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Phase 2a > ICS > Flashcards

ICS Flashcards

1
Q

Causes of Acute Inflammation

A
  • Microbial Infections (bacteria, virus)
  • Hypersensitivity Reactions (parasites)
  • Physical Agents (trauma, ionising radiation, heat, cold)
  • Chemicals (acids, alkalis, reducing agents)
  • Bacterial Toxins
  • Tissue Necrosis (ischaemic infarction)
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2
Q

Macroscopic Appearances of Acute Inflammation

A
  • Redness (rubor)
  • Heat (calor)
  • Swelling (tumor)
  • Pain (dolor)
  • Loss of function
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3
Q

Acute Inflammation Response Process

A

1) Vessels dilate & increase flow
2) Increase vascular permeability & formation of fluid exudate
3) Formation of cellular exudate - neutrophil polymorphism move into extravascular space

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4
Q

Vascular Changes in Acute Inflammation

A
  • Precapillary sphincters relax = increase blood flow
  • Increased capillary hydrostatic pressure = proteins leak = increase osmotic pressure = more fluid & protein leak out
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5
Q

Causes of Increased Vascular Permeability

A

1) Immediate transient - chemical mediators (histamine, bradykinin, nitric oxide etc)
2) Immediate sustained - severe direct vascular injury (trauma)
3) Delayed prolonged - endothelial cell injury (X-ray & bacterial toxins)

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6
Q

Stages in Neutrophil Polymorph Emigration

A

1) Margination of neutrophils
2) Adhesion of neutrophils
3) Neutrophil emigration
4) Diapedesis

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7
Q

Plasma Factors (Enzymatic Cascade Systems)

A

1) Complement
2) The Kinins
3) Coagulation factors
4) Fibrinolytic System

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8
Q

Role Of Neutrophil Polymorph in Acute Inflammation

A
  • Adhesion to microorganisms
  • Phagocytosis
  • Intracellular killing of microorganisms
  • Release of lysosomal products
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9
Q

Role of Mast Cells in Acute Inflammation

A
  • Release histamine

- Metabolise arachidonic acid into leukotrienes, prostaglandins, thromboxanes

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10
Q

Outcomes of Acute Inflammation

A

1) Resolution
2) Suppuration
3) Organisation
4) Progress to chronic inflammation

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11
Q

Systemic Effects of Inflammation

A
  • Pyrexia (fever)
  • Constitutional symptoms (anorexia, nausea, weight loss)
  • Haematological changes
  • Amyloidosis
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12
Q

Chronic Inflammation Definition

A

The subsequent and often prolonged tissue reactions to injury following the initial response. Lymphocytes, plasma cells and macrophages predominate

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13
Q

Causes of Chronic Inflammation

A
  • Primary chronic inflammation (no acute)
  • Transplant rejection
  • Progression from acute
  • Recurrent episodes of acute
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14
Q

Macroscopic Appearances of Chronic Inflammation

A
  • Chronic ulcer
  • Chronic abscess cavity
  • Thickening of the wall of a hollow organ
  • Granulomatous inflammation
  • Fibrosis
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15
Q

Granuloma

A

An aggregate of epithelioid histiocytes

- tuberculosis is the most commonest cause of granuloma

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16
Q

Cells That Regenerate

A
  • Hepatocytes
  • Pneumocytes
  • All blood cells
  • Gut epithelium
  • Skin epithelium
  • Osteocytes
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17
Q

Cells That Do Not Regenerate

A
  • Myocardial cells

- Neurones

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18
Q

Thrombosis Definition

A

The solidification of good contents that forms WITHIN the vascular system DURING life

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19
Q

Clot Definition

A

Blood coagulated OUTSIDE of the vascular system during life or AFTER death

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20
Q

Causes of Thrombosis

A

1) Change in vessel wall
2) Change in blood flow
3) Change in blood constituents

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21
Q

Clinical Effects of Arterial Thrombosis

A
  • Loss of pulse distal to thrombus
  • Area becomes cold, pale & painful
  • Tissue will die = gangrene
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22
Q

Clinical Effects of Venous Thrombosis

A
  • Area becomes tender
  • Redness
  • Swelling
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23
Q

Thrombi Can:

A

1) Resolve
2) Organised into a scar
3) Intimal cells proliferate - capillaries grow into thrombus - vessel functions again
4) Fragments break - embolism
5) Death

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24
Q

Treatment of Thrombus:

A
  • LOW DOSE ASPIRIN !!!
    (platelet aggregation inhibitor)
  • Warfarin (vitamin k aka clotting factor inhibitor) in severe cases
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25
Q

Embolism

A

An embolus is a mass of material in the vascular system able to lodge in the vessel and block the lumen

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26
Q

Venous embolism (pulmonary embolism)

A

Embolus travels to vena cava & lodges in pulmonary arteries.

  • can’t get to arterial side because blood vessels in the lungs are capillaries (can’t fit through)
  • lung acts as a filter
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27
Q

Small Emboli

A
  • May go unnoticed
  • May cause small permanent respiratory deficiency
  • Over time this may cause idiopathic pulmonary hypertension
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28
Q

Medium Emboli

A
  • May result in acute respiratory/cardiac problems
  • Chest pain, shortness of breath, area may become infarcted
  • Lung function is impaired & risk of further emboli increases
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29
Q

Massive Emboli

A
  • Sudden death
  • Usually long thrombi from leg veins
  • Often impacted across bifurcation of a major pulmonary artery
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30
Q

Arterial Embolism (systemic embolism)

A
  • Can travel to anywhere downstream
  • Generally originate from heart/artheromatous plaque
  • Thrombi may form on dead areas of cardiac muscle after MI
  • AF can cause thrombosis in heart
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31
Q

Ischaemia

A

A reduction in blood flow to a tissue or part of the body caused by constriction or blockage of the blood vessels supplying it

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32
Q

Effects of Ischaemia

A
  • Can be reversible
    Depends on:
  • duration of ismchaemic period
  • metabolic demands of tissue (cardiac myocytes & cerebral neurones are most vulnerable)
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33
Q

Infarction

A

Death (necrosis) of part or the whole of an organ that occurs when the artery supplying it becomes obstructed

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34
Q

Gangrene

A

When whole areas of limb or a region of the gut have their arterial supply cut off and large areas of mixed tissue die in bulk

1) Dry
2) Wet

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35
Q

Other Causes of Ischaemia & Infarction (other than thrombi)

A

1) Spasm
2) External compression
3) Steal
4) Hyper-viscosity
5) Vasculitis

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36
Q

Spasm

A

Spasm of smooth muscle = transient arterial narrowing
- due to decreased NO production due to cellular injury/loss
Spasm of coronary arteries - angina

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37
Q

External Compression

A
  • Can cause partial or total occlusion of vessels
  • Done intentionally in surgery to prevent haemorrhage
  • Veins are more susceptible (thin walls & low intra-luminal pressure)
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38
Q

Steal (syndromes)

A
  • Blood diverted from vital territory

- Uncommon

39
Q

Hyper-viscosity

A
  • Most effect in small vessels

- Can occur in myeloma (due to abnormally high conc. of antibodies in plasma & cylindrical shape of RBC)

40
Q

Vasculitis

A

Inflammation of vessel wall = narrow lumen

41
Q

Apoptosis (PROGRAMMED CELL DEATH)

A

Physiological cellular process in which a defined and programmed sequence of IC events leads to the removal of a cell WITHOUT the release of products harmful to surrounding cells

42
Q

Characteristics of Apoptosis

A
  • Energy dependent
  • Involved enzymatic digestion of nuclear and cytoplasmic contents
  • Phagocytosis of resultant breakdown products (still within cell membrane)
43
Q

Inhibitors of Apoptosis

A

1) Growth factors
2) EC cell matrix
3) Sex steroids
4) Some viral proteins

44
Q

Inducers of Apoptosis

A

1) Growth factor withdrawal
2) Loss of matrix attachment
3) Glucocorticoids
4) Some viruses
5) Free radicals
6) Ionising radiation
7) DNA damage
8) Ligand binding at ‘death receptors’

45
Q

Apoptosis Pathways

A 
1) Intrinsic 
OR
2) Extrinsic
then both converge in 
EXECUTION PHASE
46
Q

Necrosis

A

Traumatic cell death which induces inflammation and repair - characterised by bioenergetic failure & loss of plasma membrane integrity

47
Q

Coagulative Necrosis

A
  • Commonest form
  • Caused by ischaemia
  • Macrophages digest tissue causing it to go soft
  • Phagocytosis of myocardium can cause risk of ventricular rupture
  • Inflammatory response
48
Q

Liquifactive/Colliquative Necrosis

A
  • Occurs in the brain
  • Due to lack of supporting stroma
  • Necrotic neural tissue may totally liquify
49
Q

Caseous Necrosis

A
  • Characterises tuberculosis

- Dead tissue is structureless

50
Q

Hypertrophy

A

Increase in cell size without cell division

51
Q

Hyperplasia

A

Increase in cell number by mitosis

52
Q

Atrophy

A

The decrease in SIZE of an organ or cell by reduction in cell size and/or reduction in cell NUMBERS

53
Q

Metaplasia

A

The change in differentiation of a cell from one fully-differentiated cell type to a different fully-differentiated cell type

54
Q

Dysplasia

A

Imprecise term for the morphological changes seen in cells in the progression to become cancer

55
Q

Carcinogenesis

A

The transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

56
Q

Neoplasm

A

A lesion resulting from autonomous or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed - a new growth

57
Q

Tumours

A 
An abnormal swelling
Includes:
- neoplasm
- inflammation
- hypertrophy
- hyperplasia
58
Q

Classes of Carcinogens

A

1) Chemicals
2) Viruses
3) Ionising & Non-ionising radiation
4) Hormones, Parasites & mycotoxins
5) Miscellaneous

59
Q

Host Factors Influencing Carcinogenesis

A
  • Race
  • Diet
  • Constitutional factors - age & gender etc
  • Premalignant lesions
  • Transplacental exposure
60
Q

Oncogenes

A

Genes driving the neoplastic behaviour of cells

61
Q

Activation of Oncogenes in Tumours

A

1) Translocation
2) Point Mutation
3) Amplification

62
Q

Tumour Staging

A

T - tumour
N - node
M - metastases

63
Q

T - Tumour

A
  • refers to primary tumour
  • suffixed by number that denotes tumour size
  • number varies according to organ the tumour is on
64
Q

N - Node

A
  • refers to lymph node status
  • suffixed by a number that denotes number of lymph nodes or groups of nodes containing metastases
    E.G N0 = no nodal metastases
65
Q

M - Metastases

A
  • refers to anatomical extent of distant metastases
    E.G. M0 = no metastases
    M1 = increasing extent of distant metastases
66
Q

Innate Immunity

A
  • Non-specific
  • Rapid response
  • Instinctive
  • Resistance is NOT improved by repeat infection
  • Doesn’t depend on lymphocytes
  • Phagocytes and NK cells
67
Q

Adaptive Immunity

A
  • Specific ‘acquired’ immunity
  • Requires lymphocytes (B & T)
  • Antibodies
  • Resistance improves with repeat infection
  • Slower response
68
Q

Neutrophils

A
  • 65% of blood
  • Lifespan of 6 hours - 12 days
  • Phagocytosis
  • Primary lysosomes
  • Secondary granules
  • Fc & complement receptors
  • Secrete superoxides (toxic)
69
Q

Monocytes

A
  • 5% of blood
  • Lifespan = months
  • Differentiate into macrophages in tissues
  • Phagocytose in innate immunity
  • Antigen presenting in adaptive immunity
  • Lysosomes
  • Fc, complement receptors, PRR, TLR, mannose receptors
70
Q

Macrophages

A
  • Lifespan = months/years
  • Phagocytose & antigen presenting
  • First line of non-self recognition
  • Lysosomes containing peroxidase
  • Fc, complement receptors, TLR, mannose receptors
  • Present antigens to T cells
71
Q

Eosinophil

A
  • 5% of blood
  • Lifespan = 8-12 days
  • Associated to parasitic infections and allergic reactions
  • Granules contain major basic protein (MBP) - potent for worms
  • MBP activates neutrophils
    • induces histamine from mast cells
72
Q

Basophil

A
  • 2% of blood
  • Lifespan = 2 days
  • Express high affinity IgE receptors
  • IgE-receptor binding = histamine release
  • Parasitic infections and allergic reactions
  • Can circulate the body (not fixed like mast cells)
73
Q

Mast Cell

A
  • Only in tissues - fixed in tissue
  • Express high affinity IgE receptors
  • IgE-receptor binding = histamine release
  • Parasitic infections and allergic reactions
74
Q

T Lymphocytes

A
  • 10% of blood
  • Lifespan = hours-years
  • Adaptive
  • Antigen presenting
  • Produce cytokines
  • Bind antigen through T cell receptors
75
Q

B Lymphocytes

A
  • 15% of blood
  • Lifespan = hours-years
  • Adaptive
  • Antigen presenting
  • Differentiates into plasma cells
  • In blood, lymph nodes & spleen
76
Q

Natural Killer (NK) Cells

A
  • 15% of lymphocytes
  • Expresses CD56
  • In spleen and tissues
  • Recognise and kill virus infected cells and tumour cells - via apoptosis
77
Q

Dendritic Cells

A
  • Antigen presenting
  • Adaptive
  • Induce primary immune response in inactive/resting T cells
  • Produce cytokines
  • Promote B cell activation and differentiation
  • Found in skin (Langerhan’s cells), lining of nose, lungs, stomach, intestines
78
Q

Soluble Complement Factor

A

A complex series of interacting plasma proteins which form a major effector system for antibody-mediated immune reactions

79
Q

Purpose of Complement Pathway

A

To remove/destroy antigens - by direct lysis or by opsonisation

80
Q

Opsonisation

A

Process by which an antigen becomes coated with substances (complement) that make it more easily engulfed by phagocytic cells (macrophages have special receptors for specific complement proteins)

81
Q

Clinical Indications Related to Complement

A
  • Recurrent infections in children (pulmonary)
  • Swelling in hands/face
  • Fatigue
  • Butterfly-shaped rash on face
  • Fever, tachycardia after blood transfusion
  • Morning urine colour
82
Q

Complement Activation

A

1) Activation of C3 component

2) Activation of the lytic pathway

83
Q

Routes of Cleaving C3 (generate C3 convertases)

A

1) Classical pathway
2) Alternative pathway
3) Lectin pathway

84
Q

Classical Pathway

A
  • Antibody bound to microbe
  • Antibody dependent activation
  • Ab INdependent polyanions, gram-negative bacteria or bound-C reactive protein reactions directly with C1
  • Complement proteins: C1 (C1q, C1r, C1s), C4 & C2
  • IgM = more efficient activator of C1q than IgG
85
Q

Alternative Pathway

A
  • Complement binds to microbe
  • Consists: factor D, B, properdin (factor p), C3
  • Doesn’t need Ab, C1, C4, C2)
  • Microbial cell surfaces (endotoxin, bacterial cell walls - gram negative bacteria)
  • Innate defence (performs in the absence of pre-formed specific antibody)
86
Q

Lectin Pathway

A
  • Ab independent activation
  • Consists: mannose-binding lectin , MASP-1, MASP-2, C4, C2
  • MBL binds to mannose on bacterial cell walls, yeast walls, viruses = activates
87
Q

Opsonisation

A

Process by which an antigen becomes coated with substances (complement) that make it more easily engulfed by phagocytic cells (macrophages have special receptors for specific complement proteins)

88
Q

Clinical Indications Related to Complement

A
  • Recurrent infections in children (pulmonary)
  • Swelling in hands/face
  • Fatigue
  • Butterfly-shaped rash on face
  • Fever, tachycardia after blood transfusion
  • Morning urine colour
89
Q

Complement Activation

A

1) Activation of C3 component

2) Activation of the lytic pathway

90
Q

Routes of Cleaving C3 (generate C3 convertases)

A

1) Classical pathway
2) Alternative pathway
3) Lectin pathway

91
Q

Classical Pathway

A
  • Antibody bound to microbe
  • Antibody dependent activation
  • Ab INdependent polyanions, gram-negative bacteria or bound-C reactive protein reactions directly with C1
  • Complement proteins: C1 (C1q, C1r, C1s), C4 & C2
  • IgM = more efficient activator of C1q than IgG
92
Q

Alternative Pathway

A
  • Complement binds to microbe
  • Consists: factor D, B, properdin (factor p), C3
  • Doesn’t need Ab, C1, C4, C2)
  • Microbial cell surfaces (endotoxin, bacterial cell walls - gram negative bacteria)
  • Innate defence (performs in the absence of pre-formed specific antibody)
93
Q

Lectin Pathway

A
  • Ab independent activation
  • Consists: mannose-binding lectin , MASP-1, MASP-2, C4, C2
  • MBL binds to mannose on bacterial cell walls, yeast walls, viruses = activates

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