Respiratory System

Patho

Primary Function of Respiratory System

gas exchange (in alveoli)

True or False

O2 from air is transferred into blood

True

CO2 is _____________ into atmosphere

eliminated

Respiratory System is divided into 2 parts:

1. conducting system
2. respiratory tissues

Conducting System

air passes between atmosphere & lungs

Respiratory Tissues

where gas exchange takes place

Respiration Requires:

* ventilation
* perfusion
* diffusion

Ventilation

movement of gases into & out of lungs

Perfusion

movement of blood through the lungs

Diffusion

diffusion of gases between lungs & blood

True or False

Anatomy of respiratory tract is divided into upper & lower respiratory tract

true

Upper → organs outside thorax

* nose
* pharynx
* larynx

Lower → organs with in thorax

* trachea
* bronchi
* bronchioles
* alveolar duct
* alveoli

Physiology of Respiratory Tract

gas exchange!

* internal, external, cellular respiration

Pneumonia

inflammation of parenchymal structures of the lung in the lower respiratory tract

* 6th leading cause of death in the U.S

Etiologic Agents of Pneumonia

* infectious: S. Pneumonia, Pseudomonas, Staph __**(bacterial)**__
* Non-Infectious: inhalation of irritating fumes, aspiration of gastric contents __**(inflammation response)**__

Classification of Pneumonia

* according to setting: community or hospital acquired (Nosocomial)
* ex: “I was in the hospital for appendectomy but I also got pneumonia from the pt next door”
* according to type of agent causing the infection (typical or atypical)
* according to distribution of infection (lobar, bronchopneumonia)

Inflammatory Process of Pneumonia

* typical pneumonia → in alveoli
* atypical pneumonia → in tissues that surround the alveoli

Who gets Pneumonia?

Immunocompromised Pt:

* bone marrow/organ transplant
* cancers
* pts on corticosteroids

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Acute Bacterial Pneumonia:

* based on etiologic agent
* pneumococcal
* legionella

→ assess for loss of cough reflex, damage to ciliary endothelium, diabetes, chronic bronchitis, smoking

Bronchopneumonia

signifies a patchy consolidation involving more than one lobe

Labor Pneumonia

consolidation of a part or all of a lung lobe

Lung Cancer

disease of the lung tissue itself

* leading cause of cancer death

True or False

Cigarette smoking cause 80% of cases of lung cancer

True

* smokers can benefit at any age from smoking cessation (part of discharging a pt, to encourage a pt to not smoke anymore)

Risk for lung cancer is greater in people exposed to ________ (in old city buildings - tiles have it in ceiling)

asbestos

Tumors arise from ____________ lining of major bronchi

epithelial

Small lesions may form masses that invade ______ _______ or form large/bulky masses that extend into lung tissue

bronchial mucosa

Some masses undergo central ________ or may invade pleural cavity & chest wall

necrosis

Classify lung cancer by it being either ____ _______ or _________ lunch cancer

small cell or non-small cell

Both small cell and non-small cell can….

produce paraneoplastic syndromes

Squamous Cell Carcinoma

25-40% occurence

Adenocarcinoma

20-40% occurence

Small cell Carcinoma

20-25% occurence

Large Cell Carcinoma

10-15% occurence

Lung Cancer Symptoms

* weight loss
* anorexia
* chronic cough
* SOB
* wheezing
* hemoptysis
* pain

Diagnosis of Lung Cancer

* chest x-ray
* history/physical
* bronchoscopy
* cytological studies
* CT scan/MRI
* PET (CAT Scan with contrast)

Hypoxemia

reduction in arterial blood O2 levels = PaO2 < 95mmHg __**(not enough O2)**__

Causes of Hypoxemia

* inadequate O2
* dysfunction of neurologic system
* alterations in circulatory function

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\~if PO2 pf the tissues falls below a critical level, aerobic metabolism stops → anaerobic metabolism takes over → lactic acid is released

Symptoms of Hypoxemia

* increased heart rate
* diaphoresis (cold, clammy, sweaty)
* mental status changes
* restlessness
* confusion
* combative/agitated
* stuper/coma
* hyperventilation
* cyanosis

Diagnosis of Hypoxemia

* arterial blood gas (PaO2)
* pulse ox (good idea if someone is hypoxemia

Hypercapnia

increase in CO2 of arterial blood (PaCO2=too much CO2)

Cause of Hypercapnia

* pt not breathing enough
* alterations in CO2 production
* disturbance in gas exchange in lungs
* abnormalities in function of chest wall & respiratory muscles
* changes in neural control of respiration

Symptoms of Hypercapnia

* respiratory acidosis (decreased pH, elevated CO2)
* vasodilation of blood vessels
* CNS depression

Diagnosis of Hypercapnia

arterial blood gas (PaCO2)

Obstructive Airway Disorder (asthma)

chronic disorder of airway

Causes of Asthma Episodes

* episodic airway obstruction
* bronchial hyperresponsiveness
* airway inflammation
* in some → airway remodeling (repeated inflammation)

Risk factor for development of Asthma

* genetic disposition for development of IgE to common allergies
* family history
* antenatal exposure to tobacco smoke

Triggers for Asthma

* tobacco smoke
* dust mites
* GERD
* hormones
* cold
* emotions
* excerise

Pathogenesis of Asthma

* airway inflammation manifested by inflammatory cells (eosinophils, most cells) → damage to bronchial epithelium
* mediators associated with asthma
* cytokines: tumor necrosis, interlukins 1,4,5
* histamine
* leukotrienes
* episodes are reversible either spontaneously or with tx

Symptoms of Asthma

* airways narrow due to bronchospasm
* edema of bronchial mucosa
* FEV1 → decreased ( can’t get air out of alveoli)
* accessory muscle use
* increased work of breathing
* ineffective cough
* hypoxemia/hypercapnia
* decreased breath sounds
* wheezing
* chest tightness
* fatigue
* diaphoresis
* severe dyspnea
* acute resp. failure (inaudible breath sounds, no wheezing)

Chronic Obstructive Pulmonary Disease (COPD)

characterized by chronic & recurrent obstruction of airflow

* obstruction is progressive & accompanied by inflammatory responses

→ leading cause of death/hospitalization

Causes of COPD

* smoking
* antitrypsin (hereditary)
* asthma
* airway hyperresponsiveness

Pathogenesis of COPD

* inflammation
* fibrosis of bronchial wall
* hypertrophy of submucosal glands
* hypersecretion of mucus
* loss of elastic lung fibers & alveolar tissue
* destruction of alveolar tissue decreases surface area for gas exchange
* loss of elastic fibers impair expiration → oncrease air trapping airway collapse

2 types of COPD

1. emphysema
2. bronchitis

Emphysema

destruction of area surface of the alveoli

* enlargement of airspaces & destruction of lung tissue

→ loss of lung elasticity

→ abnormal enlargement of airspaces - air trapping

→ destruction of alveolar walls/capillary beds

→ breakdown of elastin by enzymes (protease)

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Causes of Emphysema

* smoking
* antitrypsin deficiency

Symptoms of Emphysema

“pink puffer”

* lack of cyanosis
* use of accessory muscles
* pursed lips breathing “puffer breathing”
* airways collapse during expiration → airway trapping in alveoli & lungs = barrel chest

Chronic Bronchitis

destruction of major/small airways

* increased mucus production
* chronic productive cough (last for 3 months → 2 years)
* hypersecretion of mucus in large airways
* plugging of airway lumen, inflammation
* increase in goblet cells

Causes of Chronic Bronchitis

* cigarette smoking
* dust/toxic gases

Symptoms of Chronic Bronchitis

“blue bloaters”

* cyanosis
* fluid retention with right sided heart failure (causes fluid to build up)