Pathology Flashcards
(192 cards)
1
Q
What is the role of an autopsy?
A
Who was deceased?
When did they die?
Where did they die?
Cause of death
2
Q
How is an autopsy done?
A
History External examination Evisceration Internal examination Reconstruction
3
Q
What deaths are referred to a coroner?
A
Presumed natural - death unknown
Presumed iatrogenic - peri/postoperative deaths
Presumed unnatural - accidents, unlawful killing
4
Q
What is acute inflammation?
A
Initial and often transient series of tissue reactions to injury, it’s got a sudden onset, short lived and usually resolves on its own
5
Q
Causes of acute inflammation
A
Microbial infections Hypersensitivity reactions Physical agents Chemicals Tissue necrosis
6
Q
Clinical features of acute inflammation
A
Redness (rubor) Heat (calor) Swelling (tumor) Pain (dolor) Loss of function
7
Q
What makes up the cellular exudate for acute inflammation?
A
Neutrophil polymorphs
Macrophages
Lymphocytes
8
Q
Features of Neutrophil polymorphs
A
Short lived, pus cells
First on the scene of acute inflammation
Attract other inflammatory cells
Cytoplasmic granules full of enzymes that kill bacteria
Diagnostic histological feature
9
Q
Features of lymphocytes
A
Long lived cells
Produce chemicals that attract other inflammatory cells
Immunological memory
10
Q
Features of macrophages
A
Long lived cells
Phagocytic properties
may present antigen to lymphocyte
11
Q
Features of endothelial cells
A
Become sticky in areas of inflammation so inflammatory cells adhere to them
Become porous to allow inflammatory cells to pass into tissues
12
Q
Give an example of acute inflammation
A
Acute appendicitis
13
Q
What are the benefits of inflammation?
A
Destruction of invading microorganisms and wailing off of an abscess cavity preventing infection spread
14
Q
What are the outcomes of acute inflammation?
A
Resolution
Suppuration
Organisation (fibrosis)
Progression to chronic inflammation
15
Q
What are the negatives of inflammation?
A
Autoimmunity
When it’s an over-reaction to the stimulus
Fibrosis resulting from chronic inflammation
16
Q
What is chronic inflammation?
A
Subsequent and often prolonged tissue reactions following the initial response, it has a slow onset, long duration and may never resolve
17
Q
Causes of chronic inflammation
A
Primary chronic inflammation
Transplant rejection
Progressing from acute inflammation
Recurrent episodes of acute inflammation
18
Q
Causes of primary chronic inflammation
A
Exogenous materials
Endogenous materials
Resistance of infective agent to phagocytosis and intracellular killing – TB
Autoimmune diseases – rheumatoid arthritis
Primary granulomatous diseases – Crohn’s
19
Q
What is the cellular exudate in chronic inflammation mainly made of?
A
Lymphocytes
Plasma cells
Macrophages
Fibroblasts
20
Q
What is a granuloma?
A
Group of epitheloid histiocytes which can contain lymphocytes and histolytic giant cells
Can cause caseous necrosis
21
Q
Where are granulomas seen?
A
Tuberculosis
Leprosy
Sarcoidosis
22
Q
How can you treat inflammation?
A
Aspirin, ibuprofen (NSAIDs)
Corticosteroids
23
Q
What is resolution?
A
Initiating factor removed, and tissue is undamaged or able to regenerate
24
Q
What is repair?
A
Initiating factor is still present, and tissue is damaged and unable to regenerate
25
Which organ is a good example for resolution?
Liver
26
What affects resolution of the liver?
Cirrhosis (ongoing damage resulting in abnormal architecture)
27
What cells can regenerate?
```
Hepatocytes
Pneumocytes
All blood cells
Gut epithelium
Skin epithelium
Osteocytes
```
28
What cells can't regenerate?
Myocardial cells
| Neurones
29
What happens after a skin abrasion?
Only top cell layer is removed, leaving the bottom layer/follicles/glands for scab to form and for the epidermis to eventually be regenerated
30
What are the 2 types of skin wound healing?
Healing by 1st intention (+ve)
| Healing by 2nd intention (-ve)
31
When does 1st intention healing occur?
Incision wound
32
How does healing by 1st intention work?
Edge to edge healing (heals w/ reasonable scar)
Fibrinogen exudation
Both ends are sealed together, the slight gap is filled with blood, fibrin etc which holds together a little with stitches
Epidermis regrows, fibroblasts produce collagen
Small scar forms
33
When does 2nd intention healing occur?
When tissue loss has occurred (2 edges can't be brought together nicely)
34
How does 2nd intention healing work?
Infection or haemorrhage prevent healing by first intention
Loss of tissue, granulation tissue forms and organisation occurs (phagocytosis of any debris)
Epithelial regeneration and early fibrous scar
Scar contradiction
35
What is organisation?
Repair of specialised tissue by the formation of a fibrous scar
36
How does organisation occur?
Granulation tissue is formed and dead tissue is removed by phagocytosis
Granulation tissue contracts and accumulated collagen to form a scar
37
What produces collagen?
Fibroblasts
38
Name 3 places where repair occurs and after what
Heart after an MI
Brain after a cerebral infarction
Spinal cord after trauma
39
What is a thrombosis?
Solid mass of blood constituents formed within intact vascular system during life
40
What is Virchow's triad?
Factors that can lead to thrombosis formation:
1. Change in vessel wall
2. Change in blood flow (laminar --> turbulent)
3. Change in constituents of blood
41
What does Virchow's triad do?
Predisposes to thrombosis
42
When does an arterial thrombosis normally occur?
When superimposed on atheroma
43
How does an arterial thrombus occur?
Vessel wall damage
Laminar flow disruption
Collagen exposed
Platelets stick to collagen and aggregate - positive feedback
Rbc’s can get trapped - thrombus formation and fibrin deposition (fibrinogen --> fibrin by platelet factors)
Fibrin mesh holds it all together
Thrombus can then build up and occlude artery
44
What is a vein thombus most commonly due to?
Stasis
45
What are the outcomes of a thrombus?
1. Lysis and resolution
2. Organisation – into a scar
3. Recanalisation – scar and residual thrombus
4. Embolism – breaks off
46
How can you prevent a thrombus?
Exercise
Compression stockings
Aspirin – anti platelet drug, makes endothelial cells less sticky, not a full-blown thrombus occurs
47
What does an occlusion of a coronary artery result in?
Myocardial infarction
48
What does occlusion of a cerebral artery result in?
Cerebral infarction (stroke)
49
What is laminar flow? and why is it important?
Cells travel in the centre of arterial vessels and don't touch arteries - this is important in reducing risk of blood clots
50
What is an Embolus?
Mass of material in the vascular system able to become lodged within vessel and block it
51
What is the most common cause of an embolus?
Piece of thrombus breaking off and getting lodged in a smaller vessel
52
What is the most common occurrence of an embolus?
Pulmonary embolism from deep leg vein thrombosis
53
What is Ischaemia?
Reduction in blood flow
54
What is Infarction?
Death of cells due to reduction in blood supply
55
What is infarction normally caused by?
Thrombosis of an artery
56
Explain a reperfusion injury
Occurs after ischaemia
Blood supply severely limited but cells don’t actually die
Blood flow re-established (reactive hyperaemia - cells overwhelmed with O2)
ROS production that cause damage to tissue and inflammatory response
57
Name organs with 2 blood supplies
Lungs - bronchial arteries and pulmonary arteries
Liver - portal vein and hepatic artery
Some parts of the brain
58
What areas are most susceptible to infarction?
Watershed territories
59
What are the functions of histamine?
```
Vasodilation
Emigration of neutrophils (chemotaxis)
Increase vascular permeability
Pain
Itching
```
60
Role of plasma factors
Complement system
Kinin system
Coagulation cascade (pro-clotting)
Fibrinolytic system (anti-clotting)
61
What is the microscopic appearance of chronic inflammation?
Chronic ulcer
Abscess cavity
Granulatomous inflammation
Fibrosis
62
What is a histiocytic giant cell?
Indeigestible foreign material causes macrophages to fuse together - multinucleate giant cells
Can collect and form granulomas
63
Causes of an embolus
```
Air injected
Thrombus/atheroma
Amniotic fluid
Fat
Tumour
```
64
What happens in a venous system embolism?
Goes to RHS heart
Pulmonary system
Pulmonary embolism
65
What happens in an arterial system embolism?
Goes to LHS heart
Systemic system
Embolism anywhere
66
What is end arterial supply?
Single artery supplies organ - more susceptible to infarction
67
What are watershed territories?
Parts of the brain the have a dual blood supply, but low BP can cause ischaemia
68
What is an atherosclerosis?
Build up of plague in arteries , narrows arteries
69
Where are atherosclerosis' found?
Systemic arterial system - high pressure systems
70
What are the components of an atheroma?
Fibrous cap
Cholesterol and lipid core
Smooth muscle cells surrounded by foam cells
Macrophages
71
Risk factors for atherosclerosis
Smoking - free radicals, nicotine, CO
Hypertension - increased shearing forces
Diabetes - superoxide anions and glycosylation products
Hyperlipidaemia - lipids
Increasing age
Male gender
72
What do the risk factors for atherosclerosis do?
Damage the endothelial cells
73
Explain the pathogenesis of atherosclerosis
1. Endothelial cell damage – see risk factors
2. Repeated endothelial damage -> multiple thrombi -> aggregation -> atheroma formation
3. Vascularised plaque can haemorrhage – propagates atheroma formation
74
What are the complications of atherosclerosis?
Cerebral/myocardial infarct
AAA --> weakens aorta and leads to aortic rupture
Peripheral vascular disease - gangrene
75
How can you treat atheroma?
Aspirin - anti platelet drug
Statins - lower cholesterol
Diet, exercise, control of blood pressure, smoking cessation, weight loss
76
Define apoptosis
Programmed cell death
77
Define necrosis
Traumatic cell death
78
What types of DNA damage cause apoptosis to occur?
Single/double stand break
Base alteration
Cross linking
79
Explain mechanism of apoptosis
1. P53 (gatekeeper of genome) detects DNA damage -> acts as switch for apoptosis
2. Bcl2 and Fas ligand receptor signal for capsases -> apoptosis
3. Membrane bound cell fragments engulfed by macrophages
80
Example of normal apoptosis
Removal of finger webbing during development
81
What can a lack of apoptosis cause?
Cancer - mutation in p53 means cell damage isn't detected
82
In what is excess apoptosis present?
HIV mediated T cell destruction
83
Give examples of necrosis
Myocardial/cerebral infarction
Avascular necrosis of bone - scaphoid or head of femur break
Caseous necrosis - pathological sign of TB
84
Define hypertrophy
Increase in size of a tissue caused by an increase in size of the constituent cells (eg skeletal muscle)
85
Define hyperplasia
Increase in size of a tissue caused by an increase in number of the constituent cells (eg. enlarged prostate)
86
Define atrophy
Decrease in size of tissue caused by a decrease in number of the constituent cells or a decrease in their size (eg. underuse of muscle, Alzheimers)
87
Define metaplasia
Change in differentiation of a cells from one fully differentiated type to a different fully differentiated type (eg. lung cancer - ciliated columnar --> squamous epithelium)
88
Define dysplasia
Imprecise term for the morphological changes seen in cells in the progression to becoming cancer
89
Explain spina bifida
Lack of vertebrae formation - spinal cord is exposed
| Myelomeningocele is the most severe - nerves and meninges bulge out of the back
90
What are other examples of developmental conditions?
Cleft lip/palate - cells fail to migrate and join
| Ventricular septal defect (VSD)
91
What are the signs of a VSD
Strong heart murmur
| Left ventricular hypertrophy
92
Name 3 types of development
Congenital
Inherited
Acquired
93
What is congenital development?
Present at birth - can be inherited or acquired
94
What is inherited development?
Genetic abnormality
95
What is acquired development?
Caused by external/environmental factors
96
Give an example of a chromosomal condition
Down's syndrome - trisomy 21
97
What occurs in Down's syndrome?
Increased beta amyloid production
| Causes early dementia and increase cataract risk
98
Why do growth disorders occur?
Growth hormone deficiency or excess caused by pituitary adenoma
99
Give an example of a growth disorder due to a:
1. Deficiency in GH
2. Excess of GH
1. Dwarfism
| 2. Acromegaly - increased extremity size
100
What is a telomere?
Regions at the end of a chromosome that count the number of cell replication
101
What happens to a telomere as you age?
Telomeres get shorter
102
How can age-related cell damage happen?
Free radical generation and peroxidation of cell membrane
Cross linking of DNA/proteins
Loss of Ca influx control --> mitochondrial damage
accumulation of toxic by-products
103
Explain dermal elastosis
UVB lights causes cross linking of protein (collagen) so damages cells
low elastic properties of skin = wrinkles
104
Explain osteoporosis
Decrease in normal bone matrix caused by lack of oestrogen
| Increase bone resorption and decreased bone formation
105
Why does cataracts occur?
UVB light causes lens protein cross linkage --> crystallin production --> clouding of lens
106
Why does senile dementia occur?
Cortical atrophy
| Plague and neurofibrillary tangle formation
107
What is sarcopenia?
Skeletal muscle atrophy
| Caused by decreased GH, decreased testosterone and increased catabolic cytokines
108
How does deafness occur?
Damage and subsequent loss of cochlear hair cells
109
Does apoptosis or necrosis cause an inflammatory response?
Necrosis
110
Name 5 types of necrosis
```
Caseous necrosis
Coagulative necrosis
Colliquative necrosis
Fibrinoid necrosis
Fat necrosis
```
111
Where is caseous necrosis seen?
It is a pathological sign of tuberculosis
112
What is coagulative necrosis?
Cells become firm and pale
| Seen in most tissues
113
What is colliquative necrosis?
Dead area is liquefied
| Seen in brain
114
What is fibrinoid necrosis a microscopic feature of?
Malignant hypertension - in arterioles
115
What can cause necrosis?
Ischaemia
Metabolic
Trauma
116
What is the hayflick phenomenon?
Number of times a normal human cell population will divide before cell division stops
117
What is a BCC caused by?
UVB light
118
Does a BCC metastasise?
BCC only invade locally
119
How can you treat a BCC
Complete local excision = cure
120
What lymph nodes to carcinomas spread to?
The lymph nodes that drain the site of the carcinoma (e.g. breast cancer --> ancillary lymph nodes)
121
What is leukaemia?
Tumour of WBC, circulates around the body
122
Name 5 cancers that commonly spread to bone
1. Breast
2. Thyroid
3. Kidney
4. Lung
5. Prostate
123
Give symptoms of leukaemia
```
Weight loss
Fever
Frequent infections
Fatigue and loss of appetite
Easy SOB
Night sweats
Easy bleeding and bruising
```
124
How can you confirm a breast cancer diagnosis?
Mammogram or a needle core biopsy
125
Treatment for breast cancer that has NOT spread
Remove tumour --> mastectomy
126
If axillary nodes are affected, how do you know and what treatment should be done?
Confirm by ultrasound and needle core biopsy and then remove any affected axillary nodes
127
What treatment is used if breast cancer has metastasised?
Chemo and radiotherapy
128
What is adjuvant therapy?
Extra treatment given after surgical excision
129
What is the purpose of adjuvant therapy?
Tries to remove micro-metastases that could be present even if tumour is completed excised
130
Give examples of breast cancer adjuvants
Radiotherapy after lumpectomy
| Anti-oestrogen therapy (tamoxifen) - if oestrogen receptor positive
131
Define carcinogenesis
Transformation of normal cells to neoplastic cells through permanent genetic changes
132
Features of carcinogenesis
Applies to malignant neoplasms
| Multistep process
133
What does oncogenesis refer to?
Benign and malignant tumours
134
Define carcinogen
Mutagenic (act on DNA) agents that cause (or are suspected to cause) tumours
135
What is the difference between carcinogenic and oncogenic?
```
Carcinogenic = cancer causing
Oncogenic = tumour causing
```
136
Name the carcinogen classes
Chemical
Radiation
Biological organisms
Miscellaneous
137
Give examples of chemical carcinogens
Polycyclic aromatic hydrocarbons (smoking, mineral oils) --> lung and skin cancer
138
Give examples of radiation carcinogens
UVA and B --> BCC, melanoma
Ionising radiation --> skin (radiographers – thorium), lung (uranium miners), thyroid cancer (Ukrainian children - Chernobyl nuclear explosion)
139
Give an example of a hormone carcinogen
Increased oestrogen --> mammary and endometrial cancer
140
Give an example of a mycotoxin carcinogen
Mycotoxin (Aflatoxin B1) --> hepatocellular cancer
141
Give an example of a parasite carcinogen
Parasites --> cholangiocarcinoma and bladder cancer
142
Give an example of a viral carcinogen
HPV --> cervical cancer
143
Give an example of a misscellaneous carcinogen
Asbestos --> lung cancer, asbestosis (unknown mechanism of action)
144
Name host factors for carcinogenesis
Race
Constitutional
Premalignant conditions
Transplacental exposure
145
Give examples of race as a host factor
Increased melanin in black skin --> decreased skin cancer incidence
Reverse smoking/betal nut chewing --> increase oral cancer in India, SE Asia
146
Give examples of constitutional host factors
Inherited predisposition – familial adenomatous polyposis (chr 5), retinoblastoma (chr 13)
Age – increased incidence of all cancers
Gender – breast cancer 200x more likely in females
147
Give examples of premalignant conditions as host factors
Local abnormality associated with increased risk of malignancy at that site
Colonic polyps, ulcerative colitis (bowel cancer), cervical dysplasia, undescended testes (testicular cancer)
148
Define tumour
Any abnormal swelling
| Neoplasm, inflammation, hypertrophy and hyperplasia
149
Define Neoplasm
A lesion resulting from the NEW AUTONOMOUS ABNORMAL growth of cells that PERSISTS after removal of initiating stimulus
150
What is the structure of a neoplasm?
Neoplastic cells
| Stroma - connettive tissue framework
151
What does the stroma provide of the neoplasm?
Mechanical support
Nutrition
Intracellular signalling
Contains blood vessels which perfuse the tumour
152
A tumour <2mm is known as a ...?
Avascular nodule
153
How big is a vascularised nodule?
>2mm
154
What happens when there is increased growth in tumour angiogenesis?
Increased growth = central necrosis
155
How can neoplasms be classified?
```
Behavioural = being, malignant
Histogenetic = cell of origin
```
156
Features of benign neoplasms
Localised and on-invasive
Slow growth rate - out and up
Close resemblance to normal tissue
157
Problems with benign neoplasms
```
Pressure on adjacent structures
Flow obstruction
Hormone production
Transformation to a malignant neoplasm
Anxiety
```
158
Features of malignant neoplasms
Invasive and metastases
Rapid growth rate - down and in
Poorly defined and irregular borders
159
Problems with malignant neoplasms
```
Tissue destruction
Paraneoplastic effects (symptoms not just due to cancer at the site) - weight loss
Metastasise
Pressure on adjacent structures
Flow obstruction
Hormone production
Anxiety and pain
```
160
What is the suffix for neoplasms?
-oma
161
What neoplasms do epithelial cells form?
Carcinomas
162
What neoplasms do connective tissues form?
Sarcomas
163
What neoplasms do lymphoid/haemopoietic organs form?
Lymphomas or leukaemia
164
What is a papilloma?
A benign non glandular epithelial neoplasm
165
What is an adenoma?
A benign glandular epithelial neoplasm
166
What is a carcinoma?
A malignant non glandular epithelial neoplasm
167
What is a adenocarcinoma?
A malignant glandular epithelial neoplasm
168
Name some benign connective tissue neoplasms
```
Lipoma = adipocytes
Chondroma = cartilage
Osteoma = bone
Angioma = vascular
Rhabdomyoma = striated muscle
Leiomyoma = smooth muscle
Neuroma = nerves
```
169
What is the suffix for malignant connective tissue neoplasms?
-sarcoma
170
Name some malignant connective tissue neoplasms
```
Liposarcoma = adipose tissue
Chondrosarcoma = cartilage
Osteosarcoma = bone
Angiosarcoma = vascular
Rhabdomyosarcoma = striated muscle
Leiomyosarcoma = smooth muscle
```
171
What is graded malignancy?
Carcinomas and sarcomas are further classified according to degree of differentiation (how much it resembles normal tissue)
172
What are the types of grade of malignancy?
Low grade – looks like parent tissue (well differentiated)
High grade – doesn’t look like parent tissue (poorly differentiated)
Anaplastic – unknown origin cell type
173
Name some exceptions to -oma rule
Granuloma
Melanoma - malignant
Lymphoma - malignant
Treatoma
174
What is a carcinoma in situ?
Carcinoma fills cavity but has not invaded any other tissue
175
What are the 8 stages of metastasis?
1. Detachment
2. Invasion
3. Intravasation
4. Evasion
5. Adherence
6. Extravasation
7. Growth
8. Angiogenesis
176
Explain invasion
Some cells go through the basement membrane into the extracellular matrix using enzymes (proteases, collagenase, cathepsin D, urokinase-like plasminogen activator)
177
What is intravasation?
Tumour cells move from ECM to blood/lymph vessels
178
What is evasion?
Aggregate with platelets, shed surface antigens and stick to other tumour cells
179
Explain adherence
Adherence of ells to endothelium at a remote location
180
Explain extravasation
Tumour cells move from vessels to new tissue area
181
What is angiogenesis?
Formation of blood vessels
182
Name 3 routes of metastasis
Haematogenous - by blood stream
Lymphatic
Transoelomic - in pleural, pericardial and peritoneal cavities
183
What tumours commonly metastasise to the lungs?
Most carcinomas and sarcomas (venous --> pulmonary system)
184
What tumours commonly metastasise to the liver?
Colon, stomach, pancreas, intestine (portal system)
185
What tumour never metastasises?
Basal cell carcinoma
186
What term describes a cancer that has not invaded through the basement membrane?
Carcinoma in situ
187
Give 2 promoters of tumour angiogenesis
1. Vascular endothelial growth factors
| 2. Fibroblast growth factors
188
Give 3 inhibitors of tumour angiogenesis
1. Angiostatin
2. Endostatin
3. Vasculostatin
189
Define exudate
A protein rich fluid that leaks out of vessel walls due to increased vascular permeability
190
Give 3 endogenous chemical mediators of acute inflammation
1. Bradykinin
2. Histamine
3. Nitric Oxide
191
The activity of what enzyme in the blood can act as a marker for granulomatous disease?
Angiotensin converting enzyme
192
Define abscess
Acute inflammation with a fibrotic wall
