Revision—Sealing the Cracks Flashcards
(70 cards)
1
Q
Explain the role of chemoreceptors, baroreceptors, and stretch receptors in the diving response
A
Chemoreceptors: Detect hypoxia, sending afferent signals to trigger the reflex
Baroreceptors: help mediate blood pressure as external pressure changes occur during diving
Stretch receptors: maintain lung integrity and prevent overinflation
2
Q
What occurs during the mammalian dive response?
A
- Decreased peripheral blood flow
- Apnoea
- Bradycardia
3
Q
What conditions can cause heart murmur?
A
- Atrial/pulmonary stenosis/regurgitation
- Rheumatic fever
- Anemia
- Infective endocarditis
4
Q
Describe cardiac pacemaker automaticity
A
- Cardiac pacemaker cells can transmit action potentials from other pacemaker cells
- But, in the absence of these signals, they can also create their own action potentials
5
Q
Describe cardiomyocyte action potential conduction
A
- Resting: -90mV
- (Ca2+ influx from gap junctions): -70mV
- Voltage-gated Na+ influx: +20mV
- Voltage-gated K+ outflow: 0mV
- Transient Ca2+ outflow: remains at 0mV
- Ca2+ depleted: back to -90mV
6
Q
Describe cardiac pacemaker action potential
A
- Resting: -65mV
- Na+ influx: -50mV
- Ca2+ influx: +10mV
- K+ outflow: -65mV
7
Q
How is Afib diagnosed/managed?
A
Diagnosed: “Scribbly ECG”, irregular QRS complexes, no p wave
Managed:
Rate - Beta blockers
Rhythm - antiarrhythmics
Anticoagulation - warfarin
Risk factors - alcohol, obesity, diet
8
Q
What are the two main types of bradyarrhytmia?
A
- Sinus node dysfunction
- Atrioventricular block
9
Q
What % change in FEV1 or FVC is required during a bronchodilator response in spirometry for a condition to be considered bronchodilator responsive?
A
10%
10
Q
Describe four clinical features of asthma.
A
Features:
- Coughing
- Dyspnoea
- Chest tightness
- Wheeze
11
Q
Describe the pathophysiology of acute bronchoconstriction during an asthma exacerbation
A
- Irritant inhaled
- Cross-linking IgE antibodies on mast cells
- Release of inflammatory mediators
- Constriction of smooth muscle and airway inflammation
- Constriction of airways
12
Q
List some theories on the aetiology of asthma
A
- NO2 release
- Smoking during pregnancy/childhood
- Hygiene hypothesis
13
Q
What is the FEV1/FVC ratio range that suggests COPD? What other condition is necessary for this?
A
- FEV1/FVC <0.70
- AND: bronchodilators have been given
14
Q
What cardiovascular diagnosis is often used mistakenly instead of COPD?
A
Angina; since it commonly causes breathlessness.
15
Q
Symptoms that are suggestive of COPD
A
- Exertional breathlessness
- Cough
- Sputum
16
Q
Why can people with obstructive lung diseases sometimes inhale less air?
A
- More air is trapped in the lung
- Less space for new air to be inhaled
17
Q
Common viruses that exacerbate COPD
A
- Rhinoviruses
- Influenza viruses
18
Q
Common bacteria that exacerbate COPD
A
- Haemophilus influenzaue
- Streptococcus pneumoniae
19
Q
Four main signs of asthma in terms of pathophysiology (at the level of the lungs and airways)
A
- Lung inflammation
- Airway hyper-responsiveness
- Airway remodelling
- Mucous hypersecretion
20
Q
How does the ability of cilia to clear airways change in a person with asthma?
A
- Decreases
- Leads to more mucus lining the airways
21
Q
Describe the airway remodelling that occurs during asthma
A
- Subepithelial fibrosis
- Angiogenesis
- Smooth muscle cell hyperplasia
22
Q
Describe emphysema
A
- Loss of elasticity
- Hyperinflation of lungs
- Increased airspaces (instead of many small ones), decreased SA:V
23
Q
Describe COPD Pathophysiology. How does this link to exacerbation?
A
- Inhaled irritant/toxin
- Stimulates fibroblasts -> subendothelial fibrosis
- Complex inflammatory pathways -> alveolar and capillary damage
- Mucus hypersecretion in response to inflammation
- In exacerbation, an irritant such as a bacteria or a virus simply makes this worse than normal
24
Q
What symptoms do patients present with during COPD exacerbation? Why?
A
- Increased breathlessness (airway narrowing, increased bronchospasm)
- Increased mucous production (goblet cell hyperplasia)
- Increased sputum thickness (recruitment of neutrophils or, more rarely, eosinophils)
25
List some non-pharmacological treatment methods for asthma
- Trigger avoidance
- Vaccinations
- Education
- Action plan
- Exercise + Pulmonary Rehab
26
What does SMART therapy stand for?
Single Maintenance and Reliever Therapy (both in one)
27
What adverse effects are associated with frequent SABA use?
- Beta receptor downregulation
- Decreased bronchodilator response
- Increased allergic response
28
Track 1 vs Track 2 asthma treatment
Track 1: ICS + LABA
Track 2: ICS (preventer) + SABA (reliever)
29
Extrapulmonary complications of asthma
- Obesity
- Anxiety and depression
- Osteoporosis
30
Describe airway thermoplasty
- Bronchoscope into airways
- Apply radio-frequency light to decrease smooth muscle bulk in airways
31
Describe the treatment of COPD flare-ups
- Establish goals (Palliation? Throw everything we've got at it?)
- Apply oxygen if sats below 89%
- Consider systemic corticosteroids and antibiotics
- Non-invasive ventilation (e.g. BiPAP)
32
How do you treat type 2 respiratory failure in COPD exacerbations?
CPAP or BiPAP
33
Inhaled glucocorticoid mechanism
- Bind intracellular glucocorticoid recptors
- Increased expression of anti-inflammatory genes
- Suppression of pro-inflammatory genes
34
Mucolytics mechanism of action
They break the disulfie bonds within mucous molecules
35
What is a COPD self-management plan?
A structured but personalised plan that empowers patients to control their own condition as much as possible, improving quality of life and mental health in the process.
It helps patients to:
- Understand the severity of their symptoms
- Control these symptoms themselves, where possible
- Know when to seek help
36
How do monoclonal antibodies help in chronic airway disease?
Bind to and inhibit certain key components of the inflammatory pathways (i.e. cytokines etc.)
37
Preventer vs reliever in asthma
Preventer: prophylaxis, stop symptoms from occurring
Reliever: relieves symptoms if they occur
38
List some medications that can be used in the treatment of acute asthma exacerbations
- SABAs
- Systemic corticosteroids
- Supplemental oxygen (hypoxaemia)
39
Describe the main indication for oxygen therapy in COPD patients
Hypoxaemia
40
Demographic risk factors for SCD
- Men
- Old
- African-American/Non-Asian
41
Specific conditions that can predispose to SCD
- CHD
- AF
- CKD
- Obstructive sleep apnoea
- Cardiomyopathy
- Valvular heart disease
42
Define Sudden Cardiac Arrest (SCA)
Sudden loss of all heart activity
43
List the eight reversible causes of cardiorespiratory arrest
(4 Hs, 4Ts)
Hypoxia
Hypovolaemia
Hypo/Hyperkalaemia/metabolic disorders
Hypothermia/Hyperthermia
Tension pneumothorax
Tamponade
Toxins
Thrombosis (pulmonary/coronary)
44
What are the two types of non-sustained ventricular arrythmias?
- Ventricular ectopic
- Non-sustained ventricular tachycardia (>=3 beats, <30 seconds)
45
What are the three forms of sustainted ventricular arrythmia?
- Ventricular tachycardia
- Ventricular flutter
- Ventricular fibrillation
46
Describe polymorphic VT ECG findings. What often causes it?
- Multiform QRS morphology from beat to beat (widened)
- A sign of ischaemia
47
Describe ECG findings of bidirectional VT. What can cause it?
- Beat-to-beat QRS alternation
- Can be caused by toxins/catecholaminergic polymorphic VT)
48
Describe re-entrant ventricular VT. What type of VT can it cause in terms of ECG findings?
- Circuit of slow and fast conducting myocardium created due to scarring/electrical remodelling
- Can cause monomorphic VT
49
Describe ECG findings of ventricular flutter
Sinusoidal (>300bpm), no isoelectric interval between QRS complexes
50
Describe ECG findings of ventricular fibrillation
- Rapid, grossly irregular electrical activity with marked variability in ECG waveform
- Usually >300bpm
51
Describe the positive feedback loop of a cytokine storm
- Infection
- Release of cytokines
- Recruitment of cells
- New cells released cytokines (including TNF and IFN gamma)
- PANoptosome formation
- PANoptosis (more cell death)
- PANoptosis causes further cytokine release (uh oh...)
52
ARDS symptoms/signs
- Dyspnoea
- Low O2 sat
- Tahchypnoea
- Rattling sounds when breathing
53
Risk factors for severe illness in COVID-19
- Age
- Smoking
- Pregnancy
- Male gender
- Chemotherapy
- Childhood cancer
- Diabetes
54
How does remdesivir (IV antiviral) inhibit viral replication
Inhibits activity of RdRp
55
Describe the SMART COP mnemonic for pneumonia severity
- Systolic BP <90mmHg
- Multilobar CXR involvement
- Albumin < 3.5 g/dL
- Resp Rate >30
- Tachycardia >125bpm
- Confusion
- O2 sats <90%
- pH <7.35
56
Explain the CURB-65 severity scoring
- Confusion
- Urea >7 mmol/L
- Respi rate >30
- Blood pressure (sys <90 or dia <60)
- Age: >65
57
Which enzymatic pathway is affected in myelofibrosis? Which cell does it affect?
- JAK2 pathway
- Affects haematopoietic stem cells (gene mutation)
58
Provide an outline of aplastic anaemia, including what it is, the most common cause, symptoms
- Pancytopaenia ("anemia" is technically a misnomer)
- Most common cause is autonimmune destruction of haematopoietic stem cells
- Symptoms include anaemia symptoms (from low RBC), thrombocytopaenia (from low platelets), and recurrent infections (from leukocytopaenia)
59
How can primary ciliary dyskinesia cause chronic lung inflammation?
- Mucous is static
- Bacteria multiply
- Causes pneumonia
- Repeated: chronic inflammation
60
How can cystic fibrosis cause chronic inflammation?
- Stasis of mucous due to thickness
- Division of bacteria
- Pneumonia
- Recurrent: chronic inflammation
61
How can airway obstruction (from tumours or aspirated bodies) cause chronic inflammation?
- Impairs mucociliary escalator
- Pneumonia
- Recurrent: chronic inflammation
62
How can chronic inflammation cause bronchiectasis?
- Destruction of ciliated epithelium and elastin in airway walls
- Leads to dilation
- Fibrosis only serves to make the airways stiffer and less elastic
- Stiff, mucous-filled airways cause obstructive pattern
63
How can bronchiectasis cause RV hypertrophy? What is this called?
- Widespread hypoxia -> vasoconstriction
- Pulmonary hypertension
- RV hypertrophy
- Called cor pulmonale
64
What three kinds of supportive therapy are used during pulmonary hypertension (i.e. not vasodilators)
- Supplemental O2
- Diuretics
- Anticoagulants
65
If there is a contraindication to anticoagulation in HD stable PE treatment, what treatment do we use instead?
IVC filter
66
If there is a contraindication to TpA (thrombolytics) in HD unstable PE treatment, what treatment do we use instead?
Embolectomy
67
Describe prothrombin time (PT). What is the testing performed on, what is added to it, and what are we measuring?
- Done on plasma
- Factor 3 and calcium are added
- Measures speed of clotting via extrinsic pathway and common pathway
68
What is INR?
It is a globally normalised ratio that enables us to compare prothrombin times from lab to lab
(International normalised ratio)
69
What is Factor V Leiden mutation?
Factors V and Va are resistant to cleavage by protein C
70
True or false: plasmin specifically breaks down fibrin (i.e., it is a fibrinolytic)
True
