PPT Flashcards

1
Q

How do we use CURB65 to aid management of pneumonia?

A

CURB65 score of…
0-1 - low risk so consider treatment with oral amoxicillin at home
2 - probable admission and treat with oral amoxicillin or doxycycline
3-5 - admission and manage with IV co-amoxiclav or IV clarithromycin

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2
Q

Why do we manage severe pneumonia with IV co-amoxiclav?

A

If its severe there is a higher chance of it being an atypical pneumonia - co-amoxiclav has a broader spectrum than amoxicillin

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3
Q

Why is amoxicillin the first line antibiotic for mild pneumonia?

A

As the most common microorganism is S.pneumonia

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4
Q

What is the risk of cross-reactivity between a cephalosporin and penicillin allergy? Why?

A

Up to 10%
They are both beta lactase’s

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5
Q

Outline the MOA, main and serious side effects, interactions and contraindications of penicillins?

A

Interfere with bacterial cell wall synthesis
SE - diarrhoa, n+v, hypersensitivity, thrombocytopenia, agranulocytosis, hepatic and nephritic impairment
Severe SE - severe skin reactions, anaphylaxis, pseudomembranous colitis
Interactions - warfarin, phenindione, methotrexate, acenocoumarol
Contraindications - Hx of allergy to penicillins or cephalosporins

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6
Q

Outline the MOA, main and serious side effects, interactions and contraindications of tetracyclines?

A

Allosterically bind to 30S prokaryotic ribosomal subunit
SE - angioedema, d+v+n, photosensitivity, HSP, exacerbates SLE, pericarditis
Serious SE - liver and kidney damage, intercranial hypertension
Interactions - warfarin, tretinoin, phenidione, lithium, Ciclosporin and acenocournarol
Contraindication s- pregnancy

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7
Q

Outline the MOA, main and serious side effects, interactions and contraindications of macrolides?

A

Inhibit protein synthesis by binding 50S ribosomal subunit
SE - reduced appetite, d+n+v, dizziness, hearing impairment, insomnia, pancreatitis, skin reactions, paraesthesia, vasodilation, vision disorders
Contraindications - liver disease and QT prolongation

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8
Q

Outline the MOA, main and serious side effects, interactions and contraindications of cephalosporins?

A

Bind to penicllin binding protein and interrupt cell wall biosynthesis = bacterial cell lysis
SE - abdo pain, d+n+v, dizziness, eosinophilia, leukopenia, neutropenia, thrombocytopenia, pseudomembranous colitis, skin reactions, vulvovaginal candidiasis

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9
Q

What is antimicrobial stewardship?

A

An organisational or healthcare-system-wide approach to promoting and monitoring judicious use of antimicrobial to preserve their future effectiveness

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10
Q

What are BTS recommendations for antimicrobial prescribing in pneumonia?

A

The diagnosis of CAP and the decision to start antibiotics should be reviewed by a senior clinician at the earliest opportunity.
There should be no barrier to discontinuing antibiotics if they are not indicated.
The indication for antibiotics should be clearly documented in the medical notes.
The need for IV antibiotics should be reviewed daily.
De-escalation of therapy, including the switch from intravenous to oral antibiotics, should be
considered as soon as is appropriate, taking into account response to treatment and changing
illness severity.
Strong consideration should be given to narrowing the spectrum of antibiotic therapy when specific patho-gens are identified or when the patient’s condition improves.
Where appropriate, stop dates should be specified for antibiotic prescriptions

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11
Q

What are the principles of antimicrobial prescribing?

A

Right antibiotic - what organisms could be infecting? What risk factors for resistance does this pt have?
Right pt
Right time - did you obtain cultures before? We’re antibiotics administered within an hour?
Right dose - appropriate for renal/hepatic function?
Right route - are they a candidate for oral treatment?
Least harm - are we choosing the most narrow spectrum and minimum duration and least amount of SE?

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12
Q

What types of healthcare acquired infections does the use of broad spectrum antibiotics predispose to?

A

C.diff
MRSA
E.coli infections

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13
Q

What antibiotics are typically used for atypical pneumonia?

A

Macrolide antibiotics

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14
Q

What drug therapy is given in TB?

A

Isoniazid, rifampin, Pyrazinamide and ethambutol for 2 months
Isoniazid and rifampin for 4 additional months

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15
Q

Why is TB drug therapy given in 2 phases?

A

Because TB bacteria have different growth rates and are susceptible to different drugs at different stages of their life cycle.

The first phase (intensive phase) typically lasts for 2 months - isoniazid, rifampicin, pyrazinamide, and ethambutol. These drugs are effective against actively dividing TB bacteria and help to rapidly reduce the bacterial load in the body. The intensive phase is important because it can quickly reduce the number of bacteria, reducing the risk of transmission to others.

The second phase (continuation phase), which typically lasts for an additional 4 months. isoniazid and rifampicin, which are effective against dormant TB bacteria that are not actively dividing. The continuation phase is important to ensure that all the TB bacteria in the body are eliminated, reducing the risk of relapse and preventing the development of drug-resistant TB.

By using a combination of drugs in two phases, TB treatment can effectively target both actively dividing and dormant bacteria, leading to a higher cure rate and reduced risk of relapse. It is important to follow the full course of treatment to ensure complete recovery and to prevent the development of drug-resistant TB.

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16
Q

What are the main SE of rifampicin?

A

Orange urine/tears
Hepatotoxicity

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17
Q

What are drug interactions for rifampicin?

A

can reduce plasma concentrations of oestrogen in those
taking oral contraceptives and of many other
drugs including warfarin, phenytoin and
sulphonylureas
Inducers and inhibitors of CYP3A4 (inhibitors include protease inhibitors used in HIV, macrolide antibiotics, antifungal, non-hydropyridine CCB) (inducers include anticonvulsants, st joins wort and glitazones)

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18
Q

Whats the moa of isionazid?

A

It’s a pro-drug activated by catalase–peroxidase activity within the mycobacteria. The active product inhibits enzymes involved in the synthesis of long-chain mycolic acids, which are unique to the cell wall of mycobacteria, and also inhibits enzymes required for nucleic acid synthesis.
Isoniazid is bactericidal against dividing mycobacteria, but bacteriostatic on resting mycobacteri

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19
Q

What are the main SE of isoniazid?

A

Hepatotoxic
Peripheral neuropathy

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20
Q

Why is Pyrazinamide not used as the sole treatment for TB?

A

Rapid resists acid develops

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21
Q

Which anti-TB drug works best for tuberculosis meningitis and why?

A

Pyrazinamide - it crosses the blood-brain barrier

22
Q

What are the adverse effects of ethambutol?

A

Visual disturbances
Peripheral neuritis
Hyperuricaemia and gout
Nephrotoxicity

23
Q

What non-pharmacological treatments should be discussed with asthma patients?

A

Lifestyle advice
Weight loss
Smoking cessation
Avoid triggers
Breathing exercise programmes

24
Q

What are examples of SABAs?

A

Salbutamol
Terbutaline

25
Q

When may terbutaline be used over salbutamol?

A

When the pt wants to use a dry powder

26
Q

Whats the MOA of SABA?

A

Activation of beta adrenergic receptors leads to relaxation of smooth muscle in the lung and dilation and opening of the airways
They also inhibitor mast cells and monocytes releasing mediators
They also increase mucus clearance by cilia

27
Q

What are SE of beta-2-adrenoreceptor agonists?

A

Arrhythmias and palpitations
Tremor
Headache
Hyperglycaemia
Behavioural disturbances
Hypokalaemia (rare)
Paradoxical bronchospasm

28
Q

Why are inhaled corticosteroids used instead of oral steroids in asthma?

A

They have significantly fewer side effects compared to oral steroids

29
Q

When using inhaled corticosteroid, what proportion of the drug gets inhaled and what protects you from the rest?

A

Only 10-20%
80-90% is swallowed but this is protected by first pass metabolism in the liver
This can also be decreased by using a spacer and a mouth rinse

30
Q

What are side effects of inhaled corticosteroids>

A

Oral candidiasis
Hoarse voice
Cough
Nosebleeds

31
Q

Before upping meds for asthma treatment what should you do?

A

Check adherence
Check inhaler technique
Offer a spacer device if appropriate

32
Q

Why are combination inhalers recommended for asthma?

A

They garuntee that the LABA is not taken without inhaled corticosteroid
They improve inhaler adherence

33
Q

What are the differences in NICE and BTS/SIGN guidance for asthma treatment?

A

NICE suggest using an LTA whereas BTS/SIGN recommends a LABA before this

? Maybe because NICE are more concerned about cost effectiveness and LTAs are significantly cheaper than LABAs

34
Q

Whats the main differences between formoterol and salmeterol?

A

Formoterol has a faster onset of action but they both have a long duration of action. This means formoterol can be used as a relieve and preventor
Formoterol is a full agonist of beta receptors whereas salmeterol is partial

35
Q

Whats the moa of LAMAs?

A

They bind to muscarinic receptors, reliving vagal tone on the smooth muscle which causes dilation
Used more often in COPD than asthma

36
Q

What is aminophylline?

A

A combination of theophylline and ethylenediamine - its IV

37
Q

Whats the moa of theophylline?

A

It’s a methylxanthine that inhibitors phosphodiesterase and blocks adenosine receptors

38
Q

When is theophylline indicated?

A

In status asthmaticus

39
Q

What are the issues with theophylline?

A

Causes CNS toxicity in overdose
Can cause cardiac arrest

40
Q

Whats an example of a LTA?

A

Montelukast

41
Q

What are the features of moderate acute asthma?

A

Increasing symptoms
PEFR >50-75% best or predicted
No features of acute severe asthma

42
Q

What are the features of acute severe asthma?

A

Any one of:
PEFR 33-50%
RR >=25
HR>= 110
Inahibility to complete sentences in 1 breath

43
Q

What are the features of life-threatening acute asthma?

A

Any one of:
PEFR <33%
SpO2 <92% or PaO2 <8
Normal PaCo2
Altered conscious level or exhaustion
Arrhythmia
Hypotension
Cyanosis
Silent chest
Poor resp effor

44
Q

What are the features of near-fatal acute asthma?

A

Raised PaCO2
Requiring mechanical ventilation with raised inflation pressures

45
Q

Why are beta-2-agonists given as nebulised therapy in acute asthma?

A

Faster
Drug dose is greater

46
Q

What steroids are given in acute asthma?

A

IV hydrocortisone or oral prednisolone

47
Q

What non-pharmacological management measures can you do for confined COPD?

A

Offer support to stop smoking
Offer pneumococcal and influenza vaccines
Offer pulmonary rehabilitation
Co-develop a self management pan
Optimise treatment for comorbidities

48
Q

Outline the NICE guidance for medical management of COPD?

A

1: Offer SABA or SAMA to use as needed
2: if asthmatic features/steroid responsiveness - LABA +ICS. If no asthmatic features/steroid responsiveness - LABA + LAMA
3: if asthmatic features/steroid responsiveness - LABA + LAMA + ICS. If no asthmatic features/steroid responsiveness - 3 month trial of LABA + LAM +ICS and if no improvement revert to LABA + LAMA

49
Q

Why may steroids be controversial in COPD management?

A

Due to increased risk of bacterial pneumonia

50
Q

What is the hypoxic drive?

A

a form of respiratory drive in which the body uses oxygen chemoreceptors instead of carbon dioxide receptors to regulate the respiratory cycle.

Normal respiration is driven mostly by the levels of carbon dioxide in the arteries, which are detected by peripheral chemoreceptors, and very little by the oxygen levels. An increase in carbon dioxide will cause chemoreceptor reflexes to trigger an increase in respirations.

However in cases where there are chronically high carbon dioxide levels in the blood such as in COPD patients, the body will begin to rely more on the oxygen receptors and less on the carbon dioxide receptors. In this case, when there is an increase in oxygen levels, the body will decrease the respirations
I f a person with chronic hypoxic drive enters acute respiratory distress, healthcare providers who are unaware of their condition may provide oxygen therapy as an initial treatment. The reaction to increased oxygen causes the oxygen receptors to decrease respirations, possibly to the point of respiratory arrest. For this reason, people with hypoxic drive must not receive oxygen in high concentrations or for long periods.

51
Q

SE of pyrazinamide?

A

hepatitis
hyperuricaemia
arthralgia