritis (RPGN) involves the formation of immune complexes in the kidneys?

A. Anti-GBM disease
B. Pauci-immune disease
C. Immune complex disease
D. Diabetic nephropathy

A

C. Immune complex disease

Rationale: Immune complex disease (such as lupus or postinfectious glomerulonephritis) is one of the types of RPGN, where immune complexes deposit in the kidneys, leading to inflammation and damage.

59
Q

Which of the following is a typical manifestation of rapidly progressive glomerulonephritis (RPGN)?

A. Hypertension, edema, and hematuria
B. Hypotension, weight loss, and normal urine output
C. Decreased BUN and creatinine levels
D. Hypercalcemia and hyperphosphatemia

A

A. Hypertension, edema, and hematuria

Rationale: The typical manifestations of RPGN include hypertension, edema, hematuria, and reduced urine output due to rapid kidney function loss.

60
Q

Which information in the patient history would indicate a possible cause of acute glomerulonephritis?

a. Recent bladder infection

b. History of kidney stones

c. Recent sore throat and fever

d. History of high blood pressure

A

c. Recent sore throat and fever

Rationale: Acute glomerulonephritis frequently occurs after a streptococcal infection such as strep throat. It is not caused by kidney stones, hypertension, or urinary tract infection.

61
Q

Which finding for a patient admitted with glomerulonephritis indicates to the nurse that treatment has been effective?

a. The urine dipstick is negative for nitrites.

b. The patient denies pain or burning with voiding.

c. The antistreptolysin-O (ASO) titer has decreased.

d. The periorbital and peripheral edema have resolved.

A

d. The periorbital and peripheral edema have resolved.

Rationale: Because edema is a common clinical manifestation of glomerulonephritis, resolution of the edema indicates that the prescribed therapies have been effective. Nitrites will be negative, and the patient will not experience dysuria because the patient does not have a urinary tract infection. Antibodies to streptococcus will persist after a streptococcal infection.

MS3 (22 decks)

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