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Medicine Phase 2a > Pathology > Flashcards

Pathology Flashcards

1
Q

Define Inflammation

A

The local physiological response to tissue injury

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2
Q

Why does inflammation occur

A

To bring all essential cells for healing to the area of tissue damage

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3
Q

Benefit of inflammation

A

destruction of invading microbes

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4
Q

Harmful effects of inflammation

A
  • Digestion of normal tissues
  • Swelling
  • Inappropriate inflammatory response
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5
Q

2 main types of inflammation

A

Acute

Chronic

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6
Q

Whats differs between acute inflammation and chronic

A

Duration, Cells involved, Cause

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7
Q

What causes Acute Inflammation

A
  • Tissue Necrosis
  • Microbial Infections
  • Hypersensitivity reactions (hay fever)
  • Physical Agents (Radiation)
  • Chemicals (acid)
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8
Q

What causes Chronic Inflammation

A
  • Transplant rejection
  • Persistent infection (recurrent acute inflammation) or progression from acute inflammation (e.g. suppurative if an abscess is formed)
  • Crohn’s disease/ulcerative colitis
  • Autoimmunity
  • Agent resistant to phagocytosis e.g.TB, leprosy
  • Agent indigestible i.e. fat, bone, asbestos, silica
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9
Q

Define autoimmunity

A

Immune responses of an organism against its own cells and tissues

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10
Q

Define suppurative

A

Production or causing of pus

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11
Q

*Give 5 cardinal signs of Acute Inflammation

A
  • Swelling
  • Redness
  • Heat
  • Pain
  • Loss of function
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12
Q

(cardinal signs of Acute Inflammation)

What causes Swelling?

A

Oedema - accumulation of of fluid in extravascular space (Interstitial fluid)

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13
Q

(cardinal signs of Acute Inflammation)

What causes Redness?

A

Dilation of small blood vessels within the damaged area

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14
Q

(cardinal signs of Acute Inflammation)

What causes Heat?

A

Due to Increased blood flow (HYPERAEMIA)

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15
Q

(cardinal signs of Acute Inflammation)

What causes Pain?

A

Stretching and distribution of tissues to inflammatory oedema

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16
Q

Define hyperaemia

A

increased blood flow

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17
Q

Give 5 examples of inflammation

A 
Acne
Asthma
Appendicitis
Cellulitis
Septic arthritis
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18
Q

What are key cells involved in acute inflammation and what are their functions?

A

Neutrophil Polymorphs - Phagocytose pathogens

Macrophages - Secrete Chemical Mediators essential for Chemotaxis

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19
Q 
Describe Phagocytosis (of pathogens)
and steps after
A
  • Pathogens ingested by neutrophil polymorph (np) to form phagosome (phagocytic vacuole in np)
  • Lysosomes fuse with phagocytic vacuole to form a phagolysosome
  • Enzymes of lysosome(s) digest bacterium
  • Bacterial debris released released from np and lysosomes replenished
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20
Q

What is the role of chemical mediators in acute inflammation

A

spread the acute inflammatory response (following injury of a small area)

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21
Q

Give 2 examples of chemical mediators and their functions

A

Histamine and Thrombin
both cause neutrophil adhesion to endothelial surface
thrombin also increases vessel permeability

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22
Q

What produces histamine and thrombin

A

Histamine from Mast cells

Thrombin from Platelets

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23
Q

What are the 3 main stages of acute inflammation?

A

-Changes in vessel calibre
-Fluid exudate
-Cellular exudate
(then chemotaxis)

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24
Q

**Describe the main stages of acute inflammation

A

-Vasodilation brings blood and cells into the site of inflammation
-Vessels become more permeable by vasodilation and chemical mediators (e.g.histamine, bradykinin, NO).
This allows plasma proteins to leave vessels, which decreases oncotic pressure.
This causes fluid to leave vessels, forming fluid exudate.
-Accumulation of neutrophil polymorphs into the extracellular space and enzymatic cascades
-Chemotaxis

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25
Q

What is in exudate?

A

(protein-rich)

contains antibodies and plasma proteins, such as fibrin and substances needed for inflammation

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26
Q

What are 4 enzymatic cascades (for accumulation of cellular exudate?

A
  • Complement
  • Coagulation
  • Kinin
  • Fibrinolytic
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27
Q

What is chemotaxis?

A

The attraction of cells to site (of inflammation) through release of chemicals.
Process by which neutrophils move to inflammation site, attracted to inflammatory mediators released.

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28
Q

Was are possible outcomes of acute inflammation?

A

Resolution - complete restoration of tissues to normal
Suppuration - formation of pus (also results in granulation tissue forming and scarring)
Organisation - when tissue is replaced with granulation tissue as part of healing process
Progression to chronic inflammation

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29
Q

Define suppuration

A

Formation of pus

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30
Q

Give examples of chronic inflammation

A

Ulcers, pulmonary fibrosis

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31
Q

Describe 3 general differences between acute and chronic inflammation

A

Chronic - long duration, slow onset, may not recover, fibrosis (scar tissue formation), less swelling than acute (less exudate formation)
Acute - short duration, rapid onset, often recover (also neutrophils more active here)

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32
Q

Give 2 examples of agent resistant to phagocytosis

A

TB

Leprosy

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33
Q

Indigestible agents that can cause chronic inflammation

A

Fat, Bone, Asbestos, Silica

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34
Q

What cells are involved in chronic inflammation?

A

Macrophages; Plasma cells; B-lymphocytes; T-lymphocytes

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35
Q

Define fibrosis

A

scar tissue formation

key feature of chronic inflammation

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36
Q

Why does acute inflammation have more swelling than chronic?

A

As more exudate is formed

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37
Q

What is the role of B-lymphocytes?

A

Differentiate into plasma cells to make antibodies

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38
Q

Role of T-lymphocytes?

A

Cell-mediated immunity

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39
Q

**Role of each immunoglobulin

A

IgG (gamma chains)- promote phagocytosis in plasma and activate complement system.

IgA (alpha chains)- initial defence in mucosa against pathogen agents
(found in mucosal secretions, tears, colostrum and milk)

IgM - first antibodies produced in large quantities against a pathogen. They promote phagocytosis and activate complement system.
(found on surface of B-cells so mainly in plasma)

IgE - important in allergic reactions

(IgD)

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40
Q

What is the only Ig that can cross the placenta?

A

IgG

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41
Q

Role of Plasma cells and where derived?

A

from B-lymphocytes

produce antibodies

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42
Q

Role of macrophages

A

harbour organisms
eat up debris, present cells for antibody production
longer lived than neutrophils

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43
Q

Which macrophages encourage inflammation

A

M1 macrophages

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44
Q

Which macrophages decrease inflammation and encourage tissue repair

A

M2 macrophages

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45
Q

Granuloma define

A

Aggregate of epithelioid histiocytes

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46
Q

In a granuloma, what chemical do histiocytes excrete?

A

ACE

blood marker if someone has systemic granulomatosis disease

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47
Q

4 examples of where granulomas can result

A

TB
Sarcoidosis
Leprosy
Crohn’s

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48
Q

Define thrombus

A

Solid mass of blood constituents

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49
Q

What is meant by physiological thrombus

A

thrombus as a part of haemostasis (prevents bleeding outside vessels)

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50
Q

What is meant by pathological thrombus

A

where there is an imbalance in the blood coagulation system causing a thrombus

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51
Q

3 factors affecting the formation of a thrombus (Virchow’s Triad)
Predisposing factors

A

Change in vessel wall (endothelial damage)
Change in blood flow (laminar to turbulent flow in arteries or stasis in veins)
Change in blood constituents (abnormal clotting factors, more platelets - hyper coagulability)

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52
Q

what type of inflammation and hypersensitivity is granuloma

A

Chronic

Type IV hypersensitivity

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53
Q

what is primary cause of hypercoagulability

A

genetic

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54
Q

What are causes of abnormal blood flow?

A

Atherosclerosis; Aneurysm; Dilated atria; Atrial fibrillation; Venous stasis; Varicose veins

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55
Q

What are cause change in laminar flow of artery and vein resulting in thrombus?

A

Arteries - blood flow becomes turbulent

Veins - stasis of blood (if not moving enough)

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56
Q

Causes of endothelial injury of heart vessels?

A

Myocardial infarction

Valvulitis (cardiac chambers)

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57
Q

Causes of endothelial injury

A

Atherosclerosis; Vasculitis; Hypertension; Smoking
Artery specific - Chemical irritation
Veins- prolonged recumbency and inflammation

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58
Q

*Give 3 differences between an arterial and venous thrombosis

A

Arterial:
Mostly superimposed on an atheroma
High pressure
Made up mainly of Platelets (white thrombus)

Venous:
Most commonly due to stasis
Low pressure
Made up mainly of Coagulation factors (RBC, red thrombus)

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59
Q

What thrombosis is referred to as White thrombus and why

A

Arterial thrombosis as mainly made up of platelets

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60
Q

What thrombosis is referred to as Red thrombus and why

A

Venous thrombosis as mainly made up of coagulation factors or erythrocytes

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61
Q

What can arterial thrombosis lead to?

A

Myocardial Infarction

Stroke

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62
Q

What can venous thrombosis lead to?

A 
Deep vein thrombosis (DVT)
Pulmonary embolism (PE)
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63
Q

*How to treat Arterial thrombosis (give 2 examples)

A

Anti-PLATELETS

e.g. Aspirin or Clopidogerel

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64
Q

*How to treat Venous Thrombosis (give 3 examples)

A

Anti-COAGULANTS
e.g. Warfarin, Heparin, NOACs (Rivaroxaban)

NOAC = novel oral anti-coagulant

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65
Q

What is the most important risk factor for atherosclerosis?

A

Hypercholestermia

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66
Q

What vessels does atherosclerosis affect?

A

Large and Medium

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67
Q

Name 3 modifiable and 3 non-modifiable risk factors for atherosclerosis

A

Modifiable - Smoking, hypertension, hyperlipidemia, diabetes

Non-modifiable - Age, Male sex, Post-menopausal, Family History

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68
Q

When is atherosclerosis life threatening?

A

When a thrombosis forms on a spontaneously disrupted plaque.

Atherothrombosis

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69
Q

Define Atherosclerosis

A

A disease of the arteries characterized by the deposition of fatty material on their inner walls
OR
Focal elevated lesions formed in the intima

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70
Q

*Process of Atherosclerosis

A
  • Endothelial cell dysfunction (lots of cholesterol damages wall)
  • High levels of LDL in the blood will begin to accumulate in arterial wall
  • Macrophages are attracted to site of damage and take up lipid to form foam cells (inflammatory response)
  • Formation of fatty streak (earliest stage of plaque)
  • Activated macrophages release lots of their own products e.g. cytokines and growth factors
  • Smooth muscle proliferation (to intima) around the lipid core and formation of a fibrous cap (collagen)
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71
Q

How is thrombus caused?

A

If the unstable cap of the plaque ruptures and partially occludes the vessel.
Degeneration of the walls of arteries is caused by accumulated fatty deposits and scar tissue

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72
Q

Where are plaques more vulnerable?

A

areas of high stress as there’s a thinner fibrous cap prone to rupture

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73
Q

**Define ischemia

A

inadequate blood supply to an organ or pat of the body (especially heart muscles)
OR
reduction in blood flow

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74
Q

**Define infarction

A

Ischemia (or reduction in blood flow) that leads to cell death due to lack of blood supply

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75
Q

Give complications of thrombus formation

A

Ischemia of tissue
Embolism (if thrombus is dislodged)
Aneurysm (plaques weaken wall of arteries)

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76
Q

Aneurysm of what artery can cause central abdominal pain especially in males >55

A

Abdominal Aortic Artery

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77
Q

Common places where a thrombus can result in ischemia

A

Popliteal artery

Coronary artery

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78
Q

**Define Thrombosis (3 marks)

A

Solid mass of blood constituents
formed within intact vascular system
during life

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79
Q

**Define embolus (2 marks)

A

Mass of material in the vascular system

Abel to become lodged within a vessel and block it

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80
Q

Why are the lungs, liver and some parts of brain at a lower risk of ischemia/infarction than other organs?

A

As they are all supplied by 2 blood vessels and don’t have an End Artery Supply. Therefore if embolism or thrombosis occurs in one of vessels, there other is still able to supply it.

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81
Q

What 2 vessels supply the:

a) Liver
b) Lungs

c)Brain

A

a) Portal Vein
Hepatic Artery

b) Pulmonary arteries
Bronchial arteries

c) Circle of Willis (2 internal carotid arteries)

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82
Q

Define End Artery Supply

A

An artery that is the only supply of oxygenated blood to a portion of tissue.
Extra:
Do not anastomose with their neighbours.
No collateral circulation present.

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83
Q

What is most common cause of infarction?

A

Disruption in blood flow e.g. fibrous plaque

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84
Q

Other than thrombus dislodged, what can cause an embolism?

A

Air
Fat
Foreign Body (e.g. vegetations of bacteria)

85
Q

What is pyrexia

A

fluctuating body temperature

86
Q

Examples of anti-inflammatories

A

Ibuprofen
Steroids
NSAIDs
Analgesics

87
Q

What can over-use of anti-inflammatories lead to?

A

Crohn’s, Peptic Ulcer, Ulcerative Colitis, inflamed Fallopian tubes

88
Q

Define Rheumatoid Arthritis

A

Inflammatory arthritis with granulomatous features

89
Q

Systemic effects of Inflammation (6)

A 
Pyrexia
Constitutional symptoms
Weight loss
Reactive hyperplasia of reticuloendothelial system
Haematological changes
Amyloidosis
90
Q

What are outcomes of acute inflammation

A

Resolution
Suppuration
Organisation
Progression to chronic inflammation

91
Q

What does the outcomes of acute inflammation depend on?

A
  • Type of tissue involved

- Amount of tissue destruction (this depends on the nature of the injurious agent)

92
Q

Whats meant by resolution (from cell/tissue damage)?

A

Initiating factor removed

Tissue undamaged or able to regenerate

93
Q

Whats meant by repair (how is it different to resolution)?

A

Initiating factor still present

Tissue damaged and unable to regenerate

94
Q

What cells can regenerate? (6)

A 
Hepatocytes (liver)
Pneumocytes (lungs)
All blood cells
Gut epithelium
Skin Epithelium
Osteocytes (Bone)
(PNS neurones)
95
Q

What cells don’t regenerate?

A 
Myocardial cells (heart)
Neurones (CNS)
96
Q

**Describe repair of tissue

A

Replacement on damaged tissue by fibrous tissue

Collagen produced by fibroblasts

97
Q

Examples of repair

A

Heart after myocardial infarction
Brain after Cerebral Infarction
Spinal Cord after trauma

98
Q

In lobar pneumonia, on an X-ray, what do white parts show, what is mostly present in acute inflammation of alveoli, why can lung regenerate?

A

White parts are parts gone solid
Alveoli mostly filled with neutrophils
Pneumocytes can regenerate

99
Q

If abrasion of skin is not properly sutured up, what can happen?

A

Gap can be filled with blood containing fibrin which weakly joins skin but fibroblasts eventually form collagen in gap (scar)

100
Q

Describe what can happen after 2nd intention abrasion of skin

A

(alot of layers of skin removed in area)

Fibroblasts and capillaries form granulation tissue, which can lead to scars (collagenous scar)

101
Q

Describe 1st intention abrasion of skin

A

top layer of cells scrapped off and scab can form over surface
no scar as basal layer still remains and can regenerate

102
Q

Risk factors of atherosclerosis

A

HBP (or hypertension sharing forces)
Smoking cigarettes
Hyperlipidemia (direct damage to endothelial cells)
Diabetes (superoxide)

103
Q

Give two past/current theories of atherosclerosis occurance

A

Lipid Insulation Theory

Endothelial Damage Theory (current)

104
Q

What prevents stickiness of endothelial cells of BVs

A

Teflon coating of epithelial cells

NO causes lack of stickiness

105
Q

What 3 chemicals can damage epithelial teflon coating

A

Free Radicals
Nicotine
CO

106
Q

*Define Apoptosis

A

Programmed cell death
that involves the controlled dismantling of intracellular components while avoiding inflammation and damage to surrounding cells

107
Q

Give 2 examples of fully differentiated cells that apoptose?

A

Top of villi in gut

Top of skin

108
Q

What can trigger apoptosis

A

Cells no longer have potential to divide

DNA damage

109
Q

What protein detects DNA damage

A

p53

damage to p53 gene means DNA damage undetected so cell does not apoptose - can become cancerous

110
Q

2 examples of apoptosis in disease

A

Cancer - lack of apoptosis as mutation in p53 gene

HIV - too much apoptosis as virus binds to CD4 T-helper lymphocytes then can enter cells and cause apoptosis

111
Q

*Define Necrosis

A

Traumatic cell death

112
Q

Examples of necrosis

A

Frostbite; Cerebral infarction; Avascular necrosis of bone (scaphoid bone in hand; femural head if neck supply cut off); Pancreatitis

113
Q

Types of necrosis

A

Coagulative - caused by ischemia or infarction
Liquefactive (or colliquative)
Caseous - tissue maintains cheese-like appearance

114
Q

Describe liquefactive necrosis

A

Transformation of tissue into a liquid viscous mass (focal bacterial or fungal infections)
also symptom of internal chemical burn

115
Q

What are role of caspases in apoptosis

A

Endoproteases (enzymes) that cause apoptosis by DNA fragmentation and membrane blebbing (via demolishing key structural proteins and activating other enzymes)

116
Q

Describe extrinsic apoptotic signalling network

A

Fas (transmembrane receptor) and FasL (ligand/cytokine) are members of TNF family

  • FasL binds to Fas, which brings together death domains (DD) on cytoplasmic tails.
  • ‘Fas-associated protein with death domain’ (FADD) is an adaptor protein that binds activated DD to death effector domains (DED) that bind to pro-caspase 8.
  • When pro-caspase 8s are brought together , they transactivate and cleave eachother to form Caspase 8, which leads to formation of Caspase 3.
  • Caspase 3 cleaves ICAD to form CAD (caspase activated DNAase).
  • CAD enters nucleus and cleaves DNA, resulting in apoptosis due to DNA damage.
117
Q

What is TNF family

A

Tumour Necrosis Factor family

118
Q

Describe the intrinsic apoptotic signalling network

A
  • Cellular stress, such as growth factor withdrawal and p53 cell cycle arrest induces the expression of the pro-apoptotic Bcl-2 proteins (Bax and Bak).
  • These form permissive pores on outer mitochondria causing release of Cytochrome C.
  • Cytochrome C binds to Apaf1 to form an apoptosome.
  • Apoptosome activates the initiator caspase, Caspase 9.
  • Caspase 9 then activates effector caspase, Caspase 3.
  • Caspase 3 cleaves ICAD to form CAD (caspase activated DNAase).
  • CAD enters nucleus and cleaves DNA, resulting in apoptosis due to DNA damage.

Other molecules (anti-IAPs e.g. Smac, Omi) released from damaged mitochondria counteract the effect of IAPs (inhibitor of apoptosis proteins), which would normally bind and prevent the activation of pro-caspase 3.

119
Q

What is effect of Anti apoptotic Bcl-2 protein on intrinsic apoptotic signalling network

A

Bcl2- when incorporated as a member of the Bax/Bak pore complex, renders the mitochondrial pore non-permissive to release of anti-IAPs and cytochrome C.
Prevents apoptosis.

120
Q

Cytochrome C and Apaf1 bind to form what? (Intrinsic apoptosis)

A

Apoptosome

121
Q

What is the effector caspase? (intrinsic apoptosis)

A

Caspase 3

122
Q

Binding of FasL to Fas results in formation of which Pro-Caspase and caspase? (extrinisic)

A

Pro-caspase 8 -> Caspase 8 -> Caspase 3

123
Q

What is initiator caspase? (intrinsic apoptosis)

A

Caspase 9

124
Q

What can initiate intrinsic apoptosis pathway?

A

Cellular stress, such as growth factor withdrawal and p53 cell cycle arrest

that induces the expression of the pro-apoptotic Bcl-2 proteins (Bax and Bak), causing release of cytochrome C and anti-IAPs from mitochondria.

125
Q

Give an example of apoptosis in development

A

Fingers are webbed in development and apoptosis helps separate the fingers

126
Q

What is differences between congenital, inherited and acquired deficiencies

A

Congenital - present at birth (not necessarily genetic e.g. club foot)
Inherited - Caused by an inherited genetic abnormality (e.g. Huntingtons, Down’s syndrome)
Acquired - caused by non-genetic environmental factors e.g. (Fetal alcohol syndrome)

127
Q

What are homebox genes

A

A large family of similar genes that direct the formation of many body structures during early embryonic development

128
Q

Examples of deficiencies due to problems during embryonic development

A

Spina Bifida (exposed spina cord)
also Meningocele, Myleomeningocele
Cleft palate
VSD (ventricular septal defect)

129
Q

**Define Hypertrophy

A

Increase in size of a tissue caused by an increase in SIZE of the constituent cells

130
Q

Define Hyperplasia

A

Increase in the size of a tissue caused by an increase in of NUMBER of constituent cells

131
Q

Define Atrophy

A

Decrease in size of a tissue caused by a decrease in number of the constituent cells or a decrease in their size

132
Q

Define Metaplasia

A

Change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type.

133
Q

Define Dysplasia

A

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

(change happen instead of metaplasia with severe/consistent damage or developmental abnormality)

134
Q

Example of metaplasia

A

Bronchi: ciliated columnar epithelium to squamous epithelium (smoker)
(can no longer catch microbes -> cough)

135
Q

Example of hypertrophy

A

Larger muscle but same number of myofibrils (so no change in strength, just look bigger) from steroids or condition

136
Q

Examples of hyperplasia

A

Enlarged prostate

Enlarged lining of womb (more oestrogen, less progesterone)

137
Q

Conditions that can result from age

A
  • Dermal elastosis (wrinkled skin)
  • Cataracts
  • Osteoporosis
  • Alzheimers or Vascular dementia
  • Sarcopenia
  • Deafness
138
Q

What causes dermal elastosis or cataracts

A

Increased (over time) exposure to UV-B light which causes protein cross-linking

139
Q

What causes deafness?

A

Loss of hair cells in cochlea over time

140
Q

What causes A or V dementia

A

Atrophy in the brain due to plaques of protein or neurofibrillary tangles or ishemia/infarction

141
Q

What causes osteoporosis

A

Lack of oestrogen meaning decreased bone formation and increased resorption (post menopausal women)

142
Q

What is meant by DIC?

A

Disseminated Intravenous Coagulation

in gross infections or serious traumas

143
Q

Which of these is an example of acute inflammation:

Glandular fever, leprosy, TB, appendicitis

A

Appendictis

144
Q

**Define granuloma

A

Macrophages surrounded by lymphocytes/neutrophils

145
Q

What type of inflammation is lobar pneumonia

A

Acute

146
Q

Give an example of Granulomatous inflammation

A

Crohn’s disease

147
Q

An enlarged left ventricle is an example what?

Hyperplasia, hypertrophy, atrophy

A

Hypertrophy

148
Q

Give an example of a condition you can be born with but not be genetic

A

Foetal Alcohol Syndrome

149
Q 
Which of the following has autosomal dominant inheritance?
FAP (Familial Adenomatous Polyposis)
Colour blindness
Cystic fibrosis
Sickle cell disease
A

FAP

150
Q

Which of these is not an example of apoptosis:
Graft vs Host Disease
Renal Infarction

A

Renal Infarction

cells die due to lack of blood, not due to apoptosis process

151
Q

Which of these is an example of chronic inflammation from the start:
Cholecystitis
Infectious mononucleosis (aka Glandular fever)

A

Infectious Mononucleosis which starts as lymphocytes, not neutrophils

(Cholecystitis is acute at start)

152
Q

*Which of these is NOT associated with dementia?
Huntingtons disease
Downs syndrome
Cerebral palsy

A

Cerebral Palsy

153
Q

Give an example of hyperplasia

A

Benign prostate enlargement

154
Q

Which of these cells CAN regenerate
Hepatocytes
Myocytes
Nephrons

A

Hepatocytes
(Myocytes=heart, cant regenerate)
(Nephrons=kidney “)

155
Q

Give 4 examples of DNA damage

A

Single-strand break
Double-strand break
Base alteration
Cross-linkage

156
Q

What protein detects DNA damage?

A

p53

Apoptosis triggered if DNA damage

157
Q

Describe how granulomatous tissue can develop from

A

Occurs when the immune system attempts to wall off substance but is unable to eliminate it.
This forms a granuloma (a collection of epithelioid histiocytes (macrophages))

158
Q

Most is the most common form of acute to chronic progression of inflammation

A

Suppurative type

159
Q

Describe suppurative type of progression from acute to chronic inflammation

A

Pus forms in deep-seated abscess cavity.
Drainage is delayed or inadequate and so by the time drainage occurs, the abscess will have developed thick walls composed of granulation and fibrous tissues.
Rigid walls of abscess cavity will thus fail to come together after eventual drainage and the stagnating pus within the cavity becomes organised by the ingrowth of granulation tissue, eventually to be replaced by fibrous scar.

160
Q

Example of chronic abscess

A

Osteomyelitis

Abscess in the bone, which is difficult to eradicate due to poor access by macrophages

161
Q

The presence of indigestible material can cause progression to chronic inflammation - give examples

A

Keratin (from ruptured epidermal cyst)
Fragments of necrotic bone
(both are relatively inert and resistant to lysosomal enzyme action)
Foreign body materials such as surgical suture, wood, metal or glass (chronic suppuration)

162
Q

What type of inflammation can result from foreign bodies?

A

Granulomatous Inflammation

Cause macrophages to form multinucleate giant cells called ‘foreign body giant cells’

163
Q

Example of recurrent acute inflammation resulting in chronic inflammation

A

Recurring gallstones

Result in Chronic Cholecystitis

164
Q

Commonest form of granuloma

A

Tuberculosis

165
Q

Macroscopic appearances of chronic inflammation

A 
Chronic ulcer
Chronic abscess cavity
Thickening of the wall of a hollow organ
Granulomatous inflammation
Fibrosis
166
Q

What is fibrosis and when is it most prominent

A

Macroscopic appearance of chronic inflammation
Thickening or scarring of connective tissue
Becomes most prominent when most of the chronic inflammatory cell infiltrate has subsided

167
Q

Causes of primary chronic inflammation (no acute phase)

A

Resistance of infective agent to phagocytosis and intracellular killing e.g. TB, leprosy
Endogenous materials e.g. necrotic adipose tissue, bone, uric acid crystals
Exogenous materials e.g. silica, asbestos materials, suture materials
Some autoimmune diseases
Specific disease of unknown aetiology e.g. IBD (UC)
Primary granulomatous diseases e.g. Crohns, sarcoidosis

168
Q

Autoimmune diseases that can cause primary chronic inflammation

A

Organ-specific e.g. Hashimotos thyroiditis, Chronic gastritis of pernicious anaemia
Non-organ-specific e.g. Rheumatoid arthritis
Contact hypersensitivity reactions e.g. self-antigens altered by nickel

169
Q

What does cellular infiltrate mainly consist of in chronic inflammation

A

Lymphocytes
Plasma cells
Macrophages

170
Q

Describe healing in chronic inflammation:

Paracrine stimulation of connective tissue proliferation

A
  • Involves the regeneration and migration of specialised cells
  • The predominant features in repair are angiogenesis (formation of new blood vessels) followed by fibroblast proliferation and collagen synthesis resulting in granulation tissue
  • These process are regulated by proteins called growth factors which bind to specific receptors on cell membranes and trigger a series of events culminating in cell proliferation
171
Q

**Examples of Growth factors involved in healing and repair associated with inflammation. State their specific functions also

A

Epidermal Growth Factor (EGF)
Transforming growth factor-alpha (TGF-a)
(both regeneration of epithelial cells)
TGF-beta (stimulates fibroblast proliferation and collagen synthesis; controls epithelial regeneration)
Platelet-derived growth factor (PDGF) - mitogenic and chemotactic for fibroblasts and smooth muscle cells
Fibroblast growth factor (FGF) - stimulates fibroblast proliferation, angiogenesis and epithelial cell regeneration
Insulin-like growth factor-1 (IGF-1) - synergistic effect with other growth factors
Tumour necrosis factor (TNF) - stimulates angiogenesis

172
Q

Which growth factors stimulate angiogenesis

A

TNF (Tumour necrosis factor)

FGF (Fibroblast Growth Factor)

173
Q

Which growth factors stimulate regeneration of epithelial cells

A

EGF Epidermal Growth Factor
TGF-alpha (transforming growth factor-a)
TGF-beta

174
Q

Which growth factors stimulate fibroblast proliferation

A

FGF fibroblast growth factor

TGF-beta

175
Q

Function of Platelet derived growth factor (PDGF)

A

Mitogenic and chemotactic for fibroblasts and smooth muscle cells

176
Q

Function of IGF-1

A

Synergistic effect with other growth factors

177
Q

How do macrophages moves through tissues

A

Amoeboid motion

178
Q

Important cytokines produced by macrophages

A

Interferon-alpha and -beta
Interleukin-1, -6 and -8
Tumour necrosis factor- alpha

179
Q

Role of macrophages in inflammation

A

Can ingest a wider range of materials then neutrophil polymorphs can
and, being long-lived, they can harbour viable organisms if they are unable to kill them by their lysosomal enzymes

180
Q

Example of an organism that can survive within macrophages

A

Mycobacteria:
Mycobacterium tuberculosis
Mycobacterium Leprae

181
Q

Causes of granulomas

A

Specific infections e.g. Mycobacteria (TB, leprosy), Types of fungi, Parasites, Larvae, Eggs and Worms, Syphilis
Materials that resist digestion (endogenous and exogenous)
Specific chemicals e.g. Beryilium
Drugs (Hepatic granulomas from Allopurinol, Phenylbutazone, Sulphonamides)
Others e.g. Crohn’s disease, Sarcoidosis, Wegeners granulomatosis

182
Q

Examples of endogenous materials that resist digestion

A

Keratin
Necrotic bone
Cholestrol crystals
Sodium urate

183
Q

Examples of exogenous materials that resist digestion

A 
Talc
Silica
Suture materials
Oils
Silicone
184
Q

What are histiocytic giant cells and when can they appear

A

Form when 2 or more macrophages attempt simultaneously to engulf the same particle - their cell membranes fuse and the cells unite. Resulting multinucleate giant cells with >100 nuclei have little phagocytic activity and no known function.
Form when foreign particles are too large to be ingested by a single macrophage or where particulate matter, that is indigestible by macrophages, accumulates e.g. inert materials such as silica or bacteria like tubercle bacilli

185
Q

Examples of histiocytic giant cells

A

Langerhans giant cells (characteristically seen in Tuberculosis)
Foreign body giant cells (seen in relation to particulate foreign body material)
Touton giant cells (seen when macrophages attempt to ingest lipids or in relation to xanthomas/dermatofibromas on skin)

186
Q

Role of acute inflammation in systemic conditions

A

CVS system in response to acute MI and the generation of some complication of MI such as cardiac rupture

187
Q

Role of chronic inflammation in systemic conditions

A

Initiation and propagation of cancer and in its progression e.g. in Ulcerative colitis
Involved in myocardial fibrosis after MI

188
Q

Roles of inflammation in general in systemic and organ-specific diseases

A

Atheroma development

Tissue injury and neurodegenerative disorder of CNS - multiple sclerosis

189
Q

Role of inflammation in atheroma development

A

Macrophages adhere to endothelium, migrate into the arterial intima and, with T lymphocytes, express cell adhesion molecules which recruit other cells into the area
The macrophages are involved in processing the lipids that accumulate in atheromatous plaques
(Form foam cells)

190
Q

Define chronic inflammation

A

The subsequent and often prolonged tissue reactions to injury following the initial response.
Can also be defined as an inflammatory process in which lymphocytes, plasma cells and macrophages predominate.

191
Q

Causes of chronic inflammation

A

Primary chronic inflammation
Transplant rejection
Progression from acute inflammation
Recurrent episodes of acute inflammation

192
Q

Macroscopic appearances of chronic inflammation

A 
Chronic ulcer
Chronic abscess cavity
Thickening of wall of a hollow organ
Granulomatous inflammation
Fibrosis
193
Q

Microscopic features of chronic inflammation

A

Cellular infiltrate consists characteristically of lymphocytes, plasma cells and macrophages
Some eosinophils may be present but neutrophil polymorphs are rare
Some macrophages may form multinucleate giant cells
Exudation of fluid not prominent
May be continuing destruction of tissue at same time as repair and regeneration
Necrosis can be present (granulomatous disease)

194
Q

2 lymphocytes in lymphocytic infiltrate in chronic inflammation

A

B-lymphocytes (contact with antigen, progressively transform into plasma cells that secrete antibodies)

T-lymphocytes = responsible for cell-mediated immunity; on antigen contact, produce range of soluble factors called cytokines (recruitment and activation of other cells like macrophages)

195
Q

What stain can identify tuberculosis

A

Ziehl-Neelsen stain

bright red

196
Q

What is a likely cause of granulomas with many eosinophils

A

Parasitic infection such as worms

197
Q

Locations in body of stem cells

A

Skin Epidermis in basal layer (immediately adjacent to BM), hair follicles and sebaceous glands
Intestinal mucosa near bottom of crypts
Liver between hepatocytes and bile ducts
Haemopoietic stem cells in bone marrow

198
Q

When can complete restoration occur

A

Loss of part of a labile cell population can be completely restored

199
Q

Healing of minor skin abrasion

A
  • The epidermis is lost over a limited area, but at the margins of the lesion there remain cells that can multiply to cover the defect
  • At first, cells proliferate and spread out as a thin sheet until the defect is covered
  • When a confluent layer has been formed, the stimulus to proliferate is switched off; this is known as contact inhibition, and controls both growth and movement
  • Once in place, the epidermis is rebuilt from the base up until it is indistinguishable from normal - this whole process is called healing
200
Q

What is organisation

A

The repair of specialised tissues by the formation of a fibrous scar

201
Q

**Formation of granulation tissue

A

Specialised or complex tissue is destroyed and cannot be reconstructed
Capillary endothelial cells proliferate and grow into the area to be repaired and can grow into vascular channels - these vessels are arranged as a series of loops arching into the damaged area
At the same time, fibroblasts are stimulated to divide and to secrete collagen and other matrix components. They also acquire bundles of muscle filaments and attachments to adjacent cells - these modified cells are called myofibroblasts (secrete collagen and important for contraction)
Combination of capillary loops and myofibroblasts is known as GRANULATION TISSUE

202
Q

What cells secrete collagen (in granulation tissue)

A

Myofibroblasts

203
Q

Describe wound contraction and scarring formation (also why is wound contraction important)

A

Wound contraction results from the contraction of myofibroblasts in the granulation tissue - these are attached to each other and to the adjacent matrix components, so that granulation tissue as a whole contracts and indrawn the surrounding tissues. This reduces the volume of tissue for repair and thus reduces tissue defect.
Collagen is secreted and forms a scar (replacing lost specialised tissue).

204
Q

Issues with wound contraction

A
  • If the tissue damage is circumferential around the lumen of a tube (e.g. gut), subsequent contraction may cause stenosis (narrowing) or obstruction
  • Similar tissue distortion can result in permanent shortening of a muscle (called a contracture)
  • Burns to the skin can be followed by considerable contraction, with resulting cosmetic damage and often impaired mobility
205
Q

Healing incised wound of skin - healing by first intention

A

Incision that causes little damage to tissue on either side of cut.
-Some small blood vessels will have been cut but these will be occluded by thrombosis.
-Fibrin deposited locally will bind the two sides of the wound.
-Coagulated blood on the surface of the wound will form a scab and helps to keep the wound clean (this join is very weak but is formed rapidly and is a framework for the next stage). (It is important that this framework is not disrupted thus why sutures, sticking plasters and other means of mechanical support are extremely useful.)
-Over the next few days, capillaries proliferate sufficiently to bridge the tiny gap, and fibroblasts secrete collagen as they migrate into the fibrin network.
If the sides of the wound are very close then such migration is minimal as would the amount of collagen and vascular proliferation required.
-By about 10 days the strength of the repair is sufficient to remove any plasters etc - the only residual defect will be the failure to reconstruct the elastic network in the dermis.

206
Q

Healing by second intention e.g. in tissue loss etc

A

Wound margins are not apposed
Local haemorrhage will keep the sides apart and prevent healing by first intention, infection similarly compromises healing
Involves:
- Phagocytosis to remove any debris
- Granulation tissue to fill in defects and repair specialised tissue lost
- Epithelial regeneration to cover the surface
Time scale depends on size of defect as determines amount of granulation tissue
Final result depends on amount of tissue loss and thus scarring amount

207
Q

Healing of liver architecture
When can liver heal and when can it not
What can result from damage

A

Hepatocytes are stable cell population and have good regenerative capacity.
Sometime hepatic regeneration from Liver Progenitor cells (not hepatocytes).
Liver structure cant be reconstructed if severely damaged. But condition only causing hepatocyte loss may still completely resolve, but destruction of both may not.
Imbalance between hepatocyte regeneration and failure to reconstruct the architecture may proceed to cirrhosis. However, following the partial surgical resection of the liver there can be substantial regeneration of functioning liver.

208
Q

Different things that can be an embolus

A

Solid or Gas

Eg. Cholestrol crystals from plaque, tumour amniotic fluid, fat

Medicine Phase 2a (22 decks)

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