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Dentistry Year 2 Term 2 > Henry Hopkinson > Flashcards

Henry Hopkinson Flashcards

1
Q

How many people develop cancer in their lives

How many people die from cancer

What is the most common cancers
Males, females, both

A

1 in 3

1 in 5

Males: prostate cancer
Females: breast cancer
M and F: lung cancer and bowel cancer

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2
Q

Define neoplasm

Define carcinoma

Define sarcoma

Define papilloma

A

Neoplasm- a new or abnormal growth tissue which is uncoordinated with the normal tissues, may be benign or malignant

Carcinoma- a malignant neoplasm of endodermal or ectodermal origin

Sarcoma- a malignant neoplasm of mesodermal (connective tissue) origin

Papilloma- a benign epithelial tumour

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3
Q

What does ectoderm give rise to
2

What does mesoderm give rise to
3

What does endoderm give rise to

A

Skin, nervous system

Muscles, bone, connective tissue

Linings of organs (gut, liver, lungs)

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4
Q

Define dysplasia

Define hyperplasia

Define hypertrophy

Define anaplasia

Define aneuploidy

A

Dysplasia- abnormal development in tissues which may imply potential malignancy
Hyperplasia- increased number of cells in a tissue
Hypertrophy- increase in size of cells in a tissue
Anaplasia- loss of differentiation of cells happening progressively as tumours develop
Aneuploidy- cells of a tissue possessing abnormal number of chromosomes

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5
Q

What does cancer originate from and what are these

How does a normal cell become one of these

A

Cancer stem cells: cells with the ability to self renew, they are the origin of all cells found in a tumour mass so have a high tumourigenic capacity

Genetic mutations - germline or somatic

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6
Q

What are the steps of progression of oral squamous cell carcinoma
5

A
  1. Initial genetic insult leads to transformation
  2. Deletion of 3p and 9p -genes involved in cell division
  3. Genomic instability
  4. P53 mutation (tumour suppressor gene) - leads to proliferation of genetically unstable cells
  5. Tumour heterogeneity, invasion and metastasis
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7
Q

What are oncogenes

What happens to them during cancer

Ras
Myc

A

Oncogenes are genes that normally function to promote cell growth and division in a controlled manner

When mutated they are activated causing accelerated cell cycle leading to uncontrolled cell division

Activation of KRAS/HRAS/NRAS- encodes signalling proteins which switch on proliferation and differentiation
Activation of Myc- encodes transcription factor which activates genes involved in cell proliferation

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8
Q

What are tumour suppressors

What happens to them during cancer

Rb
P53

A

Tumour suppressors are genes that normally slow down cell growth and division

In cancer they can be inactivated leading to loss of regulation of cell cycle

Inactivation of Rb- tumour suppressor that controls transition from G1 to S/differentiation/death
Inactivation of P53- detects DNA damage in cells and activates cell cycle

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9
Q

What cell death inducing genes are up regulated during cancer
1

What cell death inducing genes are down regulated during cancer
2

A

Bcl2 - anti apoptotic

BIM, BID - pro apoptotic

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10
Q

What do DNA repair genes do
At what phase of the cell cycle do they engage

What DNA repair genes are involved in breast cancer

A

DNA repair genes encode proteins that correct damage to DNA molecules
They engage after S phase

BRCA1 and BRCA2 - expressed normally but can carry germline mutations increasing risk of breast cancer

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11
Q

What cancers are associated with HPV human papilloma virus

2

A

Benign papilloma of skin

Malignant cervix carcinoma

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12
Q

What cancers are associated with EBV Epstein barr virus

2

A

Burkitts lymphoma

Nasopharyngeal carcinoma

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13
Q

What cancers are associated with HHV1 and HHV8

3

A

Oral cancer
Kaposis sarcoma
B cell lymphoma

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14
Q

What cancer is associated with Hep B
1

What cancer is associated with POX virus
1

A

Hepatocellular carcinoma

Squamous cell papilloma

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15
Q

What cancers are associated with Hep C, human T cell lymphotropic virus 1 and 2
3

A

Hepatocellular carcinoma
T cell leukaemia
T cell lymphoma

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16
Q

How many people get HPV infection

What percentage of cancers of the oral cavity test positive for HPV

What does HPV have links to

A

1 in 3

73%

Inactivation of P53 tumour suppressor leading to tumour formation and growth

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17
Q

What angiogenesis factors does the tumour mass release

4

A

Angiopoetin
FGF
VEGF
EGF

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18
Q

What is an atheroma

Where does atheroma formation take place

A

An atheroma or atheromatous plaque is an abnormal accumulation of material in the tunica intima consisting mostly of macrophages and debris containing lipids, calcium and fibrous connective tissue

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19
Q

What is thrombosis

How does a thrombus form
5 stages

What is the difference between thrombus and clot

A

Thrombosis is formation of a solid mass of blood within the circulatory system usually on the inside of the blood vessel wall

  1. Damage to endothelium exposes collagen and vWF
  2. Platelets adhere to collagen, vWF and each other to form platelet plug
  3. Endothelial cells release tissue factor and thromboplastin to initiate thrombin release
  4. Thrombin converts fibrinogen to fibrin via clotting cascade
  5. Fibrin forms network of clot

Thrombus forms in circulating blood, is firmly attached, friable and dry, pale red or red in colour and may show lines of Zahn
Clot forms in stagnant blood, it is loosely attached, soft and moist, red or yellow and doesn’t have lines of Zahn

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20
Q

What is the difference between pale thrombus, red thrombus, mixed thrombus
3 points for each

A

Pale thrombus-
Forms in fast flowing blood usually arteries
Contains mainly platelets with fibrin
Firm, pale reddish grey colour

Red thrombus-
Forms in stagnant blood where fibrin entraps RBCs
Contains many platelets, fibrin and RBCs
Soft, dark red and gelatinous

Mixed thrombus-
Forms in slow flowing blood such as veins
Contains alternating layers of red and pale layers
Lines of Zahn

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21
Q

What are the three conditions of virchows triad needed for thrombus formation

A

Hypercoagulability of blood
Vascular wall injury
Stasis of blood

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22
Q

How does vascular wall injury affect thrombosis
2

What are the physical mechanisms of wall damage
3

What are the chemical mechanisms of wall damage
2

What are the pathological mechanisms of wall damage
2

A

Damage to endothelium changes nitric oxide production which alters the balance of anticoagulant and anti-platelet mechanisms
Damage exposes ECM triggering coagulation cascade

Physical:
Ulcerated atherosclerotic plaques
Scarred valves in endocarditis
Vein injury via fractures/ muscle injury/ surgery
Chemical: (release of O free radicals)
Radiation
Cigarette smoke
Pathological:
Accumulation of cholesterol and lipids
Disease- coronary heart disease, diabetes, hypertension, hypercholesterolemia, obesity
23
Q

What is the pattern of normal blood flow and how does this prevent thrombosis

What is the effect of static blood flow on thrombosis

What is the effect on turbulent blood flow on thrombosis

What are the causes of change in blood flow
4

A

Laminar - creates dilution of clotting factors due to fast flow so dont accumulate adjacent to vessel wall

Stasis- blood flow stopped so platelets able to come into contact with epithelium and less dilution of clotting factors

Turbulence- caused by obstruction to vessel wall preventing laminar flow and leading to pockets of stasis where platelets more easily in contact with endothelium

Atrial fibrillation
Immobility or paralysis
Varicose veins
Obstruction by tumour, obesity, pregnancy

24
Q

What causes hypercoagulability of blood
7

What causes hyperviscosity of blood
3

A 
Coagulation disorders 
Obesity
Pregnancy
Hyperoestrogenic  state - oral contraceptives
Malignancy
IBS
Sepsis

Polycythemia
Deformed RBC - sickle cell
Malignancy

25
Q

What are the possible consequences of thrombosis formation

2

A

Ischemia

Infarction - myocardial infarction, stroke, pulmonary embolism

26
Q

What is an embolism

A

The lodging of an embolus inside a blood vessel usually a piece of thrombus broken off from original site and lodging elsewhere

27
Q

What is deep vein thrombosis

Symptoms (5)

Risk factors (11)

What is a possible consequence of DVT

What are non drug treatments (3)
What are drug treatments

A

The formation of a blood clot in vein usually of leg

Throbbing and cramping in one leg, swelling in one leg, warm skin, red or dark skin, swollen veins sore to touch

Over 60, overweight, smoking, contraceptive pill, cancer, heart failure, varicose veins, pregnancy, immobility, severe burns or trauma, stroke

Pulmonary embolism- clot breaks free and travels through bloodstream getting lodged in respiratory system where vessels narrow leading to low BP, fainting, arrhythmia,chest pain - in 25% of cases first presentation death

Non drug treatments - compression stockings, inferior vena cava filters, thrombectomy
Drug treatments- anticoagulants

28
Q

What is arterial thrombosis

What are the symptoms (4)

What are the risk factors (10)

A

A blood clot in an artery which can prevent blood flow to vital organs

Heart attack (myocardial infarction)
Stroke (cerebral infarction)
Transient ischaemic attack
Critical limb ischemia

Age, smoking, unhealthy diet, obesity, alcohol, high BP, high cholesterol, diabetes, south asian African or African carribean descent

29
Q

What are the short term emergency anticoagulants
2

How are they administered

What is there mechanism of action

A

Heparin - IV - inactivates thrombin and factor Xa
Streptokinase - IV - a fibrinolytic drug that activates plasminogen to form plasmin which degrades fibrin to break up thrombi

30
Q

What are the long term anticoagulants
5

What is there mechanism of action

A

Warfarin - competitively inhibits vit K to reduce synthesis of clotting factors

Dabigatran - thrombin inhibitor

Rivaroxiban - inhibits factor Xa

Apixiban - inhibits factor Xa

Edoxaban - inhibits factor Xa

31
Q

What is atherosclerosis

Where do they occur

What are the risk factors (10)

What are the treatments
6

A

The build up of fats, cholesterol and other substances in the tunica intima called plaque which can restrict blood flow or burst and cause blood clot
Occur in medium and large arteries over 2mm D

Age, male, obesity, smoking, high fat diet, lack of exercise, alcohol, diabetes, high BP, high LDL cholesterol

Statins for high cholesterol
Anti hypertensive drugs
Anti platelets -Low dose aspirin or clopidogrel
Coronary angioplasty
Coronary artery bypass graft
Carotid endarterectomy
32
Q

What is the fibrous cap of atheroma formed of
3

What is the lipid core of atheroma composed of
5

A

Smooth muscle cell
Infiltrating monocytes and macrophages
ECM

Lipids
Calcium
Cellular debris
Ox-LDL
Foam cells - transformed macrophages
33
Q

What are the phases of atheroma formation

5

A
  1. ) endocardial dysfunction
  2. ) fatty streak - yellow streak visible on luminar wall due to accumulation of fat laden foam cells in tunica intima
  3. ) simple plaque - plaque forms due to accumulation of lipids in foam cells and proliferation of smooth muscle cells, a fibrin cap forms over lesion
  4. ) stable plaque - plaque less likely to rupture with thick fibrous cap
  5. ) unstable plaque/complicated lesion- plaque more likely to rupture with thin fibrous cap and inflammation within plaque making cap less stable
34
Q

What is the dental relevance of atherosclerosis

A

PD disease has been associated with 25-50% increased risk of atherosclerosis

35
Q

Define ICP

Define RCP

Define hinge axis

Define terminal hinge axis

A

The contact that occurs when patient fits their teeth together with maximum intercuspation

The position of the mandible in relation to maxilla with condylar head in terminal hinge axis position uppermost and foremost in glenoid fossa where initial tooth contact occurs on retruded arc of closure

The axis of rotation of condyle during first few mm of mandibular opening

The axis of rotation of mandible when condyles in most superior position in glenoid fossa

36
Q

Define canine guided occlusion

Define anterior guidance

Define group function

A

During lateral excursions there is disclusion of all teeth on working side except for canine and no contacts on non working side

The functional relationship between maxillary and mandibular anterior teeth consisting of the horizontal and vertical overlaps of anterior teeth

Multiple tooth contacts on working side during lateral excursions but no contacts on non working side

37
Q

Define rest position

Define freeway space

Define Bennett’s angle

A

The habitual postural position of mandible when patient relaxed with condyle in neutral position

The space between neutral position and ICP

The angle produced by vertical movement of non working side condyle

38
Q

What is posselts envelope

What are the border movements of posselts envelope limited by

What are the maximum movements of
Opening
Lateral
Protrusion
Retrusion
A

A representation of the 3D border movements of the mandible from sagittal, frontal and horizontal planes

Border movements limited superiorly by tooth contact
Border movements limited laterally, posteriorly and anteriorly by TMJ and ligaments

Opening- 50-60mm
Lateral- 10-12mm
Protrusion - 8-10mm
Retrusion - 1mm

39
Q

What are the stages of development of OSSC and features of each
3

A

Keratosis- increased keratinisation

Dysplasia- irregular epithelium stratification, loss of basal polarity, drop shaped rete pegs, abnormal mitosis, premature keratinisation, anisonucleosis, nuclear pleomophism, anisocytosis, increased nuclear:cytoplasmic ratio

Carcinoma- local invasion by infiltration into underlying lamina propria and submucosa

40
Q

What is an oral precancerous lesion

What is an oral precancerous condition

A

A morphologically altered tissue in which cancer is more likely to occur than in its normal counterpart

A generalised state associated with a significantly increased risk of cancer

41
Q

What is leukoplakia

What are its characteristics
2

How many become malignant

What areas are of most concern

A

An abnormal white or grey area

Hyperkeratosis
Cannot be wiped off

1-5% become malignant

FOM, ventral surface of tongue

42
Q

What is proliferative verrucous leukoplakia

Where are most common sites

A

A hard to define white patch with a high incidence of long term malignant transformation

Gingiva and tongue

43
Q

What is erythroplakia

What is a characteristic

How many become malignant

A

An abnormal red area or group of red spots that forms on the mucosa

May bleed when scraped
80%

44
Q

What is erythroleukoplakia

How many become malignant

A

Speckled leukoplakia with areas of erythroplakia

30%

45
Q 
What percentage of dysplastic lesions:
Remain unchanged
Increase in size
Regress to non dysplastic state
Progress to malignancy
A

Unchanged 40%
Increase size 20%
Regress 20%
Progress to malignancy 20%

46
Q

Define carcinoma in situ

What is the process of metastasis

5

A

Cancer in which abnormal cells have not spread beyond where they first formed or broken through basement membrane

Metastasis:

  1. Local infiltration of tumour cells into adjacent tissue
  2. Intravasation - transendothelial migration of cancer cells into vessels
  3. Survival in circulatory system
  4. Extravasion
  5. Proliferation in new site leading to colonisation
47
Q

What are cadherins

What happens to cadherins during tumourogenesis
What happens to cadherins in tumour progression

A

Cadherins are transmembrane glycoproteins that mediate calcium dependent cell to cell adhesion, regulating cell growth and differentiation

Tumourogenesis- disturbed cell to cell adhesions (loss of cadherin) alters adhesion mediated signlling pathways inducing malignant phenotypes in normal cells leading to hyperplasia, dysplasia and abnormal lymphoid infiltration

Tumour progression- down regulation of E cadherin and up regulation of N cadherin plays role in early invasion and metastasis

48
Q

What are integrins

What is the role of integrins in metastasis

A

Integrins are receptors composed of alpha and beta subunits binding cells to their ECM

Metastasis- altered integrin expression leads to loss of adherence followed by metastasis

49
Q

What are matrix metalloproteinases

What is their role in metastasis
3

A

Matrix metalloproteinases are calcium dependent zinc containing molecules which are enzymes that break down proteins, they are normally found in spaces between cells and tissues

Metastasis-
Proteinase action of MMP removes physical barriers of invasion by degradation of ECM
MMPs can modulate cell adhesion so cells can move through ECM by forming new attachments and breaking old ones
MMPs can activate biological activities of ECM

50
Q

In LN metastasis where do metastatic cells enter the lymph node

Where is the first sign of LN metastasis seen

A

Afferent lymphatic vessel

Sub capsular region

51
Q

What is the process of metasstasis to red marrow of bone

4

A
  1. Tumour cells produce adhesive molecules and bind to marrow stromal cells and bone matrix
  2. Adhesive interactions direct tumour cells to increase production of angiogenic factors and bone reabsorbing factors to enhance tumour growth
  3. During bone resorption growth factors released
  4. Growth factors act in paracrine manner creating an environment where metastatic cells seed and grow
52
Q

What fraction of patients with oral cancer will present with evidence of tumour metastasis to cervicle LN

What percentage of tumours metastasise to:
level 1
Level 2
Level 3
Level 4
Level 5

What level do tumours of cheek or FOM usually metastasise to
What level do tongue and oropharyngeal cancers metastasise to

A

Half of patients

Level 1- 50%
Level 2 - 40%
Level 3 - 30%
Level 4- 15%
Level 5- 5%

Level 1

Level 2 and 3

53
Q

What are symptoms of the jaw bone of metastasis to jaw
3

What are symptoms of soft tissues of metastasis to jaw

A

Pain, swelling and paraesthesia developing over short time

Lesions resembling hyperplastic or reactive swelling such as pyogenic granuloma or fibrous epulis

Dentistry Year 2 Term 2 (4 decks)

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