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121 > Module 1C > Flashcards

Module 1C Flashcards

1
Q

Abbreviations (IL, TNF, IFN, GF, GM_CSF, PRN, OTC, IBD, SC, COX,NK cells, VLA-4, VCAM-1)

A
  • IL: interleukin
    • TNF: tumour necrosis factor
    • IFN: interferon
    • TGF: transforming growth factor
    • GM_CSF: granulocyte-macrophage colony-stimulating factor
    • PRN: as needed
    • OTC: over the counter
    • IBD: inflammatory bowel disease
    • SC: subcutaneous
    • COX: cyclooxygenase
    • NK cells: natural killer cells
    • VLA-4: very late antigen 4
    • VCAM-1: vascular adhesion molecule 1
      CYP450: cytochrome P450 enzyme system
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2
Q

What is inflammation

A
  • A physiological response to infection or tissue injury
    -Can be acute or chronic(long)
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3
Q

Is inflammation present in almost all conditions or diseases

A

Yes

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4
Q

does inflammation= infection

A

no

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5
Q

What are the signs of inflammation

A
  • Pain
    • Heat
    • Redness
      • Swelling
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6
Q

Why does the acute inflammatory response happen

A
  • Restricts damage to the localize site
    • Recruits immune cells to kill pathogens
      • Start wound repair
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7
Q

How long does the acute inflammatory response last

A
  • 24-48 hours
    -Mild and localized
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8
Q

What happens within inflammation within minutes of injury

A

Plasma proteins are activated from clotting and kinin systems

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9
Q

What activates plasma proteins

A

Clotting and kinin systems

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10
Q

what is clotting

A
  • The production of fibrin strands that accumulate to stop the spread of possible infection or bleeding to the outside
    -Keeps everything local
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11
Q

What is a kinin:

A

Produced bradykinin which induces vasodilation and increases permeability

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12
Q

What is bradykinin

A
  • Produced by kinin
    • Increases permeability and vasodilation in blood vessels
      • Allows for cells to go from blood to tissues easier
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13
Q

What do granulocytes contain

A

Contain substances that can kill a pathogen and enhance the inflammatory response

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14
Q

What do mast cells do within acute inflammation

A
  • Degranulate
    -This leads to a release of histamine and activates prostaglandins and leukotrienes
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15
Q

How does vasodilation aid in acute inflammation

A
  • It increases blood flow to the affected area
    • This leads to head, redness, and swelling (edema)
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16
Q

How does acute inflammation result in pain

A
  • The swelling and activation of nociceptors result in pain
    -It is a by product of the original injury from a nociceptor and swelling can cause pain also
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17
Q

What is diapedesis

A

The movement of leukocytes out of the blood into the site of infection or tissue damage

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18
Q

What are the 4 steps of diapedesis

A
  • Chemoattraction
    • Rolling adhesion
    • Tight adhesion
      • Transmigration
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19
Q

What is chemoattraction

A
  • Various inflammation mediators are release earlier
    Mast cells..
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20
Q

What is rolling adhesion

A
  • Carbohydrate chains on the surface of the neutrophil cause leukocytes to roll on the edge of the blood vessel rather then the middle
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21
Q

What is tight adhesions

A
  • Multiple cytokine and integrin receptors (depends on location)
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22
Q

What is transmigration

A

The leukocytes try to squeeze past the blood vessels

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23
Q

Where can leukocytes adhere to (undergo diapedesis)

A

Can only adhere to veins and not crawl through arteries

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24
Q

Different types of tissue injury

A
  • Physical agent
    • Chemical agent
      • Pathogenic microorganisms
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25
Q

Mediators of Inflammation

A
  • Capillary dilation->increased blood flow (Heat)
    • Increased capillary permeability->extravasation of fluid (Redness)
    • Attraction of leukocytes-> migration of white cells to site of injury (Swelling)
      • Systematic response->fever and leukocytes (pain)
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26
Q

What happens after leukocytes are in the tissue

A

Leukocytes phagocytize the invading pathogens and release mediators

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27
Q

What mediators are released during acute inflammation

A
  • Cytokines
    • Histamine
    • Prostaglandins
    • Leukotrienes
    • The mediators further contribute by recruiting and activating more cells, induces coagulation, further increase vascular permeability
28
Q

What is chronic inflammatory response

A
  • Continues after the acute response, cleans up debris, and facilitates healing process
    • A result from continuous exposure to offender (pathogen persistence, autoimmune disease, cancers
29
Q

What is chronic inflammatory response characterized by

A
  • The accumulation and activation of macrophages and lymphocytes, as well as fibroblasts that replace the original, damaged or necrotic tissue
30
Q

What is fibrosis

A
  • An excessive deposition of fibrous connective tissue that interferes with normal tissue function (scaring)
    • No function
31
Q

How to deal with chronic inflammation

A
  • The inflammation has now lost its helpfulness
    • Need pharmacotherapy and involves anti inflammatory
    • Want to reduce inflammatory trigger
32
Q

When treating chronic inflammation do we want to stop all inflammation?

A
  • No we don’t
33
Q

When and how are inflammatory mediators released

A
  • Released and generated during immune responses to coordinate and regulate immune cell activities
    • They are in a preformed state in granules (like granulocytes) or synthesized at time of cellular activation
34
Q

What can inflammatory mediators all do?

A
  • Have antiviral, pro inflammatory or anti inflammatory activities
    • Regulate processes
    • Self regulate
    • Can act both locally or systemically
    • They guide other cells where to go (chemoattraction in diapedesis)
35
Q

What are the four inflammatory mediators (not all of them)

A
  • Cytokines
    • Histamine
    • Prostaglandins
      • Leukotrienes
36
Q

What are cytokines

A
  • Soluble factors secreted by immune cells that are activated
    -Can be organized based on there activities
37
Q

Four groupings of cytokines and there activities

A
  • 1: promote inflammation and mediate natural immunity (recruit more cells to area, so can inhibit this group to stop some inflammation)
    IL-1, IL-6, IL-8, TNF, IFN-a
    • 2: support allergic inflammation
      IL-4, IL-5, IL-13
    • 3: Immunoregulatory activity (slow it all down, recruited late on and clean everything up after its all done, if we want to reduce inflammation we can try to boost these cells)
      IL-10, IL-12, TGF-B, IFN-y
    • 4: act as hematopoietic growth factors (tell us to get more cells, drugs can be used to affect this so it increase the amount of cells generated)
      IL-3, IL-7, GM-CSF
38
Q

What are biologics

A
  • Drugs that are produced by using biological processes
    • Complex large molecules
    • Examples are hormones, vaccines, interferon
39
Q

How do we use antibodies to target

A
  • Monoclonal antibodies can use antibodies to targe specific receptors or pathogens
    • Can attach a drug to an antibody which allows the antibody to only target specific cells and thus the drug only targets those specific cells
    • This can make therapy more effective and minimize adverse effects
40
Q

What is a way that IBD is treated

A
  • Inflammatory bowel disease
    • Infliximab (Remicade): tumour necrosis factor (TNF)- a inhibitor
    • The TNF-a inhibitor is involved in inflammation and immune responses and is in very high levels in IBD
    • Biologics have many indications and target TNF to reduce the active amounts
41
Q

What is multiple sclerosis and how is it treated

A
  • It is when immune cells destroy the myelin sheath which surrounds the axon of neurons
    • Natalizumab is a monoclonal antibody which binds to and blocks a4 integrin
    • It inhibits rolling adhesion so white blood cells are unable to get through the blood vessel and attack the neuron causing damage
42
Q

What are Histamines

A
  • A bioactive amine which is packaged into dense intracellular granules
    • Mast cells are famous for releasing it
    • When histamine is released it binds to histamine receptors
43
Q

Types of histamine receptors and there uses (what happens when you block these)

A
  • H1: within smooth muscle of the vascular system, bronchial tree, digestive track and nasal glands
    Causes allergies, allergic reactions
    Blocking H1 receptors helps with allergic rhinitis symptoms
    • H2: lining of stomach and produces gastric acid
      Blocking these reduced the amount of acidity within the stomach
    • H3: within the CNS and involved in releasing neurotransmitters such as dopamine, GABA, acetylcholine, noradrenaline, serotonin
      There is no way of blocking these as of now
44
Q

1st and 2nd generation antihistamines

A
  • 1st: block H1 receptors, shorter acting, cause drowsiness, work faster, usually used to treat allergic response
    • 2nd: longer acting, less sedating, take longer to start working, can be used everyday
45
Q

What does arachidonic acid do and where is it released from

A
  • It is released from immune cell membranes
    • It is metabolized in two different ways to generate prostaglandins/ thromboxane or leukotrienes
46
Q

What is the pathways that generate prostaglandins/ thromboxane’s vs leukotrienes

A
  • Prostaglandins= cyclooxygenase pathway
    • Leukotrienes= lipoxygenase pathway
47
Q

What are prostaglandins

A
  • Generated from arachidonic acid through the cyclooxygenase pathway
    • Have many functions including constrict/ dilate vascular smooth muscle cells, cause aggregation/ disaggregation of platelets, induce labour, release during menstruation, play an important role in mucosal production in Gi tract, act on thermoregulatory centre to produce fever
48
Q

What is cyclooxygenase (COX)

A
  • Enzyme that converts arachidonic acid to prostaglandins
    • COX-1: in all tissues and involved in platelet aggregation
    • COX-2: more specific for inflamed tissue
49
Q

Drugs that affect prostaglandins

A

NSAIDS (non steroidal anti inflammatory)

50
Q

What do NDAIDs do

A
  • Inhibit cyclooxygenase (COX)
    • This reduces prostaglandin synthesis which then inhibits inflammation
    • Have analgesic and antipyretic properties
    • Can be used to treat mild to moderate inflammation, fever, dysmenorrhea (period cramps), platelet inhibition
51
Q

What are classic NSAIDs vs COX-2 inhibitors

A
  • Classic NSAIDs: inhibit both COX-1, and COX-2
    Ibuprofen, naproxen
    • COX-2 inhibitors: more specific to inflamed tissue
52
Q

Should we take NSAIDs before or after we get pain/inflammation

A
  • Should take them before as they inhibit COX and this produces less prostaglandins
    • If we take them after pain there is already prostaglandins that were produced from COX
53
Q

What is Analgesic

A

Acting to relieve pain

54
Q

What is antipyretic

A

Used to reduce fever

55
Q

Adverse side effects of classic NSAID and COX-2 inhibitors

A
  • Classic NSAID: nausea, dyspepsia, ulcer with long term use, anti platelet action, hypertension, increase risk of cardiac events
    Can take with food and take on an as needed basis whenever possible to reduce side effects
    • COX-2 Inhibitor adverse effects: fewer GI issues but same in kidney and CV
56
Q

What are leukotrienes

A
  • Generated from arachidonic acid through the lipoxygenase pathway
    • Mostly active in smooth muscle lining of the bronchioles
    • Contribute significantly to the pathophysiology of asthma
57
Q

How do leukotriene contribute to asthma

A
  • Airflow obstruction
    • Increased secretion of mucous
    • Bronchoconstriction
    • Infiltration of inflammatory cells in airway
58
Q

What does Montelukast do

A
  • A drug affecting leukotrienes
    • Leukotriene receptor antagonists (LTRAs)
    • Reduces inflammation by blocking leukotriene receptors
    • Is preventative and doesn’t work fast enough for immediate relief
    • Adverse effects include headache, cough GI upset
    • Must be taken daily to work
59
Q

All the drugs that affect inflammation 5 types

A

• Cytokines
- Biologics (immunosuppressant/stimulant, anti-inflammatory….
• Histamine
- Antihistamines (H1)
- H2- receptor antagonists (H2RAs)
• Prostaglandins
- Non steroidal anti inflammatory drugs (NSAIDs)
• Leukotrienes
- Leukotrienes receptor antagonists (LTRAs)
• Cortisol
- Corticosteroids

60
Q

What is cortisol

A
  • A hormone released in response to stress
    • Job is to return body back to homeostasis
    • Two main effects are anti inflammatory and immunosuppressive
61
Q

Where does cortisol have receptors

A
  • All over the body and in every situation there will be the indication for the drug and adverse effects
62
Q

Explain cortisol’s anti-inflammatory MOA

A
  • Decrease production of phospholipase A, this decreases production of prostaglandins, leukotrienes, thromboxane’s
    • Decreased leukocytes means less recruitment of leukocytes to site of injury
    • Decreased bactericidal activity of phagocytes and stabilizes mast cells
63
Q

Explain cortisol’s immunosuppressant MOA

A
  • Induce apoptosis of T cells
    • This means less T cell recruitment to site of antigen
    • This increases T cell redistribution to lymph nodes and there is no B cell effects from cortisol
64
Q

What is corticosteroid and some uses

A
  • It is a synthetic version of cortisol (mimic human endogenous cortisol)
    • Has many different uses such as asthma or allergies
65
Q

Three type of corticosteroids (not all of the drugs)

A
  • Short acting: hydrocortisone, cortisone
    • Intermediate acting corticosteroids: methylprednisolone, prednisone
    • Long acting corticosteroids: betamethasone, budesonide
66
Q

Different routes of administration for corticosteroids

A
  • There are different ways to administrate to attempt to minimize adverse effects
    • Always try to use the most local way
    • Otoc (ear)
    • Oral
    • injectable
    • Inhalation
    • Topical
    • Ophthalmic (eye)

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