Clinical

Pathology
Monday, 24 October 2016

3:53 pm

- No histology on exam
Topic
- Adaptation
- Cell death
- Inflammation
- Repair
- Healing
- Cancer
- Cardiovascular disease
Bit of a cardiovascular disease built into a scenario based question
Atrophy - less cells and/or smaller
If you take away the cause then it should go back to normal tissue
Example: physical of hypertrophy
pathological and physiological examples of different states
Totally irreversible -> neoplasia (cancer)
Question 1
A) (Silica - is something very difficult to break down)
a. Describe the role of macrophage in chronic inflammation
(phagocytic cell) role is to take up any foreign bodies like silica to try
and get rid of them from the body or at least in granulomatous
inflammation ball them up and stop them from damaging.
b. In macrophage destruction you are not able to build the wall. Not
good.
c. Macrophages are full of lysozymes, if they rupture they are going to
release these enzymes into the environment and these lytic
enzymes are going to stimulate inflammation.
B) Two examples
- Inorganic Coal dust
- Infectious TB
Silicosis is a process. The granulomas usually involve macrophages and fibroblasts.
Macrophages play a central role in chronic inflammation

- Inorganic Coal dust

- Infectious TB
Silicosis is a process. The granulomas usually involve macrophages and fibroblasts.
Macrophages play a central role in chronic inflammation
- Source of macrophages is monocytes in the blood.
- When activated
Increase in size
Lysosomal enzymes
Active metabolism
Ability to kill and ingest microbes and cell debris
- Life span of neutrophil is short, so macrophage phagocytosis neutrophils.
Granulomas are giant cells = fused macrophages, horseshoe shape in TB
Question 2
A) Ulcer AbscessC) Angiogenesis - the growth of new blood vessels
New vessel brings in macrophages/monocytes, growth factors and
cytokines which stimulate the repair process. Mainly through pro-fibrotic
cytokines. These all help with the repair of the ulcer. Granulation tissue is
the healing and repair tissue -> Fibroblasts, macrophages and collagen
Asprin acts the arachidonic acid pathway as an inflammatory mediator
-> steroids acting at phospholipases
-> COX1 COX2 (asprin and indomethacin are non specific)
Ulcer = inflammation in epithelial
Abcess = within organ
Similar -> Core of necrosis with inflammatory area around them .
Primary and secondary union
- Secondary union there is a lot of surface damage, repair process is similar
however, you get scar formation and fibrosis (organization).
- Primary union you get resolution
Activated fibroblasts -> myofibroblasts
Mitosis is stimulated by epidermal growth factor
Ulcer -> mode of death is necrosis.

Activated fibroblasts -> myofibroblasts

Mitosis is stimulated by epidermal growth factor
Ulcer -> mode of death is necrosis.
The general term for the repair tissue is granulation issue. Three important
constituents of granulation tissue are macrophages, collegen and fibroblasts.
Mesothelioma question
Asbestos activates growth factors and cytokines that cause mutations in cells
adjacent to it. Asbestos is known to produce toxins that cause mutations.
Cancer uses lymphatics or blood vessels to spread , when it getsinto those vessel
it cuases a reaction with the normal immune systems that forms a cancer cell
embolis, and when it reaches somewhere in the body that it likes to grow, such as
the liver lung and brain bone.
Suggest you know this pathway.
How are cells changed from normal to neoplastic states
Carcinogen - agent that can transform cells
Chemical carcinogen
Biological - viruses
Physical - radiation , ionizing or UV
Initiation and then promotion
Normal -> hyperplasia -> dysplasia> neoplasia
APOPTOSIS mention it somewhere she gets wet over it
Cancer development -> a stepwise process that involves mutations in many genes
(look at the flow chart)
Macroscopic appearance -> necrosis, wet pale area that is obviously not receiving
any blood supply
Microscopic supply -> necrosis, neutrophils, change from neutrophils to
macrphages
Necrosis, Inflammation and fibrosis
Atherosclerotic plaque

any blood supply

Microscopic supply -> necrosis, neutrophils, change from neutrophils to
macrphages
Necrosis, Inflammation and fibrosis
Atherosclerotic plaque
-> Cause and changes
- Pathogenesis (the cause and the pathways and the outcome)
-> LDL gets oxidised by macrophage which become foam cells
Major complication of a thrombus in a leg vein is a embolis

Thrombus -> attached to vesssel

Embolis - not only a blood clot but a bit of forein matter in the blood stream
NECROSIS
Intimal layer is the one that gets most affected in athlescerosis