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MP324 > L8 - L16 > Flashcards

L8 - L16 Flashcards

1
Q

COPD Exacerbation Management

common bacterial
- Strep pneumoniae
- Haemophilus influenzae
- Moraxella catarrhalis

A
  1. Bronchodilators nebulised with air (not oxygen)
    - SABA (with SAMA if severe)
    - theophylline not recommended bc S/E
  2. Steroids
    - prednisolone 30-40mg 5-7 days

IF BACTERIAL
- give oxygen to 88-92%
- amox 500mg 3x day / doxy 200mg then 100mg daily

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2
Q

Corticosteroids

  • glucocorticoids
  • carried in the body as Transcortin
A

E.g. Prednisolone

  • transcription factor for anti-inflammatory genes
  • inhibits transcription of pro-inflammatory genes (PG + LT)
  • increases Beta adrenoreceptors in bronchial smooth muscle
  • decreases histamine release from mast cell
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3
Q

TNF-a

  • released by TH1
A
  • amplifies inflammatory response to activate IFy, macrophages & neutrophils
  • stimulates mucus secretion
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4
Q

Pulmonary Device Terms

  • MMAD, FPF, Labelled Dose
A

MMAD - mass median aerodynamic diameter

FPF - fine particle fraction

Labelled Dose - measured in each draw

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5
Q

PMDI’s

  • in solution and in suspension
A
  • made from aluminium

PMDI as solution :
-drug dissolved in propellant. becomes a homogenous phase so no need for shaking

PMDI as Suspension :
- particle size reduction by collision, and small particles leave through central discharge. need to shake

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6
Q

DPI’s

A
  • consists of micro APIs (drug) atop course carrier lactose particles
  • released by patient inhalation. inhale must be forceful enough to de-agglomerate the API from lactose
  • no propellant and environmentally friendly

aerolisation requires adhesive force between API and course carrier to be overcome. so fast and strong inhale

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7
Q

Nebulisers

  • air jet
  • vibration mesh
A

Air Jet (norm)
- uses compressed air to make fine mist
- durable but loud

Vibration Mesh
- ultrasonic vibrations passing through water to generate fine mist
- nearly silent
- can’t use with suspensions, and only handheld model

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8
Q

Severe Asthma Treatment

A

refer to hospital

  1. air nebulised SABA (+ SAMA if needed)
  2. oxygen via venturi 40-60%
  3. oral corticosteroid Prednisolone 40-50mg
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9
Q

Life Threatening Asthma Treatment

  • severe + PEFR <33% predicted
A

immediate hospitalisation

  • nebulised beta agonist + Ipratropium bromide (SAMA)
  • oral cortico Prednisolone 40-50mg
  • IV aminophylline (xanthine that inhibits PDE)
  • IV salbutamol, fluids, electrolytes

+ oxygen if SpO2 is under 92% - aim for 94-98

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10
Q

ICS Systemic Effects

  • & Ideal ICS
A
  • growth suppression
  • skin thinning and bruising
  • oral thrush
  • pharyngitis

Ideal Corticosteroid
- potent - high receptor binding
- prolonged effect with lipophilicity
- high lung deposition

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11
Q

LRT & Lipophilicity

  • LRT lung residence time
A

LRT - higher LRT means more receptor interaction
- longer MAT = better LRT of API

MAT = differencein mean residence time between inhalation and IV administration

Lipophilicity - higher LogP means better LRT

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12
Q

ICS Half-life

A
  • high protein binding results in low systemic drug concentrations
  • only unbound drug is active
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13
Q

Rofimulast Effects

  • PDE4 inhibitor
A

effects of R on cells:

  • smooth muscle relaxation
  • monocyte TNF-a release : causes more inflammation at start to engulf pathogens quickly and then itll get better
  • stops PDE breaking down cAMP so more relaxation
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14
Q

Rofimulast Biological Activity

A
  • PDE4 inhibitor
  • PDE4 inhibition causes decreased inflammatory mediator release and decreased inflammation
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15
Q

Pharmacokinetics of Rofimulast
- converted by CYP450, CYP3A4 & CYP1A2

A

Becomes active metabolite rofimulast N-oxide

  • rapid absorption after oral administration
  • max plasma conc. in 1hr
  • bioavailability 80% (immediate-release)
  • can cause weight loss
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16
Q

Treating Severe Asthma

  • PEFR 33-50%
  • unable to talk in sentences
  • RR >25 , pulse >110
A

hospital

  1. oxygen 40-60% via venturi
  2. prednisolone 40-50mg
  3. air nebulised SABA (+ SABA too if needed)
17
Q

Steroid Structure

(corticosteroid/glucocorticoid

A

Backbone : ABCD 4 ringed main body
alpha notation - in Blue & lower half of backbone
beta notation - in Red & upper side of backbone

18
Q

Adrenocorticoid Classes

  • Gluco
  • Mineralo
  • Sex Hormone
A

Glucocorticoids
- regulate carb, lipid & protein metabolism
- used for asthma relief and rheumatoid diseases

Mineralocorticoids
- salt balance & water retention

Sex Hormone
- react with androgen/oestrogen receptor

19
Q

Adrenocorticoid SAR

  • for all ac
A

all biologically active require 3-keto group & 4,5 unsaturation (double bond)

  • Gives lone pairs on oxygen which can interact with other molecules
  • Gives molecule more functionality
  • Can make double bond across pi 1 & 2 position
20
Q

Glucocorticoid SAR vs. Mineralocorticoid SAR

A

Glucocorticoid
- a-hydroxyl group on C17 in gc but not mc
- activity increased by adding 11B-hydroxyl in C-ring

Mineralocorticoid
- hydroxyl on pi position 21 in D ring

21
Q

Theophylline Effects

  • inhibits PDE’s
  • & Antagonises Adenosine Receptors
A
  1. inhibits PDE
  • PDE3 inhibition relaxes smooth muscle
  • PDE4 inhibition reduces mediator release from macrophages + blocks PDE to stop it inhibiting cAMP
  • inc. cAMP causes tissue relaxation
  1. Adenosine Receptor Antagonist
  • adenosine causes bronchoconstriction via histamine & leukotriene release
22
Q

Theophylline Pharmacokinetics & Target Conc.

  • clearance increased by - smoking, st johns wart
  • decreased by -clarithro, cardiac failure
A
  • drug clearance 0.04L/h/kg
  • oral bioavailability 100%
  • volume of distribution 0.48L/kg

10-20mg/L traditional bronchodilator effects
5-15mg/L anti-inflammatory effects

23
Q

What is Aminophylline

A
  • stable mixture of theophylline and ethylene diamine
  • used IV for severe asthma
24
Q

Autoimmune Disease Cause

A
  • Lymphocyte T-cells recognise self pathogens as foreign and attack them
  • usually they recognise small tumour growth in cells and then eradicates them
25
Q

How Rheumatoid Arthritis Happens

  • joint inflammation and destruction
  • 3x more likely in women
A

How it Happens

  • Rheumatoid antibodies activate IgE
  • citrullinated peptides activate macrophages
  • both promote inflammatory response

symptoms: fatigue, disrupted sleep, mood changes, dry eyes/mouth, joint swelling & numbness & red

26
Q

Treatments For Rheumatoid Arthritis

  • DMARD’s
  • NSAID’s
A

DMARD’s - Methotrexate + Sulfasalazine
- disease modifying antirheumatic drugs
- 1st line slows joint damage

NSAID’s - aspirin
- anti-inflammatory effect for symptom control

27
Q

MAB Treatment for RA

  • Infliximab
  • Rutiximab (mab against CD20)
A

Infliximab - anti-TNF-a
- binds to TNF-a and takes it out of circulation to reduce inflammation

Rituximab - antibody against B+T co-receptors

  • B & T cells need co-receptor activation (located between dendritic cells) to be fully activated
  • Rituximab blocks these receptors
28
Q

Lupus Erythematosus Pathophysiology

  • affects kidneys , skin , joints , CV system
A

Symptoms : mouth/nose ulcers, red patches, abdominal pain, swollen joints, hair loss

Treatment

  • DMARD’s - methotrexate
  • Corticosteroids - treats flare ups
  • Rituximab - against CD20
29
Q

Multiple Sclerosis

  • nerve cell demyelination
A

T-cells infiltrate BBB and attack myelin sheath, weakening muscle & reducing signalling

Symptom Control : IV methylprednisolone

Treatment : disease modifying IFN-b

30
Q

Biological Treatment of MS

  • Natalizumab
A

mab against cell adhesion molecule alpha-4 integrin

  • prevents T-cells crossing BBB and prevents cognitive decline
  • approved as monotherapy only
31
Q

Type 1 Diabetes Methods of Tissue Damage

  • pancreatic beta cell destruction causes loss of insulin
A
  1. CD4+ and CD8+ kill islet cells as they present antigen to cytotoxics
  2. islet of Langerhans cells contain secreting hormones specificto each cell
    - Effector T-cells recognise peptides from B-cell specific proteins & kill B-cell
32
Q

Antibodys Against Interleukins

  • Mab suffix attacks MABs (monoclonal antibodies)
A

Tralokinumab - anti IL-13 & Lebrikizumab - anti IL-13
- IL-13 produced by TH2 cells and activates eosinophils in allergic asthma

Mepolizumab - anti IL-5 antibody

Rituximab - anti CD20 (CD20 kills B-cells)

Eprotuzimab - anti-CD22

Omalizumab - anti IgE antibody
- IgE activates mast cells to release histamine which causes inflammation and allergic response

33
Q

Inside Beta-Adrenoreceptor Activation

A
  1. Beta agonists activate GS which promotes adenyl cyclase
  2. adenyl cyclase turns ATP into cAMP
  3. This activates PKA which causes beneficial effects to asthma patients

like : causing calcium efflux in SMC, inhibits raf-1 kinase

34
Q

MAB

A

Infliximab: anti-TNFa

Rituximab: mab against CD20

Epratuzumab: mab against CD22

trakolinumab + lebrikizumab: anti-il13

mopiluzimab - anti-il5

omalizumab - anti IgE

natalia - anti pyrosin

MP324 (3 decks)

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