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phar24 > week 11 > Flashcards

week 11 Flashcards

1
Q

what is asthma

A

chronic inflammatory disease of the airways =
activation of mast cells, infiltration of
eosinophils, and T helper 2 (TH2)
lymphocytes.

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2
Q

what makes asthma people different to average person

A

they have hyperresponsivness airways/over react

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3
Q

hyperplasia

A

= an increase in cell proliferation in a normal tissue or organ causing enlargement of a tissue or organ. (increase in number)

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4
Q

hypertrophy

A

= an increase and growth of muscle cells. (increase in size)

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5
Q

fibrosis

A

= thickening or scarring of the tissue. Fibrous connective tissue replaces normal tissue as a response to injury or damage (scarring).

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6
Q

oedema

A

= fluid retention

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7
Q

is asthma reversible

A

no

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8
Q

is COPD reversible

A

no

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9
Q

proteases

A

enzymes that catalyse the breakdown of proteins

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10
Q

are corticosteriods good for asthma & COPD

A

asthma yes

not for COPD

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11
Q

define COPD

A

pathological changes results on airway closure on expiration, leading to air trapping & hyperinflation

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12
Q

mainstream treatment of COPD

A

= bronchodilators

  • reduce air trapping by dilating peripheral airways
  • treatment aims to relief symptoms & reduce exacerbations
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13
Q

what can asthma be treated with

A
  • corticosteroids
  • not NSAIDs
  • antagonists of muscarinic receptors
  • agonists of adrenergic receptors
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14
Q

why are beta 2 used

A

u want the respiratory muscles to relax

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15
Q

what is the mechanism of beta 2 agonists as an effective bronchodilator

A
  1. stimulates beta2 adrenoceptors, causing the transducer (Gs) to break off and bind to aldynal cyclase, this in turn cycles ATP to cAMP which causes muscle relaxation of bronchial smooth muscle
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16
Q

what are the two classifications of B2 agonists

A
  1. SABA - salbutamol & terbutaline = short acting

2. LABA - e.b., formoterol*, indacaterol, salmeterol = long acting

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17
Q

SABA - salbutamol & terbutaline

A

= symptoms relief of asthma & COPD
= prevention of exercise induced bronchoconstriction, if taking before exercise it helps with breathless after exercise, short acting (30mins) but works straight away

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18
Q

LABA - e.b., formoterol*, indacaterol, salmeterol = long acting

A

= maintenance treatment of asthma in patients receiving inhaled corticosteroid (ICS)
= COPD

duration of action over 12 hours

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19
Q

how to minimise adverse effects of drugs used to treat asthma & COPD

A

use inhalers so it affects mainly the lungs = decreasing systemic adverse affect

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20
Q

common adverse effects of B2 agonists

A

inhalation = not problem

most common elderly = tremor, headache & palpitations = overtaken

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21
Q

what causes these adverse B2 agonist effects

A

more drugs reach the systemic circulation at higher doses leading on-target & off target effects elsewhere in the body rather then the lungs

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22
Q

B2 agonist cause tolerance & what is its effect

A

if take more then recommended = less receptors seen in the surface = down-regulation B2 receptors

does not reduce the bronchodilator response due to a large receptor reserve in airways smooth muscles

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23
Q

mechanism of action of anticholinergics

A

block muscarinic actions of acetylcholine preventing it to bind to receptor causing nerve induced bronchoconstriction & mucus secretion

= less effective then B2 agonists in asthma

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24
Q

what are the two classifications of anticholinergics

A
  1. SAMA - ioratropium (short acting)

2. LAMA - E.g., tiotropium, aclidinum, glycopyrronium

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25
Q
  1. SAMA - ioratropium (short acting)
A

symptoms relief of asthma & COPD

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26
Q
  1. LAMA - E.g., tiotropium, aclidinum, glycopyrronium
A

maintenance treatment of moderate to severe asthma as adjunct to standard treatment

  • COPD
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27
Q

what does Gq do

A

Gq is a transducer that binds to the effector, phospholipase 3 make IP3 which will lead to calcium ssensitization = msucle contraction

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28
Q

define synergistic action

A

work together to get the same outcome e.g., B2 agonists and the anticholinergics M3 working together to cause muscle relaxation

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29
Q

what are common AD of anticholinergics

A

when inhaled = little to now systemic absorption decrease chance of adverse effects

mo= dry mouth & throat irritation

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30
Q

define hyperinflation

A

increase air trapping

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31
Q

what is first line therapy for asthma

A

SABA because they are most effective

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32
Q

what are the most effective anti-inflammatory agents used in asthma

A

corticosteriods = delayed effect = will need to be taken continuously = preventers

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33
Q

corticosteriod mechanism of action x4

A
  • decreases transcription of genes that encode pro-inflammatory proteins
  • activates transcription of anti-inflammatory genes
  • directly interact with pro-inflammatory transcription factors
  • reduce inflammatory cell numbers & their activation in the airways
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34
Q

pharmacokinetics of corticosteriods

A
  • a portion of inhaled dose reaches system circulation
  • part of dose is deposited, swallowed & absorbed from gut
  • beclometasone & circlesonide are prodrugs activated by lung esterases = only active in the lungs which is where they are needed
  • budesonide & fluticasone have a greater first-pass metabolism = broken down before reaching systemic circulation
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35
Q

common AD of corticosteriods

A
  • oral candidiasis = white tongue
  • hoarseness (dysphonia)
  • facial skin irritation after nebulisation
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36
Q

bioavailability

A

amount of drug reaching systemic circulation unaltered = no first-pass metabolism

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37
Q

what receptor does SABA bind to

A

GPCR

38
Q

what receptor does corticosteroids bind to

A

glucocorticoid receptors = nuclear receptors

39
Q

what is cysteinyl-leukotriene receptor antagonist e.g., montelukast

A

blocks cysteinyl-leukotriene receptor leading to airway smooth muscle relaxation & decrease of inflammation

40
Q

common AD of cysteinyl-leukotriene receptor antagonist

A

headache, abdominal pain, diarrhea

41
Q

role of systemic corticosteriods

A

Oral corticosteroid (OCS): Prednisone or
Prednisolone used for acute exacerbations
of asthma
• Systemic adverse effects

42
Q

role of Anti-IL5 (new treatment cause corticosteroids not working) - monoclonal antibodies

A

– Mepolizumab and benralizumab
• Reduce blood and tissue eosinophils
• SC administration every 4 weeks*

43
Q

role of Anti-IgE (new treatment cause corticosteroids not working)
- monoclonal antibodies

A
  • Omalizumab
    • Binds to circulating IgE and inhibits IgEmediated reactions
    • Maintenance treatment of moderate-to severe allergic asthma
    • SC administration every 2-4 weeks
    • Generally well tolerated
44
Q

what are the bronchodilators for asthma

A
  1. beta agonists

2. muscarinic antagonists

45
Q

anti-inflammatory agents for asthma

A
  1. release inhibitors
  2. steroids
  3. antibodies
46
Q

COPD drugs

A
  1. bronchodilators
  2. steroids (anti-inflam)
  3. antibiotics (for bronchitis = inflamed broncholes)
47
Q

what is the suffix of beta-blockers

A

-lol

48
Q

mechanism of action of beta blockers x4

A

competitive antagonist of the B-adrenergic receptors

  1. negative chronotrophy
    = decreasing HR
  2. negative inotrophy = BP & cardiac contractility
  3. negative dromotrophy
    = also depress sinus node rate & slow conduction through the AV node
  4. decrease renin secretion
49
Q

are beta blockers selective

A

yes

50
Q

3 types of selective beta-blockers

A
  1. b1 receptor selective: atenolol, metoprolol (CR), bisoprolol & nebivolol
  2. non-selective (B1 & B2): propranolol, pindolol (blockage of B2 receptors may cause bronchospasm)
  3. non-selective (B1, B2, A1): carvedilol & labetalol (B-blockers commonly used in heart failure)
51
Q

define CR

A

controlled released meaning they only need to be taken once a day

52
Q

immediate-release

A

tablets need to be taken twice a day

53
Q

are Beta blockers first line therapy of hypertension

A

no anti-hypertension drugs are

54
Q

adverse affects of Beta-blockers

A
  • Bradycardia
    • Hypotension
    • Orthostatic hypotension (especially carvedilol,
    labetalol)
    • Bronchospasm
    • Cold extremities, exacerbation of Raynaud’s
    phenomenon
55
Q

what is the suffix of the alpha1 blockers

A

-ozin, prazosin

56
Q

where do the beta1 blockers mostly work

A

the heart

57
Q

where do the alpha1 blockers mostly work

A

the periphery

58
Q

mechanism of action of alpha1 blockers

A
  • decrease peripheral resistance by antagonising alpha1 adrenoceptor which leads to vasodilation = may affect both arteriolar resistance vessels & veins
59
Q

mechanism of action of centrally acting alpha2 adrenoceptor agonists e.g. chlonidine

A

• Activates α2-adrenoceptor in the CNS which leads to an inhibitory signalling, decreasing
sympathetic tone.

60
Q

what is the management if hypertension drug wise - there are four levels

A

FIRST CHOICE is a single drug = three options people could take

  1. ACE inhibitor (or angiotensin II receptor antagonist)
  2. calcium channel blocker (CB)
  3. low-dose thiazide diuretic (last one for people older than 65)

2ND CHOICE if target BP not reached = pair drugs (so take first with another type)

  1. ACE inhibitor for angiotensin II receptor antagonist + CB
  2. ACE inhibitor + low-dose thiazide diuretic

3RD CHOICE if target BP not reached = 3 medications

  1. still not work seek specialist advice
61
Q

What are the drug classes to manage hypertension (antihypertensives)

A
  1. angiotensin converting enzyme inhibitor (ACEi)
  2. Angiotensin II receptor Blocker (ARB)
  3. calcium channel blocker
  4. thiazife & thiazide-like diuretics
  5. beta blocker
62
Q

what are the two groups of calcium channel blockers

A
  1. dihydropyridine (-dipine)

2. non-dihydropyridine (verapamil & diltiazem)

63
Q

mechanism of action of calcium channel blockers

A
  • they reduce calcium entry into cells of myocardium, vascular smooth muscle & cardiac conducting system by preventing L-type calcium channel opening
64
Q

what is the binding of calcium channel blocker: dihydrophyridines

A
  • binds to alpha1 subunit = acts mainly in arteriolar smooth muscle
  • reducing BP (decreasing peripheral vascular resistance)
65
Q

what is the binding of calcium channel blocker: verapamil & diltiazem

A
  • binds to alpha1 subunit = act on cardiac muscle
  • decrease velocity of AV nodal conduction/ decrease myocardial oxygen requirement
  • with with vargina where not enough oxygen is reaching heart
66
Q

what is the type of target for calcium channel blocker target

A

voltage ion channel NOT ligand gated ion channel

67
Q

what are the adverse effects of calcium channel blockers: dihyrophyridines

A
  • nausea

- vasodilatory effects, including: headache, flushing, dizziness, hypotension, peripheral oedema (dihydropyridines)

68
Q

ACE inhibitors suffix

A

-pril

69
Q

body system used to keep blood pressure at a normal rate

A
  1. macula densa senses low fluid flow or low sodium concentration
  2. juxtaglomerular cells secrete renin
  3. kidney releases enzyme renin into blood stream
  4. will find an peptide called angiotensinogen which was previously released by the liver
  5. renin breaks down angiotensinogen into angiotensin I which will keep circulating until it reaches the pulmonary blood
  6. then will reach the angiotensin-converting enzyme (ACE) in pulmonary blood
  7. ACE converts AI into AII
  8. AII is the peptide that leads to widespread vasoconstriction & release of aldosterone in the adrenal cortex
  9. aldosterone receptors reabsorb sodium = reabsorption of water = increases blood pressure
70
Q

how do the ACE inhibitors work

A

they inhibit the angiotensin-converting enzyme ACE = decrease AII production = decreasing rest of the effects

71
Q

what is the other role of angiotensin II that causes an adverse affect when AII is inhibited

A

inhibits breakdown of bradykinin = causes it to accumulate = causes dry/non productive cough (no mucous)

72
Q

other adverse effects of ACE inhibitors

A
  • hypotension, headache, dizziness, non-productive cough, hyperkalemia (too much potassium = if increase reabsorption of sodium = decrease reabsorption potassium so if sodium isn’t been absorbed then potassium will accumulate)
  • precaution = renal failure
73
Q

what are the three drugs which can lead to acute kidney injury

A
  • one diuretic
  • one ACEi or ARB
  • one nonsteriodal anti-inflammatory drug (NSAID)
74
Q

what are the three drugs which can lead to acute kidney injury “triple whammy”

A
  • one diuretic
  • one ACEi or ARB
  • one nonsteriodal anti-inflammatory drug (NSAID)
75
Q

how does ARB work

A

they are antagonists of AII receptors

76
Q

what are the receptors of AII and which specific receptor is ARB an antagonist to

A

receptors: AT1 & AT2

competitive antagonist to type I angiotensin (AT1) receptors

77
Q

what are the effects of AT1 angiotensin II receptor

A
  • vasoconstriction
  • fiborosis
  • VSMX inflammation
  • oxidative stress
  • cardiac hypertrophy
78
Q

what are the effects of AT1 angiotensin II receptor

A
  • vasoconstriction
  • fiborosis
  • VSMX inflammation
  • oxidative stress
  • cardiac hypertrophy

= leads to disease to we want it to be blocked

79
Q

what are the effects of AT2 angiotensin II receptor

A
  • vasodilation
  • antifibriotic
  • anti-inflammation
  • decrease oxidative stress
  • antiproliferation

= leads to protection = dont want to block

80
Q

adverse effects of ARB drugs

A
  • headache, dizziness, hyperkalemia (increase potassium in blood stream)
  • renal failure
81
Q

drug interactions with ARB

A
  • loop diruetics
  • NSAIDs
  • ACEi
82
Q

use of furosemide

A

loop diruetic used for odema

83
Q

use of low-dose aspirin

A

= NSAID/antiplatelet used for acute coronary syndrome

84
Q

use of carvedilol

A

= beta-blocker used for hypertension/heart failure

85
Q

use of omeprazole

A

= proton pump inhibitor used for gastro-oesophgeal disease

86
Q

use of ramipril

A

= ACE inhibitor used for hypertension/heart failure

87
Q

role of nonsteriodal anti-inflammatory drugs (NSAIDs)

A

inhibitors of the cyclonoxygenase enzyme

88
Q

what do cyclonoxygenase enzymes produce

A

prostaglandins

89
Q

role of prostaglandins when decreased circulating volume in renal system

A

they are vasodilators of afferent renal arterioles which lead to increased renal blood flow & glomerular filtration rate = important in presence of diuretics

90
Q

how does the “Triple whammy” work to cause acute kidney failure

A
  1. diuretics reduce plasma volume, reducing glomerular filtration rate
  2. the efferent arteriole is dilated from an ACEI or ARB, reducing filtration rate
  3. the afferent arteriole is constricted from NSAID induced prostaglandin inhibition, reducing glomerular filtration rate

= hyper-perfusion = glomerular damage

91
Q

are bronchodilators relievers or preventers

A

relievers

92
Q

are anti-inflammatory drugs preventers or relievers

A

preventers of inflammation

phar24 (12 decks)

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