PATHOLOGY Flashcards
1
Q
what vascular change can occur due to acute inflammation?
A
changes in flow and vessel calibre such as vasodilation
2
Q
what can acute inflammation be caused by? (6)
A
infection injury trauma foreign bodies immune reaction necrosis of any cause
3
Q
describe vasodilation as an inflammatory response (3)
A
first involves arterioles then capillary beds
mediated by histamine and nitric oxide
results in increased heat and redness
4
Q
what does metaplasia commonly occur in response to?
A
a noxious stimulus
5
Q
what can cause a change in signals to stem cells that will cause metaplasia?
A
cytokines
growth factors
other chemicals in the cells microenvironment
6
Q
what does metaplasia represent?
A
a change in signals delivered to stem cells causing them to differentiate down a different line
7
Q
what is metaplasia?
A
the reversible change from one mature cell type to another mature cell type due to stress on the cell
8
Q
what are the precursor stages to neoplasia?
A
dysplasia
metaplasia
hyperplasia
9
Q
what occurs in epithelial malignancy?
A
malignancy goes beyond the basement membrane
10
Q
what does malignant mean?
A
neoplasm has metastatic potential which means it has the ability to spread to other sites
11
Q
where can neoplasms be found?
A
anywhere in the body
12
Q
what can a neoplasm be?
A
benign
premalignant
malignant
13
Q
is neoplasia in response to a stimulus?
A
no
14
Q
what does neoplasia mean?
A
new growth
15
Q
what can a tumour be?
A
benign
malignant
inflammatory
foreign body
16
Q
what is cancer?
A
uncontrolled cell proliferation and growth that can invade other tissues
17
Q
what are two causes of cellular necrosis?
A
oxidative stress
accumulation of toxic metabolic by products
18
Q
does apoptosis or necrosis cause a significant inflammatory response?
A
necrosis
19
Q
what cell clears up debris after apoptosis?
A
macrophages
20
Q
what happens to cells during apoptosis?
A
pyknosis
chromatin condenses and the nucleus breaks up
cytoplasm breaks up
21
Q
what is caused by too much apoptosis?
A
neurodegenerative diseases
22
Q
what is caused by too little apoptosis?
A
cancers
autoimmune diseases
23
Q
what does p53 do if DNA cant be repaired?
A
stimulates caspases and induces apoptosis
24
Q
name one protein that stimulates the caspase cascade that can be released from the mitochondria
A
cytochrome C
25
describe the intrinsic pathway in apoptosis
growth signals promote anti-apoptotic molecules in the mitochondrial membrane
when these are removed they are replaced by bak and bax
they increase the permeability of the mitochondria which leads to the release of proteins that stimulate the caspase cascade
26
what type of pathway is the intrinsic pathway?
mitochondrial
27
what do people with Fas mutations often get and why?
autoimmune diseases - Fas is involved in the recognition of self cells and can lead to apoptosis in lymphocytes
28
name two death receptors
tumour necrosis factor
| Fas
29
describe the activation of the extrinsic pathway for apoptosis
FasL binds to Fas receptor
activates Fas activated death domain
activates caspase cascade
30
what is a death receptor?
a cell membrane receptor with a death domain
31
what initiates the extrinsic pathway?
death receptors
32
what are the two mechanisms for apoptosis?
extrinsic pathway
| intrinsic pathway
33
what needs to be activated for apoptosis to occur?
the caspase cascade
34
what is pathological apoptosis in response to? (6)
```
injury
radiation
chemotherapy
viral infections
cancers
graft versus host disease
```
35
when is apoptosis physiological? (3)
part of normal growth - fingers and toes
removes self reactive lymphocytes
hormonal dependant involution - removes cells produced by hormones when not needed anymore
36
does apoptosis require energy?
yes
37
what do you ask for if someone has TB?
culture
PCR
result of Ziehl Neelson stain
38
what is caseous necrosis associated with?
TB
39
what is caseous necrosis?
granulomatous inflammation with central necrosis
40
what is liquefactive necrosis often the result of?
localised bacterial and fungal infections
| stroke in the brain
41
what happens during liquefactive necrosis?
no cell structure is left, it is all turned in to liquid
| pus is often produced
42
where is coagulative necrosis often seen?
in cardiac muscle after an MI
43
why cant processes such as proteolysis occur during coagulative necrosis?
the microenvironment formed is too toxic
44
what are dead cells consumed by in coagulative necrosis?
various enzymatic processes and cells
45
what is the most common form of necrosis?
coagulative
46
what is preserved in coagulative necrosis?
the outline of the cell
47
what are the three types of necrosis?
coagulative
liquefactive
caseous
48
what is necrosis always?
pathological
49
does necrosis require energy?
no
50
what are the two types of cell death?
apoptosis and necrosis
51
what is resolution?
complete restoration of the tissue to normal after removal of inflammatory components
52
what is what happens after inflammation dependent on and why?
the site of imjury - different capacity for repair and different vascular supplies
the type of injutry - severity
duration of injury - can it be removed, is it being sustained
53
when are mediators of inflammation produced?
only as long as the stimulus persists
54
what can progress to fibrosis?
suppuration
| chronic inflammation
55
what can occur after acute inflammation?
```
resolution
suppuration
repair
fibrosis
restitution
chronic inflammation
```
56
what cell characterises acute inflammation?
neutrophil
57
what is dolor and what is it mediated by?
pain
| prostaglandins and bradykinin
58
what is tumor and what is it caused by?
swelling
vascular changes i.e. leakiness of vessels
tumours, cysts, inflammation
59
what is calor and what is it caused by?
heat
| caused by increased perfusion, slow flow and increased vascular permeability
60
what is rubor and what is it caused by?
redness
| increased perfusion, slow flow and increased permeability of vessels
61
what are the clinical features of inflammation?
```
rubor
calor
tumor
dolor
loss of function
```
62
what do phagocytes produce that are used to kill and degrade foreign material?
reactive oxygen species - NADPH oxidase
reactive nitrogen species - nitric oxide synthase
cytotoxic granules
63
what do phagocytes use to engulf foreign material?
extensions of the cytoplasm called pseudopods
64
what are pathogens coated in that make them stand out?
proteins called opsonins
| - such as components of the complement cascade and imunoglobulin
65
what do phagocytes look for that is found on the surface of bacterial cells?
mannose
66
what are the three phases of phagocytosis?
recognition and attachment
engulfment
killing and degradation
67
what can make a chemical gradient for chemotaxis?
bacterial components
complement
leukotrienes
cytokines - interleukins
68
what is chemotaxis?
when white cells have moved out of the bloodstream and follow a chemical gradient and move along it
69
what is VEGF?
vascular endothelial growth factor
70
what mediates transcytosis?
VEGF
71
what causses endothelial contraction?
histamine
bradykinin
substance P
leukotrines
72
why do blood vessels become permeable?
endothelial contraction
direct injury
white cells causing harm to the inside of vessels
transcytosis
VEGF makes new vessels but also increases permeability
73
what does vascular permeability cause?
loss of proteins
change in osmotic pressure
water follows protein out the vessel = swelling
74
what do proteoglycans do?
increase the affinity of VCAM and ICAM for integrins
75
what do chemokines bind to?
proteoglycans on the surface of endothelial cells
76
what increases endothelial cell expression of VCAM and ICAM?
tumour necrosis factor (TNF)
| interleukin 1
77
what increases selectin expression?
histamine and thrombin from inflammatory cells
78
what increases the affinity of the ligands binding white cells to the luminal surface of blood vessels?
chemokines
79
what proteins are expressed in blood vessels and on white cells that slow flow during an inflammatory response
selectins (on endothelial cells and white cells)
integrins (bind to ICAM)
vascular cell adhesion molecule
intercellular adhesion molecule
80
what do vessels express during inflammation?
various proteins on the luminal surface that have a matching protein on the surface of the white cells
81
what is white cell margination?
larger white blood cells moving peripherally in blood vessels due to vascular dilation
82
what happens in normal blood flow?
blood flows centrally within a blood vessel
83
what cellular changes occur in acute inflammation? (5)
```
stasis
white cell margination
rolling
adhesions
migration
```
84
what are the different causes of disease?
```
vascular
infectious/inflammatory
neoplasia
drugs and toxins
iatrogenic
congenital
autoimmune
trauma
endocrine/metabolic
psychological
```
85
what is vascular disease?
disease in blood vessels including inflammation, clots and blockages
86
what does neoplasia mean?
new growth
87
what is iatrogenic disease?
caused by a doctor, medical complications
88
what is a congenital disease?
conditions someone is born with, not necessarily genetic
89
who is more likely to have a congenital disease?
young people
90
when does resolution occur? (4)
minimal cell death
tissue has the capacity to repair
good vascular supply
injurious agent easily removed
91
what is suppuration?
the production of pus
92
what does pus contain?
living, dead and dying cells
93
what is an empyema?
a space filled with pus that has been walled off
94
why wont an abscess go away by itself and why cant they be treated with antibiotics?
they have no vascular supply
95
what is needed to heal and repair any injury?
a good vascular system to deliver white cells and to remove injurious agents
96
what is organisation/restitution?
scarring
97
when does restitution occur?
when an injury produces lots of necrosis or fibrin
poor blood supply
tissue cant regenerate
98
what type of healing is favoured when the damage goes beyond the basement membrane of the epithelium?
restitution, because you need a basic structure to remain for resolution to occur
99
how does restitution occur?
defect infiltrated by capillaries and myofibroblasts
| deposit collagen and smooth muscle cells for things to be built upon
100
what can scarring and fibrosis cause?
loss of function and contraction
101
what is fibrosis in the liver called?
cirrhosis
102
what does cirrhosis result in?
liver failure, liver cant remove toxins or make proteins, disturbs large volume of blood that needs to flow through the liver
103
what does chronic inflammation not tell you anything about?
duration or severity of injury
104
what cell characterises chronic inflammation?
the lymphocyte (macrophages also present)
105
when is chronic inflammation favoured?
```
there is suppuration or scarring
persistent foreign injury
persistent infectious agent
autoimmune disease
transplant rejection
```
106
what is a granuloma?
aggregate of epithelioid histiocytes caused by an inflammatory response
107
what are granulomas caused by?
foreign bodies
endogenous substances
exogenous substances
infections such as parasites, worms, mycobacterium
