Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GEN PATH > Respi Assessment > Flashcards

Respi Assessment Flashcards

1
Q

Unilateral or bilateral bony (90% of cases) or membranous (10% of cases) septum between the nose and the pharynx

A

Choanal Atresia

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

Nonneoplastic tumefactions tgat develop as a response to chronic inflammation

A

Nasal polyps

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

The most common polyp.
Most often seen in adults with a history of IgE-mediated allergies. Nasal smear shows numerous Eosinophils

A

Allergic polyps

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

excessive snoring with intervals of breath cessation (apnea)

A

Obstructive Sleep Apnea (OSA)

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

Most common cause of OSA where Pharyngeal muscles collapse due to the weight of tissue in the neck.

A

Obesity

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

Other causes of Obstructive Sleep Apnea (OSA)

A
  • tonsillar hypertrophy
  • nasal septum deviation
  • hypothyroidism
  • acromegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Excessive snoring with episodes of apnea. Daytime somnolence often simulating narcolepsy

A

Obstructive Sleep Apnea (OSA)

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

PaO2 and O2 saturation (Sa O2) decrease and
PaCO2 increases (respiratory acidosis) during apneic episodes.

A

Obstructive Sleep Apnea (OSA)

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

Inflammation of the mucous membranes lining one or more of the paranasal sinuses.

A

Sinusitis

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

Most common malignant tumor of the nasopharynx. Male dominant
Increased in Chinese (common in adults) and African populations (common in children). Causal relationship with Epstein-Barr virus (EBV)

A

Nasopharyngeal (NP) Carcinoma

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

Occurs followed by right ventricular hypertrophy (RVH) the right ventricle becomes hypertrophied (called cor pulmonale).

A

Pulmonary hypertension (PH)

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

Hypoxemic stimulus for erythropoietin release leads to RBC hyperplasia and secondary polycythemia.

A

Secondary polycythemia

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

Location of Sinusitis

• Adult
Children

A

Adults- maxillary sinus

Children - ethmoid sinus

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

Causes of Sinusitis

A
  • Upper respiratory infections (URIs); e.g., viral, bacterial (S. pneumoniae)
  • Deviated nasal septum
  • Allergic rhinitis, barotrauma, and smoking cigarettes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pathologic findings of Nasopharyngeal (NP) Carcinoma

A
  • Squamous cell carcinoma (SCC), nonkeratinizing squamous carcinoma, or undifferentiated cancer
  • Metastasizes to cervical lymph nodes (70% of cases)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment for Nasopharyngeal (NP) Carcinoma

A

Radiotherapy

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

Risk factors Laryngeal carcinoma

A

•Cigarette smoking (most common cause)
• Alcohol (synergistic effect with smoking)
• Squamous papillomas and papillomatosis
-Human papillomavirus types 6 and 11 association.
- Majority located on true vocal cords

• Majority are keratinizing SCCs

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

Persistent hoarseness often associated with cervical lymphadenopathy

A

Laryngeal carcinoma

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

Upper Respiratory Tract disease

A
  • Choanal Atresia
  • Obstructive Sleep Apnea (OSA)
  • Sinusitis
  • Nasopharyngeal (NP) Carcinoma
  • Nasal polyps
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Loss of lung volume due to inadequate expansion of the airspaces (collapse)

A

Atelectasis

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

Airway obstruction by thick secretions prevents air from reaching the alveoli. Obstruction occurs in bronchi, segmental bronchi, or terminal bronchioles.

A

Resorption Atelectasis

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

Causes of obstruction
of Resorption Atelectasis

A
  • Mucus or mucopurulent plugs after surgery
  • Aspiration of foreign material
  • Centrally located bronchogenic carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cause of alveolar collapse

A

Lack of air and distal resorption of preexisting air. Following obstruction, circulating blood in the pulmonary capillary absorbs the preexisting air in the peripheral alveoli, leading to alveolar collapse and an airless state within a few hours.

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

Fever and dyspnea
Symptoms occur within 24 to 36 hours of collapse.

Absent breath sounds
Absent vocal vibratory sensation (tactile fremitus) Alveoli are collapsed.

A

Clinical findings of Atelectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Treatment for Atelectasis

A
  • Incentive spirometry after surgery
  • CPAP by face mask
  • Positive end-expiratory pressure (PEEP) on mechanical ventilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Air or fluid in the pleural cavity under increased pressure collapses small airways beneath the pleura

A

Compression Atelectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Examples of Compression Atelectasis

A
  • Tension pneumothorax where air compresses the lung

* Pleural effusion where fluid compresses the lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Atelectasis due to loss of surfactant.

A

Tension pneumothorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Synthesize surfactant which is stored in lamellar bodies
and synthesis begins in 28th week of gestation.

A

Type II pneumocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Has a decreased surfactant in the fetal lungs caused by prematurity (most common cause), maternal diabetes (poorly controlled)
[Fetal hyperglycemia increases insulin release.], Cesarean section (C-section) from lack of stress-induced increase in cortisol from a vaginal delivery

A

Respiratory distress syndrome (RDS) in newborns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Widespread atelectasis results in _____ from Perfusion without ventilation.

Collapsed alveoli are lined by hyaline membranes
Derived from proteins leaking out of damaged pulmonary vessels.

A

massive intrapulmonary shunting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Respiratory difficulty begins within a few hours after birth.
Grunting
Tachypnea
Intercostal retractions
Infants develop hypoxemia and respiratory acidosis.

A

Respiratory distress syndrome (RDS) in newborns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Diagnosis of Respiratory distress syndrome (RDS) in newborns

A

Chest radiograph shows a “ground glass” appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

• Increased hydrostatic pressure (HP) in pulmonary capillaries
- Left-sided heart failure, volume overload, and mitral stenosis
• Decreased oncotic pressure (OP)
- Nephrotic syndrome and cirrhosis

A

Edema due to alterations in Starling pressure (transudate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Edema due to microvascular or alveolar injury

36
Q

Noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage.

A

Adult Respiratory Distress Syndrome (ARDS)

37
Q

Due to direct injury to the lungs or systemic diseases

A

Adult Respiratory Distress Syndrome (ARDS)

Hyaline Membrane Disease

38
Q

Main causes are:
Severe Acute Respiratory Syndrome (SARS)*
Hantavirus

A

Severe Acute Respiratory Syndrome

39
Q

Other causes of SARS

A
  • heroin
  • smoke inhalation
  • acute pancreatitis
  • cardiopulmonary bypass
  • disseminated intravascular coagulation
  • amniotic fluid embolism
  • fat embolism
40
Q

Arrange the following regarding the pathogenesis of the SARS

  1. Cytokines are chemotactic to neutrophils.
  2. Neutrophils transmigrate into the alveoli through pulmonary capillaries.
  3. Capillary damage causes leakage of a protein-rich exudate producing hyaline membranes.
  4. Neutrophils damage type I and II pneumocytes.
  5. Decrease in surfactant causes atelectasis with intrapulmonary shunting.
A
  1. Cytokines are chemotactic to neutrophils.
  2. Neutrophils transmigrate into the alveoli through pulmonary capillaries.
  3. Capillary damage causes leakage of a protein-rich exudate producing hyaline membranes.
  4. Neutrophils damage type I and II pneumocytes.
  5. Decrease in surfactant causes atelectasis with intrapulmonary shunting.
41
Q

Important to distinguish ARDS from cardiogenic pulmonary edema, where PA wedge pressure is

A

> 18 mm Hg

42
Q

Bilateral interstitial infiltrates initially

Progresses to widespread alveolar consolidation with air bronchograms (80%)

A

SARS Corona Virus

43
Q

Treatment for SAR COV

A
  • Treat underlying disease
  • Hemodynamic monitoring
  • Mechanical ventilation
  • Nitric oxide inhalation, corticosteroids
44
Q

Sixth leading cause of death in the United States that the majority are caused by bacterial pathogens.
Most often due to Streptococcus pneumoniae (50%– 75% of cases)

A

Typical community-acquired pneumonia

45
Q

Microaspiration of oropharyngeal contents during sleep
• Inhalation of aerosol drops ranging in size from 0.5 to 1 µm
• Bloodstream infection

A

Typical community-acquired pneumonia

46
Q

It begins as an acute bronchitis and spreads locally into the lungs. The lower lobes or right middle lobe are usually involved. The lung has patchy areas of consolidation
with noted microabscesses

A

Bronchopneumonia

47
Q

Complete or almost complete consolidation of a lobe of lung

A

Loba pneumonia

48
Q

Syages of Lobar Pneumonia

A
  1. Congestion (1st 24hrs)- the affected lobe is red, heavy and boggy. It is vascular dilation and avoelar exudate contain bacteria in microscope
  2. Red hepatization (day 2-3)- red firm lobe (liver-like consistency). Avoelar exudate contains neutrophil, erythrocytes, fibrin
  3. Gray hepatization (4-6 days) Gray-brown firm lobe. Same with #3 but RBC disintegrate
  4. Resolution- restoration of normal architect. Enzymatic digestion of exudate
49
Q

Signs of consolidation (alveolar exudate)

A
  • Dullness to percussion
  • Increased vocal tactile fremitus
  • Sound is transmitted well through alveolar consolidations.
  • Late inspiratory crackles
  • Bronchial breath sounds, bronchophony and egophony
50
Q

gold standard screen in
Patchy infiltrates (bronchopneumonia) or lobar consolidation with a sensitivity 50% to 85%

A

Cgest radiograph

51
Q

Usually caused by Mycoplasma pneumoniae

A

Atypical community-acquired pneumonia

52
Q

Clinical findings of Atypical community-acquired pneumonia

A

•Insidious onset, low-grade fever
• Nonproductive cough
• Chest pain
• Flu-like symptoms
- Pharyngitis, laryngitis, myalgias, headache
•
No signs of consolidation

53
Q

Mononuclear infiltrate and alveolar spaces usually free of exudate

A

Patchy interstitial pneumonia

54
Q

Gram-negative bacteria- Pseudomonas aeruginosa (respirators), Escherichia coli

Gram-positive bacteria (e.g., Staphylococcus aureus)

A

Nosocomial pneumonia

55
Q

Common opportunistic infections of
Pneumonia in immunocompromised hosts

A

• Cytomegalovirus
• Pneumocystis jiroveci
-
TMP-SMX is used for prophylaxis and treatment.
• Aspergillus fumigatus

56
Q

Contracted by inhalation of Mycobacterium tuberculosis and the
Organism resides in phagosomes of alveolar macrophages

A

Tuberculosis (TB)

57
Q

Virulence factor
Of Strict aerobe, acid-fast TB

A

Cord Factor

58
Q

Purified protein derivative (PPD) intradermal skin test

Does not distinguish active from inactive disease

A

Screening of TB

59
Q

Responsible for positive PPD

A

Protein in cell wall

60
Q

Chromosome mutations involving mycolic acid

Chromosome mutations involving catalase peroxidase

A

Drug resistance in TB

61
Q

Does not distinguish active vs inactive TB

62
Q

Nodes: Subpleural location

A
  • Upper part of the lower lobes or lower part of the upper lobes
  • Ghon focus (caseous necrosis) in periphery
  • Ghon complex (caseous necrosis) in hilar lymph
63
Q

Secondary (reactivation) TB

A
  • Due to reactivation of a previous primary TB site
  • Involves one or both apices in upper lobes
  • Ventilation (oxygenation ) is greatest in the upper lobes.
  • M. tuberculosis is a strict aerobe. Reactivation TB: upper lobe cavitary lesion(s)
64
Q

Complications of Cavitary lesion due to release of cytokines from memory T cells

A

Miliary spread in lungs due to invasion into the bronchus or lymphatics

65
Q

Clinical findings
of Cavitary lesion due to release of cytokines from memory T cells

A
  • Fever
  • drenching night sweats
  • weight loss TB: drenching night sweats
  • weight loss
66
Q

extrapulmonary site TB

67
Q
  • Spread is due to invasion of pulmonary vein tributaries.
  • Kidney is the most common extrapulmonary site.
  • Adrenal involvement may result in Addison disease.
A

Miliary spread to extrapulmonary sites

68
Q

Granulomatous hepatitis, spread to vertebrae (Pott disease) TB in vertebrae

A

Pott disease

69
Q

Cavitary lesion treatment

A

• Isoniazid + rifampin + pyrazinamide
• Noninfectious in 2 to 3 weeks (3) Treat for additional 9 to 12 months

70
Q
  • Atypical mycobacterium
  • Most common TB in AIDS (often disseminates)
  • Occurs when CD4 helper T cell (T H) count falls < 50 cells/mm3 MAC: MC TB in AIDS
A

Mycobacterium avium-intracellulare complex (MAC)

71
Q

Treatment for Mycobacterium avium-intracellulare complex (MAC)

A

• Clarithromycin + rifabutin + ethambutol

72
Q

It is cuased most often due to aspiration of oropharyngeal material (e.g., tonsillar material)

A

Lung abscess

73
Q

Risk factos for Lung Abscess

A
  • Alcoholism
  • Loss of consciousness
  • Recent dental work
  • Microbial pathogens
  • Aerobic and anaerobic streptococci
    Staphylococcus
  • Prevotella
  • Fusobacterium
  • Anaerobes in 60% of cases Lung abscesses: mixed aerobic/ anaerobic infection
74
Q

From 10% to 15% of abscesses are behind a bronchus obstructed by cancer.

A

Obstructive lung neoplasia

75
Q

Infective endocarditis

A

Septic embolism

76
Q

Spiking fever and productive cough (foul-smelling sputum) are common.

Chest imaging shows cavitation with an air-fluid level

A

Lung Abscess

77
Q

Treatment for Lung Abscess

A
  • Clindamycin

* Bronchoscopy if it does not resolve

78
Q

term applied to peripheral lung nodule < 5 cm

A

Solitary Pulmonary Nodule

79
Q

Etiology of Lung Tumor

A
  • Granuloma
  • Primary lung CA
  • Bronchial Carcinoid
80
Q

Patients less than 35 years old risk:
Patients more than 50 years old risk:

A

Patients less than 35 years old risk: < 1%
Patients more than 50 years old risk: 50 to 60%

81
Q

The source of the most common lung tumor that is metastatic and appears as multiple lesions.

82
Q

Clinical Findings of Lung CA

A

Cough (75%)
Weight Loss
Hemoptysis

83
Q

Produces Horner syndrome which is a superior sulcus tumor. The tumor is usually a primary SCC located at the extreme apex of the lung.

A

Pancoast Tumor

84
Q

Is the most common fatal cancer in both men and women worldwide.

A

Primary Lung Cancer

85
Q

The most common cause of lung cancer

86
Q

Most common oncogenes

A
  • KRAS
  • MYC family
  • HER-2/ neu
  • BCL-2
  • EGFR (Epidermal Growth Factor Receptor)
87
Q

Classification of Lung Cell

A

Small Cell Carcinoma (15%)

Non Small Cell Carcinoma (85%)

GEN PATH (17 decks)

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