lec 17 - lung and heart Flashcards

1
Q

what structures are part of the upper resp tract

A

nasal cavity, pharnyx, larynx

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2
Q

what structures are part of the lower resp tract

A

trachea, primary bronchi, lungs

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3
Q

what are examples of lung infections

A

bronchitis and pneumonia

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4
Q

what are the two types of bronchitis

A

acute - viral and bacterial
chronic - airway changes associated with COPD (chronic obstructive pulmonary disease) - smoking/genetic

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5
Q

what is the treatment for bronchitis

A

inhalers and antibiotics (for bacterial infection only)

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6
Q

what is pneumonia

A

lobe infection in distal bronchioles and alveoli
can get multilobar infection from virus or bacteria

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7
Q

what is the treatment for pneumonia

A

anitbiotics or antivirals depending on type of infection

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8
Q

what is a pneumothorax

A

punctured lung
commonly spontaneous (small and heals by itself)
can be from trauma such as broken rib puncture

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9
Q

what are the symptoms of a pneumothorax

A

short of breath, possible pain

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10
Q

what is the treatment for a pneumothorax

A

small = watch and monitor
large = chest tube

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11
Q

what is a tension pneumothorax and why is it an emergency

A

air gets out of the lungs and expands the space outside the lungs
- shifts the mediastinum causing a vena cava kink
- decreases oxygenation and venous return
- emergency!!

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12
Q

what is a hemothorax

A

blood in the chest cavity
- from broken rib, bleeding vessels, sharp trauma
- marfan syndrome = from aortic aneurysm

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13
Q

what are the signs and symptoms of a hemothorax

A

short of breath and pain
decreased oxygenation
blood loss

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14
Q

what is the treatment for a hemothorax

A

chest tube at the hospital

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15
Q

what is asthma

A

reversible airway disease characterised by airway narrowing and inflammation
- provoked by allergens, exercise, fog, cold air, infection, etc

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16
Q

what are the symptoms of asthma

A

all symptoms are expiratory!
- wheezing
- coughing
- both of the above adn chest tightness with exercise

17
Q

what is the net effect of the inflammation caused in asthma

A

expiratory resistance and air trapping

18
Q

what is the number 1 issue in asthma that drives the treatment

A

inflammation

19
Q

what are the long term results of asthma

A

denudation of epithelium
collagen deposition
airway remodelling

20
Q

what is the progression/pathology of asthma

A
  1. inflammation causes disruption to ciliated epitheilum
  2. irritation causes increased mucous production
  3. mucus can’t get up the bronchioles normally because the cilia is damaged
  4. causes smooth muscle hypertrophy
  5. lumen is decreased in diameter
21
Q

what are the different types of treatment for asthma

A

anti inflammatories
- corticosteroid puffers = main
smooth muscle relaxants
- B2 agonists (need therapeutic use exemption)
— terubutaline - short acting (SABA)
— clenubterol - long acting (LABA)

22
Q

what are the recommendations for asthma treatment

A

combined inhaler with corticosteroids and LABA (clenbuterol)
- good short term control and prevents exacerbation of asthma

(traditionally treated with SABA before exercise)

23
Q

what is a PFT test (pulmonary lung function test) used for

A

usually the standard for asthma diagnosis

24
Q

what are the thresholds for tachycardia and bradycardia

A

tachy = >100 bpm
brady = <60 bpm (commonly seen in athletes)

25
Q

what is sudden cardiac death in sport

A

exercise stimulated fatal dysrhythmia
tragic - receives disproportionate degree of public scrutiny
rare event
commonly death is the first indication of problem

26
Q

what is the prevalence of sudden cardiac death in sport

A

male to female = 2:1
usually around high school and early college age
0.75 in 100 000 athletes per year (3x higher than no athletes)

27
Q

what is hypertrophic cardiomyopathy (HOCM)

A

when the heart muscle gets too big
- usually genetically transmitted
- mutations may have malignant / benign cause
- death may occur without other symptoms during moderate to severe exertion

28
Q

what does HOCM cause within the heart

A

left ventricle wall thickening
- asymmetric
- distorted cellular architecture
- abnormal coronary arteries

29
Q

what are the mechanisms of sudden death from HOCM

A

ventricular dysrhythmias
sudden hemodynamic instability
- exercise induced hypotension
- increased LV outflow obstruction
- brady dysrhythmias

30
Q

what is commotio cordis

A

blunt chest trauma over heart (sternum)
hits just before T wave (repolarisation) causing the heart to go into ventricular fibrillation (v fib)

31
Q

what is the only immediate treatment for commotio cordis

A

AED - need to shock out of v fib

32
Q

what is the greatest cause of morbidity and mortality in gen pop

A

heart disease

33
Q

what is atherosclerosis

A

decreased diameter of vessels
- increased fat, scarring, and plaques in the vessel wall

34
Q

what causes atherosclerosis

A

genetics, LDL cholesterol, triglycerides, tobacco, lack of exercise and obesity, diabetes, hypertension, old age

35
Q

what are options for screening for heart conditions

A

PAR-Q+ for those wanting to be active
- not very helpful for younger people usually
heart tests not normally required in screening
- cost implications for ECG and ECHO
history and physical exam

36
Q

what occurs during the parts of the ECG
- P wave, QRS complex, T wave

A

P wave = depolarisation of L/R atrium (SA node)
QRS complex = ventricular depolarisation
- atrial repolarisation hidden in here
T wave = ventricular repolarisation