Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine 2 > CAN Week 1 (lung Cancer) > Flashcards

CAN Week 1 (lung Cancer) Flashcards

1
Q

What is a pancoast tumour

A

Cancers that start in the apex of the lung. The tumour usually spreads into one or more structures in the upper thorax and neck, which include

  • upper ribs in the thorax
  • nerves in the upper thorax and neck
  • bundles of nerves close to the spinal cord
  • blood vessels that supply blood to the upper limb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define neoplasia

A

A synonym for tumour :
An abnormal mass of tissue
The growth of which exceeds and is uncoordinated with that of normal tissues
And which persists in the same excessive manner after the cessation of the stimulus which has evoked the change

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

What triggers neoplasia

A

Neoplasia starts when a gene changes and makes one cell or a few cells begin to grow and multiply too much which can cause a tumour / neoplasm

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

Define hyperplasia

A

An increase in the number of cells in an organ or tissue. These cells appear normal under a microscope. They are not cancer but may become cancer

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

Define dysplasia

A

The presence of abnormal cells within a tissue or organ. Not cancer but may become cancer

Can be mild, moderate or severe depending on how abnormal the cells look under a microscope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the underlying principles that determine the complexity of cancer (hallmarks of cancer)

A 
Avoiding immune destruction 
Deregulating cancer energetic 
Evading growth suppressors
Activating invasion and metastasis 
Resisting cell death 
Enabling replicative immortality 
Genome instability and mutation 
Tumour promoting inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are malignant tumours

A

Show a particular type of behaviour which leads to severe illness and without treatment will cause death (cancer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define differentiation

A

The term to describe how different in appearance the cells of a tumour are to the cell type from which they derived

Failure to achieve cellular differential is a common feature of malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define the 3 types of differentiation

A

Well differentiated tumour - composed of cells which very closely resemble the cell of origin

Poorly differentiated tumour - composed of cells which bear little resemblance to the cell of origin but just enough to enable the original cell type to be identified

Undifferentiated / anaplastic tumour - composed of cells which are so undifferentiated that their cell of origin is unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Compare benign and malignant tumours

A

Benign: do not infiltrate, grow by expansion, stay at their site of origin and do not spread to distant sites

Malignant: compress and invade adjacent tissue, can spread to distant sites of the body, will infiltrate, grow by expansion and infiltration,

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

What is metastasis

A

A malignant tumour can infiltrate and invade adjacent tissues and can spread to distant sites to form a separate Secondary tumour

It is this ability to invade ad destroy tissues and to spread to secondary sites causing further destruction there which makes malignant tumours potentially fatal

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

What are common metastatic sites

A 
Brain 
Lymph nodes 
Lung 
Liver 
Bones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are epithelial tumours called

A

Squamous benign: squamous cell papilloma
Squamous malignant: squamous cell carcinoma
Transitional benign: transitional cell papilloma
Transitional malignant: transitional cell carcinoma
Glandular benign: adenoma (colonic or thyroid)
Glandular malignant: adenocarcinoma (colonic, gastric or renal)

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

What are mesenchymal tumours called

A 
Benign bone: osteoma 
Malignant bone: osteosarcoma 
Adipose benign: lipoma 
Adipose malignant: liposarcoma 
Cartilage benign: chondroma 
Cartilage malignant: chondrosarcoma 
Smooth muscle benign: leiomyoma 
Smooth muscle malignant: leiomyosarcoma 
Striated muscle benign: rhabdomyoma 
Striated muscle malignant: rhabdomyosarcoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the names of tumours derived from different cells

A

Germ cell tumours are derived from germ cells in ovary and testis

Teratomas - germ cells containing representatives from all 3 embryological germ cell layers

Embryonal tumours - embryonic blast tissue

Glial cells of the CNS- gliomas

Melanoma - melanocytes usually in skin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Ewing’s sarcoma

A

A malignant tumour of bone seen in young people probably derived from primitive neuroendocrine cels

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

What is Hodgkin’s disease

A

A malignant proliferation of lymphoid tissues classified as a subgroup of lymphomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is kaposi’s sarcoma

A

A malignant tumour derived from endothelium and driven by infection with herpes virus 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define cellular pleomorphism

A

Variation in size and shape of cells in tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Define nuclear pleomorphism

A

Variation in size and shape of nuclei in tumour cells

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

Define nuclear hyperchromatism

A

Very dark staining nuclei due to increased nuclear DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Define high mitotic count

A

Increased numbers of cells in mitosis including abnormal mitotic forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do malignant tumours spread

A

They can invade so can gain access to lymphatics, blood vessels and serosal surfaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Common sites of blood borne metastasis

A 
Brain and cerebrospinal fluid 
Lung 
Adrenals 
Bone 
Liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are some effects of benign tumours

A 
Bleeding eg gut, bladder 
Pressure on adjacent vital structures eg in brain 
Obstruction eg in brain, bronchus 
Hormone secretion eg pituitary adenoma 
Conversion to a malignant tumour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are adenomas / polyps / warts

A

Larger growths of dysplasic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What things have to go wrong in order for a cell to become cancerous

A

Proliferation: grow independently of signals
Immortality: avoid senescence / telomere shortening
Avoiding cell death: apoptosis, they don’t do it
Angiogenesis: they must be fed
Metastasis: many activities needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the difference between sporadic and familial

A

Sporadic cancer is where there is no genetic link within the family for that specific cancer

Familial cancer is when patients inherit a predisposition to develop cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is proliferation (cell cycle control)

A

Progression through the cell cycle is regulated by checkpoints
4 checkpoints are well characterised

  • the restriction point in G1 phase
  • DNA damage checkpoints in late G1 and G2
  • metaphase checkpoint (spindle attachment checkpoint) in M
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are oncogenes and tumour suppressors

A

Oncogenes promote proliferation (via restriction point)

Tumour suppressors inhibit proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What 2 processes play a role in the intrinsic limit in the number of times a cell lineage can divide

A

Senescence - cells in G0, don’t proliferate

Apoptosis- programmed cell death as a response to DNA damage and cell stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What does excess telomere shortening lead to

A

Crisis: damage to the chromosomes will eventually make the cell unviable

  • cells undergo apoptosis if they can
  • genetic catastrophe is so severe it triggers apoptosis even in the absence of p53
33
Q

What is sustained angiogenesis

A

O2 and other nutrients supplied by vasculature are essential for cell function and survival

Newly arisen tumours must promote angiogenesis to survive

Hypoxia induced factor 1

34
Q

What is VEGF

A

Many cancers produce VEGF which induced new vessel growth and also production of endothelial precursor cells in bone marrow which travel to the tumour

35
Q

Describe the vascularisation of a tumour

A

Disorganised, probably due to the imbalance of secreted factors stimulating growth over differentiation

Leaky due to imperfect cell cell junctions

36
Q

What is the primary ramus

A

A branch of a spinal nerve. There are both ventral (anterior) and dorsal (posterior) primary rami.

Dorsal rami pass posteriorly to supply:
- a strip of skin (dermatone) extending either side of the midline of the neck or trunk and extensor muscles of the vertebral column

Ventral rami are larger and clinically more important

37
Q

How are nerve plexus formed

A

All spinal nerves (except T2-12) their anterior rami branch and rejoin forming nerve plexuses
These plexuses are formed only by anterior (not posterior) rami and occurs in cervical, brachial, lumbar and sacral regions

38
Q

How do nerve fibres regroup within a plexus

A

Branches may contain fibres from more than one spinal level (the principle of convergence)

A given spinal level may contribute to more than one branch (the principle of divergence)

Because of regrouping, damage to one spinal segment usually doesn’t lead to complete loss of function or sensation

39
Q

Cardiac plexus

A

Innervates the heart. Sympathetic nerves arise from cervical and upper thoracic parts of sympathetic trunk. Parasympathetic supply derives from vagus (X cranial) nerve. These nerves also contribute to oesophagus plexus

40
Q

Pulmonary plexus

A

Surrounds lung root and has branches from the upper thoracic sympathetic trunk and vagus nerve

41
Q

What is the difference between sympathetic and parasympathetic fibres

A

Sympathetic fibres speed up heart and dilate coronary arteries. Afferent fibres are associated with pain (eg from impaired blood supply to myocardium)

Parasympathetic fibres reduce heart rate and constrict arteries. Afferent fibres take part in cardiovascular reflexes

42
Q

Benefits and downsides of CT scans

A

Relatively quick for scanning large areas of the body and readily available

Provides good anatomical information in multiple planes

Appropriate to assess for most acute clinical problems

Larger doses of ionising radiation

Risk of allergy to iodine based contrast

Contrast resolution is relatively poor for soft tissues

43
Q

Benefits and downsides of MRI scans

A
  • excellent anatomical detail of soft tissues
  • multiple planes and sequences allow detailed evaluation
  • radiation sparing investigation
  • time consuming and expensive
  • cannot be used in all patients
  • poor assessment of air filled structures
44
Q

Benefits and downsides of ultrasound

A

Quick, expensive, radiation sparing and portable

Allows for real time assessment

Excellent for assessment of superficial soft tissue

Highly user dependent

Poor assessment of deep structures, air filled structures and bone

Limited field of view at any one time

45
Q

What scans are used for different elements of the neck

A

Bones- plain film and CT

Spinal cord and nerves - MRI

Soft tissues (glands, lymph nodes, muscles)- ultrasound, CT and MRI

Vessels - ultrasound, CT and MRI

46
Q

What scans are used for different elements of the thorax

A

Lungs - plain film and CT
Heart- ultrasound and MRI
Bone- plain film and CT

47
Q

What is the mediastinum divided into

A

Superior mediastinum - above the upper level of the pericardium and plane of Ludwig terminating at the thoracic inlet

Inferior mediastinum- below the plane of Ludwig

Anterior mediastinum - anterior to the pericardium

Middle mediastinum - within the pericardium

Posterior mediastinum - posterior to the pericardium and anterior to the vertebral column

48
Q

Describe tumour origin n

A
  • tumours arise from normal tissue
  • any tissue type can develop into a cancer
  • tissue type dictates type of cancer
49
Q

General rules of tumour origins

A
  • benign tumours have the suffix -oma (adenoma, leiomyoma)
  • malignant epithelial tumours are usually regarded as carcinomas
  • malignant mesenchymal tumours are usually regarded as sarcomas
  • many malignant tumours have benign precursors
50
Q

Tumour characteristics

A
  • many normal tissues undergo continuous turnover
  • new cells are produced by cell division from stem cells and old cells die by apoptosis (programmed cell death)
  • an imbalance between the rates of cell division and cell death will cause tumour development
  • growth control mechanisms ensure that cell division = apoptosis
  • growth control can be mediated via a number of different mechanisms:
    Levels of secreted growth factors, environmental growth inhibitory factors, levels of secreted growth inhibitors, intrinsic program of differentiation, tumour immune response
51
Q

What features does a tumour need to survive and become malignant

A
  • limitless replication / immortality
  • angiogenesis
  • invasion and metastasis
52
Q

Hallmarks of cancer

A
  • self sufficiency in growth signals
  • insensitivity to anti growth signals
  • evading apoptosis
  • limitless replicative potential
  • sustained angiogenesis
  • tissue invasion and metastasis
53
Q

Mechanisms of tumourigenesis

A
  • tumours arise from cells which were normal but not have acquired new features (such as escape from growth control)
  • acquisition of these features is mediated through disrupting gene function
  • disrupting gene function occurs through gene mutation
54
Q

How can gene mutation occur

A
  • sequence change
  • gene amplification
  • gene deletion
  • gene silencing (epigenetic)
  • gene mutation is permanent
55
Q

What does gene mutation result in

A

Chanel in protein structure or levels (or both)

This causes either gain of function (oncogenes) or loss of function (tumour suppressor genes)

56
Q

What can evasion of apoptosis occur through

A
  • upregulation of anti-apoptosic factors (Bcl2 is up regulated in follicular lymphomas due to the t(14;18) translocation
  • down regulation or pro-apoptosis factors
    Caspase 3 is down regulated in colorectal tumours
  • loss of function of pro-apoptotic factors
57
Q

3 examples of tumour markers

A

HCG- human chorionic gonadotropin from tumours with trophoblast elements
AFP- alpha fetoprotein. Liver cancer, germ cell tumours
PSA- prostate- specific antigen from carcinoma of the prostate

58
Q

What is the TNM system

A

Based upon the extent of local Tumour spread, regional lymph Node involvement and the presence of distant Metastases

Can be applied to many different types of tumour

59
Q

What are the different stagings of tumours

A

TX- primary tumour cannot be assessed
T0- no evidence of primary tumour
Tis- carcinoma in situ
T1- tumour is 2cm or less across
T2- tumour is more than 2cm but not more than 5cm across
T3- tumour is more than 5cm across
T4- tumour of any size growing into the chest wall or skin (includes inflammatory breast cancer)

60
Q

What is the staging of metastasis

A

MX- distant spread cannot be assessed
M0- no distant spread is found on X-rays (or other imaging tests) or by physical exam
M1- cancer has spread to distant organs (most often brain, bones, liver)

61
Q

Describe dukes staging for colorectal carcinoma

A

Stage A- any tumour which does not extend beyond muscular is propia (no nodal involvement)

Stage B- tumour extends beyond the muscularis propia. No nodal involvement

Stage C- any depth of tumour. Tumour present in nodes

62
Q

What is the two hit hypothesis for retinoblastoma

A

Phenotype of the mutant Rb allele is dominant at the level of the whole organism
However the phenotype of the mutant allele is recessive at the cellular level
Characteristic of the tumour suppressor gene

63
Q

Why are tumour suppressor genes associated with a loss of heterozygosity in tumours

A

Because it is highly unlikely that both gene copies are inactivated by 2 successive mutational events

The second mutation occurs by a different mutational process with a higher frequency
(Eg Mitotic recombination)

64
Q

Describe the importance of cloning the Rb gene

A

Showed that familial and sporadic cancers can share common mechanisms

Showed that theories relating to TS genes were correct

Suggested ways of identifying TS genes

  • positional cloning of genes responsible for familial cancers
  • scanning tumours for regions of LOH
65
Q

How do the tumour suppressors Rb and P53 act

A

Apoptosis:

  • when things go wrong, cells can commit suicide = programmed cell death (apoptosis)
  • this is a key mechanism to avoid cancer
  • proteins such as P53 can trigger cells to enter apoptosis if cell cycle / DNA synthesis fails
66
Q

What stresses can P53 detect and what outcomes does it trigger

A

Stresses:

  • dna damage
  • hypoxia
  • heat / cold shock
  • mitotic spindle damage

Outcomes:

  • cell cycle arrest
  • DNA repair
  • apoptosis
  • senescence
67
Q

How do oncogenes act

A

They undergo dominant activating mutations in tumours (gain of function)

68
Q

What do oncogenes do and how are they activated

A

-Translocations
-cytogenetics: chromosomal arrangements creating a novel gene: common in haematologic tumours and sarcomas
Philadelphia chromosome in 90% of patients with chronic myeloid leukaemia
- ABL is a proto-oncogene
- BCR (breakpoint cluster region) produces a novel protein kinase. This acts on many downstream signalling pathways

69
Q

How do carcinogens cause mutations

A

Reaction with free radicals (radiation)
Mechanisms of mutation: adducts, cross links, breaks etc

  • increase the rate of mutation, DNA breaks or base changes
  • leads to errors such as incorrect bases incorporated or misjoining of chromosome ends
70
Q

Examples of infectious agents that can cause cancer

A

Helicobacter pylori bacterium - stomach cancer (930,000 cancers worldwide) - cure with antibiotics

Hepatitis B virus - liver cancer (450,000 worldwide)

Human papilloma virus - cervical cancer (490,000)

Epstein- Barr virus - nasopharyngeal cancer and lymphoma (100,000) (glandular fever but cancer with malaria)

Human immunodeficiency virus - kaposis sarcoma and other rarer tumours (57,000) - treat with antivirals

71
Q

Mechanisms that cause cancer

A

Inflammation - viruses, asbestos

Immune suppression - immune suppressed individuals show small increase in cancer frequency (especially virus induced cancer)

Food, chemicals

Intrinsic causes: tissue growth- kids
Hormones

72
Q

What is the principle of an inherited cancer predisposition

A

Inherited mutation in a gene causing a defect in the machinery that guards against genome damage, either monitoring or DNA damage repair

73
Q

Examples of targeted therapies based on known features of cancer cells

A

Antibodies: to specific antigens eg herceptin, EGFR, breast cancer

Small molecule inhibitors eg Abl, leukaemias, BRAF, melanoma

Angiogenesis inhibitors: eg avastin, VEGF, colon cancer

74
Q

What are the rotator cuff muscles (SITS)

A

Supraspinatus

Infraspinatus

Teres minor

Subscapularis

75
Q

4 common physical signs of breast cancer

A

Skin dimpling

Abnormal contours

Edema (orange peal)

Nipple retraction / deviation

76
Q

What do palpable and enlarged cervical lymph nodes suggest

A

These are glands in the neck which become enlarged in infection

If they are persistent they raise suspicion of cancer (breast, lung, stomach), TB, lymphoma

77
Q

Most common symptoms of lung cancer

A
  • cough: lung cancer can cause a new cough or a change in a chronic cough
  • blood in sputum : hemoptysis- requires medical attention
  • shortness of breath
  • wheezing
  • chest pain: can develop and may be dull, sharp or stabbing
  • voice hoarseness
  • headache and swelling of the face, arms or neck
  • arm shoulder and neck pain: can be caused by a tumour in the top of the lungs (called a pancoast tumour). Other symptoms include weakening of the hand muscles (due to pressure on the nerve that stimulates the arm), a droopy eyelid and blurred vision
78
Q

Differential diagnosis for Mr jones

A

Lung cancer
Tuberculosis
Pneumonia
Hodgkin’s lymphoma

Medicine 2 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions