Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

253 > Respiratory Disorders > Flashcards

Respiratory Disorders Flashcards

(124 cards)

Start Studying
1
Q

Influenza: What type of infection? Where? What types of influenza are there? Which is most common? Incubation period? Who does it affect the most?

A

Acute viral infection. URT. A B C, A most common. 1-4 days. Elderly, young, health care workers, chronically ill.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the patho for influenza? What happens if it extends to the LRT?

A

Virus and inflammation - tissue damage of epithelial cells. Bronchial and alveolar damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are 3 complications of influenza?

A

Secondary bacterial infection, bronchitis or pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are 4 manifestations of influenza? Prophylactic measure? 3 treatment methods?

A

Cough, fever, lethargy, myalgia. Immunization. Prevent spread to others/LRT, symptomatic treatment, and antivirals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What two types of antivirals are there for influenza?

A

Amantadine (1st generation) - prevents uncoding of genetic material. Relenza (2nd generation) - prevents replication of virus and lyse of cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is another name for pneumonia? What structures are inflamed in this disease? What two forms are there? How can pneumonia be classified?

A

Pneumonitis. Alveoli and bronchioles, distal part of the respiratory tract. Infectious and non-infectious. By infectious agent or area of lung affected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are 5 etiologic factors for pneumonia and what categories can they be divided into?

A

Bacteria, virus, fungi (infectious pneumonia). Aspiration and noxious fumes (non-infectious pneumonia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the patho for pneumonia? What two problems arise in the patho of pneumonia?

A

Impaired resp defences - agent enters RT and proceeds to lungs. Inflm - pulmonary edema (exudate) - impaired gas exchange due to increased diffusion distance. 1. inflm and tissue damage 2. exudate formation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is typical pneumonia? Atypical pneumonia? Bronchopneumonia? Lobar pneumonia?

A

Microbe activity within alveoli (bacterial). Microbe activity in tissue of lungs (viral). Diffuse inflammation (throughout lung). Lobe/part of lobe affected by pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are 7 manifestations of pneumonia?

A

Fever and chills, dyspnea, sputum (exudate and mucus), headache, myalgia, lethargy, and chest pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is pneumonia diagnosed? Treatment?

A

CXR, sputum C + S. Abx and supportive treatment (oxygen).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is COPD? What two diseases is it comprised of?

A

Persistent inflammation of airways, parenchyma and vasculature in RT resulting in obstruction. Chronic bronchitis and emphysema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are 4 etiology/risk factors for COPD?

A

Smoking, recurrent respiratory infections, ageing, and genetic deficiency in alpha 1 antitrypsin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What 4 roles does cigarette smoke play in the RT?

A

Increases mucus secretion, damages cilia, causes inflammation leading to tissue damage, induces coughing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is chronic bronchitis?

A

Inflammation and obstruction of airways due to smoking and chronic/recurrent infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the two characteristics/changes in chronic bronchitis? What change happens in the large airways first and then small airways?

A

Large airways: hypertrophy of submucosal glands - increased mucus secretion/hypersecretion of mucus. Small airways: increase goblet cell number - increased mucus production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the patho for chronic bronchitis? In the V:P ratio, which factor is affected?

A

Excess mucus - mucocilary defences impaired - infection occurs easier - bronchial wall inflm - lumen obstruction - airway collapse (air is absorbed) - decreased alveolar ventilation - ventilation:perfusion (v:p) imbal - hypoxemia. V is affected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is chronic bronchitis diagnosed?

A

Chronic productive cough >3 mos/year for 2 consecutive years.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are 6 manifestations of chronic bronchitis?

A

hypoxemia and hypercapnia, activity intolerance, ++ sputum, dyspnea, wheezing and crackles (wet), prolong expiration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is emphysema? What does it result in in terms of gas exchange?

A

Destruction of alveolar tissue and capillary beds causing loss of compliance - damaged elastic tissue. Decreased surface area for gas exchange.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are two etiologic factors for emphysema?

A

Smoking, genetic deficiency of a1 antitrypsin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does a genetic deficiency for a1 antitrypsin play a role in emphysema?

A

a1 antitrypsin is an inhibitor for proteases and elastases, with it being deficient, proteases and elastases are free to break down alveolar walls.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the patho for emphysema?

A

Smoking inhibits a1 antitrypsin (inhibiting inhibitors). Smoking attracts inflammatory cells - tissue damage. Increase proteases - destruction of alveolar wall and wall of a/w - alveoli merge - decrease SA - decrease fx - air traps in between alveoli - increased dead space - increased WOB. Capillary walls destroyed - impaired perfusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

In the V:P ratio for emphysema, which factor(s) is affected?

A

V and P

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is a "bullae"? "Bleb"?
Dead space pushing upward against pleural membrane. Smaller form of bullae.
26
What is centriarcinar emphysema? Panacinar emphysema? Which is more common?
Terminal bronchioles and respiratory bronchioles are damages, alveoli largely intact. Alveoli and terminal airways affected. Centriarcinar.
27
What are 3 manifestations of emphysema?
Dyspnea, increased ventilation effort (pursed lip breathing, nasal flaring, use of accessory muscles), and barrel chest (long term).
28
What three diagnostics are used to diagnose COPD?
ABGs, CXR, pulmonary fx tests.
29
What three things can be done to manage progression of COPD?
No smoking, avoid a/w irritants, flu and pneumococcal vaccines.
30
What is the treatment regimen for COPD?
Short acting B agonist (1st line approach) and anticholinergics (bronchodilation)... then add inhaled steroid... then take away short acting B agonist and add long acting B agonist. Theophylline (bronchodilator with anti-inflm properties).
31
What two strains of bacteria cause TB? How is each spread?
Myobacterium tuberculosis hominis: human TB, spread via coughing, sneezing, talking, droplet nuclei. Myobacterium tuberculosis bovine: bovine TB, spread via milk from infected cow, initially affects GIT.
32
What is the Ghon focus? What is it comprised of?
Primary lesion. Bacillus, macrophage and other immune response cells.
33
What is the Ghon complex?
Primary lung lesion (Ghon focus) and lymph node granulomas
34
In primary TB what occurs first before the cell-mediated IR?
The bacillus enters the alveolar sacs and is engulfed by a macrophage but the macrophage is unable to phagocytize the bacillus because of the wall lipids.
35
During the cell-mediated IR of primary TB what happens?
The macrophage presents the Ag to T lymphocytes in a regional lymph node - the T lymphocyte becomes sensitized and stimulated the macrophage to increase it's lytic enzyme concentration - this results in destruction of bacillus and lung tissue - forming the primary lesion
36
When the numbers of the bacillus increases in primary TB what sort of a reaction occurs? What happens to the Ghon focus?
Hypersensitivity reaction. Central portion of Ghon focus undergoes soft, caseous necrosis (cheeselike death).
37
What occurs when the Ghon focus undergoes necrosis in primary TB? What is formed?
Tubercule bacillus drain along lymph channels affecting the tracheobronchial lymph nodes. Formation of caseous granulomas (lymph node granulomas).
38
How does secondary TB occur? What is usually the aggravating factor causing cavitation and bronchial dissemination?
Reinfection or reactivation from a healed primary lesion. Cell-mediated hypersensitivity reaction.
39
What are 4 manifestations of TB? Which manifestation is specific to secondary TB?
Wt loss, low grade fever, night sweats, fatigue. Low grade fever
40
What are two screening methods for TB? How is it diagnosed?
TB test, CXR. Sputum C+S, genotyping (identify the strain).
41
Which vaccine is given to people at high risk for TB? What is one odd treatment method used for TB that one would not expect? What are 5 other treatments?
Bacillus Calmette-Guerin (BCG) vaccine. Chemotherapy. Rifampin (inhibit RNA synthesis), ethambutol (inhibit growth), isoniazia (INH), pyrazinamide (PZA - inhibit growth), streptomycin.
42
What nasal passages are affected in rhinosinusitis?
Frontal, ethmoid, and maxillary sinuses.
43
What is the patho for rhinosinusitis?
Viral URTI or allergic rhinitis - obstructs ostia that drains sinuses - impaired mucociliary clearance mechanism
44
How is rhinosinusitis diagnosed? What are 3 treatment options?
Transillumination, CT scan. Abx, mucolytic agents, symptomatic treatment.
45
What are 2 orbital complications of rhinosinusitis? What are 5 intracranial complication?
Edema of eyelid and orbital cellulitis. Facial swelling, abnormal extraocular movements, protrusion of eyeball, periorbital edema, change in mental status.
46
What 5 virus strains are responsible for the common cold?
Rhinovirus, parainfluenza virus, respiratory syncytial virus (RSV), coronavirus, and adenovirus.
47
What is the MOT of viruses for the common cold? What are 4 manifestations of the common cold?
Contact and aerosol spread. Headache, general malaise, excessive nasal secretions, tearing of eyes.
48
Which OTC remedies for the common cold are perhaps beneficial when taken immediately as manifestations appear? Which other OTC remedies are there? Do any of them shorten length of illness?
Echinacea. Antihistamine (dry nasal secretions) and decongestants (constrict BV in nasal passage to decrease swelling). Vitamin C, Zinc. No.
49
What is asthma?
Reversible episodes of a/w obstruction d/t inflm and muscle hyperactivity
50
What form of HS is asthma?
Type 1
51
What are two etiologic factors for asthma?
Complex trait (genetic susceptibility and environmental trigger) and hypersensitivity to triggers (allergens, a/w irritants, exercise, strong odours etc)
52
What is the patho for the acute-phase response of asthma?
Exposure to allergen - Ag binds to IgE on mast cell - mediators released - inflammation attracts more inflammatory cells - intercellular junction opens - allergen enters submucosa - inc perm ince mucus - edema of a/w - bronchospasm - dyspnea and wheezing
53
What is a compensatory mechanism that occurs during asthma that really isn't compensatory? What stimulation causes bronchospasm?
A/w constriction (to prevent more irritant from entering) and PNS stimulation
54
How can the acute-phase response in asthma last?
up to 1 hour
55
Does everyone develop a late-phase response in an asthma attack?
No
56
When is the peak for the late-phase asthma response? Do the manifestations that occur during the acute-phase persist? How long can the late-phase response last?
4 - 8 hours. Yes. Days - weeks.
57
What is the patho of the late-phase response in asthma?
influx of inflm cells - epith. damage, dec mucociliary fx, hyperresponsive a/w - bronchoconstriction
58
What is a hyperresponsive a/w?
an a/w that responds to new triggers (cold air)
59
What receptors are responsible for bronchoconstriction? What about bronchodilation?
Alpha adrenergic receptors and Beta adrenergic receptors
60
What are 6 mnfts of asthma?
Dyspnea, wheezing, immobilization, bronchospasm and coughing, inc resp effort, ventilator compromise (altered resp status and ABGs)
61
How is asthma dx?
ABGs (labs), pulmonary fx tests, inhalation challenge tests (test for responsiveness to potential allergens)
62
What are 2 preventative measures for asthma? What is the 4 step method for treatment?
Avoid allergens and irritants and no smoking. Step 1: inhaled short-acting bronchodilator PRN. Step 2: add inhaled steroid. Step 3: add long acting bronchodilator to steroid and get rid of short-acting. Step 4: Short course steroid treatment (PO) + 3rd drug (leukotriene receptor antagonist or theophylline)
63
What is atelectasis? What does it impede?
Collapse of part of the lung. Filling of the lung
64
What is the patho obstructive/resorptive atelectasis? Reversible or not?
a/w obstruction (mucus) - air trapped - air absorbed into capillaries - airless - local collapse. Yes it is reversible as long as there is no structural damage.
65
What is the patho of compression atelectasis? Reversible or not?
External p on lungs (tumor) - collapse. Reversible if no structural damage
66
What is the patho of contraction atelectasis? Is it reversible?
Scar tissue contracts - lungs collapse. Harder to reverse because of scar tissue.
67
What are 4 manifestations of atelectasis?
dyspnea, tachypnea, dec chest expansion, tachycardia
68
3 dx measures for atelectasis?
CXR, CT, bronchoscopy
69
How is atelectasis treated?
Treat cause
70
What is a pleural effusion?
Fluid accumulation in pleural space
71
What is the fluid accumulation due to in pleural effusion? (Think of the 5 different fluid types)
Due to abnormal seepage or drainage of: exudate, transudate, empyema, hemothorax, chylothorax.
72
What is the etiology (4) for pleural effusion?
usually CHF, also infection, CA and pulmonary infarct
73
What is the patho for a pleural effusion?
Fluid enters via parietal capillaries - and fluid entry exceeds fluid drainage from parietal lymphatics - pleural effusion
74
What are 3 common manifestations of pleural effusion? What two other factors determine manifestations?
Dyspnea, pleuritic pain (stretched membrane), lung compression. Volume of fluid and cause determine manifestations.
75
How is a pleural effusion diagnosed?
CXR, US, CT
76
How is a pleural effusion treated?
Cause, thoracentesis (and fluid analysis), chest tube (if recurrent seepage)
77
What is pulmonary edema?
fluid accumulation inside lungs (alveoli)
78
What two issues arise with pulmonary edema?
Increased diff distance and dec ability to fill alveoli with air (decreased vol available for air)
79
What is the main etiologic factor for pulmonary edema? 4 others?
LS HF, IV fluid overload, smoke inhalation/noxious fumes, aspiration, IV drug use
80
What is the patho for pulmonary edema?
Fluid from BV - IS - alveoli - decreased resp fx
81
What are 4 manifestations of pulmonary edema?
productive cough (frothy sputum), SOB, dec compliance (less room for air in alveoli), crackles
82
What are 3 treatment methods for pulmonary edema?
Resp support, diuretic, cause
83
What is a pulmonary embolism?
a thrombus within a pulmonary vessel
84
What is the main source of a PE? what are 3 other etiologic factors?
DVT. Fat, air, amniotic fluid.
85
What is the patho of a PE?
DVT - embolus - thrombus in arterial bed - impaired perf - V:P imbal - hypoxemia - platelets aggregate and degranulate - release mediators - bronchial and pulm artery constriction - hemodynamic instability - reflexive bronchoconstriction - dec CO - loss of surfactant d/t dec BF to lungs and resources - atelectasis - RS HF (heart pumps harder to push blood through pulm circuit)
86
What are 3 common mnfts of PE? What 2 factors are the mnfts based on?
CP, tachypnea, SOB. Size and site.
87
How is a PE dx (5)?
ABGs, LDH3 (lactate dehydrogenase 3 damages lung tissue), lung scan
88
What is pulmonary HTN?
Sustained pressure increase in the pulmonary circuit
89
What is the measure in mmHg of pulm HTN?
>25 mmHg
90
What is pulm HTN usually secondary to?
cardiac or pulmonary problems
91
What are the 3 categories for etiology of pulm. HTN? Give examples of each.
Pulmonary volume increase (cardiac septal defect - increase blood going into RV from LV and into pulmonary circuit). Hypoxemia (results in vasoconstriction in the lungs to limit C02 distribution) and increased venous pressure d/t LV failure/dysfx (congestion in pulmonary circuit).
92
5 manifestations of pulm. HTN?
SOB, syncope (lack of O2 rich blood to brain), CP on exertion, RS HF, fatigue.
93
What is seen on a CXR in someone with pulm. HTN?
Distended pulm. artery and RV hypertrophy.
94
2 treatment methods for pulm. HTN?
Cause, vasodilators (with limited success - Ca+ Channel blockers). Poor prognosis with non-reversible causes.
95
What is another name for ARDS?
Post-traumatic lung
96
What structures are damaged in ARDS?
Alveolar walls and capillary walls.
97
What are 5 etiologic factors for ARDS?
Aspiration, fat embolus (trauma), smoke inhalation (fire), disseminated intravascular coagulation (DIC - liver failure), radiation.
98
What is the patho for ARDS?
Lung trauma - neutrophil influx - free radical, phospholipid and protease production - endothelial and alveolar damage - increased perm - non-defensive cells efflux, cells and fluid move into IS and alveoli - edema - decreased compliance and impaired gas exchange - surfactant deficiency and inactivation - atelectasis - thick protein and cell rich exudate lines alveoli - no gas exchange - profound hypoxemia
99
What is the thick protein and cell rich exudate that lines the alveoli in ARDS called?
Hyaline membrane.
100
What are 7 manifestations of ARDS? Which one is compensatory?
Acute onset resp. distress, SOB, tachypnea (compensatory), hypoxemia shown from ABGs, early resp. alkalosis (inc RR - dec C02 to bind to H2O to make H2CO3), late metb. acidosis (anaerobic metb), diffuse consolidation.
101
3 main treatments for ARDS?
Early intervention and identification of cause, reverse the cause, respiratory support, avoid complications.
102
In general, what are the characteristics of lung cancer?
Aggressive, invasive and metastatic.
103
What are the five major types of primary lung cancer from most prevalent to least prevalent?
Adenocarcinomas (30%), squamous cell carcinomas (30%), small cell carcinoma (22%), large cell carcinoma (12%), mixed group (5%).
104
What types of primary lung cancers fall into the Non-Small Cell Lung CA (NSCLC) group?
Adenocarcinoma, squamous cell carcinoma, large cell carcinoma.
105
What are 3 etiologic factors for lung cancer?
Smoking, toxins, genetic predisposition.
106
What are the characteristics of squamous cell carcinoma?
Arises in central bronchi (hilum area), spreads to hilar nodes, will impact heart if in L side of lung (end up with cardiac tamponade), affects males more commonly
107
What are the characteristics of adenocarcinoma?
Peripheral in origin, alveoli and bronchioles affected, common in females and non-smokers.
108
What are the characteristics of large cell carcinoma?
Peripheral in origin, premature large undifferentiated cells affected, mets early. Poorer prognosis.
109
What are the characteristics of small cell carcinoma?
Resemble oat grains (aka oat cell carcinoma), worst form, 99% smokers, aggressive, invasive, early mets, mets by dx, diffuse cells (non surgical), cells susceptible to radiation, paraneoplastic syndrome (ectopic tumor in SIADH, Cushings)
110
What is 1 common manifestation of all types of lung cancer? 2 others? Centrally located tumors?
Hemoptysis, pain d/t tumor occupying space and inflm, cardiac mnfts. Impaired ventilation (wheezing, coughing, SOB)
111
How is lung cancer diagnosed (6)?
CXR (if tumor large enough), US, CT, MRI, bronchoscopy with biopsy, cytology of bronchial wash or sputum.
112
How is NSCLC treated? SCLC?
Sx, radiation and chemo. Radiation and chemo.
113
What is cystic fibrosis?
Chloride channel defect in cell membrane resulting in abnormally thick mucus production
114
What body systems does CF commonly affect?
RT, GIT and reprod.
115
What is the etiologic factor for CF? What type of inheritance is this? Autosomal dominant or recessive.
CFTR gene mutation on chr. 7 (autosomal recessive). CFTR = cystic fibrosis transmembrane regulator.
116
What is the patho for CF?
Mutated CTR gene - cell impermeable to Cl- ions - impaired transport across CM - abnormal secretions - consistency thick and mucus cannot move along RT - mucus accum - plug a/w - decrease fx - bacterial infection - neutrophil influx and release of elastase and inflm. mediators
117
What are the 2 problem that occur because of CF? What are 3 common conditions that arise from CF?
1. obstruction of a/w and air flow 2. recurrent bacterial infections. Chronic bronchitis, bronchiectasis, and respiratory failure.
118
How is CF diagnosed (4)?
Sweat test (Na and Cl concentration is ++ in those with CF), CF in sibling, newborn screen (trypsinogen d/t overwhelmed pancreas appears in blood), GI and resp mnft.
119
Is CF curable? What are some treatments?
No. DNAase (dec mucus thickness as DNA strands that are released when cells die make mucus stickier), control infection (gamma globulin), diet mod and pancreatic enzyme supplement (pancreatic enzymes will be abn), anti inflammatory.
120
What is a complication of CF?
infection
121
What is respiratory failure?
Failure of the lungs to function. No gaseous exchange results in hypoxemia and hypercapnia.
122
What are 6 etiologic factors for resp. failure?
COPD, severe pneumonia, atelectasis, Guillan-Barre, pulm. edema, ARDS.
123
What are 3 manifestations of resp. failure?
Hypoxemia (Pa02 45), resp. acidosis, manifestations related to underlying cause.
124
How is resp. failure treated?
Restore gas exchange: 02, bronchodilator?, mechanical ventilator?, Abx

253 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions