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HSC2008 Pathophysiology & Pharmacology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the 2 types of body defence system?

A

Non-specific defence system & Specific defence system

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2
Q

What does non-specific defence system comprise of?

A

Mechanical barrier; non-specific phagocytosis; inflammation; interferons

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3
Q

What does specific defence system comprise of?

A

Humoral immunity; Cell-mediated immunity

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4
Q

What are the 6 types of cellular adaptation?

A
  • Atrophy: decrease in size
  • Hypertrophy: increase in size
  • Hyperplasia: increase in number
  • Metaplasia: change in morphology & function
  • Dysplasia: increase in number & change in cell type
  • Neoplasia (malignancy): new uncontrolled growth
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5
Q

What are the causes of cell injury?

A

Ischemia; infection; immune / allergic reaction; direct external damage (e.g. thermal, mechanical, pressure, radiation, electricity); chemical toxins; genetic factors; electrolyte balance; foreign body; nutritional factors

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6
Q

What are the 4 phases of acute wound healing?

A

Haemostasis, inflammation, proliferation, remodelling

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7
Q

What is the purpose of haemostasis?

A

To form a clot to stop bleeding

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8
Q

What are the 2 stages of haemostasis?

A
  • Stage 1 (Primary haemostasis) - platelet activation & forming platelet plug
  • Stage 2 (Secondary haemostasis) - coagulation cascade & conversion of fibrinogen to fibrin
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9
Q

What is the purpose / aim of an inflammation?

A

To eliminate the cause of injury & initiate wound repair process

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10
Q

What is released during an inflammation?

A
  • Bradykinins & histamine leading to vascular event - capillary dilation & increase permeability (swelling)
  • Macrophages & neutrophils leading to cellular event - leaving bloodstream via Chemotaxis to travel to site of injury
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11
Q

What are the cardinal signs of inflammation?

A

Redness, swelling, pain, heat

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12
Q

What occurs the during cellular event?

A
  • Exudation - release of fluid
  • Stasis - engorgement of RBC
  • Margination - adhesion of accumulated WBC to wall of vessel
  • Diapedesis - oozing of WBC outside of blood vessel
  • Chemotaxis - migration of WBC to site of injury
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13
Q

What are the function of cellular elements in an inflammatory response?

A
  • Neutrophils - phagocytosis of microorganisms
  • Basophils - release histamine leading to inflammatory response
  • Eosinophils - allergic response
  • Macrophages - migrate into tissues perform phagocytosis
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14
Q

What are the diagnostic test to determine inflammation?

A
  • Leukocyte count
  • Differential count (can distinguish viral from bacterial infection)
  • Plasma protein (increase in fibrinogen & prothrombin)
  • C-reactive protein (presence of protein that is normally not in blood)
  • Increase ESR (due to elevated plasma protein)
  • Cell enzyme (may indicate site of injury due to cell released during inflammation)
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15
Q

What are the characteristics of acute inflammation?

A
  • Sudden & short duration
  • Exudation of fluid & plasma protein
  • Migration of leukocytes (neutrophils)
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16
Q

What are the characteristics of chronic inflammation?

A
  • Period of acute inflammation & continuous tissue destruction
  • Less swelling & exudation
  • Increase leukocytes, macrophages & fibroblast
  • More severe on-going tissue destructions
  • More collagen & fibrous scar tissue
17
Q

What are the causes of chronic inflammation?

A
  • Persistent acute inflammation
  • Persistent infection
  • Persistent indigestible material
  • Immune mediated reactions (autoimmune, organ transplant rejection, unregulated immune response, hypersensitivity reactions)
18
Q

What are some treatments for inflammation?

A
  • Anti-inflammatory (i.e. asprin, NSAIDs, COX-2, GCC)
  • Analgesia (i.e. aspirin, panadol, NSIAD, COX-2)
  • Anti-pyretic (i.e. aspirin, panadol, NSIAD, COX-2)
19
Q

What are the non-pharmacological management of inflammation?

A

Rest, Ice, Compression, Elevation

20
Q

What are the side effects of Chronic use of NSAIDs?

A
  • Coagulopathy - reduced platelet aggregation; longer bleeding time
  • Gastrointestinal - ulcer, vomiting of blood, gastritis
  • Hepatotoxicity - cholestatic hepatitis, acute hepatitis necrosis
  • Haematology effects - leukopenia (low WBC), aplastic anaemia (bone marrow cannot make enough RBC), agranulocytosis (low neutrophils)
  • Kidney effects - salt & water retention, oliguria, interstitial nephritis
  • Respiratory effects - bronchospasm (sudden constriction of bronchioles)
  • Allergy, headache, dermatitis
21
Q

What are the effects of NSAIDS interaction with other drugs?

A
  • Reduced efficacy with beta-blockers, ACEi, diuretics
  • Increase effect of sulfonylureas, toxicity of aminoglycosides, cyclosporine
  • Long term of COXIB increase risk of CV events, thrombosis, MI, stroke
22
Q

What is required for the production of COX-1 & COX-2?

A

Arachidonic Acid through: binding of Phospholipase A2 to Bilayer Phospholipids

23
Q

What does COX-1 & COX-2 generate?

A
  • COX-1 (present in most tissues): Prostaglandin I2 (gastric protection) & Thrombin A2 (platelet function)
  • COX-2: Prostaglandin E2 (fever, pain, inflammation)
24
Q

What are the pharmacological effects of NSAIDs?

A
  • Anti-inflammatory - due to decrease synthesis of PG (PG plays a role in V.D)
  • Anti-pyretic - due to inhibition of COX-2 in hypothalamus leading to reduced PG (IL-1 stimulates PG in Hypo. -> increase temperature)
  • Analgesia - due to inhibition of PG synthesis (PG synthesis sensitise nociceptors which lead to inflammation)
25
Q

What are the pharmacological effects of GCC?

A
  • Inhibits NFkB - inhibit production of inflammatory mediators
  • Inhibits Phospholipase A2 & COX enzymes - reduce production of PG, thromboxane
  • increase transcription of anti-inflammatory proteins
26
Q

What are the mechanism of anti-inflammatory actions?

A
  • ASA (aspirin) - irreversible inhibits COX-1 & COX-2; weakly selective to COX-1
  • Acetaminophen (panadol) - exact mechanisms unknown; selective inhibition to COX-2
  • NSAIDS - competitive inhibitor to COX-1 & COX-2; ibuprofen & naproxen are weakly selective to COX-1
  • GCC - inhibits NFkB; increase transcription of anti-inflammatory proteins IL-1 receptor antagonist, IL-10
  • COX-2 - competitive inhibitor of COX-2 at therapeutic dose
27
Q

What are the common synthetic GCCs (produced by adrenal glands)?

A
  • Cortisone - short acting corticosteroids; T1/2 = 6-12 hrs; converted into Cortisol/ Hydrocortisone in the liver
  • Prednisone - intermediate acting drug; T1/2 = 12-36 hrs; converted into Prednisolone in the liver; 5x more potent then Cortisol
  • Dexamethasone - long acting drug; T1/2 = 36-72 hrs; 25x more potent than Cortisol
  • Betamethasone - long acting corticosteroid; T1/2 = 36-72 hrs; used topically to manage inflammatory skin condition
28
Q

What are the other effects of corticosteroid

A
  • decrease immunity
  • decrease inflammation
  • decrease Ca2+ absorption
  • decrease serotonin
  • increase blood sugar
  • retains Na+
  • regulate metabolism
29
Q

What are the 2 processes of proliferation?

A
  1. Formation of granulation tissue
    - compose of proliferating capillaries, fibroblast & residual inflammatory cells
    - cells are metabolically active with Angiogenesis & proliferating fibroblast
  2. Collagen synthesis & laydown of fibroblast
    - starts within 3-5 days of injury & continues for weeks depending of size of injury
    - collagen mass increase; cellular & vascular events decrease
30
Q

What are the key building blocks of tissue healing?

A

-Fibronectins & Proteoglycans - lay the foundation & forms a scaffold that provides tensile strength
- Elastin - cross linking to fibrils; provides elasticity to tissues
- Collagen - provide structural support & tensile strength; key determinant of structural stability

31
Q

What occurs at the stage of remodelling?

A

Parallel process of synthesis & degradation
- synthesis of collagen & extracellular metric protein
- degradation by Matrix Metalloproteinases (Type III & Type I collagen)

32
Q

What are the 3 determinants of “complete” healing?

A

The involved tissue; extent of tissue injury & nature of injury (chronic vs acute/ persistent)

33
Q

What are the 3 ‘R’s of healing?

A
  • Resolution - minimal tissue damage; able to regain original structure; intact extracellular matrix framework
  • Regeneration - occurs in cells capable of mitosis (replication); damages tissue replaced by proliferating nearby cells; new tissues are functional; no fibrosis / scarring
  • Replacement - tissue unable to generate; functional tissues replaced by connective tissues (except brain); lead to loss of function
34
Q

What are the types of healing according to regenerative ability?

A

Labile tissues
- stem / undifferentiated cells
- capable of division & replace the damaged tissue
- Eg. epithelial cells (skin, GI); haemopoietic tissues

Stable tissues
- low proliferative activity
- can undergo division if stimulated
- Eg. Parenchymal tissues (liver, kidney, pancreas)

Permanent tissues
- cannot proliferate; left the cell cycle
- Eg. skeletal & cardiac muscle; nervous tissue

35
Q

What are the factors that affect healing?

A

Promote healing
- youth
- good nutrition
- adequate Hb
- clean, undisturbed wound

Delay healing
- advanced age
- poor nutrition, dehydration
- anemia
- circulatory problems
- chronic disease / co-morbidities
- infection / foreign materials
- chemotherapy treatment
- prolonged GCC

36
Q

What is the difference between Necrosis & Apoptosis?

A

Necrosis
- Cells enlarge in size
- Nucleus goes through Pyknosis (clumping) -> Karyorrhexis (fragmentation) -> Karyolysis (dissolution)
- Plasma membrane is disrupted
- Cellular content goes through enzymatic digestion
- Frequent inflammation
- Caused by pathologic factors (e.g. inflammation)

Apoptosis
- Cells reduce in size
- Nucleus are fragmented into nucleosome-size fragments
- Plasma membrane are intact
- Cellular content are packaged into apoptatic body
- No inflammation
- Caused by physiologic factors; can be pathologic

HSC2008 Pathophysiology & Pharmacology (4 decks)

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