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Y2 EMS > 2. Methods of Disease > Flashcards

2. Methods of Disease Flashcards

1
Q

What are the 3 types of cell injury?

A

Reversible cell injury = the cell can return to full function once the cause of injury is stopped e.g. hypoxia, radiation, drugs

Irreversible cell injury = If the injury is prolonged, then the cell will die.

Ischaemic/reperfusion injury = cells that have been oxygen deprived (ischaemic) are damaged even more when blood supply resumes (reperfusion).

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2
Q

What is necrosis?

A

Unregulated cell death.

severe cell swelling followed by rupture.

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3
Q

What is apoptosis?

A

Programmed cell death.

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4
Q

What is oncosis?

A

A series of reactions after cell injury which leads to its death.

(NOT the same pathway as apoptosis)

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5
Q

How can oxygen derived free radicals cause cell injury?

A

They bind to the lipid membrane of a cell and destroy it.

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6
Q

What type of cell injury has these characteristics?

Mitochondrial swelling, lysosome swelling, membrane damage, leakage of enzymes

A

Irreversible cell injury

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7
Q

What type of cell injury has these characteristics?

Cell swelling, pallor, hydropic change (water build up), vacuolar degeneration

A

Reversible cell injury

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8
Q

What causes cellular swelling in reversible cell injury?

A

Na+ build up due to a lack of ATP (only glycolysis occurs).

This causes water to move in by osmosis.

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9
Q

In irreversible cell injury, there is membrane damage to lysosomes, cell membrane and mitochondria.
How does damage to these lead to cell death?

A

Lysosome - lysozyme enzymes leak and degrade cell.

Cell membrane - calcium ions flood the cell which activate Caspaces (pathways leading to apoptosis) and other enzymes which degrade the cell.

Mitochondria = Cyt C leaks which activates Caspaces.

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10
Q

Autophagy is when your body recycles its cells as a source of nutrients and energy.
Does this process induce an inflammatory response?

A

No

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11
Q

What are the main differences between necrosis and apoptosis?

A

Necrosis =

  1. Unregulated / ‘accidental’
  2. Affects large areas of cells in clumps
  3. Cells swell, rupture and spill contents
  4. Inflammation

Apoptosis =

  1. Programmed
  2. Affects specific cells in different areas
  3. Cells shrink and form apoptotic bodies which are phagocytosed
  4. No inflammation
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12
Q

What is the most common form of necrosis?

A

Coagulative necrosis.

Occurs in most organs but mainly in myocardium

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13
Q

What is liquefactive necrosis and where is it seen?

A

Tissue turns to liquid.

Seen in the brain.

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14
Q

What does gangrenous necrosis look like and what is its main cause?

A

Tissue rots into a black colour, usually on hands and feet.
(3 types - wet, dry, gas).

Mainly caused by infection.

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15
Q

What does caseous necrosis look like and what is its main cause?

A

Structureless dead pink tissue.

Mainly caused by tuberculosis (you can actually see the this as dark bits inside the cells on a microscope as the tuberculosis cant be destroyed).

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16
Q

What does fat necrosis look like and what causes it?

A

Loss of cell structure, looks white due to lots of vacuoles.

Caused by trauma to fatty area or enzyme action.

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17
Q

What does fibrinoid necrosis look like and where does it occur?
It is seen in what 2 conditions?

A

Occurs in blood vessels.
The wall of the artery is bright pink.

Seen in malignant hypertension and autoimmune diseases.

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18
Q

What is neoplasia?

A

Abnormal and excessive tissue growth

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19
Q 
What do these prefixes mean?
Ana-
Dys-
Hyper-
Hypo-
Meta-
A 
Ana = Absence (anaplasia)
Dys = Disordered (dysplasia)
Hyper = Excess (hyperthyroidism)
Hypo = Deficiency (hypothyroidism)
Meta = Change from one state to another (metaplasia)
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20
Q

What do these suffixes mean?

  • itis
  • oma
  • osis
  • oid
  • penia
A
  • itis = Inflammatory process (appendicitis)
  • oma = Tumour (carcinoma)
  • osis = State / Condition (osteoarthrosis)
  • oid = Bearing a resemblance to (rheumatoid disease)
  • penia = Lack of (thrombocytopenia)
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21
Q

What do these suffixes mean?

  • cytosis
  • ectasis
  • plasia
  • opathy
A
  • cytosis = Increased number of cells (leukocytosis)
  • ectasis = Dilation (bronchiectasis)
  • plasia = Disorder of growth (hyperplasia)
  • opathy = Abnormal state lacking specific characteristics (lymphadenopathy)
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22
Q

What does ‘sequela’ mean?

A

A condition which is a consequence of a previous disease/injury

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23
Q

What is the difference between ‘aetiology’ and ‘pathogenesis’?

A 
Aetiology = cause of disease
Pathogenesis = progression of disease
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24
Q

What is ‘epidemiology’?

A

Distribution of disease in a population

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25
Q

Identify the two main components of the immune system.

A

Adaptive immunity

Innate immunity

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26
Q

What is the single biggest preventable risk factor for autoimmune disease?

A

Smoking

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27
Q

Women have a stronger immune system than men, but are more susceptible to autoimmune diseases.
Why is this?

A

Women have two X chromosomes, therefore double the genes.

Resulting in a more potent immune response than men.

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28
Q

Which of these are responsible for inflammatory cytokine production?

  1. Autoreactive B cells
  2. Autoantibodies
  3. Autoreactive T cells
A

Autoreactive T cells

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29
Q

Any cell in the body can be subject to an autoimmune response.
True or False?

A

TRUE

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30
Q

What is the difference between ‘organ specific’ and ‘systemic’ autoimmune diseases?

A

Organ specific = Affects a single organ
e.g. autoimmune thyroid disease

Systemic = Affects several organs simultaneously
e.g. Connective tissue diseases

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31
Q

What is Hashimoto’s thyroiditis?

A

Autoimmune disease which gradually destroys the thyroid, leading to hypothyroidism

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32
Q

What is Grave’s disease?

A

Autoimmune disease where autoantibodies bind to TSH receptors, overstimulating them and leading to hyperthyroidism

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33
Q

What autoimmune disease is associated with ‘butterfly rash’?

A

Systemic lupus erythematosus (SLE)
or more simply…
Lupus

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34
Q

Immune complexes are more likely to cause problems where circulation is slow and there is a rich capillary network.
Why?

A

Greater chance of precipitating out and causing local inflammation.

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35
Q

Which of these is not a connective tissue disease?

  1. Systemic lupus erythematosus
  2. Scleroderma
  3. Hashimoto’s thyroiditis
  4. Polymyositis
  5. Sjogren’s syndrome
A

Hashimoto’s thyroiditis

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36
Q

What is the main advantage of testing for autoantibodies in diagnosis?

A

Early diagnosis.

You can detect autoantibodies years before someone develops an autoimmune disease.

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37
Q

What is immunosuppression?

A

A natural/artificial process of switching off the immune response partially or fully.
Can be accidental or on purpose.

Can result in immunodeficiency - susceptible to infections

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38
Q

What is the difference between primary and secondary immunodeficiency?
Give examples.

A

Primary = genetic (rare)
child who keeps getting infection suggests an immunological problem

Secondary = acquired (much more common)
e.g. transient, stress, surgery, malnutrition, drugs, infection

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39
Q

What is Severe Combined Immunodeficiency (SCID) a result of and how is it treated?

A

Defective T cells and B cells.

Bone marrow transplant
Gene therapy

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40
Q

Define allergy.

A

A damaging immune response by the body to a substance it has become hypersensitive to

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41
Q

What is the function of dendritic cells?

A

Engulf cells and present protein antigens on their cell surface.

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42
Q

What are antibodies?

A

Proteins produced by the body which identify and neutralise foreign objects.

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43
Q

What are macrophages?

A

Large phagocytes which engulf and destroy pathogens/apoptotic cells.

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44
Q

What is the immunopathogenesis for Type 1 hypersensitivity (how does the immune system respond)?

What are its clinical features?

A

Mast cells and basophils are degranulated when antigens bind to IgE antibodies on their cell surface, forming crosslinks.
Preformed inflammatory chemicals are released (histamine, proteases, prostaglandin, leukotrienes).

Clinical features:

  1. Fast onset (15-30mins)
  2. Wheal and flare
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45
Q

Identify 4 symptoms of allergy.

A
  1. Increased heart rate
  2. Swelling + inflammation
  3. Blood clots
  4. Bronchoconstriction
  5. Blood vessels dilate
  6. Increased permeability of capillaries
  7. Gastric acid secretion
  8. Adrenaline release
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46
Q

What is anaphylaxis?

A

An acute life-threatening, IgE mediated systemic hypersensitivity reaction.
(severe allergic reaction)

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47
Q

Identify 4 clinical symptoms of anaphylaxis.

A
  1. Swelling of tongue/neck
  2. Low pressure
  3. Difficulty breathing
  4. Dizziness, loss of consciousness
  5. Urticaria and angioedema
  6. Severe abdominal pain, vomiting, diarrhoea
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48
Q

How are we sensitised to an allergen (immunopathologically)?

A
  1. Dendritic cell presents the allergen to a naïve T cell.
  2. This differentiates and activates naïve B cells.
  3. Memory B cells with specific IgE for the allergen are formed which recognise the allergen on re-exposure.
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49
Q

What does the ‘Dual allergen exposure hypothesis’ suggest about allergic sensitisation and allergen tolerance?

A

Early exposure to a food protein through a disrupted skin barrier e.g. eczema leads to allergic sensitisation.

Early oral exposure (eating) to food allergen induces tolerance (less likely to be allergic).

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50
Q

Allergic responses are inherited conditions.

True or False?

A

FALSE

you might be more susceptible to an allergy, but you don’t inherit it.

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51
Q

What are the 2 most common food allergies in children?

A
  1. Milk

2 Egg

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52
Q

Food allergies are more common in adults than children.

True or False?

A

FALSE

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53
Q

How are allergies diagnosed?

A

Skin prick test

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54
Q

How is rhinitis treated?

A

(hay fever)

Nasal steroids + Antihistamines

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55
Q

Can aero-allergic stimuli such as house dust mite make asthma worse?

A

Yes

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56
Q

What is the ‘Atopic triad’?

A

Asthma
Rhinitis
Eczema

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57
Q

What is the mechanism for Type II (cytotoxic) hypersensitivity?

What are its clinical features?

Common antigen?

Diseases resulting in this hypersensitivity?

A

IgG/IgM antibodies bind to self or foreign antigens on the cell surface.
The target cell is then destroyed via:
1. Complement activation
2. Phagocytosis
3. ADCC (antibody dependent cell-mediated cytotoxicity)

Clinical features:
Onset = minutes - hours
Cell lysis + necrosis (damage + death)

Common antigen = penicillin

Diseases:

  1. Goodpasture’s nephritis
  2. Blood transfusion reaction
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58
Q

In a blood transfusion, what happens if incorrectly matched blood is given to a patient?

A

Type II hypersensitivity reaction.

  1. Patient’s antigen presenting cells detect and display foreign antigens to B cells to produce antibodies.
  2. Complement is activated and a MAC attack complex is formed which makes a hole in the cell and kills it.
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59
Q

The classic pathway of Complement is triggered by bacteria.

True or False?

A

FALSE

Bacteria trigger alternative pathway.
Immune complexes e.g. IgM, IgG, MBL trigger classical pathway.

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60
Q

What is the mechanism for Type III hypersensitivity?

What are the clinical features?

Traditional caused by?

Disease with this hypersensitivity?

A

IgG/IgM antibodies bind to SOLUBLE antigens, forming immune complexes which deposit onto tissue (e.g. endothelium of blood vessel wall).
Complement is activated which then damages/destroys these tissues.

Clinical features:
Onset = 3-8hours
Vasculitis (inflammation of blood vessels)

Serum sickness (allergic reaction to an injection)

Disease: SLE (lupus)

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61
Q

In a blood test, which components of Complement are unusually low in SLE (lupus)?

A

C3 + C4

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62
Q

What type of hypersensitivity reaction is associated with vasculitis?

Which parts of the body are particularly susceptible to this?

A

Type III

Activation of Complement leads to damage and destruction of blood vessel walls and fluid leaks out (oedema).

Kidneys + Joints + Skin

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63
Q

What is the mechanism for Type IV (delayed) hypersensitivity?

What are the clinical features?

What are the common antigens?

Disease associated with this hypersensitivity?

A

T-cell mediated cytotoxicity.
Antigen-presenting cells present a foreign body to T-cells which mediate inflammation and tissue damage.

Clinical features:
Delayed onset 48-72hours
Erythema induration (redness and hardening)

  1. Metals e.g. nickel
  2. Tuberculin test (prick skin with TB, causes reaction if previously encountered)
  3. Poison ivy

Disease: Contact dermatitis (inflammation of the skin due to an allergen/irritant)

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64
Q

Which antibody mediates Type I hypersensitivity?

A

IgE

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65
Q

What is the key difference between Type II and Type III hypersensitivity?

A

Type II is targets cells, Type III targets soluble antigens

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66
Q

SLE is an example of which type of hypersensitivity?

A

Type III

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67
Q

Which antibodies mediate Type III hypersensitivity?

A

IgG and IgM

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68
Q

Name 3 chemical mediators produced by a mast cell.

A
  1. Prostaglandins
  2. Histamines
  3. Leukotrienes
  4. Proteases
  5. Chemotactic factors
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69
Q

What is the first step in the healing process after an injury?

A

Acute inflammation

Allows immune system to enter damaged area.
Protects against infection.

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70
Q

What are the 2 possible healing outcomes following injury and how do they differ?

A
  1. Regeneration =
    Cells regrow and tissue is restored to normal structure and specialised function.
  2. Repair =
    Cells cannot regrow so a scar is formed instead, loss of specialised function.
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71
Q

What are the 3 characteristics of ‘Labile cell populations’?

Give an example.

A
  1. High cell turnover
  2. Active stem cell population
  3. Excellent regenerative capacity

Epithelia (e.g. in skin + gut)

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72
Q

What are the characteristics of ‘Stable (quiescent) cell populations’?

Give an example.

A
  1. Low normal cell turnover HOWEVER this turnover can increase massively if needed
  2. Good regenerative capacity

Liver, renal tubules

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73
Q

What are the characteristics of ‘Permanent cell populations’?

Give an example.

A
  1. No physiological turnover (cant be replaced once they die)
  2. Long life cells
  3. No regenerative capacity

Neurons, striated muscle (e.g. heart muscle)

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74
Q

Labile cells and stable cells continuously go through the cell cycle.
True or False?

A

FALSE.

Only labile cells continuously go through the cycle.
Stable cells leave the cell cycle and re-enter it depending on need.
(permanent cells do not undergo cell cycle at all)

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75
Q

The liver and renal tubules are examples of which type of cell population?

A

Stable (quiescent)

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76
Q

Neurones in the brain and cardiac muscle are examples of which type of cell population?

A

Permanent

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77
Q

What are injured/dead cells with regenerative capacity replaced by and where are these found?

A

Stem cells

Found in stem cell pool of labile and stable cell population.
Basal layers of epidermis + bottom of intestinal crypts.

78
Q

What cell type is particularly vulnerable to radiation damage e.g. radiotherapy?

A

Stem cells

79
Q

Why does liver cirrhosis occur despite liver cells having excellent regenerative capacity?

A

Constant damage to the liver over time (e.g. alcohol) results in the loss of the original architectural structure.
So although the liver can regenerate, it cannot repair the original tissue framework which results in cirrhosis.

80
Q

What does ‘contact inhibition’ refer to in the healing of a minor cut in skin.

A

The labile cells on the sides of the defect (cut) begin to proliferate, building the epidermis from the base upwards.
Once these cells cover the defect and come into contact with one another, proliferation stops.

81
Q

What 3 factors does regeneration depend on?

A
  1. Cell kinetics (labile/stable cell)
  2. Tissue architecture
  3. Stem cell survival
82
Q

What is ‘organisation’?

Give an example of when this can occur.

A

Repair of specialised tissue with granulation tissue, forming a fibrous scar.
(dead tissue is removed by phagocytosis)

Pneumonia + infarction.

83
Q

What 3 processes are occurring in granulation tissue?

A
  1. Endothelial cell proliferation = form new vessels.
  2. Phagocytes = remove dead/damaged tissue
  3. Myofibroblasts proliferate and move into area = Synthesis of collagen + ECM (extracellular matrix). Also contracts wound.
84
Q

How does granulation tissue mature over time?

A

Becomes less vascular and cellular.

The wound instead contracts and becomes stronger with more collagen + ECM.

85
Q

How does wound healing my first (primary) intention differ to healing by second (secondary) intention?

A

First intention =

  1. Clean, uninfected surgical wound.
  2. Good haemostasis (no bleeding)
  3. Edges brought together (e.g. sutures, staples, plaster)
  4. Nice clean scarring

Secondary intention =

  1. Wound edges not brought together (e.g. infection, not physically possible, extensive loss of tissue)
  2. Same fundamental process
  3. More extensive scarring
86
Q

Give 4 examples of local factors which inhibit healing.

A
  1. Infection
  2. Haematoma (clotted blood in tissue)
  3. Poor blood supply
  4. Foreign material still in tissue
  5. mechanical stress (bones)
87
Q

Give 4 examples of systemic factors which inhibit healing.

A
  1. Age (children heal better than adults)
  2. Drugs (e.g. steroids, immunosuppressants)
  3. Anaemia
  4. Diabetes
  5. Malnutrition
  6. Vit C deficiency
  7. Trace metal deficiency
88
Q

What are keloid scars a result of?

A

Excessive fibroblast production.

genetically determined

89
Q

What is the first step that occurs in the healing process after fracturing a bone?

A

Haematoma formation.
(bleeding within and around the bone provides scaffold for repair)
Necrotic fragments are removed by phagocytosis.

90
Q

Outline the process of fracture healing.

A
  1. Haematoma formation and organisation, necrotic fragments removed.
  2. Osteoblasts lay down disorganised woven bone (callus).
  3. Remodelled into stronger and more orderly lamellar bone
91
Q

Give 4 examples of what can go wrong in fractures which prevent proper healing of bone.

A
  1. Misalignment - fractures don’t unite
  2. Movement of bone - further damage + slows healing
  3. Infection - delays healing
  4. ‘pathological fracture’ - e.g. bone disease or tumour in bone prevents healing
92
Q

Damaged tissue in the brain cannot be replaced, so holes/cysts are left in the brain from its removal.
True or False?

A

TRUE

strokes also leave a cystic cavity as necrotic area is removed.

93
Q

What occurs in the brain instead of scarring?

Why is this?

A

Gliosis

Glial cells are the supporting tissue in the brain which proliferate rather than collagen + fibroblasts.

94
Q

Where is Epidermal growth factor a (EGF) released from and what is its function?

A

From = platelets, macrophages, saliva, plasma

Function = stimulates granulation tissue formation

95
Q

Neoplasia formation has the same mechanism as wound healing.

True or False?

A

TRUE

96
Q

What type of hypersensitivity reaction is Goodpasture’s nephritis an example of?

A

Type II

97
Q

What are the 5 physical characteristics of Acute inflammation?

A
  1. Rubor (redness)
  2. Calor (heat)
  3. Tumor (swelling)
  4. Dolor (pain)
  5. Functio laesa (loss of function)
98
Q

Give 4 examples of acute inflammation causes.

A
  1. Hypersensitivity
  2. Tissue necrosis
  3. Chemicals
  4. Infection
  5. Physical agents (e.g. burns, frostbite)
99
Q

What are the 3 major components of Acute inflammation and what are they caused by?

(hint: effects on vessels etc.)

A
  1. Change is vessel calibre - vasodilation (caused by histamine + NO)
  2. Increased vascular permeability resulting in fluid exudate formation
    (caused by histamine, NO, leukotriene, trauma, bacteria + toxins)
  3. Cellular exudate formation (thicker + slower blood flow due to vasodilation + fluid loss) - neutrophils stick to the endothelium and pass between these cells into interstitial tissue.
100
Q

Define ‘oedema’.

A

Excess fluid in interstitial tissue/serous cavities.
This can be exudate or transudate.
e.g. pulmonary oedema

101
Q

Define ‘exudate’.

A

Extravascular fluid with HIGH protein content (contains cellular debris).
Implies ongoing inflammation if present.

102
Q

Define ‘transudate’.

A

Extravascular fluid with LOW protein content (little/no cellular components).

103
Q

Define ‘pus’.

A

Inflammatory exudate rich in neutrophils, dead cells, and microbes.

104
Q

Hydrostatic pressure in vessels is lower in acute inflammation.
True or False?

A

FALSE

Hydrostatic pressure is higher, which forces plasma proteins out into extravascular space, therefore more fluid leaves the vessels than returns, forming exudate.

105
Q

Give 4 examples of the functions of fluid exudate.

A
  1. Dilutes toxins
  2. Allows antibodies to enter damaged tissue
  3. Allows drugs to be transported to site of injury
  4. Fibrin formation (when fibrinogen comes in contact with tissue), scaffold for granulation + also traps microbes
  5. Delivers nutrients + oxygens
  6. Stimulates immune response
  7. Constantly drained away into lymphatics and replaced
106
Q

In acute inflammation, several stimuli mediate neutrophils to leave vessels and form cellular exudate.
Give 2 examples.

A
  1. Selectins
  2. Integrins
  3. Stimuli from endothelial cells + leukocytes
  4. Chemotaxis
107
Q

Where are neutrophils produced?

A

Produced in bone marrow (most common white blood cell in blood).
Increase in acute inflammation (high levels are diagnostic).

108
Q

Which of these mediators of Acute inflammation are cell derived?

  1. Histamine
  2. Complement system
  3. Prostaglandins
  4. Lysosomal components
  5. Kinin system
  6. Leukotrienes
  7. Cytokines
  8. Coagulation system
A
  1. Histamine
  2. Prostaglandins
  3. Lysosomal components
  4. Leukotrienes
  5. Cytokines

Anything with ‘system’ at the end in plasma derived.

109
Q

What effect do steroids have on Acute inflammation pathways?

A

Steroids inhibit phospholipases.
Therefore ‘arachidonic acid’ is not produced, which stops leukotriene + prostaglandin production.

This prevents:
vasodilation + oedema (prostaglandins)
vasoconstriction, bronchospasm, increased permeability (leukotrienes)

110
Q

What effect does aspirin + indomethacin have on Acute inflammation pathways?

A

Inhibit COX enzyme, preventing prostaglandin formation.

Vasodilation inhibited.

111
Q

What is ‘pyrexia’?

A

Raised body temperature + fever.

112
Q

What are the general effects of Acute inflammation?

A
  1. Pyrexia
  2. Lymph node enlargement
  3. Nausea, malaise, anorexia
  4. Leucocytosis (increased white cell count)
113
Q

Give 3 negative effects of the Acute inflammatory response.

A
  1. Digestion of normal tissues (can be dangerous in brain)
  2. Swelling (epiglottitis can be fatal in children)
  3. Inappropriate inflammatory response (e.g. hay fever)
114
Q 
Which of these is the most common pathway of Acute inflammation?
Suppuration
Repair + organisation
Fibrosis
Chronic inflammation
Resolution
A

Resolution

115
Q

What happens if there is excessive cellular exudate formation?

A

Suppuration (pus formation)

can lead onto ‘repair + organisation’ if the pus is not discharged.

116
Q

What happens if there is excessive necrosis in Acute inflammation?

A

Repair + organisation which then leads to fibrosis.

117
Q

If the cause of Acute inflammation persists what happens?

A

Chronic inflammation

118
Q

What is ‘cholecystitis’?

A

Inflammation of gall bladder due to recurrent gall stones

119
Q

What is the term used to describe the flow of neutrophil polymorphs close to the endothelial wall?

A

Margination

120
Q

_ _ _ _ _ _ _ is an important example of a granulomatous disease.

A

Leprosy

121
Q

A class of signalling molecule secreted by activated macrophages.

A

Cytokines

122
Q

The name for an abnormal multinucleate cell that forms through the fusion of histiocytes.

A

Giant cell

123
Q

Term used to describe a cell population with the highest regenerative capacity.

A

Labile

124
Q

Define hypoxia.

A

A state of low oxygen availability in tissues which causes cell injury due to reduced aerobic oxidative respiration.

125
Q

What type of cell death does prolonged hypoxia cause?

A

Necrosis

126
Q

Give 2 examples of causes of hypoxia.

A
  1. Anaemia
  2. Carbon monoxide poisoning
  3. Low oxygen due to altitude
  4. Cardio-respiratory failure
127
Q

Define ischaemia.

A

Hypoxia in localised tissue due to a reduction in blood flow.

128
Q

What is ischaemia most commonly caused by?

A

Arterial supply obstruction by:

  1. Severe atherosclerosis
  2. Thrombosis
  3. Embolism
129
Q

Which is more damaging and why, ischaemia OR non-ischaemic hypoxia?

A

Ischaemia.

As well as not having an oxygen supply, there is also a lack of metabolites e.g. glucose in ischaemia (no anaerobic respiration either).
Tissue is injure faster + more severely than generalised hypoxia.

130
Q

What is tissue necrosis caused by ischaemia called?

A

Infarction

= tissue necrosis as a result of ischaemia

131
Q

What is a rapid primary percutaneous coronary intervention (PCI) used to treat?

A

Myocardial ischaemia/infarction

like a stent which restores blood flow

132
Q

Is the reperfusion of non-infarcted but ischaemic tissues always a good thing to do?

A

No.
Tissue reperfusion is generally good, but sometimes it can cause a reperfusion injury.
This is when reactive oxygen free radicals are generated by a sudden reperfusion of the tissue which is harmful.

133
Q

What 3 pathological effects do free radicals have on a cell?

A
  1. Lipids in the membrane are degraded
  2. Proteins are broken down / damaged
  3. DNA is damaged resulting in mutations
134
Q

Following a coronary occlusion, how long does it take for the hearts contractile function to be lost?

1 min
2 min
5 min
6 min

A

2 minutes

135
Q

Which vessel type most commonly causes infarction?

A

Arterial

venous occlusion can also occur, but it is uncommon because smaller branches (collaterals) can open up and allow blood to bypass.
Venous obstruction can lead to congestion, but rarely causes infarction.

136
Q

Which organs are vulnerable to venous occlusion causing infarction?

A

Testis / Ovaries

single venous outflow (no collaterals to allow blood to bypass)

137
Q

What type of infarction is seen in tissue with a dual blood supply?

A

Red infarction (haemorrhagic)

Single blood supply = white infarction

138
Q

What is the typical shape of an infarct?

A

Wedge-shaped.

vascular supply in a tissue is up-stream, if there is an obstruction at the start of the ‘stream’, the entire downstream area will be infarcted which creates the wedge shape.

139
Q

What type of necrosis is seen in infarction?

A

Coagulative necrosis

liquefactive necrosis in brain

140
Q

What type of necrosis is seen in a patient who dies suddenly e.g. a massive heart attack?

A

Nothing.

no time to develop a haemorrhage or inflammatory response to the infarct.

141
Q

What does a myocardial infarction look like on examination and under the microscope:
after 3-4 days?

A

Gross feature:
Yellow

Microscopic:
Coagulative necrosis with macrophage infiltration

142
Q

What does a myocardial infarction look like on examination and under the microscope:
in the first 24 hours?

A

Normal

143
Q

What does a myocardial infarction look like on examination and under the microscope:
after 1-3 weeks?

A

Gross features:
Pale + thin

Microscopic:
Granulation tissue formation

144
Q

What does a myocardial infarction look like on examination and under the microscope:
after 3-6 weeks?

A

Gross features:
Dense fibrous scar

Microscopic:
Dense fibrous scar

145
Q

What does a myocardial infarction look like on examination and under the microscope:
after 1-2 days?

A

Gross features:
Pale red / oedematous

Microscopic:
Oedema + early neutrophil infiltration

146
Q

What is low-flow infarction?

A

Infarction in areas of DIMINISHED blood flow in vulnerable anatomical regions.

e.g. watershed regions in brain (point of anastomoses between 2 vascular supplies)

(blood flow hasn’t completely cut off, so they can still function, but as soon as something goes wrong there is an infarction)

147
Q

List 5 possible causes of infarction.

A
  1. Thrombosis
  2. Embolism
  3. Steal
  4. Hyperviscosity
  5. Compression
  6. Vasculitis
  7. Spasm
  8. Atheroma
148
Q

Define shock.

What does it lead to?

A

A pathophysiological state of reduced SYSTEMIC tissue perfusion resulting in reduced oxygen delivery to the tissues.

Your whole body isn’t receiving oxygen which leads to cellular hypoxia, incorrect cellular biochemistry, and eventually organ dysfunction.

149
Q

Why is the recognition and reversal of shock clinically very important?

A

Shock is initially reversible, but rapidly become irreversible. Need to act quickly.
The end result is multi-organ failure and death.

150
Q

Shock is essentially a decrease in mean arterial pressure (MAP).
What is the equation to work this out?

A

MAP = Cardiac output X Systemic vascular resistance

MAP = CO x SVR

Anything that causes a ↓ CO/SVR can cause shock.

151
Q

What is hypovolemic shock?

What is the pathological process which leads to this?

Hence, how does the body compensate for this?

A

Vascular fluid loss.

↓ blood volume > ↓ venous return to heart > ↓ stroke volume > ↓ cardiac output > ↓ MAP = shock

Vasoconstriction to ↑ SVR =
raises MAP

You look cold and clammy

152
Q

What are some causes of hypovolemic shock?

A
  1. Haemorrhage
    (e. g. trauma, GI bleeding, fractures, ruptured vessel, ruptured haematoma)
  2. Diarrhoea, vomiting, heat stroke, burns
  3. Third spacing
    (excess loss of fluid from vessels into interstitial space or ‘third’ non-functional space between cells)
153
Q

What type of shock is associated with cardiac pump failure?

How does the body compensate for this?

A

Cardiogenic shock

↓ Cardiac output = ↓ MAP

Vasoconstriction to ↑ SVR =
raises MAP

154
Q

What are the 4 categories of causes for cardiogenic shock and an example of each?

A
  1. Myopathic (heart muscle failure e.g. MI)
  2. Arrhythmia-related (abnormal electrical activity) e.g. impaired ventricular filling / contraction = ↓ CO
  3. Mechanical (defects to blood flow in the heart)
    e. g. valve defects, ventricular wall aneurysm, atrial myxoma (tumour)
  4. Extra-cardiac (anything outside of the heart which impairs blood flow in the heart)
    e. g. massive pulmonary embolism, tension pneumothorax, severe constrictive pericarditis
155
Q

What causes distributive shock?

How does the body compensate for this?

A

↓ SVR due to severe vasodilation.

↑ heart rate + ↑ stroke volume = ↑ CO

You have a raised temp

156
Q

What causes septic shock?

A

Severe systemic infection.

Huge ↑ cytokines results in vasodilation which leads to shock.

157
Q

What type of hypersensitivity reaction is an anaphylactic shock?

A

Severe Type I

massive mast cell degranulation = vasodilation

158
Q

What causes neurogenic shock?

A

Sympathetic vascular nerve supply is cut off e.g. spinal injury = vasodilation

159
Q

S. aureus / S. pyogenes produce ‘superantigens’ which cause septic shock.
True or False?

A

FALSE

cause toxic shock syndrome

160
Q

A type of inflammation involving the innate and adaptive immune system.

A

Chronic inflammation

acute = only innate

161
Q

What are the 3 characteristic cells of chronic inflammation?

A
  1. Macrophages
  2. Lymphocytes
  3. Plasma cells
162
Q

What are 3 signs associated with chronic inflammation?

A
  1. Amyloidosis - deposition of amyloid protein aggregates in organs around the body (due to prolonged cytokine stimulation) which affects their functioning.
  2. Cachexia - Muscle weakness + weight loss (use a lot of energy to fight chronic infection)
  3. Anaemia - Constantly elevated levels of cytokines affects iron + RBC production
163
Q

Give 4 examples of how chronic inflammation can arise.

A
  1. Acute inflammation lasts so long that it progresses to chronic inflammation e.g. Helicobacter pylori
  2. Recurrent episodes of acute inflammation with little time for recovery between them e.g. chronic cholecystitis
  3. Persistent infections by microorganisms that are difficult to remove e.g. TB
  4. Prolonged exposure to toxic agents e.g. asbestos fibres, broken bone stuck in tissue
  5. Autoimmunity e.g. Hashimoto’s thyroiditis
  6. Diseases with unknown causes e.g. ulcerative colitis, Crohn’s disease
164
Q

Where do macrophages originate from?

A

Bone marrow

circulate in the blood as monocytes, become macrophages when they enter tissue

165
Q 
Which of these are a type of macrophage?
Neutrophil
Kupffer cell
Eosinophil
Microglia
Alveolar macrophages
Osteoclasts
Fibroblast
A

Kupffer cells (liver)
Microglia (CNS)
Osteoclasts (bone)
Alveolar macrophages (lungs)

166
Q

What are the functions of macrophages?

A
  1. Phagocytosis
  2. Antigen presenting cells
  3. Release cytokines
  4. Stimulate collagen production (by fibroblasts)
  5. Stimulate production of new blood vessels
167
Q

Lymphocytes, plasma cells and fibroblasts are key cells in chronic inflammation.
What are they?

A

Lymphocyte = T cell or B cell (large nucleus)

Plasma cell = B cell that produces antibodies (dotty nucleus, looks like a clock)

Fibroblasts = Produce collagen + ECM (long thin nucleus, surrounded by dense pink collagen)

168
Q

If eosinophils + mast cells are present, what is the likely cause of the chronic inflammation?

A

Due to an allergy or parasitic infection

169
Q

Angiogenesis and scarring in chronic inflammation are features of what?

A

Granulation tissue

170
Q

What does granulation tissue look like under a microscope?

A
  1. Lots of blood vessels
  2. Lots of black dots (lymphocyte nucleus’)
  3. A lot of pink material (collagen)
171
Q

How do monocytes enter a target tissue?

A

Vasodilation and change in blood flow = monocytes adhere to vessel wall and emigrate between endothelial cells into tissue.

172
Q

What is a granuloma?

A

A collection of activated epithelioid (look like epithelial cells) macrophages

173
Q

How are macrophages activated?

A

Activated by cytokines released from T-cells

174
Q

What are the features of a granuloma?

A
  1. Pink cytoplasm
  2. Indistinct cell membranes (can’t really tell where the outlines of the cells are)
  3. Oval nucleus
175
Q

What term is used for a granuloma with a necrotic centre?

A

Caseating

caseous = necrosis with a cream cheese consistency

176
Q

Many macrophages fused together.

A

Giant cell (have many nuclei)

may be present in a granuloma

177
Q

How does the structure of an early granuloma differ from a mature granuloma?

A

Both have macrophages surrounded by lymphocytes/plasma cells.

Mature granuloma:

  1. May have caseous necrosis at centre.
  2. Fibroblasts producing collagen in outer layer.
178
Q

How is granulomatous tissue formed?

A
  1. Macrophages try to phagocytose material they are not capable of.
  2. More macrophages are recruited to help (influx).
  3. Macrophages keep releasing cytokines, reactive species, enzymes which results in tissue necrosis
179
Q

Give 5 categories and their associated diseases which cause granulomatous inflammation.

A
  1. Bacterial (TB, leprosy, cat-scratch, syphilis)
  2. Parasitic (schistosomiasis)
  3. Fungal (histoplasma, cryptococcus)
  4. Inorganic metals or dust (silicosis, berylliosis)
  5. Foreign body (sutures, vascular graft)
  6. Diseases which unknown causes which cause granulomas (sarcoidosis, ulcerative colitis)
180
Q

Define atheroma.

A

A fatty deposit in the inner lining (intima) of an artery, it has a lipid core covered by a fibrous cap.

181
Q 
Atheromas commonly occur at bifurcations. Out of these commonly affected sites, where do atheromas occur most often?
Abdominal aorta
Coronary arteries
Popliteal arteries
Carotid vessels
Circle of Willis
A

Abdominal aorta

182
Q

These are the risk factors for atheroma:

Hyperlipidaemia
Age
Gender
Hypertension
Family history
Genetic abnormalities
Smoking
Diabetes
C-reactive proteins

Which of these are modifiable?

A 
Hyperlipidaemia (diet)
Hypertension (diet)
Diabetes (diet)
Smoking
C-reactive proteins (treating inflammation)
183
Q

What is atherosclerosis and what can cause it?

A

Atherosclerosis is the hardening of an artery due to an atheroma.
It begins due to damage of the inner layer of an artery which can be caused by:
1. High blood pressure
2. High cholesterol
3. Irritants e.g. nicotine (releases free radicals)
4. Certain diseases e.g. diabetes

184
Q

What is the response to injury hypothesis of atheroma formation?

A
  1. Chronic injury to endothelial layer of vessel.
  2. This layer is now permeable to blood, platelets, monocytes, inflammatory cells etc to enter the intima layer.
  3. Smooth muscle cells also start to migrate into intima.
  4. Lipoproteins carrying lipids/cholesterol enter and are eaten by macrophages to become foam cells.
  5. Smooth muscle cells + collagen proliferate to form a hard cover, this narrows the artery = ↑ BP ↓ blood flow
185
Q

What is the earliest lesion in atherosclerosis?

A

Fatty streak

these don’t actually affect blood flow and not all fatty streaks progress to become atheromas, but a good portion do.

186
Q

What is the sequelae (sequence) of atherosclerosis?

hint: what are the possible outcomes of atherosclerosis

A
  1. Rupture, ulceration or erosion - of atherosclerotic plaque results in thrombogenesis (coagulation of blood).
  2. Haemorrhage can occur into the atherosclerotic plaque.
  3. Atheroembolism - the thrombus formed can embolise.
  4. Aneurysm - due to weakening of vessel wall.

RHAA

187
Q

Define thrombus.

A

A solid mass of blood constituents formed within the vascular system.

188
Q

Compare Arterial thrombus vs. Venous thrombus.

Mechanism of formation?
Location?
Associated diseases?
What are they composed of?
How are they treated?
A

Arterial thrombus:

Mechanism - typically from the rupture of an atheromatous plaque.
Location - L heart chambers + arteries
Diseases - acute coronary syndrome, ischaemia/stroke, claudication (cramping pain due to blocked arteries)
Composition - Mainly platelets
Treatment - anti-platelets (clopidogrel, aspirin)

Venous thrombus:

Mechanism - combination of factors from Virchow’s triad
Location - venous sinusoids of muscles + valves of veins
Diseases - DVT, pulmonary embolism
Composition - mainly fibrin
Treatment - anticoagulants (heparin, warfarin)

189
Q

What is Virchow’s triad composed of?

A
  1. Endothelial injury / vessel surface (smoking, hypertension, trauma, surgery, catheter)
  2. Hypercoagulability (genetic, cancer, obesity, pregnancy, chemotherapy)
  3. Abnormal blood flow / stasis (immobility, polycythemia)
190
Q

What is the difference between a blood clot and a thrombus?

A

Blood clot = NO platelets, can occur inside AND outside a vessel, red, gelatinous, NOT attached to vessel wall (can be dislodged)

Thrombus = Platelets, occurs ONLY inside a vessel, red (venous) / pale (arterial), firm, ATTACHED to vessel wall

191
Q

What is the sequelae (sequence) of thrombosis?

hint: possible events that follow

A
  1. Occlusion of vessel - cause ischaemia
  2. Dissolve
  3. Incorporate into vessel wall - adding to astherosclerotic plaque
  4. Recanalisation - tiny tubes penetrate thrombus to allow blood flow
  5. Embolism

ODIRE

192
Q

Define embolus.

Give 4 examples of emboli.

A

A mass of material which can travel through the vascular system and lodge itself in a vessel and block it.

  1. Thrombus derived (most common)
  2. Fat
  3. Air
  4. Atheromatous plaque material
  5. Tumour fragments
  6. Amniotic fluid

Y2 EMS (4 decks)

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