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Pathophysiology 2200 > Module 6 > Flashcards

Module 6 Flashcards

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

dyspnea: shortness of breath, nostrils flare and accessory muscles of respiration are used. (sternocleiodomastoid, abs, internal intercostal muscles etc.)
orthopnea: dyspnea lying down (ab contents to put pressure on diagphragm)

PND: awakening of night w/dyspnea

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2
Q
  1. Describe 7 other symptoms/signs of respiratory disease.
A 
dyspnea
cough
abnormal sputum
hemoptysis
abnormal breathing pattern
cyanosis
clubbing
pain
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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

increase in CO2 in arterial blood, ventilation is difficult bc CO2 can diffuse faster.
Alveolar hypoventilation cab be from drugs, medullar disease, physiological dead space, emphysema.

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

hypoxemia - decrease of oxygenation of the arterial blood

hypoxia - decrease of O2 in cells

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5
Q
  1. a. Explain the 3 mechanisms that can reduce oxygenation of the blood.
A

decrease alveolar O2 delivery
O2 diffusion from alveli to blood V/Q mismatch = hypoxemia + inadequarte Q makes dead space wasted = pulmonary embolism
Anatomical L to R shunt (not uncommon)

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6
Q

b. By what two means can oxygen delivery to the alveoli be decreased? Be familiar with examples of conditions/diseases that can cause this.

A
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7
Q

What does V/Q refer to?

A 
V = alveolar ventilation
Q = Perfusion
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8
Q

d. What is the most common cause of hypoxemia?

A

V/Q mismatch

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9
Q

e. Describe the conditions of low and high V/Q and be familiar with examples of diseases that cause each.

A

High V/Q = inadequate perfusion - mostly emobli
Low V.Q = decreased diffusion across the alveolar capillary membrane, thickened membrane brought by edema or fibrosis, R-L shunt.

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10
Q

What conditions can decrease diffusion across the alveolorcapillary membrane?

A

edema, fluid in blood and alvelous instersitial or space lining which O2 cannot diffuse through it because it is fibriotic or too thick.

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11
Q

g. What is the difference between anatomical and physiological “right to left shunt”?

A

Moving blood through unventilated parts of the lungs “waste of energy”

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12
Q
  1. What causes, and is the result of, chest wall restriction?
A

decrease in tidal volume
chest is deformed, traumatized immobilized or heavy from fat accumulation.
eg. grose obese, neuromuscular diseases, polomyletitis and muscular atrophy

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13
Q
  1. Describe flail chest.
A

trauma of the chest wall, fracture of several consecutive ribs.
chest walls moves with inspiration and out with expiration = paradoxic movement with disruption it pulls outwards to the throacic cavity which prevents pulling from two sides.

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14
Q
  1. Define pneumothorax and its effect on the lung.
A

air presecnce in the pleural space, air pushes outside of the lung then collapse = the membrane space around the lungs.

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15
Q
  1. Define pleural effusion and how it usually occurs.
A

excess fluid in the pleural space and it occurs with the migration of fluid through capillary walls bordering the pleura.

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16
Q

Define empyema and how it can occur.

A

infected pleural effusion - pus collection in pleural space.

complications of pneumonia, surgery etc.

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17
Q

Describe atelectasis, its causes, and manifestations.

A

lung collapse/external compression.
eg, excess fluid in pleural space, tumour, abdominal distension, obstructed airway.
- develops after surgery
- dysnea, cough and terberculocytosis
- mostly from surgery, meds and not moving.

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18
Q

What medical procedure often results in atelectasis and what measures can be taken to improve patients’ condition?

A

surgery - make the patients get up and walk to move around, breathe deeply and move positions when laying down.

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19
Q

Describe bronchiectasis and identify some causes.

A 
Permanent dilation of the
bronchi, secondary to other
diseases that cause chronic
inflammation of bronchial wall
(e.g., TB, cystic fibrosis).
• Chronic inflammation leads to
destruction of elastic and
muscular components of bronchi
walls and permanent dilation.
• Clinical manifestations include:
chronic cough, recurring lower
respiratory tract infection,
production of purulent sputum
(cupfuls), hemoptysis and
clubbing of the fingers (due to
chronic hypoxemia)
20
Q

Describe the pathophysiology behind cystic fibrosis and its treatment.

A

Autosomal recessive disorder
• 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 (especially with Pseudomona
aeruginosa).
• Recurring infections produce bronchitis, eventually
bronchiectasis.
• Treatment: includes antibiotics to control infection, possible
replacement of pancreatic enzymes (pancreas also affected).

21
Q

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.
• Most common embolus is a clot from deep
venous thrombosis involving the lower leg.
• Embolus could also be fat, air bubble, etc.

22
Q

What does obstruction of blood flow cause in the lung and what is the result if the clot is not dissolved soon enough?

A

Obstruction of blood flow causes pulmonary
vessels to constrict, resulting in impaired gas
exchange (V/Q mismatch). If clot is not
dissolved rapidly, the resulting hypertension
could possibly lead to right heart failure.

23
Q

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
24
Q

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 (e.g., COPD)
• 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.

25
Q

What is cor pulmonale, its primary cause, and its effects?

A

Right ventricular enlargement (hypertrophy, dilation, or both),
caused by chronic pulmonary hypertension (higher than normal
pulmonary artery pressure)
• Results in increased systemic venous circulation = peripheral
edema, etc.
it can result because of low arterial circulation

26
Q

What is pulmonary edema? How is it commonly caused and how does it result in hypoxemia?

A

Excess “water” 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 and RBCs leave
capillaries and collect in the interstitial space
– 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)

27
Q
  1. Describe clinical manifestations of pulmonary edema.
A

Clinical manifestations: dyspnea, cyanosis, increased physical effort
in breathing, blood-tinged frothy sputum

28
Q

To what are obstructive lung diseases due?

A

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

29
Q

What two diseases are grouped together under the title “chronic obstructive pulmonary disease”?

A

asthma, bronchitis and emphysema

30
Q

. What are the unifying symptom and sign of obstructive lung diseases?

A

unifying symptom is dyspnea and wheezing

31
Q

Define bronchial asthma.

A

chronic inflammation - to the bronchiole mucosa that causes hypersensitivity and obstruct airways.
- genetic and environmental factors are at play

32
Q

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 (plasma 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. (See diagram). Refer also to
Module 2 – Type I hypersensitivity
– Clinical manifestations at the beginning of an attack: chest
constriction, expiratory wheezing, dyspnea, tachycardia,
coughing.

33
Q

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

Begins 4-8 hours after the early response; can be more
severe than initial attack
1. 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.
2. 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. (See diagram)
– Untreated inflammation can lead to long-term airway
damage that is irreversible.
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 blood causing hypocapnia and
respiratory alkalosis.
Impairment of respiratory muscles →
respiratory acidosis
– The continued obstruction of airways increases air
trapping (incomplete expirations), which hyperexpands
the lungs and thorax, decreasing the tidal volume and
increasing hypoxemia.
– At this point, 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).

34
Q

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

35
Q

What is chronic obstructive pulmonary disease characterized by?

A

airway obstruction that causes difficulty exhaling = both emphysema and bronchitis

36
Q

Define chronic bronchitis. What is it very commonly caused by?

A

– Very commonly caused by smoking
– Definition: Hypersecretion of mucous and
chronic productive cough for at least 3 months
of the year, for at least 2 consecutive years.

37
Q

Describe the development of chronic bronchitis.

A

The airway becomes inflamed with inspiration
of irritants. Edema occurs, along with the
production of thick, tenacious mucous.
2. Continual inflammation leads to increases in
size and number of mucous glands and goblet
cells in the airway epithelium.

38
Q

Why is the term “blue bloaters” used?

A

“blue bloaters” (hypoxemia and edema,

caused by eventual right heart failure) - no o2

39
Q

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

40
Q

What is emphysema characterized by?

A

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

41
Q

What is the difference between the physiological/anatomical causes of the obstruction of emphysema and chronic bronchitis?

A
42
Q

What are two causes of emphysema?

A

“Obstruction” results from changes in the lung
tissue (primarily loss of elastic recoil), rather than
from mucous production and inflammation, which
is the case with chronic bronchitis.
– Can be an inherited condition (minority – due to
insufficiency of alpha1-antitrypsin that combats
proteases released by normal amounts of
inflammatory cells)), or through the inhalation of
cigarette smoke, air pollution, etc. that increases
number of inflammatory cells.

43
Q

Describe the development of emphysema.

A
  1. Inflammation occurs, and inflammatory cells (neutrophils,
    macrophages) release proteases that cause destruction of
    alveolar septae. This eliminates part of capillary bed and
    increases volume of acini (alveoli cluster distal to terminal
    bronchioles).
  2. This produces large air spaces within the lungs (bullae), and
    on the surface of the lungs, next to the pleura (blebs). These
    air spaces can not function in gas exchange, which increases
    hypoxemia.
  3. 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 the lungs.
  4. This hyperexpands the thorax (barrel chest), making it difficult
    to breathe, causing hypoventilation and hypercapnia
44
Q

Define blebs and bullae.

A

air bubbles in next to pleura (blebs)

air bubbles in lungs (bullae)

45
Q

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 the disease) but
classic tripod breathing position, with lips pursed to
increase lung pressure during exhalation, in an
attempt to keep breathing passages open)

46
Q

Describe the treatment of emphysema.

A

must include cessation of smoking (if the patient
smokes), and inhalation of corticosteroids and
bronchodilating drugs.
– Oxygen therapy, if required
– Possible lung reduction surgery or transplant

Pathophysiology 2200 (7 decks)

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