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MD4001 > Week 8 > Flashcards

Week 8 Flashcards

1
Q

What is anxiety associated with?

A
  • Threatening situations (medical procedures involve huge amount of uncertainty)
  • Thoughts of threatening situations
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2
Q

List what patients are anxious about?

A
  • Anaesthesia/unconscious
  • Waking during surgery
  • Pain (e.g post-operative)
  • Life-threatening procedures
  • Post-operative outcome
  • Possibility of disfigurement
  • Threat of severe illness
  • Outcome of test results
  • Unfamiliarity of surroundings
  • Physical restriction
  • Loss of independence
  • Being away from home
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3
Q

What does Kiecolt-Glaser et al. Psychological influences on surgical recovery say?

A

Pre-operative anxiety effects outcomes of recovery

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4
Q

What are patients who experience high anxiety pre-operatively more likely to have?

A
  • More pain post-operatively
  • Use more analgesic
  • Stay in hospital longer
  • More complications
  • Anxiety & depression after surgery
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5
Q

What does Kiecolt-Glaser et al. Psychological influences on surgical recovery say regarding “Communication”?

A

Anxious patients are less likely to understand the info they are told

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6
Q

What does Kiecolt-Glaser et al. Psychological influences on surgical recovery say regarding “Adherence”?

A

Patients with anxiety are less likely to be compliant with coughing & breathing exercises (reduce likelihood of pneumonia), getting out of bed & moving around (reduce phlebitis & enhance wound healing)

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7
Q

What does Kiecolt-Glaser et al. Psychological influences on surgical recovery say regarding “Pain Management”?

A

Pre-surgery anxiety & stress can influence the type & amount of anaesthetic

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8
Q

How can we help patients who have anxiety?

A
  • Increase sense of control
  • Procedural info
  • Behavioural instruction
  • Cognitive coping
  • Sensory info
  • Modelling
  • Counselling
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9
Q

What are the benefits of procedural info & behavioural instruction according to Classic study by Egbert et al. (1964)?

A
  • Patients were discharged from hospital on average 2.7 days earlier
  • Required half as much pain medication as patients receiving usual care
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10
Q

Describe the 4 parts to the Langer, EJ, Janis, IL & Wolfer, JA. (1975) Journal of Experimental Social Psychology experiment?

A
  1. Teaching cognitive coping
  2. Procedural prep info
  3. Cognitive coping + procedural prep info
  4. Control group
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11
Q

What are the 3 positive effects of cognitive coping?

A
  1. Less analgesics
  2. Trend for early discharge (not statistically sign)
  3. Able to cope with discomfort better
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12
Q

Describe the 4 parts to the Kulik, JA & Mahler, HI. (1989) Personality & Social Psychology Bulletin experiment?

A
  1. Room with another pre-op patients, same surgery
  2. Room with another pre-op patient, different surgery
  3. Room with a post-op patient, same surgery
  4. Room with a post-op patient, different surgery
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13
Q

What are the 3 positive effects of having a room with post-op patient from same/different surgeries?

A
  1. Released more quickly
  2. Less anxious post-op
  3. More ambulatory post-op (movement)
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14
Q

Describe anxiety & non-surgical procedures?

A
  • Can be just as anxiety-provoking & distressing

- Techniques used for surgery patients can also be beneficial to prepare patients for non- surgical procedures

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15
Q

What 2 ways can you prepare a patients for endoscopy?

A
  1. Procedural & sensory info- describing endoscopy procedure & sensations to expect
  2. Behavioural instructions- teaching how to breathe & swallow to facilitate throat anaesthetisation & tube passage
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16
Q

What does the 2 methods to prepare a patient for endoscopy do?

A
  • Sensory information reduced distress
  • Combination of coping information & behavioural instructions reduced distress & reduced time required for tube passage
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17
Q

Describe how cancer patients may experience anxiety around non-surgical procedures?

A
  • Drug induced nausea & vomiting
  • Repeated chemotherapy treatments, may also experience Anticipatory Nausea & Vomiting (ANV) before chemotherapy
  • ANV may lead to discontinuing treatment
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18
Q

What are 3 ways to prepare a patient for a non-surgical procedure?

A
  1. Systematic desensitisation
  2. Information provision
  3. Relaxation training
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19
Q

What is a “Monitors” coping style?

A

Copes by seeking out detailed info

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20
Q

What is a “Blunters” coping style?

A

Copes by using avoidance to minimise the situation

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21
Q

According to a study on Women undergoing gyne exam, what happens when monitors are given little info & blunders are given a lot of info?

A

React negatively to the amount of info the received as evidence by their continued high pulse rates after the exam

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22
Q

According to a study on Women undergoing gyne exam, what happens who monitors are given more info & blunders are given low info?

A

Reacted more positively as evidenced by their reduction in pulse rates after the exam

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23
Q

What are the 2 explanations for how psychological preparation promotes recovery?

A
  1. Psychological prep –> Reduces stress –> Reduce sympathetic arousal –> Improves immunological & endocrine responses
  2. Preparations –> Reduced frequency & extent of maladaptive behaviours that unprepared patient can engage in (not doing breathing exercises)
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24
Q

What are the problems with Barbiturate drugs?

A
  • Dependence
  • Addiction
  • Misuse due to highs
  • Narrow therapeutic index
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25
Q

What 2 things are Barbiturates still used for?

A
  1. IV induction agents

2. Anti-convulsants

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26
Q

What are the 5 different classes of drugs for anxiolytics & sedatives?

A
  1. Antidepressants
  2. Benzodiazepines
  3. Z-drugs
  4. B-blockers
  5. Other ie. Melatonin, Sedating antihistamine
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27
Q

Describe Benzodiazepine drugs?

A
  • Serendipity (librium)
  • Highly lipophilic
  • Well absorbed orally
  • Highly protein bound (95%)
  • Hepatic metabolism
  • Active metabolites
  • Excreted as glucoronide conjugate
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28
Q

What are the 5 major effects of Benzodiazepines?

A
  1. Anxiolytic- reduce anxiety (α2 & α3 )
  2. Hypnotic- induce sleep (α1)
  3. Reduce muscle tone
  4. Anterograde amnesia (pros&cons)
  5. Anticonvulsant effect
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29
Q

How do you administer Benzodiazepines?

A
  • Orally or intravenously

- Not advised to be given intramuscular

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30
Q

What are the 2 categories of Benzodiazepines?

A
  1. Short acting- Lorazepam, Temazepam (t1/2 8-12hrs)

3. Long acting- Diazepam (t1/2 20-100hrs)

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31
Q

Describe the GABAa receptors?

A
  • Pentameric
  • Central ion channel pore (Chloride)
  • 18 possible subunits
  • 30 forms of receptor
  • Some subunits location specific
  • Anaesthetics & benzos allosterically activate the receptor
  • Increase frequency of opening
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32
Q

What is sedation mediated via?

A

GABAa with α1 subunit

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33
Q

What is anxiolysis mediated via?

A

GABAa with α2 & α3 subunits

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34
Q

What is Flumazenil?

A

Competitive benzodiazepine antagonist

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35
Q

Describe Flumazenil drug?

A
  • Short half life compared with benzodiazepines
  • May precipitate agitation & seizures
  • IV 100mcg increments
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36
Q

What are the side effects of Flumazenil?

A

Nausea & vomiting

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37
Q

Where do Z-drugs act?

A

Benzodiazepine receptors (very similar pharmacodynamic profile)

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38
Q

Give 3 examples of Z drugs?

A
  1. Zopiclone
  2. Zaleplon
  3. Zolpidem
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39
Q

What is the definition of Tolerance?

A

Physiological state characterized by decrease in effects of a drug with chronic administration

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40
Q

Describe the tolerance of Benzodiazepines?

A

Tolerance develops quickly for sedative effects & slowly for anxiolytic & anticonvulsant effects

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41
Q

What are the 4 mechanisms for tolerance?

A
  1. Neuro-adaptive process
  2. Desensitisation of inhibitory GABA receptors
  3. Sensitisation of (excitatory) NMDA receptors
  4. Adaptions on different time scale
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42
Q

When/How does drug dependence occur?

A
  • Induces a rewarding experience
  • Drug taking becomes compulsive
  • Psychological/ Physical dependence
  • Genetic factors
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43
Q

Describe the feelings of withdrawal?

A
  • Increased anxiety, onset / exacerbation of depression
  • Disturbed sleep
  • Pain, stiffness, muscular aches
  • Convulsions
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44
Q

What is withdrawal a result of?

A

Physical dependence (occur after relatively short courses of treatment)

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45
Q

What are Anxiolytics?

A

Medication/other intervention that inhibits anxiety

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46
Q

What are the clinical roles for sedative & anxiolytic agents/ when would you prescribe them?

A
  • Enable uncomfortable diagnostic & therapeutic procedures to be carried out
  • Management of acute alcohol withdrawal
  • Other: anticonvulsant
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47
Q

What would you prescribe for management of acute alcohol withdrawal?

A

Chlordiazepoxide 1-2 week reducing regime

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48
Q

What is the CAGE questionnaire?

A
  • Have you ever felt you should Cut down your drinking?
  • Annoyed by other people criticizing?
  • Felt Guilty about drinking?
  • Taken a drink in morning to steady nerves or ease a hangover (Eye- opener)?
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49
Q

What are the symptoms of alcohol withdrawal?

A
  • Insomnia / anxiety/ restlessness/ agitation
  • Tremor
  • Nausea & vomiting
  • Sweating/Palpitations
  • Hallucinations auditory /visual/tactile
  • Seizures
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50
Q

What are 4 investigations suggestive of chronic alcohol consumption?

A
  1. Raised MCV
  2. Pancytopenia (alcohol induced bone marrow suppression)
  3. Folate deficiency
  4. Prolonged prothrombin time
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51
Q

Describe the timeline for symptoms of alcohol withdrawal?

A
  • May start 8hrs after drop in alcohol levels

- Peak day 2

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52
Q

How do you manage insomnia?

A
  • Assessment (pain/breathlessness)
  • Good sleep hygiene
  • Hypnotics reserved for acutely distressed
  • Caution in elderly
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53
Q

Why is there caution in the elderly for using hypnotics?

A
  • Confusion
  • Falls
  • Slower metabolism
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54
Q

What is sleep hygiene?

A

Aims to make people more aware of behavioural, environmental & temporal factors that may be detrimental or beneficial to sleep

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55
Q

What should you prescribe (if you must) for insomnia?

A
  • Short acting Benzodiazepine or Z-drug
  • Lowest effective dose for shortest time
  • Inform patient no repeat prescriptions & explain why
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56
Q

How do you manage prolonged seizures?

A
  • O2 if available
  • Longer than 5 mins IV Lorazepam
  • IV not available consider rectal Diazepam or intranasal / buccal Midazolam
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57
Q

What should you consider/exlude in prolonged seizures?

A

Hypoglycaemia

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58
Q

Describe the management of acute anxiety?

A
  • Guided self help: reduce caffeine & alcohol, mantras, mindfulness, worrytime
  • Cognitive behavioural therapy
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59
Q

Should you use benzodiazepines for acute anxiety in a primary care setting?

A
  • NO, its inappropriate for “mild”

- Indicated for short-term relief of anxiety that is severe, disabling or causing patient unacceptable distress

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60
Q

Describe the effect of B-blockers for managing the somatic symptoms of anxiety?

A
  • Helps with tachycardia,
    palpitations, tremor, sweating
  • Usually Propranolol
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61
Q

What are the advantages of B-blockers?

A
  • Non-sedative

- No dependence or abuse

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62
Q

What is Gabapentin & Pregabalin used for?

A
  • NICE: consider pregabalin for generalised anxiety
  • Used to manage chronic pain
  • But misuse / abuse
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63
Q

What is Melatonin?

A

Naturally occurring hormone synthesized in pineal gland

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64
Q

What are the levels of people’s melatonin throughout the day?

A

High levels at night, low during day

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65
Q

What is Melatonin secreted in response to?

A

Input from retina

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66
Q

When is Melatonin drug used?

A
  • Children with sleep disturbance

- Licensed for insomnia > 55yrs

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67
Q

What are the laws on driving (March 2015)?

A
  • Offence to drive with certain drugs above specified levels in body, whether driving is impaired or not
  • Taking drugs as directed & driving not impaired= NOT breaking the law
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68
Q

What 3 medications can affect driving?

A
  1. Benzodiazepine
  2. Opioids
  3. Amphetamines
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69
Q

What are the 3 main categories of harm?

A
  1. Physical Harm
  2. Dependence
  3. Social harms
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70
Q

What is Doxapram?

A

Short acting respiratory stimulant used in respiratory failure

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71
Q

In what 3 scenarios would you use Doxapram?

A
  1. Post-operative respiratory depression
  2. Acute respiratory failure
  3. Neonatal apnoea
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72
Q

Describe Strychnine convulsant drug?

A
  • Poison
  • Powerful convulsant
  • Violent extensor spasms triggered by minor sensory stimuli
  • Blocks glycine receptors
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73
Q

What does small doses of Strychnine drug cause?

A

Improvement in visual & auditory acuity

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74
Q

What do Hallucinogen drugs (psyhchotomimetic drugs) act on?

A

5-HT receptors & transporters

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75
Q

Give 4 examples of Hallucinogen drugs?

A
  1. LSD (D-lysergic acid diethylamine)
  2. Psilocybin
  3. Mescaline
  4. MDMA (Ecstasy)
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76
Q

What are the main pharmacological effect of Hallucinogens?

A
  • Alter perception of sights & sounds
  • Hallucinations (visual, auditory, tactile or olfactory)
  • Sounds perceived as visions
  • Thought processes illogical & disconnected
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77
Q

What are “bad trips”?

A
  • Hallucinations can take on menacing quality

- Maybe accompanied by paranoid delusions

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78
Q

When can “flashbacks” occur due to hallucinogens?

A

Weeks or months later

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79
Q

When can a tolerance to Hallucinogen’s develop?

A

Quickly (plus cross-talk between drugs ie. LSD causes higher doses of MDMA needed for the same effects)

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80
Q

Describe the withdrawal of Hallucinogen’s?

A

No physical withdrawal syndrome, psychological effects i.e. “flashbacks & psychosis

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81
Q

What are the risks for Hallucinogen’s?

A
  • Injury & accidental death whilst intoxicated
  • Poisoning due to mistaken identity
  • Adrenergic effects with LSD
  • GI effects with Psilocybin
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82
Q

Describe Phencyclidine (PCP, “Angel Dust”) dissociative anaesthetic?

A
  • Synthesised as possible IV general anaesthetic

- Disorientation & hallucinations

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83
Q

Describe the use of Ketamine?

A

Induction & maintenance of anaesthesia

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84
Q

What effects do Phencyclidine & Ketamine dissociative anaesthetics have?

A
  • Resemble other psychotomimetic drugs
  • Analgesic
  • Stereotyped motor behaviour like Amphetamine
  • Can give “bad trip” as LSD
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85
Q

What are both Phencyclidine & Ketamine?

A

NMDA receptor antagonists

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86
Q

Describe the tolerance of dissociative anaesthetics?

A

Rapid over regular, repeated doses

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87
Q

Describe the dependence of dissociative anaesthetics?

A
  • Physical & psychological
  • Withdrawal
    syndromes with PCP
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88
Q

Describe the risks of dissociative anaesthetics?

A
  • Accidents/loss of control/automatic behaviour
  • PCP: hyperthermia, convulsions
  • Ketamine: overdose with heart attack/respiratory failure (rare)
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89
Q

What is Cannabis (cannabis sativa, indica)?

A
  • Psychotomimetic drug

- Tetrahydrocannabinol (THC) & 11-hydroxy-THC

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90
Q

Give 5 examples of psychomotor stimulants?

A
  1. Amphetamine (speed)
  2. Dextroamphetamine
  3. Methylamphetamine (crystal meth)
  4. Methylphenidate (ritolen)
  5. 3,4-methylenedioxymethamphetamine (MDMA)
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91
Q

What are the main effects of psychomotor stimulants?

A
  • Locomotor stimulation
  • Euphoria & excitement
  • Insomnia
  • Anorexia (diminishes with continued use)
  • Stereotypic behaviour (chronicuse)
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92
Q

What are the behavioural effect of Amphetamine probably due to?

A

Release of dopamine rather than noradrenaline

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93
Q

Describe the effects of Amphetamine?

A
  • Become confident, hyperactive & talkative
  • Sex drive enhanced
  • Fatigue (both physical & mental) reduced
  • Doesn’t enhance mental performance, just ability to concentrate for longer
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94
Q

Describe the mode of action of Amphetamines?

A
  • Competitive inhibitors of monoamine uptake (noradrenaline, dopamine)
  • Inhibit MAO at high concentrations
  • Cause NET to work in “reverse”
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95
Q

What are the 3 dopamine pathways in the brain & what do they do?

A
  1. Nigrostriatal- Motor control
  2. Mesolimbic & Mesocortical- behavioural effects
  3. Tuberohypophyseal system- endocrine function
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96
Q

What are the 2 noradrenaline pathways in the brain & what do they do?

A
  1. Locus coeruleus- wakefulness, alterness

2. Medulla/hypothalamus- Blood pressure regulation

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97
Q

What are the 2 serotonin pathways in the brain & what do they do?

A
  1. Locus coeruleus- sensory signals

2. Raphe nuclei- sleep, wakefulness, mood

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98
Q

Describe the tolerance of Amphetamines?

A

Rapid tolerance to euphoric & anorexic effects, slowly for other effects

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99
Q

Describe the dependance of Amphetamines?

A

Moderate dependence potential due to euphoria

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100
Q

Describe “Amphetamine psychosis”?

A
  • If taken repeatedly over a few days
  • Almost indistinguishable from acute schizophrenic attack
  • Stereotypic behaviour
  • After cessation, period of deep sleep
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101
Q

What can the subject feel after cessation of Amphetamines?

A

Lethargic, depressed, anxious & often very hungry

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102
Q

What are the risks of Amphetamines?

A
  • Vascular accidents (tachycardias, arrhythmias, ↑ BP)
  • Cerebral convulsions & coma
  • Excitation syndrome (hyperthermia/tachycardia)
  • Anorexia
  • Chronic paranoid psychosis
  • Cognitive impairment
  • Personality/mood
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103
Q

What is Khat (Catha edulis)?

A
  • Psychomotor stimulant

- Contains cathinone, an amphetamine-like stimulant

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104
Q

What is Nicotine (Nicotiana tabacum)?

A

Psychomotor stimulant

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105
Q

Where does Cocaine comes from?

A

Leaves of South American shrub, Erythroxylum Coca

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106
Q

What is Cocaine?

A

Potent inhibitor of catecholamine uptake into nerve terminals (esp. dopamine)

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107
Q

What are the effects of Cocaine (which resemble Amphetamines)?

A
  • Euphoria (related to ↓ dopamine & 5-HT reuptake)
  • Alertness & wakefulness
  • Increased confidence & strength
  • Increased sexual feelings
  • Indifference to concerns/cares
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108
Q

How can cocaine be administered?

A
  • Readily absorbed by many routes
  • Nasal damages the mucosa & septum
  • Free-base form (‘crack’) can be smoked
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109
Q

Describe the tolerance of cocaine?

A

Occurs rapidly

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110
Q

Describe the dependance of cocaine?

A
  • Physical dependence mild
  • Strong psychological
    dependence occurs
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111
Q

What are the ACUTE risks of cocaine?

A
  • Cardiovascular (↑BP, tachycardia, ventricular fibrillation, heart attack, respiratory arrest, stroke)
  • Muscle spasms, tremor
  • Hyperthermia
  • Seizures, headaches, excited delirium
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112
Q

What are the CHRONIC risks of cocaine?

A
  • Heart attacks (furring of coronary arteries)
  • Malnutrition & weight loss
  • Decreased libido & impotence
  • Personality/mood
  • “Toxic syndrome”
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113
Q

What is “toxic syndrome” from chronic cocaine similar to?

A

Acute paranoid schizophrenia

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114
Q

What contains Methylxanthines?

A

Tea, coffee, cocoa

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115
Q

What are the main 2 Methylxanthines?

A
  1. Caffeine

2. Theophylline

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116
Q

Describe the effects of Caffeine & Theophylline (Methylxanthines)?

A
  • Mild CNS stimulants
  • Diuretics
  • Cardiac muscle stimulants
  • Smooth muscle relaxants (esp. bronchial)
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117
Q

What are the main psychological effects of Methylxanthines?

A

Reduce fatigue & improve mental performance without any euphoria

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118
Q

Methylxanthines develop what to a small extent?

A

Tolerance & habituation

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119
Q

What can Theophylline be used for clinically?

A

Bronchodilator in severe asthma attacks

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120
Q

What do all endocrine glands NOT have?

A

Ducts

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121
Q

What is an endocrine secretion?

A

Hormones diffuse directly into capillaries to act on distant target organs

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122
Q

What is a paracrine secretion?

A

Hormones secreted & act more locally

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123
Q

What is a autocrine secretion?

A

Hormones which act on themselves

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124
Q

Endocrine glands are very ______?

A

Vascular (fenestrated capillaries)

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125
Q

Describe the 3 different locations of endocrine glands?

A
  1. Discrete organs (thyroid, pituitary, adrenals)
  2. Associated with other tissues (pancreas)
  3. Scattered within complex organs (ovary, kidney, gut)
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126
Q

List the major endocrine glands?

A
  • Pineal
  • Hypothalamus
  • Pituitary
  • Thyroid
  • Parathyroid
  • Thymus
  • Adrenal
  • Pancreas
  • Ovary
  • Testis
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127
Q

What are the 3 factors controlling hormone release from endocrine glands?

A
  1. Humoral
  2. Neural
  3. Hormonal
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128
Q

What are the hormones in the hypothalamus-pituitary axis?

A

Endocrine & Neuroendocrine hormones

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129
Q

What are the hormones in the adrenal cortex/medulla?

A
  • Glucocorticoids
  • Mineralocorticoids
  • Catecholamines
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130
Q

What are the hormones in the thyroid?

A
  • Thyroid hormones

- Calcitonin

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131
Q

What is the hormone in the parathyroids?

A

Parathyroid hormone (PTH)

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132
Q

What are the hormones in the pancreas?

A
  • Insulin
  • Glucagon
  • Pancreatic polypeptide
  • Somatostatin
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133
Q

What are the hormones in the gastrointestinal tract?

A
  • CCK, GIP, GLP 1&2
  • Glicentin, Gastrin
  • Bombesin
  • Secretin, VIP
  • Substance P
  • Guanylins
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134
Q

What is the hormone in the pineal gland?

A

Melatonin

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135
Q

What is the hormone in the thymus?

A

Thymopoietin

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136
Q

What are the hormone in the gonads (testes/ovaries)?

A
  • Sex steriods
  • Inhibins
  • Activins
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137
Q

What are the hormones in the heart?

A
  • Natriuretic peptides
  • ANP
  • BNP
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138
Q

What are the hormone in the liver?

A
  • Insulin-like growth factors
  • Leptin
  • Angiotensinogen
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139
Q

What are the hormones in the kidney?

A
  • Erythropoietin

- Renin

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140
Q

What is the hormone in adipose tissue?

A

Leptin

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141
Q

Describe the location of the pituitary?

A
  • Enclosed by bony
    sella turcica of sphenoid
  • Enclosed superiorly by diaphragma sellae
  • Related to cavernous sinus
  • Lies posterior to optic chiasma & sphenoid sinus
142
Q

Describe the 2 glands of the pituitary (hypophysis)?

A
  1. POSTERIOR pituitary- post lobe, neurohypophysis, pituitary stalk
  2. ANTERIOR pituitary- ant lobe, adenohypophysis, pars anterior (distalis), pars tuberalis (PT), pars intermedia
143
Q

What is Pars intermedia of the pituitary derived from?

A

Rathke’s pouch

144
Q

Describe the Pars intermedia of the pituitary gland?

A
  • Poorly developed
  • Between anterior & posterior lobes of
    pituitary
  • May contain colloid-filled, epithelial lined follicles
145
Q

What may be a connection of pars intermedia function?

A

Numerous basophilic cells, maybe connection with secretion of melanocyte stimulating hormone MSH

146
Q

Describe the embryonic development of the anterior pituitary?

A
  1. Up-growth of epithelium from oral cavity (Rathke’s pouch)

2. Rathke’s pouch loses contact with oral cavity

147
Q

Describe the embryonic development of the posterior pituitary?

A

Down-growth from the brain (infundibulum)

148
Q

How can craniopharyngiomas develop?

A

Slow growing tumours may develop along track of Rathke’s pouch

149
Q

Describe the staining of the different secretory cells of the anterior pituitary?

A
  1. Chromophils take up the stain & have 2 types- (A) Acidophils 65% GH & prolactin (B) Basophils 35%
  2. Chromophobes don’t stain (C)
150
Q

List the neurohormones controlling the secretions from the anterior pituitary?

A
  • Thyrotropin-releasing hormone
  • Corticotropin-releasing hormone
  • Growth hormone-releasing hormone
  • Somatotropin-releasing hormone
  • Somatostatin/Growth hormone release-inhibiting
  • Gonadotropin-releasing hormone
  • Follicle-stimulating hormone releasing hormone
  • Luteinising hormone releasing hormone
  • Prolactin releasing factor, TRH
  • Prolactin release inhibiting factor, Dopamine
151
Q

List the neurohormones released from the posterior pituitary?

A
  • Vasopressin (VP)
  • Anti-diuretic peptide (ADH)
  • Oxytocin (OT)
152
Q

What are the primary actions if trophic hormones?

A

On other endocrine glands

153
Q

List the trophic hormones of the anterior pituitary?

A
  • Thyrotropin/ Thyroid-stimulating hormone (TSH)
  • Corticotropin/ Adrenocorticotropic hormone (ACTH)
  • Gonadotropins: Luteinising Hormone (LH) & Follicle-stimulating hormone (FSH)
154
Q

List the hormones of the anterior pituitary acting on peripheral target cells?

A
  • Somatotropin / Growth hormone (GH)
  • Prolactin (PL)
  • α, β & γ Melanotropin / Melanocyte-stimulating hormone (MSH)
155
Q

Describe the 3 steps to controlling growth hormone release?

A
  1. Neurosecretory cells in arcuate nucleus secrete GHRH that reaches somatotrophs via hypophyseal portal blood supply
  2. Periventricular cells release somatostatin which inhibits GH
  3. GHRH causes somatotrophs to synthesise & release GH
156
Q

How does IGF-1 inhibit growth hormone (GH)?

A
  1. Indirectly by increasing secreting of somatostatin from nuclei in the periventricular region
  2. Indirectly by suppressing GHRH release from arcuate nucleus in hypothalamus
  3. Directly by suppressing somatotrophs
157
Q

What does Growth hormone (GH) inhibit and stimulate?

A
  1. Inhibits own secretion via “short-loop” feedback on somatotrophs
  2. Stimulates secreting of IGF-1 from peripheral target tissue
158
Q

What does growth hormone secretion control?

A

Circadian rhythms

159
Q

What are the 4 physiological actions of Growth Hormone (GH)?

A
  1. Increased cartilage formation & skeletal growth
  2. Increased protein synthesis, cell growth & proliferation
  3. Increased lipolysis
  4. Increase blood glucose & other anti-insulin effects
160
Q

What are the physiological consequences of Growth Hormone (GH)?

A
  • Increased linear growth & lean body mass
  • Vital for normal post-natal development & rapid growth through puberty
  • Maintenance of protein synthesis & tissue functions in adult
161
Q

What can growth hormone (GH) deficiency cause?

A

Dwarfism in children due to predictable effects on linear bone growth & decreased availability of lipids & glucose for energy

162
Q

How can Dwarfism be treated?

A

With human growth hormone

163
Q

What can growth hormone excess (acromegaly) often be due to?

A

Pituitary adenoma

164
Q

What can growth hormone excess before puberty cause?

A

Gigantism due to excess stimulation of epiphyseal plates

165
Q

What can growth hormone excess after puberty cause?

A
  • Periosteal bone growth causing larger hand, jaw & foot size
  • Soft tissue growth –> large tongue & coarsening of facial features
  • Insulin resistance & glucose intolerance
166
Q

What can growth hormone excess be treated with?

A

Synthetic long-acting somatostatins (Octreotide) with varying success

167
Q

List the physical signs of gigantism/acromegaly?

A
  • Swelling of soft tissue
  • Skin tags (wart-like growths)
  • Muscle weakness/fatigue
  • Skin changes, including thickening, oiliness, acne
  • Hirsutism (abnormal/unusual hair growth)
168
Q

List the other symptoms of gigantism/acromegaly?

A
  • Arthralgia (pain in joints) (75%)
  • Amenorrhea in women (72%)
  • Hyperhidrosis (excessive perspiration) (64%)
  • Sleep apnea (60%)
  • Headaches (55%)
  • Paresthesia/ carpel tunnel syndrome (40%)
  • Loss of libido or impotence (36%)
  • Hypertension (28%)
  • Thyroid disorders (goiter) (21%)
  • Visual field defects (19%)
169
Q

Where are Vasopressin (AVP) / Antidiuretic Hormone (ADH) synthesised?

A

Neurosecretory cells within the supra-optic nucleus (SON) & paraventricular nucleus (PVN)

170
Q

What 3 things cause ADH release?

A
  1. Increased blood osmolality (osmoreceptors in brain)
  2. Decrease blood volume
  3. Renin/ angiotensin/ aldosterone system (RAAS)
171
Q

What does ADH release do?

A
  • Recruitment of
    AQP water channels
  • Water retention (kidney collecting tubule)
172
Q

What can a deficiency in hypothalamic neurohypophysial hormones cause?

A

Diabetes Insipidus (polyuria, polydispia)

173
Q

What 2 things can cause a deficiency in hypothalamic neurohypophysial hormone?

A
  1. Cranial- 30% tumours, 30% trauma or disease induced, 30% familial disorders of NS cells
  2. Nephrogenic- sex-linked genetic defect in collecting tubule
174
Q

What produces Oxytocin?

A

Hypothalamic neurones in paraventricular & supraoptic nuclei

175
Q

Describe Oxytocin?

A
  • Bound to glycoproteins
  • Carried in axons to posterior pituitary
  • Stored in vesicles in expanded ends of axons
176
Q

What is Oxytocin release (neurosecretion) controlled by?

A

Directly by nervous impulses from hypothalamus

177
Q

Describe the 4 steps to the hypothalamic control of milk production & ejection & roles of Prolactin & Oxytocin?

A
  1. Stimulus from suckling
  2. Neurons from spinal cord inhibit dopamine release from arcuate nucleus, prolactin increases –> milk
  3. Neurons from spinal cord stimulate oxytocin
  4. Neurons from spinal cord inhibit neurons in arcuate nucleus & preoptic area causing fall in GnHR which inhibits ovarian cycle
178
Q

What does dopamine usually inhibit?

A

Lactotrophs in anterior pituitary which stops prolactin release

179
Q

Where is the pineal gland location?

A

Midline in posterior part of the roof of the 3rd ventricle

180
Q

What do pinealocytes have connections to?

A

Neural connections with hypothalamus

181
Q

Describe the functions of the pineal gland?

A
  • Darkness secretes melatonin (from tryptophan)
  • Regulates circadian rhythms (melatonin hypnotic effect)
  • Regulates reproductive processes, onset of puberty
  • Aging & regulation of immune system
  • Accumulates calcium phosphate with time, ‘brain sand’
182
Q

What is a benign neoplasia?

A

Not invasive but its expanding and can still cause damage

183
Q

What are the 3 commonest primary tumours which metastasise to the brain?

A
  1. Breast
  2. Melanoma
  3. Lung
184
Q

What are the 3 other primary tumours which metastasise to the brain?

A
  1. Kidney
  2. Gut/gastric/colorectum
  3. Lymphoma/leukaemia
185
Q

Describe the effects of metastatic brain tumours?

A
  • None
  • Space occupying lesions: fits, raised intracranial pressure, headaches, drowsiness, behavioural changes
  • Haemorrhage
186
Q

What does brain tumours do?

A

Skull can’t expand so it can destroy brain tissue or force it down the vertebral canal

187
Q

What are the 3 types of lung cancer which can metastasise to the brain?

A
  1. Small cell (aggressive)
  2. Squamous
  3. Adenocarcinoma
188
Q

What is the normal intracranial anatomy?

A
  • Brain
  • Linings ie. arachnoid membrane
  • Pituitary
  • Peripheral nerve elements: VIII cranial nerve
189
Q

What does the brain (cerebrum) contain?

A
  • Neurons
  • Astrocytes
  • Microglia
  • Oligodendroglia
  • Choroid plexus
  • Ependyma
190
Q

What is the characteristic of the commonest malignant tumour?

A

Its metastatic

191
Q

What is the commonest intracranial primary neoplasm?

A

Meningioma ~1/3

192
Q

What is the commonest primary neoplasms on a malignant spectrum?

A

Gliomas ~2/3

193
Q

What is the commonest intracranial peripheral nerve tumour?

A

Acoustic Schwannoma (acoustic neuroma) <10%

194
Q

Describe Meningiomas?

A
  • Sporadic
  • Post-irradiation (radiation)
  • Part of NF2
195
Q

Describe the location/growth of a Meningioma?

A
  • Sites of arachnoid
  • Well demarcated
  • Slowly growing
  • Not invasive, but erosive & compressive
196
Q

What are the effects of Meningiomas?

A
  • Fits
  • Drowsiness
  • Headaches
  • Raised intracranial pressure
197
Q

How can you treat meningiomas?

A

Surgical removal

198
Q

What are most Glioma’s derived from?

A

Astrocytes

199
Q

What are the 5 common Glioma’s (most common 1st)?

A
  1. Astrocytes (most common)
  2. Oligodendroglioma
  3. Ependymoma
  4. Choroid plexus tumours
  5. Medulloblastoma & PNET
200
Q

Describe Astrocytoma (glioma)?

A
  • None completely benign, always degree of malignancy

- Grading informs prognosis & treatment

201
Q

Describe the WHO grading system for Astrocytoma’s?

A

I- localised
II- diffuse
III- anaplastic astrocytoma
IV- glioblastoma multiforme

202
Q

What does PNET stand for?

A

Primitive neuroectodermal tumours

203
Q

What are the 3 different types of peripheral nerve tumours?

A
  1. Neural- neuroblastoma, ganglioneuroma
  2. Schwannoma or Neurofibroma
  3. Cranial nerve VIII- acoustic nerve
204
Q

Describe a Schwannoma & how it presents clinically?

A
  • Lump within nerve
  • Benign & not invasive
  • Cause pain due to nerve compression
  • Surgically remove it
205
Q

Describe a Neurofibroma & how it presents clinically?

A
  • Mixed between the nerve fibres
  • Benign
  • Difficult to surgically remove without sacrificing the nerve
206
Q

Describe Neurofibromatosis 1 (NF-1)?

A
  • Autosomal dominant
  • 50% spontaneous
  • White spots due to melanin disturbance
  • Hard to remove
207
Q

What are the different Neurofibromatosis 1 (NF-2)?

A
  • MISME: Multiple Inherited Schwannomas, Meningiomas & Ependymomas
  • Bilateral acoustic Schwannoma
  • Merlin NF2
208
Q

What is general anaesthesia?

A

Reversible, drug induced loss of consciousness, usually to allow a surgical procedure to be performed

209
Q

What are intravenous induction agents?

A

Agents which will

induce loss of consciousness in one arm brain circulation time

210
Q

Give 3 examples of commonly used anaesthetic agents (drugs)?

A
  1. Propofol
  2. Thiopentone
  3. Etomidate
211
Q

What is an inhalation anaesthetic agent?

A
  • Gas/vapour delivered to patient via breathing circuit
  • May be used to induce anaesthesia (children)
  • More commonly used to maintain anaesthesia
212
Q

Give 4 examples of inhalation anaesthetic agents?

A
  1. Nitrous oxide
  2. Isoflurane
  3. Sevoflurane
  4. Desflurane
213
Q

What is Entonox?

A

50 nitrous: 50 oxygen

214
Q

When might you use Entonox?

A
  • Analgesic
  • Labour
  • Trauma
215
Q

How were anaesthetics initially thought to work?

A

Due to lipid solubility

216
Q

What does MAC stand for?

A

Minimum alveolar concentration

217
Q

What is MAC?

A
  • Measure of potency of an anaesthetic

- More lipid soluble = more potent = lower MAC

218
Q

What are the more blood soluble anaesthetics?

A

Slower onset

219
Q

How are anaesthetics now thought to work via?

A

Transmitter ligand gated ion channels, principally via GABAa receptor

220
Q

What are IV anaesthetics mediated by?

A

GABA β3 subunit

221
Q

What are IV hangovers mediated by?

A

GABA β2 subunit

222
Q

What do Etomidate, Propofol & Barbiturates work on & what does this result in?

A

Excite GABAa receptors –> Decrease consciousness movement

223
Q

What does volatile anaesthetics work on & what does this result in?

A

Excite GABAa receptors, Inhibit Sodium channels, Excite Potassium channels –> decrease consciousness movement

224
Q

What does Nitrous oxide & Xenon work on & what does this result in?

A

Excite Potassium channels & Inhibit NMDA receptors –> decrease consciousness movement

225
Q

What does Ketamine (dissociative anaesthetic) work on & what does this result in?

A

Inhibits NMDA receptors –> decrease consciousness movement

226
Q

What is the main place anaesthetics target?

A

Thalamus

227
Q

How does waking up from anaesthetic work?

A

When stopping administeration concentration in brain decreases & becomes redistributed to the rest of the body –> Waking up!

228
Q

What is the main learning points regarding anaesthetics?

A

Virtually all anaesthetic agents (exception-ketamine) will to a greater/ lesser effect have a negative inotropic effect on heart & reduce systemic vascular resistance

229
Q

What can any drug causing loss of consciousness lead to?

A

Obstruction of the airway/ respiratory depression

230
Q

What does respiratory depression tend to be with IV agents?

A

Fall in respiratory rate

231
Q

What does respiratory depression tend to be with inhalation agents?

A

Fall in tidal volume

232
Q

What do we want an ideal anaesthetic agent to do?

A
  • Act rapidly
  • Pleasant
  • Cheap to manufacture
  • Stable (soda lime)
  • Analgesic effect
  • Amnesic effect
  • Minimal “hangover”
233
Q

What do we NOT want anaesthetic agents to do?

A
  • Irritant on veins/ airways
  • Emetic
  • Minimal effects on other systems (breathing, cardiovascular)
  • Produce toxic metabolites
  • Cause histamine release / anaphylaxis
234
Q

What anaesthetic agents are painful on injection?

A

Propofol & Etomidate

235
Q

What is “balanced anaesthesia”?

A

Selection of drugs & techniques bearing in mind-

  1. Health & requests of patient
  2. Properties of drugs
  3. Requirements of surgery to minimise patient risk & maximise patient safety & comfort
236
Q

What type of traumatic stressors can cause PTSD to develop?

A
  • Threaten life or well-being
  • Overwhelm coping abilities
  • Challenge the assumptions that people make about the World
237
Q

Describe the historic of “Railway spine” in the 19th century after Industrial Revolution?

A
  • Physical disorders in healthy & apparently uninjured railway accident victims.
  • Result from molecular changes in spinal cord
  • Horror of experiencing railway accident was part or all of the syndrome
238
Q

Describe the historic of “Shell shock” in World war I?

A
  • Believed that concussion of artillery shells cause CNS damage
  • Not explain cases of shock/distress among those who were not exposed to exploding shells
239
Q

List the diverse populations which are possible to find cases of PTSD?

A
  • Family & relationship abuse
  • Exposure to pathogens (HIV)
  • Assaults
  • Motor vehicle accidents
  • Natural disasters
  • Human caused disasters
  • Exposure to noxious agents (chernobyl)
240
Q

What are the evidence rates (%) of 3 different PTSD events?

A
  1. Rape: 80%
  2. Witnessing/experiencing someone’s tragic death: 30%
  3. Motor vehicle accidents with injury: 23%
241
Q

Why is it important to examine long-term experience in PTSD cases?

A

PTSD symptoms subside in many people other time & symptoms wax & wane

242
Q

What are the 4 symptoms of PTSD according to NICE CG26 p7?

A
  1. Re-experiencing symptoms
  2. Avoidance of reminders of the trauma
  3. Hyperarousal
  4. Emotional numbing
243
Q

Describe re-experiencing symptoms associated with PTSD?

A
  • Through intrusive thoughts, flashbacks/ nightmares
  • Flashbacks feel ‘real’
  • Images described as if being in a film of the incident
  • At 1st, may feel actually ‘in’ the film but perspective change to observer as they recover
244
Q

Describe the avoidance symptoms associated with PTSD?

A
  • Avoidance of thoughts, feelings, people, places, & activities related to event
  • Difficulty remembering important aspects of event
245
Q

Describe the persistent feelings of over-arousal associated with PTSD?

A
  • Irritability, anger
  • Being easily startled/ hyper-vigilant
  • Insomnia
  • Difficulty concentrating
246
Q

Describe emotional numbing associated with PTSD?

A
  • Lack of ability to experience feelings
  • Feeling detached from other people
  • Giving up previously significant activities
  • Amnesia for significant parts of the event
247
Q

Evidence shows that what 6 feelings go with PTSD (Brewin & Holmes)?

A
  1. Guilt
  2. Shame
  3. Sadness
  4. Betrayal
  5. Humiliation
  6. Anger
248
Q

Describe the onset of symptoms for PTSD?

A

Can develop immediately, in some (<15%) the onset of symptoms may be delayed

249
Q

What do some PTSD sufferers do?

A

May NOT seek help for months/years despite considerable distress

250
Q

How is assessment of PTSD challenging?

A

Many people avoid talking about their problems when presenting with associated complaints

251
Q

What are the 2 predictors of PTSD?

A
  1. Characteristics of event

2. Characteristics of person

252
Q

Describe the PTSD predictor- characteristics of the event?

A
  • Stressors of human origin more likely to cause PTSD than natural disasters
  • How deliberate human-caused stressors are judged to be, also important
253
Q

What are 4 vulnerability factors of the person which may makes them more prone to develop PTSD?

A
  1. Childhood trauma
  2. Early separation from parents
  3. Pre-existing depression / anxiety
  4. Family history of anxiety
254
Q

What are the 6 additional vulnerability factors for PTSD according to NICE clinical knowledge summaries?

A
  1. Previous trauma
  2. History of psychiatric illness
  3. Gender
  4. Younger & older age
  5. Lower SES / minority status
  6. Lower educational status
255
Q

What may be the case for vulnerability pre-existing factors?

A

May only predict PTSD in extreme cases

256
Q

What are other 5 psychological factors associated with how severe the impact of a stressor may be & how likely PTSD is to develop?

A
  1. Personal impact of event
  2. Extent of perceived control over future threats
  3. How one is prepared to deal with a stressor
  4. One’s beliefs & assumptions about trauma
  5. Social support
257
Q

What are majority of adults exposed to?

A

At least 1 potentially traumatic event in their lifetime, only a small subset of exposed adults develop PTSD

258
Q

What is Resilience?

A

Adult capacity to maintain healthy psychological & physical functioning

259
Q

Describe the 3 characteristics of resilient people?

A
  1. Process flexible adaptation to challenges
  2. Sense of continuity in their beliefs about themselves/ lives
  3. Retain ability to regenerate positive experiences
260
Q

Describe the physiology of PTSD?

A
  • Shows higher levels of catecholamine compared to without PTSD
  • Lower levels of cortisol which may interfere with body’s ability to restore itself fully after trauma & related to increased rate of physical illness in trauma survivors
261
Q

What is the physiology of PTSD similar to?

A

Stress response

262
Q

Describe the relationship of PTSD & medical conditions?

A
  1. Onset of illness can be stressful- MI, stroke etc.
  2. Diagnosis of a life-threatening disease- heart failure, HIV, cancer
  3. Prolonged treatment or unpleasant medical procedures
263
Q

What is Psychological debriefing?

A
  • Talking through trauma in a structured way with counsellor soon after trauma
  • Usually single session
264
Q

Describe how Psychological debriefing may be ineffective in preventing PTSD or actually increase the risk of the disorder?

A
  • Secondary traumatisation
  • Medicalising normal distress
  • May prevent potentially protective responses of denial & distancing
265
Q

What does NICE guidelines state for Psychological debriefing being used as prevention for PTSD?

A

Psychological debriefing should NOT be routine practice when delivering services

266
Q

What are the NICE guidelines CG26 for treating PTSD where symptoms have been present for more than 3months?

A
  • Trauma-focused psychological treatment: CBT or eye movement desentisation & reprocessing
  • Non-trauma focused interventions: relaxation or non-directive therapy, don’t address traumatic memories (not routinely offered with chronic PTSD)
267
Q

What is PTSD?

A

An anxiety disorder as a response to experiencing a traumatic event

268
Q

What are the ocular defence mechanisms?

A
  • Eyelids
  • Lacrimal system
  • Conjunctiva
  • Cornea
  • Blood-ocular barrier
269
Q

What are the bacterial conjunctivitis 3 common conditions?

A
  1. Haemophilus influenzae
  2. Streptococcus pneumoniae
  3. Moraxella spp.
270
Q

What are the 5 bacterial conjunctivitis in neonatal?

A
  1. Neisseria gonorrhoeae
  2. Escherichia coli
  3. Staphylococcus aureus
  4. Haemophilus influenza
  5. Chlamydia trachomatis
271
Q

What is the HAI bacterial conjunctivitis?

A

Pseudomonas aeruginosa

272
Q

What are the clinical features of bacterial conjunctivitis?

A
  • Hyperaemic red conjunctivae

- Mucopurulent discharge

273
Q

What samples would you take for bacterial conjunctivitis?

A
  • Conjunctival swabs

- Corneal scrapings

274
Q

What lab diagnosis would you do for bacterial conjunctivitis?

A

Culture & NAAT

275
Q

What 3 local antibiotics can you give to treat bacterial conjunctivitis?

A
  1. Fusidic acid
  2. Tetracycline
  3. Chloramphenicol
276
Q

Describe Adenovirus infections?

A
  • Purulent conjunctivitis
  • Enlargement of ipsilateral periauricular lymph node
  • Possible corneal involvement
    (punctate keratitis, subepithelial inflammatory infiltration)
277
Q

What should you avoid when treating Adenovirus infections?

A

Topical steroids

278
Q

Describe Varicella Zoster Virus (VZV) Infections?

A
  • Shingles

- Ophthalmic dermatome of 5th cranial nerve

279
Q

What are 4 the clinical features of Varicella Zoster Virus (VZV) Infections?

A
  1. Skin lesions
  2. Anterior uveitis
  3. Ocular perforation
  4. Retinal involvement
280
Q

Describe Shingles?

A
  • Chronic disease ~25%

- Very painful (post-herpetic neuralgia)

281
Q

What is the antiviral treatment for Shingles & Herpes Simplex Virus?

A

Aciclovir

282
Q

What is the treatment for severe inflammation in Shingles?

A

Topical steroids

283
Q

How would you prevent the primary infection of Shingles?

A

Live attenuated vaccine

284
Q

What is the most common infectious cause of blindness in developed world?

A

Herpes Simplex Virus (HSV) Infections

285
Q

What are the 4 clinical features of Herpes Simplex Virus (HSV) Infections?

A
  1. Ulcerative blepharitis
  2. Follicular conjunctivitis
  3. Regional lymphadenopathy
  4. Corneal involvement (not unusual)
286
Q

When may Herpes Simplex Virus relapses occur?

A

~4 years

287
Q

Describe a dendritic ulcer associated with Herpes Simplex Virus?
(marker of infection)

A
  1. Inflammation in deeper tissue
  2. Keratitis
  3. Corneal oedema
  4. Opacity
288
Q

What should you avoid in treatment of Herpes Simplex Virus?

A

Steroids

289
Q

What happens when there is repeated scarring in Herpes Simplex Virus?

A

Corneal grafting

290
Q

Describe Onchocerciasis (River Blindness)?

A
  • Caused by parasite Onchocerca volvulus

- Transmitted by blackfly

291
Q

Where especially is Onchocerciasis (River Blindness) a public health problem?

A

West Africa

292
Q

What is the international control programme for Onchocerciasis (River Blindness)?

A
  • Mass treatment of whole populations

- Invermectin & Doxycyline

293
Q

Describe Trachomatis?

A
  • Chlamydia trachomatis
  • Chronic keratoconjunctivitis
  • Largely confined to tropics
294
Q

Describe the 4 symptoms of Trachomatis, which occur 3-10d post-infection?

A
  1. Lacrimation
  2. Mucopurulent discharge
  3. Conjuntival involvement
  4. Follicular hypertrophy
295
Q

What is the treatment for Trachomatis?

A

Oral macrolides i.e. Azithromycin

296
Q

Describe the ocular manifestations of AIDS?

A
  • Cotton wool spots
  • Infarction of retinal nerve fibre layer
  • Cytomegalovirus infection late in course of HIV disease
297
Q

What is the antiviral treatment for AIDS?

A

IV Ganciclovir

298
Q

What does Endophthalmitis develop after (4)?

A
  1. Ocular operation
  2. Trauma
  3. Inoculation of foreign body
  4. Complication of systemic infection
299
Q

What are the bacterial causes of Endophthalmitis treated with?

A

Systemic antibiotics & early vitrectomy

300
Q

What are the 4 common (>50%) normal microbiota of the respiratory tract?

A
  1. Bacteroides spp.
  2. Candida albicans
  3. Oral Streptococci
  4. Haemophilus influenzae
301
Q

What are the 3 occasional (<10%) normal microbiota of the respiratory tract?

A
  1. Streptococcus pyogenes
  2. Streptococcus pneumoniae
  3. Neisseria meningitidis
302
Q

What are the 4 latent state normal microbiota of the respiratory tract tissues?

A
  1. Herpes simplex virus type I (HSV) 2. Epstein-Barr virus (EBV)
  2. Cytomegalovirus (CMV)
  3. Mycobacterium tuberculosis
303
Q

What are the 5 respiratory tract host defences?

A
  1. Saliva
  2. Mucus
  3. Cilia (muco-ciliary escalator/elevator) 4. Nasal secretions
  4. Antimicrobial peptides
304
Q

What is the common cold also known as?

A

Acute Coryza

305
Q

What is the transmission of the common cold (Acute Coryza)?

A
  1. Aerosol

2. Virus-contaminated hands

306
Q

What are the 5 causative agents for the common cold?

A
  1. 40% Rhinoviruses
  2. 30% Coronaviruses
  3. Coxsackie virus A
  4. Echovirus
  5. Parainfluenza virus
307
Q

What seasons does the common cold arise (Acute Coryza)?

A

Early autumn & mid / late spring

308
Q

List the clinical features of the common cold (Acute Coryza)?

A
  • Tiredness
  • Slight pyrexia
  • Malaise
  • Sore nose & pharynx
  • Profuse, watery nasal discharge becoming mucopurulent
  • Sneezing in early stages
  • Secondary bacterial infection in minority
309
Q

What are the 6 VIRAL causative agents for Acute Pharyngitis & Tonsillitis?

A
  1. Epstein-Barr virus
  2. Cytomegalovirus
  3. Herpes simplex virus type I
  4. Rhinovirus
  5. Coronavirus
  6. Adenovirus
310
Q

What are the 3 BACTERIAL causative agents for Acute Pharyngitis & Tonsillitis?

A
  1. Streptococcus pyogenes
  2. Haemophilus influenzae
  3. Corynebacterium diphtheriae
311
Q

Describe Cytomegalovirus (CMV)?

A
  • Transmission in body secretions & organ transplants
  • Usually asymptomatic or mild
  • Can reactivate & cause disease when cell-mediated immunity compromised
312
Q

What 3 things can be used to treat Cytomegalovirus (CMV)?

A
  1. Ganciclovir
  2. Foscarnet
  3. Cidofovir
313
Q

What is another name for Epstein-Barr Virus (EBV)?

A

Glandular fever

314
Q

What does Epstein-Barr Virus (EBV) do?

A

Replicates in B lymphocytes

315
Q

List the clinical features of What does Epstein-Barr Virus (EBV)?

A
  • Fever, Headache - Malaise
  • Sore throat
  • Anorexia
  • Palatal petechiae
  • Cervical lymphadenopathy - Splenomegaly
  • Mild hepatitis
316
Q

What are the ORAL clinical features of Epstein-Barr Virus (EBV)?

A
  • Swollen tonsils & uvula
  • Petechiae on the soft palate
  • White exudate
317
Q

What is the treatment for Glandular fever (EBV)?

A
  • NOT with antibiotics (ampicillin & amoxycillin)!

- Contact sports/ heavy lifting avoided during 1st month of illness & until splenomegaly has resolved

318
Q

What are the 3 possible complications of Glandular fever (EBV)?

A
  1. Burkitt’s lymphoma
  2. Nasopharyngeal carcinoma
  3. Guillain-Barré syndrome
319
Q

What is Tonsillitis caused by?

A

Streptococcus pyogenes

320
Q

What are the 4 clinical features of Tonsillitis?

A
  1. Fever
  2. Pain in throat
  3. Enlargement of tonsils
  4. Tonsillar lymphadenopathy
321
Q

What treatment is Tonsillitis susceptible to?

A

Penicillin

increasing resistance to erythromycin & tetracycline

322
Q

What are the 5 complications of Streptococcus pyogenes?

A 
1. Scarlet Fever
(erythrogenic
toxin from S. pyogenes)
2. Peritonsillar abscess
3. Otitis media / sinusitis
4. Rheumatic heart disease
5. Glomerulonephritis
323
Q

What is parotitis caused by?

A

Mumps virus

324
Q

List the clinical features of Parotitis?

A
  • Fever, Malaise
  • Headache
  • Anorexia
  • Trismus
  • Severe pain & swelling of parotid gland(s)
325
Q

What are the 2 primary sites of replication for Parotitis?

A
  1. URT

2. Eye

326
Q

What are the 3 forms of treatment for Parotitis?

A
  1. Mouth care
  2. Nutritional
  3. Analgesia
327
Q

What are the 2 forms of prevention for Parotitis?

A
  1. Active immunisation

2. Measles-Mumps-Rubella (MMR) vaccine

328
Q

What are the complications of Parotitis?

A
  • CNS involvement

- Epididymo-orchitis (~30% infected after puberty)

329
Q

What is Acute Epiglottitis caused by?

A

Haemophilus influenzae

330
Q

Describe the prevalence of Acute Epiglottitis?

A
  • Nasopharynx of 75% healthy people

- 88% reduction in England & Wales since Hib vaccine in 1992

331
Q

List the clinical features of Acute Epiglottitis?

A
  • High fever
  • Massive oedema of epiglottis
  • Severe airflow obstruction –> breathing difficulties
  • Bacteraemia
332
Q

Describe the diagnosis of Acute Epiglottitis?

A
  • Do NOT examine throat/ take swabs as this will precipitate complete obstruction of airway
  • Blood cultures to isolate H. influenzae
333
Q

What are the 3 possible treatments for Acute Epiglottitis?

A
  1. Life-threatening emergency
  2. Urgent endotracheal intubation
  3. IV antibiotics (ceftriaxone or chloramphenicol)
334
Q

What causes Diptheria?

A

Corynebacterium diphtheriae

335
Q

Describe Diphtheria infection?

A
  • Usually childhood disease
  • Colonises pharynx, larynx & nose (rarely skin & genital)
  • Transmission aerosol
336
Q

List the clinical features of Diphtheria?

A
  • Sore throat
  • Fever
  • Formation of pseudomembrane
  • Lymphadenopathy
  • Oedema of anterior cervical tissue (bull-neck)
337
Q

Describe the diagnosis of Diptheria?

A

Clinical grounds as therapy is usually urgently required

338
Q

Describe the 3 possible treatments of Diptheria?

A
  1. Anti-toxin therapy intramuscularly
  2. Concurrent antibiotics (penicillin or erythromycin)
  3. Strict isolation
339
Q

Describe the 2 prevention techniques for Diptheria?

A
  1. Childhood immunisation with toxoid vaccine

2. Booster doses if travelling to endemic areas if >10 years have elapsed since primary vaccination

340
Q

What are 4 possible viral origins of Laryngitis & Tracheitis?

A
  1. Parainfluenza
  2. Respiratory Syncytial
  3. Influenza
  4. Adenovirus
341
Q

What are the clinical features of Laryngitis & Tracheitis in adults?

A
  • Hoarseness

- Retrosternal pain

342
Q

What are the clinical features of Laryngitis & Tracheitis in children?

A
  • Dry cough

- Inspiratory stridor (croup)

343
Q

Describe Otitis & Sinusitis?

A
  • Blockage of eustachian tube/ sinuses
  • Mucosal swelling prevents muco-ciliary clearance of infection
  • Exacerbated by local accumulation of inflammatory bacterial products
344
Q

What are the 5 main causative agents for Otitis & Sinusitis?

A
  1. Respiratory syncytial virus (RSV)
  2. Mumps virus
  3. Streptococcus pneumoniae
  4. Haemophilus influenzae
  5. Bacteroides fragilis
345
Q

Describe the prevalence of Otitis Media?

A
  • Most common in infants & small children

- 50% viral origin, mainly Respiratory Syncytial Virus (RSV)

346
Q

List the clinical features of Otitis Media?

A
  • Fever
  • Diarrhoea & vomiting
  • Bulging ear drum & dilated vessels
  • Fluid in middle ear (“glue ear”)
347
Q

What can Otitis Media lead to?

A
  • Chronic suppurative otitis media

- Hearing difficulties & delayed learning development

348
Q

What 3 bugs is Otitis Externa favoured by?

A
  1. Staphylococcus aureus
  2. Candida albicans
  3. Pseudomonas aeruginosa
349
Q

What is the treatment of Otitis Externa?

A

Antibiotic ear drops containing Polymyxin

350
Q

Acute Sinusitis aetiology & pathology is similar to what?

A

Otitis media

351
Q

What are the 2 clinical features of Acute Sinusitis?

A
  1. Facial pain

2. Localised tenderness

352
Q

What is the treatment for Acute Sinusitis?

A
  • Ampicillin
  • Amoxycillin
  • Oral Cephalosporins (esp. with β-lactamase-producing organisms)

MD4001 (11 decks)

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