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Year 2 semester 3 respiratory system > Session 12 > Flashcards

Session 12 Flashcards

1
Q

Respiratory acidosis

A

Respiratory acidosis – • When breathing is inadequate (reduced respiratory rate and/or depth) • Inadequate ventilation • Carbon dioxide removal insufficient • CO2 retention
↑CO2 + H2O H2CO3 HCO3- + ↑ H+
• Equation moves to the right • Leads to an increase in H+ (acidosis) • Causes include: • narcotic overdose, • head injuries, neurological/muscle disease, • severe COPD,

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2
Q

Respiratory alkalosis

A

Respiratory alkalosis: • Hyperventilation (increased rate and depth of breathing) • Excessive Carbon dioxide removal • causes a reduction in plasma carbon dioxide
↓CO2 + H2O H2CO3 HCO3- + ↓ H+
• Equation moves to left • Leads to an decrease in H+ (alkalosis) • Causes of hyperventilation include: • Panic attack • Hyperventilation due to low O2 levels … e.g. Pulmonary embolism

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3
Q

Metabolic acidosis

A

Metabolic acidosis: • Extra acid formed /added to body – Diabetic ketoacidosis, lactic acidosis etc. • Or excessive loss of HCO3- from the body (GI or renal)
• Excess of H+ • Equation moves to left  More CO2 formed, HCO3- drops • Increased H+ stimulates peripheral chemoreceptors • The CO2 formed (+ more CO2) breathed out  respiratory compensation

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4
Q

Metabolic alkalosis

A

Metabolic alkalosis: • Loss of acid from body (prolonged vomiting etc.)
• Increased HCO3- retention by kidney
• loss of H+ • Equation moves to right  CO2 used up; More HCO3- formed, • Low CO2 detected by chemoreceptors, corrected by hypoventilation • But amount of hypoventilation is limited as PO2 cannot drop too much, so very limited resp. compensation
CO2

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5
Q

Renal Compensation for respiratory acidosis and respiratory alkalosis

A

pH is determined by the ratio of [HCO3- ]: [CO2] in the plasma (20:1)

Renal compensation of Respiratory acidosis
• Kidney reabsorbs all filtered HCO3• It also generates extra HCO3• For every extra HCO3- which enters blood one H+ excreted • HCO3- level rises, • Ratio returns towards 20:1 • pH returns towards normal (both CO2 and HCO3 are high but ratio normal)
insert equations when watching panopto
Renal compensation of Respiratory alkalosis
• Kidney excretes the filtered HCO3• Also stops generating new HCO3-& excreting H+ ions • HCO3- level drops • Ratio returns towards 20:1 • pH returns towards normal (both CO2 and HCO3-are low but ratio normal)

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6
Q

recovery and creation of HCO3

A

slide 8 lec 1

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7
Q

The anion gap

A

• Total anions = Total cations • But not all anions and cations are measured
• Difference between measured cations and anions = the anion gap
• ([Na+] + [K+]) – ([Cl-] + [HCO3-]) = Normally 10 – 18 mmol/L
Example: Na+ =140, Cl-=110 K+ =4, HCO3-= 24
Then (140 + 4) – (110 + 24) = 10 mmol/L
This 10 mmol/L are unmeasured anions like SO4–, phosphate, lactate, & protein anions present in the blood.
• Increased anion gap seen in metabolic acidosis (some types)
where extra acid is generated (or added to the body) e.g. • In DKA – Ketoacids ( anion: acetoacetate ) • In hypoxia –lactic acid ( anion: lactate) • In AKI /CKI – retention of acids normally excreted by kidney
• the metabolic acid (e.g. lactic acid) reacts with HCO3- , so HCO3 level drops.
Example: patient with hypoxia, with extra lactate in blood. • cations (148 + 5) = anions (110 + 15 + A- ) A- = all unmeasured anions • 153 – 125 = anion gap is 28 (higher than normal, as extra lactate is included)
Metabolic acidosis with a normal anion gap
• Due to GI or renal loss of HCO3• HCO3- is low but this is replaced by Cl- (HCO3- low, but Cl- high)
• Hence, the anion gap is unchanged e.g. renal tubular acidosis)

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8
Q

Acidosis & hyperkalaemia

A

Changes in ECF pH causes reciprocal shifts of H+ and K+ between the ECF & ICF
In all cells (muscle, liver, kidney etc)
Acidosis  shift of H+ into cells Reciprocal K+ shift  out of the cells to ECF
Acidosis leads to hyperkalaemia

In kidney this reciprocal K+ shifts out of the principal cells  low intra cellular K+
Hence renal K+ secretion is reduced Potassium is retained  Contributing to the hyperkalaemia

Similarly, changes in ECF [K+] causes reciprocal shifts in K+ and H between the ECF & ICF In all cells (muscle, liver, kidney etc)

Hyperkalaemia  shift of K+ into cells
Internal balance
Reciprocal H+ shift  out of the cells
Hyperkalaemia leads to acidaemia
In kidney this reciprocal H+ shifts out of the intercalated cells  intra cellular alkalosis
Hence less H+ secreted by intercalated cells , less HCO3 is reabsorbed / generated  Contributing to the acidaemia

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9
Q

Alkalosis and Hypokalaemia

A

Changes in ECF pH causes reciprocal shifts of H+ and K+ between the ECF & ICF

In all cells (muscle, liver, kidney etc)
K+ H+H + K+
Internal balance
Alkalosis  shift of H+ out of cells Reciprocal K+ shift  into the cells Alkalosis leads to hypokalaemia
In kidney this reciprocal K+ shifts into the principal cells  high intra cellular K+ Hence renal K+ secretion is increased Potassium is lost  Contributing to the hypokalaemia

Similarly, changes in ECF [K+] causes reciprocal shifts in K+ and H between the ECF & ICF In all cells (muscle, liver, kidney etc)
Hypokalaemia  shift of K+ out of cells
Internal balance
Reciprocal H+ shift  into the cells
Hypokalaemia leads to alkalaemia
In kidney this reciprocal H+ shifts into intercalated cells  intracellular acidosis
Hence more H+ secreted by intercalated cells , more HCO3 is reabsorbed / generated  Contributing to the alkalaemia

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10
Q

peripheral chemoreceptors and centra chemoreceptor changes

A

slide 17 panopto and slide 18 and 19

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11
Q

Some disease states leading to acidosis/ alkalosis

A

• Panic attack  increased ventilation (hyperventilation) driven by higher (emotional ) centres  low pCO2 (respiratory alkalosis)  acts on central chemoreceptors to ↓ ventilation, but higher centres overrides this to continue hyperventilation  low pCO2 & respiratory alkalosis
• High altitude low inhaled pO2  hypoxia  stimulates peripheral chemoreceptors  hyperventilation  low pCO2 & respiratory alkalosis, some improvement of pO2
• Lactic acidosis (e.g. septic shock due to pneumonia)  ↑ [H+] ions stimulate peripheral chemoreceptors  hyperventilation  low pCO2 (respiratory compensation of metabolic acidosis)
• Lung fibrosis (or pulmonary oedema)  Diffusion defect  low pO2, but pCO2 normal (since CO2 more soluble, diffuses more easily than O2)  hypoxia stimulates peripheral chemoreceptors  increased ventilation  pCO2 normal or low,
some ↑ in PO2, but hypoxia persists Type 1 respiratory failure  (with a degree of respiratory alkalosis, if pCO2 is low)
• Respiratory muscle failure (e.g. Myasthenia gravis)  HYPOVENTILATION  both hypoxia & hypercapnia
 stimulates both peripheral and central chemoreceptors (synergistic effect) 
increased neural responses from respiratory centre  but unable to increase ventilation because problem at NMJ  muscles unable to respond
Type 2 Respiratory failure  low pO2, high pCO2  Respiratory acidosis
• Similar course of events in other causes of hypoventilation with type 2 resp failure e.g:
Narcotic overdose  Resp centre depressed  reduced rate and depath of ventilation  hypoventilation  low pO2, high pCO2  stimulates both peripheral and central chemoreceptors (synergistic effect) 
but respiratory centre unable to respond appropriately  hypoventilation persists  (Type 2 Respiratory failure  Respiratory acidosis)
• Chronic severe COPD  when widespread airway narrowing  Hypoventilation of entire lung  Chronic type 2 Resp. failure
 both chronic hypoxia & hypercapnia  both peripheral and central chemoreceptors are stimulated  increased ventilation  some improvement in pO2 and pCO2  but a degree of hypoxia and hypercapnia persists, to which the body acclimatises
(eg. EPO  ↑Hb ; renal compensation of respiratory acidosis etc.)
• In Chronic hypercapnia  can result in “reset of central chemoreceptors”  the hypoxia acting via peripheral chemoreceptors is responsible for the increased rate and depth of ventilation that is needed
• Pneumonia  V/Q mismatch in part of lung  hypoxia (& initial hypercapnia)  initially stimulates both peripheral & central chemoreceptors  hyperventilation
 hypoxia not corrected, but pCO2 returns to normal or below normal  the persistent hypoxia stimulates peripheral chemoreceptors  hyperventilation continues  low pO2 persists, but normal or low pCO2
Type 1 respiratory failure  Respiratory alkalosis (if pCO2 is low)
• Similar course of events in other causes of V/Q mismatch (e.g Pulm. Embolism, acute
asthma etc)

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12
Q

Respiratory failure

A

• Type 1 Respiratory failure – hypoxia only - pO2 low, pCO2 normal or low 1. Ventilation/Perfusion mismatch
2. Diffusion defect –
• Type 2 respiratory failure - pO2 low, pCO2 high
• Hypoventilation
• NB: Type 1 may progress to Type 2 as disease progresses
• More than 1 mechanism ( eg. V/Q mismatch + diffusion defect) may be operating

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13
Q

Lobar pneumonia

A

Features on CXR • Opacity corresponds to affected lobe • Non - homogeneous opacity • Air bronchogram may be present
Air bronchogram
Air outlining the branches of the bronchial tree

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14
Q

Pleural effusion

A

Pleural Effusion • Homogenous density • Density in dependent portion • Curved upper margin (meniscus) • Upper margin higher laterally than medially (yellow arrows on image on right) • Lack of identifiable left diaphragm before and visible diaphragm after clearance of fluid
If large effusion - Mediastinal shift may be present

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15
Q

Differentiating between consolidation in lower zone (lobar pneumonia) and pleural effusion

A

Lobar pneumonia • Opacity corresponds to affected lobe • Non - homogeneous opacity • Upper border not curved • Can see outline of diaphragm

Pleural effusion - • Fluid always collects in the most dependant part – opacity is in lower zone • More dense, Homogeneous opacity • Upper border curved (meniscus) • Cannot see outline of diaphragm

Pneumonia vs Pleural effusion
Pneumonia
Pneumonia: Inflammatory exudate is inside alveoli, pleural space is clear
Pleural effusion: Fluid is in the pleural space; Alveoli are clear

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16
Q

Lobar pneumonia versus Pulmonary TB (active)

A

Lobar pneumonia
Acute illness – days High fever Cough with purulent sputum (± Haemoptysis) Pleuritic chest pain Breathlessness
Pulmonary TB
Chronic illness – weeks, months Malaise, weight loss Low grade fever Cough with scanty mucoid sputum, Haemoptysis ± High risk group

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17
Q

Pulmonary T and how its diagnosed?

A

Pulmonary TB
• Apex often involved
• Ill defined patchy consolidation
• Cavitation usually develops within consolidation
• Healing results in fibrosis
How can active pulmonary TB be diagnosed?
By demonstrating:
• Positive sputum smear for acid fast bacilli (using Ziehl –Nielson stain)
• Positive culture for TB bacilli
• Nucleic acid amplification tests (esp for smear positive patients)

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18
Q

This man has a permanent pacemaker. The pacing wires were introduced via subclavian vein What complication is seen on the CXR?
slide 38

A

Pneumothorax • Affected side (right) is hyperlucent (darker) • with absent lung markings • Edge of collapsed lung seen (arrows)-lung
collapses towards hilum
• No tracheal shift because it is a non-tension
pneumothorax

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19
Q

Tension pneumothorax vs pneumothorax

A

inser slide 39 with text

20
Q

Diaphragm normal position

A

Diaphragm – normal position
Surface marking In a live person: (at end of quiet expiration)
Dome of R/hemi diaphragm = level of 4th ICS anteriorly (some sources 5th rib anteriorly)
Dome of L/ hemi diaphragm = level of 5th ICS anteriorly
Percussion note: dull below this level
On a Chest x-ray (because CXR taken in deep inspiration)
diaphragm crosses the Anterior part of 6th rib
insert pic from slide 40

21
Q

Hyperinflated lungs (Asthma, COPD) vs Pneumothorax

A

inset slide 41

22
Q

Compare the two x-rays

slde 42 images

A

whole of slide 42

23
Q

Portions of the respiratory tract and how cells lining each part change

A

insert entire slide 47 ec 1

24
Q

The ALVEOLUS & SURFACTANT

A

Surfactant:  Lines alveoli  Mix of phospholipids and lipoproteins  Diminishes the surface tension of the water film that lines alveoli  Thereby decreasing the tendency of alveoli to collapse  and the work required to inflate them

25
Q

Dead space, pulmonary ventilation and alveolar ventilation

A

Anatomical dead space = The volume of air in the conducting airways
Alveolar dead space = air in alveoli which do not take part in gas exchange (These are alveoli which are not perfused or are damaged) - in a healthy adult alveolar dead space can be considered negligible.
Physiological dead space = anatomical dead space + alveolar dead space = the volume of ventilated air that does not participate in gas exchange
Tidal volume – amount of air inspired and expired at rest– usually about 500 ml of which ~ 350 ml occupies dead space
Total Pulmonary Ventilation (Minute ventilation)= Tidal volume x respiratory rate
Alveolar ventilation = (Tidal volume – Dead space) x respiratory rate

26
Q

Chronic bronchitis – airways disease

A

• Chronic bronchitis is a disease of the airways – from bronchi to bronchioles • Mucus hypersecretion (from goblet cells & sub mucus glands) • Reduced cilia – mucus is not cleared effectively • Effects of above lead to • airflow limitation/obstruction by luminal obstruction of small airways • epithelial remodeling, • alteration of airway surface tension predisposing to collapse • Clinical diagnosis – cough productive sputum > three months of the year for > one year

27
Q

Causes of excessive mucus in chronic obstructive pulmonary disease

A

slide 51

28
Q

COPD- Emphysema – air sacs disease

A

Definition:
 Abnormal, permanent enlargement of the air spaces distal to the terminal bronchiole
 With destruction of alveolar walls (No fibrosis)
 Inflammatory cells accumulate; which release elastases and oxidants  destroy alveolar walls and elastin
 Protease mediated destruction of elastin is an important feature
 Reduced elasticity is a key problem – airway trapping
 Also, large air spaces  reduced surface area for gas exchange

29
Q

CXR for paients with emphysema compared to normal

A

slide 53

30
Q

Chronic obstructive pulmonary disease (COPD)

A

• Chronic Obstructive Pulmonary Disease (COPD) is not one single disease but an umbrella term used to describe chronic lung diseases that cause limitations in lung airflow • People with COPD will have a mix of chronic bronchitis and chronic emphysema – but one person may have more emphysematous lungs (ie more air sacs disease) and one may have more chronic bronchitis type lungs ( ie more chronic sputum production) • Management of COPD includes • Making the diagnosis • Reducing risk factors – smoking cessation • Pharmacotherapy for COPD is used to decrease symptoms and complications – inhalers and/or oxygen • Manage exacerbations

31
Q

What is Bronchiectasis

A

• DEFINITION: Chronic IRREVERSIBLE dilatation of one or more bronchi – it is a pathological condition that can be caused by many diseases or be idiopathic- resulting in abnormally enlarged bronchi • These deformed bronchi exhibit poor mucus clearance and there is predisposition to recurrent or chronic bacterial infection
• AETIOLOGY: variety of underlying causes, with a common underlying mechanism of of chronic inflammation • Inflammation causes destruction of the elastic and muscular components of the bronchial wall and peribronchial fibrosis • RADIOLOGICAL FINDINGS • CXR - usually abnormal but inadequate in the diagnosis or quantification of bronchiectasis/ bronchial dilatation
• Gold standard diagnostic investigation = CT - specifically High Resolution CT • We find - bronchial dilatation bigger than the adjacent blood vessel, bronchial wall thickening
slide 56

32
Q

Bronchiectasis Management

A
  • PHYSIO / AIRWAYS CLEARANCE – Daily airway clearance is essential for treatment success – • Aerosolised saline solutions • Smoking cessation
  • Sputum sampling – routine culture and NTM
  • Exclude immunodeficiency / treat identifiable causes
  • Consider long-term therapies at future visits
  • Annual Flu & routine vaccinations against Haemophilus influenzae and Streptococcus pneumoniae
  • An established MDT is key
  • Management plan for infective exacerbations
33
Q

Differentiating chronic bronchitis, bronchiectasis, asthma, emphysema and bronchiolitis

A

slide 58

34
Q

Ventilation and perfusion

A

Gas exchange optimal when: • V/Q ratio of individual alveolar units ≈ 1
• 300 million alveoli - may have widely differing amounts of ventilation and of perfusion.
• Ideally, • Alveoli with ventilation should have perfusion
• Alveoli with ventilation should have perfusion
• When pulmonary capillary PaO2 is low, hypoxic vasoconstriction of pulmonary arterioles occurs this diverts blood to better ventilated alveoli • When alveolar PA CO2 is low, bronchoconstriction occurs – This diverts air to better perfused lung • BUT
• This process is not 100% efficient, so in some disease states, poorly ventilated alveoli still have significant perfusion – this is what is meant by ventilation-perfusion MISMatch

35
Q

Normal physiology of lung ventilation and perfusion

A

slide 60

36
Q

Gas composition in a normal alveolus

A

slide 61

37
Q

Consequences of Inadequate Ventilation of an alveolar unit

A

slide 62

38
Q

V/Q mismatch with V/Q ratio <1

Some causes:

A

• Asthma (airway narrowing – not uniform throughout lungs • COPD early stages – not uniform throughout lungs • Pneumonia -acute inflammatory exudate in affected alveoli • RDS in newborn -some alveoli not expanded and not uniform • Pulmonary oedema -fluid in alveoli - not uniform throughout lungs
V/Q mismatch is the commonest mechanism causing hypoxia

39
Q

oxygen-haemoglobin dissociation curve as oxygen partial pressure increases – between 10.6 kPa (80mm Hg) to 16 kPa (120 mmHg)
True or false?
As pO2 increases from 10.6 kPa to 13.3 kPa9 haemoglobin saturation markedly increases by greater than 20%
slide 64 graph

A

panopto

40
Q

Graph showing relationship between PCO2 and total CO2 content in blood
slide 65

A

 Relatively straight line in the physiological range pCO2 i.e. there is a linear relationship between pCO2 and blood total content CO2 @ 4-6kPa  This is because CO2 Is highly soluble in blood
 Unlike O2 it doesn’t require a carrier molecule – remember O2 carrier molecule is Hb
 This explains why CO2 in blood is directly proportional to alveolar minute ventilation while O2 is NOT – after a certain point can’t load more haemoglobin with O2 no matter how high pO2

41
Q

Addiction related to smoking

A
  1. Cigarette smoking is a chronic relapsing disorder that starts in adolescence 2. Nicotine causes the addiction, not the harm from tobacco
    Markers of Addiction:
    • use despite knowledge of harmful consequences • cravings during abstinence • failure of attempts to stop • withdrawal symptoms during abstinence
42
Q

Physiology of nicotine addiction

A
  • Nicotine acts on nicotinic acetylcholine receptor stimulating dopamine release
  • This results in the satisfaction associated with smoking
  • Following chronic nicotine exposure, ACh enter upregulated state - increases affinity and functional sensitivity to an agonist
  • A drop in nicotine levels leads to craving and withdrawal
  • 1-2 puffs of a cigarette binds to 50% ACh receptors
  • ACh receptors take between 6-12 weeks to desensitise after the last cigarette
43
Q

Treating tobacco related disease

A

insert slide 11
Pharmacological
treatments: nicotine patches/tablets/sprays
E-cigarettes (harm reduction):
• Smoking tobacco kills
• Harm reduction strategy can help those who can’t quit tobacco
• E-cigarettes part of a harm reduction strategy

44
Q

3 As

A

Ask - smoking staus
Advise patients of health benefits of quitting
Act on a patients response - build confidence, give information, refer prescribe, offer nhs stop smoking service.

45
Q

Arguments for and against nicotine use in smoking cessation

A

Against • Continued nicotine use • Long term effects unknown • Dual use perpetuates smoking • ‘Renormalise’ smoking • Promotes nicotine in young • Gateway to tobacco • Products unsafe • E-cigs made by tobacco companies • Joint marketing of tobacco & ecigs

For • Nicotine is a minor health risk • Negligible compared to tobacco • Quit rates continue to decrease • Normalises E-cigs not tobacco • Compared to tobacco favourable • Experimenters are same group • About to be regulated • Bigger reach for harm reduction • Regulations coming into place

Year 2 semester 3 respiratory system (13 decks)

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