CSI 1: Fresher’s Flu Flashcards

1
Q

What is a ‘differential diagnosis’?

A

Differentiating between multiple conditions associated with the same symptoms

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2
Q

Key differences between flu and cold symptoms

A
  1. Rapid onset vs slow onset
  2. First symptom: cough vs sore throat
  3. Systemic vs mainly upper respiratory tract (nose & sore throat)
  4. Sneezing, runny nose, mild phlegmy cough - cold; fatigue, aching, fever, headaches, dry cough - flu
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3
Q

What virus causes COVID-19, flu, cold?

A
  1. Coronavirus
  2. Influenza virus
  3. Rhinovirus (most common), coronavirus, adenovirus
    *Influenza C could cause very mild cold-like symptoms but doesn’t really count
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4
Q

To what does coronavirus bind to enter a cell? How does it cause symptoms?

A
  • Spike protein of SARS-CoV-2 binds to ACE2
  • When bound, ACE2 is downregulated, more angiotensin II is produced without getting cleared away -> acute lung injury and myocardial remodelling
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5
Q

What does ACE2 (angiotensin converting enzyme 2) do?

A

Clears angiotensin II from the system (by converting it into angiotensin (1-7)

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6
Q

Renin-Angiotensin System and Angiotensin II

A
  • RAS maintains blood pressure levels in blood cells and generates important hormones in the process
  • Local/systemic infection or sepsis leads to production of angiotensin I
  • Angiotensin I is converted to angiotensin II by ACE
  • Angiotensin II induces vasoconstriction and moderates vascular permeability by binding to angiotensin II type 1 receptor
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7
Q

What can excess angiotensin II in the system lead to?

A

Adverse myocardial remodelling and acute lung injury

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8
Q

How does influenza enter a cell?

A
  1. Haemagglutinin (a glycoprotein) on viral membrane binds to sialic acid on host cell membrane
  2. Virus enters cell by endocytosis
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9
Q

What are the three main molecules involved in influenza’s MOA?

A

HA, NA, Matrix-2

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10
Q

What is the purpose of neuraminidase?

A

Tis a glucoside hydrolase enzyme, which cleaves the sialic acid group that is tethering the original virus/budding virion to the host csm

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11
Q

How does rhinovirus enter a cell?

A

The multiprotein groove on the protein shell of rhinovirus binds to ICAM1 on the host cell surface membrane.

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12
Q

Key risk factors during fresher’s week

A
  • Lack of sleep
  • Alcohol (source of calories, replacing healthier food; acetaldehyde toxic breakdown product)
  • Poor diet
  • Close proximity, crowding
  • Meeting new people
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13
Q

Key risk factors for the general population

A
  • Age
  • Comorbidities, chronic illness
  • Immune disorder
  • Pregnancy
  • People living in long term facilities
  • Obesity BMI>40
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14
Q

How does exercise affect your risk of getting the common cold?

A
  1. Moderate exercise - increased levels of cortisol, improving immune function; adrenaline released has a pro-immune effect too
  2. Intense exercise - cortisol levels too high, becoming immune suppressive
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15
Q

How does stress affect your risk of getting the common cold?

A

The higher the individual’s stress, the more cortisol is released in high levels => risk of infection increases as immune system is weakened

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16
Q

How does sleep affect your risk of getting the common cold?

A

During sleep, WBCs migrate to lymphoid tissues, increasing chances of encountering viruses => the more sleep you get, the more time is allowed for the immune system to carry out its function

*Below five hours and risk of infection increases more steeply

17
Q

How are different strains of virus differentiated between?

A

Subtype, geographical origin, year of isolation, species of origin

18
Q

How do different subtypes of viruses differ from each other?

A

By their surface proteins i.e. antigenic material

19
Q

What are Zola’s triggers?

A
  1. Interpersonal crisis
  2. Interference with personal/social relations
  3. Sanctioning
  4. Interference with vocational/physical activity
  5. Temporalising
20
Q

What is an illness behaviour?

A

The way a certain individual will respond to and monitor bodily indications that they are ill (symptoms) and decide whether or not to see a doctor

21
Q

What is Helman’s Folk model of illness?

A
  1. What has happened?
  2. Why has it happened?
  3. Why to me?
  4. Why now?
  5. What would happen, if nothing is done?
  6. What should I do about it/who should I turn to for help?
22
Q

What is unique about influenza C?

A
  • It is structurally different to influenza A
  • Causes mild upper respiratory tract illness -> common cold
23
Q

What is antigenic drift?

A
  • Natural genetic mutations of a known strain that accumulate over time
  • Resulting different antigenic material that might not be recognised by an immune system
  • Could lead to gradual loss of immunity or vaccine mismatch
24
Q

What is antigenic shift?

A
  • Abrupt major change in genetic material
  • Confers a phenotypic change that needs an entirely new antigenic response
  • Risk of pandemic
  • Only in influenza A
25
Q

Why can antigenic shift only happen in Influenza A?

A
  • Influenza A can infect other organisms, not just humans
  • Human cells can only be infected by viruses with certain HAs, even though there are many avian strains
  • Pigs can be infected by both human and avian strains of influenza A
  • They act as a reservoir of genetic reassortment between HA/NA molecules
26
Q

Other than acting as way of viral entry into the cell, what can haemagglutinin do?

A
  • Act as an attachment factor
  • By binding to sialic acid on erythrocytes causing haemagglutination [a network of interconnected RBCs and viral particles]