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1Principles of Biomedicine - MD1 > 78 > Flashcards

78 Flashcards

1
Q

Effects of glucocorticoids on asthma

A

Decreases inflammatory cell number and activation.

Decreases probability and severity of episode of asthma

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2
Q 
Things that glucocorticoids suppress in inflam response
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4
A

1) Activity, recruitment and survival of eosinophils, T cells
2) Activation of mast cell cytokine production
3) Macrophage cytokine production, proliferation
4) Cytokine and collagen production by smooth muscle and fibroblasts

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3
Q 
Mechanism of glucocorticoid receptor stimulation
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3
4
A

1) Glucocortiocid enters cell
2) Binds glucocorticoid receptor, receptor dimerises
3) Binding of glucocorticoid removes inhibitory proteins from receptor, exposing nuclear localisation sequence
4) GLC/R complex enters nucleus, binds to glucocorticoid response element to stimulate or inhibit transcription.

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4
Q

Types of glucocorticoid receptors

A

Positive and negative

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5
Q

Examples of positively-regulated GREs

A

Glucocorticoid-induced leucine zipper
MAPK phosphatase-1
Inhibitor of xBa
GRE = glucocorticoid response element

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6
Q 
Examples of negatively-regulated GREs
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4
A 
Through inhibiting NFkB response element, inhibits production/release of:
IL-8
COX-2
ICAM-1
NOS2
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7
Q

IKK

A

I kappa kinase

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8
Q

IKK role

A

Phosphorylates IkappaBalpha, which results in ubiquitination of IkBa.
IkBa degraded in proteosome because of ubiquitination.

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9
Q

Protein that inhibits NFkB within a cell

A

GILZ (Glucocorticoid-induced leucine zipper)

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10
Q

How is IKK induced?

A

Cytokine receptor bound by ligand

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11
Q

Induction of AP-1
1
2
3

A

1) Cytokine receptor bound, Jun-kinase phosphorylated.
2) Kun kianse phosphorylates Jun.
3) Jun-P and Fos are subunits of AP-1, which then goes to the nucleus, binds to TRE, acts as a transcription regulator

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12
Q

IkBa

A

Bound to NFkB, prevents NFkB from entering nucleus.

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13
Q

Mechanism by which steroids lead to cellular changes

A

Transactivation

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14
Q

When are inhaled GCS indicated?

A

If beta2 agonist needed over 3 times per week (mild persistent asthma)

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15
Q

Examples of inhaled GCS available in combination with beta2 agonists

A

Budesoinde

Fluticasone propionate

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16
Q

Dose prescription strategy for inhaled GCS

A

Start at an effective dose and decrease over time (step down slowly, as onset is slow and offset from decreasing dose is slow)

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17
Q

Example of a systemic oral steroid prescribed for asthma

A

Prednisolone

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18
Q

Example of a GCS used to control severe asthma, not to prevent

A

Oral prednisolone.
For several days for severe asthma.
Chronically for severe asthma only

19
Q

Effect of GCS on peak expiratory flow over time

A

For first week of treatment very wide difference between possible peak expiratory flows. As time goes on, peak expiratory flow increases on average by a low

20
Q

Adverse effects of inhaled GCS
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3

A

1) Dysphonia (change in voice)
2) Oral candidiasis
3) Decrease in serum cortisol (not clinically significant)

21
Q 
Adverse effects of oral GCS
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A

1) Osteoporosis
2) Diabetes (stimulates gluconeogenesis enzymes in the liver, increasing blood glucose)
3) Muscle wasting
4) Hypertension
5) Growth suppression (so use cautiously in children)
6) Suppression of adrenal/pituitary/hypothalamic axis

22
Q

Protocol for taking a patient off oral GCS therapy

A

Need to wean off chronic use to avoid “withdrawal”

23
Q

Regulation of endogenous GCS

A

Cortisol negatively regulates release of GCS from adrenal gland.

Cortisol levels detected by anterior pituitary gland, which releases corticotropin.
Corticotropin negatively regulates adrenal gland release of GCS

24
Q

Why does chronic oral GCS use lead to withdrawl?

A

Exogenous GCS negatively regulates GCS release from adrenal gland, causing atrophy.

25
Q

Methylxantines mechanism of action in asthma.

A

Not really known.
Has phosphodiesterase activity, decreases cAMP in smooth muscle leading to relaxation.
HDAC2 activation.

26
Q 
Dose limiting side effects of methylxanthines and phosphodiesterase inhibitors
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A

Nausea
Vomiting
CNS stimulation (low safety margin)
Cardiostimulation (dysrhythmias)

27
Q

Example of a selective phosphodiesterase inhibitor

A

Roflumilast

28
Q

Roflumilast compared to other phosphodiesterase inhibitors

A

Reduced incidence and severity of side effects with compared to theophyline

29
Q

Drug for intermittent asthma (up to 100% FEV1)

A

SABA

30
Q

Drug for mild persistent daily asthma (under 80% predicted FEV1)

A

SABA + daily inhaled GCS

31
Q

Drugs for moderate persistent daily asthma (50%-80% predicted FEV1)

A

SABA, daily inhaled GCS and LABA

32
Q

Drugs for severe persistent asthma (50%-80% predicted FEV1)

A

SABA, increased daily inhaled GCS dose, LABA, if needed theophylline-SR and anti-leukotrienes and oral GCS

33
Q

Drugs for very severe asthma (under 50% predicted FEV1)

A

Oral prednisolone

34
Q

What are long-acting beta2 agonists always prescribed with?

A

GCS, SABA

35
Q 
Risk factors for COPD
1
2
a
b
c
d
A

1) Genes
2) Exposure to particles
a Tobacco smoke
b Occupational dusts, organic or inorganic
c Indoor air pollution from heating and cooking with biomass in poorly-ventilated areas
d Outdoor air pollution

36
Q

Effect of lung development on COPD

A

The less the lungs develop, the less ventilation you can get. This increases risk of COPD

37
Q

Type of lung disease that COPD is

A

Obstructive

38
Q

Appearance of obstructive lung disease compared to predicted FEV1

A

Much less steep FEV1 on graph, lower FVC

39
Q 
Definition of COPD 
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A

1) Preventable, treatable disesae with significant extrapulmonary effects
2) Airflow limitation that is not fully reversible
3) Progressive, airflow limitation associated with abnormal inflammatory response of the lung to noxious particles or gasses
4) Loss of lung parenchyma, small airways.
5) Inflammation, fibrosis, thickening of airways, pulmonary hypertension

40
Q

Decline of lung function with age

A

FEV1 decreases over time, to about ~75% of level at 25yo by 75yo

41
Q

Why don’t GCS work well in COPD?

A

Different inflammatory effectors than to asthma.

Inflammatory effectors are less sensitive than those in asthma (eosinophils, mast cells are sensitive)

42
Q

Effect of LABA and SABA on COPD

A

No effect

43
Q

Effect of GCS on COPD

A

Limited effect.

Used because there isn’t really another treatment

1Principles of Biomedicine - MD1 (157 decks)

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