Pathology Flashcards
What concepts does pathology include
study of the mechanisms of disease, application of laboratory methods to investigate and diagnose disease in individual patients
What gene is often found in women with breast cancer
HER2
What does HER2 do?
it encodes for a protein that promotes growth of cells
outcome
a statement of patient health or illness at a defined time
necrosis
premature death of cells and living tissue
what’s necrosis caused by
external factors such as infection, toxins or trauma
ischemia
diminished blood supply
when is necrosis no longer reversible
when the tissue is infarcted
Apoptosis
Prograammed cell death, requiring energy
Resolution
complete restoration of the tissue to normal after an episode of acute inflammation
Factors favouring resolution
minimal cell death/tissue damage, occurrence in organ/tissue with regenerative capacity, rapid destruction of causal agent, rapid removal of fluid/ debris by good local vascular drainage.
What’s healing by regeneration
is restitution with no, or minimal residual defect (no defect seen by naked eye)- replacing the cells that were originally lost
What’s healing by repair
healing wehre tissue is lost (fibrosis occurs and scar tissue is formed)
Suppuration
formation of pus
what is pus made up of?
living cells, dying cells, dead neutrophils, cellular debris and bacteria
What forms an abscess
accumulation of pus within a tissue
What’s organisation of tissues
is their replacement by granulation tissue
What factors favour organisation
large amounts of fibrin formed, substantial necrosis and exudate and when debris can’t be removed or discharged
when does resolution occur
when there’s minimal tissue damage, the damage is neutralised and there’s regrowth of cells
When does healing by repair occur
when the damage is neutralised but some tissue is damaged and so organisation occurs
when does chronic inflammation occur
when there’s a persistent damaging agent with tissue destruction and so organisation with continued inflammation
what is completely destroyed tissue replaced by
vascular granulation tissue
angiogenesis
new blood vessels
collagen synthesis
formation of scars
what are the predominant features in repairs?
angiogenesis, fibroblast proliferation and collagen synthesis
what’s the causative agent for acute inflammation?
bacterial pathogens, injured tissue
what’s the causative agent for chronic inflammation
persistent acute inflammation due to non-degradable pathogens, viral infection , persistent foreign bodies, or autoimmune reactions
what’s the onset for acute inflammation
immediate
what’s the onset for chronic inflammation
delayed
how long does acute inflammation last
few days
how long does chronic inflammation last
up to many months, or years
what’s the outcome of acute inflammation
resolution, access formation, chronic inflammation
what’s the outcome of chronic inflammation
tissue destruction, fibrosis and necrosis
What’s happens during acute inflammation in response to injury?
vascular changes, cellular changes, chemical mediators and morphologic patterns
When is organisation favoured
if there’s lots of necrosis, poor blood supply as it’s difficult to remove debris and it depends on the tissue type, as some such as liver can regenerate
What is a space that is filled with pus and walled off called?
empyema
When is healing by organisation and repair favoured instead of resolution?
When damage goes beyond the basement membrane
Why when damage goes beyond the basement membrane does resolution occur?
because organisation and repair need the basement membrane as scaffolding
What issues does scarring cause?
loss of function
cirrhosis
scarring and fibrosis in liver
What can occur from scarring in the liver?
can result in liver failure as cannot move and make the proteins it needs
job of liver
makes and breaks things
what does scarring look like under a microscope?
knobbly and denser pink strips and
chronic inflammations link with time and severity
no link
when is chronic inflammation favoured
when there’s suppuration, persistence of injury, infectious agents especially viruses and the type of injury (autoimmune)
first cell reacting to immune response
neutrophils
what’s stronger than neutrophils
macrophages
What do granulomas found in the body suggest
foreign bodies and infections
What does tuberculous granulomas do?
produce caseous necrosis (looks like cottage cheese)
Resolution
cell is as good as new
another word for organisation
scarring or fibrosis
infarction
death of tissue after loss of oxygen
What occurs during hypoxia
there’s no oxygen so ATP produced
Consequences of no ATP being produced in the cell
the Na/K ATPase fails which increases K, causing swelling. The calcium pump fails, increasing intracellular calcium. The increased calcium stimulates phospholipase activity (membrane damage), increase protease activity (membrane and cytoskeleton damage), , increases endonuclease (DNA damage and breakdown) and also increases mitochondrial permeability (releasing pro death factors)
how long is the damage reversible in the myocardium?
20 minutes
Coagulative necrosis
such sudden cell death that some structure pf the cell is still left as a ‘ghost line’ before complete phagocytosis of materials
How long for fibroblasts to finish laying down collagen?
6 weeks
how do cells cope with stress?
hypertrophy and hyperplasia
What occurs if cell stress is too severe?
Necrosis or Apotosis
does necrosis require energy
no
can necrosis be normal/ physiological ?
no
coagulative necrosis
there’s a preservation of cell outline, usually happens if death is really quick
what tissue does coagulative necrosis most often occur in
cardiac muscle
liquefactive necrosis
liquid viscous mass and there’s no cell structure remaining
where does liquefaction necrosis usually occur
the brain
caseous necrosis
cheesy necrosis
what is caseous necrosis associated with
tuberculosis
does apoptosis require ATP
yes
can apoptosis be physiological
yes, occurs during cell cycle and during ovulation
When does pathological apoptosis occur
in response to injury, radiation, chemotherapy, viral infection, cancers, graft versus host disease
The mechanisms in apoptosis
extrinsic and intrinsic pathways
extrinsic pathway
cell being told to die from outside
intrinsic pathway
cell itself sensing it needs to die off
explain extrinsic pathway
Fas ligand is present on T cells, it binds to FAS (receptor) which leads to a cascade cascade which eventually leads to apoptosis
what happens if there’s a Fas mutation
autoimmune disease
Explain intrinsic/mitochondrial pathway
growth signals normally promote anti-aptotic molecules in the mitochondrial membrane. When they’re removed they’re replaced by Fax, Back. These increase permeability in the mitochondria which release proteins (cytochrome C) which stimulates a caspase cascade and apoptosis
role of p53
halts cell cycle if there’s cell damage and the cell cannot be repaired and then it stimulates caspases and induces apoptosis
what does too much or too little apoptosis cause
too little- cancer, autoimmune disease
too much- neurodegenerative disorders
what do cells look like when undergoing apoptosis
cell shrinks, chromatin condensation occurs, the cytoplasm breaks up and then macrophages come and eat it all
What causes cellular ageing
oxidative stress- free radical damage and accumulation of metabolism by products
Tumour
swelling
difference between maligns=ant and benign tumours
malignant- harmful, asymetrical
benign- not harmful, smooth, symmetrical
neoplasia
growth that is not in response to a stimulus
is neoplasia malignant?
can be benign, premalignant or malignant
where can you get neoplasia?
anywhere
