Introduction to pathology and disease Flashcards
Define pathology
The study of disease,
Specifically the cause, origin and nature of the disease
Why is pathology relevant to being a chiropractor?
Understanding pathology can help to understanding the cause of the disease as well as the underlying mechanism of the disease. Health care providers can use this knowledge to help to diagnose and differentiate between medical conditions more accurately. It can help in the development of treatment plans. It can also help to assess the severity of the disease and help to understand the progression of the disease. This can help to predict patient outcomes therefore developing a better treatment plan
By understanding pathology we can explain more complex medical condition to the patient. Therefore, the patient can understand their diagnosis, treatment options and potential outcomes. Medicine is constantly advancing therefore staying up to date about advancing pathology can help to form the best treatment and care for the patient.
What is inflammation and name the two types
Inflammation: This is the immune systems response to harmful stimuli such as pathogens, toxins and radiation. It involves a series of complex changing Responses in order to initiate the healing response. It is a defence mechanism
Acute: Inflammation that happens over the short term
This happens when there is damage done to the vascularised tissues. It is used to help to deal with what has caused the damage. It is part of the innate immune response.
Chronic: This is inflammation that persists
Name the classifications of inflammation
Onset and duration: Acute, subacute and chronic
Severity: Mild, moderate and severe
Distribution: Focal, multifocal, locally extensive and diffuse
Predominant cell type involved
Five cardinal signs of acute inflammation
Redness, swelling, pain, loss of function and heat
Patient with painful foot
It is painful
Onset
Cardinal signs of acute inflammation
Take their tempuature
What is the cardinal signs of acute inflammation caused by?
Hyperaemia: The small blood vessels adjacent to the side of damage is intially dmaged with increased blood flow
Acute inflammatory exudate: These ocnaitn teh proetines, fluids, cells, neutrophil polymorphs, fibrin, macrophages and lymphocytes whcih destory the infectvie agent found at teh site of damage
The exudate is formed by:
Following hyperameia, the endothelial cells swell and partaill retract therfore no logner formign teh intact internal lining. The vessels beocme leaky, permtitng teh passge fo fluid, small protein includign fibrinogen and salts form teh pasma int teh dmgaed site
Fibrin is formedby teh polyermasation fo the many small fibrinogen
Emigration fo leucocytes: The cicualrigng neutrophil polymphr adher ot teh swollen endothelial cells. Then they emigrate throughteh endothelial cells jucntion by amoeboid mvoment adn then through the veneule wlals into teh tsisues spaces then into teh site of damage. Lymphcyte sand mocyets migrate teh sam way
Neutrophils
These are the main effector cells in acute inflammation.
Durign teh vascular phase of acute inflammation, the neutrophils are relased form the bone marrow.
The adhernce of neutrophils to the endothelium causes them to aggregate along the vessel walls in a process called margination.
Three stages of margination
Rolling: As blood flow slows down, the wbc rolls along the endothelial surface
Adhesive: This increases their adhesion to the endothelial cell surface. The leukocyte endothelial adhesion is caused by the expression of the activated endothelial cells. On stimulation of the endothelial cells by the proinflammatory cytokines there is the transcriptional activation of the genes encoding in these proteins
Aggregation: The adjcnet neutrophils adhere to each and change shape
Endothelium
They play a key role in acute inflammation
They are a physical barrier against the release of plasma outside teh vessles
They are activated by products from the dmaged tissues and cytokines
This leads to the activation of teh surface cell adhesion molecules which interact with complementary meolucels in the neutrophil cell membrane
They provide a normal surface for the inibition of the platelet aggregation however during acute inflammation there is the increased syntheis of Platelt activating factor which increases teh vasculr permability, increases teh nitric acid and increases the cell adheison molcules.
Main factors relased form the endothelium
Nitric acid and prostacylcin: They induce vascular relaxins and inhibit platelet aggrevation
Thrombaxane 2a, angiotensin 2, endothelin: Vascular contriction
Growth Factor, PGDF: Promote inhibitors
Chemokines
Neutrophil phagocytosis
Once the neutrophil begins to accumulate within inflammatory focus, they can now fous on removing the infective agent.
The microorganism must be covered in opsinins. The neutrophil binds to the abnormal particle using their specific receptors. The cells pushes out a pseudoposida . The pseudoposida fuses to completly fuse to surround the abnormal particle. This is called a phagosome which attaches to the neutrophile granules which discharge their contents.
Macorphages
They play a role in acute inflammatory exudate
They are derived from monocytes in teh ciruclating blood
They increase in number over time to facillate the elimination of dead materials
They have more important roles in chronic inflammation
They can survive longer due to their capacity for oxidative metabolism
Acute epiglottis
This is the inflammation ofteh upper airway by teh haemophilus bacteria.
Overpouring teh exude into the larangeal submucosa therfore narrowing teh airway. This may lead to death by asphyxia
Acute meningitis
Leptomeningeal infection by bacteria
Inflammatory response may lead to thrombosis of the local blood vessles preventing perfusion to teh cerbral cortex leading to brain damage
