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Life Support > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What is a receptor? Definition and properties

A

A receiving molecule (glycoprotein) that sends specific messages into cells once the appropriate ligand has been bound
N terminal generally the one being bound (in extracellular environment)

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2
Q

What is amplification?

A

Receptors amplify signals
They work at very low concentrations
Time scales different dependent on drug/receptor - from ms to days

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3
Q

Ligand-gated receptor/channel complexes - definition and example

A

Five subunits with pore in the middle, look like a flower from above
Each subunit has a binding site for a drug
Example: Nicotinic receptor

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4
Q

G-protein-coupled receptors - definition and example

A

one single protein that spans 7 transmembrane regions
N-terminal - ligand-binding site
C-terminal G-protein binding region
Examples: Muscarinic receptors

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5
Q

What is a G protein?

A

Guanine nucleotide (GTP/ GDP) binding proteins
3 subunits - alpha, beta, gamma
A G protein attached to GTP is active, or “on,” while a G protein that’s bound to GDP is inactive, or “off.”

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6
Q

What are the subtypes of alpha G-protein subunits?

A

Gs (stimulate), Gi (inhibit), Gq

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7
Q

Tyrosine kinase receptors - discussion and example

A

Ligand (such as insulin) binds to receptor which essentially allow glucose into fat cells to be stored / processed

Process - ligand binds, two channels move together, phosphate is added to the tyrosine on the receptor which allows the channel to open

1 protein subunit, 1 transmembrane
domain
Example - insulin

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8
Q

Intracellular (or nuclear) receptors

A

Found within the cell

Example - cortisol hormone receptor

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9
Q

What are other drug binding targets (other than receptors)? (3)

A

proteins, such as receptors, enzymes, transporters, ion channels or genetic material, such as DNA.

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10
Q

Why do we need to regulate level of breathing?

A

Adjusted to meet demand for O2 and production of CO2

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11
Q

In what circumstances does O2 requirements or Co2 production increase? 4 examples

A

Exercise, infection, injury, metabolic dysfunction

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12
Q

How do you increase amount of O2 transported?

A

Both ventilation AND increased cardiac output

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13
Q

Physiological process of breathing

A

Nerve signals sent from CNS to respiratory muscles (which are skeletal muscles) to tell them to relax and contract

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14
Q

Key respiratory muscles for inspiration and expiration

A

Inspiration - Diaphragm, external Intercostal muscles, pectorals, sterocleidomastoid, scalene
Expiration - elastic recoil of diaphragm, internal intercostals, abdominals

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15
Q

How does the brainstem dictate the basic breathing pattern?

A

Complex series of nueronal connections that interpret and determine the body’s need for oxygen

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16
Q

What factors determine the rate and depth of breathing?

A

Receptors in muscles and joints (direct rather than waiting for CO2 levels to go up)
Stretch receptors in lungs
Chemoreceptors

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17
Q

Central chemoreceptors - where, function, overview of mechanism

A

In medulla
Monitors changes in arterial CO2
Responds to changes in H in CSF but does NOT directly respond to changes in blood pH
Do not respond to changes in O2 levels

MECHANISM - negative feedback loop

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18
Q

Peripheral chemoreceptors - where, function, overview of mechanism

A

In carotid and aortic bodies
Activated by O2 levels, CO2 levels, and acidaemia (low pH)
Sends signal to respiratory centres in medulla via sensory nerves to increase ventilation
Negative feedback loop

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19
Q

What is the hypercapnic drive?

A

Predominant stimulus underlying urge to breathe

Ventilation is generally proportional to PaCO2 (because of the importance of pH to homeostsis)

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20
Q

What is hypoxic drive?

A

Occurs at VERY low PaO2

Low PaO2 stimulates increased ventilation (buth this drive only kicks in only at very low PaO2)

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21
Q

What steps are required for the initiation of breathing?

A

CNS sends message to inspiratory muscles to start breathing

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22
Q

Breathing feedback mechanisms overview (4 outlined)

A

Central chemoreceptors

Peripheral chemoreceptors

Muscles

Emotional stimuli

Irritant and stretch receptors in lungs

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23
Q

What is sleep apnoea?

A

Temporary cessation of breathing during sleep
More than 5 episodes per hour lasting more than 10 seconds
Causes tiredness, cardiovascular complications, obesity/diabetes

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24
Q

What test is used to diagnose sleep apnoea?

A 
Polysomnography
EOG
EEG
ECG
MANY TESTS
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25
Q

What are the two types of sleep apnoea? (Two types with general causes)

A

Obstructive - airways blocked
Can be caused by obesity, alcohol/sedatives, smokers

Central - dysfunction in process that initiates breathing
Stroke, drugs such as opiods can suppress neuronal activity, altitude, neonates, central hypoventilation syndrome

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26
Q

What is cheyne-stokes respiration?

A

Cheyne–Stokes respiration is an abnormal pattern of breathing characterized by progressively deeper, and sometimes faster, breathing followed by a gradual decrease that results in temporary apnea.

Often happens at high altitudes
Back and forth between peripheral and central chemoreceptors
Peripheral increase breathing in response to low O2
Central decrease breathing to respond to low pH

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27
Q

What is consent? (three legal principles)

A

Voluntary agreement to treatment, examination
Permission to examine, investigate, treat
Waiving of right to bodily integrity

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28
Q

What are the key legal issues that doctors have? (three)

A

Battery, negligence (both civil) and assault/battery (criminal)

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29
Q

What are the three aspects of VALID consent?

A

Information, voluntariness, competence

Patients must also know they can change their mind

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30
Q

What are the four features of competence? (re consent)

A
  • understand relevant information
  • retain relevant information
  • weight up relevant information
  • communication decision
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31
Q

What information should you give when getting consent?

A 
PARQ
Procedure
Alternatives
Risks
Questions
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32
Q

How much information is adequate? (three different legal models)

A

Professional practice standard - what complies with the practice standard?
Reasonable / prudent person standard - what does a hypothetical reasonable person want to know?
Subjective standard - what does this person want to know?

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33
Q

What is the significance of the Montgomery negligence case?

A

Diabetic woman had vaginal delivery and son had significant disabilities. She claimed she had not been fully informed of risks. Won £5 million

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34
Q

How did the law evolve following the Montgomery case?

A

Move away from the Bolam test to a model where they doctor is responsible to ensure the patients are aware of any material risks and alternatives - based either on a hypothetical reasonable patient or if possible, the patient themselves (if known well enough)

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35
Q

What is asthma?

A

a respiratory condition marked by attacks of spasm in the bronchi of the lungs, causing difficulty in breathing
Additional mucus caused by immune response

Common symptoms: wheeze, cough, dyspnoea (breathlessness)

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36
Q

What is the general mechanism of asthma? (5 steps)

A 
CAUSE: allergen inhalation / exercise
Immune system response
Airway inflammation
Impaired airway function
RESULT: symptoms
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37
Q

What is the general mechanism of asthma? (5 steps)

A 
CAUSE: allergen inhalation / exercise
Immune system response
Airway inflammation
Impaired airway function
RESULT: symptoms
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38
Q

What is the relationship between the radius of the airway and the resistance and airflow?

A

As airway radius DECREASES, resistance INCREASES and airflow DECREASES

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39
Q

What is the impact of asthma on the airway? Four factors

A
  • contraction of smooth muscle
  • excess mucus secretion
  • oedema / swelling
  • irritation of sensory neurons (cough)
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40
Q

What is normal vs asthmatic airflow?

A

Normal airflow - laminar flow

Asthmatic - Turbulent flow (produces wheezing)

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41
Q

Simple description of allergic response (two stages)

A 
Sensitisation
- allergen exposure
- allergen processed by immune system
- antibodies generated, immune system 'primed'
Response
- allergen exposure (same allergen)
- allergen binds to antibodies w/ immune cell activation, inflammatory response
- Symptoms
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42
Q

Simple description of allergic asthma response (two stages)

A 
Sensitisation
- allergen exposure
- allergen processed by immune system
- antibodies generated, immune system 'primed'
Response
- allergen exposure (same allergen)
- allergen binds to antibodies w/ immune cell activation, inflammatory response
- Symptoms
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43
Q

Describe the sensitisation process of allergy-induced asthma (6 steps)

A
  1. Allergen inhaled and enters airway tissue
  2. Antigen is engulfed by antigen-presenting cell (dendritic cell)
  3. Antigen presented to naive helper T cell
  4. T cell is activated and becomes Th2 cell
  5. The Th2 cell coordinates with other immune cells via cytokines (Eosinophils and B cells)
  6. B cells produce antibodies which bind to mast cells
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44
Q

List the cell types responsible in allergy-induced asthma response - name, role, inflammatory mediators involved

A

B cells - produce antibodies and IgE
Th2 cells - recruit eosinophils, activate B cells
Mast cells - Degranulate to cause inflammation, contraction, mucus
Eosinophils - Degranulate to cause inflammation, contraction, mucus

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45
Q

What happens during allergy-induced asthmatic response? (2 phases possible)

A

Primary

  1. Allergen enters airway and enters airway tissue
  2. Allergen binds receptor on mast cell, which degranulates
  3. Eosionphil degranulates
  4. Inflammation causes symptoms

Reoccurrence can be causes T CELL RESPONSE / LATE RESPONSE

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46
Q

What is the long-term impact of asthma?

A 
Ongoing, recurrent response to inflammatory mediator release
Tissue damage (chronic = airway remodelling)
47
Q

What are other cells that have recently been found to be involved in allergic asthma response? (two)

A

airway epithelial cells

group 2 innate lymphoid cells

48
Q

Paranasal sinuses (four)

A

Frontal, maxillary, thymoid, sphenoid

49
Q

Pharynx divisions (three)

A

Nasopharynx, oropharynx, laryngopharynx

50
Q

Function of the larynx (four)

A

Allow crossing over of the digestive / respiratory passages
Prevent food from entering the trachea
Contribute to voice production
Permit coughing by ‘fixing’ the thorax

51
Q

Where does the hyoid bone sit (vertebral level)

A

CIII-CIV

52
Q

Where does the cricoid bone sit (vertebral level)

A

CV-CVI

53
Q

Where does the trachea bifurcate?

A

The carina

54
Q

How do the right and left main bronchi differ?

A

Left - angled, longer, narrower (angled due to position of heart)
Right - more upright, shorter, wider - more like to inhale objects into this lung

55
Q

Describe position of the muscles of the thorax (9)

A 
Pectoralis major
Pectoralis minor
Subclavius
Serratus anterior
(Latissimus dorsi)
Diaphragm
External intercostals
Internal intercostals
Innermost intercostals
Scalenes
56
Q

Describe respiratory movements

A

Diaphragm movement during inspiration and expiration

Movement of sternum and ribs (pump handle and bucket handle)

57
Q

What cells make up the trachea and its cartilage

A

Lined with ciliated respiratory epithelium
Goblet cells (secret mucus)
Cilia and microvilli cover surface
Hyaline cartilage anterior, smooth muscle posterior

58
Q

How big are the pleural cavities in reference to the lungs?

A

The cavities extend about 2 ribs lower than the lungs to allow for expansion

59
Q

How do receptors work? (simple process with 5 steps)

A 
Chemical signal (drug) ENTERS the body
It BINDS to receptor
There is a CHANGE in receptor protein conformation
SIGNAL transduction
Cellular RESPONSE
60
Q

What are the immune cells involved in asthma sensitisation and response (4)? What is their role in asthma?

A

Th2 cells - During sensitisation - induce B cells to produce IgG
During response - coordinate immune response via cytokine release

B cells - produce allergen specific IgE

Mast cells - allergen induced degranulation which releases inflammatory mediators

Eosinophils - cytokine-induced degranulation which releases inflammatory mediators

61
Q

What is descriptive epidemiology?

A

The first stage of epidemiological investigation - focuses on describing disease distribution by place/ time / person

62
Q

Describe the findings of the ISAAC study

A

The International Study of Asthma and Allergies in Childhood
The ISAAC findings have shown that these diseases are increasing in developing countries and that they have little to do with allergy, especially in the developing world.

63
Q

Define ‘ecological study’

A

Study of a population or community (rather than individual)

64
Q

Value of geographical studies

A

Measuring exposure and disease rates helps to see changes/differences within populations (where other causal factors may be consistent)

65
Q

Impact of migration on studying geographical variation

A

Are differences in disease risk associated with adult environment or genes and early environment?

66
Q

Describe the findings of migration studies in asthma

A

People moving from low to high risk countries, they reach asthma levels of new high country
Sometime full effect not felt until second gen

67
Q

What are the pitfalls of geographic studies? (4) and how do you overcome them?

A 
Differences between countries:
Ascertainment (ability to seek medical care)
Diagnosis
Recording (of info)
Population structure (age, sex)
68
Q

What is the ecological fallacy?

A

Assuming that the findings of an ecological study apply to an individual

69
Q

Pitfalls of migration studies (3)

A

Selection bias
Information bias
Potential influence of stress of migration

70
Q

What is a period effect vs a cohort affect?

A

Period effect - recent cause of marked change in disease rate
Cohort effect - an early life cause of marked change in disease rate

71
Q

Potential pitfalls in studying time trends

A

Changes in ascertainment
Changes in diagnosis
Changes in recording of information
Changes in population structure

72
Q

Is breathing in or out more work?

A

In - inspiration is an active process

Expiration is passive

73
Q

What muscles are needed for forced inspiration and forced expiration?

A

Forced inspiration - diaphragm, muscles of the neck, including the scalenes, contract and lift the thoracic wall, increasing lung volume.
Forced expiration - abdominal, internal intercostal - (bucket handle, water pump)

74
Q

During injury, at what level would your breathing be affected?

A

Above C5/6

75
Q

What stimulates breathing?

A

When CO2 is too high, you breathe faster

76
Q

Neurogenic factors to increase breathing (5)

A

Impulses - limb receptors during exercise
Pulmonary receptors sensitive to stretch
Juxtapulmonary receptors stimulated by congestion
Impulses from receptors in muscles / joints of chest wall
Conscious changes

77
Q

Chemical stimuli to increase breathing (3) - which one is strongest?

A

Rise in CO2 (strongest)
Rise in H+ ions
Reduced pO2

78
Q

What defines respiratory failure?

A

pO2 less than 8kPa
Type 1 - hypoxic (pCO2 less than 6.5)
Types 2 - hypercapnic (pCO2 more than 6.5)

79
Q

What do hypoxic and hypercapnic mean?

A

Hypoxic - not enough oxygen

Hypercapnic - too much CO2 (not able to breathe it off)

80
Q

What characterises type 1 respiratory failure? And examples (2 types)

A

V/Q mismatch
Increased resp rate (which leads to fall in pCO2)

Alveolar unit failure (stuff in lungs prevent air getting to alveoli OR collapse)
Pulmonary oedema / pneumonia / collapse / fibrosis
Pulmonary vasculature failure (blood isn’t getting to lungs properly)
embolism / hypertension

81
Q

What characterises type 2 respiratory failure? And examples (3)

A

Ventilation failure - insufficient excretion of CO2 building up in lungs
hypoventilation

Examples - nervous system or neuromuscular failure
Airway failure (obstruction or dysfunction)
Chest wall or pleural space failure
Asthma, COPD, obesity

82
Q

What is the ventilation-perfusion match? What kind of respiratory failure does this cause?

A

Lack of air or blood to lungs

Type 1 failure

83
Q

How can you calculate pH?

A

pH is proportional to bicarbonate / pCO2

84
Q

Henderson-Hasselbach equation

A

H + HCO3– H2CO3 – H2O + CO2

85
Q

What occurs during metabolic acidosis? What about respiratory acidosis?

A

Metabolic acidosis - Increased production of acids (H+)

Respiratory acidosis - Reduced ventilation leading to raised pCO2

86
Q

What occurs during metabolic alkalosis? what about respiratory alkalosis?

A

Metabolic alkalosis - Loss of acids

Repiratory alkalosis - Increased ventilation leading to low pCO2

87
Q

What is the aetiology of asthma? (3)

A

Genetics
Immunology
Environment

88
Q

How do you make an asthma diagnosis? (3)

A
  • Classic symptoms and signs (two or more) - cough, wheeze (only caused by asthma, COPD), dyspnoea, chest tightness, sputum production, reduction in exercise tolerance
  • Tests for variability
  • Tests for eosinophilic inflammation or atopy (FeNO, blood eosinophls, skin prick test)
89
Q

What are the clinical features of asthma?

A

Cough, wheeze (only caused by asthma, COPD), dyspnoea, chest tightness, sputum production, reduction in exercise tolerance

  • Variable
  • worse at night / early AM
  • Triggers
90
Q

Examination of asthma

A

Exam can be completely normal
Expiratory wheeze may be heard
Silent chest is life threatening asthma

91
Q

Describe challenge tests for asthma

A

Mathacholine,histamine,acetylcholine challenge is a lung irritant to produce fall in FEV1 (asthma if dose provoking 20% fall is less than 16mg/mL

92
Q

What are the non-pharmacological management techniques for asthma? (4)

A
  • allergen avoidance
  • smoking cessation
  • weight loss
  • breathing technique training
93
Q

What is an asthma action plan? (4)

Peak flow values and action required (3 levels)

A

Details about asthma - peak flow, meds
How to tell when asthma control is poor
What you should do if control is poor
What to do in emergency

Of your best peak flow values:
less than 80% - ICS
less than 60% - start oral steriods, doctor within 24 hours
less than 50% - present to A&E

94
Q

How to you review asthma patients? (three first steps)

A

Make sure they have asthma
Make sure they are taking their inhaler
Make sure they are using it properly

95
Q

Questions to assess level of asthma control (7, 3 key)

A 
Does the patient have:
Daytime symptoms 
Night time wakening *
Need for rescue medication *
Asthma attacks
Limitations on activity *
Normal lung function
Side effects from meds
96
Q

Overview of immediate and subsequent management

A 
Oxygen
B2 bronchodilator (salbutamol) via O2 nebuliser
Ipratropium bromide via nebuliser
Prednisolone or IV hydrocortisone
NO sedatives

If improving, continue all
If not improving, regular doses of b2 bronchodilator and ipratropium
If still not improving, refer on

97
Q

When do you discharge patients following acute asthma?

A

xxx

People often need similar time for recovery to previous hospital stay with acute asthma

98
Q

Why does asthma still kill?

A

Because many patients are still on beta2-agonist but aren’t using longer term drug (?)
Severe can progress very quickly

99
Q

Describe: Moderate acute asthma (3)

A

Increasing symptoms
PEF > 50-75% of best or predicted
No features of severe asthma

100
Q

Describe: Acute severe asthma (4)

A 
Any of the following:
PEF > 33-50% of best or predicted
RR > 25/min
HR > 110/min
Inability to complete sentences in one breath
101
Q

Describe: Life-threatening asthma (clinical 7 and measurements 4)

A

Any one of these in patients with severe asthma:

Altered conscious level
exhaustion
arrhythmia
hypotension
cyanosis
silent chest
poor respiratory effort
PEF > 33% of best or predicted
SpO2 <92%
PaO2 <8kPa
normal PaCO2 (4.6-6)
102
Q

Describe: Near-fatal asthma

A

Raised PaCO2 and / or requiring mechanical ventilation

103
Q

DR (of DR DEAC PIMP) of asthma

A

Definition - a respiratory condition marked by attacks of spasm in the bronchi of the lungs, causing difficulty in breathing. It is usually connected to allergic reaction or other forms of hypersensitivity
Various types include adult-onset, allergic, asthma-COPD overlap, exercise-induced bronchoconstriction, noallergic, occupational

Risk factors 
Family history
Viral respiratory infections in infancy/childhood
Allergies
Occupational exposure
Smoking
Air pollution
Obesity
104
Q

Main parameters of spirometry? How is it performed? What are the main flow rates examined?

A

Common test to measure how well your lungs are working by measuring how much you inhale / exhale and how quickly. Can be used for diagnosis or to check status / response to treatment

Forced vital capacity (FVC).This is the largest amount of air that you can forcefully exhale after breathing in as deeply as you can. A lower than normal FVC reading indicates restricted breathing.

Forced expiratory volume (FEV).This is how much air you can force from your lungs in one second. This reading helps your doctor assess the severity of your breathing problems. Lower FEV-1 readings indicate more significant obstruction.

105
Q

Relationship between FVC and FEV

A

Relationship between them called the Tiffeneau-Pinelli index - FEV1/FVC

In obstructive lung disease (difficulty exhaling completely), the ratio goes DOWN

In restrictive lung disease (difficulty fully expanding lungs), ratio may be the same but both values will drop

106
Q

How should x-rays be examined?

A 
Airways
Bones / breathing
Cardiac
Diaphragm
Everything else - fluid, soft tissues, medical implements, etc.
107
Q

Different colours of sputum and what it suggests. What are the different colours suggestive of?

A

Phlegm = mucus in your chest
When you cough up phlegm = sputum
Green / yellow - generally indicates infection
Brown - brown colour generally caused by old blood
White - viral infections, GERD, COPD, heart failure
Black - Inhalation of something black (coal, tar) or fungal infection
Clear - viruses, allergies
Red/pink - Indicates blood

108
Q

What are potential causes of chest tightness in adults?

A

Many potential causes including muscle strain, anxiety, pneumonia, GERD (gastroesophageal reflux disease), asthma, ulcers, hernia, rib fracture and many others

109
Q

Describe the anatomy of the bronchiole

A

Lumen, epithelium, basement membrane, lamina propia, smooth muscle, glands, cartilage

110
Q

MICA for B2 agonists - and examples

M (2)
I (3)
C (3)
A (6)

A

B2 agonists - SHORT (Salbutamol, terbutaline) or LONG (salmeterol, formoterol) indacaterol

M: B2 receptors in smooth muscle of bronchi, gut, uterus, blood vessels
G protein couples receptor is stimulated, leading to smooth muscle relaxation
Also stimulate Na/K pumps causing shift of K from ECF to ICF

I: Asthma
COPD
Hyperkalaemia

C: B-blockers may reduce effectiveness, use alongside corticosteroids can lead to hypokalaemia
Cardiac conditions in general

A: Tachycardia, palpitations, anxiety, tremor, muscle cramps, high serum glucose levels

111
Q

MICA for corticosteriods - inhaled

M
I (2)
C (3)
A (4)

A

M: Interact with cytoplasm receptors
Activated receptor moves into nucleus, modifies transcription of genes to downregulate pro-inflammatory genes and up-regulate anti-inflammatory ones
Reduces exacerbations and symptoms

I: Asthma
COPD

C: TB, pneumonia, suppress growth in children (at very high doses)

A: Oral candidiasis (thrush)
Hoarse voice
May increase risk of pneumonia
Only causes systemic side effects in very high doses

112
Q

MICA for corticosteriods - systemic

M
I (4)
C (4)
A (5)

A

Prednisolone

M: Interact with cytoplasm receptors
Activated receptor moves into nucleus, modifies transcription of genes to downregulate pro-inflammatory genes and up-regulate anti-inflammatory ones
Direct action on suppression of monocytes / eosinophils

I: Allergic / inflammatory disorders (anaphylaxis, asthma)
Autoimmune diseases
Cancer (reduce tumour associated swelling)
Hormone replacement in adrenal insufficiency and hypopituitarism

C: Cytochrome P450 inducers- may make them less effective
NSAIDs- increase risk of peptic ulcers and GI bleeding
B2-agonists- increase hypokalaemia risk
Wide angle glaucoma

A: Immunosuppression = higher chance of infection
Metabolic side effects including diabetes mellitus, osteoporosis
Mood / behavioural changes
Hypertension / hypokalaemia
Adrenal atrophy

113
Q

MICA for antimuscarinics, bronchodilators

M
I (2)
C (3)
A (5)

A

(SHORT e.g. Ipratropium or LONG e.g. aclidnium)

M: Competitive inhibitor of acetyl choline (which normally binds to muscarinic receptor)
Bind to muscarinic receptor - blocks the action of the neurotransmitter acetylcholine
Block parasympathetic activity, reduce smooth muscle tone, increase heart rate, reduce gland secretions in GI and respiratory tracts

I: Asthma
COPD

C: Patients with: angle-closure glaucoma, arrhythmias, urinary retention

A: - Irritation of respiratory tract
- GI disturbance 
- Urinary retention
- Blurred vision
Headaches
114
Q

Give an overview of the potential treatments for asthma

A

B2 agonists
Corticosteriods (inhaled or systemic)
Antimuscarinics / bronchodilators
Aminophylline / theophylline

Both B2 agonists and antimscarinics have short and long acting versions

Life Support (5 decks)

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