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Pathophysiology & Pharmacology > Week 1A (Inflammation & Healing) > Flashcards

Week 1A (Inflammation & Healing) Flashcards

1
Q

Clinical Manifestation

A

Signs (objective) & Symptoms (subjective)

Objective = can see/measure eg: jaundice, fever
Subjective = reported by Pt eg: pain in chest
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2
Q

Diagnostic Investigation

A

Imaging (US/CT/MRI)

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3
Q

Etiology

A

Cause

Eg: high cholesterol level in bile –> formation of gallstones

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4
Q

Predisposing Factors

A

Risk Factors

Eg: High fat, low fiber diet

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5
Q

Pathophysiology

A

Mechanisms

Eg: Cholelithiasis obstruct flow of bile into cystic duct –> biliary colic and inflammation of GB

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6
Q

Course

A

Acute/Chronic

Acute: s&s appear suddenly, strong & last shortly

Chronic: s&s develop slowly & last longer

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7
Q

Treatment

A

Surgery/medications/fasting

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8
Q

Prognosis

A

Outcome/outlook

Eg: good with complete recovery if early surgical removal & bad if disease is life-threatening

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9
Q

Remission

A

Disappearance of S&S

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10
Q

Cellular Response to Stress & Injury

A
  1. Normal Cells (Homeostasis) –> Stress (Adaptation) & Injurious Stimulus (Cell Injury)
    * inability to adapt –> cell injury

2A. Cell Injury (mild, transient) –> reversible injury (recover) –> normal cells

2B: Cell Injury (severe, progressive) –> irreversible injury –> necrosis & apoptosis AKA cell death

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11
Q

6 Types of Cellular Adaptation

A
  • Atrophy
  • Hypertrophy
  • Hyperplasia
  • Metaplasia
  • Dysplasia
  • Neoplasia (Malignancy)
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12
Q

Cellular Adaptation: Atrophy

A

Reduction in size NOT NUMBER

  • vascular insufficiency
  • malnutrition
  • immobilization
  • hormone level changes

Eg:

  • bone loss
  • muscle wasting
  • brain cell loss

*reduced cell size DUE TO lower mass NOT reduced cell number

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13
Q

Cellular Adaptation: Hypertrophy

A

Increase in size NOT NUMBER
- increase functional demand

*2 cells –> 4 cells

Eg:
- heart & muscle hypertrophy

*All the hyper = increase functional demand

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14
Q

Cellular Adaptation: Hyperplasia

A

Increase in number of cells
- increase functional demand ONLY in cells capable of dividing (proliferate) / hormonal stimulation

*size small –> size large

Eg:
- during pregnancy, estrogen increases uterus thickness

*All the hyper = increase functional demand

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15
Q

Cellular Adaptation: Metaplasia

A

Change in morphology (form & structure) & function

*Square cells –> oval cells

Eg:
- smoke –> ciliated pseudostratified columnar epithelium TO stratified squamous epithelium

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16
Q

Cellular Adaptation: Dysplasia

A

Increase in numbers & change in cell types

  • 2 cells –> 4 cells + changes in cell types
  • Basal membrane integrity not breached

In chronically injured tissues, the cells are considered pre-neoplastic (pre-cancerous)

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17
Q

Cellular Adaptation: Neoplasia (Malignancy)

A

New growth (uncontrolled cell division)

*Basal membrane cell integrity breached

Eg:

  • benign (non-cancerous)
  • pre-malignant
  • malignant (cancer)
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18
Q

Causes of Cell Injury

A
  1. Ischemia (lack of blood supply) –> Infarction (blood flow completely cut off –> cell death)
  2. Infection-m/o (bacteria, virus)
    * bacteria invade tissue & release toxins –> cell lysis –> content spillage –> post-inflammatory rxn
    * virus re-direct cell biosynthesis towards viral replication
  3. Immune/allergic rxn
  4. Direct physical damage (thermal, tear, radiation)
  5. Chemical toxins (endogenous: internal OR exogenous: external)
  6. Genetics factors
  7. Nutritional factors
  8. Fluid/electrolyte imbalance
  9. Foreign bodies (splinter, glass)
19
Q

Phases of repair in acute wound healing

A
  1. Haemostasis (formation of clot)
  2. Inflammation
  3. Proliferation
  4. Remodelling
20
Q

Step 1: Haemostasis

A

Primary

  • platelet activation
  • platelet plug

Secondary

  • coagulation cascade (add on to primary)
  • fibrinogen –> fibrin
21
Q

Mechanism of Haemostasis

A

Vessels injured –> blood spillage –> injured vessels constrict (slow/block) to limit blood loss

Primary haemostasis:
Platelet activation –> injured area –> platelet plug (NOT strong enough, just a temp mesh)

Seconday haemostasis:
Coagulation cascade adds on –> coagulation factor converts fibrinogen to fibrin (stronger mesh that adds on platelet plug) –> injured area sealed

*clot has alot of active ingredients that triggers inflammatory reaction

platelet activation + complement activation –> inflammatory response

22
Q

Step 2: Inflammation Reponse

A

Tissue injury –> bradykinin released (stimulate pain)

Mast cells –> histamine, prostaglandins & leukotrienes released –> leading to 2 events

  1. Vascular events
    - Vasodilation –> increase blood flow –> increase movement/delivery of active molecules (allow movements of histamine, prostaglandins) to injury site
    - Increase capillary permeability –> endothelial cells having more gaps in between –> leaky –> swelling & redness (from increased diameter of vessels)
  2. Cellular events
    - leukocytes following chemotaxis
    - leukocytes leave circulatory system –> injury site
    - phagocytosis
23
Q

Results of Immediate Vascular Event Post Injury

A
  • Redness (increase vasodilation)
  • Heat (increase vasodilation)
  • Swelling (increase capillary permeability & protein leakage)
  • Pain (bradykinin)
  • Loss of function
24
Q

Cellular Event

A
  • Exudate of fluid from blood vessels
  • Stasis (slowing/stopping of flow due to engorgement of RBC)
  • Margination (WBC accumulate & adhere to vessel wall due to adhesion molecules)
  • Diapedesis (oozing of WBC out of blood vessel)
  • Chemotaxis (diretional migration of WBC to source of injury)
25
Q

Order of WBC

A
  1. Neutrophils (last 24 hours)

2. Monocytes & Macrophages

26
Q

Innate Immunity Cells

A

Non-specific & non-memory

  1. Neutrophils (WBC)
  2. Basophils (WBC)
  3. Eosinophils (WBC)
  4. Macrophages (Lymphocytes)

*WBC have granules to release active agents

27
Q

Activity of Neutrophils

A

Phagocytosis of m/o

*High neutrophils = pyogenic (pus producing) bacterial infection

28
Q

Activity of Basophils

A

Release histamine –> inflammatory response

*Histamine boost blood flow to area of injury

**High basophils = parasitic infection

29
Q

Activity of Eosinophils

A

Increase allergic response

*High eosinophils = allergic reaction

30
Q

Activity of Macrophages

A

Mature monocytes that migrate into tissues from blood (active in phagocytosis)

31
Q

Adaptive Immunity Cells

A

Memory cells

  1. T lymphocytes
  2. B lymphocytes

*High lymphocytes = viral infection

32
Q

Activity of T lymphocytes

A

Cell mediated immune response

33
Q

Activity of B lymphocytes

A

Produce AB

34
Q

Cell Differential Counts

A

Determine the number of cells for each types. Eg: high eosinophils will be reflected when allergic reactions are high

35
Q

Goals of inflammation

A

Early non-specific response to tissue injury

  1. Degradation & removal of necrotic tissues (neutrophils and macrophages)
  2. Secretion of chemical mediators and growth factors by inflammatory cells & macrophages
    - GF are essential for cell division during proliferative phase
36
Q

Diagnostic test for inflammation

A
  1. Leukocytosis
    - higher than normal value of WBC (esp neutrophils)
  2. Differential count
    - distinguish viral from bacterial infection
  3. Plasma proteins
    - increased fibrinogen and prothrombin
  4. CRP
    - not normally in blood but appears with acute inflammation
  5. Increased ESR (RBC sedimentation rate)
    - usually blood settle slowly at the bottom of test tube
    - if quickly = inflammation
  6. Cell enzymes
    - indicative of site of inflammation
  • 3,4 and 5 = serve as screening/monitoring parameters, unable to tell cause/site of inflammation
  • 6 = may be useful in locating site of necrotic cells (eg: ALT - liver, CK-MB - heart). However some may not be specific (eg: AST elevated in both liver diease & acute MI)
37
Q

Potential Complications of Inflammation

A
  1. Infection
    - m/o more easily penetrate into oedematous tissues
    - inflammatory exudate is an excellent medium for m/o growth
  2. Skeletal Muscle Spasm
    - protective response to pain
  3. Deep ulcers
    - Cell necrosis/lack of cell regeneration
    - Lead to complications: perforation of viscera & scar tissue formation

*Inflamamtion by itself is good (meant for cleaning & planning for wound healing –> remodelling phase) BUT when out of control = complications

38
Q

Local Effects of Inflammation

A
  1. Redness
  2. Heat
  3. Swelling
  4. Pain
39
Q

Systemic Effects of Inflammation

A
  1. Low grade fever
  2. Malaise (unwell)
  3. Fatigue
  4. Headache
  5. Anorexia (LOA)
40
Q

Acute Inflammation

A

Sudden onset + short duration

Characteristics

  • exudation of fluids & plasma protein (edema)
  • migration of WBC (esp neutrophils)
41
Q

Chronic Inflammation

A

Follows acute episode of inflammation with continued tissue destruction

Characteristics

  • less swelling & exudate
  • more lymphocytes, macrophages and fibroblasts
  • severe tissue destruction
  • more collagen and fibrous scar tissue
42
Q

Causes of Chronic Inflammation

A
  1. Persistent infection
  2. Persistent indigestible material
    - endogenous (internal)
    - exogenous (external)
  3. Immune mediated reactions
    - autoimmune reactions
    - organ transplant rejection
    - hypersensitivity reactions
  4. Repeated episodes of acute inflammation
43
Q

Acute Management of Inflammation

A

RICE

  • Rest
  • Ice
  • Compression
  • Elevate
44
Q

Drugs Used to Treat Inflammation

A
  1. ASA (eg: aspirin)
  2. Acetaminophen (eg: paracetamol)
  3. NSAID (non-steroidal anti-inflammatory)
  4. COX-2 (part of NSAID)
  5. Glucocorticoid (steroid)

Anti-inflammatory: all except acetaminophen

Analgesia (pain): all except glucocorticoids

Antipyretic (temperature): all except glucocorticoids & COX-2

Pathophysiology & Pharmacology (1 decks)

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