Pathology Flashcards
1
Q
vindicate V
A
vascular
2
Q
vindicate I
A
infection/inflammatory
3
Q
vindicate N
A
neoplastic
4
Q
vindicate D
A
drugs/toxins
5
Q
vindicate I
A
Interventions/iatrogenic
6
Q
vendicate c
A
congenital
7
Q
vindicate A
A
autoimmune
8
Q
vindicate T
A
trauma
9
Q
vindicate E
A
endocrine/metabolic
10
Q
what would neoplasia include
A
new growth
11
Q
what does Iatrogenic mean
A
something caused by a doctor
12
Q
what five things can cause inflammation?
A
trauma, injury, foreign bodies, immune reaction, necrosis of any cause
13
Q
what are vascular changes mediated by?
A
histamine and nitric oxide
14
Q
what are the four main changes to injury
A
vascular changes, cellular changes, chemical changes, chemical mediators and morphologic patterns
15
Q
what are the vascular changes in response to injury?
A
vasodilation, increased heat (calor) and increased redness (rubor)
16
Q
what are the five phases of cellular changes as a response to injury?
A
stasis, white cell margination, rolling, adhesions, migrations
17
Q
what is the change in flow during dilation?
A
the flow slows down
18
Q
why do blood cells start to stick to vessel walls during inflammation?
A
the vessels express various proteins on the lumen surface
19
Q
why do you want the blood vessels to be sticky?
A
so that WBC stick to the vessel wall and get to the tissue (lock and key ligands)
20
Q
what is margination?
A
the white blood cell moving to the vessel walls
21
Q
what do histamine and thrombin cells do from inflammatory cells?
A
they increase selection expression
22
Q
what do tumour necrosis factor and interleukin-1 do??
A
increase endothelial cell expression of VCAM and ICAM
23
Q
result of leaky vessels
A
loss of proteins, change in osmotic pressure, water follows protein and then swelling
24
Q
what is chemotaxis?
A
cells follow a chemical gradient and move along it
25
what are the three phases of phagocytosis?
recognition and attachment, engulfment and killing and degradation
26
what do bacterial surface glycoproteins and glycolipids contain?
terminal mannose residues. mammalian ones don't
27
what do opsonins do?
coat bacteria which makes them stand out from the crowd
28
what is the vesicle formation structure called?
phagosome
29
what is it called when the phagosome joins with a lysosome?
phagolysosome
30
what is the main cell of acute inflammation?
the neutrophil
31
what three things are the result of acute inflammation?
injury, vascular changes and cellular changes
32
briefly describe the vascular phase of acute inflammation?
vasodilation, increased permeability, stasis (slowing down of laminar flow)
33
wether tissues go through resolution, suppuration, repair organisation and fibrosis or chronic inflammation depends on what three things?
- site of injury. Different organs have different capacity for repair and vascular supplies
- type of injury. Severity, pathogenicity of organism
- duration of injury - can it be removed or is it sustained
34
what are the conditions for full repair (resolution)?
- minimal damage
- tissue/organ type. GI tract good but brain bad
- good vascular;ar supply for the delivery of WBC and removal of injurious agents
35
what is suppuration?
the production of pus
36
what does pus consist of?
living, dying and dead cells, neutrophils, bacteria, inflammatory debris (fibrin)
37
what is an empyema?
a space filled with pus and walled off
38
what is necrosis?
cell death
39
when will organisation of tissue happen?
when injury produces lots of necrosis (cell death) and lots of fibrin that isn't easily cleared. Also if there is a poor blood supply and debris can't be removed
40
conditions that favour suppuration?
persistence and virulence of causative agent
41
what is organisation?
replacement of damaged tissue by granulation tissue
42
common response to damage beyond the mucosae?
granulation tissue formation
43
what does granulation tissue do?
undergo organisation to form fibrous scar
44
what things are repaired with scar tissue?
severe, deep injury
cells that don't heal well
tissues with poor blood supply
45
disadvantage to scar tissue
it has no function
46
name for scarring and fibrosis in the liver
cirrhosis
47
result of liver cirrhosis
liver failure as there is a loss of liver function
48
what is chronic inflammation the result of?
- acute inflammation
- persistence of injury
- autoimmune (transplant rejection)
- viral infection
49
which type of phagocyte is better, neutrophil or macrophage?
macrophage
50
what is a granuloma
epitheliod macrophages and are surrounded by lymphocytes. They are giant
51
what can granulomas react to?
specific infections, parasites, worms, eggs, syphilis, mycobacterium (TB) and foreign bodies
52
does necrosis require energy?
no
53
what is tuberculous granulomas (TB) an example of?
caseous necrosis
54
what is the time limit for myocardium infarction that allows for a reversible change?
20 minutes
55
what are pyknotic cells?
cells that shrink
56
what do cells do first when they are damaged in MI?
shrink, become red, nucleus shrinks and becomes dark, marginal contraction bands appear
57
what vascular changes happen in the first 24 hours after MI?
vasodilation, slowing of flow, white cell margination, rolling, pavementing, diapedesis, chemotaxis and phagocytosis
58
what are neutrophils associated with? they accumulate at the site of?
acute inflammation
59
what two properties do neutrophils have?
phagocytic and cytokine production
60
what are the three types of necrosis?
caseous, liquefactive and coagulative
61
when is the greatest risk of cardiac rupture after myocardium infarction?
after 3-7 days
62
what are neutrophils replaced with during restitution?
macrophages
63
what happens when there is no atp?
the sodium potassium pump fails so there is a build up of K which leads to swelling
The calcium pump also fails. Increased calcium in the cell is bad
64
what does cardiac rupture look like?
a big hole in the heart
65
what happens after cardiac rupture? resolution? restitution?
restitution
66
what replaces macrophages during restitution?
fibroblasts
67
what do fibroblasts do?
lay down collagen and occur progressively after two weeks. Scar tissue is complete at 6 weeks
68
when you see restitution, think of....
fibroblasts laying down collagen and forming scar tissue
69
why does necrosis and apoptosis have to take over from hyperplasia and hypertrophy?
hypertrophy and hyperplasia only cope so far and they take time to happen
70
does necrosis require energy?
no, no ATP required
71
does necrosis happen normally?
no, always pathological
72
what is coagulative necrosis?
cell outline is preserved and dead cells are consumed by various enzymatic processes and cells
73
where is cogaulative necrosis often seen?
in cardiac muscle in myocardial infarction
74
what happens in liquefactive necrosis?
there is a liquid viscous mass that turns to liquid and then there is nothing left
75
what is caseous necrosis?
granulomatous inflammation with central necrosis
76
how to diagnose caseous necrosis?
ask for a culture, PCR, and look for the result of the Ziehl Neelson stain
77
does apoptosis require energy?
yes, in the form of ATP
78
examples of situations when pathological apoptosis is needed?
- in response to injury
- radiation (including UV light)
- chemotherapy
- viral infection
- cancers
- graft versus host disease
79
example of an extrinsic pathway death receptor?
tumour necrosis factor (TNF), Fas
80
what is Fas important in?
recognition of self antigens
81
what do people with Fas mutations often get?
Autoimmune diseases
82
what does p53 do if it senses cell damage that can't be repaired?
it halts the cell cycle, stimulates caspases and induces apoptosis
83
too little apoptosis leads to?
cancers and autoimmune diseases
84
too much apoptosis leads to?
neurodegenerative disorders, heart attacks and viral infections (hepatitis)
85
what are some causes for cellular ageing?
oxidative stress (free radical damage) and accumulation of metabolism by-products (lipofuscin)
86
if cells want to grow, one of two things can happen. what are the two things?
cells can produce more growth factors or produce more growth receptors
87
what is hyperplasia
an increase in the number of cells
88
what process happens for hyperplasia?
the cell cycle
89
four stages of the cell cycle
G1, S, G2, S
90
what are the three types of growth receptors?
- receptors with intrinsic tyrosine kinase activity
- 7 transmembrane G protein-coupled receptors
- receptors without intrinsic tyrosine kinase activity
91
what activates each CDK?
a specific cyclin
92
what happens during G1?
cell growth and protein synthesis
93
during G1, which cyclin activates CDK4
cyclin D
94
What does active CDK4 phosphorylate?
Rb Protein
95
normally, Rb is bound to...
E2F
96
when Rb has been activated by CDK4, it can no longer...
bind to Rb protein
97
what activates (phosphorylates) Rb protein?
CDK4
98
what will an unbound Rb protein do?
kick off cell division
99
what happens during S phase?
DNA replication
100
what does E2F do during s phase?
initiate DNA replication and increase levels of cyclin A
101
what does cyclin A do during s phase?
activate CDK2
102
What does activated CDK2 do during s phase?
promote DNA replication
103
what should the cell contain by the end of s phase?
two copies of its genome
104
what happens during G2?
more cell growth and protein synthesis
105
what do telomeres provide to chromosomes?
protection and stops chromosome fusion and degradation
106
what do telomeres consist of?
TTAGGG repeats
107
with every division, the number of repeats in telomeres gets...
smaller
108
what is the hay flick limit
50-70 divisions
109
when does compensatory hyperplasia happen and in which organs?
after loss of tissue, in the liver and bone marrow
110
when will lymph nodes undergo hyperplasia?
in response to infection
111
how can hyperplasia be reversed?
withdrawal of stimulus
112
what is hypertrophy?
increase in cell size and not cell number, often in response to mechanical stress
113
what is cell atrophy?
decrease in cell size
114
when might tissue undergo atrophy?
decreased work load, loss of function after nerve supply is removed, blocked blood supply, atherosclerosis, post menopausal uterus, inadequate nutrition, ageing, pressure due to endogenous or exogenous structures
115
what does stress on cells result in?
cellular adaptation
116
mechanisms of atrophy?
reduced cellular components, protein degradation and lysosome digestion
117
define cancer
uncontrolled proliferation and growth that can invade other tissues
118
what is neoplasia?
new growth not in response to a stimulus. Growth can be benign, premalignant or malignant
119
what is a malignant tumour?
a tumour with metastatic potential
120
what is a metastases tumour?
a tumour that has spread to other sites
121
what precursors can lead to tumours becoming malignant?
dysplasia (disordered growth), metaplasia (change from one mature cell type to another) and even hyperplasia
122
define metaplasia
reversible change form one mature cell type to another mature cell type
123
what can metaplasia be in response to?
cytokines, growth factors and other chemicals in cells microenvironment
124
what is dysplasia?
disordered growth, cells growing in an abnormal way beyond the basement membrane
125
what does CIS stand for?
carcinoma in-situ
126
what does carcinoma in-situ look like?
dysplasia affecting the whole of the epithelium
127
rank in order which is most likely to be maligant and which is least likely to be malignant? dysplasia, CIS, hyperplasia, metaplasia
```
MOST
-CIS
-dysplasia
- metaplasia
- hyperplasia
LEAST
```
