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Pathology Flashcards

1
Q

What is cancer?

A

Uncontrolled cell division that can invade other tissue and impede their function

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2
Q

What is a tumour?

A

Any swelling Can be benign or malignant

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3
Q

What is a neoplasm?

A

New growth not in response to any stimulus

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4
Q

Define malignant

A

Metastatic potential is present This involves any neoplasm invading the basement membrane

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5
Q

What is metastasis?

A

The spreading of a neoplasm to a different part of the body

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6
Q

Give three pre-malignant stages

A
  1. Dysplasia - disordered growth with no stimulus (no invasion of basement membrane)
  2. Metaplasia - change of one cell type to another
  3. Hyperplasia - increase in cell number
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7
Q

Metaplasia is a response to _____

A

Stress

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8
Q

What can initiate metaplasia?

A
  1. Injurious or noxious stimuli
  2. Cytokines and cell signals
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9
Q

Why are post-menopausal obese women at risk to hyperplasia (and cancer)?

A

Oestrogen will cause proliferation of the endometrium as part of the menstrual cycle. Cholesterol is similar in structure to oestrogen Obese women have high cholesterol which can cause proliferation in the endometrium Due to increased (an unnecessary) proliferations, these women have more “chances” for cells to begin to grown autonomously and for hyperplasia to occur

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10
Q

What occurs in dysplasia that does not occur in either metaplasia or hyperplasia?

A

A genetic abnormality is developed

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11
Q

What is carcinoma in-situ?

A

This is the final stage a neoplasm goes through before becoming malignant (invading basement membrane and spreading by metastases) This is the same as high-grade dysplasia

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12
Q

How is the N:C (nuclear:cytoplasmic) ratio affected in malignant cells affected?

A

N:C ratio is high

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13
Q

List some causes of cancer

A
  1. Genes
  2. Smoking
  3. Alcohol
  4. UV radiation, and other rdiation types
  5. Drugs
  6. Infections
  7. Obesity
  8. Burnt toast…supposedly Etc.
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14
Q

What are Weinberg Hallmarks?

A

These are “bad decisions” made by a cell that are key to becoming malignant.

  • Increased growth signals
  • Growth suppression removed
  • Avoiding apoptosis
  • Achieving immortality
  • Becoming invasive
  • Making own blood supply (angiogenesis)
  • Lose cellular DNA spellchecking
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15
Q

What is Li-Fraumeni syndrome?

A

Genetic condition affecting the tp53 gene which codes for p53. This means sufferers from LFS are unable to stop excessive growth and attempt DNA repairs (or activate apoptosis)

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16
Q

How does radiation cause cancer

A

Pyrimidine dimers are formed in DNA which are molecular lesions involving two consecutive bases on a single DNA strand to bind together ruining the normal base pairing Numerous instances can cause repair mechanisms to become overwhelmed

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17
Q

Describe briefly the cell cycle

A
  1. Cyclin D activated CDK4 (cyclin dependent kinase)
  2. CDK4 phosphorylates Rb (retinoblastoma)
  3. Rb now unbinds from DNA allowing for DNA replication to occur - access to DNA is now possible
  4. Synthesis phase now occurs involving DNA replication
  5. M phase follows after G2 and the cell divides
  6. Cytokinesis is when the cell physically divided
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18
Q

What are oncogenes?

A

A gene with the potential to cause cancer It involves increased growth

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19
Q

What are tumour supressors?

A

These are genes preventing the pathway to cancer

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20
Q

How can neoplastic cells evade DNA spellchecking?

A

Destroying spellcheck proteins such as P53

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21
Q

What happens to a tumour in the bloodstream?

A

It will aggregate with platelets This means it will eventually slow down and stop within a blood vessel and grow in this new location

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22
Q

Name 2 growth factors that can aid angiogenesis (for neoplasms)

A
  1. VEGF (vascular endothelial growth factor)
  2. PDGF (platelet derived growth factor)
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23
Q

What are the three stages involved in the pathway of mutations and neoplasm development?

A
  1. Initiation - first mutation
  2. Promotion - accumulation of mutations (dysplasia)
  3. Persistance - malignant
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24
Q

FISH is better than PCR for _____ genetic abnormalities

A

Large

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25
Q

PCR is ideal for _____ genetic abnormalites

A

Small

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26
Q

What are the functions of p53? (4)

A
  1. Cell cycle arrest at G1
  2. Increase levels of p21 to inhibit CDKs preventing Rb phosphorylation and hence DNA replication
  3. Apoptosis activation when damage is too great
  4. Activate repair mechanisms when damage is minimal
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27
Q

What are first principles in relation to identifying neoplasms?

A

These are quick decisions that can make an estimate as to whether the neoplasm appears malignant or not

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28
Q

How do benign tumour look?

A
  1. round and smooth
  2. homogenous
  3. symmetrical
  4. Normal N:C ratio
  5. Slow growth
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29
Q

How do malignant tumours look?

A
  1. Not symmetrical
  2. jagged edges
  3. heterogenous
  4. High N:C ratio
  5. Fast growth
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30
Q

What is differentiation?

A

The process by which stem cells develop into mature cells types

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31
Q

What can poor cell differentiation indicate?

A

Neoplasms Potentially malignant

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32
Q

What is pleomorphism?

A

The presence of many forms of the “same” cell type - poor differentiation has taken place

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33
Q

What is hyperchromasia?

A

A cell which has a nucleus that stains very darkly - highlights large amount of genetic material suggesting fast growth and malignancy

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34
Q

Why does rapid cell division in neoplasms impact the number of mutations developed?

A

The more divisions that take place, the more chances there is for mutation

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35
Q

What is a neoplasm of the epithelium called?

A

Carcinoma - always malignant

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36
Q

What is a benign neoplasm of glandular cells called?

A

Adenoma

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37
Q

What is a benign neoplasm of squamous cells called?

A

Papilloma

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38
Q

What is a neoplasm of bladder epithelial cells called?

A

Urothelial cell carcinoma - always malignant

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39
Q

What is a malignant neoplasm of glandular cells called?

A

Adenocarcinoma

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40
Q

What is a malignant neoplasm of squamous cells called?

A

Squamous cell carcinoma

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41
Q

What are malignant neoplasms of connective tissue (mesenchyme) called?

A

Sarcomas

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42
Q

What are the names of benign/malignant neoplasms of fat tissue?

A

Benign - lipoma Malignant - liposarcoma

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43
Q

What are the names of benign/malignant neoplasms of bone?

A

Benign - osteoma Malignant - osteosarcoma

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44
Q

What are the names of benign/malignant neoplasms of cartilage?

A

Benign - enchondroma Malignant - chondrosarcoma

45
Q

What are the names of benign/malignant neoplasms of skeletal muscle?

A

Benign - rhabdomyoma

Malignant - rhabdomyosarcoma

46
Q

What are the names of benign/malignant neoplasms of smooth muscle?

A

Benign - leiomyoma

Malignant - leiomyosarcoma

47
Q

What are the names of benign/malignant neoplasms of nerves?

A

Benign - neurofibroma (or schwannoma)

Malignant - peripheral nerve sheath tumour

48
Q

What are the names of benign/malignant neoplasms of blood vessels?

A

Benign - haemangioma

Malignant - angiosarcoma

49
Q

What are the names of benign/malignant neoplasms of the CNS?

A

Benign - gliomas

Malignant - named after benign version with malignant added in front

50
Q

What is the name of malignant neoplasms of the skin?

A

Melanoma

51
Q

What are names for blood neoplasms?

A

All are malignant Leukaemia Lymphoma

52
Q

When referring to neoplasms what does “stage” refer to?

A

Distance from origin

53
Q

In relation to neoplasms, what do karyotypes allow for?

A

Translocations to be discovered and defined

54
Q

When referring to neoplasms what does “grade” refer to?

A

Level of differentiation

55
Q

What is the difference between neoplasia and dysplasia?

A

Neoplasia - autonomous growth Dysplasia - disordered growth

56
Q

What do cancers do to the body?

A
  1. Compression/blockage of vessels/airways or ducts
  2. Impacts tissue function
  3. Haemorrhage - by infiltration
  4. Infiltrating bone marrow can weaken the immune system
57
Q

Tumours are very metabolically active using large amounts of energy, what is the name of the weight loss associated with this?

A

Cachexia

58
Q

In which two ways can growing occur?

A
  1. Hyperplasia - increase in cell number
  2. Hypertrophy - increase in cell size
59
Q

Whta causes hyperplasia?

A

An external stimulus

(when removed, growth is reversed)

60
Q

What is atrophy?

A

The decrease in cell size

61
Q

What is metaplasia?

A

The reversible change from one mature cell type to another

62
Q

Metaplasia occurs in a response to signals delivered to stem cells. What can some of these signals be due to?

A
  • Cytokines
  • Growth factors
  • Other chemicals such as noxious stimuli
63
Q

What are the four main stages in the cell cycle?

A
  • G1
  • S
  • G2
  • M
64
Q

In the cell cycle what does G1 consist of?

A
  • The cell increases in size as protein synthesis increases
  • Cyclin dependent kinase 4 (CDK4) becomes activated by cyclin D due to phosphorylation and a complex is formed between the two
  • After sufficient CDK4 is activated the cycle can proceed
  • Retinoblastoma (Rb) can be phosphorlated by the complex and it comes free from E2F
  • E2F can now act as a transcription factor
65
Q

What is retinoblastoma?

A

A transcription inhibitor

(normally binds to E2F)

66
Q

What occurs in stage S of the cell cycle?

A

DNA replication occurs

67
Q

What occurs in stage G2 of the cell cycle?

A
  • The cell grows more due to increased protein synthesis
  • P53 checks for errors in DNA replication
  • It can attempt to fix errors or initiate apoptosis if the errors are too severe
68
Q

Some cells are terminally differentiated and cannot divide or repair (e.g. neurones). What is a term to describe this?

A

Replicative senescence

69
Q

What are telomeres?

A

They consist of a TTAGGG sequence at the end of a chain

They prevent the chromosome from degrading and “unravelling”

Telomere shortening is linked to ageing

70
Q

What does the term “resolution” mean in terms of wound repair?

A

Returns tissue completely to normal

(occur when injury is minimal, there is good vascualr supply and the injurious agent is easily removed)

71
Q

What is suppuration?

A

The production of pus

72
Q

In terms of tissue repair, what does the term “organisation” mean?

A

Resolution cannot occur, and despite healing, scar tissue is present

This often occurs when the injury goes beyond the basement membrane

(occur if there is necrosis, large quantities of fibrin produced or poor blood supply)

73
Q

What is granulation tissue?

A

When tissue becomes injured, the site is infiltrated with capillaries and myofibroblasts (muscle cells)

Collagen and smooth muscle are depositied

This tissue is ganulation tissue and has a red shiny appearance

74
Q

Why does scarring occur and what is the consequence?

A

It occurs when myofibroblasts mature and produce collagen which causes the scar

This therefore means the functioning of that tissue segment is lost

75
Q

Depending on what is found pathologically during autopsy, how can the recency or cause of death be determined?

A

Presence of neutrophils mean recent injury

Granulation tissue means there has been around 2 weeks since injury

Scarring can mean anything in excess of 6 weeks

76
Q

What is scarring of the liver called?

A

Cirrhosis

77
Q

What is the consequence of cirrhosis?

A

Liver failure

(toxins cannot be removed from the blood as efficiently, and proteins are not as easily synthesised)

78
Q

What are the cell types that are most dominant in both acute and chronic inflammation?

A

Acute - neutrophils

Chronic - lymphocytes

79
Q

What are the two categories of foreign bodies?

A

Both can potentially lead to granuloma formation

  1. Exogenous - talc, asbestos, oil
  2. Endogenous - keratin, bone, crystals
80
Q

Which types of infections may lead to granuloma formation?

A
  • Parasites
  • Worms
  • Eggs
  • Syphilis
  • Mycobacterium (TB)
81
Q

Tb granuloma is cause by what?

A

Caseous necrosis (cheesy)

82
Q

What are the two types of cell death?

A
  1. Apoptosis
  2. Necrosis
83
Q

What are the three types of necrosis?

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Caseous necrosis
84
Q

Describe coagulative necrosis

A
  • Dead cells are consumed by enzymatic processes and other cells
  • Ghost outlines exist since the nucleus is no longer present
  • Cells are therefore no longer living so do not degrade properly
85
Q

Describe liquefactive necrosis

A
  • No cell structure is maintained
  • Cells are liquefied
  • This is normally associated with bacterial or fungal infections
86
Q

Describe caseous necrosis

A
  • Associated with Tb
  • A Ziehl-Neelson stain can aid identification of caseous necrosis
  • Involves granulomatous inflammation with central necrosis
87
Q

What is the key difference between apoptosis and necrosis?

A

Apoptosis requires energy, necrosis does not

88
Q

Apoptosis is normally physiological, but when may it be pathological?

A
  • Injury
  • Radiation damage
  • Chemotherapy
  • Viral infections
  • Cancers
  • After transplant
89
Q

What are the two mechanisms for apoptosis?

A
  • Extrinsic
  • Intrinsic
90
Q

Describe the extrinsic pathway for apoptosis

A
  • It involves death receptor initiation
  • FasL binds to death receptor Fas which activates caspases
  • FADD, an adapter protein, bridges the gap between the Fas receptor and the caspases
  • It is the death inducing signalling complex that undergoes conformational change when the Fas receptor is bound
  • A caspase cascade occurs
91
Q

Describe the intrinsic pathway for apoptosis

A
  • Normally growth signals promote anti-apoptotic molecules in the mitochondrial membrane
  • Growth signals become deactivated
  • They are replaced by Bax and Bak - apoptotic regulators
  • This increases the permeability of the mitochondria
  • Proteins called cytochrome C escape inducing apoptosis
92
Q

After apoptosis is induced, what then happens to the cell?

A
  • Cells shrink by pyknosis (irreversible condensation of chromatin in the nucleus)
  • The nucleus clumps and break up
  • The cytoplasm breaks up forming blebs
  • Macrophages remove debris
93
Q

How is cellular ageing caused? (3)

A
  1. Oxidative stress by free radical damage
  2. Accumulation of metabolic by products such as lipofuscin (this accumaltes with age and is toxic to cells)
  3. Finite cell divisions
94
Q

What are telomeres?

A

The TTAGGG sequence at the end of a chromosome

This prevents DNA unwinding

The number of repeats is reduced with each division and will eventually become depleted meaning cells can no longer divide

95
Q

Why do stem cells never die?

A

Telomerase continually renews the TTAGGG repeats

This maintains telomere length

Telomerase is not active in normal cells, but can be in cancerous cells conferring immortality

96
Q

After injury describe the vascular changes that occur

A
  • Vasodilatation occurs
  • Histamine and nitric oxide control this process
  • This causes calor and rubor
97
Q

What is the consequence of vasodilatation in vessels after injury?

A

Blood flow is slowed down (stasis) leading to white cell margination

98
Q

As a result of white cell margination, how do white cells interact with the endothelial wall?

A
  • They will bind, via carbohyrate groups, to selectins which are luminal proteins on the endothelial wall
  • This attraction has low affinity so the white cell rolls along the vessel wall
  • The release of chemokines, by macrophages will activate white cells allowing them to bind to selectins more strongly and also to the vessel wall via integrin to ICAM-1 and VCAM-1 which results in much stronger affinity
  • TNF and IL-1 will increase expression of ICAM-1 and VCAM-1
  • Histamine and thrombin are released from inflammatory cells which increase selectin expression
  • After coming to a halt, white cells undergo diapedesis
99
Q

During inflammation, why do vessels become leaky?

A

White cells need to undergo diapedesis and reach the site of inffection or injury

100
Q

“Leaky” vessels during inflammation is brought about by many mechanisms, what are these?

A
  • Endothelial cell contraction (muscle tissue) - this is caused by histamine, bradykinin, substance P and leukotrienes
  • Direct injury
  • White cells - self harm will release damaging toxins
  • Transcytosis - VEGF mediated, macromolecules are captured in vesicles on one side of the cell, drawn across the cell and ejected from the other side
  • New vessel formation - new vessels are weaker and leakier, their production is mediated by VEGF
101
Q

What is VEGF?

A

Vascular endothelial growth factor

102
Q

What is chemotaxis?

A

Movement of cells along a chemical gradient migrating to the source of injury

103
Q

What are the three phases of phagocytosis?

A
  1. Recognition and attachment
  2. Engulfment
  3. Killing and degredation
104
Q

Describe the recognition phase of phagocytosis

A

Bacterial surfaces express mannose receptors

Opsonins are antibodies or any other substance increasing suceptibility to phagocytes

The complement system will also surround foreign material

105
Q

Describe the engulfment phase of phagocytosis

A

Pseudopods (arms) of the phagocyte surround the foreign material forming a vesicle termed a phagosome

The phagosome will then join with a lysosome and form a phagolysosome

106
Q

Describe the killing an degredation phase of phagocytosis

A

Reactive oxygen species within lysomes kill pathogens

This ROS is created due to NADPH which oxidises oxygen

107
Q

What are the 4 clinical features of inflammation?

A
  1. Rubor
  2. Calor
  3. Tumour
  4. Dolor
108
Q

Why are neutrophils classed as polymorphs?

A

They have many lobes to their nucleus

109
Q
A

Principles (10 decks)

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