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pathology Flashcards

1
Q

define risk factor

A

Social or individual factor which increases the likelihood of you getting a disease

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2
Q

Defin aetiology

A

causes of the disease

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3
Q

Define pathogenesis

A

sequence of events from healthy state to clinical disease

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4
Q

Define sequelae

A

the range of possible outcomes of a disease process

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5
Q

Define necrosis

what does this elicit?

A

Death of tissues, pathological and elicits adjacent tissue response

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6
Q

Define coagulative necrosis

A

proteins coagulate, preservation of cell outline - MI

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7
Q

Define colliquative necrosis

A

necrotic material becomes softened and liquified (pus) - Brain necrosis

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8
Q

define caseous necrosis

A

Cheese like - TB!

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9
Q

Define gangrenous necrosis

A

cell death by necrosis and infection on top - anaerobic bacteria have the potential to grow

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10
Q

fibrinoid necrosis?

How can malignant hypertension cause this?

A

Fibre deposition - damage to blood vessel in malignant hyper tension

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11
Q

Fat necrosis? - provide an example

A

something like acute pancreatitis

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12
Q

Define apoptosis

What are the two things it can be?

A

Programmed cell death

can be either physiological or pathological

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13
Q

What can happen if p53 is lost?

What is this most likely to be?

A

can lead to the development of cancer which is most likely to be resistant to treatment

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14
Q

What is the role of p53?

What happens if mistakes are found?

A

Bit like a spell checker (G1), if mistakes are found cell cycle is paused then repair attempted

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15
Q

What are the three checkpoints of p53?

What happens at each checkpoint?

A

G1 - apoptosis can occur if DNA is damaged

G2 - mitosis will not occur if DNA is damaged or not replicated

M - mitosis will not occur if chromosomes are not aligned properly

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16
Q

If DNA can not be repaired what does P53 stimulate?

A

caspases and induces apoptosis

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17
Q

Why are chromosomes capped?
What happens to the number of repeats every division?

What does telomerase do and how is cancer caused?

A

Chromosomes are capped to prevent further degradation and fusion

Every division the number of repeats gets smaller

Telomerase adds on TTAGGG after its lost preventing cells from dying

cancer reactivates telomerase and can become immortal

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18
Q

What are free radicals produced by?

A

drugs, O2 toxicity, reperfusion injury

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19
Q

How are we protected from free radicals?

A

Protection by anti-oxidants ( scavenge free radicals)

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20
Q

What is a metabolic disorder?

How can this cause end organ damage?

A

Biochemical abnormality which may itself be deleterious, but which also causes target organ damage mostly due to the accumulation of a toxic agent

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21
Q

What kind of genetic mutation is a metabolic disorder

what does the gene encode?

A

autosomal recessive, gene encodes enzyme in metabolic pathway

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22
Q

What happens during the vascular phase and

exudative and cellular phase of inflammation?

A

vascular phase - dilation and increased permeability of blood vessels (first is arteriole)

exudative and cellular phase - fluid and cells escape from permeable venules

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23
Q

What are some positive effects of acute inflammation?

A

toxin dilution, entry of antibodies, drug transport

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24
Q

What are some harmful effects of inflammation?
digestion…
tumour
type 1 hypersensitivity

A

Digestion of normal tissues, swelling and inappropriate inflammatory response - type 1 hypersensitivity

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25
Q

What are some characteristics of chronic inflammation?

A

redness - due to dilation of small vessels

heat - increased blood flow through region

swelling - accumulation of fluid in extravascular space

pain - distortion of tissues

loss of function - inhibited by pain or swelling

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26
Q

What are acutely inflamed organ surfaces usually covered in?

A

Fibrin

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27
Q

What is the process of neutrophils getting to the site of inflammation?
margination, rolling, pavementing and diapedesis

A

1) Margination - loss of intravascular fluid and increased plasma viscosity allows neutrophils into plasma
2) rolling - WBC’s are still moving along the vessel
wall

3) Pavementing - white blood cell’s bind
tightly and flatten against the vessel wall?

4) diapedesis - is the movement of WBC’s through the vessel wall.

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28
Q

What is chemotaxis?

A

Locomotion orientated along a chemical gradient

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29
Q

Why is histamine important in chronic inflammation?

what is it released by?

What stimulates its release?

A

vascular dilation,

released by mast cells, eosinophils, and basophils

release stimulated by C3a, C5a and lysosomal proteins (released by neutrophils)

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30
Q

What can serotonin do in inflammation?

A

Increase vascular permeability

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31
Q

What do chemokines do?

A

attract various leukocytes to site of inflammation

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32
Q

What chemical mediator is involved in type 1 hypersenstivity

A

leukotrienes

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33
Q

prostaglandins?

what do they increase and what do they stimulate?

A

increase vascular permeability - simulted platelet aggregation

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34
Q

What is required for recognition of a microorganism in inflammation?

A

To be coated in opsonins

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35
Q

What is suppuration?

what is contained in this?

A

Formation of Pus - neutrophils, bacteria, cellular debris

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36
Q

What is resolution

what does it occur after?

A

complete restoration of tissues to normal after episode of acute inflammation

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37
Q

What cells are involved in chronic inflammation?

A

plasma cells, lymphocytes and macrophages

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38
Q

Detail some macroscopic appearances of chronic inflammation

TB, breach in mucosa,

A

chronic ulcer - breach in mucosa,

thickening of wall by fibrous tissue
granulomatous - chrons / TB

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39
Q

When do B lymphocytes become plasma cells?

A

on contact with antigen

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40
Q

What do T lymphocytes produce in chronic inflammation?

A

cytokines

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41
Q

Detail some examples of reversible damage of cells

lipids, tumour, pump, respiration

A

Reduced aerobic respiration/ increased anaerobic

membrane pump fails

cell swelling

accumulation of lipids

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42
Q

What is some irreversible damage done to cells?

membranes, leak, nuclear

A

Severe damage to cell membranes and mitochondria

leakage of enzymes

nuclear changes - ATP changes, cell membrane damage

43
Q

What is the progression of repair?

A

Injury and damage

attempted repair

complete (regeneration/ restitution)

incomplete (scarring)

44
Q

Where are labile(cells that multiply throughout all of life) cells found?

A

GI tract, bone marrow

45
Q

Where are stable cells found?

What are they?

A

Hepatocytes, endothelium

These cells can multiply to replace lost cells

46
Q

Where are permanent cells found?

A

neurones and skeletal muscle

Regeneration of these are not possible

47
Q

What can pluripotent stem cells differentiate into?

A

Most cell types

48
Q

What is granulation tissue

A

a tissue that undergoes organisation to form fibrous scar

49
Q

What is a granuloma?

A

Chronic inflammation, collection of macrophages (in response to foreign bodies)

50
Q

What is wound contraction caused by?( healing response that reduces the size of the tissue defect and decreases the amount of damaged tissue that needs repair.)

A

caused by the action of myofibrils

51
Q

Define differentiation

A

Acquisition of specialised function

52
Q

define Hyperplasia

A

increase in cell number

53
Q

define hypertrophy

A

increase in cell size

54
Q

Define atrophy

A

Reduction in cell size and number in an organ that was of normal size

55
Q

What is hypoplasia?

A

reduced size of an organ that never fully developed to normal size

56
Q

What is metaplasia?

A

One type of cell becomes another form of cell in response to stress (at risk site for cancer)

57
Q

What is neoplasia?

what does neoplastic material being monoclonal mean

A

NEW abnormal mass of tissue, growth which exceeds and is uncoordinated with that of normal tissues

neoplastic cells are monoclonal = derived from a single common ancestor

58
Q

What are the signs of benign neoplastic activity

A

No necrosis, nucleus to cytoplasm ratio normal, minimal pleomorphosm ( change in size or shape)
diploid

59
Q

What are some examples of benign neoplasms?

A

Adenoma or papilloma

60
Q

What are the signs of malignant neoplasms?

A

Necrosis, N:C ratio increased, pleomorphic, aneuploidy

61
Q

What are some examples of malignant neoplasms?

A

Carcinoma - cancer of epithelial cell

carcinoma in situ - not invading other tissues, confined to site of origin

sarcoma - cancer of mesenchymal cell

62
Q

What is dysplasia?

A

Disordered growth

Pre-malignant process

63
Q

What is angiogenesis?

A

formation of new, abnormal blood vessels

Successful tumours will develop their own blood supply

64
Q

What is metastasis?

A

Formation of tumour in a place discontinuous with its primary legion

65
Q

What are the two routes of metastasis?

A

lymph - carcinoma

haematogenous = sarcoma

66
Q

What is the double hit hypothesis?

A

one working gene is enough, one faulty gene puts person at increased risk…

Two faulty mutated genes will result in a functional problem

67
Q

What is stepwise progression of malignant mutations?

A

Initiation - 1st mutation
promotion - further accumulation of mutations
persistence - unregulated abnormal growth that could possibly become malignant

68
Q

Detail some examples of oncogenes that are effected by mutations (RAS, BRAF, MYC, P13K)

A

RAS (GTP binding)

BRAF - downstream (50% of melanoma are RAF mutated)

Myc (supposed to be nuclear transcription factor promoting DNA replication)

P13K most common mutated kinase in cancer - located inside the nucleus @ transcription

69
Q

What is p53, what is it activated by?

and what can it do?
regulate, cycle, death

A

p53 - guardian of the genome, transcription factor, activated by cell stress

regulates transcription of downstream target genes
cell cycle arrest - G1/s and G2/M
cell death - apoptosis

70
Q

What are the different visual appearances of malignant and benign cancers

A

malignant - rough and nasty looking

benign - rough and smooth

71
Q

What cancers are present in

epithelium(malignant), glands(benign and malignant) and in squamous cells (benign and malignant)

A

epithelium - carcinomas
glands - adenoma vs adenocarcinoma (malignant)
Squamous - papilloma vs squamous cell carcinoma

72
Q

What type of cancer is a sarcoma?

A

MALIGNANT

73
Q

What is a paraneoplastic syndrome?

A

Rare disorders that are triggered by an altered immune system response to a neoplasm

clinical syndromes involving non-metastatic systemic effects that accompany malignancy

74
Q

Detail some examples of an acquired metabolic disease

what are the complications of these

A

type 1 and 2 diabetes
obesity (central or periperal)

complications - ketoacidosis, hypoglycaemia

75
Q

What is the progression of atheroma?

A

fatty streak, fibrofatty plaque, proliferative atheroma and then complicated atheroma

76
Q

What are can cause atheroma?

A

endothelial injury - response to injury, macrophage + platelets, lipid accumulation and then smooth muscle proliferation

77
Q

What are the complications of atheroma?

TADEI

A

Thrombosis, aneurysm, dissection, embolism and ischaemia

78
Q

What are the consequences of left ventricular hypertrophy?

A

Increased LV load, poor perfusion, interstitial fibrosis,

79
Q

What is a thrombus?

A

Solid mass of blood constituents formed within a blood vessel

80
Q

What is vircow’s triad?

A

Vessel wall - loss of endothelial surface, inflammation

blood flow - stasis/ turbulence

blood constituents - platelets, coagulation proteins

81
Q

What is venous thrombosis casued by?

what is hyper coagulability caused by?

A

blood stasis - immobilised

hypercoagulability - inherited, drugs and trauma

82
Q

Define embolism

A

Mass of material in vascular system moving from its site of origin to lodge in vessels in a distant site

83
Q

When is a DVT most likely to occur?

A

Post op, bed bound, travel, oedema, pain

84
Q

Define infarction

Why is reperfusion injury possible?

How long do neurones have to live if starved of oxygen?

A

zonal necrosis due to a sudden occlusion of blood supply due to lack of oxygen and nutrient supply

reperfusion injury possible due to formation of free radicals

neurones in brain die if starved of oxygen for longer than 3 mins

85
Q 
What is:
neo-adjuvant treatment?
adjuvant treatment
palliative treatment
radical treatment
A

Neo-adjuvant treatment is given before surgery to
shrink the tumour for surgical removal.

Adjuvant treatment is given after
surgery, aimed at reducing the risk of recurrence.

Palliative treatment is non-
curative and simply aims to improve symptoms and quality of life.

Radical
treatment is intended to be curative.

86
Q

What are proto-oncogenes and when do they change in cancer?

A

Proto-oncogenes are normal genes that stimulate
cell division. In cancer, these proto-oncogenes are changed to oncogenes which
enable uncontrolled cell proliferation.

.

87
Q

What are tumour suppressor genes?

When can cancer develop in accordance to these?

A

Tumour suppressor genes are normal
genes that inhibit cell division - loss of both copies of a tumour suppressor gene
can allow cancer to develop

88
Q

What are telomeres? - what happens when cancer is present?

A

Telomeres are repeats in genetic code in normal
cells that mean they can only divide a certain number of times as each time they
divide telomere repeats decrease.

In cancer there is often a mutation that
reactivates telomerase resulting in cells gaining unlimited replicative potential.

89
Q

What are psammamoma bodies?

If these are found what is the most likely cause?

A

collections of calcium

found in biopsy samples of mesothelioma,

90
Q

What types of HPV virus causes cervical cancer?

A

types 16 and 18

91
Q

What is protective against breast cancer ?

A

Breastfeeding

92
Q

Where is cardiac muscle nuclei found?

A

In the centre of the fibre

93
Q

What is a carcinoma?

A

Malignant epithelial neoplasm

94
Q

Sarcoma?

A

Malignant neoplasms of connective tissue

95
Q

Glandular neoplasms?

A

adenocarcinomas - malignant

Adeomas - benign

96
Q

Squamous cell carcinoma

Benign squamous cell neoplasm?

A

malignant neoplasms of squamous cell

papilloma = benign

97
Q

What are the three growth receptors?

A

rectors with intrinsic tyrosine kinase activity
7 transmembrane G protein coupled receptors
receptors without intrinsic tyrosine kinase activity

98
Q

What is each step in the cell cycle controlled by?

A

cyclin dependant kinases that activate each other

99
Q

When is retinoblastoma important?

A

Normal cell growth and in malignancy

100
Q

Why is P53 important?

A

Check for mistakes, mistakes are found then cell cycle is paused, repair attempted

101
Q

What are telomeres?

A

Chromosomes are capped - provides protection and stops chromosome ends from degrading

102
Q

Does hyperplasia need a stimulus?

A

yes it needs to be in response of something

results in increased organ volume

103
Q

Why is PDL1 important?

A

inhibits T-cell proliferation which can switch off immune system so is targeted for cancer treatment

104
Q

What is Myc?

A

Myc is a nuclear transcription factor that promotes growth – DNA replication etc.
Common in lymphoma, neuroblastoma, small call carcinoma of lung

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