Cellular Pathology Flashcards

1
Q

name 2 chemical mediators of inflammation derived from cells.

A

histamine

prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

name 2 chemical mediators of inflammation from the plasma.

A

heparin, plasmin

complement proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is oedema?

A

increased leaking of fluid through permeable capillaries into the interstitial space due to oncotic or hydrostatic pressures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is exudate?

A

any fluid that filters slowly from the circulatory system into lesions or inflamed areas, normally rich in proteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is transudate?

A

not due to inflammation, liquid that has passed through a membrane especially through the wall of a capillary, has a lower protein content and lower cell count than exudate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what cells are involved in acute and chronic inflammation?

A

neutrophils, mast cells, eosinophils, basophils

lymphocytes, macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the stages of healing and repair?

A

inflammation
proliferation
maturation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is healing by primary intention?

A

wound involves epidermis and dermis without total dermal penetration, wound edges can be brought together with sutures or tape.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is healing by secondary intention?

A

wound is allowed to granulate and contract and epithelialise by itself- for wider, deeper wounds.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the stages of bone healing?

A

haematoma
fibroblast inflammatory response-granulation
chondroblasts from hyaline cartilage
woven bone
lamellar bone- cancellous bone remodelled to compact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is Virchow’s triad?

A

stasis/turbulence of blood flow
hypercoagulability
endothelial injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is an embolus?

A

circulating bolus of matter- detached from an original source

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is a thrombus?

A

matter that can cause a clot to form in a blood vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is an infarct?

A

localised area of ischaemic necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is a haematoma?

A

collection of blood beneath an epithelium or membrane due to extravasation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is hyperaemia?

A

increased redness due to perfusion

17
Q

what are petechiae?

A

smaller sub dermal collections of blood, caused by capillary haemorrhage e.g. puerperic rash, vasculitic

18
Q

what pharmacological interventions can be used for the treatment of arterial thrombosis?

A

LMWH- Dalteparin

TPA - tissue plasminogen activator- alteplase

19
Q

how can venous thrombosis in a hospital patient be avoided?

A

encouragement of early mobilisation and graduated compression stockings have been proven to reduce the risk of thrombosis.

20
Q

atheroma affects mainly which layer of the blood vessel wall?

A

tunica intima

21
Q

describe the stages of development of an atheromatous plaque

A

endothelial dysfunction/damage-espression of adhesion molecules- monocyte recruitment- macrophages and inflammatory cells- LDL ingested and oxidised by macrophages- foam cells- fatty streak formation in intima- growth into plaque of fatty deposition- release of growth factors causes smooth muscle growth in intima and fibrous tissue cap over plaque.

22
Q

main risk factors for atheroma development

A
hypertension
diabetes
dyslipidaemia
smoking
genetic susceptibility (familial hypercholesterolaemia)
23
Q

what are the causes of bowel infarction?

A

bowel obstruction- volvulus
mesenteric ischaemia- thromobosis
can cause peritonism and septicaemia.

24
Q

consequence of atheroma in aorta

A

aneurysm, cerebrovascular accident, iliac thrombosis

25
Q

consequence of atheroma in the coronary arteries

A

angina, MI

26
Q

consequence of atheroma in renal arteries

A

renal artery stenosis- hypertension

renal failure

27
Q

consequence of atheroma in cerebral arteries

A

berry aneurysm

CVA

28
Q

what are the different types of aneurysm?

A

true aneurysm- involves all three layers of the arterial wall
false aneurysm- collection of blood leaking completely out of an artery or vein but confined next to the vessel by surrounding tissue (adventitia)- extravascular haematoma communicating with intravascular space
saccular or spherical

29
Q

what causes dilatation of a vessel wall?

A

atherosclerosis erodes the vessel wall making it less flexible and weakening it- inflammation, oxygen radicals, muscle cell apoptosis- high flow and pressure

30
Q

using Laplace’s law explain why an enlarging aneurysm is dangerous?

A

a narrower lumen has increased wall tension- this means more flow will be forced into the wider and less tense aneurym- causing it to enlarge.

31
Q

what are the main features of prokaryotes?

A
single circular chromosome
no nuclear envelope
plasmids
cell walls (except mycoplasma)
70s ribosomes
no organelles
can be flagellated
32
Q

list 4 commonly used techniques to identify and classify bacteria associated with an infection.

A

growth plate culture- maconkey agar- lactose fermenter. urease etc.
Gram staining using crystal violet
microscopy- shape and motility of bacterium
genetic sequencing and PCR- rRNA or DNA analysis.

33
Q

what is the causative agent in Whooping cough and name its staining and shape.

A

Bordetella Pertussis- Gram negative coccobacillus.