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Pathology Flashcards

1
Q

What is pathology?

A

The study of disease.

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2
Q

What is aetiology?

A

The cause.

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3
Q

What is the difference between a symptom and a sign?

A

Symptom is what the patient complains of.

Sign is what the professional detects.

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4
Q

What is an idiopathic pathology?

A

The cause is unknown.

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5
Q

What is a iatrogenic pathology?

A

Caused by medial intervention.

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6
Q

What is the pneumonic for the surgical sieve? Describe each step.

A 
VIITAMIN:
Vascular,
Infective,
Inflammatory,
Trauma,
Auto-immune,
Metabolic,
Idiopathic,
Iatrogenic,
Neoplastic.
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7
Q

Name the two lineages of defence cells.

A

Myeloid and Lymphoid.

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8
Q

What type of cell can come from either lineage?

A

Dendritic cells

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9
Q

What defence cells are from myeloid origin?

A

Neutrophils,
macrophages,
mast cells,
eosinophils and basophils.

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10
Q

What defence cells are from lymphoid origin?

A

T cells, B cells and natural killer cells.

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11
Q

All myeloid cells are?

A

Granulocytes: Contain antimicrobial enzymes

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12
Q

What is the most numerous myeloid cell in the innate response?

A

Neutrophil (white blood cell)

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13
Q

What are monocytes?

A

Macrophage precursor.

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14
Q

What myeloid cells have a role in allergy?

A

Mast cells and basophils.

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15
Q

What is the function of dendritic cells?

A

Present antigens directly to T cells. (Sometimes B)

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16
Q

Where are T cells DERIVED from?

A

Bone marrow.

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17
Q

Where do T cells mature?

A

Thymus.

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18
Q

Where are mature T cells found?

A

Lymphoid organs.

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19
Q

What cells are important for immunological memory?

A

Both B and T cells.

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20
Q

What are the two types of T cells?

A

CD4 and CD8

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21
Q

What do CD8 T cells interact with?

A

MHC class 1

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22
Q

What do CD4 T cells interact with?

A

MHC class 2.

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23
Q

Where do B cells mature?

A

Bone marrow.

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24
Q

Where are mature B cells found?

A

In lymphoid organs, close to T cells.

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25
Q

What cells are phagocytic?

A

Neutrophils, macrophages, tissue dendritic cells and mast cells.

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26
Q

What cells fight parasites?

A

Eosinophils and basophils.

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27
Q

What is the innate response?

A

The immediate response.

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28
Q

What does secretory IGA bind to?

A

Antigens, flagella (preventing motility), toxins (neutralising them), itself (forming a net) and adhesion molecules (prevents adhesive properties of bacteria.

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29
Q

What occurs in the early induced innate response?

A

Mediators are released, phagocytosis is promoted and the cell is induced to express cytokines and chemokines.

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30
Q

What are cytokines?

A

Small proteins.

Act as signalling molecules that coordinate immune responses.

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31
Q

Name the 3 ways in which the cytokines can act? (Hint: ‘Crine’)

A

Autocrine: Alters behaviour of the cell they were secreted into.
Paracrine: Alters behaviour of neighbouring cells.
Endocrine: Enters the circulation and alters the behaviour of distant cells.

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32
Q

What is the purpose of chemokines?

A

Recruit immune cells and dictate where they travel to.

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33
Q

Where are leukocytes found?

A

In veins.

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34
Q

Explain neutrophil migration, more specifically the rolling mechanism.

A

Leukocytes interact with receptors on the endothelium surface of the blood vessel.
Continuous weak binding creates a rolling mechanism.
The leukocyte encounters a different receptor ICAM-1 that creates tighter binding (rolling stops.)
A signal is then sent that loosens the endothelial cell attachment.
Diapedesis occurs - neutrophil pulled though the endothelial cell wall.

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35
Q

Name the roles of neutrophils. (3)

A

Engulf and destroy pathogens.
Degranulation ( release granules that assist phagocytosis)
Create neutrophil extraceluler traps.

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36
Q

Name the 3 complement initiating pathways.

A

Classical: Antigen and antibody.
Alternative: Microbial cell wall (foreign cell surface)
Mannose: Carbohydrates on pathogen surface.

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37
Q

What region of a T cell presents an antigen binding site.

A

Variable region.

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38
Q

With regards to T cell diversity; what are the genes of the alpha section of the variable region?

A

Variable and joining.

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39
Q

With regards to T cell diversity; what are the genes of the beta section of the variable region?

A

Variable, diversity and joining.

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40
Q

Explain thymic education of T cells.

A

T cells move into the thymus expressing CD4 and 8 at low levels.
T cells move to the cortex where there are many epithelial cells expressing MHC class 1 and 2 cells.
Those T cells that can’t bind to to the MHC cells undergo apoptosis. POSITIVE SELECTION.
If the T cell binds to MHC class1 it will produce CD8 and stop producing CD4.
If T cells bind to self antigens they undergo apoptosis.
NEGATIVE SELECTION: If the T cells don’t bind to self antigens they can proceed into the body.

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41
Q

When are T cells deemed mature?

A

Once they have come into contact with a foreign antigen.

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42
Q

In terms of priming naive CD4 T cells; what dictates the type of T cell produced?

A

The cytokines produced (the 3rd signal)

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43
Q

What process results in memory cells being produced?

A

Priming.

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44
Q

How long do memory cells survive for?

A

up to 20 years.

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45
Q

In terms of B cell diversity; what is the heavy chain composed of?

A

Rearrangement of Variable, diversity and joining genes.

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46
Q

In terms of B cell diversity; what is the light chain composed of?

A

Rearrangement of Variable and joining genes.

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47
Q

What selection do B cells undergo in maturation?

A

Negative selection.

If they don’t bind to self antigens they can enter the body systems.

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48
Q

Name the 2 activated forms of the B cell.

A

Thymus dependant:T cells assist.

Thymus indépendant: No help required.

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49
Q

Where does the Thymus dependant stage occur?

A

In the Thymus.

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50
Q

Where does the Thymus independent stage occur?

A

The periphery

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51
Q

What is the stronger form of the antibody IgM?

A

IgG

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52
Q

What do Thymus independent cells differentiate into?

A

Plasma cells.

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53
Q

What do thymus independent cells lack the ability to do?

A

Create immunological memory.

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54
Q

Name the 3 processes of accute inflammation.

A

Vascular dilation.
Increased vascular permeability.
Neutrophil activation and migration.

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55
Q

What occurs in the vascular response? (3)

A

Small vessels dilate.
Endothelial cells swell and retract. Promotes immune cell passage.
Exudation. Leaky passage of water, salts and proteins.

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56
Q

Name the mediators of acute inflammation.

A

Histamine and prostaglandins.

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57
Q

What is the function of the histamine mediator?

A

Acts as a neurotransmitter.

Promotes vasodilation and retraction of endothelial cells.

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58
Q

What is the function of the prostaglandin mediator?

A

Regulates cytokine and chemokine production.
Acts on nerve fibres to generate pain.
Tissue remodelling.

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59
Q

What enzyme regulates the prostaglandin mediator?

A

Cyclo-oxygenase 2

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60
Q

What is the role of Bradykinin (plasma factor) in innate immunity?

A

Vascular permeability.
Stimulates nerves = pain
Expression of cytokines and chemokines.
Production of chemical mediators.

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61
Q

What human factor is active in intrinsic coagulation?

A

Human factor 12.

blood comes into contact with endothelial connective tissue

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62
Q

What human factor is active in Extrinsic coagulation?

A

Human factor 7.

Blood vessel damage

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63
Q

What enzyme turns fibrinogen into fibrin?

A

thrombin.

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64
Q

What deficiency do you have if you have haemophilia A?

A

Factor 8.

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65
Q

What deficiency do you have if you have haemophilia B?

A

Factor 9.

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66
Q

What characterises the Von Willebrand disease?

A

Deficiency in the Von Willebrand protein that stabilises factor 8.

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67
Q

What are the two outcomes of acute inflammation?

A

Suppuration: Pus formed by pyogenic bacteria.
Resolution: Tissue restored, rapid elimination of the causative agent.

68
Q

What is pus surrounded by to prevent spread?

A

Pyogenic membrane.

69
Q

What process occurs in unison with chronic inflammation.

A

The healing process.

70
Q

Name the classes of chronic inflammation. (2 and the subset)

A

Specific
Non-specific
Granulomatous. (specific subset)

71
Q

What type of chronic inflammation flares up regularly?

A

Non-specific.

72
Q

What is specific chronic inflammation induced by?

A

Immunological factors:
Asbestos and foreign body reactions.
Non-immunological factors:
Infective organisms, hypersensitivity, autoimmune.

73
Q

I general; What is specific chronic inflammation driven by? Name the two subsets.

A

Macrophages.

M1 and M2.

74
Q

What drives chronic granulomatous inflammation?

A

Fused epithelioid macrophages. ‘Giant multinucleate cells’

75
Q

What is oral Crohn’s/ orofacial granulomatosis?

A

Granulomas of the soft tissue within the oral cavity.

76
Q

What causes an autoimmune disease?

A

Breach of tolerance to self antigens; breakdown of immunoregulatory check points.

77
Q

Give examples of autoimmune diseases.

A

Psoriasis, Crohn’s, sjogrens syndrome and rheumatoid arthritis.

78
Q

What are the symptoms of sjogrens syndrome? Why do these symptoms occur.

A

Xerophthalmia and xerostomia.

Autoantigen attacks lacrimal and salivary gland tissue. (Auto-antibodies against ribonucleoproteins)

79
Q

In periodontitis; What drives soft tissue destruction?

A

Metalloproteinases, ROS and RNS.

80
Q

What is the purpose of metalloproteinases?

A

Remodel the fibres in the extracellular matrix. Also used for navigation.

81
Q

What enzyme breaks down the block on pro-MMPs?

A

Plasmin.

82
Q

What regulates pro-MMPs?

A

Cytokines called TIMPS. (Makes MMPs inactive again by putting the block back on)

83
Q

ROS and RNS are free radical that..

A

Damage membranes of self cells.
Cause damage to the mitochondria.
Cause damage to DNA within cells.

84
Q

In periodontitis; what drives hard tissue loss?

A

Primarily (excessive) RANKL but also (lack of) OPG.

85
Q

How does osteoclastogenesis operate?

A

RANK on infant osteoclasts becomes activated when it binds to a ligand. Starts tp resorb bone.

86
Q

How does osteoblastogenesis operate?

A

OPG inhibits the RANKL molecule. Once molecule inhibited the osteoblast comes in to repair the lost bone.

87
Q

What is an opportunistic pathogen?

A

Micro-organism will cause disease if exposed to the appropriate environmental stimuli.

88
Q

Define an endogenous infection.

A

Microbe originates from the patients own flora.

89
Q

Define an exogenous infection.

A

Microbe originates from outside the patients body.

90
Q

What protein helps E.coli bind?

A

Tamm-Horsfall

91
Q

What feature of bacteria help them attach to mucosa (i.e. bladder) regardless of the immune response?

A

Pili

92
Q

Name some encapsulated infections.

A

Meningitis, pneumonia.

93
Q

List what benefits microbes have from being encapsulated. (3)

A

Capsule prevents immune response from taking action.

Uses the capsule to adhere to surfaces.

Antibodies can’t detect the capsulated organisms.

94
Q

What is an endotoxin?

A

A toxin that is released from the cell wall of the bacteria.

95
Q

Endotoxins are released from what type of bacteria?

A

Gram negative

96
Q

What is an exotoxin?

A

A toxin that is released from the bacteria.

97
Q

Exotoxins are released from what type of bacteria?

A

Gram postive.

98
Q

What toxin is far more dangerous? (Ends/Exo)

A

Exotoxin

99
Q

What is LPS: Lipopolysaccharide?

A

An endotoxin released by gram negative bacteria.

100
Q

How does LPS cause toxic shock syndrome?

A

LPS recognised by white blood cells, the cells release signals that cause unregulated coagulation.

101
Q

What are the two healing outcomes?

A

Healing by regeneration.

Healing by repair.

102
Q

What occurs in healing by regeneration?

A

Replaced with functional cells, exact same tissue/structure restored.

103
Q

What occurs in healing by repair?

A

Forms a scar, normal structure permanently altered.

104
Q

What does the outcome of acute inflammation healing depend on?

A

Severity, location and tissue type.

105
Q

What does chronic inflammation result in?

A

Fibrosis.

106
Q

What cells shrink the wound?

A

Myofibroblasts, have contractile properties.

107
Q

Describe the process of wound healing.

A

Hemostasis: Clot formation.

Inflammatory response.

Proliferate: Granulation tissue creates the foundation for new tissues.

Remodelling: Maturation.

108
Q

What kind of wounds can result in healing by primary intentions?

A

Neat cuts.

109
Q

What kind of wounds can result in healing by secondary intentions?

A

less neat, ‘raggy’ cuts

110
Q

Describe healing by secondary intentions.

A

Larger scab

More inflammation due to larger amounts of necrotic tissue.

Larger amounts of granulation tissue (foundation tissue)

Wound contraction by myofibroblasts.

111
Q

Name and describe the 2 stages of the proliferation phase.

A

1: Vascular.
New capillaries produced.

2: Fibrous
Mature fibroblasts lay down collagen. (forms the early scar)

112
Q

What is angiogenesis?

A

Formation of new capillaries.

113
Q

Name the 2 mechanisms of capillary formation.

A

Sprouting

Intussusceptive

114
Q

What are both mechanisms of angiogenesis controlled by?

A

VEGF

115
Q

Explain fracture healing.

A

Inflammation: Blot clot forms, inflammatory cells migrate to remove debris.

Soft callus: Chondrocytes lay down collagen. Cell division and blood vessels form.
(Triggered by inflammation)

Hard callus: Odontoblasts activated. Lay down mineralised bone.
(woven bone: spongy and hard bone)

Remodelling: Cortical bone replaces softer bone. No scar on the bone due to constant remodelling.

116
Q

Define chronic inflammation.

A

Extensive deposition of collagen and formation of extra fibrous connective tissue.

117
Q

What can chronic inflammation be caused by?

A

Dysregulated healing.
Repeated damage.
Substantial damage.

118
Q

Define hypersensitivity.

A

Exaggerated immune response to a foreign agent.

119
Q

Define allergen.

A

Antigen that causes a reaction.

120
Q

Define allergy.

A

Immunological reaction.

121
Q

How many types of hypersensitivity is there?

A

4

122
Q

What type(s) of hypersensitivity are mediated by IgE?

A

Type 1

123
Q

What type go hypersensitivity causes anaphylaxis?

A

Type 1

124
Q

What is the function of a Hapten?

A

When bound to proteins can stimulate antibody formation.

125
Q

Name an example of a drug that can act as a hapten.

A

Penicillin

126
Q

What are the 2 steps in IgE mediated reaction? (hypersensitivity 1)

A

Sensitisation: Primed to response to the allergen.

Elicitation: Response is degranulation.

127
Q

Name the 2 responses in IgE mediated hypersensitivity (1).

A

Cutaneous atrophy:
‘wheal and flare’

Systemic anaphylaxis:
Degranulation all over the body.

128
Q

Describe the 3 fatal reactions of systemic anaphylaxis.

A

Laryngeal oedema = suffocation

Bronchiole constriction = suffocation.

Peripheral oedema = hypertension/heart attack.

129
Q

How is type 1 allergy tested?

A

Skin prick: ‘wheal’ appears
Patch test
Blood test: IgE levels tested
Food challenge

130
Q

How do you treat type 1 hypersensitivity reactions? (3)

A

Antihistamines.

Adrenaline injections: Relaxes muscles. Reduces effect of degranulation.

Hyposensitisation: Repeated injection of the allergen cause IgE to change to IgG.

131
Q

Describe how anti-histamines work.

A

(Histamines constantly switching from the active form to the inactive form.)

Anti-histamines stabilise the inactive form.

132
Q

What are type 2 sensitivity reactions mediated by?

A

IgM or IgG.

133
Q

Where do type 3 hypersensitivity reactions occur?

A

In the vasculature.

134
Q

What occurs in the vasculature in type 3 reactions.

A

Anti-body antigen clumps deposit in vessels.

To eradicate the clumps there is an influx of immune cells.

Immune cell influx damage the blood vessels.

135
Q

Arthur reaction is an example of a type 3 reaction, what causes this?

A

Insect bit or injecting the antigen.

136
Q

Serum sickness is an example of a type 3 reaction, what causes this?

A

Hypersensitivity reaction to penicillin.

137
Q

Oral erythema multiform is an example of a type 3 reaction, what causes this?

A

Response to drugs that act as a Hapten.

Causes blistering of the mucosa.

138
Q

What is Type 4 hypersensitivity mediated by?

A

Not antibody mediated. Mediated by T cells.

139
Q

What does type 4 involve?

A

CD4 and CD8 (from T cells)

140
Q

What is caused by type 4 hypersensitivity?

A

Crohns and TB. (granuloma formation)

141
Q

Name the anaphalatoxins from the complement pathway?

A

C3a and C5a (byproducts)

142
Q

List the 5 cardinal signs of inflammation.

A 
Redness: Rubor
Swelling: Tumor 
Heat: Calor
Pain: dolor
loss of function
143
Q

Name 2 cells with antigen presenting capabilities.

A

Macrophages

Dendritic cells

144
Q

What is the major role of natural killer cells?

A

Kill abnormal self-cells (tumour/virus infected)

145
Q

Name 2 constituents of healthy saliva that have anti-microbial properties.

A

Lactoferrin
Cystitis
Antimicrobial peptides.

146
Q

Name a pattern recognition receptor capable of recognising and responding to bacterial antigens.

A

Toll-like receptors.

147
Q

What is diapedesis?

A

Blood cells squeeze through tight endothelial cell junctions.

148
Q

What are the 3 specific signals CD4 T lymphocytes require to become activated?

A

1: Peptide antigen, presented by MHC class 2, intetacts with cognate T cell receptor.
2: CD28 interacts with CD80/86 expressed on mature dendritic cells.
3: Cytokines (differentiation)

149
Q

What class of antibody is predominant in a secondary immune response?

A

IgG.

150
Q

Where does T cell tolerance occur/maturation?

A

Thymus

151
Q

What is the term for the leaking of inflammatory exudate from blood vessels to surrounding tissues?

A

Oedema.

152
Q

In chronic inflammation; what molecule inhibits RANKL and derives osteoblast function?

A

Osteoprotogerin (OPG)

153
Q

In which stage of wound healing is granulation tissue formed?

A

Proliferative.

154
Q

In fibrosis; what is there extensive deposition of?

A

Collagen

155
Q

Name 2 microscopical characteristics of a cellular reversible injury.

A

Cloudy swelling

Fatty changes

156
Q

Which virus can induce epithelial hyperplasia?

A

HPV

157
Q

Name the 4 enzymatic cascades.

A

Complement.
Kinin
Coagulation
Fibrinolysis.

158
Q

In the complement cascade (plasma factor) what is the role of MAC: membrane attack complex?

A

Creates a pore in the cell membrane.

159
Q

In CD4 T cell priming; What signal determines the subset?

A

Signal 3/last signal.

160
Q

Name the 5 CD4 T cell subsets and their functions.

A

TH1: Supports innate immune response at the site of infection.

TH17: Supports innate response. Release-inflammatory cytokines.

TH2: Communication between T and B cells.

TFH: Communication between T and B cells.

Treg: Switch off T cell responses. Growth factors released that drives healing.

161
Q

Both TH2 and T follicular help cells allow communication between T and B cells, how do we distinguish between them?

A

TH2: Communication occurs OUTWITH the lymph node.

TFH: Communication occurs within the lymph node.

162
Q

Name 2 differences between acute and chronic inflammation.

A

Acute:

Generalised response, no long lasting immunity.

163
Q

Name 2 organisms responsible for periodontitis.

A

P.Gingivalis.

T.Forsythia.

164
Q

List the roles of macrophages.

A

Phagocytosis, clear debris.

Antigen presentation.

165
Q

What is the main function of a plasma cell?

A

Antibody secretion.

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