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Pathophysiology > Module 6: Respiratory System > Flashcards

Module 6: Respiratory System Flashcards

1
Q

is a protective reflex that helps clear the airways by an explosive expiration. Inhaled particles, accumulated mucus.

A

Cough

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2
Q

inflammation, or the presence of a foreign body
initiates the cough reflex by stimulating the_______?

A

irritant receptors

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3
Q

What type of cough?
Resolves within 2 to 3 weeks of the onset of illness or resolves with treatment of the underlying condition.

Result of
o upper respiratory tract infections
o allergic rhinitis
o acute bronchitis
o pneumonia
o congestive heart failure
o pulmonary embolus, or aspiration.

A

Acute cough

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4
Q

What type of cough?
Persisted for more than 3 weeks, although 7 or 8 weeks may be a more appropriate timeframe because acute cough and bronchial hyperreactivity can be prolonged in some cases of viral infection.

A

Chronic cough

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5
Q

Long term inflammation of the bronchial tubes caused by prolonged exposure to irritants.
- most common cause of chronic cough
- lung cancer to be considered
- ACE inhibitors

A

chronic bronchitis

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6
Q

is defined as “a subjective experience of
breathing discomfort that is comprised of
qualitatively distinct sensations that vary in intensity.

A

Dyspnea

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7
Q

Reduced oxygenation of arterial blood (reduced
Pao2), Respiratory alterations

A

Hypoxemia

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8
Q

reduced oxygenation of cells in tissues. may be caused by alterations of other systems as
well.

A

Hypoxia

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9
Q

is a bluish discoloration of the skin and
mucous membranes caused by increasing amounts of desaturated or reduced hemoglobin (which is bluish) in the blood.

A

Cyanosis

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10
Q

Cyanosis generally develops when (how many grams?) of hemoglobin is desaturated, regardless of hemoglobin concentration.

A

5g of Hb

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11
Q

Slow blood circulation in fingers and toes
- Most often caused by poor circulation resulting from intense peripheral vasoconstriction, such as that observed in persons who have Raynaud disease, are
in cold environments, or are severely stressed.

  • Best observed in the nail beds.
A

Peripheral cyanosis

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12
Q

caused by decreased arterial oxygenation (low
Pao2) from pulmonary diseases or pulmonary or cardiac right-to-left shunts.

  • Best detected in buccal mucous membranes and lips.
A

Central cyanosis

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13
Q

Is the expectoration of blood or bloody secretions.
Blood produced with coughing is usually bright
red, has an alkaline pH, and is mixed with frothy
sputum.

Bronchoscopy, combined with chest computed
tomography (CT), is used to confirm the site of
bleeding.

A

Hemoptysis

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14
Q

Vomiting of blood. Blood that is vomited is dark, has an acidic pH, and is mixed with food particles.

A

Hematemesis

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15
Q

is the selective bulbous enlargement of the end (distal segment) of a digit (finger or toe).
It is usually painless.
- Commonly associated with diseases that cause
chronic hypoxemia

A

Clubbing

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16
Q

Inflammatory condition of the lungs, infection of the pulmonary parenchyma. Leads to the air sacs in the lungs filling with pus.

A

Pneumonia

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17
Q

General Pneumonia Triad (WHO)

A
  • Fever
  • Tachycardia
  • Tachypnea (+/- Breathlessness)
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18
Q

Etiology:
- Influenza Virus A & B for adults (<10% of
pneumonia among adults)
- Most common cause of pneumonia in children
(usually RSV)

Vaccine:
FluVax is recommended Annually for Everyone

A

VIRAL PNEUMONIA
SEASONAL FLU (INFLUENZA A & B)

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19
Q

most common bacterial pneumonia
- at risk: secondary complication to a viral RTI

Sputum:
- PMNs and gram-positive oval-shaped diplococci

Clinical presentation:
- abrupt onset with fever, rigor, pleurisy, and “rusty” sputum; watch for meningeal involvement

CXR:
- classically causes a lobar consolidation (filling of lung with fluid)

A

Streptococcus pneumoniae

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20
Q

Treatment:
- penicillin G (erythromycin if penicillin allergic;
vancomycin, ceftriaxone or cefotaxime if resistant) x 7-10 days

Prevention: Pneumovax (give once only)

A

Streptococcus pneumoniae

21
Q

sudden onset bronchopneumonia
- at risk: secondary complication of influenza infection or in hospitalized patient with underlying disease, severe diabetes, drug abusers, immunocompromised

Clinical presentation:
- high fever, chills, progressive dyspnea, cyanosis, cough, pleuritic pain, quite toxic-appearing

A

Staphylococcus aureus

22
Q

Sputum:
- PMNs and gram-positive cocci in clusters, chains, and pairs

Treatment:
- Cloxacillin or vancomycin (if penicillin allergic) x 7-10 days and drain any empyema

A

Staphylococcus aureus

23
Q

most common atypical pneumonia; “walking
pneumonia”
- at risk: young adults (especially 5-15 years old)
- incubation: 12-14 days (insidious onset)

CXR:
- Classically worse than clinical presentation; usually bilateral, patchy air-space diseases

A

Mycoplasma pneumoniae

24
Q

Sputum:
- more mononuclear cells and fewer PMNs than
bacterial pneumonia, but mycoplasma not visualized

Treatment:
- macrolide, newer generation Quinolones,
Doxycycline x 10-14 days

A

Mycoplasma pneumoniae

25
Q

at risk: alcoholics
-similar to pneumococcus; bloody sputum (“red currant jelly”)

A

Klebsiella pneumoniae

26
Q

Sputum:
- large gram-negative encapsulated rods

Treatment:
- Cephalosporin and Aminoglycoside; adequate
drainage of empyema (can cause extensive scarring)

A

Klebsiella pneumoniae

27
Q

at risk: patients on immunosuppressants (e.g.
transplant recipients) or chemotherapy, AIDS when CD4 count < 200

CXR:
- diffuse interstitial infiltration, often isolated to upper lobes

A

Pneumocystis carinii

28
Q

Sputum:
- Giemsa stain; lower yield in patients on prophylaxis; diagnosis may require BAL or transbronchial biopsy

Treatment:
- TMP-SMX, pentamidine, TMP-dapsone,
clindamycin-primaquin, atovaquone; add
corticosteroids if PaO2 < 70 mm Hg or AaDO2 > 35 mm Hg

A

Pneumocystis carinii

29
Q

Development of granulomatous
reactions in the lungs, +/– local spread to lymph
nodes and hematogenous to distant organs (extrapulmonary TB, e.g. kidneys, bone)

nonspecific lower lobe calcified infiltrates, hilar and paratracheal node enlargement, pleural effusion

A

primary TB

30
Q

reactivation of dormant organisms and proliferation in aging/immunocompromised patients.

cavitation in apical regions and posterior segment of upper lobe and/or superior segment of the lower lobes +/– calcification

A

secondary/post-primary TB

31
Q

(post-primary dissemination of multiple
tiny granulomas in immunocompromised patients): fever, anemia, splenomegaly, meningitis. Uniformly distributed, very fine nodules (like seeds) throughout

A

Miliary TB

32
Q

Etiology:
- Histoplasma capsulatum, Coccidioides immitis,
Blastomyces dermatitidis

Pathogenesis:
- Primary granulomatous lung infection systemic hematogenous dissemination
- fungus is usually destroyed if patient
immunocompetent

Treatment
- Amphotericin B, itraconazole

A

PRIMARY PATHOGENIC FUNGI (Fungal Pneumonia)

33
Q

Etiology
- mostly Aspergillus fumigatus

Clinical Presentation
- allergic bronchopulmonary aspergillosis
(Pulmonary Infiltrates with Eosinophilia)
- Aspergilloma (fungus ball)

CXR: round opacity surrounded by a thin
lucent rim of air, often in upper
lobes (“air crescent” sign

A

Aspergillosis

34
Q

at risk: immunosuppressed, especially neutropenic
- severe symptoms with fever, cough, dyspnea,
pleuritic pain, tends to cavitate

CXR: local or diffuse infiltrates +/– pulmonary infarction

A

Invasive aspergillosis

35
Q

at risk: chronic lung disease. refers to a condition where the fungus Aspergillus grows within the bronchial tubes of the lungs. This can lead to inflammation, airway obstruction, and respiratory symptoms

  • chronic cough and hemoptysis
A

Endobronchial pulmonary aspergillosis

36
Q

Treatment of Aspergillosis?
CLUE: Amp and Itra

A

amphotericin B
itraconazole
resection of aspergilloma

37
Q

Etiology:
- Cryptococcus neoformans
Treatment:
- amphotericin B +/– flucytosine

A

Cryptococcosis

38
Q

Etiology:
- Candida albicans

Clinical presentation:
- fever, septicemia

CXR: diffuse, vaguely nodular infiltrate visible only when numerous abscesses are present

A

Candidiasis

39
Q

Treatment of Candidiasis?
CLUE: Amp and Fluc

A

amphotericin B
fluconazole

40
Q
  • HEAVILY ASSOCIATED WITH SMOKING
  • characterized by progressive development of airflow limitation that is irreversible/minimally reversible
  • includes chronic bronchitis and emphysema; usually coexist to variable degrees in most patients
A

CHRONIC OBSTTRUCTIVE PULMONARY
DISEASE (COPD)

41
Q

Gradual destruction of the air sacs (alveoli)
- dilatation and destruction of air spaces distal to the terminal bronchiole without obvious fibrosis
- decreased elastic recoil of lung parenchyma causes decreased expiratory driving pressure, airway collapse, and air trapping

A

Emphysema

42
Q

(respiratory bronchioles predominantly affected)
- typical form seen in smokers
- primarily affects upper lung zones

A

centriacinar

43
Q

(respiratory bronchioles, alveolar ducts, and alveolar sacs affected)
- responsible for less than 1% of emphysema cases
- primarily affects lower lobes

A

panacinar

44
Q

Long-term inflammation of bronchial tubes by exposure to irritants. A clinical diagnosis.

Chronic cough and sputum production on most days for at least 3 consecutive months in 2 successive years
- Obstruction due to narrowing of the airway lumen by mucosal thickening and excess mucus

A

Chronic Bronchitis

45
Q

Narrowing of airways. A chronic Inflammatory Disorder of the Airways >Episodic, Reversible Constriction

Clinical Features:
- Dyspnea, Wheeze, Cough
- Chest Tightness
- Tachypnea, Hyperinflation, Inc Resp. Effort
Asymptomatic between ‘Attacks’ – (But may have Allergic Rhinitis, Hives or Eczema)
- ‘Attacks’ of Severe Dyspnea & Wheezing - (Often Triggered by Allergen Pollens/Dust/Animal Dander)

A

ASTHMA

46
Q

Inhaled Corticosteroids
(Budesonide or Fluticasone) Or Inhaled
Antimuscarinic (Ipratropium Bromide) – If
ICS-Intolerant

A

Mild Asthma

47
Q

LABA + Inhaled Corticosteroid Combinations
Symbicort [Budesonide + formoterol] or
Seretide [Fluticasone + Salmeterol]

A

Moderate Asthma

48
Q

Oral Leukotriene Inhibitors
(Singulair [Montelukast])

A

Severe Asthma

Pathophysiology (7 decks)

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