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

Week 1A (Inflammation & Healing) Flashcards

(44 cards)

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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

Study These Flashcards
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

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

Step 1: Haemostasis

Study These Flashcards
A

Primary

  • platelet activation
  • platelet plug

Secondary

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

Mechanism of Haemostasis

Study These Flashcards
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

Study These Flashcards
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

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

Cellular Event

Study These Flashcards
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
Order of WBC
1. Neutrophils (last 24 hours) | 2. Monocytes & Macrophages
26
Innate Immunity Cells
Non-specific & non-memory 1. Neutrophils (WBC) 2. Basophils (WBC) 3. Eosinophils (WBC) 4. Macrophages (Lymphocytes) *WBC have granules to release active agents
27
Activity of Neutrophils
Phagocytosis of m/o *High neutrophils = pyogenic (pus producing) bacterial infection
28
Activity of Basophils
Release histamine --> inflammatory response *Histamine boost blood flow to area of injury **High basophils = parasitic infection
29
Activity of Eosinophils
Increase allergic response *High eosinophils = allergic reaction
30
Activity of Macrophages
Mature monocytes that migrate into tissues from blood (active in phagocytosis)
31
Adaptive Immunity Cells
Memory cells 1. T lymphocytes 2. B lymphocytes *High lymphocytes = viral infection
32
Activity of T lymphocytes
Cell mediated immune response
33
Activity of B lymphocytes
Produce AB
34
Cell Differential Counts
Determine the number of cells for each types. Eg: high eosinophils will be reflected when allergic reactions are high
35
Goals of inflammation
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
Diagnostic test for inflammation
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
Potential Complications of Inflammation
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
Local Effects of Inflammation
1. Redness 2. Heat 3. Swelling 4. Pain
39
Systemic Effects of Inflammation
1. Low grade fever 2. Malaise (unwell) 3. Fatigue 4. Headache 5. Anorexia (LOA)
40
Acute Inflammation
Sudden onset + short duration Characteristics - exudation of fluids & plasma protein (edema) - migration of WBC (esp neutrophils)
41
Chronic Inflammation
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
Causes of Chronic Inflammation
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
Acute Management of Inflammation
RICE - Rest - Ice - Compression - Elevate
44
Drugs Used to Treat Inflammation
1. ASA (eg: aspirin) 2. Acetaminophen (eg: paracetamol) 3. NSAID (non-steroidal anti-inflammatory) 5. COX-2 (part of NSAID) 4. 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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