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patho > alteration in pulmonary function > Flashcards

alteration in pulmonary function Flashcards

1
Q

what is ventilation

A

movement of air in and out of lungs

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2
Q

oxygenation

A

loading oxygen molecules onto hemoglobin

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3
Q

respiration

A

O2 and CO2 exchange of alveoli (external) and in cells/systemic capillaries (internal)

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4
Q

perfusion

A

delivery of blood to a capillary bed in tissue

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5
Q

dyspnea

A

breathlessness (bad breathing)
- subjective experience of difficulty breathing (symptom)
- work of breathing is greater than the actual result
- signs: flaring nostrils, use of accessory muscles, head bobbing in children
- paroxysmal nocturnal dyspnea: pulmonary condition that wakes you gasping for breath in the middle of the night

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6
Q

sputum

A

a mixture of saliva and mucus that is produced by lungs from bacterial infections
- colour provides info about progression of disease
- microscopic appearance allows microorganism identity
- excessive sputum indicates disease

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7
Q

hemoptysis

A

coughing up of blood
- usually indicates infection or inflammation of bronchiole
- if severe it can indicate cancer

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8
Q

eupnea

A

normal breathing
- rhythmic and effortless
- includes a short expiratory pause with each breath (before starting inhalation)
- occasionally people take deeper breaths or sighs

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9
Q

abnormal breathing patterns

A

patterns that automatically adjust to minimize WOB (work of body)

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10
Q

sigh

A

twice tidal volume/10 times an hour
- helps maintain normal breathing
- we consume more O2 than we produce CO2 so sighs help us equal out O2 consumption and expulsion

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11
Q

hyperpnea (kussmaul respiration)

A
  • occurs with strenuous exercise
  • increased ventilation rate/greatly increased tidal volume
  • no pause at the end of expiration
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12
Q

cheyene-stokes respiration

A

alternating deep and shallow breathing
- includes period of apnea (stopping breathing for 15-60 seconds)
- cause: reduced blood flow to brain so reduced brain impulses to respiratory center

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13
Q

hypoventilation

A

inadequate ventilation (reduced amount of CO2 exhaled)
- CO2 removed doesn’t keep up with CO2 production
- result: hypercapnia (increased CO2 in blood stream)

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14
Q

hyperventilation

A

alveolar ventilation is exceeding needs
- removal of more CO2 than is produces
- result: hypocapnia (reduced CO2 in blood)

*** hypoventilation and hyperventilation can both be determined by blood gases

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15
Q

cyanosis

A

bluish discoloration of skin
- develops when 5 grams of hemoglobin id desaturated
- cyanosis is not evident until it is severe = insensitive indicator of respiratory failure

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16
Q

peripheral cyanosis

A

poor circulation in fingers/toes due to peripheral vasoconstriction
- best seen in nail beds

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17
Q

central cyanosis

A

decreased arterial oxidation (low PaO2) from pulmonary disease
- best detected in buccal mucosa membrane and lips

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18
Q

clubbing

A

bulbous formations at the end of fingertips and toes
- from diseases that disrupts pulmonary circulation causing hypoxemia (rarely reversible)

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19
Q

pain from pulmonary disorders

A
  • almost almost localized (in chest wall)
  • can be pinpointed by a sound called the pleural friction rub
  • pleural friction rub: when the pleural walls rub together because of reduced serous fluid in the pleural cavity
  • pain can be produced by pressing on sternum/ribs
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20
Q

hypercapnia

A

increased CO2 in blood (increased PaCO2) caused by hypoventilation of alveoli

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21
Q

what does hypoventilation cause

A
  • decreased drive to breathe
  • depression of respiratory center
  • disease to medulla oblongata
  • increased work of breathing
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22
Q

hypoventilation effects

A
  • electrolyte (ionic) imbalances
  • CO2 + H2O ↔ H2CO3 ↔H+ and HCO3-
    accumulation of H+ molecules in the blood lowers pH, acidosis
  • result in dysrhythmia (irregular heart rate) and can end is coma if severe

**hypoventilation often appears normal so need to obtain blood gases to confirm it

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23
Q

hypoxemia

A

decreased O2 in blood (PaO2)
- normal PaO2 is 80-100mmHg
- severe hypoxemia is <40mmHg

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24
Q

2 causes of hypoxemia

A
  1. issue with delivery of O2 to alveoli (ventilation) and delivery of blood to the lung (perfusion)
  2. thickening of alveolar membrane or destruction of alveoli
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25
Q

diffusion of O2 from alveoli to blood is dependant on two factors

A
  1. amount of air entering alveoli (ventilation = V)
  2. amount of blood perfusing capillaries around alveoli (Q)
    an abnormal ventilation/perfusion ratio (V/Q) is the most common cause of hypoxemia
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26
Q

alveolar dead space

A

inadequate perfusion/normal ventilation
- high ratio V/Q

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27
Q

shunt

A

normal perfusion/inadequate ventilation
- very low V/Q ratio

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28
Q

acute respiratory failure

A

inadequate gas exchange
- when PaO2 is less than 60 mmHg (treat with supplemental O2)
- When PaCO2 is greater than 50mmHg (need ventilatory support)
- when pH of blood is less than or equal to 7.25

29
Q

acute respiratory failure cont

A

normal vlaues:
- pH 7.35-7.45
- PaO2 75-100 mmHg
- PaCO2 35-45 mmHg
a change in any of these values creates a potential complication in any major surgery
prevent with:
- frequent turning and position changes, deep breathing exercises, early ambulation (during surgery)
- common conditions that result in respiratory failure are pneumonia, edema, embolism

30
Q

chest wall restrictions

A

decreased tidal volume and increased breathing rate that can lead to respiratory failure
- cause: deformonty, obesity, neuromuscular disease
- result: increased work of breathing usually decrease in tidal volume
- pain from injury, surgery, disease can cause hypoventilation

31
Q

flail chest

A

fracture of consecutive ribs with or without sternum damage
- result: chest wall instability = paradoxical movement of chest when breathing

32
Q

paradoxical breathing

A

inspiration: unstable portion of chest wall moves inward (normal movement would be outward)
expiration: portion moves outward (normal movement would be inward)
- result: impaired ventilation of alveoli

33
Q

pneumothorax

A
  • air/gas in pleural space
  • cause: rupture to visceral pleural (closest layer to lung)
  • result: lung collapse (increased air in pleural cavity represses the lung - pressure against lung)
34
Q

pleural effusion

A

fluid in pleural space from blood or lymph
- diagnosis: chest x ray or thoracentesis (needle aspiration of the lung-fluid removed)

35
Q

empyema

A

infected pleural effusion by microorganisms
- indication: pus in pleural space
- cause: pulmonary lymphatic tissue becomes blocked and contaminated lymphatic fluid moves into pleural space
- result of surgery or bronchial obstruction
- TX: antibiotics and drainage of pleural space with chest tube

36
Q

restrictive lung disease

A

difficulty with inspiration (expanding their lungs)
- aspiration
- atelectasis
- bronchiectasis
- bronchiolitis
- pulmonary fibrosis
- pulmonary edema
- COVID - 19

37
Q

obstructive lung diseases

A

difficulty with expiration (difficulty retracting their lungs)
- asthma
- COPD (chronic bronchitis, emphysema)
signs and symptoms: dyspnea and wheezing

38
Q

aspiration (restrictive)

A

passage of fluids or solids into lungs
- causes: abnormal swelling mechanism, impaired cough reflex (base of trachea and alveoli)
- can lead to CNS or PNS abnormalities
- can lead to pneumonia
- TX: bronchoscopy (if this doesn’t work leads to inflammation)

39
Q

atelectasis (restrictive)

A

collapse of lung
2 types of alveoli collapse:
1. compression atelectasis: cause by external pressure (tumour or fluid)
2. surfactant impairment: decreased production of surfactant. tends to occur after surgery when using general anesthetic
- TX: deep breathing exercises: promotes ciliary removal of secretions

40
Q

bronchiectasis (restrictive)

A

persistent abnormal dilation of bronchi (large airways)
- obstruction causes: inflammation due to mucus plugs
- CI = destruction of elastic/muscular bronchi wall = permanent dilation
- symptoms: chronic productive cough, large amount of foul-smelling sputum

41
Q

bronchiolitis (restrictive)

A

inflammatory obstruction of the small airways
- can bronchiolitis obliterans: fibrosis of airways (scarring)
- can lead to BOOP: when alveoli because filled with connective tissue
- manifestation: rapid ventilatory rate and dry non-productive cough

42
Q

pulmonary fibrosis (restrictive)

A

excessive amount of fibrous/connective tissue at alveoli
- cause: scar tissue left from previous disease (Tb)
- result: deceased lung compliance and external respiration (O2/CO2 exchange)
- results from multiple injuries at different lung sites associated with abnormal healing
- symptoms: dyspnea on exertion

43
Q

pulmonary edema (restrictive)

A

excessive water on longs
- cause: left side heart disease
= reduced left side heart cardiac output
= blood backed up fro heart to lungs
= increased blood pressure in pulmonary capillaries
= fluid forced into interstitial space space between capillary and alveoli
- when fluid flow exceeds lymph system capability to remove = pulmonary edema occurs

44
Q

COVID 19 (restrictive)

A

severe COVID is manifested as viral pneumonia-induced ARDS (acute respiratory distress syndrome)
- post mortem studies reveal mortality patients had undetected viral loads (cytotoxic effects of the virus are not the main cause of death. death is caused by the host’s runaway immune response.)
- management: intubation (allows appropriate airflow)

45
Q

asthma (obstructive)

A

chronic inflammatory disorder of bronchial mucosa
- inflammation = restriction of airways. causing a hyper-immune response to irritants

46
Q

early asthma attack

A

classic immune cell response: dendritic cells, helper T cells, T cells, and B cells
- result: inflammation, increased capillary permeability and increased fluid

47
Q

late asthma attack

A

begins 4-8 hours after eaarly attack
- latent release of inflammatory mediators from original site
- result: increased damage of epithelial cells = scarring/increased mucus forming plugs/increased airway resistance

48
Q

manifestation of asthma

A

individuals normal between attacks/pulmonary function tests are normal
- if bronchospasm are not reversed by usual treatment people are considered “status asthmaticus”
- if PaCO2 is greater than 70mmHg = sign of impending death

49
Q

treatment of asthma

A

mild: short acting inhalers
persistent: inhaled corticosteroids

50
Q

pathophysiology of asthma

A
  1. inhaled antigen passes epithelial layer
  2. antigen binds to mast cells= release of mediators (histamine)
  3. mediators = mucus in production airway/broncho spasm/edema from increased capillary permeability
  4. dendritic cells present antigen to helper T cell = activate B cells which release antibodies
  5. helper T cells also active eosinophils and neutrophils. inflammation from both results in airway obstruction
51
Q

COPD (chronic obstructive pulmonary disease)

A
  • composed of chronic bronchitic and emphysema
  • most common lung disease (4th leading cause of death in world)
  • characterized by persistent airflow limitation and chronic inflammatory response to noxious particles or gas
52
Q

chronic bronchitis

A

defined as hypersecretion of mucus/chronic productive cough for at least 3 months of the year for the last 2 years
- cause: inspired irritants = inflammation/thickening of mucous membrane or reduced radius of airways = obstruction
- initially effects large airways (but eventually all airways
- airways collapse early in exhalation = air trapped in distal portions of lung = hyperinflation = hypoventilation

53
Q

emphysema

A

the permanent enlargement of gas-exchange airways and the destruction of alveolar walls
- causes obstruction (exhalation) due to destroyed walls of alveoli
- destruction of alveolar walls cause large alveolar spaces with greatly increases the distance between alveoli and capillary
- results: reduced O2 and CO2 diffusion and expiration is difficult due to loss of recoil of alveoli

54
Q

respiratory tract infections

A
  1. acute bronchitis
  2. pneumonia
  3. tuberculosis
55
Q

acute bronchitis

A

acute infection or inflammation of airways
- usually self limiting and mostly occurs due to viral infection
- symptoms: non-productive cough aggravated by cold, dry air, dusty air (similar to pneumonia)
- TX: rest, aspirin (used for relieving pain, lowering fever and reducing inflammation), cough suppressants, antibiotics

56
Q

pneumonia

A

infection of lower respiratory tract caused by microorganisms (bacteria, viruses, fungi, protozoa, parasites)
- can be HAP (hospital acquired; 2nd most common nosocomial) or CAP (community acquired)
- most common pathogen: Streptococcus pneumoniae
- common infection route: inhalation of infected individuals cough

57
Q

pathophysiology of pneumonia

A
  • in hospitals, suctioning tubes can become colonized with bacterial biofilms = suction results in seeding lung with bacteria
  • guardian cells of lower respiratory tract are cellular alveolar macrophages
  • macrophages present antigens to adaptive immune system = activation T and B cells
  • resulting immune response can fill alveoli with debris
  • microorganisms release toxins causing further damage
58
Q

tuberculosis

A
  • pathogen: Mycobacterium tuberculosis
  • leading cause of death from a curable infectious disease
  • transmitted by airborne droplets
59
Q

pathophysiology of tuberculosis

A
  1. pathogen reaches the lung and is engulfed by macrophages
  2. pathogen survives and multiplies within the macrophage, causing a chemotactic response. this response causes more macrophages to respond to the site of injury, forming a tubercle
  3. macrophages die, releasing the pathogen, and forming the center of the tubercle. DORMANT STAGE
  4. tubercle center enlarges, liquifying and filling with air. the aerobic pathogen is able to multiply outside of the macrophage
  5. liquification continues and the tubercle ruptures. the pathogen disseminates throughout the lung. NOT DORMANT
60
Q

pulmonary vascular disease

A

pulmonary blood flow disrupted causing occlusions (blocking or closing of blood vessel) = destruction of vascular bed
- causes dramatic alterations in perfusion/ventilation ratios
1. pulmonary embolism
2. pulmonary artery hypertension
3. Col Pulmonale

61
Q

pulmonary embolism

A

occlusion of portion of pulmonary vascular bed by embolism
- pathophysiology effects depend on: extent of pulmonary blood flow obstruction, size of affected vessel, nature of embolus, resulting in secondary effects

62
Q

pulmonary artery hypertension

A

mean pulmonary artery pressure greater than 25mmHg at rest (normal 20 mmHg or less)

63
Q

pathophysiology of pulmonary artery hypertension

A
  • endothelial dysfunction/overproduction of vasoconstrictors
  • increased growth factors = fibrosis = thickening of vessel wall
  • narrowing of vessels and gas exchange reduced
  • increase in pulmonary artery pressure = increased pressure in right ventricle
  • right ventricle hypertrophy = failure (Cor Pulmonale)
64
Q

Cor Pulmonale

A

enlargement of right ventricle from hypertrophy or dilation (or both)
- result of pulmonary artery hypertension
- causes increased work of right ventricle, causing increased hypertrophy of normally thin-walled heart muscles
- can cause pressure overload: dilation/hypertrophy = failure of right ventricle

65
Q

malignancies of the respiratory tract

A
  1. laryngeal cancer
  2. lung cancer
66
Q

laryngeal cancer

A

primary risk factor: smoking (risk increases when smoking combined with alcohol consumption)
- pathogen: human papillomavirus (HPV) is linked to this cancer
- pathophysiology: carcinoma of vocal cords is most common site. metastasis occurs in lymph nodes, but distant metastasis is rare
- manifestations: hoarseness, dysnpea, cough following swallowing
- diagnosis/TX: biopsy, radiation, chemo

67
Q

lung cancer

A
  • tumours on respiratory tract epithelium
  • leading cause of death in canadians
  • most common cause is smoking, then gas exposure, then second hand smoke
68
Q

pathophysiology of lung cancer

A
  • tobacco smoke contains 30 carcinogens (responsible for causeing 90% of lung cancers)
  • tumour: result of growth factors and production of free radicals
  • bronchial mucosa: suffers “hits” from tobacco smoke = epithelial damage
  • progression: metastasis to brain, bone marrow and liver

patho (4 decks)

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