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Medical Studies 1 > Revision—Sealing the Cracks > Flashcards

Revision—Sealing the Cracks Flashcards

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USMLE® Step 1 flashcards
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

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2
Q

What occurs during the mammalian dive response?

A
  • Decreased peripheral blood flow
  • Apnoea
  • Bradycardia
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3
Q

What conditions can cause heart murmur?

A
  • Atrial/pulmonary stenosis/regurgitation
  • Rheumatic fever
  • Anemia
  • Infective endocarditis
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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
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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
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6
Q

Describe cardiac pacemaker action potential

A
  • Resting: -65mV
  • Na+ influx: -50mV
  • Ca2+ influx: +10mV
  • K+ outflow: -65mV
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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

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8
Q

What are the two main types of bradyarrhytmia?

A
  • Sinus node dysfunction
  • Atrioventricular block
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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%

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10
Q

Describe four clinical features of asthma.

A

Features:
- Coughing
- Dyspnoea
- Chest tightness
- Wheeze

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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
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12
Q

List some theories on the aetiology of asthma

A
  • NO2 release
  • Smoking during pregnancy/childhood
  • Hygiene hypothesis
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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
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14
Q

What cardiovascular diagnosis is often used mistakenly instead of COPD?

A

Angina; since it commonly causes breathlessness.

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15
Q

Symptoms that are suggestive of COPD

A
  • Exertional breathlessness
  • Cough
  • Sputum
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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
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17
Q

Common viruses that exacerbate COPD

A
  • Rhinoviruses
  • Influenza viruses
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18
Q

Common bacteria that exacerbate COPD

A
  • Haemophilus influenzaue
  • Streptococcus pneumoniae
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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
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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
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21
Q

Describe the airway remodelling that occurs during asthma

A
  • Subepithelial fibrosis
  • Angiogenesis
  • Smooth muscle cell hyperplasia
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22
Q

Describe emphysema

A
  • Loss of elasticity
  • Hyperinflation of lungs
  • Increased airspaces (instead of many small ones), decreased SA:V
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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
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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)
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25
Q

List some non-pharmacological treatment methods for asthma

A
  • Trigger avoidance
  • Vaccinations
  • Education
  • Action plan
  • Exercise + Pulmonary Rehab
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26
Q

What does SMART therapy stand for?

A

Single Maintenance and Reliever Therapy (both in one)

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27
Q

What adverse effects are associated with frequent SABA use?

A
  • Beta receptor downregulation
  • Decreased bronchodilator response
  • Increased allergic response
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28
Q

Track 1 vs Track 2 asthma treatment

A

Track 1: ICS + LABA
Track 2: ICS (preventer) + SABA (reliever)

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29
Q

Extrapulmonary complications of asthma

A
  • Obesity
  • Anxiety and depression
  • Osteoporosis
30
Q

Describe airway thermoplasty

A
  • Bronchoscope into airways
  • Apply radio-frequency light to decrease smooth muscle bulk in airways
31
Q

Describe the treatment of COPD flare-ups

A
  • 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
Q

How do you treat type 2 respiratory failure in COPD exacerbations?

A

CPAP or BiPAP

33
Q

Inhaled glucocorticoid mechanism

A
  • Bind intracellular glucocorticoid recptors
  • Increased expression of anti-inflammatory genes
  • Suppression of pro-inflammatory genes
34
Q

Mucolytics mechanism of action

A

They break the disulfie bonds within mucous molecules

35
Q

What is a COPD self-management plan?

A

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
Q

How do monoclonal antibodies help in chronic airway disease?

A

Bind to and inhibit certain key components of the inflammatory pathways (i.e. cytokines etc.)

37
Q

Preventer vs reliever in asthma

A

Preventer: prophylaxis, stop symptoms from occurring
Reliever: relieves symptoms if they occur

38
Q

List some medications that can be used in the treatment of acute asthma exacerbations

A
  • SABAs
  • Systemic corticosteroids
  • Supplemental oxygen (hypoxaemia)
39
Q

Describe the main indication for oxygen therapy in COPD patients

A

Hypoxaemia

40
Q

Demographic risk factors for SCD

A
  • Men
  • Old
  • African-American/Non-Asian
41
Q

Specific conditions that can predispose to SCD

A
  • CHD
  • AF
  • CKD
  • Obstructive sleep apnoea
  • Cardiomyopathy
  • Valvular heart disease
42
Q

Define Sudden Cardiac Arrest (SCA)

A

Sudden loss of all heart activity

43
Q

List the eight reversible causes of cardiorespiratory arrest

A

(4 Hs, 4Ts)
Hypoxia
Hypovolaemia
Hypo/Hyperkalaemia/metabolic disorders
Hypothermia/Hyperthermia
Tension pneumothorax
Tamponade
Toxins
Thrombosis (pulmonary/coronary)

44
Q

What are the two types of non-sustained ventricular arrythmias?

A
  • Ventricular ectopic
  • Non-sustained ventricular tachycardia (>=3 beats, <30 seconds)
45
Q

What are the three forms of sustainted ventricular arrythmia?

A
  • Ventricular tachycardia
  • Ventricular flutter
  • Ventricular fibrillation
46
Q

Describe polymorphic VT ECG findings. What often causes it?

A
  • Multiform QRS morphology from beat to beat (widened)
  • A sign of ischaemia
47
Q

Describe ECG findings of bidirectional VT. What can cause it?

A
  • Beat-to-beat QRS alternation
  • Can be caused by toxins/catecholaminergic polymorphic VT)
48
Q

Describe re-entrant ventricular VT. What type of VT can it cause in terms of ECG findings?

A
  • Circuit of slow and fast conducting myocardium created due to scarring/electrical remodelling
  • Can cause monomorphic VT
49
Q

Describe ECG findings of ventricular flutter

A

Sinusoidal (>300bpm), no isoelectric interval between QRS complexes

50
Q

Describe ECG findings of ventricular fibrillation

A
  • Rapid, grossly irregular electrical activity with marked variability in ECG waveform
  • Usually >300bpm
51
Q

Describe the positive feedback loop of a cytokine storm

A
  • 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
Q

ARDS symptoms/signs

A
  • Dyspnoea
  • Low O2 sat
  • Tahchypnoea
  • Rattling sounds when breathing
53
Q

Risk factors for severe illness in COVID-19

A
  • Age
  • Smoking
  • Pregnancy
  • Male gender
  • Chemotherapy
  • Childhood cancer
  • Diabetes
54
Q

How does remdesivir (IV antiviral) inhibit viral replication

A

Inhibits activity of RdRp

55
Q

Describe the SMART COP mnemonic for pneumonia severity

A
  • Systolic BP <90mmHg
  • Multilobar CXR involvement
  • Albumin < 3.5 g/dL
  • Resp Rate >30
  • Tachycardia >125bpm
  • Confusion
  • O2 sats <90%
  • pH <7.35
56
Q

Explain the CURB-65 severity scoring

A
  • Confusion
  • Urea >7 mmol/L
  • Respi rate >30
  • Blood pressure (sys <90 or dia <60)
  • Age: >65
57
Q

Which enzymatic pathway is affected in myelofibrosis? Which cell does it affect?

A
  • JAK2 pathway
  • Affects haematopoietic stem cells (gene mutation)
58
Q

Provide an outline of aplastic anaemia, including what it is, the most common cause, symptoms

A
  • 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
Q

How can primary ciliary dyskinesia cause chronic lung inflammation?

A
  • Mucous is static
  • Bacteria multiply
  • Causes pneumonia
  • Repeated: chronic inflammation
60
Q

How can cystic fibrosis cause chronic inflammation?

A
  • Stasis of mucous due to thickness
  • Division of bacteria
  • Pneumonia
  • Recurrent: chronic inflammation
61
Q

How can airway obstruction (from tumours or aspirated bodies) cause chronic inflammation?

A
  • Impairs mucociliary escalator
  • Pneumonia
  • Recurrent: chronic inflammation
62
Q

How can chronic inflammation cause bronchiectasis?

A
  • 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
Q

How can bronchiectasis cause RV hypertrophy? What is this called?

A
  • Widespread hypoxia -> vasoconstriction
  • Pulmonary hypertension
  • RV hypertrophy
  • Called cor pulmonale
64
Q

What three kinds of supportive therapy are used during pulmonary hypertension (i.e. not vasodilators)

A
  • Supplemental O2
  • Diuretics
  • Anticoagulants
65
Q

If there is a contraindication to anticoagulation in HD stable PE treatment, what treatment do we use instead?

A

IVC filter

66
Q

If there is a contraindication to TpA (thrombolytics) in HD unstable PE treatment, what treatment do we use instead?

A

Embolectomy

67
Q

Describe prothrombin time (PT). What is the testing performed on, what is added to it, and what are we measuring?

A
  • Done on plasma
  • Factor 3 and calcium are added
  • Measures speed of clotting via extrinsic pathway and common pathway
68
Q

What is INR?

A

It is a globally normalised ratio that enables us to compare prothrombin times from lab to lab

(International normalised ratio)

69
Q

What is Factor V Leiden mutation?

A

Factors V and Va are resistant to cleavage by protein C

70
Q

True or false: plasmin specifically breaks down fibrin (i.e., it is a fibrinolytic)

A

True

Medical Studies 1 (90 decks)

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