unit 3 Flashcards

1
Q

How are migraines and tension headaches diagnosed?

A

There is no specific test to diagnose migraines or tension headaches. For migraines, GPs ask patients to keep diaries to identify patterns such as pulsating pain, one-sided pain, worsening with movement, sensitivity to light and sound, and nausea/vomiting.

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2
Q

What are common characteristics of a migraine headache?

A

Pulsating pain, one-sided, worsens with movement, sensitivity to light and sound, and nausea/vomiting.

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3
Q

How are tension headaches treated?

A

Tension headaches can be treated with OTC NSAIDs and paracetamol.

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4
Q

What is medication overuse headache?

A

It occurs when patients take painkillers for half of the month, which can lead to even worse headaches, encouraging them to take more painkillers.

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5
Q

What’s the key difference between migraines and tension headaches?

A

A key difference is that people with migraines cannot function well enough to carry out everyday activities, unlike those with tension headaches.

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6
Q

What are ‘red flags’ for secondary headaches?

A

These can indicate an underlying cause like a tumour. Red flags include: New headaches for patients under 10 or over 50 (e.g., temporal arthritis), Progressive headaches (e.g., intracranial lesion), Headaches in the third trimester of pregnancy (e.g., eclampsia), Worsening headaches when waking, stooping, or straining (e.g., increased intracranial pressure).

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7
Q

What should you look for if a patient has a sudden explosive headache?

A

A sudden, severe headache, like a blow to the head, could indicate a subarachnoid headache, which requires urgent medical help.

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8
Q

What other headache symptoms should raise suspicion for meningitis?

A

A headache accompanied by fever is a potential sign of meningitis.

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9
Q

What are the symptoms of primary angle-closure glaucoma?

A

Headache, nausea, unilateral painful red eye, and impaired vision.

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10
Q

What red flags should be considered for a headache in a patient taking contraceptives?

A

New headaches or headaches with motor weakness that last longer than an hour.

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11
Q
A
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12
Q

What is the “Analgesic Ladder” and its purpose?

A

The Analgesic Ladder is a framework developed to guide the rational use of analgesics, initially for cancer pain and later extended to acute and chronic non-malignant pain. It involves a 3-step approach starting with low-risk drugs and proceeding to stronger medications if necessary.

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13
Q

What are the three steps of the WHO Analgesic Ladder?

A
  • Paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs)
  • Weak opioids for mild to moderate pain (e.g., codeine, tramadol)
  • Strong opioids for moderate to severe pain (e.g., morphine, fentanyl)
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14
Q

What are the two main groups of analgesic medicines?

A
  • Non-narcotic analgesics (e.g., Paracetamol, NSAIDs)
  • Opioid analgesics (e.g., morphine, heroin)
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15
Q

What are some examples of miscellaneous drugs used to alleviate pain?

A
  • Anticonvulsant agents (e.g., gabapentin)
  • Local anaesthetics (e.g., lidocaine)
  • Tricyclic antidepressants (TCAs)
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16
Q

How do anticonvulsant agents like gabapentin work in pain management?

A

Gabapentin reduces nerve excitation and/or increases inhibitory neurotransmission, helping manage pain resulting from abnormal neuronal firing or sensitization.

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17
Q

How do local anaesthetics work to alleviate pain?

A

Local anaesthetics block the transmission of action potentials in nerve fibers by inhibiting Na+ channels, primarily affecting unmyelinated C fibers first.

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18
Q

What is the role of tricyclic antidepressants (TCAs) in pain management?

A

TCAs increase serotonin and norepinephrine levels in synapses involved in descending pain modulation and can improve mood, altering pain perception.

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19
Q

What are the main differences between paracetamol and NSAIDs?

A
  • Paracetamol provides analgesic and antipyretic effects but lacks anti-inflammatory effects and doesn’t cause gastric ulceration.
  • NSAIDs have stronger anti-inflammatory effects and may cause gastric issues.
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20
Q

What are the potential risks of paracetamol overdose?

A

Paracetamol overdose can cause severe liver damage, often fatal, and requires prompt medical intervention.

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21
Q

What is the effect of combining paracetamol with opioids like codeine?

A

Combining paracetamol with opioids can have an additive effect or a synergistic effect.

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22
Q

What are the main pharmacological actions of opioids?

A
  • Analgesia
  • Euphoria and sedation
  • Respiratory depression
  • Suppression of cough
  • Nausea and vomiting
  • Reduced GI motility, causing constipation
  • Pupillary constriction
  • Tolerance and dependence
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23
Q

What is the term ‘opioid’ and what does it refer to?

A

‘Opioid’ refers to any substance, natural or synthetic, that produces morphine-like effects.

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24
Q

migraine pain management structure

A

first line = analgesic asprin, para, nsaid

secondline = riza, sup, zolma (first line for sever/ moderate pain)

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25
Q

classification depression

A
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26
Q

Why can depression be difficult to diagnose in general practice?

A

Depression often presents with somatic (physical) symptoms that can mask the underlying depressive disorder, leading to frequent misdiagnoses. As a result, only about half of patients with major depression are correctly identified by GPs.

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27
Q

How does depression diagnosis in men differ from women?

A

Men are less likely to be diagnosed with depression but are more likely to use illegal drugs and alcohol as coping mechanisms. This can contribute to underdiagnosis or misdiagnosis in men.

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28
Q

What is the most common diagnostic test for depression?

A

The Patient Health Questionnaire (PHQ) is the most commonly used diagnostic test to identify depression in patients.

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29
Q

What are the NICE ‘Whooley’ questions used for diagnosing depression?

A
  • During the last month, have you often been bothered by feeling down, depressed, or hopeless?
  • During the last month, have you often been bothered by having little interest or pleasure in doing things?
    If a patient answers ‘yes’ to either of these questions, further investigation for depression is warranted.
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30
Q

What should be explored if a patient answers ‘yes’ to the ‘Whooley’ questions?

A

Further investigation should include checking for additional symptoms such as:
* Insomnia
* Decreased or increased appetite
* Loss of energy
* Indecisiveness
* Inappropriate guilt

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31
Q

What is the significance of somatic symptoms in depression diagnosis?

A

Many patients with depression present primarily with somatic (physical) symptoms, such as pain, fatigue, or digestive issues, which can overshadow the emotional and psychological aspects of the disorder, leading to misdiagnosis or underdiagnosis.

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32
Q

Why are men less likely to be diagnosed with depression?

A

Men are often less likely to seek help for emotional or psychological issues, and when they do, their depression may manifest through external behaviors such as substance abuse (alcohol and drugs) rather than emotional symptoms. This can result in the depression being overlooked or misdiagnosed.

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33
Q

What role does the Patient Health Questionnaire (PHQ) play in depression diagnosis?

A

The PHQ is a standardized screening tool used by healthcare providers to assess and diagnose depression based on patient responses to specific questions about mood, behavior, and symptoms over the past two weeks.

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34
Q

What is the importance of regular screening for depression in clinical practice?

A

Regular screening for depression is essential because it allows for the identification of patients who may otherwise go undiagnosed, especially when somatic symptoms dominate. Early detection and intervention are crucial for effective treatment and improved patient outcomes.

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35
Q

How is depression diagnosed according to the number of symptoms present?

A

Depression is diagnosed when a patient has at least 5 of the 9 symptoms, with at least one being a core symptom (either a depressed mood or a loss of interest/pleasure in activities).

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36
Q

What are subthreshold depressive symptoms?

A

Subthreshold depressive symptoms are present when a patient has at least 2 symptoms of depression but is still able to cope with everyday life.

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37
Q

What is persistent subthreshold depression, also known as dysthymia?

A

Persistent subthreshold depressive disorder (dysthymia) is diagnosed when a patient experiences a depressed mood for at least 2 years and has at least 2 of the 9 symptoms of depression.

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38
Q

What is Seasonal Affective Disorder (SAD)?

A

Seasonal Affective Disorder (SAD) is diagnosed when a patient experiences episodes of depression at the same time each year, usually in the winter months.

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39
Q

How do antidepressants work?

A

Antidepressants work by altering the levels of monoamines, particularly serotonin and norepinephrine, in the brain.

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40
Q

How long does it typically take to see effects from antidepressants?

A

The effects of antidepressants are typically seen within 1-2 weeks, but full benefits may take up to 4-6 weeks.

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41
Q

What should be done if there is no response to an antidepressant after 4 weeks?

A

If there is no response to an antidepressant after 4 weeks, a different antidepressant should be tried.

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42
Q

What are Monoamine Oxidase Inhibitors (MAOIs) and how do they work?

A

MAOIs inhibit the enzyme monoamine oxidase, increasing the availability of neurotransmitters like serotonin and norepinephrine in the presynaptic neurons.

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43
Q

Why are Monoamine Oxidase Inhibitors (MAOIs) not typically first-line treatments?

A

MAOIs are not first-line treatments due to their potential for severe side effects, including hypertensive crisis with tyramine-rich foods.

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44
Q

What are Tricyclic Antidepressants (TCAs), and how do they work?

A

Tricyclic Antidepressants (TCAs) block the reuptake of serotonin and norepinephrine, increasing their levels in the synapse.

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45
Q

What is a common side effect of Tricyclic Antidepressants (TCAs)?

A

Common side effects of TCAs include anticholinergic effects, sedation, and weight gain.

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46
Q

What are Selective Serotonin Reuptake Inhibitors (SSRIs) commonly used for?

A

SSRIs are first-line agents for treating depression and anxiety due to their high selectivity and reduced adverse effects. Examples include citalopram, sertraline, and fluoxetine.

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47
Q

What is the mechanism of action of SSRIs?

A

SSRIs work by selectively inhibiting the serotonin (5-HT) reuptake transporter, increasing serotonin levels in the extracellular space. At low doses, they primarily bind to the 5-HT transporter, but at higher doses, they can also bind to norepinephrine (NE) transporters.

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48
Q

How do SSRIs differ from Tricyclic Antidepressants (TCAs) in terms of selectivity?

A

SSRIs are more selective for serotonin (5-HT) transporters compared to TCAs, which makes them more specific and less likely to cause adverse effects.

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49
Q

Why are SSRIs generally better tolerated than TCAs?

A

SSRIs are better tolerated because they do not bind significantly to muscarinic, histamine, adrenergic, or dopamine receptors, which are common sites for adverse effects seen with TCAs.

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50
Q

What is a therapeutic advantage of SSRIs?

A

SSRIs have a greater therapeutic index, meaning there is a larger margin between the effective dose and toxic dose, making them safer than other antidepressants like TCAs.

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51
Q

When are Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) used?

A

SNRIs are typically used when patients do not respond to other treatments like SSRIs. They work by inhibiting the reuptake of both serotonin and norepinephrine.

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52
Q

What are the benefits of Lithium for bipolar affective disorder?

A

Lithium is effective in regulating mood and works for 3/4 of patients with bipolar affective disorder. It helps to modulate mood swings.

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53
Q

How does Lithium work in the body?

A

Lithium enters cells through sodium (Na+) channels and can increase serotonin levels. It also alters the transport of sodium in neurons, modifying neural communication.

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54
Q

What is a key challenge in using Lithium for bipolar disorder treatment?

A

Lithium has a narrow therapeutic window, meaning the difference between an effective dose and a toxic dose is small. Therefore, it requires close monitoring.

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55
Q

How can adverse effects of Lithium be avoided?

A

Adverse effects of lithium can be avoided by regularly monitoring peripheral blood levels to ensure the drug stays within the therapeutic range.

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56
Q

What are the most commonly misused legal substances?

A

Tobacco and alcohol are the most commonly misused legal substances.

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57
Q

What regulations govern substances that can lead to dependence in the UK?

A
  • Human Medicines Regulation 2012: Some prescribed and OTC medicines have potential to lead to dependence.
  • Misuse of Drugs Regulations 2001: Controlled drugs have potential to lead to dependence and some are used to treat dependence.
  • Misuse of Drugs Act 1971: Many drugs associated with dependence are illegal.
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58
Q

What is the difference between physiological and physical dependence?

A
  • Physical dependence involves tolerance and withdrawal symptoms.
  • Physiological dependence is associated with emotional and cognitive symptoms, including cravings and changes in behavior.
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59
Q

How does the WHO define substance dependence?

A

Substance dependence is defined as a need for repeated doses of the drug to feel good or avoid feeling bad.

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60
Q

What is tolerance?

A

Tolerance is the decreased pharmacological effect of a drug after continuous use, requiring higher doses to achieve the same effect.

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61
Q

What is sensitisation (inverse tolerance)?

A

Sensitisation is the phenomenon where repeated administration of a drug results in a greater effect from a given dose.

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62
Q

What happens during physical dependence and withdrawal?

A

Physical dependence results in homeostatic changes that compensate for the presence of the drug. When the drug is suddenly withdrawn, opposite effects occur, triggering withdrawal symptoms and activating the ANS stress response.

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63
Q

What is psychological dependence?

A

Psychological dependence involves resetting the brain’s reward system, leading to cravings for the drug and a higher risk of relapse.

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64
Q

What are CNS stimulants and examples?

A

CNS stimulants enhance neural activity. Examples include caffeine and cocaine.

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65
Q

What are CNS depressants and examples?

A

CNS depressants suppress or inhibit neural activity. Examples include alcohol and opioids.

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66
Q

What are hallucinogens and examples?

A

Hallucinogens induce alterations in perception, thinking, and feeling. Examples include ketamine and ecstasy.

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67
Q

What are anabolic steroids, and how are they misused?

A

Anabolic steroids are Class C drugs that mimic hormones like testosterone and stimulate muscle growth. They are misused to enhance athletic performance and speed recovery but can cause paranoia, aggression, and unwanted changes like acne.

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68
Q

How does caffeine act as a CNS stimulant?

A

Caffeine works by antagonizing adenosine receptors, increasing dopamine release and resulting in stimulating effects.

69
Q

How does cannabis affect the body and brain?

A

Cannabis affects memory and reaction times. The psychoactive component, THC, binds to CB1 receptors and affects the dopamine reward circuit, leading to tolerance and mild withdrawal symptoms like insomnia and loss of appetite.

70
Q

What are the effects of hallucinogens like ketamine and phencyclidine?

A

These substances block glutamate NMDA receptors and act at serotonin receptors, altering perceptions, causing paranoia, and resulting in flashbacks weeks after use.

71
Q

How does nicotine create dependency?

A

Nicotine activates nicotinic acetylcholine receptors in the CNS and periphery. Chronic exposure leads to desensitisation and tolerance, with withdrawal causing strong cravings and symptoms like anxiety, irritability, and increased appetite.

72
Q

What are ‘illegal highs’ and how do they work?

A

‘Illegal highs’ are synthetic substances created to mimic the effects of illegal drugs. They often target similar receptors but are now illegal due to their unpredictable effects.

73
Q

How do pharmacokinetic properties influence drug dependence?

A

Drugs that reach high concentrations quickly in the body are more rewarding, and those that are rapidly eliminated tend to be more addictive.

74
Q

What are the different types of tolerance?

A
  • Acquired tolerance: A larger dose is required for the same effects after repeated use.
  • Pharmacokinetic tolerance: Increased metabolism and excretion rates due to drug exposure.
  • Pharmacodynamic tolerance: Neuronal adaptations reduce the response to the drug.
75
Q

What are the physical and psychological aspects of dependence?

A
  • Physical dependence involves changes in cellular signaling pathways, such as activation of opioid receptors leading to changes in GABA release and dopamine activation.
  • Psychological dependence affects the reward system, causing intense cravings and a higher risk of relapse.
76
Q

What is detoxification, and how is it used to treat substance dependence?

A

Detoxification is the process of clearing a substance from the body. It is ideal but only manageable for some patients who may require longer-term treatment with prescribed medication.

77
Q

What is substitute prescribing in the treatment of substance dependence?

A

Substitute prescribing involves prescribing a less harmful drug to reduce the misuse of the primary substance. It is an effective harm reduction strategy but may take years to lead to detoxification.

78
Q

What is the recommended approach to managing benzodiazepine dependence?

A

Gradual reduction is advised to avoid abrupt withdrawal, which can cause confusion, convulsions, and toxic psychosis. Benzodiazepines are commonly prescribed for alcoholism.

No specific treatment exists for benzodiazepine dependence.

79
Q

What is Buprenorphine, and how does it help treat opioid dependence?

A

Buprenorphine is a semi-synthetic opioid used to treat opioid dependence.

  • Duration of action: 12 hours at low doses, 48–72 hours at high doses.
  • Mechanism: Partial agonist mimicking full agonists like heroin, reducing withdrawal symptoms without producing a high.

Buprenorphine can help manage opioid withdrawal symptoms.

80
Q

What is the role of Lofexidine in opioid withdrawal treatment?

A

Lofexidine is an α-2 adrenoreceptor agonist that helps reduce symptoms of opioid withdrawal, making the process more manageable.

It is effective in alleviating withdrawal discomfort.

81
Q

How does Methadone work in treating opioid dependence?

A

Methadone is a synthetic opioid agonist that helps with opioid dependence.

  • Cross-tolerance with other opioids, effective for heroin withdrawal.
  • Well absorbed when taken orally.
  • Does not damage major organs, even at higher doses.
  • Long half-life (24–36 hours), shorter than heroin.

Methadone is a key medication in opioid dependence treatment.

82
Q

What is Naloxone, and how is it used in opioid overdoses?

A

Naloxone is a short-acting opioid antagonist used to reverse opioid overdoses.

  • Available in pre-filled syringes and ampoules.
  • Used in emergency situations to quickly reverse life-threatening opioid overdose effects.

Naloxone is crucial for overdose management.

83
Q

What are the important considerations when prescribing Naltrexone for opioid dependence?

A

Naltrexone is an opioid antagonist used for opioid dependence.

  • Only prescribed to individuals opioid-free for at least 7-10 days.
  • Risks of acute withdrawal if opioid-free status is not verified.
  • Relapse risks: Overcoming receptor blocks or relapsing can cause severe complications.
  • blocks receptor so if you take opiod no euphoria= no relapse

Naltrexone helps prevent relapse but requires careful patient selection.

84
Q

How is methadone or buprenorphine started in treatment?

A

Verification: Patient’s opioid use is confirmed through urine testing.

  • Methadone: Doses are increased slowly to prevent overdose.
  • Buprenorphine: High affinity for the μ-receptor; precipitated withdrawal may occur if other opioids are present.

Initial dosing requires careful monitoring to avoid complications.

85
Q

What is supervised consumption for buprenorphine?

A

Supervised consumption ensures buprenorphine is properly absorbed.

  • The sublingual tablet must be dissolved under supervision for up to 10 minutes.
  • Ensures compliance and prevents diversion.

This practice helps prevent misuse of buprenorphine.

86
Q

What should happen if a patient misses 3 doses of buprenorphine?

A

If a patient misses 3 doses, they are at risk of overdose due to loss of tolerance.

  • Start on a lower dose to prevent overdose.
  • Precipitated withdrawal can occur if buprenorphine is missed.

Monitoring is crucial when restarting treatment.

87
Q

What are the common challenges associated with buprenorphine and methadone treatment?

A

Challenges include:

  • Buprenorphine: Precipitated withdrawal if taken too soon after using full agonist opioids.
  • Dosing adjustments: Both require careful monitoring to prevent accidental overdose or withdrawal symptoms.

Effective management requires understanding the pharmacodynamics of these medications.

88
Q

What are the main symptoms of red eye?

A

Usually affects both eyes (not always equally)
Discharge
Itchiness
Pupil is normal, and vision is not affected
Visual acuity can be checked with a standard Snellen chart

Symptoms may vary in severity and presentation.

89
Q

How do you assess the patterns of redness in red eye?

A

Use good lighting to examine the pupil, sclera, and cornea
Ask the patient to look ahead while examining
To examine the conjunctiva, ask the patient to look up while gently pulling down the lower lid

Proper examination techniques are crucial for accurate diagnosis.

90
Q

What does redness in the limbal area indicate?

A

Redness in the limbal area suggests:
* Extraocular inflammation
* Intraocular disease
* Corneal disease

Limbal redness can be a sign of serious ocular conditions.

91
Q

What does redness in the conjunctiva typically indicate?

A

Redness in the conjunctiva usually indicates conjunctivitis

Conjunctivitis can be caused by infections, allergies, or irritants.

92
Q

What are the red flags (5 Ps) to look for in red eye cases?

A

Pain
Photophobia
Poor vision
Pus in the cornea or anterior chamber
Pupil abnormality

Recognizing these symptoms is essential for timely intervention.

93
Q

How should pain be assessed in red eye cases?

A

Distinguish between actual pain and irritation/discomfort
Pain is usually associated with more severe conditions

Accurate pain assessment can guide further management.

94
Q

How do you assess photophobia in red eye patients?

A

Photophobia refers to pain when looking into light
It is usually unilateral, so ask the patient to try one eye at a time to identify the affected eye

This assessment helps determine the severity of the condition.

95
Q

How do you check for poor vision in red eye cases?

A

Check the patient’s vision using a Snellen chart
Patients may complain of blurry vision if pus is present, in which case, ask them to blink a few times to clear the vision

Blurry vision can indicate significant underlying pathology.

96
Q

What does pus in the cornea or anterior chamber signify?

A

The presence of pus is a sign of infection and should be evaluated for the amount of pus present

Pus can indicate a severe condition requiring immediate attention.

97
Q

What should be noted when assessing pupil abnormalities in red eye cases?

A

Pupils should be central, equal in shape and size
Any abnormalities (e.g., unequal pupils) should be assessed carefully

Pupil assessment is critical for diagnosing neurological involvement.

98
Q

When should a red eye patient be referred?

A

Referral is required if:
* There is trauma to the eye
* There are red flag symptoms (Pain, Photophobia, Poor vision, Pus, Pupil abnormality)

Timely referral can prevent complications and preserve vision.

99
Q

What is otitis media and why is it more severe in children?

A

Otitis media is inflammation of the middle ear, causing the eardrum to become blocked, leading to pressure and pain. It is more severe in children due to their smaller ear structures and greater susceptibility to infections.

Children are more prone to ear infections due to their shorter Eustachian tubes, which make it easier for pathogens to reach the middle ear.

100
Q

What is vertigo?

A

Vertigo is a symptom, not a diagnosis, and refers to the perception of spinning or feeling like you or your surroundings are moving.

It can be caused by various conditions affecting the inner ear or brain.

101
Q

What is the difference between peripheral and central vertigo?

A

Peripheral vertigo: Caused by a disturbance in the balance organs of the inner ear.
Central vertigo: Caused by a disturbance to the visual-vestibular interaction centers in the brain.

Peripheral causes include BPPV and vestibular neuronitis, while central causes include migraines and strokes.

102
Q

What is benign paroxysmal positional vertigo (BPPV)?

A

BPPV occurs when otolith particles become dislodged, causing movement of fluid in the inner ear, leading to vertigo.

This condition is often triggered by changes in head position.

103
Q

What is vestibular neuronitis?

A

Vestibular neuronitis is inflammation of the vestibular nerve, often occurring after a viral infection, leading to vertigo.

It typically presents with sudden onset of vertigo and may last for days.

104
Q

What is vestibular labyrinthitis?

A

Vestibular labyrinthitis is inflammation of both the labyrinth and the vestibular nerve, typically caused by a viral infection, resulting in vertigo and balance issues.

It may also be accompanied by hearing loss.

105
Q

What causes Meniere disease?

A

Meniere disease is caused by endolymphatic hypertension (increased fluid pressure) in the inner ear, leading to vertigo, hearing loss, and tinnitus.

The exact cause of the fluid buildup is often unknown.

106
Q

What is the most common cause of central vertigo?

A

Migraine is the most common cause of central vertigo, leading to dizziness and balance issues.

Vestibular migraines can occur with or without a headache.

107
Q

What is otitis media?

A

Inflammation of the middle ear causing pain and pressure.

It is a common condition, especially in children, and may require treatment with antibiotics.

108
Q

What is peripheral vertigo?

A

Disturbance in the balance organs of the inner ear.

It typically presents with sudden onset of dizziness or spinning sensations.

109
Q

What does BPPV stand for?

A

Benign paroxysmal positional vertigo.

It occurs when otolith particles become dislodged, causing fluid movement in the inner ear.

110
Q

What is vestibular neuronitis?

A

Inflammation of the vestibular nerve after a viral infection.

It often results in severe vertigo that can last for several days.

111
Q

What is vestibular labyrinthitis?

A

Inflammation of the labyrinth and vestibular nerve, often from a viral infection.

It can lead to hearing loss and balance issues.

112
Q

What causes Meniere disease?

A

Endolymphatic hypertension in the inner ear.

Symptoms include episodes of vertigo, tinnitus, and hearing loss.

113
Q

What is central vertigo?

A

Due to disturbances in the visual-vestibular interaction centers of the brain.

It can be more complex and may require neurological evaluation.

114
Q

What is a common cause of central vertigo?

A

Migraine-associated vertigo.

It can occur during or after a migraine headache.

115
Q

How should ADHD be initially managed in primary care for children with mild symptoms?

A

Self-help and simple behavioural management strategies.
* Parent support programs can be offered.
* Watchful waiting for up to 10 weeks may be an option if symptoms are causing moderate impairment.

Initial management strategies focus on non-pharmacological approaches.

116
Q

What should be assessed when ADHD is suspected in a child?

A

Social and educational impact of the symptoms.
* Self-care (e.g., hygiene, eating).
* Social interactions (friends, family relationships).
* Academic performance.
* Emotional health (anxiety, unhappiness).
* Risk behaviors (substance misuse, criminal activity).
* Safety (understanding and avoiding common hazards).

Comprehensive assessment is crucial to understand the full impact of symptoms.

117
Q

What tools can primary care practitioners use for ADHD assessment in children?

A

Strengths and Difficulties Questionnaire.
* Conners’ Rating Scale.

These tools help in quantifying behavioral issues and symptoms.

118
Q

When should a child be referred to a specialist for ADHD?

A

If symptoms are severe.
* If a period of watchful waiting is not acceptable.
* If symptoms persist with at least moderate impairment after watchful waiting or parent support.

Referral is essential when initial management does not yield sufficient improvement.

119
Q

How should ADHD be managed in adults?

A

Assess psychological, social, educational, and occupational impacts.
* If symptoms cause moderate or severe impairment, refer for assessment by a mental health specialist trained in ADHD.
* For adults with a previous ADHD diagnosis, refer to general adult psychiatric services.

Adult management is tailored to the individual’s history and current functioning.

120
Q

How is ADHD treatment managed in primary care once confirmed?

A

Specialist initiated treatment.
* Shared care arrangements for ongoing drug treatment and monitoring.
* Monitor weight, height, blood pressure, and heart rate at specified intervals (every 3–6 months).

Ongoing monitoring is crucial for safe medication management.

121
Q

What are the key monitoring requirements for ADHD medication?

A

Weight: Every 3 months in children ≤10 years, every 6 months in children >10 years and adults.
* Height: Every 6 months in children.
* Blood pressure and heart rate: Monitor before and after dose changes and every 6 months.
* Tachycardia, arrhythmia, or high blood pressure: Seek specialist advice if any occur.

Monitoring helps prevent adverse effects associated with ADHD medications.

122
Q

What lifestyle advice should be given to individuals with ADHD?

A

Encourage a healthy diet and regular exercise.
* Avoid routine elimination of artificial food colorings and additives, but keep a food diary if behavior seems linked to diet.
* Consider dietary advice if weight loss is an issue.

Lifestyle changes can support overall management of ADHD symptoms.

123
Q

What support should be offered to families of children with ADHD?

A

Positive parent-child contact and clear, consistent rules.
* Structure in the child’s day.
* Written information on self-help, local and national support groups (e.g., ADDISS, AADDUK, Mind).

Family support is integral to effective ADHD management.

124
Q

How should ADHD be managed in preschool children?

A

Group parent-training programs as the first-line treatment.
* If symptoms persist, referral to a specialist ADHD service may be needed for consideration of drug treatment.

Early intervention can lead to better long-term outcomes.

125
Q

What is the first-line treatment for school-age children and adolescents with ADHD?

A

Group-based support for parents and young people.
* Parent-training programs.
* Medication (e.g., Methylphenidate) if symptoms cause persistent impairment despite environmental changes.

Tailored approaches are essential for effective treatment.

126
Q

What are the treatment options for children with ADHD and insomnia?

A

Melatonin may be prescribed for children aged 6-17 years if sleep hygiene measures are ineffective.

Addressing sleep issues is an important aspect of overall ADHD management.

127
Q

What non-pharmacological treatments can be offered to young people with ADHD?

A

Cognitive Behavioral Therapy (CBT) to address social skills, problem-solving, self-control, and emotional expression.

Non-pharmacological treatments complement medication and can enhance coping strategies.

128
Q

What are the treatment options for adults with ADHD?

A

Medication (e.g., Lisdexamfetamine, Methylphenidate) if symptoms cause significant impairment.
* Non-pharmacological treatments in combination with medication, such as structured psychological interventions (CBT) and regular follow-up.

A comprehensive approach ensures better management of ADHD in adults.

129
Q

What advice should be given to adults taking amfetamine medications for ADHD?

A

Driving: Do not drive if feeling drowsy, dizzy, or unable to concentrate.
* It is illegal to drive with a specified amount of amfetamines in the body. Keep evidence (e.g., the prescription) in the car to show compliance with medical advice.

Safety considerations are critical for individuals on stimulant medications.

130
Q

How should ADHD be managed for adults with a previous diagnosis in childhood?

A

Refer to general adult psychiatric services for ongoing assessment and treatment.

Continuity of care is vital for effective management of ADHD across the lifespan.

131
Q

What CNS stimulants are used to treat ADHD?

A

Methylphenidate: Sympathomimetic drug for ADHD and narcolepsy.

Methylphenidate is commonly known by brand names such as Ritalin and Concerta.

132
Q

What are the contraindications for CNS stimulants?

A

Should NOT be used to treat:
* Depression
* Obesity
* Senility
* Debility
* Fatigue relief

These contraindications are important to consider to avoid exacerbating underlying conditions.

133
Q

How does Methylphenidate work to treat ADHD?

A

Blocks dopamine and norepinephrine (NE) transporters, increasing dopamine and NE levels in the brain.

This mechanism enhances focus and attention in individuals with ADHD.

134
Q

How does Atomoxetine work to treat ADHD?

A

Blocks norepinephrine (NE) reuptake, increasing NE levels in the prefrontal cortex.

Atomoxetine is not a stimulant and is often chosen for patients who may be at risk for substance abuse.

135
Q

What causes Parkinson’s disease?

A

Parkinson’s disease is caused by a selective loss of dopaminergic neurons in the substantia nigra pars compacta, leading to motor symptoms like bradykinesia, rigidity, impaired postural balance, and resting tremor.

136
Q

What are the core motor features of Parkinson’s disease?

A
  • Bradykinesia (slowness of movement)
  • Rigidity (resistance to passive movement)
  • Impaired postural balance (predisposing to falls)
  • Resting tremor (tremor when the limbs are at rest)
137
Q

Why is levodopa preferred over dopamine for treating Parkinson’s disease?

A

Levodopa is preferred because it can cross the blood-brain barrier and is converted into dopamine in the brain. Dopamine cannot cross the blood-brain barrier.

138
Q

Why is levodopa combined with carbidopa in the treatment of Parkinson’s disease?

A

Carbidopa is combined with levodopa because it prevents the peripheral conversion of levodopa to dopamine, reducing unwanted peripheral side effects while allowing levodopa to be converted to dopamine in the brain.

139
Q

What happens when levodopa is administered alone without carbidopa?

A

Without carbidopa, levodopa would be converted to dopamine in the peripheral tissues, leading to nausea, vomiting, and other unwanted side effects.

140
Q

What is the role of dopamine in Parkinson’s disease?

A

Dopamine plays a crucial role in motor control; its progressive loss in Parkinson’s disease leads to motor symptoms like bradykinesia, rigidity, impaired balance, and resting tremor.

141
Q

How much of the dopaminergic neurons are destroyed by the time Parkinson’s disease symptoms appear?

A

By the time symptoms of Parkinson’s disease first appear, at least 70% of the dopaminergic neurons are destroyed, often up to 95% at autopsy.

142
Q

What is the main advantage of levodopa in treating Parkinson’s disease?

A

Levodopa is the most effective treatment for Parkinson’s disease as it replenishes dopamine levels in the brain, alleviating motor symptoms.

143
Q

Why does levodopa cause nausea and vomiting as side effects?

A

Levodopa activates dopamine receptors in the periphery, leading to nausea and vomiting due to excessive dopamine activity outside the CNS.

144
Q

What is the mechanism of action of levodopa in treating Parkinson’s disease?

A

Levodopa acts by increasing dopamine levels in the brain after crossing the blood-brain barrier, restoring dopaminergic activity.

145
Q

What are the four major dopamine pathways in the brain?

A

Mesolimbic pathway
Mesocortical pathway
Nigrostriatal pathway
Tubero-infundibular pathway

None

146
Q

What symptoms are associated with the mesolimbic pathway in schizophrenia?

A

Positive symptoms including hallucinations and delusions due to dopamine hyperactivity

None

147
Q

What symptoms are associated with the mesocortical pathway in schizophrenia?

A

Negative symptoms and cognitive deficits such as reduced emotion, lack of pleasure, and poor attention due to dopamine hypoactivity

None

148
Q

What is the role of the nigrostriatal pathway?

A

Involved in motor control and associated with Parkinson’s disease

None

149
Q

What is the function of the tubero-infundibular pathway?

A

Involved in hormone secretion, including the regulation of prolactin

None

150
Q

What does the dopamine hypothesis of schizophrenia propose?

A

Symptoms are due to dopamine hyperactivity in the mesolimbic pathway and dopamine hypoactivity in the mesocortical pathway

None

151
Q

How do amphetamines support the dopamine hypothesis of schizophrenia?

A

They can induce hallucinations, delusions, and hyperactivity, symptoms similar to those in schizophrenia

None

152
Q

schizo treatment

A

1= chloropromazine/prochloroperazine/haloperidol

2=aripiprazole,clozapine,olanz,quetiapine

153
Q

depression treatment order

A

1= ssri
2=snri
major TCA rare due sideffect/toxic overdose

154
Q

adhd treatment order

A

1= lisdex / methylphen
2=atomoxetine intol/unresp

155
Q

What are the common symptoms of bacterial conjunctivitis?

A

Painful, gritty eyes (vision unaffected)
* Sticky discharge (mucoid)
* Both eyes usually affected (not always equally)
* Often associated with upper respiratory tract infection

None

156
Q

What are the common causes of bacterial conjunctivitis?

A

Irritants (e.g., swimming pool chlorine, contact lens use)
* Infective agents (bacteria, viruses)
* Allergens (e.g., dust, pollen, drugs, cosmetics)
* Contact with others with bacterial conjunctivitis

None

157
Q

How should bacterial conjunctivitis be examined?

A

Examine in good lighting
* Assess degree, depth, and extent of redness
* Pull down lower lid to look at conjunctiva
* Redness in limbal suggests extraocular inflammation, intraocular disease, or corneal disease

None

158
Q

What is the management for bacterial conjunctivitis?

A

Self-limiting within 1-2 weeks
* Wash sticky discharge with cotton wool and water
* Frequent hand washing
* Avoid contact lenses until infection clears
* Lubricant eyedrops (e.g., Tears Natural, Hypromellose)

None

159
Q

What are the drug treatments for bacterial conjunctivitis?

A

Chloramphenicol eye drops (OTC)
* Fusidic acid eye drops (alternative for pregnancy and young children)

None

160
Q

What are the referral criteria for bacterial conjunctivitis?

A

Symptoms last longer than 1-2 weeks or unresponsive to chloramphenicol
* Reduced visual acuity
* Photophobia
* Eye pain
* Marked redness or pus in cornea or anterior chamber
* Eye trauma

None

161
Q

What are the symptoms of dry eyes?

A

Gritty, sore feeling
* Worsens throughout the day
* Blurred vision (especially in the morning)
* Excessive watering

None

162
Q

What are the causes of dry eyes?

A

Diseases (e.g., thyroid disorder, vitamin A deficiency)
* ADR (e.g., diuretics, tricyclic antidepressants, beta-blockers, HRT, isotretinoin)
* Allergy eye disease

None

163
Q

What is the drug management for mild to moderate dry eyes?

A

Hydrating eye drops (e.g., Hypromellose, Carmellose, Carbomer gel)

None

164
Q

What is the drug management for severe dry eyes?

A

Preservative-free eye drops (e.g., Hylo-tear PF)
* Ocular ointment applied at night (e.g., wool fat lubricants)

None

165
Q

What are the red flags for dry eyes?

A

Symptoms uncontrolled for 4 weeks or more
* Reduced visual acuity
* Photophobia
* Marked redness of the eye
* Signs of corneal ulcer or scarring
* Vision deterioration

None

166
Q

What are the symptoms of Chronic Open Angle Glaucoma (COAG)?

A

No clear symptoms (silent disease)

None

167
Q

What are the first-line drug treatments for COAG?

A

Prostaglandin analogues (e.g., Latanoprost, Bimatoprost)
* Beta-blockers (e.g., Timolol)
(Apply with a 5-minute gap between medications)

None

168
Q

What are the second-line drug treatments for COAG?

A

Carbonic anhydrase inhibitors (e.g., Acetozolamide, Dorzolamide, Brinzolamide)
* Sympathomimetics (e.g., Brimonidine)
* Parasympathomimetics (e.g., Pilocarpine)

None

169
Q

What are the red flags for COAG?

A

Urgent referral if acute glaucoma symptoms are present

None