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CTB Glossary > CTB8-10 > Flashcards

CTB8-10 Flashcards

1
Q

What is anaphylaxis?

A

A severe systemic allergic reaction involving respiratory and cardiovascular systems.

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2
Q

What triggers anaphylaxis?

A

Allergens such as foods, insect stings, drugs (e.g., penicillin), and latex.

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3
Q

How does IgE contribute to anaphylaxis?

A

IgE binds mast cells and basophils, causing degranulation upon antigen exposure.

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4
Q

What mediators are released during mast cell degranulation?

A

Histamine, leukotrienes, prostaglandins, and cytokines.

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5
Q

What is the physiological effect of histamine?

A

Vasodilation, increased vascular permeability, bronchoconstriction, and itching.

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6
Q

What are the four classical signs of acute inflammation?

A

Rubor (redness), calor (heat), tumor (swelling), and dolor (pain).

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7
Q

What is loss of function (functio laesa)?

A

A fifth sign of inflammation; severe dysfunction results in systemic collapse in anaphylaxis.

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8
Q

How does anaphylaxis affect the cardiovascular system?

A

Systemic vasodilation causes hypotension and shock.

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9
Q

What happens to the respiratory system during anaphylaxis?

A

Bronchoconstriction, airway oedema, and mucus production cause dyspnoea.

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10
Q

Why is adrenaline the first-line treatment for anaphylaxis?

A

It reverses hypotension (vasoconstriction), bronchodilation, and mast cell stabilisation.

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11
Q

What are the ABC principles of anaphylaxis treatment?

A

Airway, Breathing, and Circulation.

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12
Q

What is the role of leukotrienes in anaphylaxis?

A

They sustain bronchoconstriction, inflammation, and increased vascular permeability.

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13
Q

What happens to mast cells during anaphylaxis?

A

They degranulate, releasing preformed and newly synthesised mediators.

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14
Q

How is anaphylactic shock defined?

A

Severe hypotension and tissue hypoperfusion due to systemic vasodilation.

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15
Q

What is the function of basophils in anaphylaxis?

A

They complement mast cell responses, releasing histamine and other mediators.

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16
Q

What is the role of prostaglandins in anaphylaxis?

A

They induce pain, vasodilation, and inflammation.

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17
Q

What pathway leads to IgE production?

A

Th2 cells stimulate B cells to switch to IgE production in response to antigens.

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18
Q

What are the symptoms of anaphylaxis?

A

Rashes, swelling, hypotension, bronchospasm, gastrointestinal distress, and dizziness.

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19
Q

How is anaphylaxis diagnosed clinically?

A

By acute onset of symptoms involving skin, respiratory, cardiovascular, or gastrointestinal systems.

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20
Q

What is the incidence of anaphylaxis in the population?

A

Approximately 0.05-2% of people experience anaphylaxis.

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21
Q

What does adrenaline act on to restore cardiovascular function?

A

Alpha-1 receptors (vasoconstriction) and beta-2 receptors (bronchodilation).

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22
Q

Why does vascular permeability increase in anaphylaxis?

A

Histamine and leukotrienes induce endothelial cell contraction, causing leakage.

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23
Q

How can anaphylaxis cause laryngeal oedema?

A

Increased vascular permeability causes fluid leakage into airway tissues.

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24
Q

What is biphasic anaphylaxis?

A

A recurrence of symptoms hours after the initial reaction, even with treatment.

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25
Q

Why are antihistamines used in anaphylaxis management?

A

They block histamine action, reducing swelling, itching, and rash.

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26
Q

What is the role of glucocorticoids in anaphylaxis?

A

They reduce late-phase inflammation and prevent recurrent symptoms.

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27
Q

What are lipid mediators?

A

Molecules like leukotrienes and prostaglandins produced from arachidonic acid.

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28
Q

Why is oxygen therapy important in anaphylaxis?

A

It counters hypoxaemia caused by bronchoconstriction and airway oedema.

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29
Q

What is the role of tryptase in anaphylaxis?

A

Tryptase is a mast cell-specific enzyme that can confirm mast cell activation.

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30
Q

Why is mast cell activation rapid in anaphylaxis?

A

Pre-formed mediators (e.g., histamine) are released immediately upon antigen binding.

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31
Q

What are the key inducers of anaphylaxis?

A

Foods, drugs, insect stings, and latex.

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32
Q

What mechanisms cause hypotension in anaphylaxis?

A

Systemic vasodilation and increased capillary permeability reduce blood volume.

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33
Q

How does anaphylaxis affect gastrointestinal function?

A

Smooth muscle contraction causes nausea, vomiting, abdominal pain, and diarrhoea.

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34
Q

How does IgE-mediated hypersensitivity differ from other types?

A

It is immediate, mediated by IgE, and causes mast cell degranulation.

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35
Q

How are adrenaline auto-injectors used in emergency management?

A

They deliver intramuscular adrenaline to quickly reverse symptoms.

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36
Q

Why does anaphylaxis sometimes cause wheezing?

A

Bronchoconstriction reduces airway diameter, increasing airflow resistance.

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37
Q

How do cytokines contribute to anaphylaxis?

A

They amplify inflammation by recruiting immune cells.

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38
Q

What are common anaphylaxis risk factors?

A

Previous allergic reactions, atopy, asthma, and exposure to known allergens.

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39
Q

Why does anaphylaxis need rapid treatment?

A

It can progress rapidly to shock, respiratory failure, and death if untreated.

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40
Q

What long-term strategies help prevent anaphylaxis?

A

Allergen avoidance, desensitisation therapy, and carrying an adrenaline auto-injector.

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41
Q

What is the role of IL-4 in IgE production?

A

IL-4 promotes B-cell class switching to produce IgE antibodies.

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42
Q

Why is adrenaline given intramuscularly in anaphylaxis?

A

IM administration provides rapid absorption and onset of action.

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43
Q

What causes skin rashes and urticaria in anaphylaxis?

A

Histamine induces vasodilation and increased capillary permeability.

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44
Q

How does hypoxaemia occur during anaphylaxis?

A

Airway obstruction and bronchospasm limit oxygen delivery to alveoli.

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45
Q

How does anaphylaxis affect heart rate?

A

Tachycardia occurs due to compensatory sympathetic activation.

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46
Q

Why can anaphylaxis lead to unconsciousness?

A

Severe hypotension and hypoperfusion impair brain function.

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47
Q

How does adrenaline stabilise mast cells?

A

It reduces mediator release by acting on beta-2 receptors.

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48
Q

What are the emergency steps for suspected anaphylaxis?

A

Administer adrenaline, call emergency services, provide oxygen, and monitor vitals.

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49
Q

Why are beta-blockers risky in anaphylaxis?

A

They block adrenaline’s effects, reducing treatment efficacy.

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50
Q

How does leukotriene receptor antagonism benefit anaphylaxis patients?

A

It blocks leukotriene activity, reducing bronchoconstriction and inflammation.

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51
Q

What are the key features of asthma?

A

Asthma involves airway hyperresponsiveness, chronic inflammation, and reversible airflow obstruction.

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52
Q

How does airway remodelling occur in asthma?

A

It includes smooth muscle hypertrophy, goblet cell hyperplasia, and subepithelial fibrosis.

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53
Q

What immune cells are involved in asthma?

A

Mast cells, eosinophils, and Th2 lymphocytes mediate airway inflammation.

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54
Q

What triggers asthma symptoms?

A

Allergens, pollutants, cold air, and exercise can provoke bronchospasm and mucus production.

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55
Q

How does inhaled corticosteroid therapy work?

A

It reduces airway inflammation by suppressing pro-inflammatory mediators.

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56
Q

What are the pathophysiological features of COPD?

A

Irreversible airflow obstruction due to emphysema, chronic bronchitis, and airway inflammation.

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57
Q

What role does protease-antiprotease imbalance play in COPD?

A

Excess proteases degrade alveolar walls, causing emphysema.

58
Q

How does smoking cause COPD?

A

It induces oxidative stress, neutrophilic inflammation, and tissue destruction.

59
Q

What are the clinical differences between asthma and COPD?

A

Asthma has reversible airflow obstruction, while COPD is progressive and irreversible.

60
Q

What is atherosclerosis?

A

Atherosclerosis is the accumulation of lipids, inflammatory cells, and fibrous tissue in arterial walls.

61
Q

How do foam cells form in atherosclerosis?

A

LDL oxidation causes macrophages to engulf lipids, forming foam cells.

62
Q

What are the consequences of atherosclerotic plaque rupture?

A

It can cause thrombosis, myocardial infarction, or stroke.

63
Q

How does endothelial dysfunction contribute to atherosclerosis?

A

It promotes inflammation, leukocyte adhesion, and increased permeability.

64
Q

What is pulmonary hypertension?

A

Elevated pulmonary arterial pressure leading to right ventricular hypertrophy and failure.

65
Q

What causes pulmonary hypertension?

A

Endothelial dysfunction, vascular remodelling, and vasoconstriction.

66
Q

How does pulmonary hypertension impact the heart?

A

It overloads the right ventricle, leading to hypertrophy, dilation, and heart failure.

67
Q

What role do prostacyclin analogues play in pulmonary hypertension treatment?

A

They induce vasodilation and reduce pulmonary vascular resistance.

68
Q

How do nitric oxide pathways influence pulmonary hypertension?

A

NO promotes vasodilation, and its deficiency contributes to elevated pressures.

69
Q

What therapies are available for severe COPD?

A

Bronchodilators, corticosteroids, oxygen therapy, and pulmonary rehabilitation.

70
Q

How does smoking cessation improve COPD outcomes?

A

It slows disease progression and reduces exacerbations.

71
Q

What are the key symptoms of pulmonary hypertension?

A

Dyspnoea, fatigue, chest pain, and syncope.

72
Q

What role does inflammation play in respiratory diseases?

A

Chronic inflammation causes airway damage, fibrosis, and mucus hypersecretion.

73
Q

How are biologics used in asthma treatment?

A

They target IL-5, IL-4, and IgE to reduce eosinophilic inflammation.

74
Q

What are the main goals of COPD management?

A

Symptom control, exacerbation prevention, and improving exercise tolerance.

75
Q

What causes hypoxaemia in COPD?

A

Alveolar destruction and ventilation-perfusion mismatching reduce oxygen exchange.

76
Q

What diagnostic tests confirm pulmonary hypertension?

A

Echocardiography, right heart catheterisation, and pulmonary function tests.

77
Q

What lifestyle factors contribute to atherosclerosis?

A

Poor diet, smoking, obesity, and sedentary behaviour.

78
Q

How does pulmonary vascular remodelling occur?

A

Proliferation of smooth muscle and endothelial cells thickens vessel walls.

79
Q

What are the risk factors for COPD development?

A

Smoking, air pollution, occupational exposures, and genetic predisposition (e.g., alpha-1 antitrypsin deficiency).

80
Q

How does oxidative stress contribute to respiratory and cardiovascular disease?

A

It damages cellular structures, leading to inflammation, remodelling, and dysfunction.

81
Q

What are the common comorbidities in COPD patients?

A

Cardiovascular disease, osteoporosis, and anxiety/depression.

82
Q

How does hypertension accelerate atherosclerosis?

A

Increased pressure damages vessel walls, promoting plaque formation.

83
Q

What is the impact of air pollution on respiratory diseases?

A

Pollutants trigger inflammation, airway narrowing, and exacerbations.

84
Q

What medications are used to manage pulmonary hypertension?

A

Prostacyclins, endothelin receptor antagonists, and phosphodiesterase-5 inhibitors.

85
Q

How does asthma exacerbate in response to allergens?

A

Allergen exposure triggers IgE binding to mast cells, causing degranulation and bronchospasm.

86
Q

What mechanisms lead to hyperinflation in COPD?

A

Air trapping due to collapsed airways and reduced elastic recoil of alveoli.

87
Q

What is the effect of systemic corticosteroids in asthma exacerbations?

A

They rapidly reduce airway inflammation and improve airflow.

88
Q

What role does IL-5 play in eosinophilic asthma?

A

IL-5 promotes eosinophil production and activation, contributing to airway inflammation.

89
Q

How is pulmonary hypertension classified?

A

It is classified into primary (idiopathic) and secondary forms based on underlying cause.

90
Q

How do statins help in cardiovascular disease?

A

They reduce LDL cholesterol levels and stabilise atherosclerotic plaques.

91
Q

What diagnostic tests are used for COPD?

A

Spirometry, chest X-rays, and arterial blood gas analysis.

92
Q

How does systemic inflammation link COPD and cardiovascular disease?

A

Chronic inflammation accelerates atherosclerosis and vascular damage.

93
Q

Why are beta-agonists used in asthma treatment?

A

They relax airway smooth muscle, relieving bronchospasm.

94
Q

What is the function of IL-4 in asthma?

A

It induces IgE production and Th2-mediated inflammation.

95
Q

How does pulmonary hypertension lead to heart failure?

A

Right ventricular overload causes hypertrophy, dilation, and reduced output.

96
Q

What therapies reduce inflammation in atherosclerosis?

A

Statins, anti-inflammatory agents, and lifestyle interventions.

97
Q

How does air trapping occur in COPD?

A

Narrowed airways and loss of elastic recoil prevent complete exhalation.

98
Q

What causes mucus hypersecretion in chronic bronchitis?

A

Goblet cell hyperplasia and increased mucus gland activity.

99
Q

How does endothelial dysfunction initiate atherosclerosis?

A

Loss of NO production and increased permeability allow LDL infiltration.

100
Q

What are the clinical signs of pulmonary hypertension?

A

Loud second heart sound, jugular venous distension, and peripheral oedema.

101
Q

What is precision medicine?

A

Precision medicine customises treatments based on an individual’s genetic, molecular, and cellular profiles.

102
Q

Why is precision medicine important?

A

It targets subpopulations within diseases, optimising treatment for patient-specific phenotypes.

103
Q

What are organs-on-a-chip?

A

Microfluidic devices replicating organ-level functions for drug testing and disease modelling.

104
Q

How can organs-on-a-chip reduce animal testing?

A

They allow disease simulations on human-like tissues, minimising animal model dependence.

105
Q

What is the role of the electronic nose (eNose)?

A

It detects volatile organic compounds in exhaled breath to diagnose respiratory and metabolic diseases.

106
Q

How does the iKnife improve surgical precision?

A

It analyses molecular signatures of tissues during surgery to differentiate healthy and diseased tissue.

107
Q

How does 3D printing assist in patient-specific treatments?

A

It creates customised implants, prosthetics, and anatomical models.

108
Q

How is 3D bioprinting advancing regenerative medicine?

A

It constructs tissue scaffolds and organ structures for transplantation and repair.

109
Q

What environmental changes are predicted to reduce respiratory disease?

A

Decreased pollution in developed regions will lower cases of COPD and related illnesses.

110
Q

What global disparities exist in pollution-related diseases?

A

Developing regions are expected to suffer prolonged pollution-related illnesses.

111
Q

Why is obesity a growing concern for cardiovascular diseases?

A

Obesity increases risks for hypertension, diabetes, and atherosclerosis.

112
Q

How does an ageing population sustain chronic disease prevalence?

A

Elderly patients often live with pre-existing cardiovascular and respiratory diseases.

113
Q

How do smart devices assist in monitoring patient health?

A

They collect real-time data on vitals, treatment adherence, and disease progression.

114
Q

What risks arise with digital health tools and misinformation?

A

Social media and online misinformation may reduce treatment compliance.

115
Q

How can AI improve precision medicine outcomes?

A

AI analyses large data sets to identify disease patterns and optimal treatment strategies.

116
Q

What role do biosensors play in personalised medicine?

A

They measure biomarker levels for early diagnosis and treatment monitoring.

117
Q

How can environmental policies improve cardiovascular health?

A

Reducing air pollution lowers risks for ischemic heart disease, stroke, and COPD.

118
Q

What is the role of genomics in precision medicine?

A

Genomics analyses patient-specific genetic variations to predict treatment responses.

119
Q

What challenges exist for implementing precision medicine?

A

High costs, data privacy concerns, and accessibility gaps in low-resource settings.

120
Q

How does metabolomics contribute to future diagnostics?

A

It identifies metabolic changes linked to diseases, offering biomarkers for diagnosis.

121
Q

What is telemedicine, and how does it impact care?

A

Remote healthcare delivery improves patient monitoring and access to care.

122
Q

What are wearable devices, and how are they used?

A

Devices like smartwatches monitor physical activity, heart rate, and respiratory function.

123
Q

How might robotic surgery advance future care?

A

Robotics enhance surgical precision, reducing complications and recovery times.

124
Q

What are nanotechnologies in medicine?

A
125
Q

What are nanotechnologies in medicine?

A

Nanoparticles deliver drugs precisely to target tissues, reducing systemic side effects.

126
Q

How might AI assist in cardiovascular disease risk prediction?

A

AI algorithms analyse data to predict risk factors and recommend preventive interventions.

127
Q

What future role do electronic implants have?

A

Implants monitor or regulate heart rhythms, blood glucose, and other physiological functions.

128
Q

How do stem cells contribute to regenerative medicine?

A

Stem cells differentiate into specialised cells to repair damaged tissues.

129
Q

What are CRISPR and gene editing technologies?

A

They edit genetic material to correct mutations causing inherited diseases.

130
Q

What are smart inhalers, and how do they assist asthma patients?

A

They track medication usage and deliver optimised drug doses.

131
Q

Why is global healthcare equity a concern for future technologies?

A

Advanced treatments remain inaccessible in low-resource settings, widening health disparities.

132
Q

How does ageing affect heart and lung disease prevalence?

A

Age-related loss of function increases risks for heart failure, hypertension, and COPD.

133
Q

What are bioengineered lungs?

A

Laboratory-grown lungs created using stem cells for transplantation.

134
Q

What are some future trends for drug delivery systems?

A

Innovations include nanoparticle carriers and sustained-release systems for targeted delivery.

135
Q

How can virtual reality (VR) be used in medical training?

A

VR simulates surgeries and procedures, providing a safe learning environment.

136
Q

What is personalised nutrition, and how is it relevant?

A

Tailored dietary plans aim to reduce obesity and associated cardiovascular risks.

137
Q

How will machine learning revolutionise medical imaging?

A

Algorithms improve image interpretation for early diagnosis of diseases.

138
Q

How might exosome-based therapies treat lung disease?

A

Exosomes deliver therapeutic molecules to target injured tissues for repair.

139
Q

What is the significance of global warming on respiratory health?

A

Higher pollution and allergens exacerbate conditions like asthma and COPD.

140
Q

How does patient data contribute to precision medicine?

A

Genomic and clinical data inform customised therapies and research outcomes.

141
Q

What ethical considerations arise with future medical technologies?

A

Issues include data privacy, equitable access, and consent for personalised interventions.

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