ANP1115 Midterm 2 Flashcards

Two main immune defenses

Innate immunity (non-specific), and adaptive immunity (specific/acquired)

Innate immunity

The non-specific immune defence.

Protects without recognizing a specific pathogen. Instead, it recognizes general molecular patterns on microbes (carbohydrates/lipids on cell surfaces).

It’s present at birth, is a rapid response, has no immunological memory, main response every time.

The main components are surface barriers (think skin, mucus membranes), and internal defences. (Think phagocytes, natural killer cells, inflammation, antimicrobial proteins and fever.)

Activated by PAMPs (Pathogen-associated molecular patterns), and DAMPs (damage-associated molecular patterns)

PAMPs and DAMPs alert the innate immune system that something is wrong, and don’t require identification of a specific microorganism.

Adaptive immunity:

The specific/acquired immunity.

Defined as an immune response carried out by lymphocytes that recognize specific antigens.

The key features of this type of immunity are that it’s highly specific, has memory, and develops after exposure to antigens.

There are 2 major types:

• Humoral immunity: Mediated by B cells and produces antibodies.

• Cell-Mediated Immunity: Mediated by T cells, destroys infected or abnormal cells.

Macrophages are a key player in this too. They attack antigen-presentin cells.

PAMPs (Pathogen-Associated Molecular Patterns)

Molecules found on microorganisms but not normally in the body

Eg: Bacterial cell wall molecules

Recognized by Toll-like receptors (TLRs) on phagocytes

Effects

• Trigger phagocytosis

• Trigger inflammatory response

• Notify adaptive immune system

DAMPs (Damage-Associated Molecular Patterns)

Defined as molecules located in the wrong place in the body

Example: DNA outside the nucleus or cell

They signal tissue damage even if no infection is present

Innate Defenses

These are the “surface barriers”. They are effective, but can be breached.

Acid

• Skin acidity

• Vaginal secretions

• Stomach acid

Enzymes

Lysozyme (an antimicrobial enzyme) in:

• Saliva

• Respiratory mucus

• Tears

Protein-digesting enzymes in stomach

Mucus

• Traps microorganisms in respiratory and digestive tracts

Defensins

• Antimicrobial peptides secreted by skin and mucous membranes

Other Chemicals

• Lipids in sebum

• Dermicidin in sweat

• Toxic to bacteria

Inflammation

A response to tissue injury or infection.

The four key signs of inflammation are redness, heat, swelling & pain.

Functions:

• Preventing spread of microorganisms

• Removing pathogens and cell debris

• Initiating tissue repair

• Alerting the adaptive immune system

Inflammatory chemicals (eg: histamine, kinins, prostaglandins, and complement proteins) are released by injured cells and immune cells and cause vasodilation, increased capillary permeability, and attraction of immune cells.

Leukocyte Response During Inflammation

Leukocytosis

• Increase in circulating white blood cells

Margination

• Leukocytes adhere to capillary walls

Diapedesis

• Leukocytes squeeze through capillary walls

Chemotaxis

• Leukocytes follow chemical signals to the injury site

Inflammatory Process Summary

1. Tissue injury occurs

2. Chemical mediators released

3. Vasodilation increases blood flow

4. Capillary permeability increases

5. Protein-rich fluid leaks into tissues

6. Immune cells migrate to site

7. Phagocytosis of pathogens

8. Debris cleared

9. Healing begins

Interferons

An antimicrobial protein released by virus-infected cells.

Effects:

• Diffuses to nearby cells

• Blocks viral protein synthesis

• Degrades viral RNA

It also activates macrophages, mobilizes natural killer cells and may have anti-cancer effects.

Complement system

A group of approx 20 plasma proteins circulating in inactive form

When activated, they enhance inflammation and pathogen destruction

The major effects of this system are:

• Direct destruction of microbes via membrane attack complex (MAC)

• Basodilation & increased permeability

• Chemotaxis which attracts immune cells 

• Oopsonization (coating pathogens to enhance phagocytosis)

Complement Pathways

Classical pathway

• Triggered by antibodies

Lectin pathway

• Activated by lectins binding sugars on microbes

Alternative pathway

• Activated spontaneously on microbial surfaces

Membrane Attack Complex (MAC)

Formed by complement proteins C5b–C9

It inserts into the pathogen membrane, then creates pores which causes cell lysis

Fever

• Defined as an elevated body temperature caused by resetting of the hypothalamic thermostat

• It’s caused by pyrogens released by leukocytes and macrophages exposed to pathogens

• The benefits are that it increases metabolic rate and causes the liver and spleen to sequester (isolate) iron and zinc, which limits microbial growth.

Natural Killer (NK) Cells

A type of lymphocyte in the innate immune system. It’s not antigen-specific

It targets virus-infected and cancer cells.

The mechanism of detection:

• Note that all normal cells express MHC I proteins.

• NK cells attack when MHC I is missing or reduced, or if stress markers are present.

• Many infected or cancer cells reduce MHC I expression, triggering NK.

NK cells can express toll-like receptors and respond to PAMPs or DAMPs

Lymphocytes

Derived from hemocytoblasts in red bone marrow

All of them start identical, then become B cells (mature in bone marrow) or T cells (mature in thymus).

During maturation, they develop immunocompetence and self-tolerance.

Antigen

A substance capable of mobilizing adaptive immune responses

They may have multiple antigenic determinants (epitopes)

Major histocompatibility complex (MHC)

Refers to cell surface glycoproteins which mark cells as “self”, and present antigens to T cells.

Each MHC molecule contains a groove where a self-antigen or foreign antigen can bind

Lymphocyte development

1. Origin

• Both B and T lymphocyte precursors originate in bone marrow

2. Maturation

• T cells migrate to the thymus to mature, and B cells mature in bone marrow

• During maturation, they acquire immunocompetence (recognizing and defending) and self-tolerance.

3. Seeding secondary lymphoid organs

• Naive lymphocytes migrate to lymph nodes, spleen and other lymphoid tissues

4. Antigen encounter

• When lymphocyte receptors bind their specific antigen, they become activated

5. Proliferation and differentiation

• Activated lymphocytes proliferate (clonal expansion), then differentiate into effector cells or memory cells.

• Memory cells provide long-term immunity.

T cell education in the thymus

As we know, T-cells imgrate tot he thymus where they undergo maturation.

Positive selection:

• T cells must recognize self-MHC; if it doesn’t, apoptosis occurs.

• Successful cells survive but are restricted to recognizing antigen on self-MHC.

Negative selection:

• T cells must not recognize self-antigens strongly. If they do, they undergo apoptosis to prevent autoimmune diseases.

B Cell Maturation

• The immature B cells mature in bone marrow. The self-reactive ones are eliminated.

• After maturation, B cells express unique antigen receptors, and each B cell responds only to one antigen.

• Lymphocytes become immunocompetent before encountering antigens.

Humoral immune response

Occurs when B lymphocytes respond to an antigen.

Antigen challenge usually occurs in lymph nodes or the spleen

Activation of B cells

Antigen binds to the receptor on a specific B lymphocyte

Only the B cell with the complementary receptor becomes activated

The activated B cell proliferates (clonal expansion) which produces a clone of identical cells.

After proliferation, B cells differentiate into two main types of cells. Plasma cells (effector B cells) and memory B cells.

Plasma cells

• Also known as effector B cells

• A type of B cell

• Their function is to procude large amount of antibodies

• They typically survive 4-5 days

• The antibodies circulate in body fluids, they bind antigens and mark pathogens for destruction.

Memory B cells

• A type of B cell

• Their function is to provide long-term immunity.

• They don’t immediately produce antibodies

• Remain in the body for years

• Can respond rapidly upon future exposure to the same antigen

Primary immune response

Occurs during the first encounter with an antigen

A slower response

Produces less antibodies

1. Antigen binds to B-cell receptor

2. B cells proliferate

3. Plasma cells produce antibodies

4. Memory B cells are formed

Secondary immune response

Occurs during later exposure to the same antigen

• It’s much faster

• Produces more antibodies

• Memory B cells rapidly become plasma cells

Macrophages

A type of white blood cell

They engulf athogens

Present antigen fragments to T cells

Help activate adaptive immune responses

Humoral Immunity

The immunity that has to do with B cells

• The antigen binds to B-cell receptor
  Helper T cell sends chemical signals

• B cell diffrenaites into lpasma cells

• Plasma cells release antibodies

Mechanisms of Antibody Action

Note: Antibodies don’t directly kill pathogens, rather they tag them so other immune mechanisms can destroy them.

1. Neutrization

• Antiboides bind dangerous parts of pathogens, which prevents viruses or toxins from entering cells

2. Agglutination

• Antibodeis bind multiple pathogens, causing them to clum together.

• This is easier for phagocytes to remove

3. Precipitation

• Antibodies bind double antigens, which forms complexes that settle out of solution.

4. Complement activation

• Antibodies activate compliment proteins which cause inflammation, phagocytosis and cell lysis.

Immunoglobulin classes (antibodies)

IgM

• The first antibody produced during primary response

• Indicates current infection

• Strong activator of complement

• Exists as pentamer in plasma

IgG

• Most abundant antibody in blood (75–85%)

• Major antibody in secondary immune response

• Activates complement

• Crosses placenta which provides fetal immunity

IgA

Found in body secretions:

• Saliva

• Sweat

• Intestinal fluid

• Milk

Protects mucosal surfaces

IgE

Binds to mast cells and basophils

Triggers histamine release

Important in:

• Allergic reactions

• Parasitic infections

IgD

• Found on B-cell surfaces

• They function as B-cell antigen receptors

Vaccine mechanisms

• They work by triggering a primary immune response without causing disease

• This creates memory B and T cells

• Upon a later exposure to the pathogen, it causes a rapid secondary immune response

Active immunity

• A type of immunity where the body produces it’s own antibodies

• It can either be naturally acquired (via infection with pathogen), or artificially acquired (via vaccination)

• Only active immunity produces immunological memory.

Passive immunity

• A type of immunity where antibodies come from another source

• They can be naturally acquired from the mother (fetus gets antibodies through the placenta, or infant through milk) or artifically acquired via injection of antibodies (gamma globulin)

• It provides immediate protection, but holds no memory.

T cells

• A type of cell that destroys infected or abnormal body cells

• Targeted cells include virus-infected cells, cancer cells, transplanted tissues, and cells with intracellular bacteria.

• These cells recognize antigen fragments presented on MHC molecules

Types are:

• Cytotoxic T Cells (CD8) (the killers)

• Helper T cells (CD4) (coordinate adaptive immune response)

• Regulatory T Cells (suppress or stop immune responses)

Cytotoxic T Cells (CD8)

• The killer T cells.

• They destroy infected or abnormal cells

Mechanism of killing:

• Release perforin

• Release granzymes

• Cause apoptosis (cell death)

Helper T Cells (CD4)

Most common T cells.

• They activate B cells

• Activate cytotoxic T cells

• Activate macrophages

• Release cytokines (ex: IL-2)

They basically coordinate the entire adaptive immune response./

Regulatory T Cells

They suppress or stop immune responses

They do this to prevent excessive immune activity

MHC Class I proteins

• These proteins are found on all nucleated cells.

• They are recognized by CD8 cytotoxic T cells

• These proteins display internal (endogenous) antigens… So viral and cancer proteins.

• The signal sent is basically “I belong to self, have been infected. Destroy me.”

MHC Class II proteins

• These proteins are found on antigen-presenting cells. Think macrophages, dendritic cells and B cells.

• They are recognized by CD4 helper T cells.

• They display external (exogenous) antigens.

• The signal sent is basically “I captured a pathogen. Activate immune response”

Macrophages (antigen-presenting cells)

They are derived from monocytes from bone marrow

Functions are:

• Phagocytosis (engulfing pathogens)

• Antigen presentation (displaying antigen fragments to T-cells)

• Immune activation (releasing signalling proteins, activating T cells)

Note: Activated T cells then stimulate macrophages, which creates a feedback loop.

Mechanism of Helper T Cell Mechanism

Antigen presentation

• Dendritic cell presents antigen on MHC II

Double recognition

• T-cell receptor binds antigen

• CD4 binds MHC

Costimulation

• Additional receptor interactions occur

Clonal expansion

• Helper T cells proliferate

Formation of:

• Effector T cells

• Memory T cells

Cytotoxic T Cell Killing Mechanism

1. Cytotoxic T cell recognizes antigen on MHC I

2. Releases perforin

3. Perforin creates pores in target cell membrane

4. Granzymes enter the cell

5. Trigger apoptosis

6. T cell detaches and attacks another cell/

Lines of immune defence

First line of defence: (Surface barriers):

• Skin

• Mucous membranes

• Enzymes in saliva and tears

• Stomach acid

• Mucus

Second line of defence (Innate internal defences):

• Phagocytes

• Natural killer cells

• Inflammation

• Complement

• Interferons

• Fever

Third Line of Defence (adaptive immunity)

• This line of defence provides specific, long-term protection

• Components are B cells (antibodies), T cells and memory cells

Four processes of respiration

Pulmonary ventilation

• Movement of air into and out of lungs

External respiration

• Exchange of gases between air in alveoli and blood

Transport of respiratory gases

• Blood transports O₂ and CO₂ between lungs and tissues

Internal respiration

• Exchange of gases between blood and tissue cells

Note that the respiratory system performs ventilation and external respiration, while the cardiovascular system handles transport and internal respiration

Conducting Zone

Provides a passageway for air

Filters, warms and humidifies incoming air

No gas exchange occurs here

Structures include:

• Nose

• Nasal cavity

• Pharynx

• Larynx

• Trachea

• Bronchi

• Bronchioles

• Terminal bronchioles

Respiratory Zone

The sites of gas exchange in the body

Structures include:

• Respiratory bronchioles

• Alveolar ducts

• Alveoli

Gas exchange occurs via diffusion across the respiratory membrane.

The nose

• A facial organ

• Provides an airway for respiration

• Warms and moistens the air

• Filters air

• Is a resonating chamber for speech

• Contains olfactory receptors for smell

• It has a rich blood supply (thin veins beneath epithelium), which makes nosebleeds common

• Has sensory nerves, hence why infants have a sneeze reflex

• Cold air slows cilia movement, leading to runny nose

External nose structure

• The shape of the nose is determined by nasal cartilages

• The skin covering the nose contains many sebaceous glands

• Important structures include the nasal bone, septal cartilage, major and minor alar cartilages

Air entering the nasal cavity

Air enters from the external nares (nostrils) to the nasal cavity, internal nares, and then nasopharynx. It’s divided by the nasal septum, which is made up of cartilage and bone.

Olfactory mucosa

A type of nasal mucosa

It contains receptors for smell

Respiratory Mucosa

A type of nasal mucosa

Structure is pseudostratified ciliated columnar epithelium and goblet cells, which produce mucus.

Function is trapping dust and microbes via the mucus, and cilia moves mucus towards the pharynx.

Mucus contains lysozyme, which is an antibacterial enzyme

Vibrissae

• Refers to the coarse hairs inside the nostrils

• They trap large particles

Nasal Conchae

• There are 3 pairs. Superior, middle and inferior.

• They increase surface area, create air turbulence and improve warming, humidifying, and filtering of air.

Paranasal sinuses

They are located in the bones surrounding the nasal cavity

• Frontal

• Sphenoid

• Ethmoid

• Maxillary

Their function is to lighten the skull, produce mucus and help warm and moisten air

Sinus headache occurs from sinus drainage pathways being blocked, which causes air in the sinuses to be absorbed and create a partial vacuum, causing pressure & pain.

Pharynx

A common pathway for air and food

Its walls are composed of skeletal muscle, it’s approx 13 cm long.

There are 3 regions to this:

• Nasopharynx

• Oropharynx

  • Laryngopharynx

Nasopharynx

• Located below the sphenoid bone and above the soft palate

• Allows for air passage only

• It’s structure is pseudostratified ciliated columnar epithelium

• Contains pharyngleal tonsil and pharyngotympanic (auditory) tubes, which drain into the middle ear.

Oropharynx

Extends from the soft palate to epiglottis

Connected to the mouth via the isthmus of the fauces

Provides a passageway for air and food

Has stratified squamous epithelium, which protects against abrasion

Structures include the palatine tonsils and lingual tonsils.

Laryngopharynx

• Extends from the epiglottis to the larynx

• Provides a passageway for air and food

• Has stratified squamous epithelium

• During swallowing, it directs food into the esophagus

Larynx

• The voice box

• Located between the pharynx and trachea. It’s roughly 5cm long

• It’s attached to the hyoid bone

• Functions are to maintain an open airway, switching pathway between air and food, and producing voice

• In laryngitis, the vocal cords are inflamed, which prevents normal vibration causing hoarseness

Laryngeal cartilages

There are a total of 9

Thyroid cartilage: 

• A large shield-shaped cartilage. It forms the Adam’s apple

Cricoid cartilage: 

• Located below the thyroid cartilage

Arytenoid cartilages:

• Anchor vocal cords

Epiglottis: 

• An elastic cartilage that covers the airway during swallowing.

Vocal cords

True vocal cords:

• White bands of elastic tissue, which vibrate to produce sound

False vocal cords:

• Are located above true cords and have no role in sound production

The glottis is an opening between the true vocal cords

Voice Production

• Speech occurs when expirated air passes through the vocal cords. The vocal cords open and close rapidly.

• Pitch is influenced by the length and tension of the vocal cords.

• During puberty in males, the vocal cords lengthen, hence the lower voice.

Trachea

• A flexible and mobile airway

• 10-12 cm in length, has a diameter of approx 2.5cm

• It has pseudostratified ciliated columnar epithelium

• The cilia move mucus towards the pharynx. Smoking is bad because it destroys cilia, resulting in only coughing being able to clear mucus.

Tracheal Wall Layers

Mucosa

Submucosa

• Contains seromucous glands

Hyaline cartilage rings

• 16–20 C-shaped rings

• Prevent airway collapse

Adventitia

Respiratory membrane

• Made up of alveolar wall, capillary wall and basal lamina

• It forms an air-blood barrier. Gas exchange occurs by diffusion

Type I Alveolar Cells

• Made up of simple squamous epithelial cells

• Form a thin gas-exchange surface

Type II Alveolar Cells

• Create a surfactant which reduces surface tension and prevents alveolar collapse.

Notable features of Alveolis

Elastic fibres

• These allow lungs to expand and recoil

Alveoloar pores

• These equalize air pressure between alveoli

• Provide alternate pathways if the bronchi are blocked

Alveolar macrophages

• Remove dust and pathogens

• Over 2 million macrophages are cleared per hour

The Bronchial Tree

• Refers to the branching system of airways inside the lungs. Air travelling through will become warmed, humidified, and cleansed of impurities.

• There are approximately 23 orders of branching air passages.

There are two primary bronchi, with the rIght primary bronchus being wider, shorter and more vertical. As a result, foreign objects are more likely to enter it

The bronchial tree progressively branches into smaller airways. It goes like this

1. Primary bronchi

2. Secondary bronchi

3. Tertiary bronchi

4. Bronchioles

5. Terminal bronchioles

Bronchioles and terminal bronchioles

• Bronchioles have a diameter less than 1mm, while terminal ones have a diameter less than 0.5mm (they’re the smallest structures of the conducting zone)

• After the terminal bronchioles, the respiratory zone begins

Structural changes along the bronchiole tree

Cartilage (function is keeping larger airways open):

• The trachea has C-shaped rings

• Bronchi have cartilage plates
  Bronchioles have no cartilage

Epithelium:

• Changes from Pseudostratified ciliated columnar epithelium (larger airways) to columnar and cuboidal epithelium (smaller bronchioles)

Bronchioles have no cilia or mucus-secreting cells

Smooth muscle (function is to allow bronchoconstriction and bronchodilation, which regulates airflow):

• Relative amount present increases as airway diameter decreases. 

Lung structure

• Lungs are paired organs, occupying most of the thoracic cavity

• The mediastinum lies between the lungs

• Each lung sits in its own pleural cavity

• Lungs are connected to the mediastinum through vascular and bronchial attachments

External Lung Features

Apex

• The superior tip of the lung

Base

• The inferior surface rests on the diaphragm

Hilium

• A region where structures enter and leave the lungs.

• Structures include bronchi, blood & lymphatic vessels, and nerves.

Costal surface

• Lung surface that contacts the ribs

Cardiac Notch

• An indentation in the left lung that accommodates the heart

Lung fissures

Oblique fissure

• Present in both lungs

Horizontal fissure

• Present only in the right lung

• The fissures divide lungs into lobes

Bronchoulmonary segments

Subdivided by the septum, approx 10 segments.

Each segment has its own tertiary bronchus, pulmonary artery and pulmonary vein

Lobules

• The smallest visible subdivisions of the lung

• They are hexagon-shaped

• Approx the size of a pencil eraser

• Supplied by a large bronchiole

Pulmonary circulation

• Pulmonary arteries carry deoxygenated blood to the lungs

• Pulmonary veins return oxygenated blood to the heart

• Both the parasympathetic and sympathetic nervous systems control airway diameter and other lung functions

Bronchial circulation

• Bronchial arteries deliver oxygenated systemic blood to lung tissues

Bronchial veins return blood to the right side of the heart

Pleurae

Thin, double-layered serous membranes

Parietal pleura: 

• Lines the thoracic cavity wall

Visceral pleura: 

• Covers the lung surface

They have 3 chambers, the central mediastinum and 2 lateral pleural compartments

• Pleurisy refers to inflammation of the pleural membranes, causing painful breathing.

Pleural cavity

• The space between the pleural layers

• It’s filled with pleural fluid

Functions of pleural fluid include:

• Lubricating lung movement during breathing

• Keeping lungs attached to the thoracic wall via surface tension

Physiologic Dead Space

Refers to the air that does not participate in gas exchange

Typical dead space is 150mL.

Eg: If tidal volume is 500mL, 150mL is dead sace, and 350mL is alvelolar ventilation

Anatomical dead space: Refers to air in conducting airways

Functional Dead Space: Refers to air reaching non-erfused alveoli

Pulmonary ventilation is made up of inspiration + expiration

If some alveoli are no longer functional, total dead space = 150mL + alveolar dead spaces

Atmospheric pressure

• Refers to the pressure exerted by the air around the body

• At sea level, it’s 760mmHg

• Respiratory pressures are measured relative to atmospheric pressure

• Eg: 04mmHg relative pressure = 756 mmHg absolute pressure

Intrapulmonary Pressure

• Refers to pressure inside alveoli.

• Changes during breathing.

• Eventually equalizes with atmospheric pressure.

Intrapleural Pressure

Pressure inside the pleural cavity.

Normally, about 4 mmHg lower than alveolar pressure.

This negative pressure is due to:

• Elastic recoil of lungs

• Surface tension of alveolar fluid

• Elasticity of chest wall

If intrapleural pressure becomes equal to atmospheric pressure, the lung collapses. It’s possible for only one lung to collapse because they are in separate pleural cavities.

Transpulmonary pressure

The pressure that keeps the lungs expanded

TP = Intrapulmonary pressure - Intrapleural Pressure

Quiet Inspiration

A mechanic of breathing

Muscles involved are the diaphragm and the external intercostals

Basically

• Thoracic cavity volume increases

• Intrapulmonary pressure decreases

• As a result, air flows into the lungs

The lung volume increases by about 0.5L, and intrapleural pressure drops ot about -6mmHg

Quiet Expiration

A mechanism of breathing. It’s a passive process. Depends more on the elastic recoil of the lungs

1. Inspiratory muscles relax

2. The rib cage descends

3. Lungs recoil

4. Thoracic volume decreases

As a result, intrapulmonary pressure rises to +1mmHg, and air flows out of the lungs

Deep/Forced Inspiration

• This process is assisted by accessory muscles (neck and chest)

• These muscles raise the ribs further and expand the thoracic cavity more.

Forced Expiration

• An active process

• The muscles involved are the abdominal muscles and the internal intercostals

• This process increases abdominal pressure and depresses the rib cage.

• As a result, air is forced out of the lungs.

3 major factors influencing pulmonary ventilation

1. Airway resistance

2. Alveolar Surface Tension

3. Lung compliance

Airway Resistance

A major factor influencing pulmonary ventilation

Note: Gas Flow = Pressure Gradient/Resistance

• As a result, resistance depends mainly on airway diameter.

• Resistance is greatest in medium-sized bronchi

The parasympathetic nervous system causes bronchoconstriction. This can occur during asthma attacks

The sympathetic nervous system causes bronchidilation

Airway resistance also increases with mucus, infection or tumours

Alveolar Surface Tension

• A major factor influencing pulmonary ventilation

• Surface tension occurs at the air-liquid interface in alveoli

• Water molecules are more attracted to each other than to the gas, and as a result, tend to collapse alveoli.

• They resist any force to increase surface area.

• I guess they take up space that should be occupied by air?

Surfactant

• Produced by type II alveolar cells

• A detergent-like lipoprotein

• It reduces surface tension and prevents alveolar collapse by interfering with the cohesiveness of water molecules

Infant Respiratory Distress Syndrome (IRDS)

• Occurs in premature infants

• Caused by insufficient surfactant production

• The result is alveoli collapsing, and as a result, the infants need assisted ventilation