Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PM2C: Therapeutics and Patient Care: Autumn > Cellular Interactions > Flashcards

Cellular Interactions Flashcards

1
Q

What is the inflammatory response for?

A
  1. First line of defence that’s part of the inate immune system
  2. Protects against injury
  3. Protects against infections
  4. Promotes healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 5 cardinal signs of inflammation?

A
  1. Redness
  2. Heat
  3. Swelling
    (due to increase blood flow to the area)
  4. Loss of function
  5. Pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the 3 sections of the skin structure?

A
  1. Epidermis
    - Keratinocytes
  2. Dermis
    - Fatty tissue - connective tissue
    - Capillaries
  3. Subcutaneous Layer
    - Fat
    - Larger blood vessel and nerves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What occurs when there’s an injury to the surface of the skin?

A
  1. Clots and exudate- neutrophils gather and haemorrhage too
  2. Mitosis (dividing cells)
    - Fibroblasts- create tissue to heal and create new scar tissue
    - New capillaries and macrophages
  3. Complex cascade of events occur that recruit many other cell types from the circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the purpose of inflammation occurring in injury?

A
  1. Protect from invading pathogen
  2. Penetration
  3. Burn
  4. For both part of healing process
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the purpose of inflammation occurring in insect bite?

A
  1. Protects against infection

2. Heals wound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What clinical problems may an inflammation response have?

A
  1. Insect bite: Hypersensitivity- out of controlled response
  2. Contact dermatitis: allergy
  3. Atopic Dermatitis (eczema)
  4. Urticaria (allergy/adverse reaction)- give someone a drug rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give examples of when the inflammation response goes wrong?

A
  1. Hypersensitivity (insect bite)
  2. Failure to heal
  3. Chronic inflammation (Rheumatoid arthritis- cells attacking themselves and lose function in cell)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do chemical signals cause cardinal signs of inflammation?

A

Changing cellular functions and each mediator has slightly different effects by targeting different receptors and cells

  1. Many mediators are complex as most act as drug targets
    - Receptors
    - Enzymes
    - Steroid receptors and protein expression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What mediators act as drug targets?

A
  1. Receptors
  2. Enzymes
  3. Steroid Receptors and protein expression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are mast cells and give examples of what they release?

A
  1. Cells that contain or make numerous inflammatory mediators (reside in every tissue site of the body)
  2. Histamine, 5-HT (serotonin), proteases
  3. Lipid derived mediators (prostaglandins)
  4. Cytokines (peptide mediators)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How are mast cells activated ?

A
  1. Pathogens
  2. IgE (antibodies) (immunoglobins)
  3. Complement Cascade (clotting system)
  4. Physical damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do the terms Wheal and Flare mean? And what can this lead to?

A
  1. Wheal- Swelling
  2. Flare- Reddening
  3. Leads to itch or pain- release of inflammatory mediators and activation of sensory nerves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where is histamine released? And what does an injection of it cause?

A
  1. Released by mast cells

2. Causes wheal and flare of the cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do anti-histmaines work?

A

They block the Histamine H1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do drugs target lipid mediators?

A
  1. Target the phospholipids from cell membranes which can stop inflammatory responses
  2. Targeting one pathway can stop many other pathways
  3. Example: Glucosteroids stops the production of Phospholipase A2 altogether which stops the inflammatory reaction altogether
17
Q

How do NSAIDS work in targeting the lipid mediators?

A

They inhibit the cyclooxygenase (COX) enzyme and prevent prostaglandin formation

18
Q

How does ibuprofen work in lipid mediators?

A
  1. Inhibits the cyclooxygensae (COX) which converts arachidonic acid to prostaglandins
  2. Prostaglandins work by mediating pain, inflammation and fever
19
Q

How does Aspirin work in lipid mediators?

A

Non selective inhibition of COX1 and COX2 (anti-inflammatory effect) and the irreversible inhibition of COX1 (anti-platelet)

20
Q

What side effects can NSAIDS cause and why?

A
  1. Gastric problems- prostaglandins in gut wall involved in gastric mucosa (protects GI tract) reduction which can cause GI bleeding
  2. Kidney problems- prostaglandins important in controlling blood flow to kidneys
  3. Cardiovascular problems- imbalance in prostaglandins can lead to stroke
  4. Contraindiction in ASTHMA (reducing prostaglandins)

This is mainly due to inhibition of COX 1

21
Q

What can glucosteroids (corticosteroids) do to lipid mediators for inflammation? And how do they work?

A
  1. Lipid mediators: They inhibit the induction of cycle-oxygenase which means it has a stronger effect than the NSAIDS
  2. Alter expression of proteins involved in inflammation by altering DNA transcription
  3. Promotes expression of anti-inflammatory proteins and suppresses expression of pro-inflammatory
22
Q

What is the mechanism of action of glucocorticoid?

A
  1. They normally circulate in the blood if they take are taken in orally or topically (based on the steroid of cortisol
  2. They bind to the glucocorticoid receptors into the cytoplasm which go through the nucleus to bind to different genes
  3. This affects the transcription of these different genes
  4. The activated glucocorticoid receptor complex can interfere with cell signalling pathways
  5. So doesn’t have to get translocated into the nucleus
23
Q

What does binding of the glucocorticoid do to the DNA binding dependent?

A
  1. Increases expression of the genes

2.

24
Q

What does binding of the glucocorticoid do to the DNA binding independent?

A
  1. Suppresses inflammation induced dependent gene transcription
  2. It essentially blocks the intracellular signals which stimulate gene transcription and downstream of the receptors
  3. This is stimulated by inflammatory mediators
25
Q

Explain at a lipid mediator level (by corticosteroids) how you would induce a therapeutic effect of an anti-inflammatory?

A
  1. Increase lipocortin-1 (annexin-1) synthesis

2. Block induction of COX-2

26
Q

Explain at a lipid mediator level (by corticosteroids) how you would induce a therapeutic effect of immune suppression?

A
  1. Decreases T and B cells

2. Inhibits cytokine production which are involved in recruiting and starting the immune response

27
Q

Explain the indication of hydrocortisone and the mechanism of action?

A
  1. Indication:
    - Eye- local treatment of inflammation (short term)
    - Skin- mild inflammatory disorders (eczema, nappy rash)
    - Anaphylaxis- IV with adrenaline as emergency treatment
  2. MoA:
    - Glucocorticoid receptor agonist
    - Binds to mineral corticoid receptors that regular blood pressure and volume
    (can cause many side effects hence why preferred to be used topically)
28
Q

Explain the indication of Dexamethasone and the mechanism of action?

A
  1. Indication: nurmerous, where reducing inflammation or immune suppression is beneficial e.g. joint inflammation
  2. MoA
    - Glucocorticoid receptor agonist
    - 40x more potent than hydrocortisone
    - Doesn’t bind to mineral corticoid receptors
    - Has a longer half-life than hydrocortisone
29
Q

What are some of the unwanted effects of glucosteroids being taken orally?

A
  1. Suppress proliferation of skin cells- blocks scarring- can cause permanent scarring
  2. Effects on skeleton- decreased bone density
  3. Muscle- reduces it
    - Reduce glucose uptake
    - Stimulate protein breakdown
    - Inhibit protein synthesis
  4. Adrenal suppression
    - atrophy of adrenal gland
    - Abrupt withdrawal can lead to acute adrenal insufficiency hypotension or death
30
Q

What can long term topical treatment of glucosteroids do?

A
  1. Can induce a cutaneous side effect such as atrophy of the epidermis and the dermis (skin shrinking)
  2. Disturbed wound healing
31
Q

What can long term topical treatment of glucosteroids do?

A
  1. Can induce a cutaneous side effect such as atrophy of the epidermis and the dermis (skin shrinking)
  2. Disturbed wound healing
32
Q

Which drugs target the sensory nerves?

A
  1. Opiates directly block the nerve signals that cause pain- won’t get rid of the information such as the inflammatory response
  2. Prostaglandins can reduce pain signalling by sensing the nerve
33
Q

Explain how pain occurs from the brain? And what does this cause?

A
  1. Noxious stimuli causes a C fibre activity
  2. This causes excitation of the transmission neuron which leads to pain
  3. Inflammatory response is caused

PM2C: Therapeutics and Patient Care: Autumn (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions