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Clinical Diagnosis > Respiratory Pathology > Flashcards

Respiratory Pathology Flashcards

1
Q

What is Eupnoea?

A

Normal breathing pattern

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2
Q

What is Dyspnoea?

A

Shortness of breath / laboured breathing

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3
Q

What is Orthopnoea?

A

Shortness of breath when lying down

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4
Q

What are the gasses that we breathe in?

A

78.62% nitrogen
20.84% oxygen
0.96% argon
0.04% carbon
0.5% water vapour

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5
Q

What are the gasses we breathe out?

A

78.04% nitrogen
13.6% – 16% oxygen
4% – 5.3% carbon dioxide
1% argon and other gases
5% water vapour

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6
Q

Why do we breathe?

A

Absorb oxygen and excrete CO2 .
Regulates the pH of extracellular fluid
this also affects the depth and rate of respiration.
Subsidiary functions
panting = heat loss
Laughing
yawning and sneezing.

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7
Q

What is partial pressure?

A

Lung physiology is most commonly investigated through pulmonary function and exercise tests
The end results of pulmonary ventilation is adequate tissue cell oxidation, and removal or excess carbon dioxide.
To achieve this, the partial pressure of oxygen (called PO2) in the alveoli must be above that of the blood flowing through the alveolar capillaries.
Ventilation must also lower the partial pressure of carbon dioxide (PCO2) in the alveoli below that of the alveolar capillary blood to enable excess carbon dioxide to be removed.

The Partial pressure of oxygen (PO2) and carbon dioxide (PCO) are important measures of the adequacy of oxygenation.
Lung function depends on:
Age, size and sex – and normal values vary enormously!

The total amount of air that can be expired is the: Forced Vital Capacity (FVC) which depends on:
the lung size, integrity of the respiratory muscles & skeleton.
FVC declines as we age
affected by skeletal abnormality
weak respiratory muscles
disease causing reduced lung volume (e.g. Pulmonary fibrosis or pleural effusion)
or most commonly severe airway obstruction as in emphysema and bronchial asthma.
Elastic recoil also helps expel air from the alveoli during expiration.

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8
Q

The total amount of air that can be expired is the?

A

Forced Vital Capacity (FVC)

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9
Q

What are are important measures of the adequacy of oxygenation?

A

The Partial pressure of oxygen (PO2) and carbon dioxide (PCO)

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10
Q

Respiratory Failure is defined by the presence of?

A

a low level of blood oxygen

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11
Q

The normal PO2 varies between ?

A

10-13kPa

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12
Q

Normal respiratory function maintains?

A

blood gases within physiological limits.

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13
Q

Normal PCO2 varies between?

A

4.7- 6kPa

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14
Q

Respiratory failure is defined with PO2 falls below?

A

8kPa

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15
Q

How many types of respiratory failure are there?

A

There are two types of respiratory failure
Which are defined according to whether blood carbon dioxide is also abnormal:

Type 1
PO is low, but PCO2 is within normal range

Type 2
P02 is low, and PCO2 is raised

Respiratory failure can be caused by a wide range of conditions affecting ventilation, gas exchange or perfusion of the lung.

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16
Q

What is HYPERVENTILATION?

A

ventilation exceeds metabolic demands PaCO2 of < 36 mm Hg

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17
Q

What is HYPOVENTILATION?

A

inadequate alveolar ventilation to meet demands

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18
Q

What is HYPERCAPNIA?

A

Too much co2
PaCO2 > 44 mm Hg

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19
Q

What is cyanosis?

A

Bluish skin
(>5 gm. of haemoglobin are desaturated)

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20
Q

What is HYPOXEMIA?

A

reduced PaO2 in arterial blood-caused by respiratory alterations

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21
Q

What is HYPOXIA?

A

refers to reduced oxygenation of cells in tissues
can occur anywhere in the body.

22
Q

What is ACUTE RESPIRATORY FAILURE?

A

Inadequate gas exchange results in hypoxaemia with PaO2 < 50 and PaCO2 > 50 mm Hg

23
Q

What are common causes of Low Blood CO2 (Hypoxemia)?

A

Acute respiratory Distress Syndrome
Anemia
Asthma
COPD
Pneumonia
Pulmonary Edema
Pulmonary Embolism
Pulmonary Fibrosis
Sleep Apnea

24
Q

Chronic hypoxemia has two main effects: what are they?

A

Pulmonary Hypertension
Polycythaemia

25
Q

What is Pulmonary Hypertension?

A

Due to pulmonary vasoconstriction leads to increased pulmonary artery pressure.
In time, pulmonary arteries develop intimal proliferation and narrowing.
Pulmonary hypertension leads to right ventricular hypertrophy.

26
Q

What is Polycythaemia?

A

Due to stimulation of erythropoietin release from the kidney.
This can lead to increased blood viscosity and predispose increased risk of thrombosis.
Hypercapnia, when severe, causes tremor of the outstretched hands, a bounding pulse, vasodilation and increased cardiac output & confusion leading to coma.

27
Q

A ‘collapsed’ lung is termed?

A

ATELECTASIS

28
Q

What is a collapsed lung?

A

Several conditions lead to atelectasis which has important respiratory consequences:

Obstruction of an airway leads to reabsorption of air from the lung distal to the obstruction.
Scarring in the lung may cause contraction of parenchyma and collapse.
Loss of normal surfaces leads to generalized failure of lung expansion.

29
Q

What are vascular diseases of the lungs?

A

Pulmonary Hypertension
Pulmonary Oedema
Pulmonary Emboli

30
Q

What is another name for right sided heart failure?

A

COR PULMONALE

31
Q

What is pulmonary hypertension?

A

Increased pulmonary arterial pressure in pulmonary hypertension causes irreversible structural changes in pulmonary arteries.

The leads to increased demand for work on the right side of the heart

Which causes right ventricular hypertrophy

And eventually right sided heart failure  COR PULMONALE
In long standing pulmonary hypertension, structural changes develop in the lung, including medial hypertrophy in muscular arteries and pulmonary veins.
There is narrowing or occlusion of the lumina of pulmonary arteries by intimal proliferation.
Abundance of alveolar macrophages infiltrate
Fibrosis in the interstitium of the lung eventually develops.

The clinical effects of pulmonary hypertension are breathlessness and the development of right sided cardiac failure.

32
Q

What is pulmonary odaema?

A

Pulmonary Edema is caused by an accumulation of fluid in the alveolar wall (pulmonary interstitium).
If severe, this will affect the alveolar spaces.
This leads to impaired gas exchange  lead to respiratory failure.
The main cause of pulmonary edema is left ventricular failure
Which causes increased pressure in the alveolar capillaries
Fluid leaks from capillaries into the pulmonary interstitium, and there is an increase in the flow or fluid into the pulmonary lymphatics.
This increases the stiffness of the lungs, giving rise to a subjective sensation of dyspnea.
This can remain stable for a long time

In severe left ventricular failure, fluid also leaks into alveolar spaces, resulting in severe acute impairment of respiratory function.
Capillary rupture leads to leakage of RBC into the interstiutium, as well as into the alveoli.
Haemoglobin is phagocytosed by macrophages, which accumulate iron pigment, and lie in the alveoli & interstitium

33
Q

Non Cardiogenic Causes of Pulmonary Edema include?

A

Direct damage to the lung parenchyma
trauma, inhilation of toxic gases, ARDs, choking on a foreign body, neoplasms causing lymphatic obstruction within lungs

Fluid Overload
Renal Failure, Iatrogenic

Decreased albumin in the blood
Liver disease, nephrotic syndrome, poor nutrition

34
Q

Less Common Causes of
Non Cardiogenic Causes of Pulmonary Edema include?

A

Head injury
Unclear why, thought to be due to a raised intracranial pressure
Opiate overdose
Can cause severe hypoventilation causes hypoxia then ARDs.
Altitude Sickness
Leaking capillary alveolar membranes

35
Q

What is pulmonary embolism?

A

Very common, preventable cause of death

Most emboli arise in the deep leg veins (known as deep vein thrombosis) and pass in the venous circulation through the right side of the heart and lodge in the pulmonary arteries.

The outcome of the pulmonary thromboembolism depends on the size of thrombus.

36
Q

What are promoters for embolization?

A

Long period of immobilization of an extremity
Long car or plane journeys

Right sided congestive heart Failure

Hyper- coagulable states
Cancer, post severe burns, severe trauma
Pregnancy, Oral contraceptives

Damaged endothelium
Intravenous central lines

37
Q

2 main consequences of embolism to the pulmonary arterial tree are?

A

Increase in pulmonary arterial pressure
Which puts a strain on the right side of the heart
Ischaemia of the lung
With ventilated areas not being perfused by blood.

If 60% of the pulmonary vasculature is suddenly blocked, the heart cannot pump blood through the lungs  causes rapid death (about 5% of PE cases)
10% of all PE cases, blockage of middle sized pulmonary arteries- causing chest pain & breathlessness.
Most cases, blockage of small vessels- may be asymptomatic or experience breathlessness & pleuritic chest pain.

38
Q

What is Asthma?

A

Asthma is a very common and the main reversible cause of airflow limitation

It is characterized by:
Functional obstruction of small airways- by a combination of bronchospasm & mucus plugging
Which fluctuates with time
Is frequently reversible with bronchodilator drugs

A complex inflammatory response involving eosinophils, mast cells and lymphoid cells – whatever the underlying cause.

It is an inflammatory conditions that has both acute and chronic
components affecting different structural elements in the airways.
A variety of triggers stimulate acute exacerbations.

39
Q

What are the different types of Asthma?

A

Aitiology
Most common under age of 30
Caused by IgE production following exposure to environmental allergens e.g. house dust. T- Lymphocytes mediate some of this process.

Intrinsic Asthma
Same pathology as atopy, but cold exposure & exertion can trigger.

Childhood Asthma
Often stimulated by viral infections, improves with age.

Occupational Asthma
Triggers by work environment – chemical irritant, gases etc

Aspirin Induced Asthma

40
Q

What is asthma?

A

A complex inflammatory response involving eosinophils, mast cells and lymphoid cells – whatever the underlying cause.

It is an inflammatory conditions that has both acute and chronic
components affecting different structural elements in the airways.
A variety of triggers stimulate acute exacerbations.

41
Q

What are structural changes to asthma?

A

Bronchoconstriction due to increased responsiveness of bronchial smooth muscle
Hypersecretion of mucus leading to plugging of airways
Mucosal edema leading to narrowing of airway lumen
Extravasation of plasma in submucosal tissues due to leakage from vessels contributes to mucosal edema
Infiltration of bronchial mucosa by eosinophils, mast cells, lymphoid cells & macrophages.
Focal necrosis of airway epithelium
Deposition of airway epithelium
Deposition of collagen beneath bronchial epithelium in long standing cases

42
Q

What are Inflammatory Mechanisms in Asthma?

A

Type 1 Hypersensitivity response
Mast cells are important feature in asthma, and whilst they release histamine, anti – histamines are not clinically useful in treatment.
T Tells, in particular Th2 cells are prominent in mucosal cellular infiltrate – they release a variety of cytokines.
Cytkoines orchestrate and amplify the inflammatory response.
Eosinophils migrate to the mucosa in response, and release many mediators of inflammation.
Leukotrienes constrict airways

43
Q

What is COPD?

A

A disease characterized by airflow limitation that is not fully reversible.
Airflow limitation is usually progressive, and is due to one of 2 main reasons:

Airway resistance is increased (normally due to narrowing)
Outflow pressure is reduced (elastic recoil is lost)

Three main pathologies contributing to COPD are:
Emphysema, Bronchitis, and Bronchiolitis.

44
Q

What is Emphysema (COPD)?

A

Permanent dilation of any part of the respiratory acinus with destruction of tissue in the absence of scarring.

There is a loss of elastic recoil in the lungs

As connective tissue in the alveolar walls is destroyed.

Reduced oxygen uptake, but will try and maintain blood oxygen with a rapid respiratory rate.

45
Q

What is Chronic Bronchitis (COPD) ?

A

Defined as as “Cough with productive sputum on most days, for 3 months of the year for at least 2 successive years”

Due to hypersecretion of mucus associated with hyperplasia of mucous glands.

Airway obstruction in chronic bronchitis is related to luminal narrowing and mucus plugging.

46
Q

What are the causes of COPD?

A

The most significant being lifetime smoking exposure

Other risk factors include:
Recurrent chest infections in childhood
Asthma
Occupational exposure

47
Q

What is Adult Respiratory Distress Syndrome (ARDs)?

A

occurs when the lungs become severely inflamed from either an infection or injury e.g. pneumonia, flu, sepsis, pancreatitis, near drowning.

The inflammation causes fluid to leak from the capillaries, into the alveoli
which affects perfusion- making breathing difficult
leads to hypoexemia

Is an acute restrictive lung disease caused by restrictive lung disease caused by alveolar damage.

48
Q

What is cystic fibrosis?

A

Autosomal recessive disorder
A multisystem disease
Associated with pancreatic exocrine dysfunction
Cause by the production of an abnormally viscid mucus that cannot be cleared from the lungs and causes blockage in the main pancreatic ducts
40% of cases present with respiratory disease
30% present as failure to thrive and malabsobtion
10% present with liver disease

Abnormally viscid mucus leads to:
Obstruction & stagnation of secretions leads to repeated bouts of infection – particularly staphylococcus aureus
Bronchiectasis is a frequent complication leading to hemoptyisis
Hyperinflation of lungs due to are trapping behind mucin plugs increases risk of pneumothorax
Hypoxia, scarring and destruction of the pulmonary vascular bed

The median age of survival is just over 30 years.

49
Q

What is the Pathogenesis of Cystic Fibrosis?

A

CF gene
In normal mucus secreting epithelia chloride channel open in response to increase concentration of cAMP  CFTR protein chanenel open and enables secretion of chloride, water & sodium
In the mutated CF gene, the surface protein is not present and therefore chloride secretion cannot occur… and neither can water & sodium
This means mucus is extremely viscid.

50
Q

What is Neoplastic Disease of the Lungs?

A

Carcinoma of the lungs is the most common cause of death from neoplasia.
The incidence of lung cancer is related to the main causative factor of cigarette smoking and industrial carcinogens.
Smoking increases risk of developing cancer with precursor lesions of metaplasia and dysplasia occurring in the respiratory tract after exposure to smoke.
Exposure to radioactive material, asbestos, nickel, iron oxides and coal gas plants are all known to contribute to the development of lung cancer.

51
Q

What is lung fibrosis?

A

Excessive fibrosis leads to thickening of the alveolar walls and results in reduced gaseous exchange

Causes:
Idiopathic
Occupational inhilation e.g. asbestos, silicon
Cigarette smoking
Autoimmune – rheumatoid, sarcoidosis
Radiation to chest

52
Q
A

Clinical Diagnosis (22 decks)

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