General - Pathogenesis Flashcards
1
Q
285
Dystrophic calcification (Infracus renis anemicus)
Pathogenesis
A
- Infract causes tissue damage causing inflammation, degeneration, cell death and protein denaturation
- This causes calcification
- Granulation tissue prevents further infiltration of the pathological process
2
Q
225
Hemosiderosis of spleen (Liesegang)
Pathogenesis
A
- Haemosiderin is an endogenous (yellow, beown) pigmentation
- They are released from erythrocyte breakdown
- Occurs in the spleen and other organs of monocyte-macrophage system (lymph nodes, liver, kidneys)
3
Q
33
Necrosis hepatis centrolobularis
Pathogenesis
A
- Seen under conditions of viral infection, hypoxia or anaemia from failing circulation
- Causing necrosis of the hepatocytes in a particular zone of the tubules results in dilation and congestion of the sunusoid
- Necrosis is the death of tissue in a living organism
4
Q
180
Necrosis hepatis focalis
Pathogenesis
A
- Simple coagulative necrosis occurs when trabecular structure of the tissue is preserved through the necrotic process
- Heterolysis occurs when cells are degraded by other cells
5
Q
187
Infractus renis anemicus
Pathogenesis
A
- Infract (obstruction of blood supply) causes tissue damage leading to necrosis, nuclear karyolysis is present in coagulative necrosis
- Affected areas of kidney are surounded by normal structures and function
6
Q
223
Chronic passive hyperemia of liver
Pathogenesis
A
- Any cause of increase of pressure within the hepatic beins and sinusoids, disturbes blood drainage causing congestion
- Leading to hepatocellular hypoxia, kupffer cell activation and collagen deposition = liver fibrosis
- Eventually the reduced blood flow exacerbates heparic dysfunction
7
Q
25
Pleuritis fibrinosa (repair by organisation)
Pathogenesis
A
- Inflammatory stimulus leads to mediator release and the pleural blood vesel permeability increases
- Fibrin deposition occurs an accumulates in the pleural space, and eventually organises into fibrous scarring
- Often accompanied by crupous inflammation in the lungs
8
Q
148
Fibrosis myocardii
Pathogenesis
A
- Repair of damaged myocardium, when arising granulation tissue mature to high differentiated connective tissue during healing
9
Q
255
Bronchopneumonia purulenta
Pathogenesis
A
- Infectious agent, usually bacteria, triggers inflammatory response
- Exudate then forms with neutriphils predominating as main cell population
- Accumulation causes consolidation of the lung tissue
10
Q
253
Pericarditis fibrinosa
Pathogenesis
A
- Small amount of fibrin leaves the vessels and settles in the pericardium, where it proliferates
- Demonstrates acute stadium of serosal fibrinous inflammation
- Production of fibrous tissue represents healing of fibrinous inflammation
11
Q
166
Cirrhosis hepatis
Pathogenesis
A
- Fibrous tissue originates from interlobular spaces and moves into lobule centers, causing press atrophy of parenchyma
- Proliferation of interstitial tissue leads to fibroblasts forming fibrous connective tisue
- Biliary hyperplasia is associated with peribiliary fibrosis
12
Q
201
Actinomycosis
Pathogenesis
A
- Affects one part of the jaw, in tisse and bone (“lumpy jaw”)
13
Q
263
Pneumonia TBC miliaris - poultry
Pathogenesis
A
- Formation of tiny granulomas in the lungs lead to respiratory signs after infection with Mycobacterium
14
Q
264
Pneumonia TBC miliaris - poultry with Ziehl-Nielson
Pathogenesis
A
- Formation of tiny granulomas in the lungs lead to respiratory signs after infection with mycobacterium
- During gerneralised TBC process, the lungs tend to be the last organ receiving tubercule dissemination
15
Q
219
Adenoma and adenocarcinoma sabaceum
Pathogenesis
A
- In adenomas there may be necrotic changes in the nuclei
- In adenocarcinoma the alveolar centers undergo regressive changes such as dystrophy and necrosis
