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Patho > Respiration Disease > Flashcards

Respiration Disease Flashcards

1
Q

What is the role of the respiratory system

A

Gas exhange and regulating pH
You need
- To acquire oxygen.
- To remove carbon dioxide
- To control blood pH

The way you do that is through efficient gas exchange between the blood and the atmosphere

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2
Q

Integrated components of the respiratory system

A

Controller (Sensor of O2, pH, and CO2) => Chest wall (pump-diaphram, ribs, …) => Lung (gas exchanger) => Controller =>

This is the cycle and it keep happening to keep everything undercontrolled

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3
Q

Respiratory Tract Anatomy

A

Two major components:
- Conduits (airway-just get gas)
–Bronchi
– Bronchioles
– Alveolar ducts
- Blood-gas interface (alveoli)
– Where gas exchange take place

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4
Q

Respiratory Tract

A

Upper respiratory tract
Lower respiratory tract

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5
Q

Upper Respiratory Tract

A

Anatomy of the Conduits
- Upper airway
– Nasal Cavity
– Pharynx
– Larynx

Nose => Turbinates => Filter in nose particles deposited and do not enter lungs
Nose => warm up air to room temp

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6
Q

Lower Respiratory Tract

A

The Respiratory Tree (got more than one gen)
Trachea
Primary bronchi
Lungs (exhange)

Trachea (orign => divide into right and left bronchi)
Primary bronchi: Conducting airways ( At gen 16 it turn into bronchiloes which help with respiration)
- Turn into bronchioles (respiratory airways) and Acini (the gas exchange unit)

Bronchioles gonna turn into alveolus to max surface area

Conduct; differ w/chest being there

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7
Q

Structure of Extrapulmonary Airways (Outside of Lung)

A

Cross Sectional View of Bronchi
- Cartilagenous ring anterior
- Muscular wall posterior (trachealis mus.)

Longitudinal view of bronchi
- Cartilage on first 2nd - 3rd divisions
– first few branches are semi rigid to prevent collapse during coughing

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8
Q

Airway Structure

A
  • Globlet Cells and Glands: produce mucus for lining
  • Ciliated Cells: Move upward => more muscus out (keep lung clear)
    – Lose when smoking
  • Hyaline cartilage: Stiff for Structure
  • Smooth muscles: Change amount of air

Respiratory Bronchioles (gen 16 - need to be as thin as possible)
- gonna turn into alveoli (need epitherlia & elastic fiber)

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9
Q

What Gen 16 do to cross sectional area and Resistance

A

It decrease resistance and drastically increase total cross section area (Gen-15 have high resistance and low to non total cross section area; called conducting zone)

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10
Q

Cells of the Airway

A
  • Large conducting airway
  • Small conducting airway
  • Alevolus
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11
Q

Large Conducting Airway

A

Ciliated epithelium; globlet cells; mucous glands; cartilage
- All these try to clear the air and keep it clear

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12
Q

Small Conducting Airway

A

Ciliated epithelium (type I)
- Also try to filture the air

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13
Q

Alevolus

A

Non ciliated epithelium
- Where exchange of O2 and CO2 happen with blood
- There is also macrophages that act as last line of defense of phagocytkines (if smokin/breathing kil them)

Surfactant secretion (type II)
- control surface tension
- Cytokines and protein that regulate

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14
Q

Pulmonary Acinus

Blood-gas interface

A

One terminal bronchiole with associated respiratory bronchioles and alveoli (fixed ad doesn’t regulate airflow)
- Alveolar neck is always open in the absense of disease

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15
Q

Cells of the Alveolus

A

Components of the Alveolar Wall
- Endothelium (barrier)
- Mesenchymal
- Alveolar type I and Type II

Cells in alveolar lumen
- Pulmonary alveolar macrophage
- Lymphocyte

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16
Q

Surfactant and Alveolar Filling Pressure

A

T=Surface Tension
R=Radius (smaller R lead to more pressure)
P=Pressure=2T/r
- Surfactant reduces tension as alveoli expand by increasing lipid incorporation
– Without it small alveoli would empty into larger especially at low volume

Alveoli connected so gas can move from one to another

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17
Q

Lung Vasculature

Anatomy of the Circulatory System

A

Two Systems:

Bronchial
- Supplies the lung

Pulmonary: for gas exchange
- Pulmonary artery (deoxygenated blood)
- Capillary
- Pulmonary vein (oxygenated blood)

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18
Q

Lung Vasculature

Circulation

A

Pulmonary Circulation:
- Arteries and Bronchi travel together
- Capillaries are designed to maximize gas exchange (move in upper repiratory)

Bronchial Circulation:
- Separate circulation to lung
- Supplies bronchi
- Arises from aorta (carries oxygenated blood)

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19
Q

Anatomy of the Pump

A
  • Right Lung (3 lobes)/Left Lung (2 Lobes)
  • Pleural Membrane (surrounds lung and puts it into cavity space)
  • Chest wall
    – Skeletal (ribs, sternum, vertebrae)
    – Muscles (diaphragm (main muscle), Intercostal muscles (internal and external)

Abdomial muscles => used in forced expiration

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20
Q

Chest Wall

Diaphragm, Intercostal Muscles and Ribs

A

Diaphragm: Main muscle of respiration
- flattens => lungs expand

Intercostal muscles:
- Two types (int. & ext.) used for expiration (internal) and inspiration (external)

Abdominal muscles: used in forced
expiration

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21
Q

Lung Volumes (Statics) and Flow (Dynamics)

A

Lung Vol: Conducting airway (dead space); alveoli (vol of lung)
Ventilation (ml) & flow (ml/min)
- Tidal volume (Vt); vol of normal breath
- Dead space (Vd); not used in gas exchange

Minute ventilation = Vt * Freq
Alveolar ventilation = (Vt-Vd) * Freq

V/Q = 1
- If too much V or too much Q (flow) is bad

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22
Q

Subdivisions of Lung Volume

A
  • Total Lung Capacity (TLC): Vol in lung at maximal inspiration
  • Forced Vital Capacity (FVC): Vol expired from maximal inspiration to maximal expiration
  • Functional Residual Capacity (FRC): Vol in lung at resting position (no force applied)
  • Expiratory Reserve Volume: Vol of air that can be expired maximally beyond resting position
  • RV: mostly dead space
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23
Q

Spirometer

A

Measure of the Lung Volume
- Measure FVC, ERV
- FRC - ERV = Residual Volume (RV)

Nitrogen washout:
- Measures FRC

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24
Q

Flow Rates

A

Timed Volumes: Spirometer tracing while the paper is moving
- FEV1: Forced expiratoy volume in one sec (80% of air comes out here)
- Major index of obstruction: FEV1/FVC
- Major index of restriction: reduced lung volume with normal FEV1/FVC ratio

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25
Q

Diffusion Capacity

A

Measure of the gas transfer across alveolar-capillary epithelium
- Principle: Carbon monoxide (CO) is a gas that is bound irreversibly to hemoglobin ( makes blood red)
- Measurment: Dilute concentration of CO is inhaled, breath is held for 10 sec., and CO uptake is computed
- Interpretation: CO uptake (D(L)CO) is low when BARRIER IS THICKEND or when ALVEOLAR surface area is DECREASED

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26
Q

Control of Ventilation

A

Respiration is:
- Automatic (paced rate of breathing)
- Continually adjusted to maintain levels of oxygen and carbon dioxide tension within a narrow range
- Can override at any time and decide how much you hold

Respiration is controlled by a feedback system:
- Components: controller, effector, sensor
- Output: ventilation (muscle force & frequency, airway tone)
- Input: levels of acid (pH, H+) and O2

Proprioceptors, Lung and upper airway receptor tell the brain how much the lung is expanded
- CNS medullary signal if breathing is too fast or too slow

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27
Q

CO2 and O2 importance in the Control of Ventilation

A

Small changes in CO2 are detected better
- Lung control pH

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28
Q

Acid Base Changes

A

Elements maintaining acid base balance
- Lung: regulate CO2, a weak acid
- Kidney: Regulate HCO3, a base (very slow at changing pH)
- Blood and tissues: buffering capacity

Regulation
- Lung: CO2 levels change quickly
- Kidney: HCO3 takes longer

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29
Q

pH equation

Lung and Kidney

A

pH = Metabolic (kidney)/Respiratory (Lung)
HCO3-/Pco2

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30
Q

Alveolar Ventilation and pCO2 relationship

A

They are inversely related
pCO2 =K/V(alv)
K is a constant

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31
Q

Normal Acid base balance

A

Lung: 1.2 of dissolved CO2
Kidney: 24 of HCO3-
- pH = 7.4

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32
Q

Respiratory Acidosis and Acidemia

A

Failure in the lung function
- Not blowing off CO2

Lung: 2.4 Dissolved CO2
Kidney: 24 of HCO3-
- pH = 7.2

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33
Q

Compensated Respiratory Acidosis

A

Kidney Compensate

Lungs: 2.4 dissolved CO2
Kidney: 40 of HCO3-
-pH normal again

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34
Q

Anatomy of the Pulmonary Vessels

A

Pulmonary arteries are thinner and have less smooth muscle than systemic arteries
- Offer less resistance
- More distensible

Much lower Intervascular Pressure
- More compressible

Located within the Thorax (not outside the chest)
- Subject to pulmonary pressue (alveloar and intrapleural pressure)

Pulmonary Vascular Resistance (PVR) is determined by more than pulmonary vascular tone

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35
Q

Pulmonary and Systemic Circuits

A
  • PAP is much smaller than systemic pressure (1/10)
  • Distrubution of pressure through systemic and pulmonary vasculature uneven
  • Requirement for systemic head pressure not present in lung
  • Differential organ flow systemically

The reason why it’s so much lower is because you really don’t need so much pressure. All what the PAP need to do and send is already in the lung

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36
Q

Determination of Pulmonary Vascular Resistance

A

Pouseille’s Law: Pi - Po = Q x R
- R= P1-P2/Q
– P1= pressure at beginning of tubles
– P2 = pressure at end of the tubles
– Q = Flow
– R= Resistance

PVP= MPAP(mean pulmonary arterial pressure) - MLAP(mean left atrial pressure)/PBF (pulmonary blood flow)

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37
Q

Increased Cardiac Output change PVR

A

Wehn Cardiac Output increases (like in excercises) => PVR decreases
- Increased output mediates reduction in PVR passively (isolated lung)

Mechanism:
- Recuritment:
– Significant effect on dead space ( Normally we only use 1/3 of the vessel) => Increase gas exchange surface
- Distension: The vessel is flexable so it can stretch and become wider which reduce pressure

38
Q

Regulation of Pulmonary Vascular Resistance

A

Increased Lung Volume (Above FRC): Increase PVR
- Mechanism: lengthening and compression of alveolar vessels

Decreased Lung Volume (under FRC): Increase PVR
- Mechanism: Compression of and less traction on extraalveolar vessels

Increased Pulmonary artery pressure: Decrease PVR
- Recruitment and distention

Gravity: Decrease PVR
- Hydrostatic effect lead to recruitment and distention

Positive-pressure ventilation: Increase PVR
- Compression and derecruitment of alveolar vessels

39
Q

V/Q match is

A

A Continuum; Ventialation/Perfusion must be 1
- When there is CO2 but no O2 => decreased V/Q
- When there is CO2 and O2 => normal V/Q
- When there is no CO2 but there is O2 => Increased V/Q

Both V and Q are better in the lower portion of the lung bc of gravity (has more effect on vessels)

40
Q

Hypoxic Pulmonary Vasocontriction

A

When you in a low oxygen area the lung will contract the vessel on it’s own to max gas exchange and help you adapt
- Principle mech of V/Q match
– Poorly executed due to low smooth muscle content
– Can help in total lung hypoxia

41
Q

Shunts Qs/Qt Ratio

A

Qs is the oxygenated blood flow
Qt is the total blood flow
- Increased right to left shunt (Qs;Qt would not be the same; you will have less blood with oxygen)
– Anatomic (common in infants; blood bypass the lung)
– Intrapulmonary (bypass the intrapulmonary circulatio)

Caused by
- Increased ventilation-perfusion mismatch (COVID)
- Imparied diffusion
- Shift of oxyhemoglobin dissociation curve (doesn’t pick up O2 as well)

42
Q

Pulmonary Pathology

A

There are a number of lung specific disease
- Bronchitis
- Pneumonia
- Emphysema
- Asthma
- COPD
- Lung cancer is one of the most common visceral malignancies

The lung is involved in almost all forms of terminal disease

43
Q

Symptoms of Lung Disease

A
  • Dyspnea: Difficulty breathing
  • Stridor: Crowing sound on inspriation
  • Wheeze: whistling sound on expiration
  • Cough: Dry, or productive
  • Sputum production
44
Q

Signs of Lung Disease

A
  • Cyanosis: Blue coloration of skin (esp. eyes)
    – Indicating greater deocyHb and inadequate oxygen delivery
  • Percussion note
    – Dull; fluid or consolidation of the lung
    – Hyperresonant: hyperinflation of the lung as a result of emphysema or asthma
  • Prolonged expiration: Ratio of inspiration/expiration protonged > 1:2
  • Wheezing: airway obstruction
  • Rales: cellophane paper sound indicating fluid in lungs
  • Friction rub: sandpaper like sound indicating inflammation of the pleura (surface)
45
Q

Patterns of breathing

Lung Disease

A

Bradypnea: slow breathing
Apnea: absence of breathing
Tachypnea: rapid breathing
Hyperventilation: rapid and deep beathing
Periodic (cheyne-stokes) breathing: apnea followed by periods of rapid breathing (not regulating CO2 and pH properly)

46
Q

Atelectasis

Collapse or loss of lung space

A

Absorption: part of lung is gone
- Associated with infection

Compression: fluid pushing on lung
- Associated with Cardiac Disease

Contraction: Not filling th esame space; loss of volume
- Associated with inflammation; Fibrosis

Patchy: Lung is patchy
- RDS: Respiratory distress syndrome

47
Q

Disease of Vascular Origins

A

Pulmonary Congestion and edema
- Indirectly from hemodynamic disturbances
- Primarily from increased hydrostatic pressure (increased fluid in lung) as in cardiac failure)
- Directly from Microvascular Injury and increased capillary permeability (lung leaky
– No change in hydrostatic or osmotic pressure as in ARDS

48
Q

Mechanism of Pulmonary Edema

A

Screenshot

49
Q

Pulmonary Edema

A

Result in a heavy wet Lung
- Fluid accumulate in the lower lobes (bc of gravity)
- Interstitial space fills before alveoli
- Presence of fluid in alveoli (exudate) => decreased pulmonary function (less diffusion) and predisposes to infection

50
Q

Adult Respiratory Distress Syndrome

A

Many Synonyms:
- Shock Lung; Acquired Respiratory Deficiency Syndrome; Acute alveolar Injury; Diffuse alveolar damage (same disease)

Caused by diffuse alveloar damage==> effect include:
- Respiratory insufficiency, Cyanosis; Severe arterial hypoemia; refractory to oxygen therapy

Often leads to multi-organ system failure => death
Associated with a variety of other clinical conditions

51
Q

ARD; Clinical Association

A
  • Diffuse Pulmonary Infection
  • Inhalation of irritant gas (smoke, oxygen)
  • Drug toxicity
  • Aspiration of gastric fluid
  • Near drowing (salty or regular water)
  • Pulmonary embolism (Increase in hydrostatic pressure)
  • Shock/Trauma
  • Sepsis/Pancreatitis
  • Excessive burns
  • Radiation Therapy

Damage alveolar diffusing; cause neutrophils to be called (problem)
- Hyaline membrane will be damaged

52
Q

Type L Covid ARDS

A
  • Low elastance: Amount of gas in lung is nearly norma
  • Low ventilation to perfusion (VA/Q) ratio: As the gas volume is normal; hypoxia is best explained by loss of regulation of perfusion and loss of hypoxic vasoconstriction.
    – Pulmonary artery pressure is almost normal
    – Systemic hypoxia => ventlation helps
  • Low lung weight: Only ground glass densities (large amount of fluids) are present on zct scan, primarily located subpleurally and along lung fissures
    – Lung weight only moderately increased
  • Low lung recruitability: the amound of non aerated lung is low
53
Q

Type H Covid ARDS

A
  • High elastance: The decrease of gas volume due to increased edema account for increased lung elastance
  • High right-to-left shunt: This is due to fraction of cardiac output perfusing the non aerated tissue => develop in dependent lung region due to increased edma and superimposed pressure
  • High lung weight (>1.5kg): fluid accumulate; on the order of magnitude of sever ARDS
  • High Lung recruitability: The increased amount of non-aerated tissue is associated, as in sever ARDS, with increased recruitability
54
Q

Temporal Aspects of COVID

A

Screenshot

55
Q

Pulmonary Hypertension

A

Caused by endothelial dysunction
- Primary: idiopathic, autoimmune, toxic (Fen-Phen)
- Secondary: increased shear, thromboembolism

Primary most common in women adged 20-40
- Dyspnea, fatigue, cyanosis, ventricular hypertrophy
- Fatal in 2-5 years in 80% of patients
- NO, prostacyclin, Heart-lung transplant

56
Q

Restrictive Disorders

A

FVC = 2.56 L (5.65 is normal)
FEV = 2.14 L (4.18 is normal)
FEV/FVC =84% (slightly high-74% is normal)
- The problem here is that FVC and FEV is low ( the lung is not expanding fully)

57
Q

Obstructive Disorders

A

FVC=4.20L
FEV=1.09L
FEV/FVC =26% (very low)
- Inability to expire air properly

58
Q

Obstructive vs. Restrictive Disease

A

Obstructive:
- Increased resistance to airflow within airway
- Result from complete or partial obstruction anywhere in respiratory tree

Disease
- Emphysema
- Chronic bronchitis
- Bronchietasis
- Asthma

59
Q

Obstructive vs. Restrictive Disease

Restrictive

A

Restrictive
- Reduced expansion of lung
- Acute or chronic interstitial infltraties/inflammation
- Chest Wall disease

Disease:
- ARDS
- Dust disease
- Pneumoconioses

60
Q

Chronic Bronchitis

COPD

A
  • Site: Bronchus
  • Changes:
    – Mucus gland hyperplasia
    – Hypersecretion
  • Etiology: Tobacoo smoke, air pollutants
  • Signs
    – Cough
    – Sputum production
61
Q

Branchiectasis

A
  • Site: Bronchus
  • Changes:
    – Airway dilation
    – Scarring
  • Etiology: Persistant or sever infection
  • Signs
    – Cough
    – Purulent sputum
    – Fever
62
Q

Asthma

A
  • Site: Bronchus
  • Changes:
    – Smooth muscle hyperplasia
    – Excess mucus
    – Inflammation
  • Etiology: Immunologic
  • Signs
    – episodic wheezing
    – cough
    –dyspnea
63
Q

“Small Air way disease” Bronchiolitis

A
  • Site: Bronchiole (respiratory portion)
  • Changes:
    – Inflammatory Scarring
    – Obliteration
  • Etiology: Tobacoo smoke, air pollutants, misc
  • Signs
    – Cough
    – Dyspnea
64
Q

Emphysema

A

Definition: abnormal enlargement of the airspace distal to the terminal bronchiole without obvious fibrosis (21 gen of lung-bottom)
Four Types
- Centricacinar, Panacinar (most common two)
- Paraseptal
- Irregulat

65
Q

Centrilobular Emphysema

A

The Respiratory bronchiole will get extended and will lose elasticity eventually
- Primarily affects the upper lobes of the lungs.
- Characterized by damage to your respiratory passageways.

66
Q

Panacinar Emphysema

A

Alveolus will get a lot of excess air space
- Hyperresonant lung sound (drum like)
- Air trapped and unable to be foced out
- Loss of elastic property

67
Q

Emphysema Causes

A

Lung insult: Oxidant => Elastin and collagen fiber damage
- Cigarette smoke
- Endogenous oxidants

Lung Defense:
- Antioxidant => go to elastin and collagen fibers => damage it in while fighing oxidant
- Antielastases: a1(antiprotease), a2(macrogloblin), Bronchial mucous inhibitor => MMPs elastase <= Macrophages and neutrophil

Elastin and collagen fiber damage => Emphysema

68
Q

Emphysema Signs/Symptom

A

Signs not seen until 1/3 parenchyma is damaged (significant loss)
- Dyspnea is first symptom
- Cough and wheeze (easily confused with asthma)
- Slowed forced expiration (pinched, doubled over)
- Can develop congestive heart failure and secondary hypertension
– Death occurs as a result of respiratory acidosis/heart failure/lung collapse

Other types:
- Compensatory
- Senile
- Bullous
- Interstitial

69
Q

Chronic Bronchitis

A

Definition: persistent cough with sputum production for at least 3 month in at least 2 consecutive years
- Original thought of as benign can lead to:
– Chronic airway obstruction, Heart failure, dyspalsia and epithelial malignancy
- Often associated with emphysema (smoking; can happen together; screen shot)
- Higher incidence in urban areas

70
Q

Chronic Bronchitis: causes

A

Two main causes:
- Inhalation of substances
- Microbial infection

Result in
- Hypersecretion of mucus
- Increase goblet cells in smaller airways
- Increased alveolar Mphages
- Inflammatory infiltration/Fibrosis (infection is secondary)

71
Q

Bronchial Asthma

A

Definition: Hyper reactive airway, leading to episodic bronchoconstriction, owing to increased responsiveness of the tracheobronchial tree to various stimuli (hyper responsiveness)
Types;
- Extrinsic: initiated by type I hypersensitivity to extrinsic antigen (atopic, occupational, aspergillosis)
- Intrinsic: initiated by diverse mechanism including asprin, pollutant, stress, infection, exercise

Result from chronic airway inflammation involving multiple cell types

72
Q

Mechanisms of Bronchial Asthma

A

Antigens incite lymphoid cells => antigen specific IgE antibodies that bind to mast cells
- Mast cell (w/subsequent exposure) degranulate and release inflammatory mediators
- Mediators stimulate contraction of smooth muscle cells through adneyl cyclase
- Mediators also increase vascular permeability and cause airway edema

73
Q

Clinical Aspects of Asthma

A

Symptoms are attacks of wheezing, chest tightness and cough
- Usually last hours and are followed by raising of copious mucous (can lead to death)

74
Q

Status asthmaticus

A

Sever cause of asthma; attack can last days or weeks
- Usually only disabling rather than lethal
– More severe forms lead to other pulmonary disease such as emphysema and infection based bronchitis (more material in lower part of lung)

75
Q

Bronchiectasis

A

Definition: chronic necrotizing infection of the bronchi and bronchioles leading to abnormal dilation of airway
- Signs are cough, fever, and foul smelling spumtum
- Dilation is permanent-remodel airway (reversible dilation is associated with pneumonias)

Causes:
- Bronchial obstruction (tumor, foreign bodies, mucous)
- Congenital disease (CF Immunodeficiency states)
- Necrotizing Pneumonia (tubercle bacillus, staphyloccoci)- necrosis of epithlial suface

76
Q

Cystic Fibrosis

A

Definition: Autosomal recessive disease that result from defective epithelial chloride ion transport
- Mucus plugging from increased production and altered biophysical properties
- Chronic Inflammation/Infection
– Long term damage, abnormal cytokines, TNF, & Interleukins
- Increased goblet cels and submucosal glands

77
Q

Cystic Fibrosis: Causes

A

Delta CFTR => Altered Mucus Production => Inflammation and infection => bronchiectasis & ancreased Neutrophils & Elastase (gonna feed back into inflammation and the bronchiectasis)
- Strucural protein damage

78
Q

Peneumonia

A

Definition: Acute infection of the lower respiratory tract caused by anything biological
- Incidence and mortality are highest in immunocompromised patient
– Elderly, smoking, intubation, alcoholism, very young, malnutriton
- Causative microorrganism affect presentation

79
Q

Pneumonia; Types

A

Community Acquired Pneumonia (CAP)
- Step.pneumonia most common form (rarely fatel except in elderly)
- Mycoplasma pneumonia; often seen in young
- INfluenza; most common viral form; usually mild although does predispose to secondary bacterial infection
- Legionella

Nosocomia (hospital acquired):
- Pseudomona aeruginosa most common form
- Staph. Aureus

In the sick Pneumocystis carinii occurs (HIV)

80
Q

Bacterial Pneumonia

A

Consolidation results from bacterial invasion
- Host response may be suppurative or fibrinous (produce fluid material to fight off or seal it off)

Two types of gross anatomic distribution
- Bronchopneumonia: patchy distrubution
- Lobar pneumonia: acute bacterial infection of a lobe (infrequent now due to antibiotics)

81
Q

How much we breath

A

Inhale 10000 liters per day of air (full of contaminant particles)
- Large particles 10um or greater => trapped in nose and upper airway
- 3-10um lodge in trachea or bronchi
- 1-5 um reach terminal airway and alveoli

82
Q

Why we generally infection free

A

Nasal Clearance:
- Coughing/sneezing
- Swallowing

Tracheobronchial clearance:
- Mucocliary action
- Swallowing/expectoration

Alveolar clearance:
- Alveolar macrophages
- Phagocytosis/lymph

83
Q

Why we get eventually get infected

A
  • Suppresstion by coma, anesthesia, neuromuscular disorder, or drugs is possible
  • Injury to mucocilary action by smoking, inhalation of hot or corrosive gaes, viral disease or genetic disease
  • Phagocytic action is inhibited by smoking, alcohol, anoxia, or oxygen toxicity
84
Q

Viral & Myocplasma Pneumonia

Primary Atypical Pneumonia

A

Rare in healthy;
- Organisms involved such as influenza, RSV and mycoplasma uusually ONLY infect UPPER respiratory tract
- Result in cellular invation of the alveoli, loss of wall integrity
- Low mortality except with exceptional virulent organism

85
Q

Tuberculosis

A

Infection with Mycobacterium tuberculosis
- Transmitted via aerosol

Most causes; infection is isolated and does not spread (primary)
– In some, infection may spread locally or to other parts of the body (more common in adult; secondary)
– If managed to spread to other organs => can be fatal

Symptoms: Chronic illness with cough, fever, sweats, sputum and coughing blood

86
Q

Diffuse Interstitial Lung Disease

A

Definition: a group of disease of widely different origin characterized by chronic involvement of pulmonary connective tissue
Causes;
- Occupational and environmental inhalants
- Drugs and toxins
- Infections
- A number of unknown cause including sarcoidosis, Goodpasture’s syndrome
- Typically present as restrictive lung disease
- Eventually result in secondary hypertension and right heart failure

An injury happen=> growth factors go to fix it => the barrier gets bigger from all the collage fibers => stiff => can’t diffuse & breath well (check screen shot)

87
Q

Lung Cancer

A

Major type of cancer in men and 2nd in women
- Variety of benign and maligenant tumors may arrise in lung but >90% are bronchogenix
– Squamous cell carcinoma (25-40%)
– Adenocarcinoma (25-40%)
– Small cell (20-25%)
– Large cel (10-15%)
- Directly linked to smoking (esp. small cell)
- Often spreads to other organs before diagnosed
- Survival is poor (>15% alive at 5 year)

88
Q

Bronchogenic tumors of main stem

A

Most arise in large airways
- Erodes epithelial lining
- Cause sever obstruction
- Metastasize through the lymph and blood to adrena, liver, brain, and bones

89
Q

Bronchiloalveolar Carcinoma

A

Occures in respiratory airways
- Typically adenocarcinoma (beyond 16 gen)
- Occur at any age of 20 and higher
- Often present as interstitial pneumonitis
- Good survival rates (75% at 5 years)
- If metastasize =>45% survival

90
Q

Pleural Tumors

A

Primary is rare although often occur as secondaries to lung, breast, and ovarian carcinoma
- Derive from mesenchymal cells
– Can either be stromal or epithelial
- Most common form of primary malignant mesothelioma derives from asbestos exposure
- Present as restrictive lung disease

Patho (17 decks)

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