Pathology Flashcards
1
Q
What is acute inflammation?
A
Initial response of tissue to injury
2
Q
Describe the onset of acute inflammation.
A
Early onset (seconds to minutes)
3
Q
How long does acute inflammation last?
A
Short duration (hours to days)
4
Q
What cells are involved in acute inflammation?
A
Neutrophils and monocytes
5
Q
What steps are involved in acute inflammation?
A
Vascular and exudative component and recruitment of neutrophil polymorphs
6
Q
What is the vascular component of acute inflammation?
A
Dilation of vessels
7
Q
What is the exudative component of acute inflammation?
A
Vascular leakage of protein-rich fluid
8
Q
What are the causes of acute inflammation?
A
Microbial infections, hypersensitivity reactions, physical agents, chemicals, bacterial toxins and tissue necrosis
9
Q
What are some causes of microbial infections?
A
Bacteria, viruses
10
Q
What are some causes of hypersensitivity reactions?
A
Parasites
11
Q
What physical agents can cause acute inflammation?
A
Trauma, heat, cold
12
Q
What chemicals can cause acute inflammation?
A
Corrosives, acids
13
Q
Give a cause of tissue necrosis.
A
Ischaemic infarction
14
Q
What are the 5 characteristics of acute inflammation?
A
Rubor (redness), calor (heat), tumor (swelling), dolor (pain) and loss of function
15
Q
What is rubor?
A
Redness
16
Q
What is calor?
A
Heat (only peripheral in acute inflammation)
17
Q
What is tumor?
A
Swelling
18
Q
What is dolor?
A
Pain
19
Q
What causes redness in acute inflammation?
A
Dilation of small vessels
20
Q
What causes swelling in acute inflammation?
A
Oedema or a physical mass
21
Q
How are vessels affected in the acute inflammatory response process?
A
Changes in vessel calibre (gets wider) which increases vessel flow
22
Q
How is vascular permeability affected in the acute inflammatory response process?
A
Increased vascular permeability which leads to formation of fluid exudate
23
Q
How do neutrophil polymorphs reach the site of acute inflammation?
A
Increased vascular permeability which allows for the formation of cellular exudate
24
Q
What are the stages of neutrophil polymorph emigration?
A
- Migration of neutrophils
- Adhesion of neutrophils
- Neutrophil emigration
- Diapedesis
25
Why do neutrophils migrate in acute inflammation?
Due to increase in plasma viscosity and slowing of flow due to injury
26
Where do neutrophils first migrate to in acute inflammation?
Plasmatic zone
27
What happens once neutrophils have migrated to the plasmatic zone in acute inflammation?
Adhesion to the vascular endothelium occurs in venules (pavementing)
28
What happens after pavementing during acute inflammation?
Neutrophils pass through endothelial cells, onto the basal lamina and then the vessel wall
29
What happens in diapedesis in acute inflammation?
RBCs may also escape from vessels. This is a passive process and indicates severe vascular injury
30
What are the outcomes of acute inflammation?
1. Resolution
2. Suppuration
3. Organisation
4. Progression
31
What is resolution in terms of acute inflammation?
- The complete restoration of tissues to normal
| - There is minimal cell death and rapid destruction of the causal agent
32
Give an example of a disease where resolution is seen after acute inflammation.
Acute lobar pneumonia
33
What is suppuration?
- Formation of pus
| - This becomes surrounded by a pyogenic membrane, which is the start of healing
34
What does suppuration lead to?
Scarring
35
What is organisation in terms of acute inflammation?
- Replacement by granulation tissue
| - New capillaries grow into the inflammatory exudate, macrophages migrate and fibrosis occurs
36
What is progression in terms of acute inflammation?
Causative agent is not removed so there is progression to chronic inflammation
37
What is chronic inflammation?
Subsequent and prolonged response to tissue injury
38
What cells are involved in chronic inflammation?
Lymphocytes, macrophages and plasma cells
39
When does chronic inflammation occur?
Longer onset
40
How long does chronic inflammation last?
Long last effects
41
What are the causes of primary chronic inflammation?
- Resistance of infective agent
- Endogenous materials
- Exogenous materials
- Autoimmune conditions
- Primary granulomatous diseases
- Transplant rejection
42
What infective agents could cause chronic inflammation?
TB, leprosy
43
What endogenous materials could cause chronic inflammation?
Necrotic tissue
44
What exogenous materials could cause chronic inflammation?
Asbestos, silica
45
What autoimmune conditions could cause chronic inflammation?
Hashimoto's, rheumatoid arthritis
46
What primary granulomatous diseases could cause chronic inflammation?
Crohn's, sarcoidosis
47
What is the macroscopic appearance of chronic inflammation?
- Chronic ulcer
- Chronic abscess cavity
- Granulomatous inflammation
- Fibrosis
48
What is the microscopic appearance of chronic inflammation?
- Characteristically lymphocytes, plasma cells and macrophages
- Evidence of continuing destruction
- Possible tissue necrosis
49
What microscopic feature of acute inflammation is not seen in chronic inflammation?
Exudation (are others but cba lol)
50
What do macrophages do?
Respond to chemotactic stimuli
| Produce cytokines
51
What cytokines do macrophages produce?
Interferon alpha and beta, IL1, 6, 8, TNF-alpha
52
In what type of inflammation are granulomas seen?
Chronic
53
What are granulomas?
Aggregate of epithelioid histocytes (clump of macrophages surrounded by lymphocytes)
54
What conditions can cause granulomas?
TB, leprosy, Crohn's and sarcoidosis
55
What is the most common condition to cause granulomas?
TB
56
What stain can be used to identify TB granulomas?
Ziehl-Neelsen stain
57
What does the combination of granulomas and eosinophils indicate?
A parasite
58
What happens to the cells involved in acute inflammation?
Neutrophil extravasation
59
What happens to the cells involved in chronic inflammation?
- Cellular infiltrate of lymphocytes, macrophages and plasma cells
- Possible granulomas
60
What is thrombosis?
The solidification of blood contents that forms within the vascular system during life
61
What are the features of platelets?
- No nucleus
| - Alpha granules and dense granules
62
What are platelets derived from?
Megakaryocytes
63
What do alpha granules do?
Involved in platelet adhesion e.g. fibrinogen
64
What do dense granules do?
Cause platelets to aggregate e.g. ADP
65
What do platelets do once activated?
Release their granules when they come into contact with collagen
66
What happens if platelets are activated within an intact vessel?
A thrombus is formed
67
What is the result of chronic inflammation?
Fibrosis and scar tissue
68
What is the first stage of thrombosis?
Platelet aggregation (starts the clotting cascade)
69
Why are platelet aggregation and the clotting cascade hard to stop?
Both have positive feedback loops
70
What factors contribute to thrombosis?
Virchow's triad:
1. Reduced blood flow
2. Increased coagulability
3. Blood vessel injury
71
Give some examples of causes of reduced blood flow.
```
Atrial fibrillation
Long distance travel
Varicose veins
Venous obstruction (e.g. pregnancy)
Immobility
Ventricular/venous insufficiency
```
72
Give some examples of causes of increased coagulability.
Sepsis
Smoking
Coagulation disorders
Malignancy (e.g. cancer)
73
Give some examples of causes of blood vessel injury.
Trauma (especially orthopaedic)
Orthopaedic or major surgery
Hypertension
Invasive procedures (e.g. cannulation
74
Referring to Virchow's triad, what causes thrombosis?
2 factors from Virchow's triad
75
What is the first stage of arterial thrombosis?
An atheromatous plaque that results in a change in the vessel wall
76
What might atheromatous plaques have?
A fatty streak - yellow streaks on arterial wall
77
What happens after the formation of the atheromatous plaque and consequent change in the arterial wall?
Over time, the plaque grows and protrudes into the lumen which causes a degree of turbulence in blood flow
78
Describe normal blood flow.
Laminar flow - red blood cells flow through the middle of the vessel and do not collide with the endothelium
79
What does turbulent blood flow cause?
Loss of intimal/endothelial cells which exposes collagen
80
What happens after intimal cells are lost as a result of turbulent blood flow?
Fibrin deposition and platelet clumping occurs. Platelets adhere to exposed collagen and activate
81
What happens once platelet aggregation has commenced on the arterial endothelium?
Formation of the platelet layer (first layer of thrombus)
82
What does the first layer of thrombus allow for?
Precipitation of a fibrin meshwork in which RBCs get trapped
83
What happens to the fibrin meshwork formed during thrombosis?
The structure protrudes further into the lumen causing more turbulence and more platelet deposition
84
In what direction do thrombi grow?
In the direction of blood flow - propagation
85
Do atheroma form in veins?
No - there is lower blood pressure in veins
86
Where do thrombi begin in veins?
Valves
87
How can veins become damaged and cause thrombosis?
Valves produce a degree of turbulence and can be damaged e.g. trauma, stasis
88
What happens in the veins if blood pressure falls?
Flow through the veins slows, allowing for a thrombus to form
89
What are the clinical features of arterial thrombi?
Loss of pulse distal to thrombus
Area becomes cold, pale and painful
Possible gangrene
90
What are the clinical features of venous thrombi?
Tender
| Area becomes reddened and swollen
91
What can happen after thrombus formation?
Resolution
Organisation
Recanalisation
Embolus
92
What happens in the resolution of a thrombus?
Body dissolves and clears it
93
What happens in the organisation of a thrombus?
Becomes a scar - results in slight narrowing of the vessel lumen
94
What happens in recanalisation of a thrombus?
Intimal cells may proliferate
| Capillaries may grow into the thrombus and fuse to form larger vessels
95
How does a thrombus turn into an embolus?
Fragments of the thrombus break off into the circulation
96
What is an arterial thrombus most commonly caused by?
Atheroma
97
What is a venous thrombus most commonly caused by?
Stasis
98
What type of blood pressure causes arterial thrombi?
High
99
What type of blood pressure causes venous thrombi?
Low
100
What are arterial thrombi mainly made of?
Platelets
101
What are venous thrombi mainly made of?
RBCs
102
What conditions can arterial thrombi lead to?
MI/stroke
103
What can venous thrombi lead to?
DVT/PE
104
How are arterial thrombi treated?
Anti-platelets e.g. aspirin
105
How are venous thrombi treated?
Anti-coagulants e.g. warfarin
106
What is an embolism?
A mass of material in the vascular system able to lodge in a vessel and block its lumen
107
What type of embolism do arterial embolisms cause?
Systemic embolism
108
Where can arterial emboli travel to?
Anywhere downstream of its entry point
109
Where can mural thrombi in the left ventricle go?
Anywhere
110
Where can cholesterol crystals from an atheromatous plaque in the descending aorta go to?
Any lower limb or the renal artery
111
What conditions can thrombi in the left ventricle cause if they form emboli?
Cerebral infarct (stroke)
Renal infarct
Ischaemic bowel
Ischaemic foot (dry gangrene)
112
What type of embolism do venous embolisms cause?
Pulmonary emboli
113
Where do emboli travel to in the venous system?
The vena cava and lodge in the pulmonary arteries (pulmonary embolism)
114
What conditions can small pulmonary emboli cause?
Idiopathic pulmonary hypertension
115
Why might small pulmonary emboli go untreated?
May occur unnoticed
116
What conditions can large pulmonary emboli cause?
Acute respiratory or cardiac problems
117
What symptoms do large pulmonary emboli cause?
Chest pain and shortness of breath
118
How quickly do large pulmonary emboli resolve?
Slowly
119
What can massive pulmonary emboli result in?
Sudden death
120
Where are massive pulmonary emboli often impacted?
Across the bifurcation of one of the pulmonary arteries
121
What do massive pulmonary emboli tend to be?
Long thrombi derived from the leg veins
122
What is ischaemia?
The reduction in blood flow to a tissue or part of the body
123
What causes ischaemia?
Constriction or blockage of the blood vessels supplying the tissue
124
What is infarction?
Necrosis of part of the whole of an organ that occurs when the artery supplying it becomes obstructed
125
Can the effects of ischaemia be reversed?
Yes
126
How long do ischaemia attacks last?
Briefly
127
What cells are most vulnerable to ischaemic attacks?
Cardiomyocytes and cerebral neurons
128
Why are most organs susceptible to infarcts?
They only have a single artery supplying them
129
Which organs are less susceptible to infarcts and why?
Liver, brain and lungs because they have a dual supply
130
What is a reperfusion injury?
Damage to tissue during reoxygenation
131
What is atherosclerosis?
Disease characterised by the formation of atherosclerotic plaques in the intima of large and medium sized arteries e.g. coronary arteries
132
How does atherosclerosis present?
Often asymptomatic
133
What accumulates in the intimal atherosclerotic plaques?
Lipids, macrophages and smooth muscle cells
134
How can atherosclerosis cause life threatening damage?
If a thrombus forms on a disrupted plaque
135
What conditions can atherosclerosis cause?
```
Cerebral infarction
Carotid atheroma, leading to TIAs
MI
Aortic aneurysm (can cause sudden death)
Peripheral vascular disease
Gangrene
```
136
What is the first stage of atherosclerosis?
Endothelial cell dysfunction (lots of cholesterol damages wall)
137
What happens once the arterial wall has been damaged by cholesterol?
High levels of LDL in the blood will begin to accumulate in the arterial wall
138
How does the site of atherosclerosis become inflamed?
Macrophages are attracted to the site of damage and take up liquid to form foam cells (inflammatory response)
139
What is formed after the recruitment of macrophages in atherosclerosis?
A fatty streak
140
What is the earliest stage in the formation of a plaque?
Fatty streaks
141
What do the activated macrophages in atherosclerosis release?
Cytokines and growth factors
142
What is the final stage of atherosclerosis?
Smooth muscle proliferation (to intima) around the lipid core and formation of a fibrous cap (collagen)
143
What are the risk factors for atherosclerosis?
```
Hypercholesterolaemia (most important risk factor)
Smoking
Hypertension
Diabetes
Male sex
Increasing age
```
144
How can you prevent atherosclerosis?
```
Smoking cessation
Blood pressure control
Weight reduction
Low dose aspirin
Statins
```
145
Why should aspirin be used to prevent atherosclerosis?
Inhibits aggregation of platelets
146
Why should statins be used to prevent atherosclerosis?
Cholesterol reducing drug
147
What is apoptosis?
A cellular process in which a defined and programmed sequence of intracellular events leads to the removal of a cell without the release of products harmful to surrounding cells
148
What inhibits apoptosis?
Growth factors
Extracellular cell matrix
Sex steroids
149
What induces apoptosis?
```
Glucocorticoids
Free radicals
Ionising radiation
DNA
damage
```
150
What does the intrinsic apoptosis pathway use?
Pro/anti-apoptotic members of the Blc-2 family:
Bax
p53
151
What happens in the intrinsic apoptosis pathway?
Bax forms Bax-Bax dimers which enhance apoptotic stimuli
152
What determines the cell's susceptibility to apoptotic stimuli?
Bcl-2:Bax ratio
153
What does the intrinsic apoptosis pathway respond to?
Growth factors and biochemical stress
154
What is the role of the p53 gene in intrinsic apoptosis?
Induces cell cycle arrest and initiates DNA damage repair
155
What induces apoptosis if DNA damage is difficult to repair?
p53 gene
156
What happens in extrinsic apoptosis?
Ligand-binding at death receptors on the cell surface
157
Give some examples of death receptors involved in extrinsic apoptosis.
TNFR1 and CD95
158
What does ligand-binding in extrinsic apoptosis result in?
Clustering of receptor molecules on the cell surface and the initiation of signal transduction cascade
159
What molecules trigger extrinsic apoptosis?
Caspases once activated
160
What is the purpose of extrinsic apoptosis?
Used by the immune system to eliminate lymphocytes
161
What is necrosis?
Traumatic cell death which induces inflammation and repair
162
What is necrosis characterised by?
Bioenergetic failure and loss of plasma membrane integrity
163
What is the most common type of necrosis?
Coagulative necrosis
164
Where can coagulative necrosis occur?
Most organs
165
What is coagulative necrosis caused by?
Ischaemia
166
Where does liquefactive necrosis occur?
In the brain due to its lack of substantial supporting stroma
167
What does caseous necrosis cause?
A 'cheese' pattern
168
What disease is characterised by caseous necrosis?
TB
169
What is gangrene?
Necrosis with rotting of the tissue
170
How does gangrene present?
Affected tissue appears black due to deposition of iron sulphide (from degraded haemoglobin)
171
What is hypertrophy?
Increase in cell size without cell division
172
Where is muscle hypertrophy commonly seen?
In athletes due to increased muscle activity
173
Where is uterine hypertrophy seen?
Pregnancy
174
What is hyperplasia?
Increase in cell number by mitosis
175
In what cells can hyperplasia occur?
Only in cells that divide - can't happen in myocardial cells or nerve cells
176
Where is hyperplasia of bone marrow cells seen?
In those living at high altitudes
177
What is atrophy?
The decrease in the size of an organ or cell either by reduction in cell size and/or number
178
Where does atrophy occur naturally?
During the development of the GU tract
179
Give an example of a disease where atrophy occurs.
Muscle atrophy in ALS
180
What is metaplasia?
The change in differentiation of a cell from one fully-differentiated cell type to another
181
When does metaplasia occur?
In response to alterations in the cellular environment
182
Give some examples of metaplasia.
- Ciliated columnar cells in epithelium of bronchi in smokers become simple squamous
- Squamous epithelium of oesophagus can become columnar epithelium in response to stomach acid (Barrett's oesophagus)
183
What is dysplasia?
Morphological changes seen in cells in the progression to becoming cancer (not cancer but could become cancer)
184
What is carcinogenesis?
The transformation of normal cells into neoplastic cells through permanent genetic alterations or mutations
185
What is a neoplasm?
A lesion resulting from the autonomous or relatively autonomous abnormal growth of cells
186
In what cells can neoplasms not occur?
RBCs because they don't have nuclei
187
What is a tumour?
Any abnormal swelling
188
What is a carcinogen?
An environmental agent participating in the causation of tumours
189
What can cause lung tumours?
Smoking
190
What can cause bladder cancer?
B-naphthylamine (dyes and rubber industry)
191
What can cause scrotal cancer?
Polycyclic aromatic hydrocarbons (soot exposure)
192
What can cause Burkitt's lymphoma?
EBV
193
What can cause cervical cancer?
HPV
194
What can cause skin cancer?
UV radiation
195
What can cause hepatocellular carcinoma?
Aflatoxins (mycotoxins)
196
What can cause mesothelioma?
Asbestos
197
Describe the growth of benign tumours.
Don't invade basement membrane and exophytic (grows outwards)
198
Describe the mitotic activity of benign tumours.
Low mitotic activity
199
What type of tumour is circumscribed?
Benign - malignant are poorly circumscribed
200
In what type of tumour is necrosis and ulceration common?
Malignant - they are rare in benign
201
Describe the growth of malignant tumours.
Invades the basement membrane and endophytic (grows inwards)
202
How are tumours classified?
Behaviour and histogenesis
203
What are cancers of epithelial cells called?
Carcinomas
204
What are cancers of connective tissues called?
Sarcomas
205
What are cancers of lymphoid called?
Lymphomas or leukaemia
206
What is a grade 1 cancer?
Well differentiated (most closely resembles parent tissue)
207
What is a grade 2 cancer?
Moderately differentiated
208
What is a grade 3 cancer?
Poorly differentiated
209
What is the suffix of epithelial tumours?
-oma
210
What is a papilloma?
Benign tumour of non-glandular tissue
211
What is an adenoma?
Benign tumour of secretory tissue
212
What is a carcinoma?
Malignant tumour of epithelial cells
213
What is an adenocarcinoma?
Malignant tumour of glandular epithelium
214
What connective tissues can be affected by cancer?
```
Adipocytes
Striated muscle
Smooth muscle
Cartilage
Bone
```
215
What is a lipoma?
Benign tumour of adipocytes
216
What is a rhabdomyoma?
Benign tumour of striated muscle
217
What is a leiomyoma?
Benign tumour of smooth muscle cells
218
What is a chondroma?
Benign tumour of cartilage
219
What is an osteoma?
Benign tumour of bone
220
What is a liposarcoma?
Malignant tumour of adipocytes
221
What is a rhabdomyosarcoma?
Malignant tumour of striated muscle
222
What is a leiomyosarcoma?
Malignant tumour of smooth muscle
223
What is a chondrosarcoma?
Malignant tumour of cartilage
224
What is an osteosarcoma?
Malignant tumour of bone
225
What is metastasis?
The process whereby malignant tumours spread from their site of origin to form other tumours at distant sites
226
What type of cancer never metastasises?
Basal cell carcinoma
227
What is the first stage of metastasis?
Detachment of tumour cells from their neighbours
228
What happens in metastasis once tumour cells have detached from their neighbours?
Invasion of the surrounding connective tissue to reach conduits of metastasis
229
What happens once tumour cells have invaded surrounding connective tissue?
Intravasation into the lumen of vessels
230
What happens in metastasis after intravasation?
Evasion of host defence mechanisms, such as NK cells
231
What happens in metastasis after the evasion of host defence mechanisms?
Adherence to endothelium at remote location
232
What happens in metastasis after tumour cells have adhered to endothelium elsewhere?
Extravasation of the cells from the vessel lumen into the surrounding tissue
233
What happens after extravasation in metastasis?
Tumour cells proliferate in the new environment and grow their own blood supply
234
What cancers metastasise to bone?
Lung, breast, kidney, thyroid, prostate
235
Which secondary cancer is common?
Secondary tumours in lymph nodes - lymphatic metastasis
236
How do carcinomas tend to spread?
Lymphatic spread
237
How do sarcomas tend to spread?
Haematogenous spread
238
How are tumours staged?
TMN staging
239
What is the 'T' in TMN staging?
Primary tumour size
240
What is the 'M' in TMN staging?
Metastatic status - extent of distant metastases
241
What is the 'N' in TMN staging?
Lymph node status - degree of lymph node involvement
242
What does exudate contain?
Leukocytes and high in protein and lactate dehydrogenase (LDH)
243
Why causes formation of exudate?
Occurs due to inflammation and increased capillary permeability
244
In what conditions is exudate found?
Pneumonia, cancer, TB, viral infection, PE, autoimmune conditions
245
What is transudate?
Transudates accumulate due to increased hydrostatic pressure or low plasma oncotic pressure
246
What does transudate contain?
Low in protein and lactate dehydrogenase (LDH)
247
In what conditions is transudate found?
Congestive heart failure (CHF), cirrhosis, nephrotic syndrome, PE, hypoalbuminaemia
248
When does hyperacute transplant rejection take place?
Occurs minutes to hours following revascularisation of the graft
249
Why does hyperacute transplant rejection occur?
Due to performed circulating cytotoxic antibody which reacts with MHC class I antigens in the donor organ
250
What does hyperacute transplant rejection cause?
Complement mediated endothelial injury
251
How is hyperacute transplant rejection resolved?
In most cases the graft will have to be removed as it is usually damaged too much by the recipient immune system
252
When does acute transplant rejection occur?
Occurs a few days or weeks following transplantation
253
What percentage of all transplants result in acute rejection?
Up to 20% of all transplants
254
What is acute transplant rejection associated with?
Increased expression of MHC class I and class II antigens in inflamed grafts, and with early infiltration of CD8+ T lymphocytes
255
When does chronic transplant rejection occur?
Seen after months or years
256
How is chronic transplant rejection resolved?
Not thought to be immunologically mediated, and doesn't respond to immunosuppressive therapy
257
Which cells play a central role in organ rejection?
CD4+ T lymphocytes
258
What are the two phases of organ rejection?
- An afferent phase (initiation or sensitising component)
| - An efferent phase (effector component)
259
What happens in the afferent phase of organ rejection?
Donor MHC molecules within the graft are recognised by the recipient CD4+ T cells - this is known as allorecognition
260
What happens in the effector phase of organ rejection?
The effector phase of rejection is orchestrated by CD4+ T cells which enter the graft and recruit effector cells responsible for the tissue damage of rejection
261
What are the effector cells involved in organ rejection??
- Macrohages
- CD8+ T cells
- Natural killer cells
- B lymphocytes
262
What are the most important cytokines in graft rejection?
Interleukin-2 and interferon-gamma
263
What are the critical targets of graft rejection?
Microvasculature and the specialised parenchymal cells or the organ, such as renal tubules, pancreatic islets of Langerhans and cardiac myocytes
264
What do the endogenous chemical mediators cause in acute inflammation?
- Vasodilation
- Emigration of neutrophils
- Chemotaxis (the attraction of neutrophil polymorphs towards certain chemicals e.g at the site of inflammation)
- Increased vascular permeability
- Itching & pain
265
What are the endogenous chemical mediators of acute inflammation?
```
Histamine and thrombin
Lysosomal compounds
- Eicosanoids - type of prostaglandin
- 5-hydroxytryptamine (serotonin)
- Chemokine (chemotactic cytokines)
```
266
Which cells can regenerate?
- Hepatocytes
- Pneumocytes
- All blood cells
- Gut epithelium
- Skin epithelium
- Osteocytes
267
Which cells can't regenerate?
- Myocardial cells
| - Neurones
268
What is the difference between a thrombus and a clot?
```
Thrombus = the solidification of blood contents that forms within the vascular system during life
Clot = blood coagulated outside of the vascular system or after death
```
269
What is gangrene?
When whole areas of a limb or a region of the gut have their arterial supply cut off and large areas of mixed tissue die in bulk
270
What can ischaemic damage cause?
- Cerebral infarction
- Carotid atheroma - emboli causing transient
ischaemic attacks or cerebral infarcts
- Myocardial infarction
- Aortic aneurysm - rupture causes certain death
- Peripheral vascular disease
- Gangrene
271
What is an aneurysm?
A localised permanent dilation of part of the vascular tree
272
What are some apoptosis inhibitors?
- Growth factors
- Extracellular cell matrix
- Sex steroids
- Some viral proteins
273
What are some apoptosis inducers?
- Growth factor withdrawal
- Loss of matrix attachment
- Glucocorticoids
- Some viruses
- Free radicals
- Ionising radiation
- DNA damage
- Ligand-binding at ‘death receptors’
274
How do benign tumours cause morbidity and mortality?
Pressure on adjacent structures (e.g. bening meningeal tumour causing epilepsy)
Obstruction to the flow of fluid (e.g. benign epithelial tumour blocking duct)
Production of a hormone (e.g. benign thyroid tumour causing thyrotoxicosis (excessive thyroid hormone)
Transformation into a malignant neoplasm
Anxiety & stress since patient thinks the lesions may be something more sinister
275
How do malignant tumours cause morbidity and mortality?
Pressure on and destruction of adjacent tissue
Formation of secondary tumours (metastases)
Blood loss from ulcerated surfaces
Obstruction of flow (e.g. malignant tumour of the colon causing intestinal obstruction)
Hormone production
Paraneoplastic effects resulting in weight loss and debility
Anxiety and pain - many cancers cause no pain until quite late into the disease
276
What are the 3 major families of proteinases in neoplastic invasion?
- Interstitial collagenases; degrade types I,II & III collagen
- Gelatinases; degrade type IV collagen and gelatin
- Stromelysins; degrade type IV collagen and proteoglycans
277
What do proteinases do in neoplastic invasion?
These enzymes are secreted by malignant neoplastic cells, enabling them to digest the surrounding connect tissue
278
What cancers are there screening programmes for in the UK?
- Cervical cancer
- Breast cancer
- Colorectal cancer
279
What is lead time bias?
Earlier detection does not affect the inevitable fatal outcome, but prolongs the apparent survival time
280
What is length bias?
Preferential detection of slow growing tumours with intrinsically better prognosis
281
What is overdiagnosis bias?
Diagnosis of lesions that, although histologically malignant, are
clinically relatively harmless
282
What is selection bias?
Volunteers for screening are more at risk of good-prognosis tumours
283
What is atopy?
Inherited tendency for overproduction of IgE antibodies to common environmental antigens
284
What do you find within a granuloma?
- Multinucleate giant cells
- Lymphocytes
- Epithelioid histocytes
