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Flashcards in Respiratory + Pain Drugs Deck (92)
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1
Q

What do you use paracetamol for

A

1) 1st line - acute and chronic pain

2) Antipyretic

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

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

4
Q

What inhibits the action of paracetamol

A

peroxides

5
Q

Adverse effects of paracetamol

A

Generally very safe

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

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

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

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

9
Q

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

A

Test INR, ALT and creatinine

10
Q

Name strong opioids

A

Morphine, Oxycodone

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

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

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

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

15
Q

Interactions of strong opioids

A

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

16
Q

Name opiate compounds

A

Co-codamol

Co-dydamol

17
Q

Indications for opiate compounds

A

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

18
Q

Overdose effects of opiate compounds

A

Hepatotoxicity - paracetamol

Neurological and respiratory depression - opiods

19
Q

Warnings of opiate compounds

A

Extreme caustion in significant respiratory disease

Dose reductin in renal/hepatic impairment

20
Q

What should we avoid prescribing opiate compounds with

A

Other sedating drugs (tricyclic antidepressants, benzodiazepines, antipsychotics)

21
Q

Name weak opiods

A

Codeine, Dihydrocodeine, Tramadol

22
Q

How do weak opiates work

A

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

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

24
Q

What is tramadol

A

Synthetic analogue of codeine

25
Q

What effects does tramadol have

A

As well as opiate effect also acts via adrenergic and serotonin pathways
Prevents the reuptake of noradrenaline and serotonn

26
Q

Adverse effects of weak opiods

A
Nausea
Constipation
Dizziness
Drowsiness
Neurological and respiratory depressoin

Tramadol causes less constipation and respiratory depresssion

27
Q

What route should you never give codeine/dihydrocodeine

A

IV - causes a severe reaction, similar to anaphylaxis but it is actually mediated by histamine

28
Q

Caution in giving weak opiods in

A

1) Significant respiratory depression
2) renal/hepatic impairment –> need a dose reduction
3) Epilepsy and unvontrolled epilepsy –> tramadol lowers the seizure thresholds

29
Q

Interactions of weak opiods

A

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
Q

Name inhaled corticosteroids

A

Beclometasone, Budesonide, fluticasone

31
Q

Uses of inhaled steroids

A

1) Asthma –> decreases airway inflammation

2) COPD –> controls symptoms and reduces exacerbations

32
Q

How do steroids work

A

Downregulate pro-inflammatory interleukins, cytokines and chemokines
Upregulate anti-inflammatory proteins

Reduces mucosal inflmation, widens airways and reduces exacerbations and mucus secretions

33
Q

Adverse effects of inhaled steorids

A

Oral candidiasis
Hoarse voice
Increased risk of pneumonia in COPD

34
Q

Is asthma or COPD steroid responsive?

A

Asthma - generally steroid responsive and stops disease progression

COPD - generally poorly responsive to steroids and dose not stop disease progression

35
Q

Warnings of using inhaled steroids

A

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
Q

Name systemic corticosteroids

A

Dexamethasone
Prednisolone
Hydrocortisone

Usually oral except give IV dexamethasone for cerebral oedema due to cancer

37
Q

Uses of systemic corticosteroids

A

1) Allery/inflammatory disorders
2) suppression of autoimmune diseases
3) Cancer
4) Hormones replacement

38
Q

What metabolic effects do systemic corticosteroids have

A

Increase gluconeogenesis from circulationg amino acids and fatty acids

39
Q

What mineracorticoid effects do systemic corticosteroids have?

A

Act like aldosterone

Cause sodium and water retention and potassium excretion

40
Q

Adverse effects of systemic corticosteroids

A

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
Q

Caution of systemic steroids in who

A

In infection ad children

42
Q

Interactions of systemic steroids

A

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
Q

What shall we consider the use of in long term systemic steroids use

A

Bisphosphonates –> stops osteoporosis
PPI –> prevents ulcers

In long term also monitor HbA1c and DEXA scans

44
Q

Name topical corticosteroids

A

Hydrocortisone, betamethasone

45
Q

Uses of topical steroids

A

Inflammatory skin conditions e.g. eczema

46
Q

Adverse effects of topical steroids

A

Potent can cause thinning of skin, striae, telangextasia, contact dermatitis
Perioral dermatitis and acne exacerbation if on face

47
Q

Contraindiciations of topical steroids

A

Infection present

Facial lesions

48
Q

How long can you use topical steroids for

A

2 weeks max, 1 week if on face

49
Q

Name NSAIDS

A

Naproxen, ibuprofen, diclofenac and etroicoxib

50
Q

What is etoricoxib

A

A Slective COX-2 Inhibitor

51
Q

What do you use NSAIDS for

A

As needed traetment for pain

Regular treatment of pain related inflammation

52
Q

What should you take NSAIDS with

A

FOOD –> avoids stomach upset

53
Q

How do NSAIDS work?

A

Inhbiit COX enzymes –> prevents the synthesis of prostaglandins from arachadonic acid

54
Q

What do the 2 different types of COX do?

A

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
Q

Whcih COX enzyme inhbition causes therapetic effects and which causes adverse effects

A

COX - 1 = adverse effects

COX - 2 = therapeutic effects

56
Q

Adverse Effects

A

GI toxicity
Renal Impairment
Cardiovascular events

Hypersensitivity
Fluid retention (espesically if given with loop diuretics)
57
Q

Who should we avoids NSAIDS in

A
Renal impairment
Heart failure
Peptic ulcer disaese
Liver failure
Hypersensitivity
58
Q

Interactions of NSAIDS

A

GI ulceration –> low-dose aspirin, corticosteroids
GI bleeding –> anticoagulants, SSSRIS, venlafaxine
Renal Impairment –> ACEi, diuretics

59
Q

Who should we consider gastroprotection in for NSAIDS?

A

1) OVer 65
2) Previous peptic ulcer disease
3) Other drugs with GI effects, particularly low dose aspirin and prednisolone

60
Q

Name some anticholinergics/antimuscuranics

A

Ipratropium

Tiotropium, glycopyronium (long acting)

61
Q

Uses of anticholinergives

A

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
Q

How do anticholinergics work?

A

Competitive inhibitor of acetylcholine at the muscarinic receptor!!

Normally receptor stimulation causes parasympathetic effects

63
Q

What happens when you block the anticholinergic receptor?

A

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
Q

Adverse effects of anticholinerigcs

A

Dry mouth

65
Q

Caution of using antichlinergics

A

Angle-closure glaucome
Can precipitate a dangerous rise in intraoccular pressure

Caution if arrhytmias

66
Q

Interactions of antibholinergics

A

Generally none as little systemic absoprtion as it is inhaled

67
Q

Name Beta-2-agonists

A

Salbutamol, terbutaline (short acting)

Salmeterol, formaterol (long acting)

68
Q

Indivations of beta 2 agonists

A

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
Q

How do beta - 2- agonists work

A

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
Q

Adverse effects of beta-2-agonists

A

Causes sympathetic response –> tachycardia, palpitations, fine tremore

Promotes glycogenolysis
Increaess serum lactate levels
Muscle cramp –> in long acting beta - 2- agonists

71
Q

Caution of using beta-2-agonists

A

Only give long acting with inhaled corticosteroids

Caution in patients with V –> tachycardia may provoke angina arryhythimias

72
Q

Interactions of beta-2-agonists

A

beta blockers reduce their effectiveness

Concommitant use of high dose nebulises beta 2 agonsit with theophylline and corticosteroids can cause hypokalaemia

73
Q

What is seretide

A

combo of long acting beta - 2 agonists and a corticosteroid

74
Q

Who do we give oxygen too

A

Hypoxaemia
Pneumothoraw
CO Poisonin

75
Q

How does oxygen treat a pneumothoraw

A

decreaesse the partial pressure of nitrogen in alveolar gas hence accelerates its diffusions out of the body

76
Q

How does oxygen treat CO poisoning

A

It competes with CO to bing to Hv therefore shortens the half life of carboxyhaemoglobin

77
Q

Adverse effects of oxygen

A

mainly due to the felivery methods e.g. discomfort from face mask
Dry throat due to lack of humidity

78
Q

Warnings of giving oxygen

A

Type 2 respiratory failure e.g. CO2, they have a hypoxic drive to breathe not hypercapnic

Heat sources/naked falmes

79
Q

Target oxygen saturations§

A

94-98% for normal

88-92% for COPD

80
Q

Name mucolytics

A

Carbocysteine

81
Q

Indicationsf or mucolytics

A

Respiratory disoders characterised by excessive, viscous mucus

82
Q

mechanism of carbocysteine

A

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
Q

Adverse effects of mucolytics e.g. carboysteine

A

Skin rashes
Hypersensitivity
Stomach bleeding

84
Q

Contraindications of mucolytics

A
Cough suppressants (antitussives)
Active peptic ulcer disaese
Lactose/fructose intolerance as contins these
85
Q

Interactions of carbocysteine

A

Increased risk/severity of adverse effects when combined with chloramphenicol, disulram, gliclazide, ketoconazole, metronidazole, griseofulvin

86
Q

What is theophylline

A

A methylxanthine

87
Q

What do we use theophylline to treat

A

Severe asthma/treat nocturnal asthma symtpoms

88
Q

How does theophylline work

A

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
Q

GI adverse effects of theophylline

A

Nausea, vomiting, anorexia

90
Q

Cardiovascular effects of theophylline

A

Dilatation of vascular smooth muscle –> headaches, flushing and hypotension
Tachycardia and cardiac dysrhytmias

91
Q

CNS effects of theophylline

A
Insomnia
Hypervenitlation
Anxiety
Agitations
Headaches
Fits
92
Q

Interactions of theophyliine

A

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)