The Correct option is E

Papillary necrosis is complication of pyelonephritis.
Kidney stones formation or urolithiasis is comprised of calcium carbonate crystals in the presence of hypercalciuria and a common complication is chronic pyelonephritis.

The Correct option is B

Fanconi Syndrome (Toni-Debre-Fanconi Syndrome)

Fanconi syndrome is a generalized disorder of the PT. The defect can lead to glycosuria, aminoaciduria, phosphaturia, bicarbonaturia and excessive urinary loss of K+, Na+, Ca++, Mg++, uric acid and other organic acids.

It appears that the common denominator in most of the inherited forms is that a toxin builds up in the tubular cells (e.g. cystinosis--cystine in lysosomes, Wilson’s disease-copper). In the idiopathic forms, the presumed tubular toxin is unknown. Because of the number of different transport mechanisms involved in Fanconi syndrome, it is likely that individual transporters themselves are affected. It is speculated that a generalized membrane defect exists (permeability theory), or alternatively, there is a defect in intracellular energy production or utilization (energy theory). In experimentally induced Fanconi syndrome (maleic acid), decreased intracellular ATP has been noted.

Clinical signs of Fanconi syndrome include polyuria and those secondary to electrolyte and bicarbonate losses. In children growth retardation and rickets may develop. Idiopathic Fanconi syndrome often progresses to chronic renal failure.

The Correct option is B

Renal Carcinoma

• Renal Cell Carcinoma – hypernephroma/Grawitz tumour
• Arises from proximal renal tubular epithelium
  

Epidemiology

• 90% renal cancers
• Mean age 55 years, male: female is 2:1
• 15% those on renal dialysis develop renal cell carcinoma
  

Clinical features

• 50% incidental findings during abdominal imaging for other symptoms
  
• Haematuria, loin pain, abdominal mass, anorexia, malaise, weigh loss and PUO may all occur
  
• Rarely, invasion of left renal vein compresses testicular vein causing a left varicocele
  
• Spread may be direct, via lymph nodes, or haematogenous (bone, liver, brain)
  

Tests

• Bloods – FBC (polycythemia from epo secretion), ESR, U+E, alk phos (bony mets)
• Urine – RBC, cytology
• Imaging – USS, CT/MRI, IVU (filling defect in kidney and calcification)
• Renal angiography if partial nephrectomy or palliation are being considered
• CXR – cannon ball mets

The Correct option is C

Minimal change disease

Is a commonest cause of nephrotic syndrome in children in whom this disease occur frequently. Despite massive proteinuria, the renal function remains normal. Over 90% of patients are corticosteroid sensitive while small numbers of patients are corticosteroid dependent or resistant. The later can be treated by immunosuppressive agents. The disease is characterized by normal appearing glomeruli on light and immunofluorescence microscopy and the only abnormality detected is effacement of epithelial cell foot processes which is identified on electron microscopy only. No immune-complexes are identified and so the disease is not an immune complex in origin but several associated features suggests immune mediation. The current hypothesis is that the cell-mediated immunity seems to play an important role where T-lymphocytes are said to produce vascular permeability factor which is responsible for massive proteinuria.

The Correct option is A

IgA NEPHROPATHY

General: a.k.a Berger Disease. Causes: Nephrotic syndrome

Epidemiology/At risk individuals: Most common type of GN worldwide, occurs 1-2 days after URTI/GIT infections in patients

Clinical features / course: There is an acquired or genetic defect in regulating production of IgA antibodies. After URTI / GIT infection, too much IgA is produced à forms immune complexes à trapped in mesangium à elicit alternate complement pathway à injury. Proteinuria + haematuria (Nephrotic syndrome). Progress to ESRF in 25-50% of patients.

Morphology: LM: mesangial proliferation, matrix deposition. IF: IgA in mesangium + C3.

Treatment: none.

The Correct option is C

“Extrahepatic bile duct obstruction” is a blockage of the biliary tree at the level of the extrahepatic or common bile duct or at the level of the liver bile ducts (may involve one, several, or all ducts, depending on the disorder) that results in the flow of bile being decreased or stopped (known as “cholestasis”)

CAUSES

· Associated with diverse disorders

· Presence of hard, solid material in the bile duct or gall bladder (known as “cholelithiasis”)

· Inflammation of the common bile duct (known as “choledochitis”); the extrahepatic or common bile duct empties into the upper small intestine

· Cancer

· Malformation of bile ducts

· Parasitic infestation (flukes)

· Compression of the bile duct from surrounding tissues (such as lymph nodes, cancer, inflammation of the pancreas [pancreatitis], diaphragmatic hernia)

· Scarring of the bile duct (known as “duct fibrosis”), such as secondary to trauma, inflammation of the lining of the abdomen (known as “peritonitis”), inflammation of the pancreas (pancreatitis); major duct involvement in some cats with inflammation of the bile duct or biliary tree (known as “cholangitis”) and inflammation of the bile ducts and liver (known as “cholangiohepatitis”)

· Narrowing of the bile duct, secondary to blunt trauma, surgical manipulations/procedures

The Correct option is A

Explanation:

Primary biliary cirrhosis (PBC)

first stage- destructive inflammatory lesions of multiple interlobar and septal small bile ducts characterized by granulomatous inflammation accompanied by dense mixed infiltrate in portal tracts

progressive lesion- global involvement of hepatic portal tracts with secondary obstructive changes and eventually with development of cirrhosis

end stage- indistinguishable from other forms of cirrhosis

The Correct option is E

Explanation:

Chronic active hepatitis- more progressive liver destruction

Micro: severe portal and periportal infiltrates of lymphocytes, plasma cells and macrophages, active destruction of hepatocytes in the vicinity of portal tracts- so-called piecemeal necroses, fibrosis and cirrhosis it is getting to be evident now that both forms are related may overlap

The Correct option is B

Explanation:

Patients with unconjugated hyperbilirubinemia should be examined for evidence of hemolysis. This includes reticulocyte count, examination of a peripheral smear, serum level of lactic dehydrogenase, and haptoglobin levels. The diagnosis of exclusion for unconjugated hyperbilirubinemia is Gilbert’s disease, which is a benign disease of a partial defect in the enzyme uridine diphosphoglucuronyl transferase (UDPGT), characterized by mild, chronic, and intermittent unconjugated hyperbilirubinemia.