Pathology disorders Flashcards
What is the difference between lobar pneumonia and bronchopneumonia?
which of the 2 involves MORE than one lung?
- Lobar pneumonia affects all or part of a lobe with other areas generally normal.
- Bronchopneumonia is especially seen in young and old patients. It has a patchy distribution and generally i_nvolves more than one lobe_ and often both lungs.
Broncho>both
Which organism most commonly causes lobar pneumonia?
Describe the 4 pathological stages of lobar pneumonia.
What complications can arise following lobar pneumonia? (5)
More than 90% are due to Streptococcus pneumoniae. or hemphilus influenza, mycobacterium TB
- Congestion – the lobe is heavy, red and boggy. There is vascular congestion. Proteinaceous fluid, scattered neutrophils and many bacteria are present in the alveoli.
- Red hepatisation – occurs after a few days. The affected lung has a liver-like consistency. The alveolar spaces are packed with neutrophils, red cells and fibrin. There is a fibrinous or fibropurulent exudate (pus) on the adjacent pleura.
- Grey hepatisation – the lung tissue is dry, grey and firm. Red cells get lysed, fibrous exudate persists within alveoli.
- Resolution – the exudate is enzymatically digested and resorbed or expectorated. The basic architecture of the lung is left intact.
COMPLICATIONS
Bacteraemia which can result in meningitis, arthritis or endocarditis.
Lung abscesses.
Empyema.
Pleural effusion.
Lung fibrosis.
Inherited angio-oedema
extremely rare autosomal dominant condition in which sufferers have an inherited deficiency of C1-esterase inhibitor ((component of compliment system))
-They also experience recurrent abdominal pain which is due to intestinal oedema.
- Patient experiences attacks of non-itchy cutaneous angio-oedema (rapid oedema of dermis, subcutaneous tissue, mucosa and submucosal tissues)
- Family history of sudden death (laryngeal involvement).
what is Chronic granulomatous disease
genetic condition, where phagocytes can’t generate the free radical ‘superoxide.’ As a result, bacteria is phagocytosed but not killed! (no oxygen burst) >> leads to chronic infections
There is a deficiency in the nadph oxidase enzyme.
Chronic suppurative granulomas (collections of macrophages surrounded by mononuclear cells) or abscesses affecting the skin, lymph nodes, sometimes lung and liver and osteomyelitis.
Alpha-1 antitrypsin deficiency
- What it is
- PAthophysiology
- Presentation
- Complication
This is an autosomal recessive disorder
LOW levels of alpha-1 antitrypsin, (a protease inhibitor which deactivates enzymes released from neutrophils at the site of inflammation).
liver makes a version of α1-antitrypsin that is incorrectly folded.> cannot be packaged by ER & accumulates within this organelle and is not secreted by the liver.
proteases in the lung can act unchecked > EMPHYSEMA as lung tissue is broken down.
Treatment: Therapeutic phlebotomy
Complications: emphysema, COPD, Cirhossis (due to the accumation of the uncorrectly folded protein
What are Chemical mediators of acute inflammation that cause
- Increased blood flow
- Vascular permeability
- Neutrophil chemotaxis
- Phagocytosis
acute appendicitis
