Respiratory System Flashcards

1
Q

what host defences protect us from respiratory diseases

A

saliva, lymphoid tissue eg tonsils, alveolar macrophages

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2
Q

give an example of a disease causing sinusitis and how does it work

A

adenovirus, damages adhesions to cells, allows it to get through to mucosa and penetrate

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3
Q

give a virulence factor of streptococcus pyrogenes

A

exotoxins are haemolysis, break down blood cells, also protein m forming capsule

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4
Q

how does rheumatic fever result from strep pyrogenes

A

capsule is protective mechanism, form antibodies to this, but these are self reactive, attack sacrolemma of cardiac tissue, damages heart tissue

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5
Q

what is the difference between acute and chronic bronchitis

A

acute - happens over winter months due to virus

chronic - continuous cough for 3 months over 2 years

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6
Q

how does tb cause disease

A

has a thick capsule, macrophages engulf the bacteria, cannot lyse the capsule, so the bacteria continues to replicate inside the macrophages, giant cells form, if these liquify, the disease will spread in the body

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7
Q

what is pneumonia

A

inflammation of alveoli air sacs in lungs

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8
Q

how might pneumonia be acquired and what are pathogens are associated with disease

A

community - streptococcus pneumonia

hospital - staph aureus

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9
Q

what are 2 virulence factors of streptococcus pneumonia and how to they contribute to disease

A

pneumolysin - cleavage of proteins, allows adherence to alveoli cells, breaks down blood cells
capsulated - immune system can see bacteria but cannot get to it to attack it, chronic inflammatory disease

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10
Q

what are the treatments available for pneumonia

A

antibiotics - beta lactams, erythromycin
but resistance to these is increasing
so developing vaccine

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11
Q

how are drugs given by inhalation absorbed

A

powder which is topically by the airways, doesnt reach alveoli, is absorbed before then

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12
Q

how do bronchodilators aid respiratory disease

A

they act on beta 2 receptors as an agonist, opens up the airways, increase diameter, allows for better ventilation. or anticholinergic drugs block muscarinic nerve transmission to increase patency

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13
Q

how do anti-inflammatory’s aid respiratory disease

A

break down mucous being secreted, this prevents a blockage in the airway

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14
Q

what triggers an asthma attack

A

mast cell degranulation

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15
Q

what is chromoglycate used for

A

mast cell stabiliser

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16
Q

what drugs impair respiratory function

A

opiods and benzodiazepines

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17
Q

what are the 2 types of inhalers

A

Metre dosed inhaler - puffer, powder in air is pressed out an inhaled, but can go at a high velocity so more absorbed in mouth than airways
breath activated device - blow into the inhaler, activates the powder, this is then inhaled, much slower velocity, more likely to be absorbed in airways

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18
Q

what can be given with a puffer to improve efficacy

A

spacer - slows down velocity and allows for a higher concentration of dose to be given

19
Q

what are the 2 types of beta agonist inhalers

A

short acting - salbutamol, immediately opens airways, good in asthma attack, but only lasts up to 4 hours
long acting - salmeterol, takes 2 hours to start working but lasts 12-15 hours, may have affects on heart so must be used with steroid inhaler

20
Q

what is an anticholinergic inhaler available

A

ipratropium - grey, improves bronchodilation

21
Q

what steroid inhalers can be used

A

brown - beclomethasone, different shades of brown for different concentrations, indications of how severe asthma is
orange - fluticosone, pink - mometasone

22
Q

what inhalers would give an indication that the asthma is not too bad

A

blue only or green and brown

23
Q

what inhalers would indicate more severe asthma

A

orange or pink with green

24
Q

why are compound preparations useful

A

patients tend to stop taking brown inhaler as dont feel it is doing anything, take green only, compromise heart. so these can be put together in one inhaler to ensure patient receives both drugs

25
Q

what are symptoms of obstructive disease

A

cough - either dry or producing

wheezing or stridor, pain or dysponea - distress whilst breathing

26
Q

what are signs of obstructive disease

A

respiratory rate - normally 12-15 breaths per minute, but will be much higher if breathing is insufficient
chest movement, vocal resonance - speaking heard whilst sounding chest

27
Q

what investigations can be done into obstructive disease

A

peak expiratory flow rate - maximum flow
forced expiratory flow - in one second
chest x-ray

28
Q

what is vq mismatch

A

blockage in ventilation so not all alveoli receiving oxygen, blockage in arteries so not all alveoli being perfused, the alveoli being perfused are not being ventilated - results in no oxygen delivery to blood

29
Q

what is asthma

A

a reversible airflow obstruction

30
Q

what causes asthma

A

hyper-reactivity to un-harmful substance, e.g. cold air or exercise. causes mast cell degranulation resulting in inflammatory mediators - causes inflammation, mucous production and constriction of airway smooth muscle.

31
Q

what do patients with asthma complain of

A

shortness of breath, wheezing and coughing

32
Q

why can asthma be described as diurnal

A

when measuring PEFR this is lowering in the morning - ventilation is poor and more likely to have an attack. this then improves throughout the day.

33
Q

why can asthma be described as biphasic

A

first phase - due to bronchial constriction of smooth muscle

second phase - inflammation and mucous production narrows airways due to inflammatory mediators

34
Q

what drugs work at each phase

A

first phase - short acting beta agonist

second phase - corticosteroid

35
Q

what drugs are indicitve of severe asthma

A

long acting beta agonist, theophyline, oral steroid or been admitted to hospital due to asthma attack

36
Q

why are corticosteroids the most effective for preventing asthma

A

they attack the triad that causes obstruction - mucous production, inflammatory mediators and constriction

37
Q

what is a copd

A

combination of obstructive disease and destructive disease, irreversible

38
Q

what is destructive disease

A

emphysema - destruction of alveoli, the existing alveoli dilate to fill in space, results in reduced surface area for gas exchange - less oxygen into blood

39
Q

what causes copd

A

smoking is biggest cause - pack years related to worse disease, lower fev
may be occupational related - asbestos, resulting in fibrosis

40
Q

how is copd managed

A

bronchodilators and corticosteroids. or increasing oxygen delivery in severe copd

41
Q

what is the importance in dentistry with copd and asthma

A

inhalers - increased candida infections

oxygen - need to get it 24 hours a day, including during treatment

42
Q

what drives breathing in type 1 respiratory failure

A

hypercapnia - levels of carbon dioxide get too high

43
Q

what drives breathing in type 2 respiratory failure

A

hypoxia. chronic poor breathing, levels of carbon dioxide have been high so desensitised to it, dont recognise high levels to stimulate breathing so its low levels of oxygen that drive breathing