Pathophysiology of lung disease + Functions of Alveoli

Question 1

describe the role of surfactant

4

Answer 1

1-prevents collapse of small alveoli
2-decreases surface tension ( air-water interface—>lipid-water interface) - hence reduces work of breathing
3-prevents transfer of fluids from capillaries
4-stabilised pulmonary capillaries

Question 2

what factors effect lung compliance/ expansibility ?

8

Answer 2

1- surface tension , if it is deceased then the lung can expand more = increasing compliance
2-elastin fibres = cause recoil but also help with expanding . Normal and low levels of these = increase compliance
3-Collagen fibres = stiff = cause the compliance to decrease
4-increased surfactant increases compliance
5-alveolar size = bigger alveoli compliance increases
6-lung volumes=more air decreases compliance ( remember small alveoli = large sa: v ratio )
7-Hysteresis= difference in between inspiration (compliance increases) and expiration (decreases)
8-disease =
-restrictive decreases compliance ( more stiff lungs due to an increase in collagen )
-obstructive increases compliance ( more elastase which breaks down the elastin , hence like an old sock = air is trapped inside and can’t get out = no elastic recoil )

Question 3

what are alveoli dependant on ?

2

Answer 3

1-Elastic fibres

2-Surface tension

Question 4

What is the law of laplace?

2

Answer 4

When you blue into the balloon , the first breath is the hardest !
- P=2T/RADIUS
Laplace’s law states that the pressure inside an inflated elastic container with a curved surface, e.g., a bubble or a blood vessel, is inversely proportional to the radius as long as the surface tension is presumed to change little.
- big radius = smaller pressure
-Small radius = greater pressure

Question 5

outline the properties of an obstructive lung disease
(old sock )
(8)

Answer 5

1-Obstructive diseases =OBSCURE RATIO
2-Increased compliance as elastin is broken down= so the alveoli can’t recoil
3- Airway resistance increases =small airways collapse due to the lack of elastin
4- FEV1 =Forced expiratory volume =LOW
FVC= Forced Vital Capacity =LOW
FEV1/FVC=LOW=Obstructive OPRESSES ( cant get air out)
TOTAL LUNG CAP= BLOATERS, BARRALLED CHEST = air trapped inside so it increases
Vital capacity = Low , cant exhale out
Residual volume =HIGH -air trapped

Question 6

Outline restrictive lung disease
pulmonary fibrosis
symptoms and investigation
(10)

Answer 6

COMPLIANCE DECREASES = lung is stiff as collagen replaces elastin
CAN NOT GET AIR IN
1- Extrinsic or intrinsic restrictive disease ie : pulmonary fibrosis
2-FEV1= LOW because they cant get air in hence less volume out
3-FEV1/FVC ratio =high
RESTRICTIVE RAISES
TOTAL LUNG CAP=LOW
VITAL CAP=LOW
Residual volume = low

symptoms :
1-dyspnoea 
2-dry cough 
3-fine inspiratory crepatation 
4-deceased Transfer factor ( more collagen fibres increase diffusion distance so gas transfer rate is slow)

Investigations :
1- chest x-ray
2-high resolution CT ( Marking on the bases = shaggy )

Question 7

Outline what happens in asthma!
physiology of the process
(10)
MAIN 5 outcomes?

Answer 7

1- The allergen , dust or stimulus enters the body and is picked up by the APC dendritic cells –> phagocytosis occurs and it becomes a MHC2 complex ( APC presenter)

2- T helper 2 cells react :
- CD4+ receptor + MHC2 receptor
-TH2 receptor + allergen
these cause the production of interleukin 4 and interleukin 5 :

3- INTERLEUKIN 4 - activates antibodies IGE

• > IgE + mast cell —> releases mediators such as histamine, leukotrienes = cause inflammation of the airways and vascoconstriction
• smooth muscle constriction = bronchoconstriction
• mucous builds up= to get rid of the pathogen or allergen = hypertrophy of goblet cells
• MUCOSA ( epithelium and lamina propria ) = inflamed with fluid and eosinophils
• vascular permeability increases =capillaries are leaky = due to inflammatory cytokines
• hypertrophy of basement membrane and smooth muscle

4- Interleukin 5 = makes eosinophils that secrete proteases that can cause excessive tissue damage
- also secretes leukotrienes, cytokines, histamines and increase WBC = increased inflammation and permeability of the blood vessels

MAIN 4 OUTCOMES
1-smooth muscle constriction
2-mucosa is filled with fluid
3-thickening of the ar way wall, leading to the narrow lumen (high-level x tryptase released by mast cell)
4-mucous builds up, causing more hypertrophy of goblet cells
5-eosinophilic inflammation

Question 8

what happens in COPD
(10)
symptoms
pathophysiology ( due to 2 main disease, decrease what happens in each )

Answer 8

symptoms :
1-progressive breathlessness , cough , sputum could become darker, repeated infections
2-course crepatations ( small explosive sounds of air bubbling through mucous )
3- wheeze

COPD due to :
chronic bronchitis and emphysema = obstructive disorder
1- Chronic Bronchitis - due to smoking, airways narrow and mucous production increases
->hypertrophy and hyperplasia of the mucous glands and goblet cells
->ciliary shortening ( less able to move mucous ) leads to mucous plugs
->air trapping
->V:Q mismatch leads to hypoxemia and hypercapnia
->stagnant mucous causes increased risk of pneumonia and repeated infection as you cant get rid of pathogens

2- EMPHYSEMA
->smoking leads to neutrophils->increased elastase and decreased ELASTIN in the alveolar walls = less able to recoil
= air trapping, increased compliance
= Air ways collapse due to the loss of elastin
-> alpha 1 anti trypsin deficiency = autosomal dominant
- normally A1 Anti trypsin =inhibits the actions of elastase , this means elastin numbers are controlled and normal
= deficiency = lots of elastase, hence very low elastin = alveoli = weak and make big ballooned areas ( SA decreased , gas exchange is impaired !)
- eventually leads to hypoxemia and hypercapnia

Question 9

outline pulmonary hypertension 
(10)
causes 4
symptom 1
pathophysiology 3
clinical examination 3

Answer 9

causes :
1-unknown
2-hypoxia
3- Thrombo embolism = blood clots which blocks arteries
4-Schitosmia ( parasite which causes vasculature to be blocked )

symptoms :
- non specific ie : exercise intolerance , fatigue , pain , cough , , blood in cough

pathophysiology :
1-back pressure increases ie : LH heart failure , weak LV cant empty the pulmonary veins = blocked veins !
2-Increased flow from left to right heart ( shunt ) or Hole in heart
3-V:Q mismatch ( hypoxia and hypocapnia )

Clinical examination :

1-You can hear a 2nd heart beat = LOUD as the pulmonary artery is lower pressure than LH so valve closes slowly = in disease there will be a shorter gap in the sound as RV pressure increases)
2- Right ventricle heave
3-chest x -ray and echocardiogram (rounded heart and apex above diaphragm )

Question 10

what is bronchiectasis ?
pathophysiology 4
causes 3
clinical observations 4

(10)

Answer 10

1- swelling of the bronchi = more than 2mm 
- bronchial wall becomes enflamed
and weakened
-collapses during expiration 
- poor clearance of secretion 
= OBSTRUCTIVE DEFECT

causes :
1- infection and CF
2-ciliary dyskinesia
3-gamma globulin deficiency

clinical observations:
1-cought and increases sputum , may be blood in cough 
2- course crepitations 
3- chest X-ray 
4-High res CT

Question 11

how can we differentiate asthma from another obstructive disease ?via test ?
(4)

Answer 11

spirometry may be normal
1- 15% increase in FEV1 shows be seen after inhalation of B2 agonist
= ASTHMA
2- if spirometry is normal but they have history of airway obstruction :
- Metacholine test challenge test :
provocative concentration of metacholine = causes a 20% fall in FEV1,