Respiratory + Pain Drugs Flashcards

1
Q

What do you use paracetamol for

A

1) 1st line - acute and chronic pain

2) Antipyretic

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2
Q

How does paracetamol work

A

Weak inhibitor of COX
In the CNS COX Inhibition appears to increase the pain threshold and reduce prostaglandin concentration in the thermoregulatory centre of the hypothalamus

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3
Q

Which COX is paracetamol specific for?

A

COX 2 –> however it is only a weak inhibitor as its actions are inhibited by peroxides

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4
Q

What inhibits the action of paracetamol

A

peroxides

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5
Q

Adverse effects of paracetamol

A

Generally very safe

This is because lack of COX-1 inhibition prevents, GI, renal and CV implications

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6
Q

How is paracetamol metabolised

A

By CP450 enzymes in the liver
Metabolised to NAPQI that is conjugated with glutathione
In overdose NAPQI builds up causing hepatocellular necrosis

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7
Q

When should we reduce paracetamol dose

A

In those at risk of liver toxicity e.g.
Increased NAPQI production –> chornic excessive alcohol use or inducing enzymes
Decreased glutathione stores –> malnutrtion, low body weight, severe hepatic impairment

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8
Q

What does patacetaml interact with

A

CP450 Inducers e.g. carbamazepine and phenytoin

This increase the rate paracetamol is metabolised hence increased NAPQI production and risk of liver toxicity

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9
Q

How do we establish the efficacy of n-acetylcysteine in treating paracetamol overdose?

A

Test INR, ALT and creatinine

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10
Q

Name strong opioids

A

Morphine, Oxycodone

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11
Q

What do we use strong opioids for

A

Acute severe pain - rapid onset e.g. post-op and MI
Chronic pain –> step 3
Breathlessness –> relieves it in end of life care
Acute pulm oedema –> with furosemide and oxygen and nitrates

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12
Q

How do strong opioids work

A

Activation of opioud mu receptors in the CNS
Decreases neuronal excitability and pain transmission
In the medulla they blunt the response to hypoxia and hypercapnia –> hence redce breathlessness

AS they relieve pain also decrease sympathetic stimulation –> this may reduce cardiac work and oxygen demand hence relieving symptoms in MI and pulm. oedema

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13
Q

Adverse effects of strong opiods

A

1) Respiratory depression
2) Neurological symptoms
3) Nausea and vomiting –> as they activate chemoreceptor trigger zone –> usually decreases with time but offer them an anti-emetic
4) Pupillary constriction –> activate the Edinger-Westphal nucleus
5) Constipation –> decrease motility and increase smooth muscle tone
6) itching, urticaria, vasodilation and sweating –> as may cause histamine release
7) Toelrance
8) Withdrawal reaction –> anxiety, pain, breathlessness, pupils dilate, cold and dry skin

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14
Q

Warnings of strong opioids

A

Redice dose in hepatic or renal impairment
Avoid in respiratory failure
Avoid in biliary colic –> can cause smooth muscle contraction and spasm of Sphincter of Oddi –> worsens pain

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15
Q

Interactions of strong opioids

A

Dont use with other sedating drugs e.g. anti-psychotics, benzodiazepines or tricyclic antidepressants.

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16
Q

Name opiate compounds

A

Co-codamol

Co-dydamol

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17
Q

Indications for opiate compounds

A

Treatment of mild-moderate pain –> when paracetamol is insufficient

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18
Q

Overdose effects of opiate compounds

A

Hepatotoxicity - paracetamol

Neurological and respiratory depression - opiods

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19
Q

Warnings of opiate compounds

A

Extreme caustion in significant respiratory disease

Dose reductin in renal/hepatic impairment

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20
Q

What should we avoid prescribing opiate compounds with

A

Other sedating drugs (tricyclic antidepressants, benzodiazepines, antipsychotics)

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21
Q

Name weak opiods

A

Codeine, Dihydrocodeine, Tramadol

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22
Q

How do weak opiates work

A

Codeine and dihydrocodeine metabolised by the liver to produce small amounts of morphine/dihydromorphine

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23
Q

Why do some poeple find opiates ineffective

A

10% of caucasians have an enzyme CP450 2D^ that is less active hence don’t metablise it

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24
Q

What is tramadol

A

Synthetic analogue of codeine

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25
What effects does tramadol have
As well as opiate effect also acts via adrenergic and serotonin pathways Prevents the reuptake of noradrenaline and serotonn
26
Adverse effects of weak opiods
``` Nausea Constipation Dizziness Drowsiness Neurological and respiratory depressoin ``` Tramadol causes less constipation and respiratory depresssion
27
What route should you never give codeine/dihydrocodeine
IV - causes a severe reaction, similar to anaphylaxis but it is actually mediated by histamine
28
Caution in giving weak opiods in
1) Significant respiratory depression 2) renal/hepatic impairment --> need a dose reduction 3) Epilepsy and unvontrolled epilepsy --> tramadol lowers the seizure thresholds
29
Interactions of weak opiods
1) avoid with other sedating drugs (anti-psychotics, benzodiazepines, tricyclic antidepressants) 2) Dont use tramadol with other drugs that lower the threshold potential (SSRIs and tricyclic antidepressants)
30
Name inhaled corticosteroids
Beclometasone, Budesonide, fluticasone
31
Uses of inhaled steroids
1) Asthma --> decreases airway inflammation | 2) COPD --> controls symptoms and reduces exacerbations
32
How do steroids work
Downregulate pro-inflammatory interleukins, cytokines and chemokines Upregulate anti-inflammatory proteins Reduces mucosal inflmation, widens airways and reduces exacerbations and mucus secretions
33
Adverse effects of inhaled steorids
Oral candidiasis Hoarse voice Increased risk of pneumonia in COPD
34
Is asthma or COPD steroid responsive?
Asthma - generally steroid responsive and stops disease progression COPD - generally poorly responsive to steroids and dose not stop disease progression
35
Warnings of using inhaled steroids
1) COPD With history of pneumonia --> caution in high dose steroids 2) CHildren - high dose steroids shouldn't be used in children unter 16
36
Name systemic corticosteroids
Dexamethasone Prednisolone Hydrocortisone Usually oral except give IV dexamethasone for cerebral oedema due to cancer
37
Uses of systemic corticosteroids
1) Allery/inflammatory disorders 2) suppression of autoimmune diseases 3) Cancer 4) Hormones replacement
38
What metabolic effects do systemic corticosteroids have
Increase gluconeogenesis from circulationg amino acids and fatty acids
39
What mineracorticoid effects do systemic corticosteroids have?
Act like aldosterone | Cause sodium and water retention and potassium excretion
40
Adverse effects of systemic corticosteroids
Immunosuppresion Metabolic: DM and osteoporosis Increased catabolism causes proximal muscle weakness, skin thinning, easy brusising Mood changes: insomonia, confusion, psychoisis Mineracorticoid effects Lhypertension, low potassium and oedema Adrenal atrophy
41
Caution of systemic steroids in who
In infection ad children
42
Interactions of systemic steroids
1) NSAIDS --> increased risk of pepetic ulcers and GI bleeds 2) Beta 2 agonists, theophylline, loop/thiazine diuretics - all cause low potassium 3) Cytochrome P450 inducers (carbamazepine, phenytoin, rifampicin) --> this reduces corticosteroids efficacty 4) Vaccines --> reduces immune response
43
What shall we consider the use of in long term systemic steroids use
Bisphosphonates --> stops osteoporosis PPI --> prevents ulcers In long term also monitor HbA1c and DEXA scans
44
Name topical corticosteroids
Hydrocortisone, betamethasone
45
Uses of topical steroids
Inflammatory skin conditions e.g. eczema
46
Adverse effects of topical steroids
Potent can cause thinning of skin, striae, telangextasia, contact dermatitis Perioral dermatitis and acne exacerbation if on face
47
Contraindiciations of topical steroids
Infection present | Facial lesions
48
How long can you use topical steroids for
2 weeks max, 1 week if on face
49
Name NSAIDS
Naproxen, ibuprofen, diclofenac and etroicoxib
50
What is etoricoxib
A Slective COX-2 Inhibitor
51
What do you use NSAIDS for
As needed traetment for pain | Regular treatment of pain related inflammation
52
What should you take NSAIDS with
FOOD --> avoids stomach upset
53
How do NSAIDS work?
Inhbiit COX enzymes --> prevents the synthesis of prostaglandins from arachadonic acid
54
What do the 2 different types of COX do?
COX - 1, the constitutive form Stimulates prostaglandin synthesis that is essential to rpeserve integrity of the gastic mucosa, maintain renal perfusion (as dilates the afferent glomerular arteriole) and inhibits thrombus formation at the vascular endothelium COX-2 inducible form expressed in response to inflammatory stimuli --> stimulates production of prostaglandings that cause inflammation
55
Whcih COX enzyme inhbition causes therapetic effects and which causes adverse effects
COX - 1 = adverse effects COX - 2 = therapeutic effects
56
Adverse Effects
GI toxicity Renal Impairment Cardiovascular events ``` Hypersensitivity Fluid retention (espesically if given with loop diuretics) ```
57
Who should we avoids NSAIDS in
``` Renal impairment Heart failure Peptic ulcer disaese Liver failure Hypersensitivity ```
58
Interactions of NSAIDS
GI ulceration --> low-dose aspirin, corticosteroids GI bleeding --> anticoagulants, SSSRIS, venlafaxine Renal Impairment --> ACEi, diuretics
59
Who should we consider gastroprotection in for NSAIDS?
1) OVer 65 2) Previous peptic ulcer disease 3) Other drugs with GI effects, particularly low dose aspirin and prednisolone
60
Name some anticholinergics/antimuscuranics
Ipratropium | Tiotropium, glycopyronium (long acting)
61
Uses of anticholinergives
1) COPD --> short acting used to relieve brethlessness, long acting to prevent breathelssness 2) ASthma --> short acting used as an adjuvant for breathlessness during acute exacerbations Long acting are added at step 4 of chronic asthma treatment
62
How do anticholinergics work?
Competitive inhibitor of acetylcholine at the muscarinic receptor!! Normally receptor stimulation causes parasympathetic effects
63
What happens when you block the anticholinergic receptor?
Decreased Heart rate Decreased smooth muscle tone Decreased secretions from respiratory and GI tract ALSO CAUSES RELAXATION OF PUPILLARY CONTRICTOR AND CILIARY MUSCLES --> causes pupilllary dilation and prevents the accomodation reflect
64
Adverse effects of anticholinerigcs
Dry mouth
65
Caution of using antichlinergics
Angle-closure glaucome Can precipitate a dangerous rise in intraoccular pressure Caution if arrhytmias
66
Interactions of antibholinergics
Generally none as little systemic absoprtion as it is inhaled
67
Name Beta-2-agonists
Salbutamol, terbutaline (short acting) | Salmeterol, formaterol (long acting)
68
Indivations of beta 2 agonists
1) Asthma: Short acting PRN for step 1, long acting as step 3 (but always give in combo with a steroid) 2) COPD: - short acting to relieve breathlessness, long acting = step 2 3) Hyperkalaemia urgent tratment: give with glucose, insulin and calcium gluconate
69
How do beta - 2- agonists work
Stimulates the receptor fround in the GI tract, bronchus, uterus and blood vessles Causes smooth muscle relaxation Also stimulates the Na/K ATPase pump (like insulin) causing potassium to be moved from extracellular to intracellular
70
Adverse effects of beta-2-agonists
Causes sympathetic response --> tachycardia, palpitations, fine tremore Promotes glycogenolysis Increaess serum lactate levels Muscle cramp --> in long acting beta - 2- agonists
71
Caution of using beta-2-agonists
Only give long acting with inhaled corticosteroids Caution in patients with V --> tachycardia may provoke angina arryhythimias
72
Interactions of beta-2-agonists
beta blockers reduce their effectiveness Concommitant use of high dose nebulises beta 2 agonsit with theophylline and corticosteroids can cause hypokalaemia
73
What is seretide
combo of long acting beta - 2 agonists and a corticosteroid
74
Who do we give oxygen too
Hypoxaemia Pneumothoraw CO Poisonin
75
How does oxygen treat a pneumothoraw
decreaesse the partial pressure of nitrogen in alveolar gas hence accelerates its diffusions out of the body
76
How does oxygen treat CO poisoning
It competes with CO to bing to Hv therefore shortens the half life of carboxyhaemoglobin
77
Adverse effects of oxygen
mainly due to the felivery methods e.g. discomfort from face mask Dry throat due to lack of humidity
78
Warnings of giving oxygen
Type 2 respiratory failure e.g. CO2, they have a hypoxic drive to breathe not hypercapnic Heat sources/naked falmes
79
Target oxygen saturations§
94-98% for normal | 88-92% for COPD
80
Name mucolytics
Carbocysteine
81
Indicationsf or mucolytics
Respiratory disoders characterised by excessive, viscous mucus
82
mechanism of carbocysteine
Reduces the viscosits of sputum to help relieve symptoms by alllowing the sufferer to bring up the sputum more easily Targets glutathione S-transferase P protein
83
Adverse effects of mucolytics e.g. carboysteine
Skin rashes Hypersensitivity Stomach bleeding
84
Contraindications of mucolytics
``` Cough suppressants (antitussives) Active peptic ulcer disaese Lactose/fructose intolerance as contins these ```
85
Interactions of carbocysteine
Increased risk/severity of adverse effects when combined with chloramphenicol, disulram, gliclazide, ketoconazole, metronidazole, griseofulvin
86
What is theophylline
A methylxanthine
87
What do we use theophylline to treat
Severe asthma/treat nocturnal asthma symtpoms
88
How does theophylline work
Raises intracellular cAMP by competitvely inhibiting phosphodisesterase --> relaxes airway smooth muscles and inhibits mediator release from mast cells Antagonism of adenosine (a potent bronchoconstrictor) at alpha 2 receptors Anti-inflammatory activity on T-lymphocytes by reducing release of platelet-activating factors
89
GI adverse effects of theophylline
Nausea, vomiting, anorexia
90
Cardiovascular effects of theophylline
Dilatation of vascular smooth muscle --> headaches, flushing and hypotension Tachycardia and cardiac dysrhytmias
91
CNS effects of theophylline
``` Insomnia Hypervenitlation Anxiety Agitations Headaches Fits ```
92
Interactions of theophyliine
Many drugs inhibit the CYP1A2 hepatic enzymes that eliinate theophylline e.g. macrolides, fluoroquinolones, interferon, cimetidine CYP450 inducers (phenytoin, carbamazepine, rifampicin) increase the metabolism of theophylline therefore reducing its efficacy)