Pathology And Microbiology

Front 1

What are the types of aquired disease?

Back 1

Haemodynamic, Degenerative, Inflammatory, Disordered immunity, Metabolic and Growth disorders

Front 2

What are the signs of inflammation?

Back 2

Pain, redness, swelling, heat and loss of function

Front 3

Single cells are affected. Is this apoptosis or necrosis?

Back 3

Apoptosis

Front 4

Cells swell. Is this apoptosis or necrosis?

Back 4

Necrosis

Front 5

Cytoplasm and nucleus have increased density. Is this apoptosis or necrosis?

Back 5

Apoptosis

Front 6

Loss of intracellular features. Is this apoptosis or necrosis?

Back 6

Necrosis

Front 7

Dyes enter the cell. Is this apoptosis or necrosis?

Back 7

Necrosis

Front 8

There is acute inflammation. Is this apoptosis or necrosis?

Back 8

Necrosis

Front 9

What are the 6 types of necrosis?

Back 9

Fat, Causeous, Liquefaction, Ischaemic and Coagulation

Front 10

What causes Fat necrosis?

Back 10

Trauma, surgery or pancreatitis

Front 11

What causes causeous necrosis?

Back 11

TB

Front 12

What causes liquefaction necrosis?

Back 12

Proteolytic enzymes

Front 13

What happens in coagulation necrosis?

Back 13

All cytoplasmic proteins are denatured to form 'tombstones'

Front 14

How is cell death defined?

Back 14

Loss of membrane integrity, impairment of energy metabolism and paralysis of protein synthesis

Front 15

How does capillary permeability increase in acute inflammation?

Back 15

Endothelial contraction, transcytosis, direct injury and gaps opened by leukocyte enzymes

Front 16

How so leukocytes break through endothelium?

Back 16

Using collagenase

Front 17

What does histamine do?

Back 17

Dilutes arterioles and increases venule permeability

Front 18

Give examples of vasoactive amines

Back 18

Histamine and serotonin

Front 19

Which complement proteins form the membrane attack complex?

Back 19

C6,7,8, and 9

Front 20

What is the role of C3b?

Back 20

An opsonin

Front 21

What do C3a and C5a do?

Back 21

Vasodilators

Front 22

What is produced by the clotting cascade?

Back 22

Fibrin and thrombin

Front 23

What is produced from arachdonic acid and which enzymes are used?

Back 23

Lipogenase makes leukotrines and cyclooxygenase make prostaglandins

Front 24

Which cells produce NO?

Back 24

Endothelial cells, macrophages and brain neurons

Front 25

What are the effects of NO?

Back 25

vasodilation, reduced platelet aggregation and reduced leukocyte adhesion

Front 26

What is the effect of bradykinin?

Back 26

Increased vascular permeability

Front 27

Which chemical mediators cause fever?

Back 27

IL-1, IL-6 and TNF

Front 28

What are the effects of platelet activating factor?

Back 28

Platelet activation, bronchoconstriction, leukocyte adhesion, chemotaxis, degranulation and oxidative burst

Front 29

What are the 4 types of inflammation?

Back 29

Serous, fibrinous, suppurative and ulcers

Front 30

How can chronic inflammation occur?

Back 30

Chronic from outset, progression from acute, and recurrent acute episodes (due to prolonged exposure or persistent infection)

Front 31

How is chronic inflammation characterised?

Back 31

Mononuclear cells, tissue destruction and repair

Front 32

What are the outcomes of chronic inflammation?

Back 32

Abscess formation, fibrous healing or complete resolution

Front 33

What is a foreign body granuloma?

Back 33

Foreign material is in the centre

Front 34

What is seen in a granuloma?

Back 34

Central necrosis, mononuclear inflammatory cells, macrophages and giant cells

Front 35

What are the two types of healing?

Back 35

By first and second intention

Front 36

What are potential complications in healing?

Back 36

Keloid, malunion, or non-union

Front 37

What is immunopathology?

Back 37

Tissue damage caused by an excessive immune response

Front 38

What is immunoprivilege?

Back 38

Reduced immune response in important tissues

Front 39

What do eosinophils release?

Back 39

Myeloperoxidase

Front 40

Which cell kills by oxygen dependent and independent killing?

Back 40

Neutrophils

Front 41

What methods are included in oxygen independent killing by neutrophils?

Back 41

acid, lysozyme, cationic proteins, lactoferrin, vitamin B12

Front 42

What are the humoral components of the innate immune system?

Back 42

Complement, acute phase proteins and interferons

Front 43

What are the functions of the complement system?

Back 43

Allows eosinophils to recognise parasites, opsonisation, recruits phagocytes, promotes inflammation and forms a membrane attack complex

Front 44

Which interleukines stimulate B and T cell division?

Back 44

1 and 6

Front 45

Which interleukin stimulates neutrophil migration?

Back 45

8

Front 46

Which interleukin stimulates phagocyte production?

Back 46

3

Front 47

What is the function of interferon?

Back 47

Inhibits protein translation in nearby cells when infected by a virus

Front 48

How are B cells activated?

Back 48

Antibodies on surface cross linking

Front 49

Which antibodies neutralise pathogens by blocking receptors?

Back 49

G,A and M

Front 50

Which antibodies are opsonins (as phagocytes have Fc receptors)

Back 50

G and A

Front 51

What process involves antibodies activating NK cells?

Back 51

Antibody dependent cellular cytotoxicity

Front 52

C1q binding to antibodies activates what?

Back 52

Complement

Front 53

What does IgE do?

Back 53

Activates mast cells to degranulate and activates eosinophils

Front 54

What does a killer T cell bind to?

Back 54

CD8 and MHC class I

Front 55

Which molecules are involved with killer T cells mode of action?

Back 55

Perforin, Granzymes and Fas protein

Front 56

Which type of T cell is affected by HIV?

Back 56

CD4 Helper

Front 57

What is the costimulatory signal for T cells?

Back 57

B7 to CD28

Front 58

What is IL-2 a growth factor for?

Back 58

T cells

Front 59

How do Th1 and Th2 inhibit each other?

Back 59

Th1 releases IFN gamma and Th2 releases IL-4 and IL-10

Front 60

What do Th1 cells release?

Back 60

IFN gamma, TNF alpha and beta and IL-2

Front 61

What do Th2 cells release?

Back 61

IL-4, 5 and 10

Front 62

What does IFN gamma do?

Back 62

Activates macrophages, increased MHC expression andNK cell activation

Front 63

What does TNF alpha do?

Back 63

Macrophage activation and activation of the endothelium

Front 64

What does TNF beta do?

Back 64

Macrophage activation, neutrophil activation and kills tumour cells

Front 65

What does IL-4 do?

Back 65

B cell activation and division, T cell growth, mast cell generation

Front 66

What does IL-5 do?

Back 66

IgA synthesis, eosinophil growth and differentiation

Front 67

What does IL-10 do?

Back 67

Inhibits macrophage activation and promotes mast cell growth

Front 68

What are interleukins?

Back 68

Hormone-like messengers produced by leukocytes

Front 69

What is hypersensitivity?

Back 69

An excessive immune response

Front 70

Explain the progression of an allergic response.

Back 70

Soluble antigens cause B cells to release IgE. They bind to mast cells causing release of inflammatory mediators

Front 71

Why is genetics important in allergy?

Back 71

It is mediated by Th2 and suppressed by Th1, and the balance of Th1 and 2 responses is controlled by genetics

Front 72

What are the three types of cytotoxic hypersensitivity?

Back 72

Phagocytosis, ADCC and compliment activation

Front 73

Which type of hypersensitivity is haemolytic disease of the newborn?

Back 73

Type II

Front 74

What causes the activation complex of compliment to be activated?

Back 74

Recognition unit binding the Fc region of antibodies

Front 75

Explain the progression of an immune complex hypersensitivity reaction.

Back 75

Soluble antigens bind antibodies forming insoluble microcrystals. These lodge in capillaries which results in compliment and leukocytes destroying epithelial cells.

Front 76

What type of hypersensitivity is rheumatoid arthritis?

Back 76

Type 3

Front 77

What type of hypersensitivity is hepatitis?

Back 77

Type 3

Front 78

What type of hypersensitivity is herpes?

Back 78

type 4

Front 79

What type of hypersensitivity is TB?

Back 79

Type 4

Front 80

What type of hypersensitivity is type 1 diabetes?

Back 80

Type 4

Front 81

Explain delayed hypersensitivity.

Back 81

Th1 produces cytokines and along with CTL and macrophages they cause harm to host cells

Front 82

Why does immunodeficiency usually present in children over 4 years old?

Back 82

Because prior to that the mother's immunity is passed

Front 83

What do myeloid progenitors eventually become

Back 83

Innate immunity components

Front 84

Which autoimmune disease acts on desmosomes causing blisters?

Back 84

Pemphis vulgaris

Front 85

What are the side effects of steroids?

Back 85

Hirstutism, stretch marks, poor healing, diabetes, heart attacks and strokes

Front 86

How are monoclonal antibodies made?

Back 86

A lab animal is injected with antigen, they produce antibodies. these are fused with myeloma and screened for antibodies which are cloned.

Front 87

What is reticular dysgenesis?

Back 87

Stem cell defects

Front 88

Which thyroid disorder causes overactive metabolism?

Back 88

Hyperthyroidism

Front 89

What causes oral granulomas?

Back 89

TB, Crohn's disease, sarcoidosis

Front 90

Which antibody crosses the placenta

Back 90

IgG

Front 91

What are the causes of primary immunodeficiency in children?

Back 91

Transient hypogammaglobulinaemia, Bruton's X-linked agammaglobulinaemia

Front 92

What are the causes of primary immunodeficiency in adults?

Back 92

IgG subclass deficiency and selective IgA deficiency

Front 93

Which syndrome results in an underdeveloped or absent thymus?

Back 93

Digeorge syndrome

Front 94

What is absent in Chedik-Higashi syndrome?

Back 94

Phagocytes

Front 95

What are potential causes of secondary immunodeficiency?

Back 95

Malnutrition, Immunosuppresive drugs, aging, metabolic disease, iatrogenic causes or infection.

Front 96

What are T cell precursors called?

Back 96

Thymocytes

Front 97

What does double negative mean?

Back 97

Expressing neither CD4 or CD8

Front 98

Explain positive selection

Back 98

Double positive thymocytes interact with MHC from specialised cortical epithelial cells. 95% don't interact so are destroyed by apoptosis

Front 99

Explain negative selection

Back 99

Remaining thymocytes are checked by specialised dendritic cells that MHC affinity isn't too strong so there isn't autoimmunity

Front 100

What are the two peripheral mechanisms of self tolerance?

Back 100

Anergy (no co-stimulation) and exclusion from privilege sites

Front 101

Which hypersensitivity response are systemic autoimmune diseases associated with?

Back 101

Type III

Front 102

What does Sjogren's syndrome destroy?

Back 102

Lacrimal and salivary glands

Front 103

What are the 3 shapes of bacteria?

Back 103

Coccus, bacilus and spirochete

Front 104

Is bacterial DNA single or double stranded?

Back 104

Single

Front 105

Which type of bacteria does penicillin act on?

Back 105

Gram positive

Front 106

What inhibits penicillin?

Back 106

beta lactamase

Front 107

What inhibits beta lactamase?

Back 107

Clauvulanic acid

Front 108

What ribosomes do bacteria have?

Back 108

70s

Front 109

What synthesised the cell wall?

Back 109

The cell membrane?

Front 110

What are the functions of the cell wall?

Back 110

Rigidity and prevents lysis

Front 111

What is present in gram positive bacteria?

Back 111

Peptidoglycan, teichoic acid, lipoteichoic acid

Front 112

What is present in gram negative bacteria?

Back 112

LPS, pores, virulence enzymes

Front 113

Do gram positive or negative bacteria secrete the exotoxin?

Back 113

Both

Front 114

Which antibody blocks bacterial adhesion?

Back 114

IgA

Front 115

What do OPA proteins bind to?

Back 115

CEACAM receptors

Front 116

What is the function of the bacterial capsule?

Back 116

Prevents phagocytosis and opsonisation

Front 117

What binds iron so it isn't available for bacteria?

Back 117

Lactoferrin

Front 118

What is the role of pilli?

Back 118

Attachment

Front 119

What is antigenic diversion?

Back 119

Bacteria release 'blebs' which are attacked by the immune system instead

Front 120

What is phase variation?

Back 120

Switching on and off a surface component on a bacterial wall

Front 121

What do Factor H and C4 do?

Back 121

Inhibit C3 convertase, found on bacterial membrane

Front 122

What are the three types of exotoxin?

Back 122

Cytotoxins, neurotoxins and enterotoxins

Front 123

What do static antibiotics do?

Back 123

Stops bacteria growing

Front 124

How does Tetracycline work?

Back 124

Prevents tRNA binding to ribosomes

Front 125

How does Chloramphenicol work?

Back 125

Blocks growth of the peptide chain

Front 126

How does Aminoglycoside work?

Back 126

Causes misreading of mRNA

Front 127

How does Rifampicin work?

Back 127

Inhibits RNA polymerase

Front 128

How does flouroquinolone work?

Back 128

Inhibits DNA uncoiling

Front 129

How does Cycloserine work?

Back 129

Inhibits cell wall synthesis

Front 130

How does sulphonamide work?

Back 130

It is an antimetabolite

Front 131

What are the 5 mechanisms of antibiotic resistance?

Back 131

1) Expels through efflux pumps

2)Inactivate antibiotics by enzymes

3)Drug no longer binds

4)Bacterial envelope made less permeable to antibiotics

5)Bypassing a metabolic pathway targeted by the drug

Front 132

How can you sterilise something?

Back 132

Heat (dry or steam), Gas plasma, Formaldehyde, or gamma irridation

Front 133

How does the baltimore system group viruses?

Back 133

By multiplication cycle

Front 134

What is the viral envelope made up of?

Back 134

Lipid membrane with glycoproteins

Front 135

What are the 4 direct methods of detecting a virus?

Back 135

PCR, direct antigen detection (using monoclonal antibodies), electron microscope visualisation, and virus isolation

Front 136

How can you indirectly detect a virus?

Back 136

Using antibodies

Front 137

Which sialic acid analogue treats influenza?

Back 137

Zanamivir

Front 138

Give an example of an acute virus.

Back 138

Influenza

Front 139

Give an example of a persistent virus.

Back 139

Hepatitis

Front 140

Give an example of a latent virus.

Back 140

Herpes

Front 141

Give an example of slow virus.

Back 141

Measles

Front 142

What are the three types of fungi?

Back 142

Moulds, yeasts and mushrooms

Front 143

What distinguishes yeasts?

Back 143

They are unicellular

Front 144

What distinguishes moulds?

Back 144

They are filamentous

Front 145

What are filaments called?

Back 145

Hyphae

Front 146

How does candida albicans pass through the gut wall

Back 146

By persorption

Front 147

What is tinea corporis commonly known as?

Back 147

Ringworm

Front 148

What does clostridium difficile cause?

Back 148

Colitis and diahorrea

Front 149

Which bacteria are mutualistic in the vagina?

Back 149

Lactobacilli

Front 150

What is endogenous infection?

Back 150

One caused by your own microbiota

Front 151

What is the term for a disease always present in a population?

Back 151

Endemic

Front 152

Which is more important? Virulence or immune status of the host?

Back 152

Immune status of the host

Front 153

What is the index case?

Back 153

The first person to get a disease

Front 154

Is Polio a live or dead vaccine?

Back 154

Live

Front 155

Is diptheria a live or dead vaccine?

Back 155

Dead

Front 156

What does flucloxacillin treat?

Back 156

Cellulitis

Front 157

How do you diagnose an upper respiratory tract infection?

Back 157

Culture aspirates, stain for viral antigens ehwn replicate by PCR

Front 158

Pneumonia, broncholitis, CF and empyema are examples of what type of infection?

Back 158

Lower respiratory tract infections

Front 159

What are the 4 types of pneumonia

Back 159

Immune compromised host, aspiration, hospital acquired, community acquired (triggered by a virus)

Front 160

Which type of hepatitis is caught from close personal contact?

Back 160

A

Front 161

Which type of hepatitis is divided into chronic persistent, chronic active, cirrhosis and hepatocellular carcinoma?

Back 161

B

Front 162

Which type of hepatitis is tested for by looking for the HCV antibody and in the acute phase may give a false negative?

Back 162

C

Front 163

Which type of hepatitis is only present alongside B?

Back 163

D

Front 164

Which type of hepatitis is acute?

Back 164

E

Front 165

Where does herpes simplex persist?

Back 165

In the trigeminal ganglion.

Front 166

In which disease is Karposi's sarcoma seen?

Back 166

HIV

Front 167

Where are peyer's patches found?

Back 167

In the ileum

Front 168

How may antibiotic use result in GI tract infection?

Back 168

It wipes out normal flora

Front 169

In which 4 ways may pathogens infect the GI tract?

Back 169

Toxins, attachment, direct invasion, impaired reabsorption

Front 170

Dehydration, electrolyte disturbances and sepsis are complications of which disease?

Back 170

Gastroenteritis

Front 171

Which disease has an AB5 toxin - with a toxogenic alpha subunit, and immunomodulatory beta subunit

Back 171

Cholera

Front 172

What is septic arthritis an infection of?

Back 172

The joints

Front 173

What is osteomyelitis?

Back 173

Bone infection

Front 174

Which bacteria causes chronic monoarticular arthritis?

Back 174

Mycobacterium tuberculousis

Front 175

Which 4 ways can osteomyelitis reach bone?

Back 175

Haematogenous spread, adjacent spread, trauma and iatrogenic

Front 176

What is osteomyelitis treated by?

Back 176

Antibiotics

Front 177

What is a Brodie's abscess and where does it form?

Back 177

Fibrous capsule surrounding pus. Formed around osteomyelitis.

Front 178

How is osteomyelitis treated?

Back 178

Surgery and antibiotics

Front 179

What is bacteraemia?

Back 179

Bacteria in the (usually sterile) blood

Front 180

How is bacteraemia detected?

Back 180

Blood culturing in an incubator

Front 181

What circumstances make bacteraemia significant?

Back 181

Virulence factors, large numbers of bacteria, immunocompromised individuals

Front 182

Neisseria meningitidies can cause which two conditions?

Back 182

Sepsis and meningitis

Front 183

What is sepsis defined as?

Back 183

Clinal signs of infection plus systemic inflammatory response syndrome

Front 184

What does severe sepsis turn into?

Back 184

Septic shock

Front 185

What does polio virus destroy?

Back 185

CNS

Front 186

How can organisms reach the CNS?

Back 186

Blood, direct spread, and neuronal spread from peripheral nerves

Front 187

Polymorphs are seen in which type of meningitis?

Back 187

Bacterial

Front 188

Mononuclear cells are seen in which type of meningitis?

Back 188

Viral

Front 189

What do you see increasing in meningitis?

Back 189

CSF cell number and protein

Front 190

What is wrong with plain polysaccharide vaccinea?

Back 190

They have a short lived immune response with no memory

Front 191

What is the medical term for a birth mark?

Back 191

Hamartoma

Front 192

Where do you see a mass of disorganised by mature specialised tissue indigenous to the site?

Back 192

Hamartoma

Front 193

What features are seen in dysplasia?

Back 193

Hyperchromasia, increased mitosis, and high nuclear-cellular ratio?

Front 194

What is severe dysplasia known as?

Back 194

Carcinoma in-situ (doesn't invade basement membrane)

Front 195

After a stimulus has been removed, does neoplasm persist?

Back 195

Yes

Front 196

Which type of tumour doesn't show dysplasia?

Back 196

Benign

Front 197

Which type of tumour has no defined border and invades surrounding tissue?

Back 197

Malignant

Front 198

Which type of tumour is highly differentiated?

Back 198

Benign - it resembles parent tissue

Front 199

Benign epithelial tumours with a round shape are called...?

Back 199

Adenoma

Front 200

Benign epithelial tumours with a fingerlike shape are called...?

Back 200

Papilloma

Front 201

What are malignant epithelial tumours called?

Back 201

Carcinoma

Front 202

What type of tumour is a fibroma?

Back 202

Benign mesenchymal - of fibroblasts

Front 203

What is a sarcoma?

Back 203

Malignant mesenchymal

Front 204

Grade 1 tumours are...?

Back 204

Well differentiated

Front 205

Staging of tumours is what?

Back 205

Spread

Front 206

What happens after terminal differentiation?

Back 206

The cells are stuck in G0

Front 207

What is balanced in tissue homeostasis?

Back 207

Cell birth and death

Front 208

Stem cells turn into transit amplifying cells, how do they differ?

Back 208

SC cycle slowly, TAC cycle quickly

Front 209

What happens during 'commitment'?

Back 209

Cells drop out into G0

Front 210

What is Rb protein?

Back 210

A tumour suppressor

Front 211

If retinoblastoma tumour is unilateral and late onset what does this signify?

Back 211

That it is unilateral

Front 212

What is Knudson's two hit hypothesis?

Back 212

There has to be mutations in both alleles for cancer to occur

Front 213

In which 3 ways can transcription factors be activated?

Back 213

Cytokines binding to membrane receptors, diffusible factors binding to nuclear receptors and cell-cell/cell-ECM contact

Front 214

What are the 4 stages of the cell cycle?

Back 214

G1,S,G2 and M

Front 215

What causes aneuploidy?

Back 215

Anaphase before chromosomes are properly aligned

Front 216

Do cyclins and CDKs vary or remain constant throughout the cell cycle?

Back 216

Cyclins vary, CDKs remain constant

Front 217

How are cyclins degraded?

Back 217

By polyubiquitination

Front 218

What is polyubiquitination?

Back 218

Ubiquitin monomers label the target so it can be recognised by the 26s proteosome which degrades it.

Front 219

Which CDKs do the INK family of inhibitors inhibit?

Back 219

4 and 6

Front 220

Explain how Rb releases E2F.

Back 220

Hypophosphorylated by CDK4/6 and cyclin D. CDK2 and cyclin E hyperphosphorylate at the R checkpoint so Rb can't hold E2F so it is released. This trancribes S phase genes so is a positive feedback cycle

Front 221

What does loss of Rb lead to?

Back 221

E2F release

Front 222

p16 inhibits which CDK?

Back 222

4/6

Front 223

What is frequently lost in (HPV negative) oral SCC?

Back 223

p16

Front 224

What do E1A, Large T and E7 target?

Back 224

Rb

Front 225

What is invasion?

Back 225

Growth of malignant tumour cells in adjacent tissues

Front 226

What is metastasis?

Back 226

Formation of a secondary tumour in a different part of the body

Front 227

What are the 4 stages of tumour invasion?

Back 227

Detachment by downgrading E-cadherins, attchement to matrix by integrins, degradation of ECM by proteolytic enzymes and migration.

Front 228

How do tumours evade the immune response?

Back 228

Reduced MHC class I expression and ICAM1 shedding

Front 229

In which ways can a tumour spread?

Back 229

Direct, hematogenous, lymphatic, transcoelomic, seeding

Front 230

HPV, Hep B and HTLV-1 are examples of what?

Back 230

Cancer causing viruses

Front 231

Where does HPV insert on the genome? and what does this gene usually code for?

Back 231

The E2 gene which codes to supress E6 (p53 degradation) and E7 (Rb degradation)

Front 232

Which virus is associated with Burkitts lymphoma, hodgkin's disease and nasopharyngeal carcinoma?

Back 232

Epstein-Barr virus

Front 233

What happens to the lymphocyte genome in Epstein-Barr?

Back 233

It becomes circular (and B cells become immortalised)

Front 234

What is burkitt's lymphoma a tumour of?

Back 234

B cells

Front 235

Giant R-S cells (seen in hodgkin's lymphoma) are linked to which virus?

Back 235

EBV

Front 236

Hepatocellular carcinoma is linked to which virus?

Back 236

Hep B (indirect cancerous effect)

Front 237

Which type of UV causes cancer in humans?

Back 237

UVB

Front 238

Mining, radiotherapy and atomic bombs are sources of which type of radiation?

Back 238

Ionising radiation

Front 239

What do pro-carcinogens need?

Back 239

Metabolic activation

Front 240

Are alkylating and acylating agents examples of direct or indirect chemical carcinogens?

Back 240

Direct

Front 241

Aromatic hydrocarbons, aromatic amines and azo dyes are examples of what?

Back 241

Pro-carcinogens

Front 242

What activates aromatic amines, amides and azo dyes?

Back 242

p-45

Front 243

Betanphythylamine is responsible for a 50 fold increase in what?

Back 243

Bladder cancer§

Front 244

Aflatoxin B1 is an artificial carcinogen, true or false?

Back 244

False, it is naturally occurring (but is a carcinogen)

Front 245

Inhalation of metals may cause cancer of which part of the body?

Back 245

Lung

Front 246

Arsenic is associated with which cancer?

Back 246

Skin cancer

Front 247

What are the 3 phases of carcinognesis?

Back 247

Initiation, promotion and progression (each stage may involve genetic changes)

Front 248

At which stage or carcinogenesis does multiplication and transformation into a malignant cell occur?

Back 248

Promotion

Front 249

Name the 7 hallmarks of a cancer cell.

Back 249

Self sufficient

Insensitive to anti-growth signals

apoptosis resistant

angiogenesis

immortality

invasion and metastasis

evasion of the immune system

Front 250

In which 3 ways do oncogenes differ from their proto-oncogene?

Back 250

Different gene product

Gene expressed at the wrong place/time

Too much protein produced

Front 251

What does cyclin D do?

Back 251

Pushes the cell into the cell cycle

Front 252

Name an oncogene.

Back 252

C-Myc

Front 253

How can oncogenes be activated?

Back 253

Point mutations

Gene amplification

Chromosome translocation

Chromosome relocation

Front 254

C-Myc moves chromosomes in which disease?

Back 254

Burkitts lymphoma

Front 255

Explain the epidermal growth factor receptor pathway.

Back 255

It is activated by a growth factor, and causes Ras to be converted to Raf, Map kinases cause changes in gene expression

Front 256

The EGFR can be activated by autocrine signalling, true or false?

Back 256

True

Front 257

What doea Wnt bind to?

Back 257

Frizzled receptor

Front 258

What does Wnt cause inactivation of?

Back 258

APC (which prevents beta-catenin being downgraded - so there is proliferation)

Front 259

What does TGF-beta result in?

Back 259

Growth inhibition

Front 260

What is Fas?

Back 260

A death ligand

Front 261

In which 4 ways does caspase cause cell death?

Back 261

Cuts off contact with surrounding cells

Reorganises the cytoskeleton

Disrupts the nuclear skeleton

Induces the cell to display phagocytic markers

Front 262

What is p53?

Back 262

A tumour suppressor

Front 263

What does p53 code for?

Back 263

Cell cycle arrest, DNA repair and apoptosis

Front 264

What is primary cancer prevention?

Back 264

Preventing cancer occuring

Front 265

What is secondary cancer prevention?

Back 265

Preventing premalignancies

Front 266

What is tertiary cancer prevention?

Back 266

Preventing spread of the cancer

Front 267

Is actinic chelitis malignant?

Back 267

No - premalignant

Front 268

What does aflavtoxin target?

Back 268

p53

Front 269

What does cetuximab inhibit?

Back 269

EGFR

Front 270

What hormone is linked to breast cancer?

Back 270

Oestrogen

Front 271

What hormone is linked to endometrial cancer?

Back 271

Oestrogen

Front 272

Testosterone promotes which cancer?

Back 272

Prostate cancer

Front 273

What is a functional hormone?

Back 273

Produced by an endocrine tumour

Front 274

What is an ectopic hormone?

Back 274

A hormone produced by a tumour that doesn't normally produce hormones

Front 275

What hormone is produced in testicular cancer?

Back 275

HCG

Front 276

Which 6 scans can be used to detect cancer?

Back 276

X-ray

Ultrasound

CT scan

MRI

PET

Radio-isotope scan

Front 277

Which ways (other than scans) can you diagnose cancer?

Back 277

Tumour markers in blood

Cytology

Biopsy

Front 278

What does a PET scan show?

Back 278

Radioactive substance in metabolically active areas

Front 279

What is incidence?

Back 279

Number of new cases

Front 280

What is prevalence?

Back 280

Number of people with a disease at a certain time

Front 281

What is radiotherapy?

Back 281

Strong x-rays

Front 282

Why are cancer cells targeted in radiotherapy?

Back 282

They divide more rapidly and aren't as good at repairing

Front 283

Why is radiotherapy given in small doses each day?

Back 283

To allow normal cells to recover and to allow cancer cells to move through the cycle so they are all targeted

Front 284

What does radiotherapy on the jaws increase risk of?

Back 284

Osteoradionecrosis (characterised by benign chronic ulceration)