The Respiratory System Flashcards by Deleted Deleted

RESPIRATORY TRACT

Upper

Humidify & warm air
Defence – mucus and cilia
Sensory
Speech

Lower

GAS EXCHANGE
Defence
Metabolic

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WHAT IS THE FUNCTION OF THE LARYNX?

To generate different sounds

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WHAT PARTS OF THE LUNGS ARE KNOWN AS THE ‘CONDUCTING ZONES’?

The tubes (e.g. trachea and primary bronchus)

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LOWER RESPIRATORY TRACT

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WHAT IS THE PARENCHYMA?

The part of the lungs where gas exchange occurs

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LUNG BRANCHES

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AIRWAY RESISTANCE

Proportional to 1/radius⁴
But conduction summative

–huge numbers of respiratory bronchioles

–small airways make a small contribution to total Resistance

•Conducting zone bronchioles largest influence

Inversely proportional to conductance; higher the resistance, the less efficient conduction.

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AIRWAY RESISTANCE IS INCREASED IN MANY DISEASES

Smooth muscle contraction
Obstruction with mucus
Collapse
Structural changes occur in the conducting airways
Smooth muscle growth
Fibrosis

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LUNG EPITHELIUM

Lining cells in airway
Specialisation changes down the airway

–Bronchi

•ciliated, goblet, glandular

–Bronchioles

•ciliated, non-ciliated, goblet, club cells

–Alveoli

•Squamous, cuboidal

Ciliated= waft

Goblet cells secrete mucus (as do glandular cells)

Club cells (secretory cells)

Highly specialised cells in the alveoli (specialised for gas exchange).

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AIRWAY STRUCTURE

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AIRWAY INNERVATION

Sensory (afferent) nerves FROM the airway epithelium and smooth muscles signal to the brain.

Autonomic fibres TO glandular epithelium and smooth muscle from CNS

Parasympathetic branches of the vagus nerve (vagus nerve is the main nerve supplying the lungs).
Excitatory (e) and inhibitory (i)
Very little sympathetic innervation (most nerves are parasympathetic).
ß-adrenoceptors on airway smooth muscle are stimulated by circulating adrenaline.

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THE RESPIRATORY UNIT

•Massive network of airways and air sacs (around 500 million) to maximise surface area (50-100 m²).

Pneumocytes are very thin, flat cells to allow maximum _ exchange.

Also surrounded by dense _ network= gas exchange.

Capillary

Gas

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ALVEOLAR EPITHELIUM CELLS (PNEUMOCYTES)

•Type I (Gas exchange cells)

–Very large surface area

cover 95% of alveolus
10% of cells

–squamous

–gas exchange

•Type II cells (secrete surfactant, they also replace TI cells when the TI cells die)

–cuboidal

•majority of cells

–secretory

•surfactant

–precursors for type I

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WHAT DO TYPE II CELLS SECRETE?

Surfactant

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SURFACTANT

•Produced by type II alveolar epithelial cells

–Lipid (90%) – mostly phospholipid

–Proteins – SP-A, -B, -C, -D

•Reduces surface tension

–prevents alveolar collapse (atelectasis)

Innate immunity function
Instilled into babies with Infant Respiratory Distress Syndrome

–Beractant (bovine)

–Pumactant (synthetic, lipid only)

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LUNGS AT BIRTH

Lung epithelium develops in last trimester of pregnancy.
Maturation stimulated by _ in premature babies
Lung is fluid filled in foetus - must rapidly empty

–Surge in corticosteroids and catecholamines at birth

–Activation of absorptive channels

•Epithelial Sodium Channels (ENaC)

–Pressure changes (squeeze through birth canal)

•Caesarian section – reduced drive for fluid absorption

Corticosteroids

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BLOOD SUPPLY TO THE LUNGS

•Pulmonary circulation

–Artery flows directly from the right ventricle

LOW oxygen
HIGH flow
_ pressure

–Capillaries pass around the alveoli

–Pulmonary _ returns oxygenated blood to left heart

•Bronchial circulation

–From aorta (left ventricle)

–HIGH pressure

–Supplies oxygen and nutrients the conducting airways

–Not involved systemic respiration processes

–Only 2% of cardiac outflow

Low

Vein

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VENTILATION IS AUTOMATIC AND CONTROLLED BY THE CNS.

TRUE OR FALSE?

TRUE

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NEURONAL CONTROL OF BREATHING

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MUSCLE INNERVATION

Somatic motor nerves

Innervate skeletal muscles in the thorax

Phrenic
innervates the diaphragm
irritation => hiccough
Intercostal

Autonomic nerves

Bronchial

•supply smooth muscle & secretory cells

–branch from vagus

–reflex bronchospasm and mucus secretion

–important in asthma

Sensory output

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RESPIRATORY MUSCLES

Intercostals are between the _.

External intercostals contract to lift ribs _.

Internal intercostals contract to pull ribs down again and to force air out.

Ribs

Upwards

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SENSORY AFFERENT PATHWAYS FROM THE LUNG (MYELINATED)

•Send impulses via vagus to medullary centres

Slowly adapting

–Stimulated by stretch receptors in airway smooth muscle

–Elicit reflexes

Shortened inspiration
Hering-Breuer reflex

–Promotion of expiration following steady inflation

–Prevents over-inflation of lung

Rapidly adapting stretch receptors

–Stimulated by sudden, sustained inflation

–Also by ‘irritant receptors’ among epithelium

–Elicit reflexes:

Cough
Bronchoconstriction
Mucus secretion

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WHAT STIMULATES RAPIDLY ADAPTING STRETCH RECEPTORS?

Sudden, sustained inflation of the lungs

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**_SENSORY AFFERENT PATHWAYS (NON-MYELINATED FIBRES)_** * Pulmonary and bronchial C fibres * Located close to blood vessels (J receptors) * **Exogenous stimuli** –Noxious agents in air **•Endogenous stimuli** –inflammatory agents generated by the body **•Reflex bronchoconstriction & mucus secretion**

WHAT DO J RECEPTORS CAUSE?

Cause changes in blood flow in specialised regions

**_COUGH REFLEX_** •Stimulation of irritant receptors –Sensory nerves conveys signal to medulla * Motor nerves signal to _ muscles * Glottis closes * Abdominal and _ intercostal muscles contract rapidly * Intrapulmonary pressure rises * Glottis opens

Skeletal Internal

**_PLEURAL MEMBRANES_** * Double membrane surrounding the lungs * Left & right pleura anatomically distinct –Collapsed lung (pneumothorax) usually only affects one lung •Normally very small amounts of pleural fluid between membranes (few ml) –Serous fluid •Lubricant

**_VENTILATION_** * Fluid in the pleural sac helps the lung wall “stick” to the inside of the thorax. * Contraction of the _ and the external intercostal muscles. –Increased lung \_. –Internal pressure falls (Boyles Law) –Air drawn into lungs •Exhalation is passive at rest –Elastic recoil

Diaphragm Volume

IN TERMS OF VENTILATION, WHAT HAPPENS WHEN YOUR DIAPHRAGM AND EXTERNAL INTERCOSTAL MUSCLES CONTRACT?

1. Lung volume increases 2. Internal pressure falls 3. Air is drawn into the lungs

**_PULMONARY COMPLIANCE_**

**_METABOLIC FUNCTION OF THE LUNG_** •Club cells _ inhaled substances –cyt p450 •Vascular cells **inactivates** some circulating hormones –prostaglandins •Vascular cells **activate** angiotensin I –Biologically inert Ang I converted to pressor Ang II (Angiotensin Converting Enzyme) •Fibrinolytic function

Detoxify

WHAT DO CLUB CELLS DO IN THE LUNGS?

Detoxify inhaled substances

**_NEURAL AND CHEMICAL CONTROL OF RESPIRATION_** ## Footnote **Neural control** Central rhythm generator in medulla * Receptors in respiratory tract causing sneezing, coughing and hyperpnoea * Nociceptors **Chemical control** •Central and _ chemoreceptors

Peripheral

**_NEURONAL CONTROL OF BREATHING_** **Medulla** –Ventral and Dorsal Respiratory Group: * Discharge rhythmically * efferent neurons to motor nerves * receives afferent input from periphery and pons * Little activity in expiratory centre at rest **Pons** –Apneustic centre: * Prolongs medullary centre firing * Hence depth of breathing increased –Pneumotaxic centre: * Inhibits apneustic centre * Controls rate of breathing

WHAT DOES THE APNEUSTIC CENTRE IN THE BRAIN DO?

Prolongs medullary centre firing= increases depth of breathing

WHAT DOES THE PNEUMOTAXIC CENTRE OF THE BRAIN DO?

Inhibits apneustic centre Controls rate of breathing

**_RHYTHMIC DISCHARGE OF PRE-BÖTZINGER COMPLEX_** * Region of the ventral respiratory group in the \_. * Spontaneous rhythmic discharge. * Stimulates rhythmic discharge of motor nerves. * Results in contraction of \_.

Medulla Diaphragm

WHAT IS ONDINE'S CURSE?

Loss of automatic control of ventilation

**_VOLUNTARY CONTROL OF BREATHING_** Via the Cerebral Cortex. * Sends signals direct to respiratory motor neurones * Sensitive to: –Temperature –Emotion

**_LUNG TRANSPLANT_** * Motor innervation is to skeletal muscles, so ventilation maintained * Preservation of cough from tracheal stimulation * Loss of cough stimulation from lower airway * Loss of Hering-Breuer reflex

WHAT TWO TYPES OF RECEPTORS CONTROL RESPIRATION?

Central Chemoreceptors (respond to [H⁺] and also the concentration of CO₂) Peripheral Chemoreceptors- Carotid and Aortic bodies (Primary signal is O₂ but there is also some input from [H⁺].

WHAT IS THE NORMAL AIR CONCENTRATION OF CO₂?

0.04% (0.3 mm Hg)

WHAT IS THE NORMAL ATMOSPHERIC CONCENTRATION OF OXYGEN IN THE AIR?

21% (160mm Hg)

WHAT DOES PaO₂ AND ALSO PaCO₂ STAND FOR?

Partial pressure of arterial oxygen (normally about 80-100mm Hg) Partial pressure of arterial CO₂(normally about 40mm Hg)

WHAT DOES PAO₂STAND FOR?

Concentration of alveolar oxygen

**_CENTRAL CONTROL OF RESPIRATION_** ## Footnote **Carbon Dioxide Stimulates the Chemosensitive Area** Although carbon dioxide has little direct effect in stimulating the neurons in the chemosensitive area, it does have a potent indirect effect. It does this by reacting with the _ of the tissues to form carbonic acid, which dissociates into _ and bicarbonate ions; the hydrogen ions then have a potent direct stimulatory effect on respiration. **Why does blood carbon dioxide have a more potent effect in stimulating the chemosensitive neurons than do blood hydrogen ions?** The blood-brain barrier is not very permeable to hydrogen ions, but carbon dioxide passes through this barrier almost as if the barrier did not exist. Consequently, whenever the blood PCO₂ increases, so does the PCO₂of both the interstitial fluid of the _ and the cerebrospinal fluid. In both these fluids, the carbon dioxide immediately reacts with the water to form new hydrogen ions. Thus, paradoxically, more hydrogen ions are released into the respiratory chemosensitive sensory area of the medulla when the blood carbon dioxide concentration increases than when the blood hydrogen ion concentration increases. For this reason, respiratory center activity is increased very strongly by changes in blood carbon dioxide levels. (PIC SHOWS WHAT OCCURS IN THE CSF)

Water Hydrogen Medulla

HOW DOES CARBON DIOXIDE (INDIRECTLY) STIMULATE THE NEURONS IN THE CHEMOSENSITIVE AREA?

. It does this by reacting with the water of the tissues to form carbonic acid, which dissociates into hydrogen and bicarbonate ions; the hydrogen ions then have a potent direct stimulatory effect on respiration

THE BLOOD-BRAIN BARRIER IS VERY PERMEABLE TO HYDROGEN IONS BUT NOT TO CARBON DIOXIDE. TRUE OR FALSE?

FALSE It isn't very permeable to hydrogen ions but carbon dioxide can pass through it a though it almost doesn't exist.

WHAT DOES CSF STAND FOR?

Cerebrospinal fluid

**_HENDERSON-HASSELBACH EQUATION_** (TURN OVER TOO)

**_REGULATION OF CO₂ DURING SUSTAINABLE EXERCISE_** **•Ventilation increases prior to rise in blood CO₂** The presumed reason that the ventilation forges ahead of the buildup of blood carbon dioxide is that the brain provides an “\_” stimulation of respiration at the onset of exercise, causing extra alveolar ventilation even before it is necessary. However, after about 30 to 40 seconds, the amount of carbon dioxide released into the blood from the active muscles approximately matches the increased rate of \_, and the arterial PCO₂ returns essentially to normal even as the exercise continues. * Arterial PCO₂ levels fall * As exercise proceeds, more CO₂ generated * CO₂ passes from muscles into venous \_ * Efficiently removed in lung * When exercise ceases, ventilation falls rapidly

Anticipatory Ventilation Blood

**_PERIPHERAL CONTROL RESPIRATION_** Fall in O₂ stimulates glomus cells in carotid and aortic bodies. * Contain O₂ sensitive K+ channels and dopamine * O₂ fall * O₂ sensitive K+ channels CLOSE * Depolarisation * DA release * Stimulates afferent fibres * Signals to medulla

**_REGULATION OF AFFERENT FIBRE ACTIVITY FROM THE CAROTID BODY BY O₂_**

**_RESPIRATORY STIMULANTS_** **Doxapram** Closes K+ channels on glomus cell (carotid body) •Glomus cell depolarises - sends afferent signals to medullary respiratory centre Central action at high dose Use in respiratory failure (rarely) **Caffeine** (& other xanthines) –Non-specific CNS stimulation, including respiratory centre –Bronchodilator (via phosphodiesterase inhibition?) –Used in sleep apnoea and premature babies. **Acetazolamide** Carbonic anhydrase inhibitor. Stimulates respiration by creating mild metabolic acidosis via decreased renal reabsorption of bicarbonate and hence reduced acid buffering. Carotid bodies respond to decreased pH (although fall O2 is primary drive)

WHAT ARE THREE EXAMPLES OF RESPIRATORY STIMULANTS?

Doxapram Caffeine Acetazolamide

ALCOHOL IS A STIMULANT. TRUE OR FALSE?

FALSE It is a depressant

**_RESPIRATORY DEPRESSANTS_**

**_WHY DO WE BREATHE?_** •O₂ needed for aerobic respiration –Krebs’ cycle cannot proceed without regeneration of \_. –\_ Transport Chain crucially dependent on O₂ •ATP generated by respiration required for all active processes –Active transport * Ionic gradients * Nutrient uptake –Anabolic reactions –Muscle contraction –Phosphorylation of targets –Precursor for cAMP •O₂ also needed to pay ‘oxygen debt’ after bursts of _ metabolism

Anaerobic NAD+ Electron

**_PARTIAL PRESSURE OF GAS_**

**_HOW MUCH O₂ IS CONSUMED?_**

**_BLOOD TRANSPORT_** ## Footnote CO₂ production measured in arterial blood •Normal arterial PCO₂ is about 37 mm Hg so Alveolar oxygen pressure PAO₂ = O₂ inspired – O₂ consumed = O₂ inspired – (CO₂ produced/RQ) = 150 – (37/0.8) mmHg = 104 mm Hg

**_DIFFUSION OF OXYGEN INTO TISSUES_**

HOW MANY OXYGEN MOLECULES CAN ONE HAEMOGLOBIN MOLECULE BIND?

**_OXYGEN RELEASE IN TISSUES_** * As oxygenated arterial blood reaches capillaries, O₂ released * Consumed by cells * Arterial PO₂ 100 mmHg * Venous PO₂ 40 mmHg

HAEMOGLOBIN BINDS CO-OPERATIVELY. TRUE OR FALSE?

TRUE

**_CO₂ TRANSPORT_** * CO₂ transported mainly (70%) as HCO₃^- * 7% as dissolved \_ * 23% as carbamino haemoglobin (HbCO₂) * CO₂ from tissues diffuses into plasma. * Most of this (80%) enters red blood cells and is converted to bicarbonate by carbonic \_. * When CO₂ production increased (exercise or disease) * Fraction of CO₂ increases relative to HCO₃^- * Passage into CSF and detection by central \_.

CO₂ Anhydrase Chemoreceptors

WHAT IS MOST CO₂ (70%) TRANSPORTED IN THE FORM OF?

HCO₃^-

**_GAS PRESSURES IN ALVEOLI AND BLOOD_** •PO2 same in alveolus and pulmonary vein, but much higher than in systemic veins (and hence the pulmonary artery) • •PCO2 higher in veins than alveolus and systemic arterial blood

**_GAS PRESSURES IN ALVEOLI AND BLOOD_** ## Footnote * PO₂ same in alveolus and pulmonary vein, but much higher than in systemic veins (and hence the pulmonary artery) * PCO₂ higher in veins than alveolus and systemic arterial blood

WHAT HAPPENS WHEN OXYGEN BINDS TO HAEMOGLOBIN?

* Haemoglobin becomes more acidic * Less formation of Hb.CO2 * Excess H+ bind bicarbonate to form carbonic acid * CO2 released

**_VENTILATION-PERFUSION MATCHING_**

WHAT IS HYPOXAEMIA?

Low oxygen levels

WHAT IS HYPERCAPNIA?

Increased CO₂ levels

**_CAUSES OF HYPOXAEMIA_** ## Footnote •Shunting –Anatomical –Unventilated alveoli * Ventilation-perfusion mismatch * Diffusion abnormalities –thickened alveolar wall •Hypoventilation –Neuronal defect or muscle weakness –Obstruction –drug-induced **_CAUSES OF HYPERCAPNIA_** Increased dead space -pulmonary embolus Hypoventilation

**_PHYSIOLOGICAL RESPONSE TO LOW INSPIRED OXYGEN_** **•Increased ventilation (immediate)** –Driven by peripheral chemosensors –Not sustained **•Pulmonary vasoconstriction (rapid and sustained)** –Homeostatic mechanism designed to shunt blood away from poorly ventilated areas –Not useful if the whole lung is hypoxic! **•Increased haematocrit (red cell fraction of blood \> 50%)** –HIF (hypoxia inducible factors) activation –HIF regulates oxygen-sensitive gene transcription * Erythropoetin production by kidneys * EPO stimulates bone marrow to make red blood cells

WHAT ARE THE THREE PHYSIOLOGICAL RESPONSES TO LOW INSPIRED OXYGEN?

Increased ventilation Pulmonary vasoconstriction Increased haematocrit

**_ALTITUDE SICKNESS_**