Case 4 Flashcards
What are the 4 main components of blood
RBCs- erythrocytes
White blood cells- leukocytes
Platelets- thrombocytes
Fluid-plasma
What is the haematocrit
The proportion of the blood that is taken up by red blood cells
What is the erythrocyte sedimentation rate
The rate at which RBCs settle in a tube under the forces of gravity
With anaemia, is the erythrocyte sedimentation rate greater or smaller
Greater
How wide is an erythrocyte
6-8mm
How long does an average erythrocyte live
120 days
How long do platelets last in the circulation
7-14 days
What is the proteins role in the plasma (5)
Reserve supply of amino acids Carriers for other molecules Act as buffers Help blood to coagulate Oncotic pressure
What are globulins
Proteins in the blood plasma that transport lipid and vitamins with some being immunoglobins
What is albumin
A negatively charged protein making up 60% of the blood
Has a role in maintaining oncotic pressure and transporting substances
How does oncotic pressure vary as you go along a capillary bed
It stays the same (slight raise towards venous end as fluid volume decreases)
What are electrolytes role in the blood
They maintain osmotic balance
What other substances are in the blood beyond proteins, electrolytes and blood cells
Glucose for energy Amino acids for protein synthesis Hormones Dissolved gases Vitamins and minerals Urea and uric acid
How does hydrostatic pressure vary as you go through a capillary
It decreases
How can heart effect hydrostatic pressure in a capillary why
There may be increased hydrostatic pressure at the venous end as there is a back up in the system which may result in less fluid going back into the capillary at this end
How can nephrosis alter oncotic pressure
This may decrease it as there will be decreased albumin synthesis
What visible symptoms caused by a change in increased hydrostatic or reduced oncotic pressure result in
An oedema
How can a compromised immune system result in an oedema
Localised oedema can occur upon the removal of a lymph node
The immune system may also form an oedema on injury to allow an influx of chemical mediators into the site of injury to fight off any potential infection
Where is the spleen situated
In the left hypochondrium
What arteries supply the spleen
The splenic artery and vein
What is the function of white pulp in the spleen
It is part of the immune system and is mainly made up of white blood cells
What is the function of red pulp in the spleen
It is made up of connective tissue and filters the blood for antigens, microorganisms and defective red blood cells
What are the main key functions of the spleen
It's a lymphoid organ for the immune system Removes old erythrocytes in the red pulp Screens for pathogens in the white pulp Stores platelets Stores iron
Where are antigens found on erythrocytes and what are they
The surface attached to glycolipids or glycoproteins
they are short sugar chains
What synthesises antigens
glycosyltransferases- different types lead to different antigens
Why is blood group O considered a ‘universal donor’
Because it contains no antigens on it’s surface
What blood can patients with blood type A and blood type B receive
Group A or O however A is preferable
Same idea however with B
What blood groups can blood group AB receive
All blood groups as it contains antigen A and B on its surface so won’t react when transfused
What antibodies are present in blood type AB
There are no antibodies present
What complication does giving the wrong blood type lead to
Haemolytic disease
What percentage of the population are rhesus positive
85%
How can complications arise in pregnancy if the father and mother have differing blood types and how can this be combatted
If the mother and father have conflicting rhesus types this may lead to haemolytic disease of the newborn
This can be prevented by giving an injection that neutralises antigens the mother produces that may attack the foetus’ blood
What does the suffix poiesis refer to
making of a substance
What is granulopoiesis
The making of WBCs
What are granulocytes
neutrophils, eoisinophils and basophils
What are mononuclear cells
Monocytes and lymphocytes
What is the site of primitive haematopoiesis
The yolk sac
Where is the major site of haematopoiesis
The bone marrow however this retracts with age and is replaced by fat
Where, beyond the bone marrow, can the body naturally make blood cells
Peripheral blood stem cells
What procedure can occur to transfer many stem cells into the peripheral blood cells of adults
Using an umbilical cord
What are committed progenitors
These are stem cells that are going to become a specific cell and this path cannot be altered
What are precursors
These are cells that have lost the ability to make any other cells and look almost exactly like the mature cell they are about to develop into
What is the lineage-primed model of haematopoiesis
Stem cells tend to differentiate in a certain way and have their path set out for them, if the environment is altered in a certain way this path may be changed however if not then they will differentiate to form the cell they intended
Whta defines a stem cell
They are self renewing so can copy themselves indefinitely
They are pluripotent so can differentiate into many different cell types
What results in a stem cell differentiating from the bone marrow
If one of the daughter cells the stem cell produces becomes unattached from its specific niche within the bone marrow
What controls stem cell differentiation
Transcription factors control the expression of specific genes
Growth factors act as extrinsic factors that influence cell fate
What specific transcription factors dictate RBC differentiation and leukocyte differentiation
GATA 1 forms an erythrocyte and PU. 1 tends towards a leukocyte
How are the transcription factors in stem cells regulated
Through positive feedback loops
If there is a slight imbalance of one specific transcription factors between daughter cells of stem cells what occurs
The daughter cell with greater levels of this transcription factor will continue to produce more and the one with less will have that transcription factor inhibited
What is EPO
Erythropoietin is the colony stimulating factor for erythrocytes
What is G-CSF
Granulocyte colony stimulating factor
What is TPO
thrombopoietin
When would EPO be clinically treated to combat disease
Renal failure, bone marrow failure and may help blood shortages
When would G-CSF be administered clinically
After chemo or for stem cell mobilisation
Where is erythropoietin produced and how is it regulated
The kidneys
Dependent on the amount of oxygen in the body
What are reticulocytes
immature red blood cells
When does reticulocytosis occur
When there is a sudden need for RBCs such as extreme bleeding or haemolysis
What four stresses drive the production of G-CSF
Infection
Inflammation
Immunity
Infarction
What does the activation of high levels of G-CSF result in
Progenitor expansion
Toxic granules
Left shift (mobilisation of immature cells)
What are the four components of the mononuclear phagocyte system
Blood monocytes
Mobile tissue macrophages
Fixed tissue macrophages
Dendritic cells
What are the roles of macrophages (6)
Developing blood, brain and bone Storing iron Clearing debris Detecting pathogens Priming immunity Immune response
How is the mononuclear phagocyte system important in disease and infection
There are specialised macrophages in each part of the body to deal with and pathogens coming in to that specific part
How does the state of haem change upon the binding of oxygen
The haem goes from a ‘tense’ to a ‘relaxed’ state and this allows further O2 to bind as it increases its affinity to O2
How does p.p. affect oxygen release by haem
The lower the p.p. the mroe oxygen is given off
Therefore organs that require a lot of oxygen have low p.p.
How does an increase in temp. decrease in pH or increase in 2-3 DPG levels affect the oxygen dissociation curve
It shifts it to the right
What is 2-3 DPG
A product of glycolysis
Why is a tissue affected by a shift in the oxygen haemoglobin dissociation curve but an alveolus isnt
Because a tissue is usually at 5-7kPa whereas an alveolus is at 14kPa so it is barely affected
What do metabolically active tissues give off that results in a shift of the oxygen haemoglobin curve to the right and why does this assist them
Very active metabolic tissues require a lot of oxygen they give off heat due to metabolic processes and this shifts the curve to the right
As a result oxygen dissociates from haemoglobin more readily and the affinity of oxygen for Hb is reduced
How is pH linked to the Bohr effect
A lower pH occurs due to an increase in CO2 in the bloodstream due to respiratory acidosis
This shifts the oxygen haemoglobin curve to the right alongside an increase in the presence of CO2
How does 2-3 DPG result in a shift to the right of the oxygen haemoglobin curve
It interacts with amino acids on beta chains and this destabilises the interaction of Hb with O2
How does altitude affect 2-3DPG
Higher altitudes increase 2-3DPG production so more oxygen goes to the tissues
What are the three main forms of CO2 carriage in the bloodstream
Dissolved in the plasma
Bicarbonate
Bound to haemoglobin
How does carbonic anhydrase promote the Bohr effect
Carbonic anhydrase catalyses the reaction CO2 + H2O -> HCO3- + H+
This H+ can bind with haemoglobin instead of some oxygen which decreases Hb affinity for oxygen
What does carbon dioxide form when combined with haemoglobin
Carbaminohaemoglobin
What groups are mainly affected by sickle cell disease
Those of African, Caribbean, Middle Eastern and Indian descent
What are the three main types of sickle cell anaemia and what are their genotypes
Sickle cell anaemia (HbSS)
Sickle haemoglobin-C disease (HbSC)
Sickle beta Thalassemia
What is the inheritance pattern in sickle cell anaemia
Autosomal recessive
How does sickle haemoglobin C disease affect a patient
Similar symptoms to sickle cell however less anaemia in general
Where is the mutation in the haemoglobin in sickle cell anaemia
On the beta globin chain
What is the nature of the mutation that codes for HbS
A single base substitution on the sixth codon of the beta-chain gene
How does the HbS mutation result in a sickle shaped RBC
It forms polymers under deoxy conditions so the erythrocyte distorts and collapses in on itself
This occurs when it is cold, infection, hypoxia and exercise but if these episodes reccur then the cells amy become irreversibly sickled
What is the disadvantage of the sickle cell RBCs
They are stickier and less flexible than normal RBCs so can form clusters and get stuck, blocking and damaging blood vessels
What is a sickle cell crisis
This is the clustering of sickle cells in blood vessels and is characterised by harsh pain
What is the lifespan of a sickle cell
around 17 days
How does Sickle cell anaemia present
Usually in early childhood
Variable severity
Half the sufferers experience sickle cell crisis with most having a few each year
Anaemia and infection common
Chronic manifestations can be seen by ischaemia and infarction due to blocking of blood vessels by sickle cells
Why do children in general not present with sickle cell in the first 6 months
They are protected by elevated levels of HbF
How can FBC and blood film indicate sickle cell disease
They will present with a high percentage of reticulocytes and then sickled RBCs
What does the sickle solubility test do but what is it’s limitation
This exposes RBCs to a deoxygenating agent that gives a cloudy appearance in the presence of HbS
however it doesn’t differentiate between sickle cell disease and sickle trait
How can you confirm sickle cell disease after a positive sickle solubility test
You can analyse with electrophoresis or high-performance liquid chromatography
What is the only curative treatment of sickle cell disease
Bone marrow transplant
What is dactylitis, a symptom of sickle cell disease
This is hand and foot swelling, mainly in infants
What is an aplastic crisis
When the body doesn’t produce enough new RBCs to replace the old ones
How can sickle cell anaemia affect the eyes
Vision loss or even blindness may occur when sickle cells become blocked in the retina so sufferers should have their eyes checked
What is spherocytosis
The presence of sphere shape RBCs instead of bioconcave discs
What causes spherocytosis
Genetic or various forms of haemolytic anaemia
What is the pattern of inheritance of spherocytosis
It is autosomal dominant
What is the defect cause that leads to the spherical shaped blood cells in spherocytosis
A defect in one or more of the coupling proteins that connect the cytoskeleton and lipid bilayer membrane
This means the lipid bilayer isn’t supported by the cytoskeleton
What consequences can arise as a result of spherocytosis
This results in a smaller surface area for gas exchange and less efficient oxygen transportation
What occurs in the spleen to spherocytes
These cells are often caught in there and promote phagocytosis by splenic macrophages leading to extravascular haemolysis, shortened lifespan and subsequent anaemia
How may spherocytosis be discovered if not found in early life
This may be of an incidental finding of haemolysis, haemolytic anaemia or spherocytes on the blood smear
What is the life expectancy of sickle cell disease
40-60 years
What is the life expectancy of those suffering from spherocytosis
Generally normal
What are qualitative abnormalities with globin chains
Structual variations to the Hb molecule
What are quantitative abnormalities to the Hb chain
There is a quantitative decrease in the production of alpha or beta globin chains
Chains are structurally normal
Known as Thalassemias
What is alpha thalassemia
A reduction in alpha globin chain synthesis
What is beta thalassemia
A reduction in beta globin chain synthesis
How many types of alpha thalassemias are there and how are they dictated
There are 4 different types characterised by the mutation of a number of alpha globin genes on each chromosome as there are four different genes that can be affected
How does a single deletion of an alpha globin allele affect sufferers
Hardly, asymptomatic
How does a two gene alpha globin gene deletion affect sufferers of alpha thalassemia
Very rarely majorly however they may present with mild hypochromic anaemia
How does a three gene deletion on the alpha globin allele affect sufferers
This leaves one normal gene and therefore excess beta globin chains form HbH
How does HbH affect an RBC
It which has a high affinity for oxygen which results in the RBCs being ineffective at delivering oxygen to hypoxic tissues
It also is prone to oxidation which results in intracellular occlusions that may promote haemolysis
What does a four gene deletion fo the alpha globin gene result in
Severe lack of HbF- extremely important in gestation
Gamma chains take place and form gamma tetrameters which cannot deliver oxygen as their affinity of O2 is too high
Baby is stillborn and has hydrops fetalis- full body oedema
How can you diagnose alpha thalassemia
Complete blood count and blood smear
Haemoglobin analysis such as electrophoresis determines what type is present
How is beta thalassemia inherited normally
In the autosomal recessive manor
What classifies patients who have beta thalassemia intermedia from major
If they are transfusion dependent (major) or not (intermedia)
Why are newborns asymtomatic despite having the beta thalassemia genotype
Because they have HbF as their major haemoglobin source
What occurs in beta thalassemia major to the RBCs
The unpaired alpha chains may precipitate to form inclusions
This leads to anaemia and inefficient erythropoiesis due to earlier breakdown by the spleen and apoptosis of inclusions
What are the symptoms of beta thalassemia major
Abdominal swelling
Bony deformities due to erythroid hyperplasia
Palor and jaundice
Exercise intolerance
How can you diagnose beta thalassemia
The complete blood count and peripheral blood smear
How can you cure beta thalassemia
If identified early you can do a stem cell transplant
What is the most common form of anaemia in the Uk
Iron deficiency anaemia
What causes iron deficiency anaemia
Pregnancy or child growth spurts Heavy menstrual periods Poor absorption of iron Bleeding from the gut Eating a poor or restricted diet
What are causes of anaemia beyond iron deficiency
Lack of vitamin B12 and folic acid
RBC problems
Bone marrow problems
RA and chronic kidney disease
How do you treat iron deficiency anaemia
Oral iron salts (100-200mg) given daily
Folic acid and iron for pregnant women
What can you administer if the patient can’t take oral iron
Parenteral iron
What dose of folic acid should be taken daily for adults suffering with anaemia
5mg
What drug can be taken for those with pernicious anaemia
Hydroxocobalamin
Should you ever take hydroxocobalamin daily
No
What side effects does hydroxocobalamin generally cause
Diarhhoea dizziness headache Hot flush Nausea
What forms of anaemia result in microcytic anaemia
Iron deficiency anaemia
Anaemia due to chronic infection
What forms of anaemia result in megaloblastic anaemia
Folic acid deficiency
Vitamin B12 deficiency
What form of anaemia results in normocytic anaemia
Anaemia due to bone marrow or renal failure
What is the normal daily requirement of iron
5mg in men
15mg growing children and menstruation
2-10x more in pregnant women
What B vitamin is folic acid
B9
Where can you find folic acid in your diet
Leafy green vegetables and folic acid preparations
What can a lack of folic acid in pregnancy cause
Neural tube defects
What is the role of vitamin B12 in the body
Normal DNA synthesis
Haematopoiesis
Maintenance of myelin in the nervous system
Where does absorption of vitamin B12 occur
The terminal ileum
What drugs can be administered to control the differentiation of pluripotent stem cells
Haemopoietic factors such as erythropoietin and colony stimulating factors
How are haematopoietic factors administered
Intravenously
What are examples of erythropoietin haematopoietic factors
Epoietin and darbepoetin
What is an example of a granulocyte-macrophage-CSF
Sargramostim
What are common side effects to erythropoietins
Flu-like symptoms
iron deficiency
increased blood viscosity
What are common side effects to leukocyte stimulating factors
Fever and chills
Rash
GI effect
Bone pain
What are examples of G-CSFs given clinically
end in -grastim
What does Oprelvekin stimulate the production of
Megakaryocyte
Thrombopoiesis
If there is too high levels of abnormal HbS what drug can be taken and what is its mode of action
Hydroxycarbamide acts to inhibit synthesis of HbS
What is a tumour
An abnormal mass of tissue that the growth of it is uncoordinated and exceeds natural tissue size
What is a papilloma
A benign epithelial tumour that grows exophytically
What is an adenoma
A benign tumour that arises in glandular tissue
What is a carcinoma
A malignant tumour that arises in the epithelial tissue of the skin or internal organs
What is a sarcoma
A malignant tumour arising in connective or non-epithelial tissue
What is dysplasia
A pre-cancerous increased cell division that results in abnormal looking cells and is reversible
What is neoplasia
Uncontrolled cell proliferation resulting in an abnormal cell structure and function and is irreversible
What is a carcinoma in situ
Neoplastic cells remain growing and contained within their original site and haven’t invaded the basement membrane
What is intraepithelial neoplasia
This describes the difference between invasive and non-invasive neoplasms
What is metastasis
The development of secondary neoplastic growths in non-neighbouring tissues
How are cancers staged and what does each stage represent
Stage 0: carcinoma in situ Stage 1: localised Stage 2: locally invasive Stage 3: Local spread to lymph nodes Stage 4: metastasised
What is the grading of cancer and what does each grade mean
1: nearly normal cells
2: Some abnormal cells
3: many abnormal cells
4: very few normal cells
5: completely abnormal cells
What is the transformation of cells with neoplasia
The changes that normal cells undergo as they become malignant
What is clonality
When multiple cells are derived from a single cell and are genetically identical
What is a carcinogen
Any substance that promotes transformation of a cell
What are the two types of carcinogens
Initiators: mutagenic and promote DNA mutations
Promoters: Non-mutagenic and act by stimulating cell division to increase the mutant population
What is an oncogene
This is a mutated gene that contributes to drive neoplasia
What is a proto-oncogene
an unaltered cellular counterpart of an oncogene
What is a viral oncogene
A virally encoded protein that contributes positively to neoplasia
What is a tumour-suppressor gene
a gene involved in regulating cell growth and division that is usually inactivated by cancers
Why does a mutation in a gene responsible for regulating the cell cycle mean further mutations of this cell are likely
Because the cell is dividing much more rapidly and replicating DNA at a faster rate, increasing the chance of mutations
Eventually the mutations will result in the cell dividing in an uncontrollable way that results in a clonal cellular mass
Why are tumour cells damaging
They don’t perform their original function
How can tumour cells interfere with adjacent cells
They can release toxins to create a necrotic environment
They compress organs and neighbouring organs
They can result in complete colonisation
What is hyperplasia
Increased cell division but cells look and act normal
What are post-mitotic cells
These are cells that have left the cell cycle and don’t know how to divide
What occurs in the G1 phase of the cell cycle
Increasing in size and number of organelles
What is the S phase of the cell cycle
Where the DNA is replicated
What is the G2 phase of the cell cycle
Where the cell grows and prepares for mitosis
Checks if the DNA has been replicated correctly
What occurs in the M phase of the cell cycle
the division of the cell to form two new cells
What are the stages of mitosis and what occurs at each one
Prophase: chromosomes condense to become more compact
Prometaphase: chromosomes organise themselves within the cell and nuclear membrane breaks down
Metaphase: chromosomes align
Anaphase: the chromosomes are pulled to either pole
Telophase: the nuclear membrane reforms around each daughter cell
What pulls the chromosomes apart from the centromeres
The mitotic spindle
Where are the 4 checkpoints of the cell cycle
The point between G1>S
In S-phase
G2>M checkpoint
The metaphase to anaphase transition
What does the G1/S checkpoint check
If the environment is favourable and in a growth stable environment
What does the S phase checkpoint check for
Problems with DNA replication
What does the G2/M phase checkpoint check for
If the DNA has been replicated correctly and if the environment is favourable for mitosis
What does the metaphase-anaphase checkpoint check for
If the spindle is correct and that the chromosomes are aligned in an optimal way to divide
What enzymes drive the cell cycle
Cyclin dependent kinases
What proteins activate Cdks and how
Cyclins are needed to form complexes with the Cdks to activate them
How do cyclin-Cdk complexes trigger events in the cell cycle
They phosphorylate target proteins
In G1 what cyclin binds to what CDKs
Cyclin D to CDK 4 and then 6
What cyclin binds at the end of G1 to what cyclin
Cyclin E to CDK 2
What cyclin binds to what CDK at the end of S phase
Cyclin A to CDK2
What cyclin binds to what CDK during G2
Cyclin A to CDK 1
What cyclin binds to what CDK during M phase
Cyclin B binds to CDK1
What occurs if the correct cyclin isn’t present
The cell will not have the right enzymatic reaction to go through the cell cycle
What activates the transcription and binding of cyclins to CDKs
The binding of growth factors to the CSM
This activates a MAP kinase signalling cascade
This activates transcription that codes for cyclins
What proteins can inhibit the cell cycle
INK4 or Cip/Kip
What are mitogens
Growth factors that stimulate cell division
Why is P53 referred to as the guardian of the genome
Because it acts as an inhibitor of the cell cycle
What is an example of a tumour suppressor gene
P53
When is P53 active
If there are: errors in mitosis DNA damage Cell stress Oncogene activation Excessive mitogenic pressure
Why aren’t telomeres effective in cancer cells
cancer cells can continue to divide even if the telomeres are too short
What is the first step of cancer cell production
A carcinogen initiates a cell through initiation
What occurs after initiation of a cancer cell
a genetic change occurs to form a pre-neoplastic that then undergoes a genetic change to form a malignant cell
What can genetic mutations in cancerous cells lead to
Loss of function Silencing tumour suppressors Expression of oncogenes Loss of sensitivity to growth inhibition factors Evasion of cell death Limitless replication potential
Why can there be a selection of tumour cells in a patient
Because they may be undergoing different selection pressures
Why may chemo not kill all the cancerous cells
Some may adapt to the selection pressure of chemo and not be killed from it
Why is a cancer relapse harder to treat
Because the cells have undergone chemo and may be more resistant to it as they have survived and can then multiply
What are the 6 hallmarks of a cancerous cell
Self stimulus to growth Evading growth suppressors Resisting cell death Replicative immortality Angiogensis (own blood supply) Invasion and metastasis
What are the two types of mutations that cause cancer cells
Somatic mutation (carcinogens or oncogene viruses) Germ line (inherited)
How can direct DNA damage cause mistakes in the DNA
There may be imperfect repairing of the DNA
What can a carcinogen do to DNA
directly damage DNA crosslinking
Mutate DNA bases
Produce free radicals that damage the DNA
What are examples of viral oncoproteins that inhibit tumour suppressor genes
E6 inhibits P53
E7 inhibits retinoblastoma
How do oncogenes promote constant cell division
When active they phosphorylate target proteins that allow continuation through the cell cycle
What are the clear differences between malignant and benign cells
Malignant don’t really look like normal tissue
They grow endophytically
Have an enlarged nuclear:cytoplasm ratio
Fast growth rate
Poorly defined border
What is the key difference with regards to invasion between benign and malignant tumours
Invasion through the basement membrane
How does the differentiation of tissues vary with benign and malignant tumours
benign tumours are well differentiated and malignant are not
What is anapalstic tissue
Tissue destroyed by tumour so much so that it doesn’t represent the original tissue
How do the levels of necrosis vary between benign and malignant tumours
There is a much higher level of necrosis in malignant tumours due to high cell turnover and replication
What is an adenocarcinoma
A malignant tumour in the glandular tissue
What is Burkitt’s lymphoma
A cancer of B cells that affects the lymphatics system
What is Ewing’s sarcoma
An ulcerating cancer of the bone
What is Hodgkin’s lymphoma
A certain type of lymphoma that is characterised by the presence of Reed-Sternberg that are cells that contain more than one nucleus
What are blastomas
Tumours of the blast cells
What are harmatomas
These affect connective tissue and cause cells in the connective tissue to grow larger as the patient grows
They don’t cause any symptoms but appear as tumours on scans
What is the most common symptom of endocrine tumours
Excessive hormone production
What is a cyst
A fluid filled space that is lined by epithelium
What is a teratoma
A tumour of an egg cell or sperm cell
What are cells bound to each other by normally
Adhesion molecules
How can malignant cells separate from surrounding cells
They lose expression of adhesion molecules
How do malignant cells break down connective tissue
They secrete proteolytic enzymes
How do malignant epithelial cells produce mobility in order to spread and move more effectively
They produce enzymes usually produced by the more mobile mesenchymal cells
What is contact inhibition and how does it apply to malignant cancer cells
This is that if a moving cell bumps into another cell it will stop moving through contact inhibition
Malignant cells don’t have movement inhibition so keep moving
What are secondary tumours
These are metastases located in distant organs from the primary cancer
Why are metastases more aggressive than primary tumours
Because for a malignant cell to spread around the body it has to undergo many mutations
What are the three main ways malignant cells can spread
Haematogenously
Lymphatically
Transcoelemic
Why may you feel enlarged lymph nodes in metastatic cancer
Because some malignant cells may congregate in the lymph nodes
What is the transcoelomic route of metastatic spread
This is through the cavities of the body:
The pleural, pericardial or peritoneal cavities
What determines the grading of a cancer
Mitotic activity
Nuclear size
Hyperchromasia (how dark the nucleus appears)
What does TNM staging look at
tumour size, nodal involvement and metastases
What is the Duke’s staging used for
Colorectal cancers
What is public health
The science and art of promoting health and preventing disease by organised efforts of society
What is primary intervention
Reducing the risk of disease in areas
What is secondary intervention
Identifying and managing diseases early
What is tertiary intervention
Preventing chronic or disabling effect of chronic disease
What is screening
Identifying healthy people who may be at risk of a condition and offering them information, further tests and appropriate treatment to reduce the risk of complications
What are the potential weaknesses of screening
False negatives and positives
People getting the all clear on their unhealthy lifestyles
Over diagnosis of disease
Health inequalities may increase
What are the main cancer screening tests offered by the NHS
Bowel cancer screening
Breast cancer
Cervical cancer
What are the main non-cancer screening tests offered by the NHS
Diabetic eye Fetal anomaly (structural) Infectious diseases in pregnancy Newborn and infant physical examination Newborn blood spot (heel prick) Newborn hearing Sickle cell and thalassemia
What are the three main categories of screening
Proactive, targeted screening
Voluntary
Opportunistic- e.g. attending the GP and screening for cholesetrol
What are the 4 criteria for screening
The disease
The test
Sensitivity
Specificity
What criteria must the disease fulfil in order for it to be satisfactory for screening
It should be a serious, frequent disease
Its history should be understood It should be treatable
There should be a long period between when it’s detected and when treatment becomes no longer effective
What criteria must the screening test fulfil in order to be satisfactory
It must be valid, simple and cheap, safe, acceptable and reliable
What is sensitivity
The ability to test correctly those who have the disease
What is specificity
The ability to test correctly those who have the disease
How should the program be apparent to combat disease
There must be evidence it’s reducing disease
The opportunity cost must not outweigh it Participants must be able to make an informed choice about participating
Quality assessed by the SQAS
What occurs in the bowel cancer screening program
FIT testing- end of test is dipped into a single bowel motion
gFOB testing where two samples are collected from three separate bowel movements
There may be heavy bleeding or perforations in rare cases
What are the principles of cancer surveillance
There must be a clear definition of the case
The cases can be identified through various sources
There must be a systematic collection of data for cases
The data and summary statistics must be analysed
What are the risk factors of bowel cancer
Age>50 Previous CRC Strong family history of CRC Longstanding IBD Inherited symptoms Type 2 diabetes Unhealthy lifestyle
What are symptoms of bowel cancer
Maybe none Often iron deficiency Rectal bleeding Change in bowel habit Pain
Where does foregut pain present
On the left side
Where does hind and mid gut pain present
Higher up than the foregut on the right side
At what point can a bowel cancer not be removed by endoscopy
When it reaches the muscle layer
What does a positive bowel cancer screening test lead to
A colonoscopy
