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Pathology Flashcards

1
Q
  • osis
A

disease/condition

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2
Q
  • itis
A

inflammation of

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3
Q

Diverticulitis
diverticular disease

A

diease –> Digestive conditions that affects the large intestine (colon).
Small bulges or pockets (diverticula)develop in the lining of the intestine

X + itis, is when these pockets become inflamed or infected.

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4
Q

Causes of inflammation

A
  • Microbial infections
  • Hypersensitivity reactions (some parasitic infections + TB)
  • Physical agents (trauma, heat injury, radiation)
  • chemicals (Acids, bacterial toxins, corrosives)
  • tissue necrosis ( secondary to ischaemia)
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5
Q

Bacterial Endotoxin

exotoxin

A

endo - associated with bacterial cell walls, stimualting inflamamtion

chemicals release by bacteria, stimualting inflammation

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6
Q

Cardinal signs of acute inflammation

A

R - Redness (Rubor)
H - Heat (calor)
S - Swelling (tumor)

P - Pain (dolor) –> due to release of some chemical mediators (PROSTAGLANDIN + BRADYKININ) ++ due to physical distortion of tissue
L - Loss of Function (functio laesa)

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7
Q

synonym for redness

A

rubor

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8
Q

synonym for heat

A

calor

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9
Q

synonym for swelling

A

tumor

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10
Q

synonym for pain

A

dolor

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11
Q

Stages of inflammation

A
  1. Release of chemical mediators
  2. Vasodilation
  3. Increased vascular permeability
  4. Fluid accumulation
  5. Cellular recruitment
  6. Phagocytosis
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12
Q

synonym for exudate

A

pus

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13
Q

exudate

A

fluid that leaks out of blood vessels into nearby tissues is named…

it is made up of cells, protein and solid materials.

it may ooze from cuts or from areas of infection or inflammation

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14
Q

process called exudation

A

name of process when vascular changes in acute inflammation includes:

increased vascular permeability +++ increased net flow of fluid and cells our of vessels

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15
Q

Margination

A

the adhesion of white blood cells to the walls of damaged blood vessels.

caused by the loss of intravascular fluid, which slows the flow to the site, thus allowing leukocytes e.g. neutrophils to marginate

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16
Q

Synonym for adhesion

A

Pavementing

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17
Q

the process of diapedisis

A
  1. marginatoin of neutrophiles
  2. pavementing of neutrophils (adhesion)
  3. pass between endothelial cells (emigration)
  4. pass through basal lamina and migratie into adventitia
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18
Q

HIstamin functions

A
  1. regualtes sleep wake cycle + cognitive function
  2. role in allergies
  3. causes vascular dilation + permeability

released mainly by mast cells

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19
Q

function of prostaglandins

A

derived from arachidonic acid

some cause paltelet aggregation
some cause increased vascular permeability
PAIN

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20
Q

function of Seratoning

A

vasoconstrictor

released by platelets

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21
Q

leukotrienes function

A

vasoactive properties

often made in neutrophils from arachidonic acidfun

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22
Q

funciton of Bradykinin (plasma factor)

A

peptide mediation vasodilation + pain
activated by coagulation factor XII

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23
Q

Plasma factors
4 enzyme cascade systems in plasma

A

these 4 enzyme cascade systems in plasma are called X:

  1. Coagulation system ( fibrinogen to fibrin)
  2. Kinins (activated by caogulation factor XII), includes Bradykinin
  3. Fibrinolytic system (removes fibrin from the vascular system preventing clots from occluding the vessel.)
  4. COmplement system
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24
Q

Chemical mediators of acute inflammation

A
  1. Early chemical events
    - Histamine + - Thromin released by inflammatory stimulus

—> causing upregulation of P-SELECTIN on endothelial cells + PAF on endothelial cells

—> allowing ligands onthe neutrophil surface to engage with the P-SELECTIN, starting to roll along the endothelial wall

  1. PAF (platelets activating factor)
    – docks with corresponding receptor on neutrophil and promotes expression of otehr molecules —-> endresult is a firm adhesion onto the endothelial surface
  2. Histamine
    – vascular dilation + permeability
    – released by mast cells
  3. Lysosomal compounds
    – vascular permeability
    – stimualte histamine release from mast cells
    – released by neutriphils
  4. Leukotrienes
    – vasoactive properties
    – often made by neutrophils from arachidonic acid
  5. Prostaglandins
    – dervied from arachidonic acid
    – increased vascualr permeability
    – plateelt aggregation
  6. Seartonin
    – vasoconstrictor
    – released by platelets
  7. Chemokines
    – attarcting more WBCs to site of inflammation
    – IL-8 attracts neutrophils
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25
Q

cellular senescence

A

when the cell stops dividing as it ages
ascribed to progressive shortening of telomeres

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26
Q

HeLa cell line

A

cervical cancer cells taken without consent from Henrietta Lacks.

have active version of tolomerase which copies telomeres and prevents shortening

No Hayflick limit = cellular immortality

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27
Q

Function of telomerase

A

RESTORES telomeres
(so not present in normal cells, which have Hayflick limit)

hTERT gene - human telomerase reverse transcriptase, upregulation means more telomerase

hTERT mutations associated with many cancers

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28
Q

Clinicopathological features of Ageing: SKIN

A
  • contains less elastin
  • less collagen
  • atrophy of dermis
  • sun damage;photoageing
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29
Q

Clinicopathological features of Ageing: CARDIO

A

Ratio of ellastin to collagen decreases
reduced ability of conduit arteries to distend = increased systolic bood pressure

(aorta and major branches need to be able to stretch in response to internal pressure(compliance) and go back again (elasticity))

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30
Q

Clinicopathological features of Ageing: immune cells

A

immunosenescence
more memory cells, less naive cells ( decreased abiltiy to respond when encountering novel pathogens)

Thymus atrophy
less naive T cells

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31
Q

Clinicopathological features of Ageing: osteoarticular ageing

A

Osteoporosis
Normal mineralisation of bone matrix, BUT trabeulae are thinned

  • prone to fractures
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32
Q

Clinicopathological features of Ageing: nervous

A

Neurodegenerative
CNS damage as a result of hypoxia/haemorrhage

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33
Q

Cell Size Feature of Necrosis

A

Increased (swollen)

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34
Q

Cell Size Feature of Apoptosis

A

Reduced (celll shrunken(

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35
Q

Nucleus Feature of Apoptosis

A

Fragemtnation / Condensatoin

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36
Q

Nucleus Feature of Necrosis

A

Pyknosis, Karyohexis, Karyolysis

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37
Q

Plasma Membrane Feature of Necrosis

A

Disrupted

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38
Q

Plasma Membrane Feature of Apoptosis

A

Intact

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39
Q

Nearby inflammation feature of Necrosis

A

almost always

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40
Q

Nearby inflammation feature of Apoptosis

A

Never

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41
Q

Causes of cell injury

A

Physical damage ( trauma)
Oxygen deprivation
Microbial
Immunological
Chemical

  • strong acid contact (coagulates tissue proteins(
  • CO inhalation (prevents O2 transport)
  • Paracetamol overdose (Metabolites bind to liver cell prtoeins and lipoproteins)
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42
Q

How are cells damaged?

A

ATP depletion / reduced synthesis
Mitochondria damage
Intracellular calcium
Free radical (ROS) damage
Defective membrane permeability
Protein misfolding

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43
Q

Casues of Hypoxia

A

Ischaemia (most common cause – also compromises delivery of glyogen substrates, so double whammy)

Reduction in oxygen carrying capacity of the blood
Eg anaemia, CO poisoning

Inadequate blood oxygenation
Eg pneumonia

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44
Q

What happens in hypoxic Injury

A
  1. Reduction in intracellular generation of ATP
    Sodium pump activity is reduced, so sodium accumulates in the cell
    This causes isoosmotic gain of water and acute cellular swelling
  2. Increase in anaerobic glycolysis (bc of deceased ATP)
    Rapid depletion in glycogen stores
  3. Ribosomes detach from the rough ER
    Polysomes dissociate into monosomes
    Reduction in protein synthesis
  • cytoskeleton breaks down
  • loss of ultrastructural features
  • irreversible daamge
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45
Q

Causes of Mechanical Injury

A

Direct mechanical damage
Cell membranes rupture, cytoplasm spills out

Freezing
Intracellular and cell membranes perforated by ice crystals

Osmotic imbalance
Rupture as a result of rapid change in osmotic pressure

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46
Q

hyperplasia
metaplasia
dysplasia + SYNONYMS
atrophy
hypertrophy

A

increased no, of cells

  • conversion from one type of normal adult cell to another type of normal adult cell. (The most common types of metaplasia observed by pathologists involve the conversion from squamous to glandular cells and vice versa) // disordered growth ((premalignant, precursor lesion, potentially malignant) ——- usually referring to squamous epithelium (NOT INVASIVE MALIGNANCY, has NOT breached the membrane)

-refers to the abnormal development of cells within tissues or organs.

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47
Q

1.hyperplasia
2. metaplasia
3.dysplasia
4.atrophy
5. hypertrophy

A
  1. “Increase in the number of cells in an organ or tissue”
  2. “Reversible change in which one adult cell type is replaced by another adult cell type.”
  3. “Shrinkage in the size of a cell by the loss of cell substance”
  4. Increase in the size of cells and consequently an increase in the size of the organ”
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48
Q

Coagulative necrosis
- what it is
- causes

A

Tissue with connective tissue  basic arrangement preserved

Caused by ischemia

Ischemia results in decreased ATP, increased cytosolic Ca++, and free radical formation, which each eventually cause membrane damage

e.g. Infarct: localized area of ischemic necrosis - myocardial infarct

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49
Q

caseous necrosis
- what it is
- causes

A

Cheese’-like necrotic debris contained within

Coagulated tissue no longer resembles the cells, but is in chunks of unrecognizable debris

Usually giant cell and granulomatous reaction

Example: Tuberculosis

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50
Q

colliquative necrosis
- what it is
- causes

A

Tissue with minimal connective tissue  ‘liquifies’

Often in brain because lack of supporting stroma predisposes to total liquefaction when necrotic

Usually caused by focal bacterial infections, because they can attract polymorphonuclear leukocytes (neutrophils)

The enzymes in the neutrophils are released to fight the bacteria, but also dissolve
the tissues nearby, causing an
accumulation of pus
effectively liquefying the tissue

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51
Q

Gangrenous necrosis

A

DRY – sterile coagulative necrosis e.g. distal limb

WET – coagulative necrosis with superimposed infection

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52
Q

Fat necrosis

A

Release of enzymes from pancreas or gut or traumatic

Enzymes (lipases) release free fatty acids, which with calcium produce soapy deposits in tissuesP

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53
Q

Physiological examples of Apoptosis

A

Embryogenesis (shaping organs, eliianting webbing between fingers)
Menstrual cycle (elimination of cells from funtional layer of endometrium)
Immune system –>
- Death of post-inflammatory neutrophils
- Removal of self-reactive lymphocytes
- Death of virally infected cells

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54
Q

Clinical diagnosis of myocardial infacrtion ( cell death)

A

Myocyte necrosis  enzymes released (troponins, CK-MB, LDH)

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55
Q

Labile cells
(Regeneration

A

good capacity to regenerate ( e.g. surface peithelial cells(

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56
Q

Stable cells
(Regeneration)

A

Divide at a slow rate, but can regenerate if needed (e.g. hepatocytes in liver)

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57
Q

Permanent cells
(Regeneration)

A

no means of effective regeneration
e.g. nerve cells, striated muscle cells

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58
Q

Suppuration

A

formation of pus
lots of neutrophils accummulating
mix of neutrophils, debris, bacteria

forms abscess if it gets walled off

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59
Q

Outcomes of inflammation

A
  • Resolution
  • Suppuration
    -Scarring / Fibrosis
  • Chronic inflammation
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60
Q

Granulation tissue

A

a new connective tissue with microscopic blood vessels and myofibroblasts that develop at the wound site in the process of healing. It grows from the base of the wound and helps in filling the wounds. It is important for the contraction of the wound and epithelial cell migration.

New capillaries, leading to more macrophages, leading to proliferation of fibroblasts, leading to fibrosis and/or scarring

61
Q

Skin Healing - primary intention

A

in x Fibrin joins the edges together weakly
Over time, epidermal regrowth and collagen synthesis makes a stronger join

62
Q

Skin healing - secondary intention

A

Tissue defect filled in by granulation tissue
Epithelial regrowth over the surface
Fibrous scar forms and contracts over time

63
Q

Bone Healing

A

Break
Haematoma / inflammatory response
Callus formation (woven bone)
Replaced eventually by stronger lamellar bone

64
Q

Which parts of the kidney can regenerate, and which parts not?

A

Epithelium can regenerate, architecture can’t
Similar to liver
Loss of tubular epithelium only can regenerate/repopulate cells
Destruction of glomerulus or damage to interstitium usually results in scarring / impaired function

65
Q

Which smooth muscle cells can regeneration?

A

Vascular smooth muscle cells can regenerate
Other smooth muscle cells … not so much
Damaged muscle is replaced by scar tissue

66
Q

Examples of primary granulomatous disease

A

Crohns
sarcoidosis

67
Q

Resistance of microorganism to phagocytosis and intracellular killing

examples

A

TB
Leprosy

68
Q

Macroscopic signs of chronic inflammation

A

Chronic ulcer
chronic abscess cavity
fibrosis/ thickening of tissueC

69
Q

cells of chronic inflamamtion

A

lymphocytes(B and T)
plasma cells
macrophages
sometimes eosinophils

70
Q

Histology - recognising a lymphocyte

A

Small purple dots

71
Q

Histology - recognising a plasma cell

A

fried eggs

72
Q

Histology - recognising a macrophages

A

bigger blobby ones

73
Q

Histology - recognising a eosinophils

A

tomatoes with sunglasses

74
Q

Which cytokine promotes apoptosis

A

TNF

75
Q

which cytokine promotes anti viral defences

A

interferon

76
Q

Granuloma

A

collection of histiocytes

77
Q

difference between granuloma + granualtion tissue

A

A granuloma is a small, organized collection of immune cells, primarily macrophages, that forms in response to chronic inflammation, particularly when the body tries to isolate and contain a substance or infection it cannot eliminate.
– Contains and isolates difficult-to-remove substances
e.g. TB, Crohns (inflammation of bowel disease), Sarcoidosis

Granulation tissue is new connective tissue and microscopic blood vessels that form on the surface of a wound during the healing process, particularly in open wounds
– Repairs tissue and promotes wound closure
e.g. skin wounds

78
Q

Giant cells - what are they, how they form

describe the types
- Langhans
- Foreign body type
- Touton type

A

when macrophages collide, ending up with huge multinucleated cells

Langhans - horsehow nuclei (seen in TB)

Touton type - neat little circles of nuclei , lipid breakdown and xanthoma

foreign body - nuclei randomyl scattered

79
Q

Xanthoma

A

a skin condition in which certain fats build up under the surface of the skin

80
Q

Intrinsic Pathway of Apoptosis

A
  1. Cytochrome C released during apoptosis
    (mitochondrial protein)
  2. Binds with other factors
    - ATP (Apoptotic Protease activating factor)
    - Pro-caspace 9
    (MAKING AN APOPTOSOME)
  3. Pro-caspase 9 -> cleaved into -> caspase 9
  4. Caspase 9 cleaves
    procaspase 3 -> caspase 3 (active form)
    CASPASE 3 triggers CELL DEATH
81
Q

Extrinsic pathway of apoptosis

A

TNF PATHWAY:
1. tumor necrosis factor BINDS to TNF receptor

  1. TNF receptor associates with death domain (TRADD)
    FADD (Fass associated death domain)
    - forms complex with procaspase 8
    - caspase activation, procaspase 8, caspase 3
    - triggers cell death

FAS PATHWAY:
1. first apoptotic protein
FAS Ligand + FAS receptr

  1. Formation of FADD complex
    procaspsase 8/10
    death inducing signalling complex ( DISC)
    leading to caspase activaton
    - triggers cell death
82
Q

Mesenchyme
Mesenchymal cells

A

Multipotent stem cells
Progenitor cell which differentiates to all types of connective tissue –> e.g. fibroblast, osteoblast, chondroblast, preadipocytes

produce ECM that consists mainly of a simple ground substance rich in hyaluronic acid.

ECM + mesenchymal cells = MESENCHYME

EMBRYO: type of embryonic conenctive tissue that gives rise to all other connective tissues of the body during early development.

ADULT: present in small quantities as part of loose connective tissue in
- umbilical cord
- bone marrow
- adipose tissue
serve to give rise to fibroblasts + new blood vessels

83
Q

synonym for neoplasia

A

tumour

84
Q

tumour meaning

A

swelling

85
Q

ONCO / OLOGY
oncology

A

study of tumours ( i.e. swellings)

86
Q

Malignant neoplasm

A

potentially lethal
has ability to invade and metastasise

exceptions e.g.
- malignang tumor (BASAL CELL CARCINOMA) does not metastasise

87
Q

Benign neoplasm

A

does NOT have ability to metastasise

  • does NOT always mean harmless - some can be v locally destructive
88
Q

anaplastic tumour

A

the least differentiated tumour

DIFFERENTIATION TOPIC: the extent to which neoplastic tissues resemble their corresponding normal tissue of origin

as tumors become less well differentiated, anaplastic features become more prominent

89
Q

Anaplastic/Undifferentiated tumorsq

A

BAD BOYS
cannot be identified by morpholgy alone
– immunohistochemistry needed, to look at their lineage
– subtyping important for diagnosis and treatment

90
Q

Features of poor differentiation
(Grade 3 classification)

A

NUCLEUS, abnormal:
- high nuclear: cytoplasmic ratio
- clumped chromatin
- prominent nucleoli

Nuclear pleomorphism:
- varibaility in nuclear size/shape

increased mitotic activtiy

Loss of polarity

NECROSIS - bad sign

91
Q

Dysplasia

A

earliest form of precancerous lesion, describing confined neoplastic change(mostly epithelia) , with nuclear plyomorphism /architectural disruption

confined withi nthe basement membrane

it is NOT cancer, but can sometimes become cancer
- can be low/high grade

can regress, not alway sleading to malignancy

92
Q

Carcinoma in-situ

A

severe form of dysplasia
WIHTOUT invasion ( basement membrane of dysplastic epithelium not penetrated)
full thickness of epithelium

not actually carcinoma (just terrible name)

93
Q

x happens when the tumour is growing so fast that the blood supply cannot keep up

A

Necrosis

94
Q

adjectives to describe BENIGN local invastion

A

well circumscribed
enapsualtoin (fibrous capsule)

slow growing
noninvasive -nonmetastatic

Exophytic growth direction

sometimes they are NOT harmless, they can be very locally destructive

95
Q

adjectives t odescribe MALIGNANT local invasion

A

infiltrative
invasive

karge
rapidly growing with hemorrhage + necrosis
metastatic

Endophytic growth direction (fown the way into connective tissue in an invasive manner)

96
Q

Benign tumours (not just epithelial)

A

Suffix “-OMA”

97
Q

Benign tumour of glandular / secretory epithelium

A

ADENOMA

98
Q

Benign tumour of non-glandular / surface epithelium

A

PAPILLOMA

99
Q

Mesenchymal tissues
benign mesenchymal tumours prefixes + suffix OMA:

Smooth muscle
skeletal muscle
adipose
blood vessel
bone
cartilage
fibrous

A

leiomyo
rhabdomyo
lipo
haemangio
osteo
chondro
fibro

100
Q

suffix for malignant epithelial tumors

A

CARCINOMAS

101
Q

suffix for benign epithelial tumors

A

OMA

102
Q

malignant mesenchyma tumours called

A

SARCOMAS

103
Q

benign mesenchyma tumours suffix

A

OMA

104
Q

malignant mesenchymas tumours suffix

A
  • sarcoma
105
Q

TERATOMAS

A

TUMORS COMPOSED of well-differentiated tissues e.g. bone, mnuscle , teeth, hair

contains cells representing ALL 3 germ cell layers

REMINDER: well differentiated, behave better
the anaplastic are the bad boys

106
Q

HAMARTOMA

A

NON-NEOPLASTIC DISORDERED OVERGRWOTH OF NORMAL TISSUE

indigenous to site of occurence

e.g. PORT WINE STAIN

107
Q

CHORISTOMA

A

heterotropic rests
bening normal tissue but seen in abnormal location

e.g. pancreas nodule in stomach

108
Q

Myeloma

A

malignancy of plasma cells

109
Q

LYMOHOMA

A

Malignancy of B / T cekk origin, often beginning in lymph nodes

110
Q

Leukemia

A

Malignancy of WBCs, beign in bone marrow

111
Q

Melanoma

A

malignancy of melanocytes (producing pigment in the skin/0

112
Q

Melanocytic naevus

A

benign proliferation of melanocytes

113
Q

How do neoplastic cells become immortal?

A
  1. AUTOCRINE GROWTH STIMULATION
    - abnormal expression of oncogenes / inactivation of tumor ruppressor genes, which normally inhibit growth pathways
  2. REDUCED APOPTOSIS
    - abnormal expression of genes that inhibit apoptosis (BCL-2)
  3. TELOMERASE
    normally onoly present in germ cells and stem cells, but NOT in normal cells

normal cells usually undergo telomeric shortening with each cell division, resitricting the number of cell division cycles.

telomerase prevents the shortening

114
Q

example of gene that inhibits apoptosis

A

BCL2

115
Q

Normal location of telomerase

A

germ cells + stem cells
prevents the shortening of telomeres (repetitive DNA sequences at the end of a chromosome)

116
Q

examples of tumour suppressor genes

A

TP53, which encodes for p53 protein(the guardian of the cells)
(both caretaker + gatekeeper function)

binds to oncoportein encoded by DNA viruses

complexes of normal p53 with mutant –> normal protein gets inactivated

MUTATIONS INCLUDE:
- nonsense (unreadable gene)
- missense (defective protein)

  1. repairs DNA damage
  2. induces apoptosis
  3. cell cycle arrest growth (G1), via p21(providing the stop signal for cell division)
    ____________________________________________
    pRb
117
Q

the 3 types of tumour suppressor genes

A
  1. inhibit neoplastic growth
  2. caretaker genes (Repair DNA damage)
  3. gatekeeper genes (stop damaged cells from dividing (by inhibiting proliferation OR inducing apoptosis)
118
Q

5 groups of oncogenes/oncoproteins

A
  1. Growth factors
  2. receptors for growth factors
  3. DNA binding TFs (regualting cell proliferation)
  4. signalling mediator with tyrosine kinase activtiy
    - tyrosine kinases regulate cell survival and proliferation
  5. signalling mediator with nucleotide binding activity
119
Q

Aneuploidy

A

when cell contains INEXACT multiple of chromosomes

usually we have diploid (normal amount of DNA, 2 copies of each chromsome)

might have
- additional chromosomes
- chromosomal transloactions/rearrangements

120
Q

examples of oncogenes

A

Ras

121
Q

Chemical contained in SMOKING + cancer caused

A

carcinoma (lung, skin, mouth)
- polycyclic aromatic hydrocarbons

122
Q

Chemical contained in rubber/dye industries+ cancer caused

A

bladder cancers
- aromatic amines

123
Q

Chemical contained in tobacco/cured meats + cancer caused

A

GI cancer
- nitrosamines

124
Q

Chemical contained in some azo dyes+ cancer caused

A

bladder, liver ca

125
Q

Chemical contained in pvc manufacture+ cancer caused

A

liver agiosarcoma
- vinyl chloridea

126
Q

angiosarcoma

A

cancer that forms in the lining of blood vessels and lymph vessels. It often affects the skin and may appear as a bruise-like lesion that grows over time

127
Q

Nitrate heavy food examples

indirect carcinognes

A

cured meats

dietary nitrates conerted into NITROSAMINES by GI tract bacteria

NO3- => N-N=O

128
Q

papilloma

A

a benign (non-cancerous) tumor arising from an epithelial surface and usually known to grow in an outward direction

129
Q

Human Papillomavirus
HPV

A

High risk: HPV 16/17
- squamous cell carcinoma

Low risk: HPV 6/11
- squamous cell papilloma

anogenital region
head cancer
neck cancer

e.g. cervical cancer

–> HPV E6 oncoprotein acts on TP53, which makes p53 tumour suppressor gene
–> HPV E7 oncoprotein binds on pRB

–> virus integrates with host genome

130
Q

Mode of action of p53

A

G1/S checkpoint
- prevents cell from entering S phase (DNA synthesis) if there is DNA damage
- if damage is irreparable, induces apoptosis or senescence to prevent propagation of faulty DNA
—> mediated through p21 activation (providing the stop signal, which signals G1 cell cycle arrest)

G2/M checkpoint
- prevents cell from entering mitosis if DNA damage/incomplete DNA replication
- allows additional time for repair before mitosis /// triggers apoptosis if repair fails

131
Q

tumour suppressor gene RB which codes for retinoblastoma protein - function

A

Rb inihbits cell cycle progression unitl a cell is ready to divide
G1-S checkpoint

132
Q

Epstein Barr Virus

A

type of herpesvirus
causes glandular fever = mononulceosis

associated with some lymphomas + carcinomas

Latent EBV can reactivate drive B cells to proliferate —> EBV driven lymphoproliferative disorder

  • can infect squamous cells (skin/mucosa)
  • can act in combination with environmental factors e.g. smoking, to promote nasopharyngeal carcinoma

common initiating event for carcinomas:
-> inactivation of p16/CDKN2A ++ TGFBR2

133
Q

Burkitt lymphoma

A

high-grade B cell lymphoma

134
Q

malaria

A

infection caused by a parastie
does not spread from person to person, but only from mosquitos

135
Q

type of UV radiation implicated in skin cancer

A

UVB

ASSOCIATED WITH
- basal cell carcinoma
- malignant melanoma

136
Q

cells that arise from the neural crest

A

The neural crest is a transient embryonic structure in vertebrates that gives rise to

  1. most of the peripheral nervous system (PNS)
  2. several non-neural cell types, including
    - smooth muscle cells of the cardiovascular system,
    - pigment cells in the skin,
    - craniofacial bones,
    - cartilage,
    - connective tissue
137
Q

melanocytes

A

neural crestt derived cells
in basal layer of epidermins
produce melanin pigment

malignant transformation can occur following UV damage

pale skin people more susceptible to UV damage
- melanin has protective effect against UV damage

138
Q

Tissues most sensitive to carcinogenic effects of ionising raditaion

A

Thyroid
Breast
Bone
Haemoatopoietic tissue

CHORNOBYL DISASTER – explosion of nuclear power plant in Ukraine -1986
- fatal doses
- initial deaths from radiation exposure
- LT increase in childhood thyroid cancers
- clonal DNA ds breaks

139
Q

bacterium linked with carcinogen

A

Helicopater Pylori
- gastric adenocarcinomas
- some lymphomas
- toxins released activated oncoproteins

140
Q

Fungi and carcinogens example

A

aflatoxin carcinogen
hepatocellular carcinoma

(food, crops, animals feed, milk)

141
Q

Hormones and carcinogenesis

A

excess oestrogen (breast, endometrail, excess adipose tissue, obesity a risk factor in some cancers)
- excess adipose tissue means higher levels of growth hormones, oestrogen etc

anabolic steroids
- liver neoplasms

Grwoth hormone / IGF1 (breast, prostate, colon)

142
Q

2 reasons why cancer is most common in old age

mostly epithelial in origin

A
  1. loss of immune competence
  2. increasing somatic genetic mutations
143
Q

in children

A

epithelial cancers (carcinoma) VERY rare

acute leukemias / primitive CNS neoplasms common

retinoblastoma (small blue round cell tumours)

Wilms tumour (nephroblastoma) - kidney cancer

144
Q

Properties of invasiveness

A
  1. Decreased cellular adhesion
  2. Secretion of proteolytic enzymes
  3. Abnormal / increased cellular motility
145
Q

the 6 steps of metastasis

A
  1. detachment from main tumour body
  2. local invasion of surroudnign tissue
  3. intravasation into vessels
  4. evasion of host cell defences

dissemination

  1. adherence to endothelium elsewhere
  2. extravasation of cells from vessel in to surrounding tissue

colonization

146
Q

intravasation

A

The movement of a cell or a foreign substance through the wall of a blood or lymph vessel into the vessel itself

147
Q

transcoelomic metastasis

A

“across the peritoneal cavity”) metastasis refers to the dissemination of malignant tumors throughout the surfaces and organs of the abdominal and pelvic cavity covered by \peritoneum

148
Q

routes of metastasis

A
  1. Haematogenous
  2. Lymphatic
  3. Transcoelomic (across the peritoneal cavity)
149
Q
A

FoM (14 decks)

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