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Medicine 1 > Week 10 - Infection and inflammation > Flashcards

Week 10 - Infection and inflammation Flashcards

1
Q

What are the 5 cardinal symptoms associated with tissue damage?

A
  • Redness
  • Pain
  • Heat
  • Loss of function
  • Swelling
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2
Q

What substances are involved in vascular resistance / arteriolar tone?

A

Noradrenaline + sensory nerves = constrictor / dilator factors

Endocrine and pancreatic hormones

pO2 + pCO2

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3
Q

What happens during the acute imflammatory state?

A

Inflammatory vasodilators override arteriolar tone influencers (from tissue fluid, tissue cells, nerve endings, leukocytes)

Histamine (skin mast cells –> vasodilation)-REDNESS

Bradykinin (vasodilation and endothelial prostaglandin release + stimulation of nociceptors)-PAIN

Vasodilator peptides in sensory nerves (substance P, VIP, CGRP)

Each = + blood flow and temperature

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4
Q

What happens during microcirculation in acute extravasation?

A

All cells = contractile elements

Arteriolar endothelium = even protein distribution

Venular endothelium = selective distribution around pores

Venular site = low hydrostatic pressure and large SA

Oedema from plasma protein and fluid leakage into extracellular space -SWELLING

Endothelial damage

Postcapillary venule pore modulation

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5
Q

What happens during microcirculation in intermediate extravasation?

A

Acute inflammation = =2 hours

Tumour necrosis factor released

Complement 5 activation, attracting neutrophils to site of injury

Cytokines activate vascular endothelium and interleukin-8 release

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6
Q

What happens during acute modulation of venular permeability when it is + and -?

A

+ venular permeability = Ca2+ elevated, contracting pore proteins

Histamine, Bradykinin, Leukotriene C4 / D4, Platelet activating factor

  • venular permeability = pore proteins relax by cyclic AMP

‘B’2-adrenoceptor agonists, PGI2

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7
Q

What happens during the triple response?

A

Flush – histamine release from mast cells and vasodilation

Flare - + vasodilation and redness, sensory nerve orthodromic activation (pain + itching), antidromic activation of branches –> P, CGRP, VIP release

Wheal – oedema in damaged area, protein extravasation

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8
Q

What happens during neutrophil-dependent extravasation?

A

Release of IL-8 from activated endothelium

Stimulate neutrophil G protein coupled chemokine receptor

Permits interaction between integrin and endothelial Ig CAM

Promotes adhesion of neutrophil to endothelium (2 hours after injury)

Neutrophils cross endothelium (diapedasis) and migrate towards chemoattractant at site of injury

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9
Q

What happens when there are + neutrophils?

A

+ phospholipase A2 regulation and cyclooxygenase–2 induction

+ blood flow

IL-1 and TNF release, activating endothelial receptors

Endothelial-leukocyte adhesion molecule production for monocytes –> conversion into macrophages

Induction of Nitric Oxide Synthase II

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10
Q

What happens during the late phase?

A

Cytokines from activated neutrophils and macrophages = degradation of damaged tissue + site of injury preparation for healing

Breakdown of tissue for repair = lead by leukocyte production of proteolytic enzymes and oxygen radicals

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11
Q

What is the role of cytokines in injury response?

A

Act centrally to pyrogenic response –> receptors in hypothalamus (fever)

Elevate corticosteroids as ‘stress response’, promoting inflammation in short-term

+ hepatic protein

Bone marrow stimulation

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12
Q

What happens during the proliferative / granulation phase?

A

Growth factors produced by macrophages and platelets

Granulation of tissue caused by proliferation of + cells

Macrophages, fibroblasts + neovascularisation = in loose collagen matrix

Failure to stop phase = rheumatoid arthritis, scleroderma –> calcification and ossification of cartilage

Fibroblasts = produce collagen for structure

Blood vessel proliferation = for oxygen and nutrient supply

Cell movement in site of injury stimulated by metalloproteinases

Angiogenesis = inhibited by methotrexate

Affected by sex hormones

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13
Q

What happens during the maturation phase?

A

Remodelling of tissue

Macrophages involved

Reduced vascularisation = - nutrient demand and – tissue metabolic activity

Collagen remodelling and reinnervation by nerves = + tissue strength and sensation

Scar tissue = caused by lack of elastin

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14
Q

How do NSAIDS work?

A

Cyclooxygenase inhibitors:

  • Reduces inflammation by supressing PG synthesis
  • Reduce vasodilation and hyperaemia
  • Reduce hydrostatic pressure in venules
  • Reduce protein leakage into extracellular space
  • Reduce pain
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15
Q

How do glucocorticoids work?

A
  • Inhibit inflammation with long-term treatment
  • Reduced cell adhesion molecule expression
  • Reduced chemotaxis of neutrophils
  • Reduced cytokine production
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16
Q

How do selective COX-2 inhibitors work?

A
    • prostanoid and thromboxane A2 levels
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17
Q

What are the functions of skin?

A

External damage protection (UV)

Barrier (waterproof)

Sensation

Metabolic (subcutaneous fat energy store)

Thermoregulation (insulation)

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18
Q

What are the 3 layers of the skin and how are they structured?

A

Epidermis (epithelium) –> stratified squamous keratinised

Dermis (connective tissue) –> dense, irregular connective tissue (fibroblasts, collagen I, elastin, blood, nerves, receptors), divided into papillary and reticular dermis

Hypodermis / subcutis (fascia) –> adipose tissue and main blood supply

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19
Q

What are the 5 epidermis keratinocyte layers?

A
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20
Q

What are the epidermis barriers?

A

Tight junctions (prevent paracellular diffusion)

Desmosomes and hemidesmosomes (mechanical and sheer)

Keratin (microorganisms)

Phospholipid (waterproof)

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21
Q

How do the 5 epithelial keratin layers form?

A

Basal layers divide

Differentiate as they rise through layers

Intermediate layers produce keratin and lose organelles and nucleus, becomming stratum corneum flattened cells

Hemidesmosomes tether basal layer to dermis

Intermediate layers have + desmosomes

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22
Q

What are the types and properties of keratinocyte cancers?

A

Basal cell carcinoma (approx. 80%) from basal layer

Squamous cell carcinoma (approx. 20%) from upper epidermal layers

Both are curable

Linked to total cumulative sun exposure

Common on head, neck and hands

In people of all skin colours

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23
Q

What are the properties of keratinocytes and melanocytes?

A

Keratinocytes: 95% of cells

Stratified squamous keratinising epithelial cells

Produce keratin

Melanocytes:

pigment synthesising cells responsible for skin and hair colour

Neural crest derived cells lying in the stratum basale

Melanosomes in cytoplasm contain melanin and are passed to keratinocytes – scattering of UV light

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24
Q

What are the properties of langerhans cells and merkel cells?

A

Langerhans cells:

All layers and upper dermis-prominent in spinosum. Bone marrow derived. Dendritic, antigen presenting cells-migrate to regional lymph nodes and communicate with the immune system.

Merkel cells:

Clear cells in stratum basale. Plentiful in touch areas. Connected to keratinocytes and afferent nerves. Neuroendocrine function

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25
Q

What are the 4 skin cell types?

A

Keratinocytes

Melanocytes

Langerhans cells

Merkel cells

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26
Q

What are examples of skin pigmentation disorders?

A

Lentigo maligna

Albinism: Lack of melanin due to lack of enzyme required to make melanin: tyrosinase

Vitiligo: macules of de-pigmented skin enlarging over time. Cause unknown

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27
Q

What are the properties of a melanoma?

A

Asymmetry

Border

Colour

Diameter

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28
Q

How does the skin stay on?

A

+ surface area from interdigitation between epidermis and dermis

Epidermis and dermis adhered by hemidesmosomes

Basement membrane between epidermis and dermis

29
Q

What are the properties of the dermis?

A

Dense connective tissue:

collagen 70%

Papillary: conical papillae (rete ridges), richly vascularised (capillaries), lymph and nerve

Reticular: Horizontal collagen and elastin fibres

Contains hair and gland structures

30
Q

How is skin varied?

A

Thin skin:

  • Most locations
    • eccrine glands and thin keratin layer
  • Less well defined rete ridges

Thick skin:

  • Fingertips + soles of feet
  • Thick epidermis and keratin layer and well developed rete ridges
    • eccrine glands, no hair

Hairy skin:

  • Thin epidermis and lots of hair follicles and sebaceous glands
31
Q

What are the skin specialisations?

A
32
Q

What is the main virus structure?

A

Simple

Nucleic acids

Proteins

Lipids

No organelles

33
Q

What are the properties of virus metabolism?

A

Metabolically inert

Rely on host cell

Are obligate intracellular parasites

34
Q

What are the properties of virus replication?

A

Independent component part synthesis

Can be in separate parts of cell

Under separate control

Assembly into new particles

35
Q

What are the properties of virus nucleic acids?

A

DNA –> double / single stranded, circular / linear, 3kb-200kb

RNA –> ds / ss, ss = +ve / -ve polarity, linear / segmented, 5kb-10kb

36
Q

What are the functions of proteins in viruses?

A

Capsid formation –> symmetry (icosahedral / helical)

Attachment –> specific cellular receptor and viral ligand interaction, determines viral tropism (preference to infect certain cell types)

Enzymes –> macromolecular synthesis enzymes

Interference with cell function –> i.e. stop apoptosis, avoid immune recognition

37
Q

What are the functions of the lipid envelope of viruses?

A

From host cell membranes

Needs to contain external attachment proteins

Loss of infectivity if envelope stripped

Virus more fragile if enveloped

38
Q

What is virus clasification based on?

A

Nature of genetic material

Nature of capsid

Enveloped

Size / shape

Families, genera, strains

39
Q

What are the stages of viral replication?

A

Attachment (cellular receptor / viral ligand)

Entry (endocytosis, fusion)

Uncoating

Macromolecular synthesis (multiple viral genome and viral protein copies (requiring +ve ss RNA))

Assembly

Release (budding (yielding enveloped virus), cell lysis)

40
Q

What is a virion?

What is positive / negative polarity of RNA?

What is a viral tropism?

A

Virion = mature virus particle –> nucleic acid, protein coat (capsid), lipid envelope

-ve polarity = can be translated at a ribosome

Viral tropism = specificity of a virus to a specific host cell

41
Q

What are the anti-viral effects of antibodies?

A

Antibodies = block entry and binding to cells, activate intra-cellular degradation via TRIM21

Antibodies + complement = damage enveloped viruses, opsonisation for phagocytosis

Antibody bound to infected cells = antibody-dependent cellular cytotoxicity

42
Q

What is antigenetic shift?

A

Recombination between 2 different viruses, forming a totally new one

43
Q

What are the functions of interferons?

A

Type 1 = enhance HLA class 1 protein expression and activate natural killer cells

Interferons produced by infected cells bind to receptors on uninfected cells

Uninfected cell is resistant to viral cell replication

Protein synthesis is inhibited in cell and viral mRNA is degraded

44
Q

How do cytotoxic T cell work?

A

Have CD8 receptors on surface

Viral cell proteins degraded by protease, forming peptides

Peptides are expressed on infected cell surface HLA class 1 proteins

Cytotoxic T cells bind to the HLA class 1 protein and kill infected cell

45
Q

How do natural killer cells work?

A

Have kill activating receptor molecules

Have kill inhibition receptor molecules too

Binding to normal cell = don’t kill as stronger inhibition signal

Abnormal cells = kill signal is dominant

46
Q

How is an enveloped RNA virus formed?

A
47
Q

What are the criteria for screening a population?

A
  1. The condition sought should be an important health problem
  2. There should be an accepted treatment for patients with recognized disease, and treatment should be better at an earlier stage
  3. Facilities for diagnosis and treatment should be available
  4. There should be a recognizable latent or early symptomatic stage
  5. There should be a suitable test or examination
  6. The test should be acceptable to the population
  7. The natural history of the condition, including development from latent to declared disease, should be adequately understood
  8. There should be an agreed-upon policy on whom to treat as patients
  9. The cost of case-finding (including diagnosis and treatment of patients diagnosed) should be economically balanced in relation to possible expenditure on medical care as a whole
  10. Case-finding should be a continuing process and not a “once and for all” project.
48
Q

What are the benefits of screening programmes?

A
  1. Screening may produce earlier diagnoses
  2. Earlier diagnosis may improve prognosis for those who develop disease
  3. In some cases disease may be prevented
  4. If treating early is cheaper than treating late, then screening may sometimes save money
49
Q

What are the disadvantages of screening programmes?

A
  1. Screening programmes cost money
  2. Screening may induce anxiety in the well
  3. Tests my cause harm directly
  4. No screening test will detect all disease
  5. A screen negative patient may delay presenting symptomatic disease if falsely reassured
  6. There will be false positives
  7. There will be over diagnosis
50
Q

What is lead time bias?

A

Time between when a disease can be detected through screening and when it can be clinicaly detected

51
Q

What is length bias?

A
52
Q

What are the 4 outcomes of virus infection?

A

Cell death –> cytolytic or cytocidal infection (Rhinovirus)

Chronic infection –> continuous viral replication in cell, cell survives (Hep B)

Latency –> No replication of virus, no viral protein production, always infected once infected, reactivation of virus replication can occur, primary and secondary infections (herpes)

Transformation –> cell immortalisation (Epstein-Barr virus)

53
Q

How are viruses spread to hosts?

A

Skin

Mucosal surfaces

Respiratory tract

Gastrointestinal tract

Placenta

54
Q

How are viruses spread within hosts?

A

Skin – vesicles

Respiratory tract – droplets

Gastrointestinal tract – saliva, faeces

Urogenital tract – urine, semen, female genital tract secretions

Blood – BBV incl HBV, HCV, HIV

Breast milk

55
Q

What is cytolytic infection?

What is cytopathic effect?

A

Where a cell is destroyed

Change in host cell structure caused by viral infection

56
Q

What happens during hypertrophy?

A

Increase in the size of cells

Can be physiologic/pathologic

No new cells-just bigger

Cells that don’t divide e.g. Cardiac and skeletal muscle

Examples: exercise, hypertension

57
Q

What happens during hyperplasia?

A

Increase in the number of cells

Breast development at puberty/liver regeneration after resection/wound healing

Eg psoriasis leads to thickened skin

58
Q

What do hypertrophy and hyperplasia both result in and when do they occur at the same time?

A

Both adaptations individually result in enlargement of tissue

Example of both together:

Uterine enlargement (hypertrophy) during pregnancy is a consequence of smooth muscle hypertrophy and hyperplasia

59
Q

What is atrophy?

A

Shrinkage in cell size due to loss of cell substance

Functionally diminished but alive

Eg immobilised or aging limb muscle

60
Q

What is involution?

A

Reduction in number of functioning cells

Due to reduction in functional demand (myometrium of uterus post partum)

Usually by programmed cell death (apoptosis)

61
Q

What is metaplasia?

A

Change in type of cell - reprogramming of stem cells

Survival mechanism in response to injury e.g. Smoking

Specialised function is lost

Can predispose to neoplasia

Reversible

+ cancer risk

62
Q

What is the purpose of acute inflammation?

A

A protective mechanism that functions to:

Eradicate cause of injury

Remove damaged cellular material

Initiate repair process

63
Q

What are the 3 steps of acute inflammation?

A

1. Vasodilation

Slowing the local blood flow to the area

(allowing time for plasma containing mediators to leave and for neutrophils to come into contact with the vessel wall)

Enabling cells to contact the capillary endothelium

Generating heat and redness

2. Increased vascular permeability

Allowing plasma carrying mediators out

Causing swelling (oedema/tumor/turgor)

3. Cellular activation and migration

Neutrophils are activated to migrate from the vessels. They have a great capacity for phagocytosis

Short lived so need to be replaced

64
Q

What are the outcomes of acute inflammation?

A

Resolution –> minimal damage, normal tissue restored

Repair –> damage too severe (scar forms)

Chronic inflammation –> persistent stimulus

Abscess forms

65
Q

What are the 3 types of cells?

A

Labile – replicate throughout life –> i.e. skin (resolve)

Stable – Non-dividing in normal circumstances but capable of regeneration –> i.e. liver and kidney (resolve or scar)

Permanent – non-dividing cells –> i.e. neurons and heart (always scarring)

66
Q

What happens during fibrosis?

A

Granulation tissue –> macrophages + fibroblasts + new blood vessels

Fibrosis + scar formation –> matrix laid down by fibroblasts, + collagen laid down forming scar to strengthen tissue

Remodelling –> reduction in number of vessels so pale scar remains

67
Q

What is the process of wound healing?

A

Inflammatory phase –> macrophages producing growth factors for next phase

Proliferative phase –> granulation tissue, fibroblasts secrete matrix components + growth factors for angiogenesis, regrowth of epithelial cells over wound

Remodelling –> - vascularity, wound contraction

68
Q

What are the functions of growth factors?

A
  • Mediators of repair
  • Stimulate cell proiliferation, differentiation and maturation
69
Q
A

Medicine 1 (28 decks)

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