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Biology 2401 > RESP PATHO > Flashcards

RESP PATHO Flashcards

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1
Q
  1. Describe dyspnea, orthopnea and paroxysmal nocturnal dyspnea (PND).
A

Discomfort in breathing (shortness of breath)

Signs include flaring of the nostrils, use of accessory muscles of respiration

Orthopnea: dyspnea upon lying down (causes abdominal contents to put pressure on diaphragm, plus redistribution of blood to the lungs)

PND: awaking at night with dyspnea

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2
Q
  1. Describe 7 other symptoms/signs of respiratory disease.
A

Cough – initiated by irritant receptors in the airway. There are few of thesis in the distal portions of the “respiratory tree”, so it is possible for significant secretions to build up before the cough reflex occurs

Abnormal sputum – changes in the amount, colour and consistency (microscopic observation can reveal cellular debris and microorganisms)

Hemoptysis: coughing up of blood (bright red, alkaline pH, frothy sputum)

Abnormal breathing pattern: hypo – or hyperventilation

Cyanosis: bluish discolouration of skin and mucous membranes, caused by increased amounts of deoxygenated hemoglobin in the blood

Clubbing: selective bulbous enlargement of the end of a digit

Pain: originates in pleurae, airways or chest wall. Caused by infection, inflammation, stiff muscles from coughing

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3
Q
  1. Define hypercapnia (hypercarbia), its immediate cause, and three occurrences that can bring the immediate cause to happen.
A

Increased carbon dioxide in the arterial blood

Caused by hypoventilation of the alveoli (CO2 passes very readily from the blood to the alveolar space (20x more readily than with O2, so is affected only by exchange in alveolar gases that occurs with ventilation))

Can be a result of anything decreasing drive/ability to breathe, including:

Drugs, diseases of the medulla, chest injuries

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4
Q
  1. Define hypoxemia and explain the difference from hypoxia.
A

Reduced oxygenation of arterial blood

Different from hypoxia, which is reduced oxygenation of tissues

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5
Q
  1. Explain the 3 mechanisms that can reduce oxygenation of the blood, including the following questions: a. By what two means can oxygen delivery to the alveoli be decreased? Be familiar with examples of conditions/diseases that can cause this. b. What does V/Q refer to? c. What is the most common cause of hypoxemia? d. Describe the conditions of low and high V/Q, and be familiar with examples of diseases that cause each. e. Be familiar with conditions that can decrease diffusion across the alveolocapillary membrane.
A

Hypoxemia results from defects in one or more of the 3 mechanisms of oxygenation: oxygen delivery to the alveoli, diffusion of oxygen from the alveoli into the blood, and anatomical right to left shunting

Oxygen delivery to the alveoli: decreased oxygen in the air/decreased ventilation (a problem with unconscious individuals, those with disease that restricts chest expansion, COPD) & decreased diffusion across the alveolocapillary membrane (due to thickened membrane brought about through edema, or fibrosis)

V: alveolar ventilation & Q: perfusion (the amount of blood perfusing the alveolar capillaries

A mismatch of the V/Q ratio

High V/Q: inadequate perfusion of well-ventilated area, producing alveolar dead space (wasted ventilation) most common cause is pulmonary embolism & low V/Q: inadequate ventilation of well-perfused area of lung (atelectasis, asthma, pulmonary edema)

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6
Q
  1. What is the result of, and what causes chest wall restriction? Describe flail chest.
A

Results in a decrease in tidal volume

Occurs when the chest wall is deformed, traumatized, immobilized or heavy from the accumulation of fat (grossly obese, neuromuscular disease)

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7
Q
  1. Define pneumothorax and its effect on the lung.
A

Presence of air in the pleural space caused by a rupture in the visceral or parietal pleura

Negative pressure of pleural cavity is destroyed and lung tends to recoil and collapse towards hilum

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8
Q
  1. What is tension pneumothorax, and how does it develop?
A

Preventing air from escaping the pleural cavity with exhalation

Develops when a lung or chest wall injury is such that it allows air into the pleural space but not out of it (one-way valve)

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9
Q
  1. Define pleural effusion and how it usually occurs.
A

Presence of excess fluid in the pleural space

Usually through migration of fluid through walls of capillaries bordering the pleura

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10
Q
  1. Define empyema and how it can occur.
A

Infected pleural effusion

Complication of pneumonia, surgery

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11
Q
  1. Describe atelectasis, its causes and manifestations.
A

Collapse of lung tissue

External compression (e.g. fluid in pleural space, tumor, abdominal distention), obstructed airways (air is absorbed form obstructed alveoli and they collapse), inhalation of concentrated oxygen (increases rate of absorption of gases, leading to collapse), decreased production of surfactant

Dyspnea and cough

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12
Q
  1. What medical procedure often results in atelectasis and what measures can be taken to improve patients’ condition?
A

Tends to develop after surgery (patients that are in pain breathe shallowly. Viscous secretions can result from anaesthesia)

Post-surgery patients are advised to breathe deeply, become ambulatory asap, and change positions frequently when lying down to prevent the thick bronchial secretions produced by narcotics and anaesthesia from obstructing an airway

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13
Q
  1. Describe bronchiectasis and be familiar with some causes.
A

Permanent dilation of the bronchi (secondary to other diseases that cause chronic inflammation of bronchial wall)

Chronic inflammation leads to destruction of elastic and muscular components of bronchi walls and permanent dilation

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14
Q
  1. Describe the pathophysiology behind cystic fibrosis and its treatment.
A

Mutation produces inability of cell membranes to transport chloride ion. This causes a series of events, resulting in increased absorbance of sodium and water from respiratory secretions. This produces very thick mucous, which is difficult for cilia to move. The mucous then accumulates, increasing the risk of infections

Includes antibiotics to control infections, possible replacement of pancreatic enzymes

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15
Q
  1. What is a pulmonary embolism, and of what is the most common embolus comprised?
A

Occlusion of a portion of the pulmonary vascular bed by an embolus

Is a clot from deep venous thrombosis involving the lower leg

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16
Q
  1. What does obstruction of blood flow cause in the lung?
A

Obstruction of blood flow causes pulmonary vessels to constrict, resulting in impaired gas exchange (V/Q mismatch) and hypoxemia.

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17
Q
  1. What is the result if the clot is not dissolved soon enough?
A

If clot is not dissolved rapidly, the resulting hypertension could possibly lead to right heart failure

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18
Q
  1. What are the clinical manifestations of a pulmonary embolism?
A

Depends upon size and location of obstruction

Small emboli may go unnoticed unless patient’s health is otherwise compromised

Moderate emboli: sudden onset chest pain, dyspnea, tachypnea, tachycardia

Massive emboli: sudden collapse, crushing chest pain, shock – often fatal

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19
Q
  1. Define pulmonary hypertension, and explain how hypoxemia and certain heart conditions can lead to this condition.
A

Elevated mean pulmonary artery pressure

Most cases develop as a serious complication of many acute and chronic pulmonary disorders, a common cause is continued exposure of pulmonary vessels to hypoxemia, which causes these vessels to constrict (unlike systemic vessels, which dilate)

Can also be caused by mitral valve disorders or left ventricular diastolic dysfunction, which raise left atrial pressure

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20
Q
  1. What is cor pulmonale, its primary cause and its effects?
A

Right heart failure brought about through lung disease or chronic pulmonary hypertension

Increased work of the right ventricle causes hypertrophy and eventual failure

Results in systemic venous congestion, peripheral edema, fatigue

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21
Q
  1. What is pulmonary edema, and describe how this is commonly caused.
A

Excess fluid in the lungs

Most common cause is left-sided heart failure. Failure of left ventricle causes increased filling pressure, which causes back-up of blood in lungs, increasing pressure in lung capillaries. When this exceeds osmotic pressure of lung capillaries, fluid & RBCs leave capillaries and collect in the interstitial space

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22
Q
  1. Why does pulmonary edema result in hypoxemia?
A

When there is too much interstitial fluid for lymph system to collect, edema occurs. Fluid eventually leaks into the alveoli: fewer alveoli available to expand with air, means a reduction in surface area of respiratory membrane, thickening of available respiratory membrane (increased distance for oxygen molecules to diffuse) -> results in reduced oxygen diffusion rate

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23
Q
  1. Describe clinical manifestations of pulmonary edema.
A

Dyspnea, cyanosis, increased physical effort in breathing, blood tinged frothy sputum

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24
Q
  1. To what are obstructive lung diseases due?
A

Due to airway obstruction that is worse with expiration – emptying of the lungs is slowed

25
Q
  1. What two diseases are grouped together under the title “chronic obstructive pulmonary disease”?
A

Asthma, chronic bronchitis, emphysema

26
Q
  1. What are the unifying symptom and sign of obstructive lung diseases?
A

Symptom: dyspnea

Sign: wheezing

27
Q
  1. Define bronchial asthma.
A

Chronic inflammatory disorder of the bronchial mucosa that causes hypersensitivity and constriction of the airways

28
Q
  1. Describe the early response stage of an asthma attack, including clinical manifestations.
A

Usual type I hypersensitivity response: allergen exposure to the bronchial mucosa activates B cells to produce IgE which complexes with mast cells

Further exposure cross-links the IgE, causing the mast cells to release a host of chemicals, which cause vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction and mucous secretion

Clinical manifestations at the beginning of an attack: chest constriction, expiratory wheezing, dyspnea, tachycardia, coughing

29
Q
  1. Describe the 4 steps in the late response stage of an asthma attack, including how respiratory alkalosis can arise in the late stage of an asthma attack, and how this can develop into respiratory acidosis.
A

Release of inflammatory chemicals: chemokines released by cells in early response call other inflammatory cells: neutrophils, eosinophils and lymphocytes to the area, inflammatory chemicals released by these cells cause further bronchospasm, edema and mucous secretion

Cell damage + mucous accumulation: damage from these chemicals occurs to ciliated epithelial cells. Mucous accumulates and cellular debris forms plugs in the airways impeding alveolar ventilation. Untreated inflammation can lead to long-term airway damage and hyper-responsiveness

Air trapping -> hypoxemia -> respiratory alkalosis: the obstructed airway makes it more difficult to expire, causing air to be trapped in alveoli, increasing alveolar gas pressures. This causes decreased perfusion of blood over the alveoli (capillaries collapse), leading to hypoxemia. The hypoxemia stimulates the respiratory centre -> hyperventilation, CO2 diffuses out of the blood causing hypocapnia and respiratory alkalosis

Impairment of respiratory muscles -> respiratory acidosis: continued obstruction of airways increases air trapping (incomplete expirations), which hyperexpands the lungs and thorax, decreasing the tidal volume and increasing hypoxemia, CO2 levels will rise, leading to hypercapnia and respiratory acidosis; the situation is life-threatening if treatment does not reverse the process quickly (mechanical ventilation may be required), mainstays of treatment are avoidance of allergens, and inhalation of anti-inflammatories, bronchodilators and adrenaline in acute attack

30
Q
  1. What are the mainstays of treatment for asthmatics?
A

mainstays of treatment are avoidance of allergens, and inhalation of anti-inflammatories, bronchodilators and adrenaline in acute attack

31
Q
  1. What is chronic obstructive pulmonary disease characterized by?
A

Airway obstruction that causes difficult exhalation

32
Q
  1. What is chronic bronchitis very commonly caused by?
A

Smoking

33
Q
  1. Define chronic bronchitis.
A

Hypersecretion of mucous and chronic productive cough for at least 3 months of the year, for at least 2 consecutive years

34
Q
  1. Describe the development of chronic bronchitis.

7

A

The airway becomes inflamed with inspiration of irritants. Edema occurs, along with the production of thick, tenacious mucous -> continual inflammation leads to increases in size and number of mucous glands and goblet cells in the airway epithelium -> continual inflammation brings in macrophages and neutrophils that release proteases, which harm ciliated epithelial cells -> due to impairment of the ciliary function, the mucous cannot be cleared (may have low grade fever) -> the airways are constricted by thickened bronchial wall (increased gland size) and mucous. Expiration becomes more difficult as airways are narrowed during this part of respiratory cycle -> obstruction eventually leads to hypoxemia -> eventually airways collapse early in expiration, causing air trapping. This expands the thorax, making expiration even more difficult = decreased tidal volume, hypoventilation and hypercapnia

35
Q
  1. Describe the treatment of chronic bronchitis.
A

Bronchodilators and expectorants as needed to control cough and reduce dyspnea, stop smoking, chest physical therapy, eventually antibiotics (infection), steroids (last resort), home oxygen therapy

36
Q
  1. Why is the term “blue bloaters” used?
A

Hypoxemia and edema, caused by eventual right heart failure

37
Q
  1. What is emphysema characterized by?
A

Characterized by a loss of lung elasticity and abnormal enlargement of the airspaces distal to terminal bronchioles, with destruction of the alveolar walls and capillaries

38
Q
  1. What is the difference between the physiological/anatomical causes of the obstruction of emphysema and chronic bronchitis?
A

Obstruction results from changes in the lung tissue (primarily loss of elastic recoil), rather than from mucous production and inflammation of the airways, which is the case with chronic bronchitis

39
Q
  1. What are two causes of emphysema?
A

Can be inherited (due to insufficiency of alpha 1-antitrypsin that combats proteases released by normal amounts of inflammatory cells) or through the inhalation of cigarette smoke, air pollution that increases number of inflammatory cells

40
Q
  1. Describe the development of emphysema.
A

Inflammation occurs & inflammatory cells release proteases that cause destruction of alveolar septae. This eliminates part of the capillary bed and increases volume of acini (alveoli cluster distal to terminal bronchioles) -> this produces large air spaces within the lungs (bullae), and on the surface of the lungs, next to pleura (blebs). This air spaces cannot function in gas exchange, which increases hypoxemia -> damage from inflammation includes a loss in the elastic lung tissue, which helps to keep air passages open. This results in expiration becoming difficult, thus trapping air in lungs -> this hyperexpands the thorax, making it difficult to breathe, causing hypoventilation & hypercapnia

41
Q
  1. Define blebs and bullae.
A

Bleb: blister filled with serous fluid

Bullae: air pockets

42
Q
  1. Describe the treatment of emphysema.
A

Must include cessation of smoking, and inhalation of corticosteroids and bronchodilating drugs

Oxygen therapy, if required

Possible lung reduction surgery or transplant

43
Q
  1. Why is the term “pink puffer” used?
A

“pink puffers” there is initially little hypoxemia (increased breathing can keep up with oxygen demand until late stages of disease) but use is often made of the classic tripod breathing position, with lips pursed to increase lung pressure during exhalation, in an attempt to keep breathing passages open)

44
Q
  1. Describe Acute Lung Injury and Acute Respiratory Distress Syndrome and be familiar with causes.
A

Both involve acute lung inflammation and injury to the alveolocapillary membrane, leading to severe pulmonary edema and hypoxemia

Caused by sepsis, trauma, pneumonia, drug overdose, smoke inhalation, aspiration of gastric contents

45
Q
  1. What is the difference between these two conditions?
A

ARDS is more severe aspect of ALI

46
Q
  1. Describe the development of these conditions.

ARDS & ALI

A

As a response to injury, neutrophils release inflammatory chemicals that damage the alveolocapillary membrane and greatly increase capillary membrane permeability, allowing blood to leak into the interstitial spaces and alveoli = edema

There is surfactant inactivation, causing collapse of alveoli, which adds to decrease in gas exchange

A hyaline membrane forms, impairing gas exchange

If injury is extensive, repair of tissues may produce fibrosis

47
Q
  1. Describe clinical manifestations of ALI/ARDS, and the treatment.
A

A rapid onset of respiratory distress (marked dyspnea, rapid, shallow breathing, inspiratory crackles (a “popping open” of small airways and alveoli collapsed by fluid), hypoxemia), usually within 12-18 hour of injury. There may be a systemic response as the inflammatory compounds spread through body

48
Q
  1. Define Acute Respiratory Failure (there are three parts to the definition).
A

Inadequate gas exchange, leading to lower PaO2, with/without higher PaCO2 accompanied by decreased pH (<7.30)

49
Q
  1. Identify the two types of ARF and their general causes.
A

Hypercapnic/hypoxemic: due to failure of ventilation

Causes: an increase in arterial CO2 (reducing ventilation by half causes a doubling of the PCO2) = hypercapnia & a decrease in arterial O2 = hypoxemia

Hypoxemic: due to failure of gas exchange within the lungs

Causes: ventilation/perfusion mismatch – often seen in people with COPD, where a lung region may not be perfused or not ventilated, impaired diffusion – often seen in interstitial lung diseases, ARDS, pulmonary edema, treated usually with administrating high concentrations of oxygen (increases the diffusion gradient)

50
Q
  1. What medical procedure can often cause acute respiratory failure? Be familiar with the problems that this procedure can cause that may result in acute respiratory failure.
A

Important potential complication of surgery - most common post-op problems causing ARF are atelectasis, pneumonia, pulmonary edema and pulmonary embolism

51
Q
  1. Describe how hypercapnic/hypoxemic respiratory failure can be brought about, and how it is usually treated.
A

Anything interfering with the ventilation mechanism can bring this about: diseases of the nervous system, disorders of the respiratory muscles, COPD

Treated with mechanical ventilation

52
Q
  1. Describe how hypoxemic respiratory failure can be brought about, and how it is usually treated.
A

Causes: ventilation/perfusion mismatch – often seen in people with COPD, where a lung region may not be perfused or not ventilated, impaired diffusion – often seen in interstitial lung diseases, ARDS, pulmonary edema

treated usually with administrating high concentrations of oxygen (increases the diffusion gradient)

53
Q
  1. What is croup characterized by?
A

Inspiratory stridor, hoarseness and a barking cough, as a result of subglottic inflammation and edema

54
Q
  1. Define stridor.
A

Wheezing tone produced during inspiration, indicating obstruction of upper respiratory pathway

55
Q
  1. What is the most common cause of croup?
A

Laryngotracheobronchitis (LTB) caused by viruses

56
Q
  1. What is a retraction?
A

Severe croup results in severe retractions (indentations of skin around ribs and sternum, showing use of accessory muscles of respiration)

57
Q
  1. Define bronchiolitis and give its cause.
A

Inflammation of small airways (bronchioles)

Caused by virus

58
Q
  1. Define epiglotitis, and give its cause.
A

Swelling of larynx, epiglottis

Caused by bacterial infection

59
Q
  1. To what is respiratory distress syndrome in infants due?
A

Premature infants, due to surfactant deficiency

Biology 2401 (30 decks)

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