Respiratory Failure Flashcards

Question

Clinical features of Hypercapnia

Answer 1

Variable patient to patient Irritability Headache Papilloedema Warm skin Bounding pulse Confusion Somnolence (tiredness/sleepy) Coma

Answer 2

Airway patency Oxygen delivery Primary cause (eg antibiotics for pneumonia) Treatment with O2 may be more difficult eg COPD rely on hypoxia to stimulate respiration

Answer 3

Invasive (facial mask) and non invasive (endotracheal tube)

Answer 4

Inadequate PaO2 despite increasing FiO2 Increasing PaCO2 Patient tiring

Answer 5

Under tongue

Answer 6

5-10 litres/min face mask or 2-6 litres/min nasal cannulae Aim for SpO2 of 94-98% If saturation <85% and not at risk of hypercapnic respiratory failure 10-15 litres / minute reservoir mask Patients with COPD and other risk factors for hypercapnia; Aim for SpO2 of 88-92% pending blood gases Adjust to SpO2 of 94-98% if CO2 normal unless previous history of high CO2 or ventilation

Answer 7

Pneumonia Asthma

Answer 8

Overdose Trauma

Answer 9

Fibrosing lung disease

Answer 10

COPD neuromuscular

Answer 11

Patients have a new baseline due to habituation (normal level is hypoxaemia) Giving oxygen will get rid of drive to breathe Also, will change V/Q ratio due to reduced hypoxia related arterial vasoconstriction

Answer 12

Loss of taste

Answer 13

5-10 L/min

Answer 14

10-15 L/min If saturation <85% and not at risk of hypercapnic respiratory failure

Answer 15

88-92 % pending blood gases 94-98% if CO2 normal unless previous history of high CO2 or ventilation

Answer 16

Controlled oxygen therapy Known FiO2

Answer 17

Uncontrolled oxygen delivery More stable patients Unknown FiO2- pockets of high FiO2 develop in nasopharynx

Answer 18

During hyperventilation, large volume of CO2 lost—> as CO2 is acidic causes blood to become more alkaline (raising pH) To compensate for loss of CO2, kidneys begin to secrete alkaline HCO3- into the urine in exchange for H+ ions

Answer 19

Increases due to reduced elastic recoil of lung tissue due to reduced elastic tissue

Answer 20

Hypoxic drive

Answer 21

Grain Wood Laboratory Animals Fish Latex Enzymes

Answer 22

Glutaraldehyde Isocyanates Paints metal working fluids Metals Chemicals Sterilising agents

Answer 23

common chronic inflammatory disease of the airways characterized by variable and recurring symptoms reversible airflow obstruction and bronchospasm. common symptoms include wheezing, coughing, chest tightness, and shortness of breath

Answer 24

wheezing, coughing, chest tightness, and shortness of breath

Answer 25

5-16% of people worldwide have asthma Wide variation between countries Increase in prevalence second half of the 20th century Now plateaued mostly US study; Poorer individuals, African-Americans Many studies identify a wide range of risk factors Hygiene hypothesis, Berlin

Answer 26

Emergency attendances Atlanta Poaceace (grass) and Quercus (oak) species investigated Levels associated with emergency room attendances Oak pollens particularly important in children aged 5-17 years old Australian thunderstorm data

Answer 27

Farm life protected the subsequent development of asthma Early and in utero life seem to have an important role Specific agents not identified, but likely to be a mix of bacterial and other agents, potentially altering gastrointestinal immune response Airway bacteria may also play a role in causing asthma, role of rhinovirus

Answer 28

Important roles in the development of allergic illnesses Birth cohort study Development and severity of asthma @ 7 years Children’s home sampling aged 8 months 24% had asthma aged 7 Associations with fungal exposure (aspergillus and penicillium) and subsequent asthma

Answer 29

Cat ownership and exposure most implicated Exposure at home is associated with sensitisation as judged by IgE, but; Timing and intensity to pet exposures appear important

Answer 30

Air pollution; aggravating lung diseases; Responses to pollutants can be analogous to viral responses Asthma hospitalisations relate to PM2.5 and PM10 Air pollution; inducing allergy less clear Swedish birth cohort study NO exposure in the first year of life related to pollen sensitisation at 4 years old Increasing evidence

Answer 31

is an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled agents Acute, sub acute and chronic forms (fibrotic, non fibrotic) Immune complex related disease Antigen reacts with antibody Normally IgG response Very significant environmental influences; farmers lung, bird fanciers lung, metal working fluids

Answer 32

Farmers lung (eg animals, mouldy straw and hay) Bird fanciers lung Metal working fluids Musical instruments Microbiological and chemical agents from the environment and work place

Answer 33

Hot tub use in general identified as a cause of EAA (hypersensitivity pneumonitis) One of the first descriptions; 1997 (Kahana et al 1997) Two recent cases of HP Case of a 49 year old male, 2 months of fever, weight loss, shortness of breath and cough Regular hot tub use Sputum grew Mycobacterium fortuitum The hot tub drain and shower drain swabs were smear positive, with cultures demonstrating M fortuitum Re-presented with further problems 2 months later, and admitted a relapse of his ban on hot tubs

Answer 34

type of obstructive lung disease characterized by chronically poor airflow. It typically worsens over time, with the main symptoms include: shortness of breath, cough, and sputum production

Answer 35

Tobacco smoking main cause (contains cadmium) Other causes include occupational exposures such as; Silica, Coal, Grain, Cotton, Cadmium PAH, Isocyanates, Iron/steel processing, Agricultural dust, biomass fuels, Wood dust

Answer 36

Lungs susceptible to infection from inhaled microbiological agents (i) bacteria [e.g. pseudomonas], viral [e.g. COVID-19]

Answer 37

Silica Coal Grain cotton Cadmium

Answer 38

Pleural plaques Pleural thickening Benign pleural effusions Asbestosis Lung cancer Malignant mesothelioma

Answer 39

Regional variation in the lung Inflammation of bronchioles

Answer 40

Turkish denim sandblasters

Answer 41

Genetics Preterm birth Early life environmental exposures LRTI Childhood persistent asthma

Answer 42

Asthma runs in families Children of asthmatic parents are at increased risk of asthma Asthma is not caused by a single mutation in one gene Transmission of the disease through generations does not follow simple Mendelian inheritance typical of classic monogenic diseases New genotyping technologies has made it possible to sequence the human genome for asthma-associated variants

Answer 43

Individualise pharmacotherapy based on genetic polymorphisms Certain drugs are administered only to those patients who are most likely to respond Harmful effects are avoided in patients who are most likely to experience toxicity and adverse reactions Candidate genes for such studies are those encoding receptor proteins and enzymes involved in drug transportation, processing, degradation and excretion.

Answer 44

Chronic genetic disease Multi-organ involvement In UK >10,000 people affected Median age of death improving Most common lethal autosomal recessive genetic disorder in Caucasians Static incidence with an increasing prevalence

Answer 45

Defect in long arm of chromosome 7 coding for the cystic fibrosis transmembrane regulator (CFTR) protein (anion channel) >1600 mutations of CFTR gene identified 90% within a panel of 70 mutations F508del most common mutation causing CF

Answer 46

Transport protein on membrane of epithelial cells Abnormal CFTR protein leads to dysregulated epithelial fluid transport 80% Lung and gastrointestinal involvement 15% Lung alone

Answer 47

Bronchitis —> bronchiectasis —>fibrosis

Answer 48

Genetic profile and neonatal screening (day 5 IRT) Clinical symptoms – frequent infections, malabsorption, failure to thrive Abnormal salt / chloride exchange – raised skin salt Late diagnoses via infertility services – azoospermia or via gastroenterology team with recurrent pancreatitis / malabsorption 50% diagnosed @ 6 months 90% diagnosed @ 8 years of age

Answer 49

Persistent cough with productive thick mucus Wheezing and shortness of brewth]frequent chest infections Sinusitis Nasal polyps

Answer 50

Bowel disturbances Weight loss Obstructive Constipation

Answer 51

Osteoporosis Arthritis

Answer 52

95% men and 20% women are infertile

Answer 53

FEV1 increases to 100% as you age up until mid-20s as lungs are still growing Lung function then plateaus and begins to decrease

Answer 54

blockage of exocrine ducts, early activation of pancreatic enzymes, and eventual auto-destruction of the exocrine pancreas Most patients require supplemental pancreatic enzymes

Answer 55

Does NOT follow Mendelian inheritance But runs in families

Answer 56

Bulky stools can lead to intestinal blockage

Answer 57

mucus retention, chronic infection, and inflammation that eventually destroy lung tissue There are multiple hypotheses regarding the pathogenesis of lung disease, each of which is supported by data in vitro and in vivo Lung disease is the most common cause of morbidity and mortality

Answer 58

Long arm of chromosome 7 7q

Answer 59

F508del 2 abnormal genes

Answer 60

Does not move Cl-, causing sticky mucus to build up on the outside of the cell Leads to dysregulated epithelial fluid transport

Answer 61

Respiratory tract infection (microbial insults OR defect in host defence) —> bronchial inflammation—> respiratory tract damage —> more liable onto infection… Progressive lung disease

Answer 62

Frequent infections Malabsorption Failure to thrive

Answer 63

A mild electrical current pushes medicine into skin to cause sweating Sweat is collected and salt content measured

Answer 64

Maintenance and prevention management Rescue Personalised approaches

Answer 65

Segregation Surveillance- frequent reviews minimum every 3 months Airway clearance- physio and exercise Nutrition- pancreatic enzymes, diet high calorie and fat, supplements including vitamins, percutaneous feeding Psychosocial support

Answer 66

Class I: no functional CFTR protein is made (e.g. G542X) Class II: CFTR protein is made but it is mis-folded (e.g. F508del) Class III: CFTR protein is formed into a channel but it does not open properly (e.g. G551D) Class IV: CFTR protein is formed into a channel but chloride ions do not cross the channel properly (e.g. R347P) Class V: CFTR protein is not made in sufficient quantities (e.g. A455E) Class VI: CFTR protein with decreased cell surface stability (e.g. 120del123) More than 2000 CF - causing CFTR mutations have been found Most common of which is F508del [a class II mutation found in up to 80% to 90% of patients]

Answer 67

Different classes of genotype abnormality for development of CTFR protein Class I- Class VI

Answer 68

Suppression of chronic infections – antibiotic nebulisation Bronchodilation – salbutamol nebulisation Anti inflammatory – azithromycin, corticosteroids Diabetes – insulin treatment Vaccinations – influenza, pneumococcal, SARS CoV 2

Answer 69

2 week course IV antibiotics Home vs hospital Issues with frequent antibiotics Allergies Renal impairment Resistance Access problems

Answer 70

Allergies Renal impairment Resistance Access problems

Answer 71

Individual tailored or targeted medicine Move away from a ‘one size fits all’ approach Stratified based on predicted response or risk of disease Genetic information major factor Monogenic disorder (i.e. is the result of mutation(s) in a specific gene) Well-characterised pathophysiology with clear therapeutic targets Genotype directed therapies Targeted treatments based on infectious organisms and resistance patterns

Answer 72

CFTR potentiator- potentiates chloride secretion via increased CFTR channels opening time Class III mutations

Answer 73

CFTR corrector - corrects cellular misprocessing of CFTR (e.g. folding) to facilitate transport from the endoplasmic reticulum Class II mutation - F508del/F508del

Answer 74

Bacteriophage therapy is the use of lytic phases to kill infectious diseases

Answer 75

adherence to treatment High treatment burden High cost of certain treatments Allergies/intolerances to treatment Different infectious organisms and resistance to drugs

Answer 76

Autosomal recessive genetic disorder 80 different mutations of SERPINEA1 gene on chromosome 14 Serum antiprotease M phenotype normal and healthy S and Z phenotypes major disease associations

Answer 77

SERPINEA1 gene on chromosome 14

Answer 78

Normal and healthy PiMM

Answer 79

Major disease associations

Answer 80

Early onset emphysema (proteases in lung breakdown lung proteins) and bronchiectasis Liver cirrhosis Unopposed action of neutrophil elastase in the lung

Answer 81

Sign of emphysema

Answer 82

Sense of awareness of increased respiratory effort Inappropriate

Answer 83

Breathless on lying down

Answer 84

Increased respiratory rate

Answer 85

Reduced respiratory rate

Answer 86

Inappropriate over breathing

Answer 87

Episodes of shortness of breath

Answer 88

Is not caused by a single mutation (at least chromosome 2,6,9,15,17 and 22 are involved)

Answer 89

• involves low oxygen, and normal or low carbon dioxide levels. (hypoxaemia (PaO2 <8 kPa / 60mmHg) with normocapnia (PaCO2 <6.0 kPa / 45mmHg)) • It usually occurs due to ventilation/perfusion (V/Q) mismatch – the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lung tissue • As a result of the ventilation/perfusion mismatch, PaO2 falls, and PaCO2 rises. The rise in PaCO2 rapidly triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 due to the different shapes of the CO2 and O2 dissociation curves.

Answer 90

Type II respiratory failure

Answer 91

COPD causes habituation of high PaCO2 Begin to rely on low PaO2 for drive to breathe

Answer 92

PaCO2 Small changes causes difference as very sensitive

Answer 93

Hypoventilation —> increase PCO2 (acidic) —> increase H2CO3 —> decrease pH Respiratory acidosis

Answer 94

CO2 moving into RBCs combines with H2O- carbonic anhydride converts to H2CO3 which dissociates into HCO3 -

Answer 95

Renal: Increased HCO3 - reabsorption Increased H+ excretion in ammonia (NH3+ -> NH4)

Answer 96

Renal failure GI HCO3 - loss eg cholera Diabetic ketoacidosis Dilution of blood with H2O Failed H+ excretion (hypoalosteronism)

Answer 97

Decreased pH—> chemoreceptors increase respiratory rate —> decreases PCO2 —> decreases H2CO3

Answer 98

Vomiting (HCL loss) Alkali ingestion Renal acid loss: hyperaldosteronism, hyperkalaemia

Answer 99

Increased pH —> chemoreceptor inhibition —> decrease’s respiratory rate- hypoventilation—> increases PCO2 —> decreases pH

Answer 100

Hyperventilation—> decreases PCO2 (acidic) —> decreases H2CO3 —> increases pH Respiratory alkalosis

Answer 101

Renal: Decreased HCO3 - reabsorption Decreased H+ excretion

Answer 102

Pulmonary oedema

Answer 103

Interstitial fibrosis

Answer 104

Shunt V/Q= 0

Answer 105

Decreased V/Q Local hypoxia

Answer 106

V/Q = infinty

Answer 107

Increased V/Q

Answer 108

Local Bronchoconstriction Hypoxic pulmonary vasoconstriction (weak-little muscle) diverts blood to better-oxygenated lung segments

Answer 109

Marker of eosinophilic airway inflammation >50 ppb

Answer 110

Inflammation Increased mucus

Answer 111

Decreased lung surface area Destruction of alveoli and capillaries Decreased elastic recoil Distended thorax (barrel chest)

Answer 112

Misfolded CFTR Eg F508del (most common)

Answer 113

CFTR channel doesn’t open properly

Answer 114

Antiproteases inhibit neutrophil elastase from damaging elastin

Answer 115

Increased airways resistance - chronic obstructive pulmonary disease Reduced breathing effort (drug effects, brain stem lesion, extreme obesity) A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis) Neuromuscular problems

Answer 116

Mesothelioma

Answer 117

low pO2, normal/low pCO2

Answer 118

low pO2, high pCO2, normal-high HCO3-

Answer 119

Low ambient oxygen (e.g. at high altitude) Ventilation-perfusion mismatch (parts of the lung receive oxygen but not enough blood to absorb it, e.g. pulmonary embolism) Alveolar hypoventilation due to reduced respiratory muscle activity, e.g. in acute neuromuscular disease (this form can also cause type 2 respiratory failure if severe) Diffusion problem (oxygen cannot enter the capillaries due to parenchymal disease, e.g. in pneumonia) Shunt (oxygenated blood mixes with non-oxygenated blood from the venous system, e.g. right to left shunt)

Answer 120

Right main bronchus

Answer 121

Chemoreceptors in the carotid bodies detect low blood oxygen and send signals via cranial nerves to the dorsal respiratory group. Motor output is sent via the phrenic nerve to stimulate contraction of the diaphragm and increase respiratory rate

Answer 122

Central chemoreceptors in dorsal medulla less able to respond to carbon dioxide levels Body becomes reliant on peripheral chemoreceptors and hypoxic drive

Answer 123

PaO2 <8 KPa PaCO2 > 6KPa

Answer 124

Decrease in compliance as pulmonary oedema occurs

Answer 125

Increases due to loss of elastic tissue

Answer 126

Sign of CO2 retention - type 2 respiratory failure

Answer 127

Respiratory acidosis

Answer 128

Respiratory alkalosis

Answer 129

V/Q mismatch

Respiratory Failure Flashcards

(168 cards)