LO2 description, aetiology and pathophysiology

Question 1

describe COPD

Answer 1

-persistent and chronic airflow limitation
-usually progressive
-can lead to chronic bronchitis or emphysema

Question 2

what is chronic bronchitis?

Answer 2

• a cough that produces sputum
• lasts 3 months of the year
• for 2 years or more
  -not due to specific resp disease eg bronchiectasis

Question 3

pathology of chronic bronchitis

Answer 3

-repeated inhalation of smoke
-irritation of sensitive linings
-inflammation

Question 4

what is emphysema?

Answer 4

-abnormal permanent enlargement of the air spaces distal to the terminal bronchioles
-destruction of alveolar walls

Question 5

pathology of emphysema

Answer 5

-inhalation of noxious particles cause inflammation
-induces release of neutrophils
-breaks down alveolar septa
-this reduces surface area for gas exchange and reduced elastic recoil

Question 6

clinical features of copd?

Answer 6

-progressive dyspnoea (sob)
-chronic productive cough
-sputum production
-limited exercise capacity

Question 7

aetiology of copd

Answer 7

-smoking
-inhaled environmental irritants (smog/dust/chemicals)
-chronic asthma
-alpha-1 antitrypsin deficiency (genetic)

Question 8

pathophysiology of copd

Answer 8

-increased mucus production
-mucus gland hypertrophy
-destruction of ciliated epithelial cells
-chronic inflammatory changes
-increase in bronchial smooth muscle
-chronic inflammatory changes
-small airway fibrosis

Question 9

epidemiology of copd

Answer 9

gender: men>women

location: 90% in low/middle income countries
<scotland and north of england

age: mean age= 67yrs
9% >70yrs

Question 10

describe pneumonia

Answer 10

-inflammatory condition
-primarily affects the alveoli - fill with pus or fluid
-can be lobar or bronchial
-can be community, hospital or ventilator-acquired

Question 11

clinical features of pneumonia

Answer 11

-breathlessness
-fatigue/confusion
-fever (pyrexia)
-tachicardia/tachypnoea
-sputum production
-pleuritic pain

Question 12

aetiology of pneumonia

Answer 12

-normally caused by infection:
bacterial (streptococcus pneumonia), viral or fungal

-invasion or overgrowth of pathogens in lung parenchyma = intra-alveolar exudates
-depressed conscious states or swallowing difficulties (aspiration pneumonia)

Question 13

pathophysiology of pneumonia

Answer 13

-acute inflammatory response due to invasion of pathogens in lungs

4 stages:
-congestion (first 24hrs)
-red hepatisation (day 2-5)
-grey hepatisation (day 4-8)
-resolution (day 8-10)

Question 14

what is the congestion (first 24 hrs) stage of pneuomia?

Answer 14

-bacteria in lungs
-white blood cells unable to fight infection

Question 15

what is the red hepatisation (days 2-5) stage of pneumonia?

Answer 15

-presence of many erythrocytes, neutrophils and fibril in alveoli
-are of lung becomes dry, granular and airless

Question 16

what is the grey hepatisation (day 4-8) stage of pneumonia?

Answer 16

-fibrin and red blood cells begin breaking down
-results in fibro-purulent fluid like exudate in alveoli
-macrophages appear

Question 17

what is the resolution (days 8-10) stage of pneumonia?

Answer 17

-fluids and broken-down products from cell destruction reabsorbed
-macrophages help clear away neutrophils and cell debris

Question 18

what is lobar pneumonia?

Answer 18

-infection localised and confined to one or two lobes
-normally caused by streptococcus pneumonae

Symptoms:
-pleuritic pain, sudden onset, high fever and rusty sputum

Question 19

what is bronchopneumonia?

Answer 19

-diffuse pattern of infection in both lungs
-commonly in lower lobes
caused by multiple microorganisms

symptoms:
-insidious onset, moderate fever, productive cough with yellow or green sputum, fine crackles in lower lobes

Question 20

what is community acquired pneumonia (CAP)?

Answer 20

pneumonia acquired outside a hospital

Question 21

what is hospital acquired pneumonia (HAP)?

Answer 21

pneumonia apparent more that 48hrs after hospital admission

Question 22

what is ventilator associated pneumonia (VAP)?

Answer 22

pneumonia becomes apparent after 48hrs of intubation

Question 23

diagnosis of copd?

Answer 23

-fever
-malaise
-persistent cough
-pleuritic pain
-secretions
-cxr changes

Question 24

what is spasticity?

Answer 24

-a positive feature of the upper motor neurone syndrome
-increase in tone (hypertonia) and stiffness in muscle group
-increased resistance to voluntary and/or passive movement
-velocity-dependant increase in tonic stretch reflexes

Question 25

clinical features of spasticity

Answer 25

-hyperexcitability of stretch reflex -velocity dependent - the faster the muscle is moved or stretched the greater the resistance to stretch or passive elongation -impaired movement - lower limb pattern = plantar flexion and inversion of ankle with hamstring tightness, limiting knee ROM and adductor spasticity -upper limb pattern = shoulder adduction, internal rotation, elbow flexion, forearm pronation with wrist and elbow flexion

Question 26

aetiology of spasticity

Answer 26

-disruption and damage to areas of the brain involved in sensory processing, motor planning and motor control -altered sensory input from poor alignment, poor muscle activation, inappropriate proprioceptive input from muscle spindles/joint kinaesthetic receptors and altered cortical input -Disruption in communication to the reticular formation, affecting its ability to modulate muscle tone properly. -Damage or lesion to descending motor pathways (e.g., corticospinal tract, reticulospinal tract) leading to loss of normal tone regulation

Question 27

pathophysiology of spasticity

Answer 27

-Normal tone regulation: Controlled by reticular formation in brainstem, input from the cerebellum and basal ganglia regarding movement and required muscle tone. Reticulospinal Tracts: Medial reticulospinal tract is excitatory onto the stretch reflex, inc response. Lateral reticulospinal tract is inhibitory onto the stretch reflex, helping to modulate the muscle tone. Interplay between tracts: Normally, there's a balance between the excitatory medial tract and the inhibitory lateral tract to maintain the desired muscle tone. Disruption of balance: there is a disruption in communication (due to damaged sensory input, improper alignment, or altered motor input), the interaction between these two tracts is disrupted, leading to an imbalance in muscle tone. Lack of descending inhibition: There is a lack of descending inhibition from the lateral reticulospinal tract onto the stretch reflex, causing unopposed excitatory action from the medial tract. Hyper-reactive muscle spindles: Muscle spindles become hyper-reactive, feed into cycle of increased tone, stimulating alpha motor neurons and contributing to spasticity. Intrinsic muscle changes (soft-tissue adaptations): Loss of viscoelastic properties in the muscle. Loss of sarcomeres (the contractile units of muscle). Increase in non-contractile collagen in the muscle tissue, leading to stiffness and loss of muscle flexibility.

Question 28

description of stroke

Answer 28

-cardiovascular accident (CVA) -acute focal change in cerebral function of presumed vascular origin -symptoms last longer than 24 hours -85% are ischaemic (thrombolytic and embolytic) -15% haemorrhagic (intracerebral)

Question 29

what is a TIA?

Answer 29

a 'mini' stroke with symptoms that last less than 24 hours

Question 30

clinical features of a stroke

Answer 30

-upper motor neurone syndrome -hyperreflexia -clonus -positive Babinski -tonal changes -hemiparesis -sensory loss may also have: -visual disturbances -disturbances in balance -dysphagia

Question 31

aetiology of stroke

Answer 31

non-modifiable: age, sex, ethnicity, genetics modifiable: hypertension, diabetes, hypercholesterolemia, cardiac factors (AF), smoking, obesity, excessive alcohol, sedentary behaviour

Question 32

pathophysiology of stroke

Answer 32

-disruption of blood in the brain -lack of oxygen and nutrients leads to necrosis of neurons -build up of toxins (glutamate) exacerbates cell death -penumbra - area of viable tissue supporte by collateral circulation (circle of Willis) -most common site is MCA -MCA supplies frontal, parietal, temporal lobes, basal ganglia and internal capsule -frontal - executive functions/planning, motor cortex -parietal - processing, sensory -temporal - memory, speech (Broca = expressive; Wernicke's = receptive)

Question 33

thrombotic stroke

Answer 33

blood clots that forms in arteries suppling brain blood large vessel thrombosis -long term atherosclerosis -high cholesterol is risk small vessel disease or lacunar infarction -high bp

Question 34

embolic stroke

Answer 34

-clot or plaque fragment forms somewhere in body and travels to brain -clot blocks vessel passage

Question 35

ischaemic penumbra

Answer 35

-tissue surrounding core area of infarction (cell death) where damage is reversible -blood supply maintained by collateral circulation -"rescued" through reperfusion

Question 36

haemorrhagic stroke

Answer 36

-a blood vessel bursts within the brain -a blood vessel on the surface of the brain busts and causes subarachnoid haemorrhage -15% of cases are caused by bleeding in or around the brain -usually higher mortality rates

Question 37

what is bronchiectasis?

Answer 37

-irreversible widening of medium to small-sized airways (bronchi) -characterised by inflammation, destruction of bronchial walls and frequent colonisation of bacteria

Question 38

clinical features of bronchiectasis

Answer 38

-chronic cough -productive phlegm (normally purulent) -repeated chest infections -breathlessness -fatigue -finger clubbing

Question 39

pathophysiology of bronchiectasis

Answer 39

-permanent abnormal dilation of bronchi and bronchioles -associated with chronic bacterial infection -blockage of mucus/pus -alveoli collapse -elastic tissue degenerates = fibrous non-elastic tissues replace -inspired air increases pressure proximal to blockage site -dilation occurs -worsened by persistent coughing

Question 40

aetiology of bronchiectasis

Answer 40

-50% idiopathic -previous lower respiratory tract infection -1:200 adult sin the UK -women>men ->70yrs