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BDS2 BAMS > respi meds > Flashcards

respi meds Flashcards

1
Q

2 components of respi system

A

ventilation and gas exchange

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2
Q

what affects ventilation

A

airway patency ie diameter
active muscles

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3
Q

what affects gas exchange

A
  • adequate number of alveoli
  • no fibrosis of alveolar wall
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4
Q

what is ventilation

A

moving gas from outside to inside px

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5
Q

whhat is gas exchange

A

exchange gas with blood at alveoli

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6
Q

if the lungs are filled with air, what colour is the lungs on xray

A

radiolucent

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7
Q

costaphrenic recess/angle

A

first place where fluid collects in lungs if got problem

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8
Q

function of ribs

A

main function is not protection

it is changing the intrathoracic volume to increase vol for air to enter

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9
Q

number of lobes in right lung

A

3

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10
Q

main muscles of respi

A

inter/ext intercostal muscles
oblique

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11
Q

accessory muscles function in breathing

A

prim function is not breathing but if needed example got breathing problem/ times of stress then it can be activated to assist

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12
Q

type of diffusion of gas

A

simple passive diffusion

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13
Q

how might you tell a patient is experiencing breathing difficulties (related to accessory muscles)

A

gripping arms by the side

pectoral accessory muscles activated for breathing, arms cannot move

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14
Q

type1 vs type 2 respi failure

A

type 1 gas exchange

type 2 ventilation failure

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15
Q

type 1 respi failure cause

A

gas exchange failure
- fibrosis
- inadequate number of alveoli
- VQ mismatch

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16
Q

type 2 respi failure cause

A
  • muscle problem
  • airway patency narrow
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17
Q

symptoms and signs of respi probems

A

symptoms - cough, sputum, blood, wheezing, stridor, dyspnoea, pain

signs - chest movement, rate of resp, vocal resonance, percussion

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18
Q

what is the appearance of the sputum in respi failure

A

sticky thick mucus may be bloody

heart failure sputum difference -> white frothy

CF -> thick sticky

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19
Q

what could pain be caused by when breathing

A

fracture, pneumonia, inflammation in chest wall

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20
Q

what could blood in cough be caused by

A

tumour, TB

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21
Q

normal rate of respi (bpm)

A

12-15 breaths per minute

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22
Q

in normal ppl shld there be vocal resonance and percussion when using stethoscope?

A

yes u shld hear vocal resoncance, otherwise means there is consolidation of a solid/liquid

dull instead of resonant percussion is bad because might mean liquid r solid filling the lung

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23
Q

respi investigations types

A

sputum
CT scan
spirometry
PEFR
bronchoscopy
VQ scan using radioisotopes

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24
Q

3 types of respi drug administration

A

inhalation
IV
oral

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25
Q

drugs used for ventilation and drugs used for gas ex

A

ventilation = bronchodilators, anti inflammatory ie steroid and cromoglycate/leukotriene

gas exchange = oxygen

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26
Q

types of bronchodilators

A
  1. B2 agonist
  2. anticholinergic
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27
Q

difference between B2 agonist and anticholinergic?

A

B2 binds to B2 receptors in airway and causes bronchodilation

Anticholinergic inhibits muscarinic nerve and reduces mucus, relaxes tone of smooth muscle

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28
Q

what do Cromoglycate inhaler and Leukotriene tablet do?

A

They reduce inflammatory mediators, by preventing mast cell degranulation,

they are more preventative measures, to prevent release of chemical mediators in the bronchial walls that initiate asthma

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29
Q

Drugs that impair ventilation

A
  • ** beta blockers**
  • respiratory depressants like opioids or benzodiazepines (used in iv sedation, need to monitor respi rate)
  • respi depressants reduce ventilation rate and causes smooth muscle relaxation
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30
Q

blue vs green B2 agnoist

A

blue short acting green long acting

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31
Q

most common bronchodilator

A

most commonly blue salbutamol (b2 agonist) for acute asthma attacks and

brown beclomethasone (corticosteroid) for preventative

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32
Q

Types of inhalers

A
  1. Meter dose
    a. with or without spacer
  2. Breath activated
    a. spinhaler
    b. turboinhaler
  3. Nebuliser
    a. gas bubbled through liquid
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33
Q

problem with meter dose

A

is that it fires all over oral pharynx and may cause local immunosuppression and sometimes candidiasis

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34
Q

why does long acting b2 agonist need to be taken with steroids

A

otherwise high risk of ACS

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35
Q

bronchitis vs Bronchiectasis

A

Bronchitis is an inflammatory disorder of the trachea and bronchial tubes. (mucus and infla)

Bronchiectasis is a disorder in which the bronchi widen and become destroyed due to infection. (damaged, scarred, thickened, widened, infection, cannot clear mucus, reduced dimeter, loss of normal lung structure )

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36
Q

Side effects of corticosteroids

A

adrenal suppression

candidiasis

osteoporosis?

SPACER recommended for every metered dose inhaler

37
Q

most effective asthma treatment

A

corticosteroids

but be aware of the side effects like risk of fungal,bact,viral infctions, osteoporosis, adrenal suppression?

38
Q

what is CF

A

recessive gene; genetic disease that causes Production of excess sticky mucus in various organs, but mainly lungs and pancreas

Defect of chloride ion channels (either opens abnormally or cannot open at all)

39
Q

what mutation in CF

A

F508del mutation of CFTR gene on chromosome 7

Recessive gene

40
Q

in CF sweat test, what ae we looking out for

A

Sweat test – higher chloride ion conc in sweat => most likely have CF

41
Q

best test for CF

A

CFTR gene testing

42
Q

symptoms of CF

A

Pulmonary infection (Staphylococci)

Coughing

Chest infections

Malnutrition due to pancreatic insufficiency

Poor weight gain

Prolonged diarrhoea

Asthma with clubbing and bronchiectasis

43
Q

why would someone with CF have osteoporosis

A

Osteoporosis due to lack of vitamin D

Deficient in pancreatic enzymes, cannot absorb fat dependent vitamins (ADEK)

44
Q

how is CF linked to diabetes and liver dysfunction

A

mucus to build up and block bile ducts in the liver. This prevents bile from leaving the liver, which causes inflammation and produces scarring. permanent scarring of the liver, called cirrhosis

The build-up of sticky mucus caused by cystic fibrosis can lead to inflammation and scarring of the pancreas. This can damage the cells that produce insulin and lead to high blood glucose (sugar) levels. As the pancreas can’t produce enough insulin, blood sugar levels may continue to rise.

45
Q

tx for CF

A

physio therapy to drain excess mucus

medications

exercise to improve lung function and build bone mass

transplatn

46
Q

meds used in CF

A

bronchodilators

antibiotics (but try not to overprescribe can cause ABR)

steroids

pancreatic enzyme replacement

nutritional supplements

**CFTR modulators **

stem cell therapy

47
Q

CFTR modulators best used on which px

A

px with F508del mutation

48
Q

is asthma reversible

A

yes REVERSIBLE airflow obstruction

49
Q

what is asthma

A

Bronchial hyper reactivity, changes in bronchial walls restricting air flow in and out

Allergen -> T cell-> B cell-> IgE production-> mast cell degranulation -> histamine and leukotrienes -> bronchoconstriction, oedema and mucus secretion

1 Bronchial SM constriction
2 Oedema in mucosa
3 Mucus secretion into airway lumen

50
Q

causes of asthma

A

unknown/

infections/

environmental stimuli like dust and smoke/

warm->cold air/

atopy ie hypersensitivity allergy

51
Q

dental risk assessment for asthma patients

A

full medical history

severity

triggers to avoid

position patient in emergency

emergency drug kit

when to call ambulance

52
Q

symptoms of asthma

A

Cough caused by mucus causing irritation

Wheeze

SOB

Diurnal variation **worse in overnight and early morning

More problems with exhaling than inhaling since there are muscles to support inhalation

53
Q

what is biphasic response in asthma

A

early/acute
breathlesses wheezing
B2 agonists used

late
corticosteroids used to prevent the late response in severe acute asthma attacks

54
Q

meds used for asthma

A

1 blue/green SA/LA bronchodilators B agonists

2 brown/purple/others LD/HD corticosteroids
For most severe asthama, given daily steroids

3 Regular montelucast

4 Pulsed oral steroid - prednisolone
leukotriene inhibitor
prevents mast cell degranulation

5 Monoclonal antibodies therapy

55
Q

Look at the colour of their inhaler to help determine severity of their asthma

A

Blue and brown -> SA B2 agonist and LD corticosteroid

Green and purple -> LA B2 agonist and others (moderate to severe asthma)

56
Q

types of lung tumours

A

Central tumours

Peripheral tumours

ALL ARE MALIGNANT

1 Small cell

2 Non small cell
- SCC (most common, centrally located, SMOKING biggest cause)
- Large cell
- Adenocarcinoma

57
Q

causes of lung tumours

A

smoking,

genetics,

radiation,

chemicals,

pollution,

other lung diseases like COPD or pulmonary fibrosis

58
Q

symptoms of lung cancer

A

Cough

SOB

Fatigue

Haemoptysis (blood stained sputum)

Pneumonia and repeated respi infections (occlusion of main bronchi)

Metastasis

dysphagia

SVC obstruction

Recurrent laryngeal nerve palsy -> hoarseness

59
Q

how does lung tumours cause dysphagia and SVC obstruction

A

Central tumour compresses oesophagus and SVC as it passes the mediastinum

for svc obstruction, prevents blood retuning from upper part of body, oedema in arms head neck

60
Q

when is lung tumours usually found

A

stage 3 and 4 which is too late, poor prognosis

Stage 3 involves both side of the bronchus

Stage 4 involves oedema, fluid, pneumonia, metastasis

61
Q

what is sleep apnoea

A

Airway obstruction when sleeping

10sec or more

Muscle tone drops -> tongue falls back and blocks airways by occluding back of the pharynx

people with OSA experience a collapse of their airways during sleep. When this causes their breathing to completely stop or reduce to 10% of normal levels for at least 10 seconds, it is called an apnea.

62
Q

sleep apnea px are at risk of what?

A

Increased risk of MI

do not get enough oxygen, continual periods of hypoxia

63
Q

how to measure sleep apnoea

A

Measure with AHI

The apnea-hypopnea index (AHI) represents the average number of apneas and hypopneas you experience each hour during sleep.

Key to long term survival is to have lesser episodes per night

64
Q

management of sleep apnea

A

1 Mandibular advancement appliance

2 CPAP – continuous positive airway pressure
NOT a ventilator , provides pressure to keep space between tongue and pharynx

3 Sleep apnoea positional therapy

65
Q

what is COPD

A

COPD has damage both to the airways and the alveoli, so less ability to ventilate and gas exchange

Chronic bronchitis (inflammation and mucus) non reversible damage

Emphysema (destruction of alveoli, enlarged sacs, reduced SA for gas exchange) non reversible

Asthma component REVERSIBLE

66
Q

causes of copd

A

Smoking

Pollution

Genetics

Age

Chemicals

Chronic bronchitis

Asthma

67
Q

diagnosing copd

A

CAT = COPD assessment test

Exacerbation history

No. of symptoms

Spirometer

Airflow limitation

FEV

68
Q

exacerbation of chronic obstructive pulmonary disease (COPD)

A

An acute exacerbation of chronic obstructive pulmonary disease (COPD) is a sustained worsening of a person’s symptoms from their usual stable state

cause by infection (viral, bacterial) or

non infection (noncompliance with meds or environmental factors)

69
Q

symptoms of copd

A

Productive chronic cough

Green sputum

SOB

Dyspnoea

Chest discomfort

Fatigue

Mucus

70
Q

what can copd lead to

A

Heart failure

Pneumonia

ARDS (acute respiratory distress syndrome)

type 1 or 2 respiratory failure

71
Q

how does copd lead to pneumonia

A

Chronic inflammation interferes with the body’s natural ability to clear and destroy bacteria that enter into the lung, leading to infection

72
Q

ARDS

A

severe inflammation of the lungs causing fluid to leak into the BV in the airways

can be fatal

73
Q

treatment for copd

A

Fundamental tx method is NON drug based

  • Offer smoking cessation
  • Flu vaccinations prevents infection
  • Pulmonary rehabilitation (graded exercise programmes)

if they dont work then use inhalers (bronchodilators, steroids, oxygen)

74
Q

when to use steroid in copd

A

Steroids if FEV<50% (used if there is significant airway inflammation)

75
Q

what to watch for when using oxygen theraoy for copd

A

When using oxygen, make sure to watch respiratory rate because oxygen reduces body drive to breathe

76
Q

***rmb that for asthma, can determine severity based on medication they use eg colour of inhaler

But for COPD, cannot assess severity based on their medications, every person is different

A
77
Q

when to prescribe antibiotics to copd patients

A

ANTIBITOICS may be prescribed for severe COPD patients to use in the case of acute exacerbations

78
Q

Dental implications for copd

A

Have oxygen in clinic

Be careful oxygen is flammable

Inhaled steroids candida risk

Use spacer for MDI inhalers

Smoking cessation advice

Smokers have increased oral cancer risk so should screen

79
Q

Home oxygen therapy for COPD useful?

A

Effective if used 24h each day, significant increase in survival

Intermittent use of NO help -> low level hypoxia throughout the day make ACS events more likely (cvs risk of sudden death)

80
Q

pinkpuffer and blue bloater are which type of respi failure?

A

pink puffer => type 1 (gas exchange failure)

blue bloater => type 2 (ventilation failure)

81
Q

is pink puffer emphysema or chronic bronchitis?

A

emphysema

blue bloater -> chronic bronchitis

82
Q

is type 1/2 respi failure hypoxaemia or hypercapnia

A

type 1-> pink puffer (hypoxaemia)

type 2-> blue bloater (hypercapnia)

83
Q

Hypoxaemia

A

Hypoxaemia ie low oxygen (PaO2 <8kPa or SaO2 <90%)

84
Q

Hypercapnia

A

Hypercapnia (PaCO2 >6.7kPa

CO2 retention due to ventilation failure)

85
Q

symptoms of pink puffers

A

hyperventilation
pink because oxygenated
minimal cough

Reduced SA for gas exchange
Thickening of alveolar barrier
Diffusion abnormality
VQ mismatch

86
Q

symptoms of blue bloaters

A

cyanosis
wheezing
productive cough chronic
purulent sputum
Exacerbations caused by oedema and mucus

87
Q

is type 1 or 2 ACUTE respi failure

A

type 2

88
Q

CO2 retention

A

blue bloater
ventilation failure
co2 cannot be expelled

89
Q

Why and when is emergency supplemental oxygen supplied and not supplied to a patient in reference to COPD?

A

If the patient is Hypoxic (low blood oxygen), then oxygen can be given to patients suffering from acute COPD

however emergency oxygen cannot be used for patients with chronic COPD

BDS2 BAMS (27 decks)

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