1
Q
What is inflammation?
A
Inflammation is the body’s process of fighting things that harm it such as infections, injuries and toxins.
2
Q
What are the types of inflammation?
A
Acute and chronic inflammation.
3
Q
What is acute inflammation?
A
The initial tissue reactions to injury which may last from a few hours to a few days.
4
Q
What is acute inflammation mediated by?
A
Neutrophils
5
Q
What is chronic inflammation?
A
The subsequent and prolonged tissue reactions to injury following acute inflammation.
6
Q
What is chronic inflammation mediated by?
A
Macrophages and lymphocytes.
7
Q
What is inflammation characterised by?
A
The 5 cardinal signs.
8
Q
What are the 5 cardinal signs?
A
- Rubor (redness)2. Dalor (pain)3. Calor (heat)4. Tumor (swelling)5. Function loss
9
Q
What are the 3 stages of acute inflammation?
A
- Increased vessel calibre - vasodilation by cytokines (bradykinin, NO, prostaglandins)2. Fluid exudate - Leaky vessel, fluid forced out3. Cellular exudate - Neutrophils become abundant
10
Q
What do neutrophils do in acute inflammation?
A
- Margination - To edge of vessel2. Adhesion - Neutrophils bind to endothelium of vessel3. Emigration - Neutrophils move out of vessel4. Chemotaxis - phagocytosis, phagolysosome, macrophage clears debris.
11
Q
What are the four outcomes of acute inflammation?
A
- Resolution - Tissue restored to normal2. Supportation - Pus formation3. Organisation - Granulation tissue and fibrosis.4. Progression - Excessive recurrent inflammation; becomes chronic and fibrotic tissue.
12
Q
What are granulomas?
A
They’re aggregates of macrophages in response to chronic inflammation.
13
Q
What is the significance of granuloma shape?
A
- Central necrosis - TB2. No central necrosis - Crohn’s, leprosy, sarcoidosis
14
Q
What is the marker for granulomas?
A
ACE as they secrete it.
15
Q
What is thrombus?
A
A mass of blood constituents (platelets) forming in vessels.
16
Q
How does a thrombus form?
A
- Vasospasm2. Primary platelet plug - VWF binds to exposed collagen; platelets bind to this.3. Coagulation cascade
17
Q
What is Virchow’s triad?
A
Three factors in the contribution of thrombosis. Only one is needed but it’s usually two or three.
18
Q
What are the factors in Virchow’s triad (with examples)?
A
- Endothelial injury - Trauma, smoking, MI, surgery.2. Hypercoagulability - Sepsis, atherosclerosis, pregnancy, malignancy.3. Decreased blood flow - AF, immobility.
19
Q
What are the different types of thrombosis?
A
Arterial and venous thrombi.
20
Q
How does an arterial thrombus form?
A
Forms by atherogenesis.
21
Q
How does a venous thrombus form?
A
Forms by venous stasis.
22
Q
What are the fates of thrombi?
A
- Resolution - degrades2. Organisation - leaves behind scar tissue3. Embolism - fragments of thrombi break away and lodge in distal circulation
23
Q
What is an embolus?
A
An embolus is a fragment of a thrombus which has broken off.
24
Q
What are the types of emboli?
A
Arterial and venous.
25
What is an example of an arterial embolus?
A thrombus from AF embolises and lodges in the carotid artery causing an ischaemic stroke.
26
What is an example of a venous embolus?
A DVT thrombus embolises and lodges in the pulmonary artery causing a PE.
27
What is atherosclerosis?
Fatty plaque that forms in the intima and media of arteries, hardening and narrowing them over time.
28
What causes atherosclerosis?
Chronic inflammation and activation of the immune system in the artery wall.
29
What are the contents of an atherosclerotic plaque?
Lipids, smooth muscle, macrophages, platelets, fibroblasts.
30
What are the non-modifiable and modifiable risk factors for atherosclerosis?
Non-modifiable: age, family history, gender.Modifiable: smoking, alcohol, poor diet, low exercise, obesity, poor sleep and stress.
31
What is the name of the formation of a plaque?
Atherogenesis.
32
What are the four steps of atherogenesis?
1. Endothelial injury2. Fatty streak3. Inflammatory reaction4. Fibrous cap
33
How does a fibrous cap in atherosclerosis cause further narrowing?
If the fibrous cap ruptures, there is continuous plug formation which occludes the lumen leading to narrowing.
34
What is apoptosis?
Apoptosis is non-inflammatory genetically programmed cell death without any harmful product release.
35
How do cells appear in apoptosis?
Cells shrink, organalles are retained, cytoplasm stays intact, chromatin is unaltered, fragmented for phagocytosis.
36
What are the mechanisms for apoptosis?
1. Intrinsic2. Extrinsic3. Cytotoxic
37
What is necrosis and what causes it?
Inflammatory unprogrammed cell death due to adverse event such as infarction, burn, frostbite, infection and trauma.
38
How do cells appear in necrosis?
Cells burst, organelles splurge, cytoplasm is damaged, chromatin is altered, and the cell is FUCKED.
39
What are the different patterns of necrosis?
1. Coagulative2. Liquefactive3. Caseous4. Gangrene
40
What is hypertrophy?
Cell gets bigger without cell division.
41
What is hyperplasia?
Number of cells increase via mitosis.
42
What is atrophy?
Number or size of cells decreases
43
What is metaplasia?
Replacement of one cell type to another.
44
What is dysplasia?
Morphological changes seen in cells progressing to become cancerous.
45
What is ischaemia?
Decreased perfusion to tissue without infarction.
46
What is infarction?
Death of tissue due to severe and prolonged ischaemia.
47
What is carcinogenesis?
Transformation of normal cells to neoplastic cells through permanent mutation.
48
What is a neoplasm?
An abnormal and persistent new growth which can only arise from nucleated cells (not RBCs).
49
What is a tumour?
Any abnormal swelling.
50
How can tumours be classified?
By behaviour and histogenesis.
51
How can tumours be divided by their behaviour?
Benign or malignant.
52
What are the differences between benign and malignant cells?
Benign - slow growing, localised, well circumscription, outward growing, rare ulceration and necrosis.Malignant - Very fast growing, poor circumscription, invade nearby tissues, inward growing, common ulceration and necrosis.
53
What does tumour histogenesis measure?
The origin cell of tumours.
54
What are carcinomas?
Tumours of epithelia.
55
What are sarcomas?
Tumours of connective tissue.
56
What are lymphoid tumours?
Leukeamia and lymphoma (always malignant).
57
Which cancers are screened for?
Cervical - SwabBreast - MammogramsColorectal - Fecal sample
58
How are most tumours staged?
By TNM (tumour, nodes, metastases)-Primary tumour measured (T1-4)-Nearby lymph nodes measured for cancer (NX, N0, N1)-Metastases measured (MX, M0, M1)
59
What are the classes of carcinogens?
1. Chemicals (paints).2. Viruses (HPV).3. Ionising/non-ionising radiation (UVB light), 4. Hormones (oestrogen).5. Miscellaneous (asbestos).
60
Which tumours are pathological?
Malignant and benign. Benign tumours can also put pressure on local structures, secrete hormones and cause obstruction like malignant tumours.
61
What are the five main cancers that metastasise to bone?
BLTKP - Breast, lung, thyroid, kidney, prostate
62
What are the methods of tumour spread?
1. Haematogenesis - Via blood.2. Lymphatic - Secondary formation in lymph nodes.3. Transcolemic - Via exudate fluid accumulation.
63
What is the pathway of metastasis?
1. Detachment from primary tumour2. Invasion of other tissue3. Invasion of blood vessels4. Evasion of host defence and adherence to blood vessel endothelium5. Extravasation and colonisation
64
What is the name of a non-glandular benign tumour?
Papilloma
65
What is the name of a non-glandular malignant tumour?
Carcinoma
66
What is the name of a glandular benign tumour?
Adenoma
67
What is the name of a glandular malignant tumour?
Adenocarcinoma
68
What is the name of benign and malignant adipocyte tumours?
Benign - lipomaMalignant - liposarcoma
69
What is the name of benign and malignant striated muscle tumours?
Benign - rhabdomyomaMalignant - rhabdomyosarcoma
70
What is the name of benign and malignant smooth muscle tumours?
Benign - leiomyomaMalignant - leiomyosarcoma
71
What is the name of benign and malignant cartilage tumours?
Benign - chrondromaMalignant - chondrosarcoma
72
What is the name of benign and malignant bone tumours?
Benign - osteomaMalignant - osteosarcoma
73
What is a melanoma?
Malignancy of melanocytes
74
Which cancer never spreads to other parts of the body?
Basal cell carcinoma
75
What is a suitable treatment for leukaemia and why?
Chemotherapy as leukaemia is systemic
76
What is an example of a carcinoma that spreads to the axillary lymph nodes?
Breast carcinomas
77
What is a pro and con of conventional chemotherapy?
Pro: Effective against fast dividing tumours.Con: Non-selective for tumour cells, normal cells also get killed (diarrhoea, N+V, hair loss)
78
What is the theory behind targeted chemotherapy?
It exploits the differences between cancer cells and normal cells; this means it is more effective and has less side effects.
79
Which type of cancers is targeted chemotherapy most suited to?
Slow growing cancers.
80
What is myeloma?
Cancer of plasma cells.
81
What is multiple myeloma?
When a myeloma affects multiple parts of the body.
82
What is carcinoma in situ?
When a carcinoma is still contained and hasn't invaded the basement membrane.Often referred to as stage 0 cancer.
83
What is a mesothelioma?
Malignancy of mesothelial cells of pleura.
84
What is a major risk factor and features of mesothelioma?
Asbestos inhalation.Very large latent period (up to 45 years).Very poor prognosis.
85
How long does acute inflammation last for?
Hours to days.
86
How long does chronic inflammation last for?
Months to years.
87
Give two examples of things that may cause acute inflammation.
Infections and hypersenstivity.
88
Give two examples of things that may cause chronic inflammation.
Autoimmunity and recurrent infections.
89
Which two tissues never resolve?
Cardiac tissue and neurons - most become granular tissue and fibrotic.
90
What would raised eosinophils and granulomas indicate?
A parasite infection.
91
What can arterial thrombi cause?
MI, angina, ischaemic strokes and PVD.
92
What are the three signs of an arterial thrombi?
Cold, pale and loss of pulse.
93
What do venous thrombi cause?
Mainly DVTs which can cause PEs.
94
What are the three signs of a venous thrombi?
Tender, swollen and red.
95
How are thrombi treated?
Antiplatelets (aspirin) and anticoagulants (warfarin, DOACs).
96
What causes endothelial injuries at the start of atherogenesis?
Due to smoking, T2DM, hypertension, and increased LDL in blood.
97
Describe a fatty streak in atherogenesis.
Plaque precursor, LDL phagocytosed by macrophages to form foam cells in intima; this builds up over time.
98
What are foam cells?
LDL phagocytosed by macrophages which accumulate in a fatty streak.
99
Describe the inflammatory reaction in atherogenesis.
WBCs infiltrate the fatty streak and it gets larger.
100
Describe a fibrous cap in atherogenesis.
Fibroblasts produce smooth muscle fibrous cap which covers internal lumen of plaque.
101
What happens when a fibrous cap is damaged?
There is continuous platelet plug formation over the damaged fibrous cap, forming a large thrombus.-This occludes the artery and if in the heart - MI.
102
To which tissues does hypertrophy most commonly occur?
Muscles (including the heart).
103
What is an example of metaplasia?
Barrett's oesophagus.-From simple squamous to columnar epithelia.
104
How are leukaemias and lymphomas staged?
Ann arbor staging.
ICS
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