Pathology Flashcards

(108 cards)

1
Q

State the 2 types of inflammation

A
  1. Acute
  2. Chronic
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2
Q

What is the onset and duration of acute inflammation?

A

Early onset - seconds to minutes
Short duration - hours to days

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3
Q

Which cells are involved in acute inflammation?

A
  1. Neutrophils
  2. Monocytes
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4
Q

What is the function of acute inflammation?

A

Initial response of tissue to injury

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5
Q

What are the 3 steps of acute inflammation?

A
  1. Vascular component - dilation of vessels
  2. Exudative component - vascular leakage of protein-rich fluid
  3. Neutrophil polymorph - cells type recruited to tissue
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6
Q

State the 6 causes of acute inflammation

A
  1. Microbial infection - bacteria, viruses, etc
  2. Hypersensitivity reactions - parasites
  3. Physical agents - trauma, heat, cold
  4. Chemicals - corrosive, acid
  5. Bacterial toxins
  6. Tissue necrosis - ischemic infarction
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7
Q

What is the vascular component of acute inflammation?

A

Dilation of vessels

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8
Q

What is the exudative component of acute inflammation?

A

Vascular leakage of protein rich fluid

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9
Q

What is the neutrophil polymorph component of acute inflammation?

A

Cells type recruited to tissue

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10
Q

What are the 5 ways of characterising the appearance of acute inflammation?

A
  1. Rubor - redness
  2. Calor - heat
  3. Tumor - swelling
  4. Dolor - pain
  5. Loss of function
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11
Q

What are the 4 stages of neutrophil polymorph emigration in acute inflammation?

A
  1. Migration (margination) of neutrophils
  2. Adhesion of neutrophils
  3. Neutrophil emigration
  4. Diapedesis
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12
Q

What happens during the migration of neutrophils stage of neutrophil polymorph emigration in acute inflammation?

A
  1. Plasma viscosity increases
  2. Flow slows due to injury
  3. Neutrophils migrate to plasmatic zone
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13
Q

What happens during the adhesion of neutrophils stage of neutrophil polymorph emigration in acute inflammation?

A

Adhesion of the neutrophils to the vascular endothelium in the venules

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14
Q

What is the term for the adhesion of neutrophils to the vascular endothelium during the neutrophil polymorph migration stage of acute inflammation?

A

Pavementing

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15
Q

What happens during the neutrophil emigration stage of neutrophil polymorph emigration in acute inflammation?

A

Neutrophils pass through endothelial cells onto basal lamina and then the vessel wall

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16
Q

What happens during the diapedesis stage of neutrophil polymorph emigration in acute inflammation?

A

RBCs escape from vessels as a passive process; indicates severe vascular injury

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17
Q

What are the outcomes of acute inflammation?

A
  1. Resolution
  2. Suppuration
  3. Organisation
  4. Progression
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17
Q

Describe resolution as an outcome of acute inflammation

A
  1. Complete restoration of tissues to normal
  2. Minimal cell death
  3. Rapid destruction of causal agent
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18
Q

Describe supporation as an outcome of acute inflammation

A
  1. Formation of pus
  2. Becomes surrounded by pyogenic membrane (start of healing process)
  3. Leads to scarring
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19
Q

Describe organisation as an outcome of acute inflammation

A
  1. Replacement of granulation tissue
  2. New capillaries grow into inflammatory exudate
  3. Macrophages migrate
  4. Fibrosis occurs
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20
Q

Describe progression as an outcome of acute inflammation

A
  1. Causative agent agent not removed
  2. Progression to chronic inflammation
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21
Q

What are the 2 possible outcomes of healing?

A
  1. Resolution
  2. Repair
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22
Q

What circumstances lead to repair as an outcome of healing?

A

When resolution impossible

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23
Q

What are the cells involved in chronic inflammation?

A
  1. Lymphocytes
  2. Macrophages
  3. Plasma cells
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24
What are the 2 major causes of chronic inflammation?
1. Primary chronic Inflammation 2. Transplant rejection
25
What are the 5 subtypes of primary chronic inflammation?
1. Resistance of infective agent 2. Endogenous materials 3. Exogenous materials 4. Autoimmune conditions 5. Primary granulomatous diseases
26
Give examples of resistance of infective agent as a cause of primary chronic Inflammation
1.TB 2. Leprosy
27
Give examples of endogenous materials as a cause of primary chronic Inflammation
Necrotic tissue
28
Give examples of exogenous materials as a cause of primary chronic Inflammation
1. Asbestos 2. Silica
29
Give examples of autoimmune conditions as a cause of primary chronic Inflammation
1. Hashimoto's 2. Rheumatoid arthirtis
30
Give examples of primary granulomatous diseases as a cause of primary chronic Inflammation
1. Chron's 2. Sarcoidosis
31
State the macroscopic appearance of chronic inflammation
1. Chronic ulcer 2. Chronic abscess cavity 3. Granulomatous inflammation 4. Fibrosis
32
State the microscopic appearances of chronic inflammation
1. Presence of lymphocytes, plasma cells and macrophages 2. Exudation NOT a common feature 3. Evidence of continuing destruction 4. Possible tissue necrosis
33
What is the function of B lymphocytes in chronic inflammation?
Transform into plasma cells and produce antibodies
34
What is the function of T lymphocytes in chronic inflammation?
Responsible for cell mediated immunity
35
What is the function of macrophages in chronic inflammation?
1. Respond to chemotactic stimuli 2. Produce cytokines
36
Which stain can be used to identify TB granulomas?
Ziehl-Neelsen stain
37
What does the presence of granulomas and eosinophil indicate?
Parasite
38
Define thrombosis
The solidification of blood contents that forms within the vascular system during life
39
Describe platelets
1. Derived from megakaryocytes 2. Contains alpha granules and dense granules 3. When platelets activated, granules released when they come into contact with collagen
40
What is the function of alpha granules
Platelet adhesion
41
What is the function of dense granules
Platelet aggregation
42
What is the trigger for thrombosis formation?
First stage - platelet aggregation Next stage - clotting cascade
43
What type of feedback loop do platelet aggregation and clotting cascade have?
Positive loop
44
What are the 3 corners of Virchow's Triad
1. Reduced blood flow 2. Increased coagulability 3. Blood vessel injury
45
What are 6 factors that cause reduced blood flow?
1. Atrial fibriliation 2. Long distance travel 3. Varicose veins 4. Venous obstruction (e.g. pregnancy) 5. Immobility 6. Ventricular/venous insufficiency
46
What are 4 that increase coagulation?
1. Sepsis 2. Smoking 3. Coagulation disorders 4. Malignancy (e.g. cancer)
47
What can venous thrombus lead to?
DVT/PE
48
What is treatment for arterial thrombus?
Anti-platelets (aspirin)
49
What is treatment for venous thrombus?
Anti-coagulants (warfarin)
50
What is an embolism?
A mass of material in the vascular system able to lodge in a vessel and block its lumen
51
Describe arterial embolism
1. Systemic embolism 2. Arterial emboli can travel anywhere downstream of entry point 3. Mural thrombi in left ventricle can go anywhere 4. Cholesterol crystals from atheromatous plaque in descending aorta can go to any lower limb or renal artery
52
Describe venous embolism
1. Pulmonary embolism 2. Emboli travels to vena cava and lodge in pulmonary arteries 3. Results in PE
53
What are the 3 types of emboli?
1. Small 2. Large 3. Massive
54
What are the characteristics of a small venous emboli?
1. May occur unnoticed 2. Can cause idiopathic pulmonary hypertension
55
What are characteristics of a large venous emboli?
1. Can result in acute respiratory/ cardiac problems 2. Resolves slowly 3. Chest pain 4. Shortness of breath
56
What are characteristics of a massive venous emboli?
1. Sudden death 2. Long thrombi derived from leg veins 3. Often impacted across the bifurcation of one of the pulmonary arteries
57
Define ischaemia
ischaemia is the reduction in blood flow to a tissue or part of the body caused by constriction or blockage of blood vessels supplying it
58
Define infarction
Infarction is the necrosis of part or whole of an organ that occurs when the artery supplying it becomes obstructed
59
Describe ischaemia
1. Effects can be reversible 2. Duration of ischaemia attack is brief 3. Cardiomyocytes and cerebral neurone most vulnerable
60
Describe infarction
1. Usually macroscopic event 2. Most organs have single artery supply therefore susceptible to infarcts 2. Liver, brain and lungs have dual supply --> less susceptible 3. Repercussion injury = damage to tissue during re-oxygenation
61
Define atherosclerosis
Disease characterised by formation of atherosclerotic plaques in the intimate of large and medium sized arteries
62
Describe atherosclerosis
1. Often asymptomatic 2. Accumulation of lipids, macrophages and smooth muscle cells in intimal plaques 3. Can cause life-threatening damage if thrombus forms on disrupted plaque
63
State the risk factors of atherosclerosis
1. Hypercholesterolaemia (most important risk factor) 2. Smoking 3. Hypertension 4. Diabetes 5. Male sex 6. Increasing age
64
What drugs help in atherosclerosis prevention?
1. Low dose aspirin --> inhibits aggregation of platelets 2. Statins --> cholesterol reducing drug
65
Define apoptosis
Apoptosis is 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
66
What are the inhibitory regulators of apoptosis?
1. Growth factors 2. Extracellular cell matrix 3. Sex steroids
67
What are inductive regulators of apoptosis?
1. Glucocorticoids 2. Free radicals 3. Ionising radiation 4. DNA damage
68
What are the 2 pathways to apoptosis?
1. Intrinsic 2. Extrinsic
69
Which receptors are involved in extrinsic apoptosis?
1. TNFR1 2. CD95
70
Define necrosis
1. A traumatic cell death which induces inflammation and repair 2. Characterised by bioenergetic failure and loss of plasma membrane integrity
71
State the 4 types oof necrosis
1. Coagulative 2. Liquefactive 3. Caseous 4. Gangrene
72
Describe coagulative necrosis
1. Most common type 2. Can occur in most organs 3. Cause by ischaemia
73
Describe liquefactive necrosis
Occurs in brain due to lack of substantial supporting stroma
74
Describe caseous necrosis
1. Causes a 'cheese' pattern 2. TB characterised by this form of necrosis
75
Describe gangrene as a type of necrosis
1. Necrosis with rotting of tissue 2. Affected tissue appears black due to deposition of iron sulphide (from degradation of haemoglobin)
76
Describe hypertrophy
1. Increase in cell size without cell division 2. Uterine hypertrophy observed in pregnancy
77
Describe hyperplasia
1. Increase in cell number by mitosis 2. Only occurs in dividing cells 3. Hyperplasia of bone marrow cells observed at high altitude
78
What cells cannot undergo hyperplasia?
1. Myocardial cells 2. Nerve cells
79
Describe atrophy
1. Decrease in size of an organ or cell and/or reduction in cell size/ number 2. Natural occurrence during GI tract development 3. Occurs in disease
80
Describe metaplasia
1. Change in differentiation of a cell from one fully-differentiated cell type to another 2. Response to alterations in cellular environment
81
Describe dysplasia
Morphological changes seen in cells in the progression to becoming cancer
82
Define carcinogenesis
Transformation of normal cells into neoplastic cells through permanent genetic alterations or mutations
83
Define neoplasm
Lesion resulting from autonomous abnormal growth of cells
84
Define tumour
Any abnormal swelling
85
Why can neoplasm not occur in erythrocytes?
No nuclei
86
Which cancer can be caused by B-naphthylamine?
Bladder cancer
87
What cancer can be caused by polycyclic aromatic hydrocarbons?
scrotal carcinoma
88
What cancer is linked to Epstein-Barr Virus (EBV)?
Burkett's lymphoma (cancer of lymphatic system)
89
What cancer is linked to HPV?
Cervical cancer
90
What cancer are aflatoxins linked to?
hepatocellular carcinoma
91
What is mesothelioma linked to?
Exposure to asbestos- Cancer of mesothelium; covering of many organs
92
What are the properties of a benign neoplasm?
1. Does not invade basement membrane 2. Exophytic (grows outwards) 3. Low mitotic activity 4. Circumscribed 5. Necrosis and ulceration rare
93
What are the properties of a malignant neoplasm?
1. Invades basement membrane 2. Endophytic (grows inwards) 3. High mitotic activity 4. Poorly circumscribed 5. Necrosis and ulceration common
94
What are the 2 aspects that neoplasm classification is based on?
1. Behaviour (benign vs malignant) 2. Histogenesis
95
What is histogenesis classification based on?
Specific cell or origin of the tumour
96
What do neoplasms in epethelial cells form?
Carcinomas
97
What do neoplasms in connective tissue form?
Sarcomas
98
What do neoplasms in lymphoid form?
Lymphomas or leukemia
99
State and define the histological grading of neoplasms
Based on extent to which neoplasm resembles original parent cell histology Grade 1 - Well differentiated (close resemblance to parent cell) Grade 2 - Moderately differentiated Grade 3 - Poorly differentiated
100
What is adenocarcinoma?
Malignant tumour of glandular epithelium
101
State the 2 benign epithelial neoplasms and their location
1. Papilloma - non glandular tissue 2. Adenoma - secretory tissue
102
State the 5 types of connective tissue neoplasms
1. Lipoma - adipocytes 2. Rhabdomyoma - striated muscle 3. Leiomyoma - smooth muscle cells 4. Chondroma - cartilage 5. Osteoma - bone
103
Define metastasis
Process of malignant neoplasms spreading from site of origin to form neoplasms at distant sites
104
Which is the only neoplasm that does not metastasise?
Basal cell carcinoma
105
State some routes of metastasis
1. Bone metastasises from cancer originating from - lung, breast, kidney, thyroid, prostate 2. Lymphatic metastasis common 3. Carcinomas prefer lymphatic spread 4. Sarcomas prefer haematogenous spread
106
What is tumour staging?
1. Staging = extent of tumour spread 2. Determined by histopathological examination and clinical examination
107
How is tumour staging classified?
-T - Primary tumour size -N - Lymph node status -M - Metastatic status