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renal phatho

Descriptive (70 Questions)

Q1. What is an ectopic kidney?

Ans: An ectopic kidney is a condition in which the kidneys fail to migrate to its
normal position and remains in the pelvis or at the pelvic brim.

Q2. What is Drug Induced Tubulointerstitial Nephritis?

Ans: Drug Induced Tubulointerstitial Nephritis is an adverse reaction to any one of an

increasing number of drugs, such as penicillins (methicillin, ampicillin), other
antibiotics (rifampin), diuretics (furosemide), proton pump inhibitors (omeprazole),
nonsteroidal anti-inflammatory agents, and numerous other drugs (phenindione,
cimetidine, etc). It is characterized by interstitial inflammation, often with abundant
eosinophils, and edema.

Q3. What is the nephrotic syndrome?

Ans: The nephrotic syndrome is a glomerular disease characterized by heavy

proteinuria (excretion of >3.5 gm of protein/day in adults), hypoalbuminemia(<3
g/dl), severe edema, hyperlipidemia, and lipiduria (lipid in the urine).

Q4. What are the possible pathogenetic mechanisms in Ischemic Acute

Renal Failure?

Ans: The possible pathogenetic mechanisms in Ischemic Acute Renal Failure include
Tubule epithelial cell injury, persistent and severe disturbances in blood flow
(intrarenal vasoconstriction), resulting in diminished oxygen and substrate delivery
to tubular cells, and increased sodium delivery to distal tubules which can stimulate
a tubuloglomerular feedback mechanism and contribute to afferent arteriolar
vasoconstriction and a decrease in GFR.

Q5. What is chronic kidney disease?

Ans: Chronic kidney disease (previously called chronic renal failure) is defined as the
presence of a diminished GFR that is persistently less than 60 mL/minute/1.73 m2
for at least 3 months, from any cause, and/or persistent albuminuria. It results from
progressive scarring in the kidney of any cause.

Q6. What is the pathogenic hallmark of IgA Nephropathy (Berger

Disease)?

Ans: The pathogenic hallmark of IgA Nephropathy (Berger Disease) is the deposition
of IgA in the mesangium.

Q7. What is tubulointerstitial nephritis?

Ans: Tubulointerstitial nephritis (TIN) is a group of inflammatory kidney diseases that

primarily involve the interstitium and tubules. It can be caused by bacterial infection,
drugs, metabolic disorders, irradiation, viral infections, and immune reactions.

Q8. What is Nephrotic Syndrome?

Ans: Nephrotic Syndrome is a clinical and laboratory syndrome characterized by

massive proteinuria with the daily loss of 3.5gm/day, hypoalbuminemia (plasma
albumin levels less than 3 gm/dL), generalized edema, hyperlipidemia and lipiduria.
It may accompany any glomerular disease or injury and is caused by a derangement
in the capillary walls of the glomeruli that results in marked prolonged increase in
permeability to plasma proteins.

Q9. What is glomerular disease?

Ans: Glomerular disease is a class of diseases that affect the glomerulus, a small
structure in the kidney that is responsible for filtering waste from the blood.
Glomerular disease can be primary or secondary, with the primary form being the
more common. Chronic glomerulonephritis is one of the most common causes of
chronic kidney disease in humans.

Q10. What are the histological findings of Post streptococcal

Glomerulonephritis (PSGN)?

Ans: Histologically, Post streptococcal Glomerulonephritis (PSGN) is characterized by

increased cellularity of the glomerular tufts that affects nearly all glomeruli,
infiltration of leukocytes and proliferation of endothelial, mesangial and epithelial
cells, and necrosis in severe cases. Electron microscopy shows deposited immune
complexes arrayed as subendothelial, intramembranous, or, most often,
subepithelial humps nestled against the glomerular basement membrane.

Q11. What is Minimal Change Disease (Lipoid Nephrosis)?

Ans: Minimal Change Disease (Lipoid Nephrosis) is a relatively benign disorder that is
the most frequent cause of the nephrotic syndrome in children. It is characterized by
diffuse loss of foot processes of epithelial cells in glomeruli that appear virtually
normal by light microscopy and is usually associated with secondary causes such as
respiratory infections, cancer, drug ingestion, and immunizations. It usually responds
well to corticosteroid therapy.

Q12. What is autosomal dominant (adult) polycystic kidney disease?

Ans: Autosomal dominant (adult) polycystic kidney disease is a hereditary disorder

characterized by multiple expanding cysts of both kidneys that ultimately destroy the
renal parenchyma and cause renal failure. It is caused by mutations of three
separate genes and is associated with mitral valve prolapse, congenital cystic liver,
and congenital cerebral berry aneurysms.

Q13. What is acute kidney injury (AKI)?

Ans: Acute kidney injury (AKI) is the abrupt onset of renal dysfunction characterized
by rapid reversible decline in GFR (within hours to days) with an acute increase in
serum creatinine often associated with oliguria or anuria (decreased or no urine flow)
and electrolyte balance.

Q14. What is the etiology and pathogenesis of Post streptococcal

Glomerulonephritis (PSGN)?

Ans: Post streptococcal Glomerulonephritis (PSGN) develops in a child 1 to 4 weeks

after recovery from a group A streptococcal infection of throat or, less commonly,
the skin(impetigo). The etiology and pathogenesis involves immune complex
deposition, with the formation of immune complexes in the circulation or in situ
(binding of antibodies to bacterial antigens planted in the GBM). Low complement
C3 levels and granular deposits of IgG and complement on the GBM are seen.

Q15. What is the most common cause of reflux?

Ans: The most common cause of reflux is congenital complete or partial absence of
the intravesical ureter (B).

Q16. How does dialysis work?

Ans: Dialysis works by removing excess fluid and waste products from the blood and
circulating it through a dialyzer. The blood is then bathed by dialysate. Hemodialysis
and peritoneal dialysis are the two types of dialysis.

Q17. What is the Pathogenesis of Ischemic ATI/N?

Ans: The Pathogenesis of Ischemic ATI/N begins with hypoperfusion, which initiates
cell injury that often leads to cell death. This is most prominent in the straight
portion of the proximal tubules and thick ascending limb of the loop of Henle. The
reduction in the GFR occurs not only from reduced filtration due to hypoperfusion
but also from casts and debris obstructing the lumen, causing blockage of urine flow
and back leak of filtrate through the damaged epithelium (ineffective filtration). In
addition, ischemia leads to decreased production of vasodilators (i.e. nitric oxide,
prostacyclin) and increased release of the endothelial vasoconstrictor endothelin by
tubular epithelial cells, leading to further vasoconstriction and hypoperfusion.
Q18. What is Azotemia?

Ans: Azotemia is a biochemical abnormality that refers to an elevation of blood urea

nitrogen (BUN) and creatinine levels, and is related largely to a decreased glomerular
filtration rate (GFR). It is a typical feature of both acute and chronic (obstruction)
kidney injury.

Q19. What is compensatory hypertrophy?

Ans: Compensatory hypertrophy is the enlargement of the remaining kidney when

one kidney fails or is removed. This is done to increase the effectiveness of the
functioning kidney.

Q20. What is Rapidly Progressive (Crescentic) Glomerulonephritis?

Ans: Rapidly Progressive (Crescentic) Glomerulonephritis is a clinicopathologic

syndrome caused by the accumulation of cells in the Bowman space in the form of
crescents accompanied by a rapid, progressive loss of renal function (severe oliguria)
and death within weeks to months if untreated. It is commonly associated with
severe glomerular injury with necrosis and GBM breaks and subsequent proliferation
of parietal epithelium (crescents).

Q21. What is IgA Nephropathy (Berger Disease)?

Ans: IgA Nephropathy (Berger Disease) is the most common type of

glomerulonephritis worldwide and is characterized by recurrent microscopic or gross
hematuria. It typically affects children and young adults and begins as an episode of
gross hematuria that occurs within 1 or 2 days of a non-specific upper respiratory
tract infection. Associated with flank pain, mild proteinuria is usually present, and
the nephrotic syndrome may occasionally develop.

Q22. What is Focal Segmental Glomerulosclerosis (FSGS)?

Ans: Focal Segmental Glomerulosclerosis (FSGS) is a disorder of the glomerulus in

which the capillary walls are thickened and the capillaries are narrowed or closed. It
is characterized by proteinuria, hematuria, and hypertension, and is often associated
with a collapsing variant glomerulopathy. It has a poor prognosis and can lead to end
stage renal disease in most patients.

Q23. What are the mediators of glomerular injury?

Ans: Mediators of glomerular injury include cells such as neutrophils, macrophages,

lymphocytes, platelets, and resident glomerular cells, as well as soluble mediators
such as chemotactic and complement components, eicosanoids, nitric oxide,
endothelin, cytokines, chemokines, and the coagulation system.

Q24. What is Henoch Sch nlein purpura?

Ans: Henoch Sch nlein purpura is a systemic syndrome involving the skin (purpuric
rash), gastrointestinal tract (abdominal pain), joints (arthritis), and kidneys. It is
characterized by IgA deposition and is associated with an abnormality in IgA
production and clearance.

Q25. What is the clinical manifestation of prerenal azotemia?

Ans: Prerenal azotemia is encountered when there is hypoperfusion of the kidneys.

Its clinical manifestation includes an elevation of blood urea nitrogen (BUN) and
creatinine levels, and is related largely to a decreased glomerular filtration rate (GFR).

Q26. What is the clinical course of IgA Nephropathy (Berger Disease)?

Ans: The clinical course of IgA Nephropathy (Berger Disease) typically begins as an
episode of gross hematuria that occurs within 1 or 2 days of a non-specific upper
respiratory tract infection. The hematuria lasts several days and then subsides, only
to recur every few months. Associated with flank pain, mild proteinuria is usually
present, and the nephrotic syndrome may occasionally develop.

Q27. What is Xanthogranulomatous Pyelonephritis?

Ans: Xanthogranulomatous Pyelonephritis is an uncommon form of chronic

pyelonephritis characterized by the accumulation of foamy macrophages with
lymphocytes, plasma cells, neutrophils, and occasional giant cells. It is often related
to gram-negative Proteus infection.

Q28. How can vesicoureteral reflux be demonstrated?

Ans: Vesicoureteral reflux can be demonstrated radiographically by a voiding

cystourethrogram. The bladder is filled with a radio opaque dye, and films are taken
during micturition.

Q29. What are the three complications of acute pyelonephritis that

are seen in special circumstances?

Ans: The three complications of acute pyelonephritis that are seen in special
circumstances are complete urinary tract obstruction usually at high levels, diabetes,
and sickle cell anemia.

Q30. What factors increase the risk of developing pyelonephritis?

Ans: Factors that increase the risk of developing pyelonephritis include being
debilitated, immunosuppressed, receiving immunosuppressive therapy, having a
lower urinary tract obstruction, neurogenic bladder dysfunction, and being pregnant.

Q31. What are the clinical features of autosomal dominant (adult)

polycystic kidney disease?

Ans: The most common presenting complaint is flank pain or a heavy, dragging
sensation. Intracystic hemorrhage or progressive dilation of the cysts may produce
abdominal pain and mass. Intermittent gross hematuria commonly occurs. The most
important complications, because of their deleterious effect on already marginal
renal function, are hypertension (which is usually difficult to control with treatment)
and secondary urinary infection.

Q32. What is the main characteristic of colloid casts?

Ans: The main characteristic of colloid casts is that they resemble thyroid colloid
(thyroidization).

Q33. What are the common causes of chronic kidney disease?

Ans: : The common causes of chronic kidney disease include chronic

glomerulonephritis, chronic pyelonephritis, urinary tract obstruction, renal tumors,
and urinary tract infection.

Q34. What is Chronic Glomerulonephritis?

Ans: Chronic Glomerulonephritis refers to end stage glomerular disease due to the
progression of various types of glomerulonephritis, such as poststreptococcal GN,
RPGN, membranous GN, focal glomerulosclerosis, MPGN, and IgA nephropathy. It is
an important cause of end stage renal disease, presenting as chronic renal failure.
On examination, the kidneys are symmetrically contracted and diffusely granular
with a thinned cortex and increased peripelvic fat. The glomeruli may still show
evidence of the primary disorder.

Q35. What is Nephrotoxic ATI?

Ans: Nephrotoxic ATI is toxic injury to the tubules caused by endogenous (e.g.,
myoglobin, hemoglobin, monoclonal light chains, bile/bilirubin) or exogenous agents
(e.g., drugs, radiocontrast dyes, heavy metals, organic solvents). Most of the
pathophysiological features of ischemic ATI/N are shared by the nephrotoxic forms.

Q36. What is Post streptococcal Glomerulonephritis (PSGN)?

Ans: Post streptococcal Glomerulonephritis (PSGN) is a type of acute proliferative

glomerulonephritis that develops in a child 1 to 4 weeks after recovery from a group
A streptococcal infection of throat or, less commonly, the skin(impetigo). It is
characterized by evidence of a recent streptococcal infection (culture of the
organism, raised ASOT) and low complement C3 levels, that return to normal after 6
8 weeks.
Q37. What is the collapsing variant of focal segmental
glomerulosclerosis (FSGS)?

Ans: The collapsing variant of FSGS is a severe form of FSGS that is associated with
HIV infection. It is characterized by cystic dilation of tubules, diffuse thickening of
capillary walls, and sometimes glomerular and vascular damage.

Q38. What is pyelonephritis?

Ans: Pyelonephritis is a form of tubulointerstitial nephritis caused by bacterial

infection and is one of the most common renal diseases. It involves the tubules,
interstitium and renal pelvis and can be acute or chronic.

Q39. What is a horseshoe kidney?

Ans: A horseshoe kidney is a rare congenital condition in which both kidneys are
fused together usually along the lower poles by renal or fibrous tissue. Congenital
double ureters and double renal pelvis are common anomalies associated with this
condition.

Q40. What is thyroidization?

Ans: Thyroidization is a histopathological picture due to dilation of tubules which

contain eosin staining proteinaceous material (colloid).

Q41. How does acute pyelonephritis morphologically manifest?

Ans: Acute pyelonephritis morphologically manifests with patchy interstitial

suppurative inflammation, intratubular aggregates of neutrophils, tubular necrosis,
and an irregular distribution (with poles being common).

Q42. What is cystic disease of the kidney?

Ans: Cystic disease of the kidney is a heterogeneous group of disorders that may be
hereditary, developmental but nonhereditary, or acquired. It is important to
understand these disorders as they are quite common and can represent diagnostic
problems for clinicians, radiologists, and pathologists.

Q43. What is end stage renal disease (ESRD)?

Ans: End stage renal disease (ESRD) is irreversible loss of renal function requiring
dialysis or transplantation typically due to severe progressive scarring in the kidney
from any cause. In end stage renal disease (ESRD) the GFR is less than 5% of normal.

Q44. What is Membranous Glomerulonephritis (Membranous Nephropathy)?

Ans: Membranous Glomerulonephritis (Membranous Nephropathy) is a form of

chronic immune complex nephritis characterized by diffuse glomerular wall
thickening due to slow progressive in situ immune complexes deposition along the
subepithelial side of the basement membrane. It is the most common cause of
nephrotic syndrome in adults and can be either primary or secondary, with
secondary forms resulting from infections, malignant tumors, autoimmune
conditions, exposure to inorganic salts, or drugs.

Q45. What is the difference between chronic pyelonephritis and

vascular sclerosis?

Ans: The difference between chronic pyelonephritis and vascular sclerosis is that the
kidney is usually irregularly scarred in chronic pyelonephritis, whereas the scarring is
symmetrical in vascular sclerosis.

Q46. What is glomerulonephritis?

Ans: Glomerulonephritis is a type of kidney disease that affects the glomeruli, the
tiny filters in the kidneys. It is caused by damage to the glomeruli and can result in a
variety of symptoms, including proteinuria, hematuria, hypertension, and reduced
glomerular filtration rate.

Q47. What is the typical presentation of acute pyelonephritis?

Ans: : The typical presentation of acute pyelonephritis is a sudden onset of pain at
the costovertebral angle and systemic evidence of infection, such as fever and
malaise, as well as pyuria, WBCs casts, and a positive urine culture.

Q48. What are the clinical presentations of chronic renal disease?

Ans: The clinical presentations of chronic renal disease include fluid and electrolytes
imbalance, edema, hyperkalemia, metabolic acidosis, dehydration,
hyperphosphotemia, hypocalcemia, secondary hyperparathyroidism, anemia,
bleeding, hypertension, congestive heart failure, pulmonary edema, nausea,
vomiting, gastritis, colitis, peripheral neuropathy, encephalopathy, pruritus,
dermatitis, and reduced immunity.

Q49. What are the clinical features of Chronic Pyelonephritis?

Ans: The clinical features of Chronic Pyelonephritis can present acutely or insidiously.
Acute symptoms include back pain, fever, pyuria, and bacteruria. Patients may seek
medical attention when developing hypertension, renal insufficiency, or when
subject to urinalysis (pyuria, WBC casts, and bacteruria). Reflux nephropathy is a
common cause of hypertension in children.

Q50. What is autosomal recessive (childhood) polycystic kidney

disease?

Ans: Autosomal recessive (childhood) polycystic kidney disease is characterized by

multiple epithelium-lined cysts in the kidneys and liver with portal fibrosis as well as
proliferation of portal bile ducts. Patients who survive infancy may develop a
peculiar type of hepatic fibrosis called congenital hepatic fibrosis.

Q51. What are the four basic tissue reactions to glomerular injury?

Ans: : The four basic tissue reactions to glomerular injury are hypercellularity,
basement membrane thickening, hyalinosis, and sclerosis. Hypercellularity refers to
an increase in the number of cells in the glomerular tufts, basement membrane
thickening refers to an increase in the thickness of the capillary walls, hyalinosis
denotes the accumulation of homogenous and eosinophilic material, and sclerosis is
characterized by the accumulation of extracellular collagenous matrix.
Q52. What is HIV nephropathy?

Ans: HIV nephropathy is a type of kidney disease caused by HIV infection or heroin
abuse, which is superimposed on another primary glomerular disease, such as
morbid obesity, hypertension, or sickle cell disease. It is a maladaptation associated
with loss of renal mass nephropathy.

Q53. What are the mediators of glomerular injury in

glomerulonephritis?

Ans: : Mediators of glomerular injury in glomerulonephritis include cells such as

neutrophils, macrophages, lymphocytes, platelets, and resident glomerular cells, as
well as soluble mediators such as chemotactic and complement components,
eicosanoids, nitric oxide, endothelin, cytokines, chemokines, and the coagulation
system.

Q54. What is the most common cause of clinical pyelonephritis?

Ans: The most common cause of clinical pyelonephritis is ascending infection from
the lower urinary tract. The principal causative organisms are the enteric gram
negative bacilli/rods from the patient's own fecal flora, with Escherichia coli being
the most common.

Q55. What is Focal Segmental Glomerulosclerosis?

Ans: Focal Segmental Glomerulosclerosis is characterized by scarring/sclerosis of

some but not all glomeruli (focal) and in the affected glomerulus only a portion of
the capillary tuft is involved (segmental). It is associated with heavy proteinuria and
progressive renal failure and is the predominant cause of idiopathic nephrotic
syndrome in adults.

Q56. What is diabetic glomerulosclerosis?

Ans: Diabetic glomerulosclerosis, also known as diabetic nephropathy, is a type of

kidney disease that is caused by diabetes and is the leading cause of chronic renal
failure in the industrialized world. It is characterized by capillary basement
membrane thickening, diffuse glomerulosclerosis, nodular glomerulosclerosis, and
ischemic damage to tubules and interstitium.

Q57. What are the hallmarks of chronic pyelonephritis?

Ans: The hallmarks of chronic pyelonephritis are coarse, discrete, corticomedullary

scars overlying dilated, blunted, or deformed calyces, and flattening of the papillae.

Q58. What is the Classification of the major causes of acute kidney

injury?

Ans: The Classification of the major causes of acute kidney injury includes Prerenal,
Intrinsic renal and Postrenal. Intrinsic renal causes can result from glomerular,
interstitial, vascular or acute tubular injury. Acute Tubular Injury/Necrosis (ATI/N) is
the most common intrinsic/intrarenal cause of acute kidney injury (AKI).

Q59. What is acute proliferative glomerulonephritis?

Ans: Acute proliferative glomerulonephritis is a condition characterized histologically

by diffuse proliferation of glomerular cells, associated with influx of leukocytes and
clinically by the syndrome of acute nephritis. It is typically caused by immune
complexes and the inciting antigen may be exogenous or endogenous.

Q60. How is pyelonephritis caused?

Ans: Pyelonephritis is caused by bacterial infection and can be caused by two routes:
hematogeneous (seeding of kidneys from distant foci) and ascending infection from
the lower urinary tract.

Q61. What is HIV-associated nephropathy?

Ans: HIV-associated nephropathy is a type of kidney disease that is associated with

HIV infection and is characterized by a severe form of the collapsing variant of FSGS.
It can lead to acute renal failure, acute interstitial nephritis, thrombotic
microangiopathies, postinfectious glomerulonephritis, and other renal disorders.
Q62. What are the principal causes of Acute Tubular Injury/Necrosis
(ATI/N)?

Ans: The principal causes of Acute Tubular Injury/Necrosis (ATI/N) are Ischemic
ATI/N and Nephrotoxic ATI. Ischemic ATI/N is due to persistent decreased or
interrupted blood flow, and can arise from decreased effective circulating blood
volume or reduced intrarenal blood flow. Nephrotoxic ATI is toxic injury to the
tubules caused by endogenous or exogenous agents.

Q63. What is the most common cause of chronic pyelonephritis?

Ans: The most common cause of chronic pyelonephritis is chronic reflux associated
pyelonephritis (reflux nephropathy).

Q64. What is agenesis hypoplasia?

Ans: Agenesis hypoplasia is a disorder characterized by the absence or

underdevelopment of an organ or tissue. In the case of the kidney, it refers to the
absence or underdevelopment of the kidney.

Q65. What is the clinical course of Post streptococcal

Glomerulonephritis (PSGN)?

Ans: The classic clinical course of Post streptococcal Glomerulonephritis (PSGN) is a

young child abruptly developing malaise, fever, nausea, oliguria and (smoky or cocoa
colored urine) 1 to 2 weeks after recovery from a sore throat [the nephritic
syndrome]. Red cell casts in the urine, mild proteinuria periobital edema, mild to
moderate HTN are also present. More than 95% of affected children eventually
recover and 1-2% may undergo slow progression to chronic GN. In adults, the
disease is less benign.

Q66. What is Membranoproliferative Glomerulonephritis?

Ans: Membranoproliferative Glomerulonephritis (MPGN) is a pattern of immune-

mediated injury characterized by thickened capillary loops and proliferation of
glomerular cells. It is divided into type I and type II, with type I being more common
and caused by circulating immune complexes with subendothelial antigen, and type
II being caused by excessive complement activation. It is a persistent and slowly
progressive condition.

Q67. What are the two critical events that underlie both ischemic
and nephrotoxic ATI/N?

Ans: : The two critical events that underlie both ischemic and nephrotoxic ATI/N are
Tubule epithelial cell injury and persistent and severe disturbances in blood flow
(intrarenal vasoconstriction).

Q68. What are the four basic morphologic components of the kidney?

Ans: The four basic morphologic components of the kidney are Glomeruli, Tubules,
Interstitium, and Blood Vessels.

Q69. How does chronic pyelonephritis manifest microscopically?

Ans: Microscopically, chronic pyelonephritis manifests with widespread tubular

atrophy, hypertrophy or dilation in some areas, dilated tubules with flattened
epithelium filled with glassy appearing PAS positive casts, patchy mononuclear
interstitial inflammation, and prominent interstitial fibrosis involving cortex and
medulla.

Q70. What is interstitial nephritis?

Ans: . Interstitial nephritis is a type of tubulointerstitial nephritis that is non-bacterial

in origin and is caused by drugs, metabolic disorders, irradiation, viral infections, and
immune reactions. It is characterized by interstitial inflammation and can result in a
variety of symptoms, including proteinuria, hematuria, and hypertension.

Fillups (59 Questions)

Q71. The glomeruli may be spared altogether or affected only late in

the __________.
 1. primary TIN

2. secondary TIN

3. interstitial nephritis

4. pyelonephritis

Q72. Microscopically, the papillary tips show coagulative necrosis

surrounded by a ____________ infiltrate.

1. Mononuclear

2. Lymphocytic

3. Neutrophilic

4. Plasma cell

Q73. The most common presenting complaint of Autosomal Dominant

(Adult) polycystic kidney disease is _____.

1. Flank pain

2. Abdominal pain

3. Intermittent gross hematuria

4. Fluid retention

Q74. The kidney is a good target for toxins because it has a rich
blood supply, receiving _____ of CO.

1. 10%
 2. 15%

3. 20%

4. 25%

Q75. In pyelonephritis, scarring is often _________, versus

symmetrical scarring in vascular disease.

1. Symmetric

2. Discrete

3. Asymmetric

4. Coarse

Q76. Pathogenesis of ischemic ATI/N involves cell injury and death

which is prominent in ________.

1. Glomeruli

2. Straight portion of the proximal tubules and thick ascending limb of loop of
Henle

3. Interstitium

4. Vascular

Q77. Glomerular diseases progressing to chronic glomerulonephritis

include __________.

1. HIV nephropathy

2. Poststreptococcal GN
 3. Focal glomerulosclerosis

4. All of the above

Q78. Urinary tract obstruction and renal tumors have ___________.

1. Diminished GFR

2. Varied clinical manifestations

3. An increase in the blood urea nitrogen (BUN) concentration

4. An increase in the plasma or serum creatinine (SCr) concentration

Q79. Hyalinosis is a consequence of _____.

1. Chronic endothelial or capillary wall injury

2. Chronic mesangial wall injury

3. Chronic glomerular wall injury

4. Chronic renal tubular wall injury

Q80. Glomerular diseases manifesting with nephrotic syndrome include

__________.

1. Membranous nephropathy

2. Focal segmental glomerulosclerosis

3. Collapsing variant glomerulopathy

4. All of the above

Q81. End stage renal disease is __________.

1. Irreversible loss of renal function requiring dialysis or transplantation

2. The presence of a diminished GFR that is persistently less than 60

mL/minute/1.73 m2

3. An increase in the blood urea nitrogen (BUN) concentration

4. An increase in the plasma or serum creatinine (SCr) concentration

Q82. The most common cause of reflux is congenital complete or

partial absence of the __________.

1. Bladder

2. Ureter

3. Intrarenal reflux

4. Pylonephritis

Q83. In the case of TIN caused by bacterial infection, the renal

pelvis is prominently involved hence the more descriptive term
__________.

1. Pyelonephritis

2. Interstitial nephritis

3. Glomerulosclerosis

4. Diabetic nephropathy
Q84. Two critical events underlying both ischemic and nephrotoxic
ATI/N are ________ and persistent and severe disturbances in blood
flow.

1. Tubule epithelial cell injury

2. Hypovolemic shock

3. Reduction in GFR

4. Increase in nitric oxide, prostacyclin

Q85. Urinary tract infection (UTI) is characterized by ___________.

1. Heavy proteinuria

2. Bacteriuria and pyuria

3. Edema

4. Hypoalbuminemia

Q86. Response to fluid repletion can help distinguish between

prerenal azotemia and ischemic ATN with _______.

1. Reduced intrarenal blood flow

2. Obstruction of tubular lumen with Tamm Horsfall protein

3. Return of renal function within 24-72 hours

4. Increase in nitric oxide, prostacyclin

Q87. In children, 20% of chronic kidney failure is due to

___________.
 1. Renal dysplasia or hypoplasia

2. Chromosomal disorder

3. Renal agenesis

4. Hypoplasia

Q88. Autosomal Recessive (Childhood) polycystic kidney disease may

present with _____.

1. Polycystic liver

2. Congenital hepatic fibrosis

3. Subarachnoid or intracerebral hemorrhage

4. All of the above

Q89. Acute kidney injury is characterized by ___________.

1. Rapidly reversible decline in GFR

2. An increase in the blood urea nitrogen (BUN) concentration

3. An increase in the plasma or serum creatinine (SCr) concentration

4. An increase in urine volume

Q90. Glomerular diseases constitute some of major problem in _____.

1. Radiology

2. Nephrology
 3. Pathology

4. Cardiology

Q91. Kidneys affected by chronic glomerulonephritis show a

symmetrically __________ cortex.

1. Granular

2. Thinned

3. Normal

4. Thickened

Q92. Pyelonephritis is much more common in females because of

__________.

1. a combination of reasons

2. short length of urethra

3. urethral trauma

4. hormonal changes

Q93. The inciting antigen in type I membranoproliferative

glomerulonephritis is __________.

1. Ab against phospholipase A2 receptor

2. C3 nephritic factor

3. Unidentified
 4. Nonsteroidal anti inflammatory agents

Q94. Focal segmental glomerulosclerosis is characterized by

__________.

1. Increased mesangial matrix

2. Obliterated capillary lumens

3. Hyalinosis

4. All of the above

Q95. The two routes by which bacteria can reach the kidney are
__________ and __________.

1. ascending infection, hematogeneous

2. pyelonephritis, renal pelvis

3. renal pelvis, ascending infection

4. hematogeneous, pyelonephritis

Q96. Primary focal glomerulosclerosis is found in __________ of

cases.

1. 10%

2. 40%

3. 50-80%

4. 100%
Q97. Type II membranoproliferative glomerulonephritis is also known
as __________.

1. Mesangiocapillary GN

2. Dense deposit disease

3. Heymann nephritis

4. C3 nephritic factor

Q98. Urine analysis of Acute pyelonephritis may reveal ___________.

1. Granulomatous interstitial inflammation

2. Casts

3. Pyuria

4. Pale gray necrosis

Q99. Extensive disease, however, eventually also destroys the

glomeruli, and fungal pyelonephritis (e.g., Candida) often affects
___________.

1. Tubules

2. Interstitium

3. Glomeruli

4. Papillae

Q100. Characteristically, discrete, yellowish, raised abscesses are

grossly apparent on the renal surface in _____________
 1. Chronic obstructive pyelonephritis

2. Reflux Nephropathy

3. Chronic Reflux Associated Pyelonephritis

4. Acute pyelonephritis

Q101. __________ is a morphologic entity in which predominantly

interstitial inflammation and scarring of the renal parenchyma is
associated with grossly visible scarring and deformity of the
pelvicalyceal system.

1. Chronic Reflux Associated Pyelonephritis

2. Reflux Nephropathy

3. Chronic obstructive pyelonephritis

4. Chronic pyelonephritis

Q102. HIV can result directly or indirectly to __________.

1. Acute renal failure

2. Acute interstitial nephritis

3. Pyelonephritis

4. Glomerulosclerosis

Q103. The most common organism responsible for acute pyelonephritis

is __________.

1. Enterobacter
 2. E. coli

3. Proteus

4. Pseudomonas

Q104. Immune mechanisms are the underlying cause of _____.

1. Primary glomerulopathies

2. Secondary glomerular disorders

3. Systemic diseases

4. Hereditary diseases

Q105. Response of membranous nephropathy to corticosteroid therapy

is __________.

1. Variable

2. High

3. Poor

4. Spontaneous

Q106. The most frequent route by which bacteria reach the kidney is
__________.

1. hematogeneous

2. pyelonephritis
 3. ascending infection

4. renal pelvis

Q107. The experimental model of membranous GN is __________

nephritis.

1. Heymann

2. Dense deposit

3. MPGN

4. IgA

Q108. Nephrolithiasis (renal stones) is manifested by ___________.

1. Heavy proteinuria

2. Spasms of severe pain (renal colic) and hematuria

3. Edema

4. Hypoalbuminemia

Q109. The principal causes of acute tubular injury are _______.

1. Hypovolemic shock

2. Ischemia, due to persistent decreased or interrupted blood flow, and

nephrotoxins

3. Reduction in the GFR

 4. Decreased effective circulating blood volume

Q110. The characteristic histologic feature of acute pyelonephritis

is ______________.

1. Interstitial fibrosis

2. Tubular necrosis

3. Suppurative necrosis or abscess formation

4. Coagulative necrosis

Q111. The renal lesions associated with HIV include __________.

1. Glomerulosclerosis

2. Bacterial urinary tract infection

3. Collapsing variant of FSGS

4. Acute interstitial nephritis

Q112. Hemodialysis and peritoneal dialysis ___________.

1. Remove excess fluid & wastes from blood

2. Increase the blood urea nitrogen (BUN) concentration

3. Increase the plasma or serum creatinine (SCr) concentration

4. Reduce urine volume

Q113. The two major diseases that involve tubules and interstitium
are __________ and __________.

1. Pyelonephritis, Acute renal failure

2. Acute renal failure, Glomerulosclerosis

3. Inflammatory involvement, Ischemic or toxic tubular injury

4. Glomerulosclerosis, HIV associated nephropathy

Q114. Pathology of glomerular disease can be _____.

1. Primary

2. Secondary

3. Both primary and secondary

4. Chronic

Q115. Primary membranous glomerulonephritis is found in __________

of cases.

1. 10%

2. 15%

3. 85%

4. 50%

Q116. The surfaces of both kidneys demonstrate multiple

microabscesses from hematogenous spread of a ______ infection.
 1. Fungal

2. Bacterial

3. Viral

4. Parasitic

Q117. Chronic kidney disease is defined as ___________.

1. The presence of a diminished GFR that is persistently less than 30

mL/minute/1.73 m2

2. The presence of a diminished GFR that is persistently less than 60

mL/minute/1.73 m2

3. An increase in the blood urea nitrogen (BUN) concentration

4. An increase in the plasma or serum creatinine (SCr) concentration

Q118. The constellation of changes, broadly termed acute kidney

injury/Acute renal failure, manifests clinically as sudden decreased
in GFR with concurrent elevation of serum creatinine often
associated with a reduction in urine volume and ______.

1. Polyuria

2. Pyuria

3. Oliguria

4. Anuria

Q119. The clinical manifestations of renal disease can be grouped

into ____________.
 1. Prerenal azotemia

2. Rapidly progressive glomerulonephritis

3. Reasonably well defined syndromes

4. Uremic gastroenteritis

Q120. Acute Tubular Injury/Necrosis (ATI/N) is classified into two

categories, namely ___________.

1. Ischemic ATI/N and Prerenal Azotemia

2. Ischemic ATI/N and Nephrotoxic ATI

3. Intrinsic Renal and Postrenal

4. Prerenal, intrinsic renal and Postrenal

Q121. Cellular proliferation is a common feature of _____.

1. Hyalinosis

2. Glomerular sclerosis

3. Hypercellularity

4. Basement membrane thickening

Q122. Acute Tubular Injury/Necrosis (ATI/N) is a clinicopathologic

entity characterized by damage to tubular epithelial cells and an
acute decline in renal function, often associated with ___________.

1. Hypovolemic shock
 2. Shedding of granular casts and tubular cells into the urine

3. Persistent decreased or interrupted blood flow

4. Obstruction of tubular lumen with Tamm Horsfall protein

Q123. Basement membrane thickening is best seen by _____.

1. Light microscopy

2. Ultrasound

3. PAS staining

4. X-ray

Q124. The PKD1, PKD2 and PKD3 gene are located on _____.

1. Chromosome 1

2. Chromosome 12

3. Chromosome 16

4. Chromosome 18

Q125. The etiology of non-bacterial TIN includes __________.

1. bacterial infections

2. metabolic disorders

3. viral infections
 4. drugs, metabolic disorders, viral infections, and immune reactions

Q126. The nephrotic syndrome is characterized by ___________.

1. Diminished GFR

2. Heavy proteinuria

3. Edema

4. Hypoalbuminemia

Q127. In focal glomerular disease, the lesion involves _____.

1. Only some of glomeruli

2. Most or all glomeruli

3. Part of the glomerulus

4. Entire glomerulus

Q128. Nephrotoxic injury to tubular cells occurs by multiple

mechanisms including _______.

1. Intrarenal vasoconstriction

2. Intratubular obstruction

3. Direct toxic injury

4. Hypovolemic shock
Q129. The histopathological picture referred to as "thyroidization"
is due to __________.

1. The accumulation of foamy macrophages

2. Dilation of tubules containing eosin staining proteinaceous material

3. Obstruction of tubular lumen with Tamm Horsfall protein

4. Urate nephropathy