Henry Hopkinson Flashcards

(53 cards)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What cancers are associated with HPV human papilloma virus

2

A

Benign papilloma of skin

Malignant cervix carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What cancers are associated with EBV Epstein barr virus

2

A

Burkitts lymphoma

Nasopharyngeal carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What cancers are associated with HHV1 and HHV8

3

A

Oral cancer
Kaposis sarcoma
B cell lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What cancer is associated with Hep B
1

What cancer is associated with POX virus
1

A

Hepatocellular carcinoma

Squamous cell papilloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What angiogenesis factors does the tumour mass release

4

A

Angiopoetin
FGF
VEGF
EGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Hypercoagulability of blood
Vascular wall injury
Stasis of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
What are the possible consequences of thrombosis formation | 2
Ischemia | Infarction - myocardial infarction, stroke, pulmonary embolism
26
What is an embolism
The lodging of an embolus inside a blood vessel usually a piece of thrombus broken off from original site and lodging elsewhere
27
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
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
What is arterial thrombosis What are the symptoms (4) What are the risk factors (10)
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
What are the short term emergency anticoagulants 2 How are they administered What is there mechanism of action
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
What are the long term anticoagulants 5 What is there mechanism of action
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
What is atherosclerosis Where do they occur What are the risk factors (10) What are the treatments 6
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
What is the fibrous cap of atheroma formed of 3 What is the lipid core of atheroma composed of 5
Smooth muscle cell Infiltrating monocytes and macrophages ECM ``` Lipids Calcium Cellular debris Ox-LDL Foam cells - transformed macrophages ```
33
What are the phases of atheroma formation | 5
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
What is the dental relevance of atherosclerosis
PD disease has been associated with 25-50% increased risk of atherosclerosis
35
# Define ICP Define RCP Define hinge axis Define terminal hinge axis
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
# Define canine guided occlusion Define anterior guidance Define group function
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
# Define rest position Define freeway space Define Bennett's angle
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
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 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
What are the stages of development of OSSC and features of each 3
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
What is an oral precancerous lesion What is an oral precancerous condition
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
What is leukoplakia What are its characteristics 2 How many become malignant What areas are of most concern
An abnormal white or grey area Hyperkeratosis Cannot be wiped off 1-5% become malignant FOM, ventral surface of tongue
42
What is proliferative verrucous leukoplakia Where are most common sites
A hard to define white patch with a high incidence of long term malignant transformation Gingiva and tongue
43
What is erythroplakia What is a characteristic How many become malignant
An abnormal red area or group of red spots that forms on the mucosa May bleed when scraped 80%
44
What is erythroleukoplakia How many become malignant
Speckled leukoplakia with areas of erythroplakia 30%
45
``` What percentage of dysplastic lesions: Remain unchanged Increase in size Regress to non dysplastic state Progress to malignancy ```
Unchanged 40% Increase size 20% Regress 20% Progress to malignancy 20%
46
# Define carcinoma in situ What is the process of metastasis | 5
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
What are cadherins What happens to cadherins during tumourogenesis What happens to cadherins in tumour progression
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
What are integrins What is the role of integrins in metastasis
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
What are matrix metalloproteinases What is their role in metastasis 3
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
In LN metastasis where do metastatic cells enter the lymph node Where is the first sign of LN metastasis seen
Afferent lymphatic vessel Sub capsular region
51
What is the process of metasstasis to red marrow of bone | 4
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
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
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
What are symptoms of the jaw bone of metastasis to jaw 3 What are symptoms of soft tissues of metastasis to jaw
Pain, swelling and paraesthesia developing over short time Lesions resembling hyperplastic or reactive swelling such as pyogenic granuloma or fibrous epulis