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Pathology Flashcards

1
Q

Describe acute inflammation

A

Sudden onset
Usually resolves by itself
Neutrophils are normally the main cells on site
Can progress to chronic inflammation

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2
Q

Describe chronic inflammation

A

Slow onset or following acute inflammation
Long duration
Might never resolve
Usually involves lymphocytes and macrophages as well as neutrophils

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3
Q

Describe the progression of acute inflammation

A

Injury/infection
Neutrophils arrive - phagocytosis and enzyme release
Macrophages arrive - phagocytosis
Resolution OR progression to chronic inflammation

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4
Q

Describe the progression of chronic inflammation

A

Macrophage or lymphocyte mediated inflammation or progression from acute inflammation
No/few neutrophils
Macrophages, lymphocytes present
Fibroblasts present
Resolution if no tissue damage OR repair/scar tissue formation if tissue is damaged

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5
Q

What is inflammation?

A

The body’s response to injury or infection, involving different types of cells

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6
Q

What are the causes of inflammation?

A

Injury
Infection
Autoimmunity
Over-reaction to a stimulus

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7
Q

What are the signs of inflammation?

A

Rubor - redness
Calor - heat
Dolor - pain
Tumour - swelling
Loss of function (as a result of these)

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8
Q

What is a granuloma?

A

An aggregate of epithelioid histiocytes
When macrophages cluster together to kill something but are ineffective. They get surrounded by lymphocytes

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9
Q

Describe granuloma formation in TB

A

The mycobacteria infect alveolar macrophages
Infected macrophages are surrounded by foamy macrophages, other macrophages, lymphocytes and fibrin
TB lies in dormancy and doesn’t spread
As CD4 and TNFa depletion, granuloma becomes unstable and fail
TB spreads around the body

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10
Q

What is fibrosis?

A

The accumulation of fibrous connective tissue in inflamed or damaged tissue

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11
Q

What do fibroblasts produce?

A

Collagen

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12
Q

Describe healing by 1st intention

A

A weak fibrin joint first (red)
Gradually replaced by a strong collagen joint (white)
Happens when the edges of the wound fit together well

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13
Q

Describe healing by 2nd intention

A

A large fibrin mesh forms which fills the wound
Granulation tissue forms
Bright dots of capillaries and fibroblasts grow in

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14
Q

Define atherosclerosis

A

The accumulation of fibrolipid plaques in systemic arteries (not pulmonary arteries)

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15
Q

Describe the pathophysiology of atherosclerosis

A

Endothelial damage theory:
ECs are damaged - hyperlipidaemia, shearing forces, free radicals from cigarette smoking, glycosylation products from poorly controlled Diabetes Mellitus
LDLs enter the endothelium and are oxidised
Macrophages engulf lipoproteins forming a foam cell
Foam cells form a fatty streak
Continued damage, macrophage recruitment, and lipid accumulation, forming a lipid core -> atheroma
Fibrotic tissue forms on the lesion an calcifies -> fibroatheroma

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16
Q

What is a thrombosis?

A

A solid mass of constituents formed within intact vascular system during life

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17
Q

Describe the pathophysiology of thrombosis

A

Endothelial cell damage
Platelets stick to the collagen underneath
Platelet aggregation
This causes turbulent flow in the vessel
RBCs get trapped
Formation of blood clot -> thrombus
Deposition of fibrin helps trap the RBCs, solidifying the thrombus

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18
Q

Why does thrombosis happen in veins more than arteries?

A

Arteries have laminar flow so cells rarely touch the sides
In veins, cells scrape along the sides causing EC damage

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19
Q

What is Virchow’s triad and what are the components?

A

The 3 factors increasing likelihood of thrombosis
- Change in vessel wall
- Change in blood flow
- Change in blood constituents

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20
Q

Define embolism

A

The process of a solid mass in the blood vessels being carried through the circulation to the place where it gets stuck and blocks the vessel
E.g. thrombus, air, cholesterol crystals, amniotic fluid, tumour

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21
Q

Where could a venous embolus go?

A

Through vena cava to pulmonary arteries

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22
Q

Where could an arterial embolus go?

A

Anywhere downstream of its entry point

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23
Q

Define ischaemia

A

A reduction in blood flow

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24
Q

Define infarction

A

A reduction in blood flow causing a subsequent death of cells

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25
What is apoptosis?
Programmed cell death (affects an individual cell)
26
Give an example of pathology relating to apoptosis
Cancer - lack of apoptosis HIV - causes apoptosis of CD4 cells
27
Define necrosis
Traumatic cell death (whole sheets of cells)
28
Give an example of a pathology relating to necrosis
Frostbite Cerebral infarction (stroke) Pancreatitis
29
Define Atrophy
A decrease in the size of a tissue caused by a decrease in the number of constituent cells or the size of constituent cells, or both
30
Give an example of a pathology relating to atrophy
Cerebral atrophy in Dementia Muscular atrophy Optic atrophy
31
Define hypertrophy
An increase in the size of a tissue caused by an increase in the size of constituent cells
32
Give an example of a pathology relating to hypertrophy
Myofibril or sarcophagi can hypertrophy in muscles Left ventricular hypertrophy in heart
33
Define hyperplasia
An increase in the size of a tissue caused by an increase in the number of constituent cells
34
Give an example of a pathology relating to hyperplasia
Benign prostatic hyperplasia Endometrial hyperplasia
35
Define metaplasia
A change in the differentiation of a cell from one fully-differentiated type to another fully-differentiated type
36
Give an example of a pathology relating to metaplasia
Bronchi changing from ciliated columnar epithelium to squamous due to smoking Barret’s Oesophagus - epithelium changes from squamous to columnar due to GORD
37
Define dysplasia
The morphological changes seen in cells in the progression to becoming cancer
38
Define a tumour
Any abnormal swelling
39
Define neoplasm
A lesion resulting from the autonomous or relatively autonomous new growth of cells which persists after the initiating stimulus has been removed
40
What spectrums are neoplasms measured on?
Benign to malignant Subclinical to fatal
41
What is angiogenesis?
The growth or new blood vessels Essential to tumour growth beyond around 2mm
42
What are methods of tumour classification?
Behavioural and histogenic
43
What is tumour behavioural classification divided into?
Benign, borderline and malignant
44
Describe benign tumours
Non-invasive Localised Close resemblance to normal tissue Low mitotic activity Circumscribed Often normal nuclear morphometry Necrosis, ulceration is rare Mucosal surface growth is usually exophytic
45
Describe malignant tumours
Invasive Metastasises Rapid growth rate/increased mitotic activity Variable resemblance to normal tissue Poorly defined Hyperchromatic and pleomorphic nuclei Necrosis and ulceration is common Mucosal surface growth is usually endophytic
46
What is the histogenesis of a neoplasm?
The specific cell type of origin of the neoplasm
47
What is a carcinoma?
Malignant epithelial neoplasm
48
What is a papilloma?
Benign, non-glandular/non-secretory, epithelial neoplasm
49
What is an adenoma?
Benign, glandular/secretory, epithelial neoplasm
50
What is a lipoma?
Benign connective tissue neoplasm of adipocytes
51
What is a chondroma?
Benign connective tissue neoplasm of cartilage
52
What is an osteoma?
Benign connective tissue neoplasm of bone
53
What is an angioma?
Benign connective tissue neoplasm of vascular tissue
54
What is a rhabdomyoma?
Benign connective tissue neoplasm of striated muscle
55
What is a leiomyoma?
Benign connective tissue neoplasm of smooth muscle In the uterus, this is called a fibroid
56
What is a neuroma?
Benign connective tissue neoplasm of nerve cells
57
What is a Liposarcoma?
Malignant connective tissue neoplasm of adipose tissue
58
What is a chondrosarcoma?
Malignant connective tissue neoplasm of cartilage
59
What is an osteosarcoma?
Malignant connective tissue neoplasm of bone
60
What is an angiosarcoma?
Malignant connective tissue neoplasm of vascular tissue
61
What is a rhabdomyosarcoma?
Malignant connective tissue neoplasm of striated muscle
62
What is a leiomyosarcoma?
Malignant connective tissue neoplasm of smooth muscle
63
Which cells does Burkitt’s Lymphoma affect and what causes it?
B cells Caused by Epstein Barr Virus
64
Which cells does Ewing sarcoma affect?
Long bones
65
Which cells does Grawitz tumour affect?
Renal cell (carcinoma)
66
Which cells does Kaposi’s sarcoma affect and what causes it?
The skin or mucosal membranes of GI tract from the mouth to the anus Human Herpes 8 Virus
67
What is a melanoma?
A malignant neoplasm of melanocytes
68
What is a mesothelioma?
A malignant neoplasm of mesothelial cells
69
What is a lymphoma?
A malignant neoplasm of lymphoid cells
70
What is a myeloma?
A malignant neoplasm of myeloid cells
71
How are malignant tumours graded?
By how closely they resemble the tissue of origin High grade = poor resemblance = poorly differentiated
72
What does it mean if a neoplasm is anaplastic?
The cell type of origin can’t be determined
73
What is tumour staging?
How much a tumour has spread
74
What are the three categories in tumour staging?
Tumour- the size and extent or depth of the tumour Nodes - the extent of lymph node metastases Metastases - the extent of metastases/spreading to the rest of the body
75
What is carcinogenesis?
The transformation of normal cells to neoplasticism cells through permanent genetic mutations/alterations - only malignant tumours
76
What is oncogenesis?
The transformation of normal cells to neoplasticism cells through permanent genetic mutations/alterations - benign and malignant tumours
77
What is a carcinogen?
An agent known or suspected to cause tumours
78
Define mutagenic
Capable of causing a mutation
79
What are the host factors that increase the risk of cancer?
Ethnicity Diet and lifestyle Age Gender Underlying conditions Transplacental exposure
80
What are the classes of carcinogens?
Chemical Biological Radiant Viral Miscellaneous
81
Give some examples of biological carcinogens
Hormones e.g. anabolic steroids, oestrogen Mycoproteins produced by fungi Parasites e.g. shistosoma
82
Give some examples of radiant carcinogens
UVA, UVB, x-rays, gamma rays
83
Give some examples of viral carcinogens
DNA viruses e.g. HH8V, EBV, HBV, HPV, MCV, RNA viruses e.g. HTLV-1, HCV
84
Give some examples of miscellaneous carcinogens
Asbestos Some metals e.g. arsenic
85
What is a carcinoma in situ?
A carcinoma that hasn't breached the basement membrane
86
What is a micro-invasive carcinoma?
A carcinoma that has only invaded the basement membrane a little bit so only has a small risk of spreading
87
What is an invasive carcinoma?
A carcinoma that has invaded the basement membrane
88
How do carcinomas invade through the basement membrane?
1. Neoplastic cells produce proteases that break down collagen in the basement membrane 2. they then use cell motility to move across the basement membrane and into the extracellular matrix
89
Define metastasis
The development of secondary malignant growths at a distance from the primary site of cancer
90
Describe the process of metastasis
1. Invasion (of vessels like lymphatics and venules) 2. Evasion of host immune response 3. Extravasation (leaving the vessel) 4. Invasion of the extracellular matrix 5. Tumour growth
91
Describe the ways that neoplastic cells can evade the host immune response
1. Aggregation with platelets to disguise themselves 2. Releasing antigens to 'confuse' lymphocytes 3. Adhesion to other neoplastic cells to protect the ones at the centre
92
What are the types of autopsy?
Hospital Medico-legal (corneal and forensic)
93
When are deaths referred to the coroner?
1. If the cause of death is unknown (but presumed natural) and they haven't seen a doctor within the past 14 days 2. If the death is presumed iatrogenic 3. If the death is presumed unnatural
94
What is the purpose of an autopsy?
To identify the deceased To find out when they died To find out where they died To find out how they died
95
What is the clotting cascade?
A series of reactions in response to bleeding which ultimately produces a blood clot. It stabilises the platelet plug.
96
Describe platelet plug formation
1. Endothelial injury 2. Exposure of collagen and release of Von Willebrand factor 3. Adhesion of GP1B surface proteins on platelets to Von Willebrand factor 4. Activation of platelets 5. Aggregation of platelets to fibrinogen
97
Draw the clotting cascade
98
What causes the intrinsic pathway of the clotting cascade
Collagen exposure
99
What causes the extrinsic pathway of the clotting cascade
Damage to endothelial tissue releasing tissue factor
100
What are the Vitamin K dependent clotting factors?
X, IX, VII, II 10, 9, 7, 2
101
What is Prothrombin Time (PT)?
The time taken for fibrin to form via the extrinsic pathway of the clotting cascade
102
What is the normal range for prothrombin time?
9-12 seconds
103
Name some causes of prolonged prothrombin time?
Disseminated intravascular coagulation (DIC) Vitamin K deficiency Chronic Liver Disease
104
What is International Normalised Ratio (INR)?
The patient's prothrombin time compared to a normal PT
105
What is Activated Partial Thromboplastin Time (APTT)?
The time taken for fibrin to form via the intrinsic pathway of the clotting cascade
106
What is the normal range for the activated partial thromboplastin time?
23-28 seconds
107
What are some causes of prolonged Activated Partial Thromboplastin Time?
Disseminated Intravascular Coagulation (DIC) Clotting factor deficiencies Von Willebrand's Disease Lupus anticoagulation

Phase 2a (9 decks)

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