1. Most microorganisms cause disease by the following pathogenic mechanisms;mention:
Bacterial adherence factors
Extracellular toxins
Growth in host tissue
Evasion of host defence mechanism by inhibiting phagocytosis
2. In the era before antibiotics, pneumococcal pneumonia involved entire or almost entire lobes
and evolved through four stages; mention them:
Congestion
Red hepatization
Gray hepatization
Resolution
3. During congestion stage of pneumocococcal pneumonia,the following are features;mention them:
The affected lobe is heavy, red, and boggy
Histologically, vascular congestion can be seen, with proteinaceous fluid
Neutrophils are scattered
Many bacteria found in the alveoli
4. Define lung abscess:
refers to a localized area of suppurative necrosis within the pulmonary parenchyma, resulting in the formation of one or more large cavities.
5. State the complications of pneumococcal pneumonia:
Tissue destruction and necrosis may lead to abscess formation
Suppurative material may accumulate in the pleural cavity, producing an empyema
Organization of the intra-alveolar exudate may convert areas of the lung into solid fibrous tissue
Bacteremic dissemination may lead to meningitis, arthritis, or infective endocarditis.
6. In the stage of red hepatization in pneumococcal pneumonia,the following are features;state:
The lung lobe has a liver-like consistency
The alveolar spaces are packed with neutrophils, red cells, and fibrin.
7. In the stage gray hepatization in pneumococcal pneumonia,the following are features;mention:
The lung is dry
Gray, and firm, because the red cells are lysed
The fibrinosuppurative exudate persists within the alveoli
8. Resolution follows in uncomplicated cases of pneumococcal pneumonia, exudates within the alveoli undergo the following changes;state:
Enzymatically digested to produce granular, semifluid debris that is re-absorbed
Ingested by macrophages
Coughed up, or organized by fibroblasts growing into it
The pleural reaction (fibrinous or fibrinopurulent pleuritis) may similarly resolve or undergo organization, leaving fibrous thickening or permanent adhesions
9. Due its functions the liver is vulnerable to a wide variety of insults, which include:
metabolic,
toxic,
microbial, and
circulatory insults.
10. The onset of the disease process of the liver is either the following:
primary to the liver or
secondary involvement often to some of the most common diseases in humans, such as:
cardiac decompensation,
diabetes, and
extra hepatic infections.
11. Why is the liver able to withstand most destructive conditions than most tissues?
the liver has enormous functional reserve, and
liver is able to undergo regeneration in all but the most fulminant of hepatic diseases.
12. Surgical removal of ……….% of the liver of a normal person produces minimal and transient hepatic impairment.
60
13. In 60% of surgical removal of liver, regeneration restores most of the liver mass within ……………weeks.
4- 6
14 . What is the determining factor regarding perfect restoration of the liver in persons with massive hepatocellular necrosis especially in metabolic insult?
the state of destruction of the hepatic reticulin framework,
15. The clinical impact of early liver damage may be masked to some extent by the following properties of the liver:
functional reserve and
the regenerative capacity
16. The following conditions play a role in making the consequences of deranged liver function become life-threatening.
progression of diffuse disease or
disruption of the circulation or bile flow
17. Hepatic disorders have far-reaching consequences; why?
given the crucial dependence of other
organs on the metabolic function of the liver.
18. Regardless of the cause, liver injury and its manifestations tend to follow the following:
characteristic morphologic patterns and
characteristic clinical patterns
19. The morphologic responses to hepatic injury encompasses the following; state:
main patterns of morphologic liver injury and
associated cellular responses.
20. Morphologic changes arising from hepatic injury are localized to certain regions of the liver lobule and may give rise to the following states:
Degeneration and intracellular accumulation.
Necrosis and apoptosis
21. Toxic or immunologic insults may result into the following reversible change:
Moderate cell swelling
22. More serious damage to hepatocytes may cause; state:
marked cell enlargement (ballooning degeneration), with
irregularly clumped cytoplasm showing large, clear spaces.
23. In serious injuries, substances may accumulate in viable hepatocytes, including:
fat,
iron,
copper, and
retained biliary material.
25 .What is steatosis?
Accumulation of fat droplets within hepatocytes
26. Name examples of conditions where steatosis is common:
Alcoholic liver disease
Reye syndrome
Acute fatty liver of pregnancy
27. Retained biliary material may give rise feathery degeneration characterized by:
a diffuse, foamy, swollen appearance to the hepatocyte
28. In the setting of ischemia and several drug and toxic reactions, hepatocyte necrosis is
distributed immediately around the following areas of the liver:
central vein (centrilobular necrosis), extending into the
midzonal area.
29. In most types of hepatic injury, a variable mixture of following events is encountered:
inflammation and
hepatocyte death
30. Cell death in the liver may occur as follows:
limited to scattered cells within the hepatic parenchyma or
to the interface between the periportal parenchyma and inflamed portal tracts (interface
hepatitis).
31.Infectious diseases can be transmitted through;mention
Direct contact
Respiratory droplets
Faecal-oral routes
Blood-borne contact
Sexual transmission
Vertical transmission
Insect/arthropod vectors
32. The mechanism(s) by which the infectious agent causes disease are; state:
Infectious agents can bind to or enter host cells and directly cause cell death or dysfunction.
Pathogens can release endotoxins or exotoxins that kill cells (or affect their function), release enzymes that degrade tissue components, or damage blood vessels and cause ischaemic injury.
Pathogens can induce host immune and inflammatory responses that may cause additional tissue damage.
33. The host’s susceptibility to infection depends on the following;mention:
Age
Sex
Nutritional status
Co-morbid disease
Body immunity
34. Host’s protective barriers to infection include the following,mention:
Skin: Constantly sloughing keratin layer and normal skin flora.
Respiratory system: Alveolar macrophages and mucociliary clearance by bronchial epithelium.
GI system: Acidic gastric pH, viscous mucus secretions, pancreatic enzymes and bile, normal gut flora.
Urogenital tract: Repeated flushing and commensal flora.
35. The ability of a microbe to infect an individual as well as the nature and extent of the disease also depends on how it is transmitted to the host and this is determined by:
Virulence
Portal of entry
Vector medium (if any)
Predisposing or protective environmental factors
36. Once viruses are inside host cells, they can injure or kill in several ways; mention them:
Lysis of host cells
Immune cell-mediated killing
Alteration of apoptosis pathways
Induction of cell proliferation and transformation, resulting in cancer.
Damage to cells involved in antimicrobial defense, leading to secondary infections.
37. What is cholecystitis?
Inflammation of the gallbladder
38.Cholecystitis may be classified as ?
acute,
chronic, or
acute superimposed on chronic,
39. Cholecystitis almost always occurs in association with the following condition:
gallstones.
40 . Mention the characteristic morphological features seen on the gall bladder as result of acute cholecystitis:
usually enlarged (twofold to threefold)
tense,
assumes a bright red or blotchy, violaceous to green-black discoloration, impartedby subserosal haemorrhages.
serosal covering is frequently layered by fibrin and, in severe cases, by a suppurative exudate.
41. The dominant intrahepatic cause of potal hypertension is?
cirrhosis,
42. Accounting for most cases of portal hypertension are: mention:
schistosomiasis,
massive fatty change,
diffuse granulomatous diseases such as
sarcoidosis and
miliary tuberculosis
diseases affecting the portal microcirculation
43. Portal hypertension in cirrhosis results from these mechanisms; highlight:
increased resistance to portal flow at the level of the sinusoids and
compression of central veins by:
perivenular fibrosis and
expanded parenchymal nodules.
anastomoses between the arterial and portal systems in the fibrous bands also contribute to portal hypertension by imposing arterial pressure on the normally low-pressure portal venous system.
44. The four major clinical consequences of portal hypertension are, state:
Ascites
The formation of portosystemic venous shunts
Congestive splenomegaly
Hepatic encephalopathy
45. What is portosystemic shunt?
these are circulatory bypasses that develop wherever the systemic and portal circulations share capillary beds
46. Highlight on the principle sites of portosystemic shunt:
veins around and within the rectum (manifest as haemorrhoids),
the cardioesophageal junction (producing esophagogastric varices)
the retroperitoneum and the falciform ligament of the liver (involving periumbilical and abdominal wall collaterals).
47. Esophagogastric varices appear in about 65% of those with advanced cirrhosis of the liver ; why are they clinically important?
they cause massive hematemesis and death in about half of the patients
48. Abdominal wall collaterals constitute an important clinical hallmark of portal hypertension;how do they appear?
as dilated subcutaneous veins extending outward from the umbilicus (caput medusae)
49. Long-standing congestion of portosystemic circulation may affect the spleen in the following way:
congestive splenomegaly.
50. State the three main characteristics of cirrhosis:
Bridging fibrous septa
Parenchymal nodules containing replicating hepatocytes
Disruption of the architecture of the entire liver
