203 L1 Flashcards
Intro to the study of disease
Pathology is the study of the —– and —— of the disease.
Is the study of the cause and the mechanism of the disease.
What is the progression of pathology?
Morbid anatomy
Histopathology
Molecular pathology
Anatomical pathology is the ——— and ——- study of tissue obtained by biopsy at surgery or post-mortem.
It’s an ——- science.
Anatomical pathology is the microscopic and macroscopic study of tissue obtained by biopsy at surgery or post-mortem.
It’s an observational science.
General pathology is the investigation of processes underlying ——– conditions.
This is an ——– science
General pathology (mechanisms of disease) is the investigation of processes underlying disease conditions.
This is an experimental science
What is the pathogenesis of the disease?
The mechanism of its development from its earliest stages to its final advanced stages.
What is aetiology?
The cause of disease/ the underlying risk factors that can provoke the development of the disease.
Crohns disease
Is an ——— ——- disease.
It first appears in ———– or ——- ——-.
It can occur anywhere in the ——— but commonly occurs in the ——- of the ——- intestine.
Affected areas are ——
The ———- lining (——- surface) ——— (tissue is eaten away through long term damage).
The ——– wall may be damaged and undergo ——- thickening (there is extensive damage and scar tissue is layed down. The ——— narrows with ———– (is stenosed). ——– (fissures) develop through the ——— wall and drain into ——filled ——- (abscesses), or form ——- (fistulas) into nearby loops of ——–. The ———- system is activated, with ———- follicles and macrophages, and enlarged lymph nodes.
The probability of developing —– (neoplastic disease) is increased.
Crohns disease
Is an inflammatory bowel disease.
It first appears in adolesents or young adults.
It can occur anywhere in the gut but commonly occurs in the ileum of the small intestine.
Affected areas are inflamed
The epithelial lining (mucosal surface) ulcerates (tissue is eaten away through long term damage).
The colon wall may be damaged and undergo fibrotic thickening (there is extensive damage and scar tissue is layed down. The lumen narrows with obstruction (is stenosed). Cracks (fissures) develop through the colon wall and drain into pus-filled cavities (abscesses), or form channels (fistulas) into nearby loops of colon. The immune system is activated, with lymphoid follicles and macrophages, and enlarged lymph nodes.
The probability of developing cancer (neoplastic disease) is increased.
Outline of the pathogenesis of CD
An ———- trigger may damage the ———- which stops bacteria from getting into the tissues.
Injury by a ——— results in a breach in ——– lining and ——— tissue (submucosa) causing ——- ———– due to neutrophils, resulting in ——– and immunological tolerance
People with a genetic deficiency in ——- —— or ——— function may be unable to ——– the damage or eliminate ——— from the submucosa. This results in an uncontrolled ——- response against commensal bacteria which may damage the —— wall
An environmental trigger may damage the mucosa which stops bacteria from getting into the tissues.
Injury by a pathogen results in a breach in epithelial lining and connective tissue (submucosa) causing acute inflammation due to neutrophils, resulting in healing and immunological tolerance
People with a genetic deficiency in innate immunity or barrier function may be unable to repair the damage or eliminate microbes from the submucosa. This results in an uncontrolled immune response against commensal bacteria which may damage the colon wall
Multiple aetiological factors are implicated in CD.
Genetic contribution. The NOD2 gene is mutated. The NOD2 protein is a receptor that recognises bacterial products. So there is impairment in eliminating intracellular bacteria by autophagy, and for the antimicrobial activity of Paneth cells.
Environmental factors. Diet, NSAIDs, tobacco, and increased hygiene (altering the balance of commensal microbes).
Microbial factors may reflect altered communities of commensal bacteria, altering the ecology of the gut, and pathogenic infections as triggers.
Uncontrolled immune responses to commensal bacteria damage the bowel (overactive TH1 cells which secrete TNF, or under-active Treg cells).
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