Pathology basis of disease Flashcards
What is the 5 pathological processes?
- cell injury, necrosis
- immunology, inflammation and repair
- circulatory disturbance
- disorders of growth
- pigmentations and deposits
What is the 4 groups of changes in circulatory disturbances?
- fluid distribution imbalance
- oedema - disorder of haemostasis
- haemorrhage
- inappropriate coagulation (thrombosis/ bleeding disorder) - hyperaemia and congestion
- infarction and ischaemia
What is disease?
- it is an abnormality of tissue structure or function (lesion)
- the outcome of the host-pathogen-environment interactions
What are the factors of H-P-E interactions?
- agent of disease
- effect on host
- host response
- environment
what is the 4 stages of infectious disease?
- exposure
- colonisation
- sub-clinical
- clinical
what will free radical do to skin?
free radical formation in skin causing cell membrane damage and subsequent cell death, leading to inflammation.
what does cell injury first starts with?
cell injury first starts with biochemical alterations. morphological. changes lag behind biochemical changes so a cell showing chnages consistent with moderate cell injury may already be dead.
What is the difference between clinical pathology and anatomical pathology?
clinical pathology:
- attempt to detect biochemical changes
Anatomical pathology:
- attempt to detect morphological changes
when will cell injury occur?
once the cell’s adaptive capacity is surpassed, it is unable to respond to functional demands for homeostasis: cell injury occurs.
cell injury can be reversible (recovery), but past that point the cell dies (irreversible injury)
cell degeneration and necrosis can lead to:
- cell injury (cell degeneration)
- mainly cytoplasmic changes for degeneration (reversible) cloudy swelling, hydropic change, fatty degeneration. - cell death (necrosis and apoptosis)
- follows mainly detecting nuclear changes e.g. pyknosis, karyorrhexis, karyolysis for cell death
what is the causes of cell injury
- physical agents
- heat, radiation, cold
-the extent of the injuries may be increased by local hypoxia associated with vascular damage - chemical agents
- toxins, poisons, drugs, metabolites
- free radicals - genetic factors
- often operate through deviant biochemical mechanisms that lead to atrophy, dystrophy or even cell death e.g. storage diseases. - infectious agents
- virus, bacteria, fungi, protozoa, algae, metazoan parasites, prions/infectious proteins - by-products of inflammation/ immunity
2 major causes of cell injury:
- membrane damage
- plasma and/or organelle membranes- due to altered biochemical synthesis or structural disruption of molecules - energy (ATP) depletion
how is membrane being damaged?
- many agents damage cell membranes via intermediates known as free radicals.
- free radicals are highly reactive oxygen species with very short half lives
- chain reaction such as lipid peroxidation can cause widespread membrane damage and more.
list anti-oxidants in cells.
- superoxide dismutases
- catalases
- vitamin E
- glutathione
- selenium
- ascorbate
How will energy (ATP) depletion leads to cell injury?
- Na-K-ATPase ion pump fails if ATP production is disrupted.
- membrane damage is followed by influx of Na2+, Ca2+ and H2O into the cell and its organelles
- this leads to cellular and mitochondrial swelling which further disrupts aerobic respiration
- water influx leads to cellular swelling and mitochondria swelling which will have an on going effect on energy production
- hypoxia is the most common reason for ATP depletion, as oxygen is vital for energy production.
what may hypoxia develop?
hypoxia may develop with a leision anywhere from the nostrils down to mitochondrial enzymes and so may involve:
1. air not reaching the lungs
- oxygen not reaching the blood
- oxygenated blood not reaching the tissues
- circulatory disturbance
- reduced O2 carrying capacity of blood - respiratory poisons acting at specific cellular sites in the respiratory pathway
How can ATP be produced in hypoxia?
- in hypoxia, ATP is produced by anaerobic glycolysis which yields much less energy and produces lactic acid which lowers cell pH and inhibits enzymic activity
- cells with higher metabolic rates (e.g. neurons, myocardial fibres, hepatocytes, renal epithelium) are more susceptible to hypoxia
What is the light microscopic changes of cell injury seen in the cytoplasm?
- membrane failure leads to cytoplasmic swelling (cloudy swelling) - often sublethal and reversible
- hydropic degeneration as water accumulates fine vacuoles
- small or large lipid droplets (vacuoles) can accumulate (fatty change/ fatty degeneration)
- Vacular change (water or lipid) is reversible up to point, but then becomes irreversible leading to cell death.
when does reversible cell injury become irreversible?
- become irreversible when it loses the ability to restore mitochondrial function
- ATP depletion
- profound disturbances in membrane function
- ATP is likely yo be the critical substrate determining irreversible cell damage.
state the 2 mechanisms in irreversible cell injury (necrosis).
- oncosis (swelling) = continuum with sublethal cell injury [nuclei can be pyknotic/ karyorrhectic and finally karyolytic]
- Apoptosis = programmed cell death
what things are with brown pigments?
- haemosiderin
- bile pigments
- copper
- melanin
- lipofuscin
- artefact- acid haematin
etc
