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CPAT > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What are the two types of airflow obstruction?

A

Reduced functional airway diameter

Reduced elasticity of parenchyma

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2
Q

What is serous? What is its role?

A

Watery protenatious anti-pathogen fluid

Makes a layer of fluid allowing the cilia to beat (critical for success of the organ)

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3
Q

T/F:

Asthma is a primary immune response to an antigen

A

False

Secondary immune response

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4
Q

What type of antibodies are commonly seen in asthmatics?

A

IgE

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5
Q

T/F:

Mast cells bind to IgE coated antigen and are activated. They remodel the ECM (in asthmatics)

A

True

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6
Q

List what mast cells release upon activation

A

They manufacture and release secondary mediators:
Lipid mediators
Cytokines
Chemokines

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7
Q

T/F:

bronchospasm is a remote effect in asthmatics

A

False

local effect

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8
Q

List some local effects seen in asthmatics

A

Brochospasm
Vasodilation
Endothelial permeability
Mucus secretion

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9
Q

List some remote effects seem in asthmatics

A

Recruitment of leukocytes

Local secretion of mediators by epithelium, endothelium, leukocytes

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10
Q

What role does the late phase reaction play during asthma?

A

Amplify the reaction
Sustains the response without the antigen being present
Intervention is the only cause of action

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11
Q

What type of cells are recruited during the late phase response of asthma?

A

Leukocytes- eosinophils, neutrophils, monocytes, lymphocytes

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12
Q

Describe some of the histological characteristics of asthma

A 
Smooth muscle proliferation
Vascularisation
Mucus plugs
Destruction of the epithelium due to degranulation
Oedema
Trapping of air due to mucus plugs
Congested vessels
Leukocyte infiltration
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13
Q

T/F:

Emphysema is overinflation

A

False

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14
Q

Emphysema is ______ of air spaces

A

abnormal enlargement

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15
Q

In emphysema, bronchiolar/alveolar walls are destroyed- what is a consequence of this?

A

Reduced gas exchange (lose surface area)
Lose blood vessels
Lose cross sectional area = pulmonary hypertension

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16
Q

What happens if you are deficient in alpha1 anti-trypsin or don’t have control over your production of proteases?

A

Breakdown of epithelia and basement membranes
destruction of alveolar walls
contributes to emphysema

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17
Q

How does smoking contribute to the onset of emphysema?

A

Smoking incites peripheral cells (macrophages and neutrophils)
They release lots of proteases= increased elastic/collagen destruction
Smoking also decreases effects of alpha1 anti-trypsin
Smoking also decreases activity of the proteases as well

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18
Q

In emphysema, what happens when elastin in the alveolar/bronchiole walls is lost?

A

Makes it harder to exhale air, need to use your muscles to exhale the air
Obstruction of the outflow of air

19
Q

T/F:

emphysema involves obstruction of air inflow

A

false

air outflow

20
Q

Chronic bronchitis is a _____ cough

A

productive cough

21
Q

What is a consequence of excessive mucus production when individuals are suffering chronic bronchitis?

A

Can lead to infections

22
Q

T/F:

A common histological sign of chronic bronchitis is muscularis mucosa hypertrophy

A

False
this layer is not affected
this layer is however affected in asthmatics

23
Q

Describe some histological characteristics of chronic bronchitis

A 
Thickened basement membrane
Vascularisation (more so than asthmatics)
Oedema
Leukocyte infiltration
Increased goblet cells
Increased activity of serous glands
Destruction of epithelial layers
Remodelling
No hypertrophy
24
Q

T/F:

Emphysema is a promixal disease and chronic bronchitis is a distal disease

A

False
Emphysema= distal (alveoli)
Chronic bronchitis= proximal (bronchioles)

25
Q

T/F:

infection is a commonality between emphysema and chronic bronchitis

A

False

infection is present in chronic bronchitis but not emphysema

26
Q

What are the three common features between chronic bronchitis and emphysema?

A

loss of air exchange surface area= reduced air exchange
loss of elastic recoil= obstructive outflow
loss of airway diameter= obstructive outflow

27
Q

What was a great advancement in medicine that changed survival rates of pneumonia?

A

Antibiotics

however there is now resistance so problem isn’t fixed as it once was thought to be

28
Q

T/F:

Classical pneumonia is bacterial

A

True

there are some viral cases as well though don’t forget

29
Q

T/F:

Pneumonia involves only an innate immune response

A

False

both innate and adaptive

30
Q

T/F:

Pneumonia involves lung consolidation with transudate

A

False
in pneunomia it is specifically exudate (full of proteins)
lung consolidation= filling of the alveoli with fluid

31
Q

What are the two types of pneumonia?

A

Broncho (diffuse and confluent)
Lobar (patchy and focal)

They type depends on the organism, immune response and treatment

32
Q

What types of defence mechanisms are compromised that might lead to pneumonia?

A

Cough reflex= ie CNS depression
Decreased mucocillary apparatus
Decreased phagocytic activity
Presence of viral infections, hospital based infections

33
Q

T/F:

Bronchopneumonia often occurs in healthy young patients where as lobarpneumonia is more commonly seen in the debilitated

A

False

other way round

34
Q

T/F:

Red hepatiziation is a sign of the clearance of pneumonia

A

False

grey hepatization is

35
Q

How does pneumonia progress?

A

Congestion
Red hepatization
Grey hepatization
Resolution

36
Q

List some features of red hepatization

A 
Exudation
Leakage of vessels
RBC extravasation
Reduced air exchange 
Consolidation
37
Q

List some features of grey hepatization

A

RBC number is decreasing due to clearance by macrophages
Exudation and fibrin
Neutrophils reduce in number as bacteria have been eliminated

38
Q

List some features of resolution (last stage of pneumonia)

A

RBC decreasing
digestion of exudate and fibrin
Macrophages are removing debris
Resorption and expectoration of the liquid exudate

39
Q

What three factors determine the outcome of lobar or broncho pneumonia

A

Dosage (ie how much bacteria infect you)
Virulence (how good is the bacteria at infecting you)
Immune status

40
Q

List some complications that may arise from broncho or lobar pneumonia

A

Abcess formation
Empyema = pus in the pleural cavity
Organisation= leads to fibrosis
Haematogenous dissemination to critical organs

41
Q

What are the two main causes of pulmonary congestion and oedema?

A

Haemodynamic

Microvascular injury

42
Q

List some haemodynamic causes outside of the lung

A

Increased hydrostatic pressure

  • left sided cardiac failure
  • mitral stenosis
  • pulmonary vein obstruction
  • volume overload

Decreased onotic pressure

  • Some diseases result in reduced proteins in the blood= water leaks out
  • Nephrotic syndrome (kidney disease and can’t contain albumin)
43
Q

List some haemodynamic causes inside of the lung

A

Increased hydrostatic pressure

  • fibrous scar tissue in the lung
  • chronic inflammation
  • loss of cross-sectional vascular area
44
Q

Explain how microvascular injury, specifically diffuse alveolar capillary damage, contributes to lung diseases of vascular origin

A

endothelial damage can impede fluid and protein movement
lose the barrier to maintain the fluid/protein volume
results in adult respiratory distress syndrome

CPAT (9 decks)

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