21+22 Flashcards
the 5 cardinal signs of inflammation?
pain, redness, swelling, loss of function, and heat
3 components of acute inflammation
- vascular dilation (more blood flow to area)
- endothelial activation (edema by protein leakage)
- neutrophil activation and migration
transudate vs exudate, regarding leakage
transudate = increased hydrostatic pressure, thus fluid leaks out
exudate = protein and fluid leakage
What mediators lead to vasodilation?
prostaglandins, NO and histamine
what mediators increase permeability
histamine, serotonin, bradykinin, leukotrienes
what mediators help with chemotaxis and leukocyte recruitment
cytokines, chemokines, leukotrienes, bacterial products
what mediators lead to fever
prostaglandins and cytokines
what mediators lead to pain
prostaglandins and bradykinin
what mediators lead to tissue damage
NO, leukocyte enzymes, and reactive oxygen species
pyrogenic bacteria? examples?
promote purulent inflammation
example: acute appendicitis, lobar pneumonia
components of purulent exudate and fibrous exudate?
purulent = mainly neutrophils, with few macrophages and fibrin
fibrous = mainly fibrin with few neutrophils
serous inflammation?
In this pattern of acute inflammation the main tissue response is accumulation of fluid with a low plasma protein and cell content (transudate)
can be seen in response to a burn and in serous membrane-lined cavities
outcomes of acute inflammation?
- resolution (occurs when CT framework is intact)
- healing by fibrosis (damage to CT framework or tissues cannot regenerate)
- abscess formation (collection of pus due to extensive tissue damage or pyrogenic bacteria)
- progression to chronic inflammation
determined by severity of damage, the capacity of cells to duplicate, and type of tissue damage
acute vs chronic abscess
acute = Expansion is limited by organization & repair at the margins of the abscess
chronic = The abscess may become encapsulated by
granulation & fibrous tissue
what cells are seen in chronic inflammation
plasma cells, lymphocytes, macrophages, eosinophils, and fibroblasts
Chronic Granulomatous Inflammation
A granuloma is a cellular attempt to contain a persistent agent that is difficulty to eradicate
seen to have epithelioid macrophages and giant cells
foreign body giant cells: nuclei are central
langhans giant cells: nuclei are in periphery
Tuberculosis Granuloma
due to mycobacterium tuberculosis
morphology: central necrosis epithelioid macrophages langhans giant cells lymphocytes
Oxidative phase of the PPP?
irreversible reactions
forms NADPH and pentose phosphate
enzyme is G6PD
pathway:
1. glucose 6-phosphate is converted to 6-phosphogluconate by G6PD (regulated step)
- 6-phosphogluconate is converted to ribulose 5-phosphate by 6-phosphogluconate dehydrogenase
non-oxidative phase of PPP
reversible reactions
takes place when pentoses are not needed
pathway:
1. Xylulose 5-P is converted to glyceraldehyde 3-P by transketolase. ribose is converted to sedoheptulose 7-P by same enzyme
2. glyceraldehyde 3-P is converted to fructose 6-P by transaldolase. Sedoheptulose 7-P is converted to erythrose 4-P (same enzyme)
3. erythrose 4-P is converted to glyceraldehyde 3-P by transketolase
how is ribulose 6-P converted to ribose 5-P
isomerase
How is ribulose 5-P converted to xylulose 5-P
epimerase
what does transketolase need in order to function?
TPP or thiamine as a coenzyme
those with beriberi have low thiamine; which can be tested by transketolase activity
Uses of NADPH
- detoxification of hydrogen peroxide and reactive oxygen species
- phagocytosis in WBC’s
phagocytosis in WBC’s pathway?
- oxygen is converted to superoxide by NADPH oxidase (respiratory or oxidative burst)
- superoxide is converted to hydrogen peroxide by superoxide dismutase
- H2O2 can be converted to HOCl by myeloperoxidase
H2O2 can also go through the fenton reaction to create hydroxyl radicals
HOCl is toxic to fungi
HOCl and hydroxyl radicals are toxic to bacteria
Chronic granulomatous disease
NADPH oxidase deficiency
severe persistent fungal and bacterial infections due to defective respiratory burst
Myeloperoxidase deficiency
increased risk of fungal infections
normal respiratory burst, but decreased HOCl formation
RBC detoxification of H2O2
H2O2 is converted to water by glutathione peroxidase
(the hydrogen is donated by reduced glutathione or GSH)
selenium containing enzyme
oxidized glutathione (GS-SG) can be converted back to the reduced form by glutathione reductase
how does acute hemolysis occur and signs?
G6PD deficiency (X-linked recessive)
Heinz bodies are seen in the RBC’s
accumulation of reactive species
increased bilirubin (yellow eyes) less hemoglobin and brown/red urine
sulfonamides and some antimalarial drugs lead to increased oxidative stress, thus acute hemolysis may occur.
what does catalase do?
found in the peroxisome
uses hydrogen peroxide for detoxification
ALS or amyotrophic lateral sclerosis
10 percent of the time this disease can be due to a deficiency in the enzyme SOD (superoxide dismutase)
Candida albicans
more likely to get recurrent infections from this fungi when one has a myeloperoxidase deficiency
reduced formation of HOCl
NO and cell defense
NO synthase can convert NO to peroxynitrite
can kill invading bacteria
rate-limiting step of the PPP?
G6PD
lack of this enzyme leads to the impairment of NADPH formation.
RBC is not protected form oxidative damage
