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PAT 90- Flashcards

1
Q

patterns of liver cell injury

A
  1. degenerative
  2. apoptosis
  3. necrosis of hepatocytes
  4. Regeneration of lost hepatocytes
  5. Scar Formation and Regression
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2
Q

how is the degeneration of liver cell injury

A

potentially reversible changes, such as
1. hydropic degeneration
2. accumulation of fat (steatosis)
3. bilirubin (cholestasis)

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3
Q

name of acidophilic apoptotic bodies in yellow fever

A

Councilman bodies

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4
Q

how the apoptosis occur in liver cells

A
  1. The hepatocytes undergo shrinkage,
  2. nuclear chromatin condensation (pyknosis),
  3. fragmentation (karyorrhexis),
  4. and cellular fragmentation into acidophilic apoptotic bodies
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5
Q

The principal cell type involved in scar
deposition in liver

A

hepatic stellate cell

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6
Q
A
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6
Q

what is the hepatic stellate cell in its quiescent form and in acute and chronic injury

A

In its quiescent form, it is a lipid (vitamin A) storing cell. However, in several forms of acute and chronic injury, the stellate cells can become activated and are converted into highly fibrogenic myofibroblast

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7
Q

viruses cause viral hepatitis

A

Epstein Barr virus [EBV], cytomegalovirus, and yellow fever virus
ABCDE hepatotropic viruses

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8
Q

hepatic viruses transmitted fecco oral

A

HAV
HEV

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9
Q

trasmission of HBV and HCV

A

a. By blood, blood components and contaminated instruments e.g. in intravenous (IV) drug abuse.
b. Sexual transmission
d. Transplacental transmission.

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10
Q

transmission of HDV

A

HDV infection can develop only when there is concomitant HBV infection

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11
Q

the most common cause of chronic hepatitis in Egypt

A

HCV

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12
Q

viral infection of increased hepatocellular carcinoma

A

HBV

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13
Q

causes fatal fulminant hepatitis in pregnant
women

A

HEV

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14
Q

hepatic viral infection do not cause chronic disease

A

HAV and HEV

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14
Q

hepatic viral infections are frequently sub-clinical

A

HAV and HBV

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15
Q

Acute asymptomatic infection with recovery in viral heaptitis based on

A

elevated transaminases, or by anti-viral antibody titers

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16
Q

Acute asymptomatic hepatic viral infection with recovery caused by

A

HAV and HBV

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17
Q

Acute symptomatic hepatic viral infection with recovery

A

HEV, HBV or HCV

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18
Q

The carrier state the of viral hepatitis caused by

A

HBV or HCV

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18
Q

Gross of acute viral hepatitis

A

Liver is enlarged and greenish yellow

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19
Q

Microscopic picture of acute viral hepatitis

A
  1. Liver cell injury :
    * Hydropic degeneration (ballooning) of hepatocytes.
    * Apoptosis of individual cells, resulting in acidophil bodies, usual with adjacent T cells (lobular hepatitis).
    * Focal necrosis (drop out), leaving collapsed reticulin network behind.
    Scavenger macrophages mark the sites of dopout.
    * In severe cases, confluent necrosis occurs, commonly centrilobular, or even central-portal bridging necrosis.
  2. Cholestasis:
    Accumulation of bile in the liver cells and bile canaliculi (obstructed by swollen hepatocytes)
    Kupffer cells engulf bile and undergo hyperplasia.
  3. Portal tract inflammation: In the form of mild mononuclear cell infiltration.
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20
Q

Clinical picture of acute viral hepatitis

A

Nausea, vomiting, abdominal pain followed by jaundice.

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21
Q

gross of Acute Massive Necrosis

A

Shrunken liver, mottled yellow (necrosis) and red (hemorrhage) areas, with wrinkled capsule

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22
Q

microscopic picture of Acute Massive Necrosis

A

Massive diffuse liver cell necrosis, sinusoidal rupture,
inflammatory cells (lymphocytes, macrophages, plasma cells)

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23
Q

patient develop post necrotic cirrhosis

A

patient that have survived from Sub massive Necrosis

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24
Q

def of chronic hepatitis

A

Chronic hepatitis is defined by the presence of symptomatic, biochemical, or serologic evidence of continuing or relapsing hepatic disease for more than 6 months, with histologically documented inflammation and necrosis

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25
Q

Etiology of chronic hepatitis

A
  • Viral etiology (most common): HBV (+ HDV) or HCV. Mixed infection may occur.
  • Autoimmune: Caused by autoantibodies as antinuclear antibodies & anti-actin antibodies.
  • Drug induced: Isoniazid, methyl dopa
  • Metabolic diseases as :
    (a) α 1 antitrypsin deficiency
    (b) hemochromatosis
    (c) Wilson’s diseases.
  • Cryptogenic (undetermined etiology).
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26
Q
A
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27
Q

Gross of chronic viral hepatitis

A

mild hepatomegaly

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28
Q

Def of chronic viral hepatitis

A

A chronic necro-inflammatory disease caused by** HCV or HBV**.
The pathological changes characteristically start at ‘the interface’, which is the **parenchymo- mesenchymal interface **between hepatic lobules and portal tracts

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29
Q

microscopic picture of chronic viral hepatitis

A

1) Inflammation: (in variable degrees)
* Portal inflammation: Expansion of the portal tracts by chronic inflammatory cells; mainly lymphocytes. Bile duct walls may be inflamed (mainly in HCV infection).
* Lobular inflammation (lobular hepatitis): Usually mild.

2) Necrosis: It may be:
* Piecemeal necrosis (interface hepatitis): This is inflammation with destruction of the liver cells at the limiting plates of liver lobules (i.e. the parenchymomesenchymal interface). The liver cells become detached.
* Spotty ( focal )
Confluent, bridging, or multiacinar necrosis occurs in severe cases.
* Apoptosis may also occur
3) Fibrosis: It may be:
Portal fibrosis, bridging fibrosis, or bridging fibrosis accompanied by regeneration nodules (cirrhosis)

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30
Q

Steatosis of hepatocytes related to

A

HCV

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31
Q

Ground glass hepatocytes related to

A

HBV

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32
Q

Complications of chronic viral hepatitis

A
  1. Post hepatitic cirrhosis.
  2. Liver failure.
  3. Hepatocellular carcinoma
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33
Q

Grading of Chronic Hepatitis based on

A

extent of interface hepatitis,
the degree of bridging necrosis,
the frequency of hepatocyte apoptosis
the density of portal inflammation

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33
Q

The most popular grading & staging systems are

A
  • Ishak scores the grade out of 18, and the stage out of 6. 6/6 is cirrhosis.
  • Metavir scores the grade from A0 to A4 and the stage from FO to F4. F4 is cirrhosis
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34
Q

solitary liver abscess

A

¨ Amoebic abscess.
¨ Infected hydatid cyst.
¨ Complicating cholecystitis.
¨ Traumatic (penetrating Injury)

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35
Q

Multiple liver abcesses

A

¨ Amoebic abscess.
¨ Abscesses of ascending cholangitis.
¨ Actinomycosis.
¨ Pyemic abscesses.

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36
Q

Etiology of amoebic liver abscess

A

Amoeba trophozoites enter portal venous radicals in colonic submucosa to reach liver

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37
Q

Gross of Amoebic Liver Abscess

A

§ Single, but may be multiple, large being mostly in right lobe.
§ Wall is necrotic & the lining is shreddy.
§ Its contents is a brown liquid material (chocolate pus).

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38
Q

microscopic picuture of Amoebic Liver Abscess

A
  • Amoeba in the liver causes necrosis, which becomes secondarily infected & purulent (the grossly yellow pus quickly turns brown due to excessive hemorrhage).
  • The wall of the abscess is composed of necrotic liver tissue with frequent vegetative forms of amoeba surrounded by a clear halo due to lytic enzymes secreted from the amoeba.
  • The inflammatory reaction consists of lymphocytes, plasma cells & macrophages.
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39
Q

etiology of Ascending Cholangitic Abscesses

A

Caused by mixed flora: E coli, staphylococcus aureus & anaerobic bacilli

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40
Q

pathological features of Ascending Cholangitic Abscesses

A
  • Multiple, yellow, small, abscesses,
  • mostly in portal tract areas around the bile ducts.
  • The bile ducts show all features of an acute suppurative Inflammation &
  • their lumen contains pus
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40
Q

liver abscess lined by irregular yellow membrane

A

Pyemic Abscesses

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41
Q

GRANULOMATOUS DISEASE of liver

A

tuberculosis, sarcoidosis, bilharziasis and primary biliary cirrhosis

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42
Q

Def of liver cirrhosis

A
  • Progressive necrosis of liver cells with destruction of liver architecture (framework).
  • Repair in liver cells by regeneration (regeneration nodules) and in framework by fibrosis.
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43
Q

Etiology and Types of liver cirrhosis

A

1- Post-Hepatitic Cirrhosis: Chronic viral hepatitis B and C
2- Post-Necrotic Cirrhosis
3- Nutritional and Alcoholic Cirrhosis (Laennec’s Cirrhosis)
4- Primary biliary cirrhosis ( intrahepatic biliary obstruction )
5- Secondary Biliary Cirrhosis
6- Cirrhosis caused by congenital metabolic disorders
7- Cirrhosis due to chronic venous congestion of the liver (cardiac cirrhosis)
8- obstruction of hepatic veins due to veno-occlusive disease and budd-chiari

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44
Q

other name of Nutritional and Alcoholic Cirrhosis

A

Laennec’s Cirrhosis

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45
Q

causes of Post-Necrotic Cirrhosis

A

due to viral hepatitis or toxic hepatitis caused by drugs as isoniazid or chemicals as carbon tetrachloride

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46
Q

carbon tetrachloride causes…….

A

Post-Necrotic Cirrhosis

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46
Q

causes of Secondary Biliary Cirrhosis

A

A Congenital biliary atresia.
S Gall stones.
C Compression by large lymph nodes

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47
Q

congenital metabolic disorders causes cirrhosis

A
  • Pigment cirrhosis: due to hemochromatosis (bronzed diabetes).
  • Wilson’s disease. Inherited disease, failure of liver to excrete copper in bile and copper accumulates in liver and brain).
  • Alpha 1 antitrypsin deficiency.
  • Glycogen storage disease.
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48
Q

main complications of cirrhosis

A

1) Liver cell failure.
2) Portal hypertension.
3) Hepatocellular carcinoma.

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48
Q

Gross of liver cirrhosis

A
  1. The liver is decreased in size and weight due to loss of liver tissue & fibrous tissue shrinkage.
  2. The surface and cut section are nodular. According to size of regeneration nodules , cirrhosis is classified into :
    * Micronodular cirrhosis: 1-3 mm in diameter. .
    * Macronodular cirrhosis: >3 mm in diameter.
    * Mixed micro and macro nodular cirrhosis.
  3. The color is :
    * Yellow in cases of nutritional or alcoholic cirrhosis (fatty change).
    * Green in case of biliary cirrhosis
    * Dark brown in case of hemochromatosis.
  4. Consistency is firmer than normal, edges are sharp & retracted cut section (due to fibrosis)
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49
Q

causes mixed nodular cirrhosis

A

post hepatitic cirrhosis

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50
Q

causes macro nodular cirrhosis

A

post necrotic
wilson

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51
Q

the color of the liver is yellow in which type of cirrhosis

A

nutritional or alcoholic cirrhosis and post hepatitic

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52
Q

the color of the liver is green in which type of cirrhosis

A

biliary cirrhosis

53
Q

the color of the liver is dark brown in which type of cirrhosis

A

hemochromatosis.

54
Q

microscopic picture of cirrhosis

A

1) Regeneration nodules:
- Regenerating hepatocytes are arranged in collections trying to simulate a liver lobule but the sinusoids are irregular and the central vein may be absent, and these masses of regenerating hepatocytes are totally surrounded by fibrous bands
- - Liver cells proliferate haphazardly so that the liver cell plates, which are normally one cell thick, are two cell thick and not radiating from the central vein.
- Regenerating liver cells may be binucleated & may also undergo dysplastic changes (predisposes to carcinoma).
- Other changes that may be observed according to the cause: necrotic foci, fatty change, hydropic changes, Mallory bodies or ground glass appearance of virus B infection.
2) Fibrosis:
- in the form of bands of collagen encircling the regenerating nodules & involving the portal areas.
- According to the presence or absence of inflammatory cells within the fibrous septae, cirrhosis is either active (i.e. contain lymphocytes, plasma cells & macrophages) or inactive.
3) The portal tracts are widened by the fibrosis, the inflammatory cells & show proliferating bile ducts & angiomatoids (opening of anastomosis between arteries and portal vein). In case with active. cirrhosis apart from inflammation , piecemeal necrosis ( interface hepatitis ) at the limiting plate may also be seen

55
Q

etiology of Primary Biliary Cirrhosis

A
  • This is an autoimmune disease.
  • In 95 % of cases serum anti-mitochondrial antibodies are detected.
  • The disease mostly affects middle-aged females.
55
Q

Gross of primary biliary cirrhosis

A

Liver is enlarged, green (bile-stained) with micronodular cut surface

56
Q

microscopic picture of primary biliary cirrhosis

A

4 stages:
1) Lymphocytes and plasma cells surround and infiltrate the medium. sized ducts, and granulomas may develop around the ducts . Finally most of the ducts disappear (ductopenia).
2) As result of ductopenia, proliferation of the small ductules occurs.
3) Stage of scarring: progressive fibrosis.
4) Stage of established cirrhosis: Cirrhosis is due to progressive liver injury caused by bile retention (cholestasis) due to ductopenia. Regeneration nodules are usually micronodular.

57
Q

There are three (overlapping) forms of alcoholic related liver disease

A

§ Hepatic steatosis (fatty liver).
§ Alcoholic steato-hepatitis.
§ Alcoholic cirrhosis.

57
Q

Etiology of alcoholic liver disease

A
  • Alcohol is metabolized in the hepatocytes producing toxic acetaldehyde.
  • This along with the malnutrition associated with chronic drinking results in acute liver disease
57
Q

NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD) is associated to

A

insulin resistance, diabetes mellitus, hypertension and dyslipidemia

57
Q

mechanism of alcoholic liver disease

A

Toxicity of alcohol leads to decreased fatty acid oxidation, increased synthesis of triglycerides & impaired secretion of lipoproteins by liver cell.
The associated malnutrition causes increased fat mobilization from stores & decreased lipotropic factors which results in steatosis.

58
Q

Liver failure is characterized clinically by

A

a. Hypoalbuminemia
b. Easy bruising due to clotting factor deficiency.
c. Jaundice
d. Ascitis:
e. Hyperestrenism
f. Encephalopathy
h. Hepatorenal syndrome

58
Q

cause of ascites caused by renal failure

A

hypoalbuminemia, portal hypertension and salt and water retention

59
Q

Hyperestrenism manifestions

A
  • spider nevi and telangiectasia
  • Loss of chest hair, change in distribution of pubic hair, testicular atrophy & gynecomastia (breast enlargement)
59
Q

Cause of portal hypertension in liver cirrhosis

A
  • Obstruction of portal blood flow by fibrosis and regeneration nodule
  • Transmission of arterial pressure to portal circulation via anastomosis between the arterial and portal veins in the fibrous septae of the liver.
  • Splanchnic arterial vasodilatation leading to increase in portal venous flow Effect of portal hypertension
60
Q

nodularity of cirrhosis causing hepatocellular carcinoma

A

macronodular

61
Q

breath odor of patient with liver failure

A

(rotten apple) called fetor hepaticus

62
Q

pre sinosoidal causes of portal hypertension

A

Portal vein thrombosis
- Tumor
- Infection
Portal tract fibrosis
- Schistosomiasis
- Sarcoidosis
- Biliary cirrhosis

63
Q

sinosoidal causes of portal hypertension

A

Cirrhosis

64
Q

post sinosoidal causes of portal hypertension

A
  • Veno-occlusive disease ( bush tea, some drugs )
  • Budd-Chiari syndrome ( hepatic vein thrombosis )
65
Q

portosystemic shunts leads to

A

Esophageal varices
Rectum (hemorrhoids)
Falciform ligament and umbilicus (caput medusa)

66
Q

f

A
67
Q

types of gall bladder stones

A

① Cholesterol stones:
Associated with hypercholesterolemia , obesity . diabetes and pregnancy .
So it is common in fatty fertile females in their forties.
② Pigment stone ( bilirubin stone ):
§ Pure pigment stone is associated with hemolytic anemia with increased excretion of bilirubin .
③ Mixed stones :
§ Cystic duct obstruction , producing 2ry infection & water absorption from the wall of gall bladder .
Contents become concentrated & the bile salts deposit around shedded epithelial cells & inflammatory exudate forming a mixed type of stone containing all components of the bile (cholesterol , pigment & calcium carbonate)

67
Q

Clinical Consequences Of Portal Hypertension

A

Ascites
Portosystemic shunts
Splenomegaly
Hepatic encephalopathy

68
Q

what is the combined galls stone

A

It is a cholesterol stone, which changes its appearance at the start of 2ry infection of the bile i.e. central cholesterol stone with outer mixed stone shell

69
Q

Morphology of cholesterol stone

A

Cholesterol stone
* is usually single 1-5 cms, yellowish-white, large & has a mamillated surface .
* On section, it has a radiating crystalline center .
* By X - ray it is radioluscent ( can’t be seen & needs a dye to be observed )

70
Q

morphology of Pigment stone

A
  • Pigment stones ( bilirubin stones ) : Multiple , small ,
  • dark & have a smooth surface .
  • On section, they are very dark.
  • By X ray, they are radiopaque.
71
Q

morphology of mixed stones

A
  • The stones are multiple , soft-firm , resulting in flattening of some surfaces when in contact with one another i.e. faceted .
  • On section they have a laminated cross section with different colored layers.
  • By X-ray it is radiopaque.
72
Q

Complications of Gall bladder stones

A

Predisposes to carcinoma
cholecystitis
Acute pancreatitis
obstruction of the common bile duct causing colic and jaundice
obstruction in the intestine by gall stone passing through fistula
obstruction of cystic duct causing mucocele and hydrops

1 carcinoma 2 inflammation 3 obstruction

73
Q

Etiology of acute cholecystitis

A

obstruction of cystic duct

74
Q

Complications of acute cholecystitis

A

1) Gangrene
2) Perforation resulting in septic peritonitis
3) Adhesions and fistulous tract between gall bladder and duodenum leading to passage of gall stone to the intestine.
4) Chronic cholecystitis

75
Q

Rokitansky-Aschoff sinuses related to

A

CHRONIC CHOLECYSTITIS

76
Q

Complications of chronic cholecystitis

A

1- Repeated acute attacks.
2- Gall stone formation.

77
Q

Definition of Acute Hemorrhagic Pancreatitis

A

Acute inflammation of the pancreas

77
Q

Most gallbladder carcinomas are

A

adenocarcinomas

77
Q

microscopic picture of chronic cholecystitis

A

Rokitansky-Aschoff sinuses

78
Q

diagnostic marker of acute hemorrhagic pancreatitis

A

marked elevation of serum amylase

79
Q

morphology of acute hemorrhagic pancreatitis

A
  1. Early the gland is swollen , edematous and hyperemic .
  2. Proteases digest the wall of blood vessels with extravasation of blood , and the inflammation becomes hemorrhagic. Amylase is released in the blood and is a diagnostic marker of the condition.
  3. Lipases cause fat necrosis of peri - pancreatic fat which can be quite extensive within the abdomen .
    Fat necrosis appears as chalky white areas due binding of calcium
80
Q

Etiology of acute hemorrhagic pancreatitis

A

Pancreatic necrosis , hemorrhage and inflammation may be due to :
1- Obstruction of ampulla of Vater by gall stone .
Thus bile passes into pancreatic duct and activates trypsinogen into trypsin which digests the pancreatic tissue .
2- Excess alcohol abuse may lead to increased secretion of pancreatic juice and
contraction of sphincter of oddi leading to rupture of pancreatic duct.
3- Accidental surgical injury of pancreas.
4- Hyperparathyroidism.
5- Polyarteritis nodosa.
6- Viral and bacterial infection

81
Q

Complications acute hemorrhagic pancreatitis

A
  • Death ( 5 % of patients ) can occur from shock , acute respiratory distress syndrome or acute renal failure .
  • Pancreatic pseudocysts can result from accumulation of liquefied necrotic material.
81
Q

Complications of chronic Pancreatitis

A

1- Malabsorption.
2- Diabetes mellitus.
3- Pseudocysts.

82
Q

the most common secondary tumors of peritoneum

A

ovarian and pancreatic adenocarcinomas are the most common

83
Q

Majority of pancreatic cancers arise in which part of pancreas

A

head of the gland, followed by the
body then the tail

84
Q

congenital anomalies of kidney

A
85
Q
A
86
Q

complete absence of one kidney

A
86
Q

Failure of the kidney to develop to the normal size

A

Hypoplasia of kidney

87
Q
  • Double or extra renal pelvis,
  • Anomalies in renal arteries &
  • Double ureters
A

Miscellaneous
anomalies

88
Q

cause of adult polycystic kidney

A

failure of fusion of convoluted
and collecting tubules

89
Q

account for 20% of renal failure in
children

A

Renal dysplasia and renal hypoplasia

90
Q

disease associated with congenital cystic liver & congenital cerebral aneurysms

A

Adult Polycystic Kidney

91
Q

Both kidneys are fused together

A

Horse shoe
kidney

91
Q

kidney fails to migrate up to normal position
& remains in the pelvis.

A

Ectopic
kidney

92
Q

Gross of Adult Polycystic Kidney

A
  • Kidneys:
     enlarged & may reach enormous size
     may weigh up 4 Kg
  • Cysts:
     variable sizes
     clear or bluish content.
     may be communicating together but not with the renal pelvis.
93
Q

microscopic of Adult Polycystic Kidney

A
  • Cysts:
    lined by flat or cubical epithelium
  • Nephrons:
    detected between the cysts.
94
Q

type of congenital anomaly of infantil polycystic kidney

A

autosomal recessive
anomaly

94
Q

is the most common cause of chronic renal
)ملحوظه هامه( failure

A

Chronic glomerulonephritis

95
Q

is the most common type of glomerular injury as glomerular deposits of immunuglobulins

A

Antibody mediated injury

95
Q

Two forms of antibody mediated injury of glomerular

A

➢ The antibodies react directly with intrinsic tissue antigens (Anti GBM nephritis) or planted antigens (IgA nephropathy).
➢ Deposition of circulating antigen antibody complexes in the glomeruli

96
Q

clinical picture of adult poly cystic kidney

A

 Hematuria
 Hypertension
 Secondary infections
 Chronic Renal Failure (CRF)

97
Q

clinical picture of nephritic syndrome

A

➢ hematuria
➢ hypertension (mild/ moderate )
➢ proteinuria
➢ edema
➢ oliguria

98
Q

nephritic syndrome is presenting feature of

A

acute post
streptococcal glomerulonephritis

99
Q

clinical picture of nephrotic syndrome

A

proteinuria( more than 3.5 gm/day) :-
➢ hypoalbuminemia
➢ severe edema
➢ hyperlipidemia
➢ lipiduria (lipid in urine)

100
Q

Acute Diffuse Proliferative GN is caused by

A

group A beta hemolytic streptococci

101
Q

location of deposition of ADPGN

A

subepithelial humps

102
Q

Etiology of Rapidly Progressive G.N

A

) Post infectious:
▪ follow acute diffuse proliferative GN, especially in adults
2) systemic disease:
▪ as poly arteritis nodosa (PAN) SLE &Good pasture syndrome.
3) Idiopathic.

103
Q

microscopic of ADPGN

A
  • Glomeruli
    Enlarged and hypercellular due to proliferation of endothelial mesangial and epithelial cells
  • the tubules
    show hydropic degeneration and may contain red Cell and granular casts.
  • The interstitium
    is edematous and may be infiltrated by neutrophils
104
Q

Course of Acute diffuse

A

1) Complete recovery in
▪ 95% of children and
▪ 65% of adult.
2) Severe hypertension leading to:
▪ acute heart failure (AHF) or
▪ acute renal failure (ARF).
3) Progress to
▪ rapidly progressive GN or
▪ chronic GN

104
Q

Gross of rapidly progressive GN

A

kidneys are pale, enlarged with petechial hemorrhages on the outer surface

105
Q

Micro of rapidly progressive GN

A

➢ Glomeruli :-
 enlarged,
 hypercellular showing proliferation of endothelial , mesangial,
epithelial cell & leucocytic infiltration.
 glomerular necrosis and may be glomerular capillary thrombosis.
➢ Crescents :-
 formed in the Bowman space and compressing the tufts.
 They are formed of proliferating parietal epithelial cells, fibrin and
migrating monocytes and leucocytes
➢ By immunofluorescence microscopy(I/F) :-
 in Goodpasture syndrome there is linear deposition
of IgG andC3 along GBM.

106
Q

Course of rapidly progressive GN

A

 Acute renal failure.
 Hypertension.
 Pulmonary hemorrhage in Goodpasture syndrome

107
Q

It is one of the most common cause of nephrotic syndrome in adult

A

Membranous Nephropathy

108
Q

infections causes Membranous Nephropathy

A

Hepatitis B & C and Bilharziasis

109
Q

Etiology of membreanous GN

A

A) Idiopathic 85% of patient.
B) It may occur in association with:
✓ systemic disease as carcinoma SLE,
✓ infections (Hepatitis B & C and Bilharziasis )
✓ metabolic disorders.
✓ Drugs

110
Q

GN that deposit IgG and C3

A

ADPGN
RPGN
MGN
MPGN 1 and 3

111
Q

It is the most common cause of NS in children (2-6 years)

A

Minimal Change Disease

112
Q

diseases considered Nephrotic

A

minimal change
membranous GN

113
Q

diseases considered nephritic

A

ADPGN
RPGN

114
Q

diseases considered mixed

A

MPGN
focal segmented
focal proliferative
IgA nephropathy

115
Q

types of MPGN

A

type 1: Sub endothelial and mesangial deposits of IgG and C3
type 2: rregular electron dense deposits of C3 in the GBM and mesangium
type 3: Sub epitheial ,mesangial and some subendothelial deposits of IgG and C3

116
Q

definition of Focal Segmental Glomerulosclerosis

A

It is characterized by sclerosis of only portion of the capillary tuft (segmental) in some glomeruli(focal)

117
Q

Secondary causes of FSGS

A

heroin abuse or AIDs.

118
Q

location of sclerosis and hyalinosis in FSGS

A

Juxtamedullary ones

119
Q

IgA deposition

A

IgA nephropathy
FPGN

120
Q

IgM and c3

A

FSGS

121
Q

C3 only

A

MPGN 2

121
Q

IGM and C3

A

FSGS
FPGN

122
Q

etiology of FPGN secondary to

A

➢ Upper respiratory tract infections
➢ PAN
➢ SLE
➢ Henoch-Shoenlein purpura

PAT (5 decks)

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