Q3- 1998)

1) The pathophysiology of generalised edema in congestive heart

failure

2) -Congestive heart failure causes generalized edema

3) -the pathogenesis of cardiac failure is complex and the main contributory

factor is increase venous hydrostatic pressure

4) -in congestive cardiac failure, the cardiac output is reduced and it

translates into renal perfusion and trigger RAA axis

5) -in RAA axis, renin is secreted by JGA and it stimulate the conversion of
angiotensinogen to angiotensin 1.angiotensin converting enzyme convert
angiotensin 1 to angiotensin 2

6) -angiotensin 2 increases the sodium and water retention by kidney and it

consequently increase volume of the blood.

7) -if the heart cannot increase the cardiac output,the extra fluid load causes
increase venous pressure and eventually edema.

8) Reference: notes edema (increase hydrostatic pressure)

9)

(Q1,2 1997)

Short note (1997)

(carcinogen and their role in carcinogenesis)

1. Carcinogen is an agent known or suspected to participate in the causation

of tumors

2. Site of action : DNA

3. Carcinogen is a mutagen

4. More than one carcinogen necessary to produce tumor

5. The process are several steps=multistep hypothesis

6. 85% of cancer risk is due to environmental agents

7. Carcinogen may identified from:

- Epidemiological studies
 - Assessment of occupational risk

- Direct accidental exposure

- Carcinogenic effects in laboratory animals

- Transforming effects on cell cultures

8. Carcinogenic agents are the agents that cause genetic damage and induce
neoplastic transformation include:

- Chemical carcinogen

- Radiant energy

- Oncogenic viruses and some other microbes

9. Carcinogenesis is the process which result in the transformation of normal

cell to neoplastic cell by causing permanent genetic alterations

10.Tumors arise from a single cell due to cumulative mutational events and it
is a multistep process

11.Involves stages of initiation and progression

VENOUS THROMBOSIS

• Mainly by coagulation cascade

• Platelets play a secondary role

• Form in sluggish venous circulation

• Most occur in lower extremities. About 90%

• Thrombophlebitis. For example, superficial varicose vein

• It is associated with stasis

• Always occlusive

• Easily detachable

• Embolisation

• Tributaries always present.

(Q1 -2004)
1. Shock

Definition; a clinical syndrome characterized by systemic hypoperfusion which is

caused by either reduced CO or by reduced effective circulating blood volume.
The end results are; hypotension, impaired tissue perfusion and cellular hypoxia.
There are 4 type of shock;

1- Cardiogenic shock
a. Cause: any form of heart damage
b. Eg: MI, acute mitral regurgitation, myocarditis

2- Hypovolemic shock
a. Cause: any condition providing a major reduction in blood volume
b. E.g. : internal and external hemorrhage, severe burns, dehydration

3- Septic shock
a. Cause: infection or other causes of systemic inflammatory response
that produce widespread endothelial damage with vasodilation,
atrivenous shunting, microvascular occlusion and tissue oedema
b. E.g. : resulting in organ damage

4- Anaphylactic shock
a. Cause: inappropriate vasodilation triggered by an allergen
b. E.g. : bee sting, allergic reaction

5- Neurogenic shock
a. Cause: caused by major brain or spinal injury of brain stem and
neurogenic vasomotor control
b. E.g. : maybe associated with neurogenic pulmonary edema

(Q1- 1999)
QUESTION 1

Malignant neoplasms are characterized by a wide range of parenchymal

cell differentiation from a surprisingly well differentiated to completely
undifferentiated. For example, the adenocarcinoma colon are malignant tumour
varies in differentiation.

Malignant neoplasms that are composed of undifferentiated cells are said

to be anaplastic. Anaplastic cells display marked:

-Pleomorphism:-cellular pleomorphism

-nuclear pleomorphism

-Nuclear hyperchromasia

-Nuclear cytoplasmic ratio

-Presence of larger nucleoli

-Number of mitosis

-Presence of tumour giant cell

-Disorientation
-Abnormal karyotype

The characteristics of mode of growth of malignant tumours by the:

-Infiltrative, crab-like, claw-like extensions into adjacent tissue

-No capsule

-Extend and infiltrate lymphatics, vascular spaces, perineural

sheaths

QUESTION 2

2) a) Define embolism

An embolus is a detached intravascular solid, liquid, or gaseous mass that is

carried by the blood to a site distant from its point of origin. the vast
majority are part of a dislodged thrombus

b) List the type of embolism

Pulmonary Thromboembolism

• 95% of cases, venous emboli originate from deep leg vein thrombi
above the level of the knee .They are carried through progressively
larger channels and pass through the right side of the heart before
entering the pulmonary vasculature.

• the patient who has had one pulmonary embolus is at high risk of having
more

• Rarely, entering the systemic circulation.

Systemic Thromboembolism

• emboli in the arterial circulation

• Most (80%) arise from intracardiac mural thrombi, remainder originate

from aortic aneurysms, thrombi on ulcerated atherosclerotic plaques, or
fragmentation of valvular vegetations

• arterial emboli can travel to a wide variety of sites; the site of arrest
depends on the point of origin of the thromboembolus and the relative
blood flow through the downstream tissues

• The major sites for arteriolar embolization are the lower extremities (75%)
and the brain (10%), with the intestines, kidneys, and spleen affected to a
lesser extent
Fat Embolism
• Microscopic fat globules can be found in the circulation after fractures of
long bones (which contain fatty marrow) or after soft-tissue trauma

Air Embolism
• Gas bubbles within the circulation can obstruct vascular flow (and cause
distal ischemic injury)

• A particular form of gas embolism, called decompression

sickness, occurs when individuals are exposed to sudden changes in
atmospheric pressure. Scuba and deep-sea divers, and underwater
construction workers are at risk.

Amniotic Fluid Embolism

• cause is entry of amniotic fluid (and its contents) into the maternal
circulation via a tear in the placental membranes and rupture of uterine
veins

• contain - squamous cells shed from fetal skin, lanugo hair, fat from
vernix caseosa, and mucin derived from the fetal respiratory or
gastrointestinal tracts

SOURCES: 1.Lecturer’s notes

2.Robins Basic Pathology

(Q1-2006)
The pathogenesis of hepatic steatosis in alcohol abuse.

• Hepatic steatosis is also known as fatty liver

• It is an accumulation of small lipid droplets in hepatocytes which can be
seen as fatty globules under the microscope.
• It is an early, asymptomatic and reversible consequence of chronic alcohol
assumption.
• Initially, the hepatocytes presents small fat vacuoles ( liposomes ) around
the nucleus – microvesicular fatty change in this stage, liver cells are filled
with multiple fat droplets that do not displace centrally located nucleus.
 • In the late stages, the size of vacuoles increases pushing the nucleus to
the periphery of the cell giving characteristics signet ring appearance –
macrovesicular fatty change. These vesicles are well-delineated and
optically “empty” because fats dissolve during tissue processing.
• Macroscpically, the fatty liver of chronic alcoholism is large ( <4-6 kg ),
soft, yellow, and greasy.
• Although there is no or little fibrosis at the outset, with continued alcohol
intake, fibrous tissue develops around the central veins and extends into
adjacent sinusoids.
• Until fibrosis appears, the fatty change is completely reversible if there is
abstention from further intake of alcohol.
• The metabolism of ethanol is required for hepatic injury to occur, although
variations in ethanol metabolism do not completely explain the variable
susceptibility to alcoholic liver disease.
• Ethanol first metabolized I liver to acetaldehyde, this process primarily
occurs in the hepatocyte cytosol via reaction catalyzed by the enzyme
alcohol dehydrogenase (ADH ). There are multiple forms of dimeric ADH
molecule,
• Large amounts of alcohol enhance lipolysis because of direct stimulatory
effect on adrenal and pituitary axis.
• Clinical features : hepatomegaly with mild elevation of serum bilirubin and
alkaline phosphatase.

(Q2 -2008)

THE OUTCOMES OF ACUTE INFLAMMATION

The acute inflammatory response is aimed at neutralizing or inactivating the

agent causing the injury. There are several possible outcomes:

1) Resolution: in uncomplicated acute inflammation, tissue returns to normal

in a process of resolution, in which the exudate and cellular debris are
liquefied and removed by macrophages and lymphatic flow.

2) Repair: when tissue necrosis has occurred before the agent is neutralized,
repair ensues, and dead cells are either replaced by regeneration or
repaired by scar formation.

3) Suppuration: in virulent bacterial infections, exaggerated emigration of

neutrophils with liquefactive necrosis occurs (suppurative inflammation).
 The liquefied mass of necrotic tissue and neutrophils is called pus. When
an area of suppuration becomes walled off, an abscess results.

4) Chronic inflammation: when the noxious agent is not neutralized by the

acute inflammatory response, the body mounts an immune response,
which leads to chronic inflammation

(Q3-2009)
1. Gross and microscopic features of benign and malignant neoplasm.

- Anaplastic cells display marked pleomorphism (i.e., marked variation in

size and shape).

- Nuclear pleomorphism.

- The nuclei are extremely hyperchromatic (darkly stain) and large.

- The nuclear-to-cytoplasmic ratio may approach 1:1 instead of the

normal 1:4 or 1:6.

- Presence of larger nucleoli.

- Presence of tumour giant cell.

- Mitoses are often numerous and distinctly atypical; anarchic multiple

spindles may be seen and sometimes appear as tripolar or quadripolar
forms.

- Fails to develop recognizable pattern of orientation to one another.

- Abnormal karyotype.