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My Phase 2a > Pathology > Flashcards

Pathology Flashcards

1
Q

What is inflammation

A

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

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2
Q

What are the types of inflammation

A
  • Chronic and acute AKA neutrophil-mediated inflammation and macrophages/lymphocyte mediated inflammation
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3
Q

What are neutrophil polymorphs

A

White blood cells made in the bone marrow with a very short lifespan

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4
Q

What is the rough lifespan of a neutrophil polymorph

A

2-3 days

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5
Q

Describe the shape of a neutrophil polymorph

A

Polylobed nucleus

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6
Q

Function of polymorphs

A

Phagocytose debris and bacteria and kill and digest them using lysosomes

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7
Q

What cell responds first in acute inflammation

A

Neutrophil polymorphs

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8
Q

What is a macrophage

A

A type of white blood cell

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9
Q

How do macrophages differ to neutrophils

A

Macrophages have a longer lifespan than neutrophils

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10
Q

Function of neutrophils

A
  • phagocytose debris and bacteria.
  • produce and release pro-inflammatory factors to recruit more immune cells
  • They also transport material to lymph nodes and may present the material to lymphocytes so a secondary immune reaction is induced.
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11
Q

Give 3 examples of types of macrophages

A
  1. Kupffer cells in liver
  2. Osteoclasts in bone
  3. Microglial cells in brain
  4. Alveolar macrophages
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12
Q

What is a lymphocyte

A

A type of WBC with long lifespan

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13
Q

Function of lymphocytes

A
  • produce chemicals involved in controlling inflammation and antibodies.
  • Immunological memory of the body to scale up an immune response against a previously seen microorganism
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14
Q

Function of a fibroblast

A

Produce collagenous connective tissue in scarring following some types of inflammation.

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15
Q

What are the 5 cardinal signs of inflammation?

A
  1. swelling
  2. pain
  3. heat
  4. loss of function
  5. redness
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16
Q

Stages of inflammation

A
  1. increased vessel permeability inflammatory cytokines mediate vasodilation - e.g. bradykinin, prostacyclin and nitrous oxide
  2. fluid exudate the vessel becomes leaky and fluid is forced out of the vessel
  3. cellular exudate neutrophils become abundant in the exudate
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17
Q

Sequence of chronic inflammation

A

• either progresses from acute inflammation or starts as ‘chronic’ inflammation such as infectious mononucleosis (thus better term is macrophage/lymphocyte-mediated inflammation)
• no or very few neutrophils
• macrophages and lymphocytes, then usually fibroblasts
• can resolve if no tissue damage (e.g. viral infection like glandular fever) but often ends up with repair and formation of scar tissue

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18
Q

What is a granuloma

A
  • particular type of chronic inflammation with collections of macrophages/histiocytes surrounded by lymphocytes
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19
Q

When are granulomas commonly seen?

A
  • MYcobacterial infections
    • Tb
    • Leprosy
  • Chrohns
  • sarcoidosis
  • may be seen around foreign material in tissues
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20
Q

Broad pattern of acute inflammation

A

Polymorph neutrophils first then macrophages later.

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21
Q

cells involved in chronic inflammation

A

• Lymphocytes, plasma cells, macrophages.
• Epithelioid macrophages can sometimes be seen as granulomas

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22
Q

Name five causes of inflammation

A
  1. Necrosis
  2. Infection
  3. Chemical agents, other physical agents or radiation
  4. Autoimmune reactions, especially hypersensitivity
  5. Hypersensitivity reactions
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23
Q

Why does inflammation occur

A

To bring all the cells needed for healing to the site of inflammation

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24
Q

Name 5 causes of acute inflammation

A
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25
Q

Name 4 causes of chronic inflammation

A
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26
Q

How does smoking increase risk of formation of atherosclerotic plaques

A

Endothelial damage by releasing free radicals nicotine and CO into the body and blood

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27
Q

How does hypertension cause atherosclerotic plaques

A
  • It increases the pressure in the blood vessels which damages the endothelial wall through shear forces
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28
Q

Where are blood vessels most susceptible to shearing forces

A

At a bifurcation of the vessels

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29
Q

How does diabetes increase risk of atherosclerosis

A

Diabetes increases dyslipidemia and causes hyperglycaemia which:
- Increased LDLs and free radicals
- Increases oxidised LDLs —> depositing in the tunica intima
- Reduced NO -> increased BP and reduced blood flow. NO normally relaxes blood vessels and increases blood flow.

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30
Q

How does obesity increase risk of atherosclerosis

A

Increased pro inflammatory cytokines

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31
Q

How does exercise affect the risk of atherosclerosis

A
  • Helps to rebalance the ratio of LDL:HDL
  • reduces BP
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32
Q

Stages of acute inflammation

A
  1. Changes in the vessel calibre
    • vasodilation ➡️ increased blood and cells at the site of inflammation
  2. Fluid exudate
    • vasodilation AND chemical mediators make the blood vessels more permeable
    • chemical mediators include: NO, histamine and bradykinin.
  3. Cellular exudate
    • neutrophils polymorphs accumulate in the extra cellular space.
  4. Chemotaxis in later stages
    • release of chemoattractants ➡️ increase of cells at the site of inflammation ➡️ macrophages arriving and phagocytosis debris and the pathogen.
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33
Q

What is exudate

A

Fluid that leaks out of the blood vessels into nearby tissues due to inflammation or local cellular damage.
It is composed of cells, proteins and solid materials

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34
Q

What are the outcomes of acute inflammation

A
  • Resolution = complete restoration of tissues to normal.
  • Suppuration = formation of pus. Seen with excessive exudate.
  • Organisation = inflamed tissue is replaced with granulation tissue as part of the healing process. Seen with excessive necrosis + results in fibrotic scar tissue
  • Progression to chronic inflammation
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35
Q

How can chronic inflammation begin

A
  • progression from acute inflammation
  • originating as chronic inflammation e.g. infectious mononucleosis.
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36
Q

Causes of chronic inflammation

A
  • agents resistant to phagocytosis e.g. TB and leprosy
  • agents that can’t be digested (fat, asbestos,silica)
  • autoimmune diseases
  • Crohn’s disease and UC
  • transplant rejections
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37
Q

T/F neutrophils are not involved in chronic inflammation

A

True

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38
Q

What cells are involved in chronic inflammation

A

Mainly macrophages and lymphocytes
Fibroblasts are also involved later.

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39
Q

What are the outcomes of chronic inflammation

A
  • if no tissue has been damaged then chronic inflammation can resolve.
  • most cases result in repair and scar tissue formation.
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40
Q

Define thrombosis

A

The formation of a solid mass from blood constituents in an intact vessel in a living person

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41
Q

Define embolism

A

A solid mass in the blood being carried by the circulation to a place where it gets stuck and blocks the vessel

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42
Q

What factors prevent the formation of blood clots all the time

A
  1. Laminar flow: cells travel in the centre of the arterial vessel and don’t touch the sides
  2. Endothelial cells lining the blood cells are not sticky when healthy.
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43
Q

Describe how a thrombus forms

A
  1. Platelet aggregation
  2. Platelets release chemicals when they aggregate ➡️ other platelets sticking to the AND invitation of the cascade of clotting proteins in the blood
  3. Clotting cascade ➡️ formation of fibrin, a large protein that makes a mesh for RBCs to become entrapped in.
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44
Q

What are the factors that make up Virchow’s triad and what causes them

A
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45
Q

What is transudate

A
  • Fluid that leaks out of the blood vessels due to high blood pressure pushing the fluid out
    (systemic conditions that alter the pressure in blood vessels, causing fluid to leave the vascular system)
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46
Q

Causes of embolisms

A
  • Thrombus
  • Air
  • Cholesterol crystals from atheromatous plaques
  • tumours
  • amniotic fluid
  • Fat
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47
Q

What causes an arterial vs venous thrombus

A
  • Arterial: forms on an atheromatous plaque.
  • venous: stasis
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48
Q

Where does a venous thrombus travel

A

Venous system ➡️ vena cava ➡️ pulmonary arteries and gets stuck there depending on size ➡️ pulmonary embolism it never enters arterial circulation

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49
Q

Where does an arterial thrombus embolism travel

A
  • travels anywhere downstream of the entry point
  • can travel any where in the body once it reaches the left ventricle
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50
Q

What are the potential outcomes of an arterial thrombus

A
  • MI
  • Stroke
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51
Q

What are the potential outcomes of an venous thrombus

A
  • Pulmonary embolism
  • DVT
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52
Q

Arterial thrombus treatment and why

A
  • Anti platelet Tx (aspirin and clopidogrel)
  • as the thrombus is made up mainly of platelets
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53
Q

Venous thrombus treatment

A
  • Anti-coagulants (warfarin, heparin, DOACs)
  • as mainly made up of coagulation factors and RBCs
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54
Q

Define ischaemia

A

Inadequate blood flow to a tissue

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55
Q

Define infarction

A

Reduced blood flow to a tissue to the point where cells can not be maintained ➡️ cell death.

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56
Q

Which organs are less susceptible to infarction and why

A
  • the lungs, the liver and the brain because they have dual/multiple blood supplies, so a thrombus cannot block the end arterial supply.
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57
Q

describe the time course of atherosclerosis

A

time course of atherosclerosis
* birth - no atherosclerosis
* late teenage/early 20s - fatty streaks in aorta, may not progress to established atherosclerosis
* 30s/40s/50s - development of established atherosclerotic plaques
* 40s-80s - complications of atherosclerotic plaques e.g. thrombosis, intraplaque haemorrhage

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58
Q

what are the risk factors of atherosclerosis

A
  • hypertension
  • hyperlipidaemia
  • cigarette smoking
  • poorly-controlled diabetes mellitus
  • obesity
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59
Q

what can damage endothelial cells

A

easily damaged by:
* cigarette smoke,
* shearing forces at arterial divisions
* hyperlipdaemia,
* glycosylation products

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60
Q

What are the potential outcomes of thombi

A
  1. Resolution - break down, normal
  2. Organisation - leaves scar tissue behind
  3. Embolism - dislodges and travels round to another part of the body and causes a blockage.
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61
Q

What do apoptosis and necrosis have in common

A

Both cause cell death

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62
Q

Define apoptosis

A

Programmed cell death in single cells ➡️ cell turnover.
* controlled by cellular signals
* no associated inflammation or secondary tissue damage

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63
Q

Why is apoptosis important

A

It prevents the accumulation of genetic damage caused by repeated divisions which could ➡️ cancer cell development.

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64
Q

How does a cell decide to apoptose?

A

The protein P53 can detect the amount of DNA damage in a cell and uses this to trigger apoptosis

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65
Q

How does apoptosis occur

A

If apoptosis is deemed necessary, the cell triggers a cascade of proteins that ➡️ the release of enzymes that auto digest the cell.
- the cell shrinks, organelles are retained and chromatin is fragmented for easy phagocytosis

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66
Q

What are the mechanisms of apoptosis

A
  1. Intrinsic
    • Bax acts on the mitochondrial membrane to release cytochrome C ➡️ release of caspases ➡️ apoptosis
  2. Extrinsic
    • Fas ligand binds to the Fas receptor expressed on the cell membrane ➡️ release of caspases ➡️ apoptosis
  3. Cytotoxic
    • CD8+ cells bind to the cell and release granzyme B ➡️ release of perforins ➡️ release of caspases ➡️ apoptosis
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67
Q

Role of apoptosis in health

A

Important for:
* Normal cell turnover e.g. intestinal villi cells at the tips are removed and replaced by the cells below
* Development e.g. removal of interdigital webs.

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68
Q

Role of apoptosis in disease

A
  • cancer cells don’t apoptose when they should ➡️ tumour generation that increase in size and genetic mutation
    • usually due to mutation in P53 gene meaning DNA damage isn’t detected and apoptosis isn’t triggered
  • HIV virus can induce apoptosis in CD4 helper cells ➡️ major reduction in their numbers ➡️ immunodeficiency
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69
Q

Define necrosis

A

The destruction of numerous cells by an external factor such as injury or disease.
Mediated by extracellular factors

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70
Q

4 clinical examples of necrosis

A

• Infarction due to loss of blood supply e.g. myocardial infarction, cerebral infarction
• Frostbite
• Toxic venom from reptiles and insects
• Pancreatitis

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71
Q

What are the outcomes of necrosis

A
  • macrophages phagocytose dead cells to clear up
  • the necrotic tissue is replaced with fibrous scar tissue if the tissue is unable to regenerate
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72
Q

Give one example of a type of necrosis

A

Caseous necrosis - soft cheese
* can be caused by TB

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73
Q

What happens if necrosis is left long term

A

Inflammation and decreasing blood supply ➡️ tissue death (gangrene) ➡️ death
* e.g. myocardial infarction

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74
Q

Define hypertrophy

A

Increase in the size of an organ due to an increase in the size of its constituent cells

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75
Q

Where is hypertrophy seen

A

In organs where cells can’t divide
E.g. skeletal muscle in athletes

76
Q

Define hyperplasia

A

An increase in the size of an organ due to an increase in the number of its constituent cells

77
Q

Where is hyperplasia seen

A

In organs where the cells can divide
E.g. BPH and endometrial hyperplasia

78
Q

What is mixed hypertrophy/hyperplasia and where can it be seen

A
  • Increase in the size of an organ due to an increase in the size and number of its constituent cells.
  • seen in organs where the cells can divide
  • e.g.smooth muscle cells of the uterus during pregnancy
79
Q

Define atrophy

A

A decrease in the size of an organ due to a decrease in the size AND/OR number of the organ’s constituent cells

80
Q

Give 2 examples of atrophy

A
  1. Alzheimer’s dementia
  2. Quadriceps muscle atrophy after a knee injury
81
Q

Define metaplasia

A

A change in cell type from one fully differentiated cell type to another

82
Q

What causes metaplasia

A

Usually a constant change in the environment of an epithelial surface
E.g. Barrett’s oesophagus

83
Q

What is Barrett’s oesophagus?

A

Continued acid reflux from the stomach ➡️ oesophageal squamous epithelium changing ➡️ columnar glandular epithelium

84
Q

3 examples of metaplasia

A
  1. Barretts oesophagus oesophageal squamous epithelium changing ➡️ glandular columnar epithelium
  2. bronchial epithelium from ciliated columnar epithelium ➡️ squamous epithelium due to continued cigarette smoke.
  3. the uterine cervix from columnar epithelium ➡️ squamous epitheli- um at puberty when it is exposed to the acidic environment of the vagina
85
Q

Metaplasia can lead to cancer T/F

A

False
Metaplasia itself is a benign, non-cancerous condition; however, if left untreated, the cells undergoing metaplasia can become dysplastic (i.e., atypical in shape and size), which can eventually lead to cancer

86
Q

Define dysplasia

A

Abnormal changes in cellular shape size or organisation that may progress onto cancer.
features seen in histopathological exam with light microscope

87
Q

Types of dysplasia

A

Mild
Moderate
Severe
Carcinoma in situ
Invasive cancer

88
Q

Why is identification of dysplastic cells important

A

If identified early, treatment can be given to eradicate dysplasia and prevent development of cancer e.g. cervical screening programme.

89
Q

define neoplasia

A
  • A lesion resulting from the autonomous, or relatively autonomous, abnormal growth of cells which persists after the initiating stimulus has been removed
90
Q

what causes neoplasia

A
  • carcinogens
91
Q

give 5 examples of carcinogens

A
  1. chemicals
  2. viruses
  3. non/ionising radiation
  4. hormones
  5. bacteria, fungi and parasites
92
Q

define carcinogenesis

A

the transformation of normal cells to neoplastic cells through permanent genetic alterations /mutations.

93
Q

erythrocytes can become neoplastic T/F

A

False
carcinogenesis and neoplastic cells can only arise from nucleated cells therefore the erythrocytes cannot undergo carcinogenesis BUT their precursors can -> neoplastic erythrocytes.

94
Q

types of neoplasia

A

benign and malignant

95
Q

features of benign neoplasia

A
  • slow growing
    • have low mitotic rate
  • often well circumscribed
    • no invasion of surrounding lymph or tissue
    • no metastaiss to other areas
  • they resemble the cell of origin
    • rarely necrotic or ulcerate
96
Q

what are the consequenses of a longterm benign growth

A
  • pressure on adjacent tissues
  • obstruction of flow in ducts/hollow organs
  • production of hormones
  • transformation into malignant neoplasms
  • anxiety
97
Q

what are the properties of malignancy

A
  1. Invasive
  2. fast growing with a high mitotic rate of division
  3. can metastasis to other areas
  4. poorly defined borders with irregular infiltrative borders
  5. variable resemblance to cell of origin
    • commonly necrotic
    • commonly ulcerates
98
Q

describe the structure of a neoplasm

A
  • neoplastic cells
    • monoclonal cells derived from nucleated cells
    • growth pattern similar to parent cell
    • synthetic activity related to parent cell i.e. producing hormones, mucin etc.
  • stroma
    • connective tissue network that provides mechanical support and nutrition
99
Q

how do tumours survive and grow

A

they produce factors such as TAF to stimulate angiogenesis to bring nutrients and blood to itself- tumour angiogenesis factor

100
Q

what is essential for the growth of tumours

A

angiogenesis

101
Q

features of malignant neoplasms

A
  • hyperchromatic nuclei
  • pleomorphic nuclei
  • increased mitotic activity
  • necrosis and ulceration are common
  • growth on mucosal surfaces and skin is often endophytic
102
Q

define endophytic growth

A

growth down and inwards

103
Q

why are malignant neoplasms concerning

A

they cause morbidity and malignancy by:
* destruction of adjacent tissue
* blood loss from ulcers
* obstruction of flow
* hormone production
* paraneoplastic effects such as clubbing
* anxiety and pain.

104
Q

define histogenesis

A

the specific cell of origin of a tumour

105
Q

what can neoplasms arise from

A
  • epithelial cells
  • connective tissues
  • lymphoid/ haematopoietic organs
106
Q

what does the suffix “oma” indicate?

A

a neoplasm

107
Q

how is the prefix of a neoplasm determined

A

by behavioral classification and cell type

108
Q

define a papilloma

A

benign tumour of non-glandular, non-secretory epithelium

109
Q

define an adenoma

A

benign tumour of glandular or secretory epithelium

110
Q

define a carcinoma

A

malignant tumour of epithelial cells

111
Q

define an adenocarcinoma

A

carcinomas of glandular epithelium i.e. malignant tumour of glandular epithelium

112
Q

7 types of benign connective tissue neoplasms and their origins

A
  1. lipoma → adipocytes
  2. osteoma →bone
  3. chondroma → cartilage
  4. angioma → vascular
  5. rhabdomyoma → striated muscle
  6. leiomyoma → smooth muscle
  7. neuroma → nerves
113
Q

6 types of malignant connective tissue neoplasms

A
  1. liposarcoma → adipocytes
  2. osteosarcoma →bone
  3. chondrosarcoma → cartilage
  4. angiosarcoma → blood vessels / vascular
  5. rhabdomyosarcoma → striated muscle
  6. leiomyosarcoma → smooth muscle
114
Q

whats the difference between a carcinoma and a sarcoma

A
  • carcinomas form in the epithelial cells
  • sarcomas form in the bone and soft/ connective tissue cells
115
Q

what is an anaplastic tumour

A

where the cell type of origin is unknown

116
Q

what do you call a tumour with an unknown cell type of origin

A

an anaplastic tumour

117
Q

True /False: all “-omas” are neoplasms

A

False
exceptions = granuloma, mycetoma, tuberculoma

118
Q

All malignant tumours are carcinomas or sarcomas True/False

A

False:
* melanoma: malignant neoplasm of melanocytes
* Mesothelioma: malignant neoplasm of mesothelial cells
* lymphoma: malignant neoplasm of lymphoid cells

119
Q

T/F: melanomas can be benign and/or malignant

A

False - no such thing as a benign melanoma

120
Q

how are tumours graded

A

based on similarity to the parent cell

121
Q

define the stage and grade of a tumour

A
  • The stage of a cancer describes the size of a tumour and how far it has spread from where it originated.
  • The grade describes the appearance of the cancerous cells.
122
Q

what are the gradings of tumours

A

grade 1 : cancer cells that resemble normal cells and aren’t growing rapidly.
grade 2 : cancer cells that don’t look like normal cells and are growing faster than normal cells.
grade 3: cancer cells that look abnormal and may grow or spread more aggressively

123
Q

what are the number stages of a tumour

A

stage 0 – the cancer is where it started (in situ) and hasn’t spread
stage 1 – the cancer is small and hasn’t spread anywhere else
stage 2 – the cancer has grown, but hasn’t spread
stage 3 – the cancer is larger and may have spread to the surrounding tissues and/or the lymph nodes (or “glands”, part of the immune system)
stage 4 – the cancer has spread from where it started to at least 1 other body organ, also known as “secondary” or “metastatic” cancer

124
Q

how are tumours staged?

A
  • number stages
  • TNM stages
125
Q

what is the TNM system

A

a method of staging a cancer
* T describes the size of the tumour, with numbers 1 to 4 (1 = small, 4 = large)
* N stands for lymph nodes, with numbers 0 to 3 (0 = no lymph nodes have cancer, 3 = many lymph nodes do)
* M stands for metastases or whether the cancer has spread to another part of the body, with numbers 0 or 1 (0 = it has not spread, 1 = it has)
* e.g. an advanced cancer that has spread may be T4 N3 M1.

126
Q

T/F: carcinogenesis is a single step process

A

FALSE its a multistep process

127
Q

difference between oncogenic and carcinogenic agents

A
  • oncogenic = tumour causing (not necessarily cancer)
  • carcinogenic = cancer causing
    • act on DNA ∴ are mutagenic
128
Q

define atherosclerosis

A

plaques forming in the tunica intima and media of high pressure blood vessels - arteries.

129
Q

what is in an atherosclerotic plaque

A
  • cholesterol
  • smooth muscle
  • foam cells
  • platelets
  • fibroblasts
  • macrophages
130
Q

decribe the formation of an atherosclerotic plaque

A
  1. Endothelial cell dysfunction (high cholesterol damages endothelium)
  2. High levels of LDL in the blood will begin to accumulate in the arterial wall in the tunica intima . the cholesterol becomes oxidised and causes an inflammatory response.
  3. Macrophages are attracted to the site of damage and take up lipid to form foam cells (the inflammatory response)
  4. Formation of a fatty streak = earliest stage of plaque
  5. The foam cells release lots of their own products - cytokines and growth factors→ proliferation which causes:
    1. Smooth muscle migration AND proliferation to intima.
    2. Increased collagen production around the lipid core → collagen formation of a fibrous cap –> stable atheroma
    3. an increase in the plaque size and level of vascular occlusion
131
Q

define exophytic growth

A

growth outwards and upwards

132
Q

Basal cell carcinoma never metastasises
True/ False

A

True

133
Q

describe the steps of metastasis

A
  1. Detachment of tumour cells from their neighbours
  2. Invasion of the surrounding connective tissue to reach conduits of metastasis
  3. Intravasation into the lumen of vessels
  4. Evasion of host defence mechanisms, such as NK cells
  5. Adherence to endothelium at a remote location
  6. Extravasation of the cells from the vessel lumen into the surrounding tissue
  7. Tumour cells proliferate in the new environment
134
Q

define metastasis

A

The process whereby malignant tumours spread from their site of origin to form other tumours at distant sites

135
Q

cancers which commonly metastasise to the liver

A
  • colon
  • retum
  • stomach
  • pancreas
136
Q

tumours that commonly metastasise to the bone

A

BLT KP
* breast
* lung
* thyroid
* kidney
* prostate

137
Q

define a micro-invasive carcinoma

A

a carcinoma that crosses the basement membrane

138
Q

define an invasive carcinoma

A

tumour crosses the basement membrane and enters the stromal tissue, giving it access to blood vessels and lymphatics

139
Q

define carcinoma in situ

A

cancer cells held in place by a basement membrane, meaning it has no access to blood vessels and lymphatics

140
Q

what agents + features does a tumour use to invade the basement membrane

A
  • proteases - matrix metalloproteinases
    • collagenase
    • cathepsin D
    • urokinase-type plasminogen activator
  • cell motility
    • tumour cell derived motility factors
    • breakdown products of extracellular matrix.
141
Q

define intravasation

A

tumour cells gaining entry to and moving through blood and lymphatic vessels

142
Q

what agents do tumour cells use for intravasation

A
  • collagenases
  • cell motility
143
Q

how do tumour cells evade the immune system

A
  • aggregation with platelets
  • shedding of surface antigens
  • adhesion to other tumour cells
144
Q

define extravasation

A

the movement of tumour cells from the inside of the vessel into the tissue of an organ

145
Q

what do cancerous cells use to carry out extravasation

A
  • adhesion receptors
  • collagenases
  • cell motility
146
Q

how do cancerous cells grow at a metastatic site?

A

they produce and use growth factors to promote their growth

147
Q

classes of carcinogens

A
  1. chemical
  2. viral
  3. ionising
  4. Biological agents: hormones, parasites and mycotoxins
  5. miscellaneous - asbestos
148
Q

methods of tumour spread

A
  1. haematogenous
    • via blood
  2. lymphatic
    • secondary formation in lymph nodes. e.g. lymphoma
  3. transcolemic
    • via exudative fluid accumulation, spread through pleural, pericardial and peritoneal effusions
149
Q

how do chemical carcinogens cause cancer

A
  • some act directly on DNA
  • most are metabolically converted from pro-carcinogen →ultimate carcinogens.
    • the enzymes needed for this may be ubiquitous or confined to certain organs
150
Q

5 examples of chemical carcinogens

A
  1. alkylating agents
  2. polycyclic aromatic hydrocarbons
  3. aromatic amines
  4. nitrosamines
  5. dyes, paint rubber etc
151
Q

examples of viral carcinogens

A
  1. human herpes 8 virus → Kaposi sarcoma
  2. Epstienn Barr virus → Burkitt lymphoma
  3. Hep B/ Hep C→ hepatocellular carcinoma
  4. human papillomavirus → squamous cell carcinoma of the cervix, penis, anus, head and neck.
152
Q

examples of ionising carcinogens

A
  • UVA and/or UVB exposure increases risk of basal cell carcinoma, melanoma and squamous cell carcinoma.
  • uranium exposure
  • nuclear material exposure
  • radiograph material
153
Q

types of biological carcinogens with examples

A
  1. hormones
    • rise in oestrogen →increased risk of mammary/ endometrial cancer.
    • anabolic steroids can → hepatocellular carcinoma
  2. mycotoxins
    • Aflatoxin B1 → hepatocellular carcinoma
  3. parasites
    • shistosoma → bladder cancer (SCC)
154
Q

examples of miscellaneous carcinogens

A
  • asbestos
  • metals
155
Q

risk factors for developing cancer

A
  • ethnicity
  • diet and lifestyle
  • premalignant lesions
  • Constitutional factors - age, gender, genetics etc.
156
Q

how could lifestyle influence cancer risk

A
  • diet and exercise:
    • excess alcohol increases cancer risk of liver colon breast mouth
    • obesity increases risk of breast, colon and kidney cancer
    • exercise lowers risk of colon and breast cancer
  • sexual behaviour
    • unprotected sex increases risk of HPV-related cancer
  • smoking
157
Q

examples of premalignant conditions that increase risk of cancer

A
  • colonic polyps
  • cervical dysplasia
  • ulcerative colitis
  • undescended testes.
158
Q

how do sarcomas typically spread

A

via blood = haematoogenous

159
Q

how do carcinomas typically spread

A

mostly lymphatic

160
Q

what are the steps in neutrophil polymorph emigration?

A
  1. margination
  2. pavementing
  3. pass between endothelial cells
  4. pass through basal lamina and migrate into the adventitia
161
Q

what is margination of neutrophils?

A

caused by loss of intravascular fluid and increase in plasma viscosity with slowing down of flow at the site of acute inflammation
neutrophils flow in plasmatic zone

162
Q

what is pavementing of neutrophils?

A

adhesion of neutrophils to the vascular endothelium, occurring at sites of acute inflammation

163
Q

where does pavementing occur?

A

only seen in venules

164
Q

What are these signs indicative of:
- Organelles to be damaged
- Cell lysis
- Inflammation
- Altered chromatin

A

necrosis

165
Q

4 signs of necrosis

A
  • Organelles to be damaged
  • Cell lysis
  • Inflammation
  • Altered chromatin
166
Q

An adenocarcinoma is …

A

a malignant neoplasm of glandular origin

167
Q

a leiomyoma is…

A

a benign neoplasm of smooth muscle

168
Q

a rhabdomyoma is…

A

a benign neoplasm of striated muscle

169
Q

a malignant neoplasm of glandular origin =

A

An adenocarcinoma

170
Q

a benign neoplasm of smooth muscle =

A

a leiomyoma

171
Q

a benign neoplasm of striated muscle =

A

a rhabdomyoma

172
Q

a benign neoplasm of striated muscle =

A

a rhabdomyoma

173
Q

what is a proto-oncogene

A
  • a normal gene
  • Genes that encode proteins that function to stimulate cell division, inhibit cell differentiation, and halt cell death.
174
Q

what is an oncogene

A
  • An abnormal proto-oncogene that drives the neoplastic behavior of cells.
  • Can be due to mutations or over-expression.
175
Q

what is a tumour suppressor gene

A
  • A gene which inhibits the transformation of a cell into a neoplastic state.
176
Q

Types of tumour supressor genes

A
  • Caretaker gene which is involved in repairing DNA.
  • Gate keeper genes which promote apoptosis.
177
Q

how do mutations in tumour supressor genes → cancer

A

Mutations in tumour suppressor genes
prevent DNA repair → mutations and therefore → excessive cellular proliferation.

178
Q

how do mutations in proto-oncogenes → cancer

A

Mutations in proto-oncogenes
prevent apoptosis from occurring.

179
Q

which cancers are screened for in the UK and how

A
  • breast cancer - mammograms
  • bowel cancer -FIT test
  • cervical cancer - smear test
180
Q

tumours which more commonly metastasise to the lung

A
  • sarcomas
  • any common cancer
181
Q

tumours which more commonly metastasise to the liver

A
  • colon,
  • stomach,
  • pancreas,
  • carcinoid tumours of intestine
182
Q

tumours which more commonly metastasise to bone

A
  • prostate
  • breast
  • thyroid
  • lung
  • kidney
183
Q

How do liver metastases access the liver

A

Through the hepatic portal vein

184
Q

How do lung metastases reach the lung

A

From the body through the vena cava ➡️ the heart ➡️ pulmonary artery➡️ lungs

185
Q

describe the process of anaphylais

A
  1. Allergen binds to (Fab region on) IgE (1),
  2. which stimulates mast cells to produce HISTAMINE + tryptases/leukotrienes (1),
  3. which results in increased vessel permeability/bronchoconstriction/vasodilation [any 1 of these] (1)

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