Pathology assignment

1st Term exam

Maha Khan

Roll No# 99

3rd Year MBBS

Submitted to: Dr. Bushra

Q7 a) vascular events of acute inflammation.

Ans: 1) vasoconstriciton
2) vasodilation
3) changes in vascular flow
4) increased permeability

Vasoconstriction: Before the phase of vasodilation, the vessels constrict for a short time
Vasodilation and changes in vascular flow : induced by mediators mainly, histamine. It
involves arterioles which then lead to opening of new capillary beds. This leads to increased blood
flow. Permeability of vessels also increases which will lead to the outflow of exudate. Low blood
volume leads to slow movement of blood, viscosity increases, leading to stasis of blood.
Increased permeability: contraction of endothelial cells leads to increased interendothelial
spaces. Elicited by histamine, bradykinin and leukotrienes.

b)
acute inflammation chronic inflammation
Causative agent pathogens, tissue injury acute-inflammation persists,
foreign pathogen not
eliminated,
cells involved neutrophils macrophages

mediators vasoactiveamines, eicosanoids Interferon gamma, cytokines

onset immediate delayed

Q8
a) a mass of granulation tissue, typically produced in response to infection, inflammation, or the
presence of a foreign substance.
it contains immune cells, mainly macropages.

b) immune granuloma: It has a T cell mediates immune response. Macrophaes activate T cells
which produce cytokines eg, IL2 and IFN-gamma. INF-gamma or IL4 transform the cells into
epithelioid cells and multinuclear giant cells thus forming granuloma.

C) leprosy and sarcoidosis.

Q9
a) phases of cutaneous healing: inflammation, proliferation and cutaneous healing.

Rapid activation of coagulation pathways to stop bleeding and also allows the migration of cells.
VEGF leads to increased vessel permeability.
Within 24hrs neutrophils migrate towards the fibrin clot. They clear the debris by releasing
enzymes. Within 24 to 48 hrs epithelial cells from both margins move towards each other along
the dermis.
By day 3, neutrophils are replaced by macrophages and granulation tissue progresses.
Collagen fibers are seen.
During 2nd week the process of blanching begins.

b) Local factors
growth factors trapping or deficiency
tissue hyoxia
Excessive exudates
Necrotic tissue
Systemic factors:
Diabetes mellitus
Malnutrition
Obesity
Anemia
Age

Q10
a) labile tissues: continuously dividing cells replaced by maturation from stem cells
examples : hematopoietic cells, surface epithelium
Stable tissues: cells are quiescent( G0phase) minimal prolidlferative activity
Examples: liver, kidney
Permanent tissues: cells are terminally differentiated and non proliferstive
Example neurons and heart cells.

b) infection, diabetes, nutritional status, poor profusion, type and extent of injury

Q11a) Shock is defined as a state of cellular and tissue hypoxia due to either reduced oxygen
delivery, increased oxygen consumption or inadequate oxygen utilization.
There is circulatory failure manifested as hypotension and reduced tissue perfusion
b) pathogenesis of septic shock

C) cardiogenic shock. MI, arrhythmia

Hypovolemic shock. . Fluid loss, vomiting
Shock with systemic inflammation microbial infection, trauma
Neurogenic shoc. Anesthesia, spinal cord injury
Anaphylactic shock IgE mediated

Q12
a) Infarction is obstruction of blood supply to an organ or region of tissue typically by a thrombus
or emboli

b)
Factors influencing infarct development :
nature of vascular supply
rate of development of occlusion
vulnerability of a given tssue to hypoxia
blood oxygen content

C) Renal infarct morphology :

Well-demarcated, wedge shaped.
triangular areas of coagulative necrosis
neutrophills and mononuclear cells infiltration patches in areas of necrosis
Fibrosis and capsule cell depressions spoted in chronic cases.