RS Lecture 9 and 10 - Acid Base Regulation and Sensory Aspects of Respiratory Disease Flashcards Preview

LSS 1 - Thorax anatomy, Respiratory and Circulatory system > RS Lecture 9 and 10 - Acid Base Regulation and Sensory Aspects of Respiratory Disease > Flashcards

Flashcards in RS Lecture 9 and 10 - Acid Base Regulation and Sensory Aspects of Respiratory Disease Deck (67):

What is alkalaemia?

Raised pH of blood


What is acidaemia?

Lowered pH of blood


What is alkalosis?

Describes circumstances that will decrease [H+] and increase pH


What is acidosis?

Described circumstances that will increase [H+] and decrease pH


What is the main equilibrium in the body?

H2O+CO2 H2CO3 H+ + HCO3-


What is the blood's buffering capacity?

It is huge and reacts almost immediately to imbalances


What is the equation for pH and [H+]?

pH= --log10[H+] [H+]= 10^-pH


What are the 2 types of acids in the body?

Respiratory acid (CO2) and metabolic acid (pyruvic acid, etc)


What is the Henderson equation and the Henderson-Hasselbalch equation?


What can we tell from an arterial blood gas sample?

Changes in pH, PaCO2, PaO2, BE


What are the values for PaO2 in the blood?

>10kPa is normal, 8-10 mild hypoxaemia, 6-8 moderate hypoxaemia, and


What are the 2 compensatory mechanisms?

Changes in ventilation can stimulate a RAPID compensatory response to change CO2 elimination and thus alter pH. Changes in HCO3- and H+ retention/secretion in kidneys can stimulate a SLOW compensatory response to increase/decrease pH


How can you compensate acidosis/alkalosis?

Acidosis needs alkalosis. Alkalosis needs acidosis.


What are the 2 compensatory mechanisms for respiratory acidosis?

Acute: CO2 moves into RBC , to combine with H2O to from H+ and HCO3- which is transported via the AE1 transporter into the blood, where they join with the excess H+ to form conjugate acid, increasing pH Chronic: Increasing reabsorption of HCO3- in the nephron


How is metabolic alkalosis compensated for (graph)?


How is metabolic acidosis compensated for (graph)?


How is respiratory alkalosis compensated for (graph)?


How is respiratory acidosis compensated for (graph)?


What are the 4 basic disturbances and what do they cause?

Hypoventilation -> respiratory acidosis. Hyperventilation -> respiratory alkalosis. Diarrhoea -> metabolic acidosis. Vomiting -> metabolic alkalosis


How do you interpret ABG?

Type of imbalance (alkal/acidaemia); aetiology of imbalance (respiratory, metabolic or mixed); homeostatic compensation present (UC, PC, FC); oxygenation (hypoxaemia, normoxaemia, hyperoxaemia)


What are the normal values of [Hb], pH, PCO2, PO2, HCO3-, BE and standard BE?


How do you interpret blood gases? -> chart


Work out these acid-base problems:


What is the prevalence of cough, chest pain and shortness of breath as respiratory symptoms?

Cough -> 3rd most common complaint heard by GP. Chest pain -> most common pain for which medical attention is sought. SOB: 6-27% of general popn; 3% of visits to GP


What are some signs and symptoms that can be seen in respiratory diseases?

Symptoms: cough, chest pain, shortness of breath. Signs: hyperinflation of chest, dullness on percussion of chest wall, increased resp rate, reduced movement of chest wall


What is the physiologic/pathologic stimulus leading to conscious sensation pathway?

Sensory stimulus -> transducer (sensor) -> excitation of sensory nerve -> integration of CNS -> sensory impression (neurophysiology) => sensory impression -> perception -> evoked sensation (behavioural psychology)


What is a cough?

Crucial defense mechanism protecting the LRT from inhaled foreign material and excessive mucous secretion


When does a cough occur?

Secondary to mucociliary clearance (usually), but is important in lung disease when mucociliary function is impaired and mucous production is increased


What is the function of the expulsive phase of cough?

Generates high velocity of airflow, which is facilitated by bronchoconstriction and mucus secretion


Where are cough receptors located and what are they?

Nerve profile - rapidly adapting irritant receptors; located within airway epithelium, most numerous on posterior wall of trachea -> present at main carina and branching points of large airways, less numerous in more distal airways, absent beyond bronchioles -> possibly in pharynx, external auditory meatus, eardrums, paranasal sinuses, diaphragm, stomach, pleura, pericardium


What is the stimuli for cough receptors?

Laryngeal and tracheobronchial receptors respond to chemical and mechanical stimuli


What are the 3 types of sensory receptors in the lung and airways?

Slowly adapting stretch receptors, rapidly adapting stretch receptors and C-fibres


What are c-fibre receptors?

Free nerve endings -> small unmyelinated fibres


Where are c-fibre receptors located?

Larynx, trachea, bronchi, lungs


What stimulates C-fibres and what do they release in response?

Stimulates: chemical irritants, inflammatory mediators. Release: neuropeptide inflammatory mediators Substance P, neurokinin A, calcitonin gene related peptide


Where are the rapidly adapting stretch receptors present and what are they?

Naso-pharynx, larynx, trachea, bronchi -> small myelinated nerve fibres


What stimulates the rapidly adapting stretch receptors?

Mechanical, chemical irritant stimuli and inflammatory mediators


Where are the slowly adapting stretch receptors present and what are they?

In airways smooth muscle, predominantly in trachea and main bronchi -> myelinated nerve fibres


What stimulates the slowly adapting stretch receptors?

They are mechanoreceptors so respond to lung inflation


What are the 2 types of receptors innervating the trachea and what do they react to?

Mechanoreceptors (mechanical displacement, citric acid) and Nociceptors (Capsaicin, bradykinin, citric acid, cinnamaldehyde)


What are the afferent neural pathways for cough?

Stimulation of irritant receptors or cough receptor by mechanical or chemical stimuli


What is the cough pathway?


What are the mechanics of cough?

Inspiratory phase -> glottic closure -> expiratory phase (sound)


How do the sounds of cough form?

2 phases with initial explosive phase that is the first cough sound, followed by an intermediate phase with decreasing sound -> additional 3rd phase called the voiced/glottal phase gives rise to second cough sound


What are the common causes of cough?


What is an acute cough caused by and what are some symptoms associated with it?

Caused by common cold - present for cough, post nasal drip, throat clearing, nasal blockage/discharge


What is a chronic persistent cough caused by?

> 3wks -> asthma/eosinophilic related (25%), Gastro-oesophageal reflux (25%), rhinosinusitis (20%), chronic bronchitis (8%), bronchiectasis (5%), drugs (ACE inhibitor 1%), post-viral (3%), idiopathic (10%), others (3%)


What is chronic cough?

Indication of increased cough reflex -> cough hypersensitivty syndrome -> irritation in the throat/upper chest, cough paroxysms difficult to control (not throat clearing)


What triggers cough hypersensitivity syndrome to cough?

Deep breath, laughing, talking too much, vigorous exercise, smells, cigarette smoke, eating crumbs, cold air, lying flat


What is plasticity of neural mechanisms?

Excitability of afferent nerves increased by chemical mediators, increase in receptor/VGC's, NT increase


What are the mechanisms of chronic cough?



What are the current antitussive types?

Symptomatic suppressant therapies, disease-specific therapies


What are some examples of symptomatic suppressant therapies for antitussives?

Central action: opiates -> dihydro/phol/codeine, dextromethorphan (dia/morphine). Peripheral action: eosinophil-associated -> inhaled corticosteroids; GORD -> H+ pump inhibitors, H2 antagonists; post-nasal drip -> topical steroids, antihistamines; bronchiectasis -> postural drainage, Ab


How do we manage cough hypersensitivity syndrome?

As sensory neuropathic cough -> Speech pathology management: ^ voluntary control, decrease cough sensitivity/laryngeal irritation/laryngeal muscle contraction; Pharmacology -> amitryptiline, gabapentin, opiates


What is the sensory input to the lungs, airway and chest wall?

Nose (CNV), pharynx (CNIX/X), larynx/lungs (CNX), chest wall (spinal nerves)


How does pain sensation reach the brain?

NB: the nerves change sides in the dorsal horn (contralateral)


How does touch sensation reach the brain?

NB: the nerves change sides in the medulla


What are the different types of pain?

Visceral pain is difficult to localise, diffuse and referred to somatic structures. Somatic pain is like that from skin. Much less number of visceral afferents than somatic


What can cause chest pain in the respiratory system?

Pleuropulmonary disorders: pleural inflammation, pneumothorax, malignancy. Tracheobronchitis -> infections, inhalation of irritants. Inflammation or trauma to chest wall -> Rib fracture, muscle injury, malignancy, herpes zoster.


Where does diaphragmatic irritation refer to?

Shoulder tip


What non-respiratory disorders can cause chest pain?

CVD: myocardial infarction, pericarditis, dissecting aneurysm, aortic valve disease. GID: oesophageal rupture, GORD, cholecystitis, pancreatitis. Psychiatric disorders: panic disorder, self-inflicted


What is dyspnoea?

Shortness of breath, occurring at inappropriately low levels of exertion and limits exercise tolerance


What is the clinical dyspnea scale?


What is the modified Borg scale?


What are the 3 types of breathlessness?

Air hunger, work/effort and tightness


Which disorders present with dyspnoea?

Impaired pulm function (airflow obstruction, restriction of lung mechanics, extrathoracic pulmonary restriction, NM weakness, gas exchange abdnormalities); imparied CV function (Myocardial disease leading to HF, valvular/pericardial /pulm vascular/ congenital vascular disease); altered central ventilatory drive/perception (systemic/metabolic disease, metacidosis, anaemia)


How do you treat dyspnoea?

Treat the cause, therapeutic options: add bronchodilators, drugs affecting brain, lung resection, pulmonary rehabilitation

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