General Practice Flashcards

1
Q

Tx - Trigeminal Neuralgia

A

1st line - carbamezapine
Surgical Interventions are possible for persistent symptoms

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2
Q

what causes hormonal headaches? how do they present- describe the distribution of the headache? When do they occur?

A

Hormonal headaches are related to low oestrogen.

They have similar features to migraines, with a unilateral, pulsatile headache associated with nausea. They are sometimes called menstrual migraines.

They may occur:
- Two days before and the first three days of the menstrual period
- In the perimenopausal period
- Early pregnancy (headaches in the second half of pregnancy should prompt investigations for pre-eclampsia)

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3
Q

hormonal headaches - Tx

A

Triptans and NSAIDs (e.g., mefenamic acid)

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4
Q

What is Cervical Spondylosis and how does it present?

A

Cervical spondylosis is a common condition caused by degenerative changes in the cervical spine.

Sx :
- neck pain, usually made worse by movement.
- often presents with headaches.

Sponylosis just means spinal degeneration (thinning of intervebral disks), not to be confused with spinal stenosis (narrowing)- spondylosis leads to spinal stenosis , spondylitis (inflammation of vertebra), spondylolisthesis (lateral displacement)

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5
Q

Tension headaches management, including chronic

A
  • Reassurance
  • Simple analgesia (e.g., ibuprofen or paracetamol)

Amitriptyline is generally first-line for chronic or frequent tension headaches.

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6
Q

What is a hemiplegic migraine, how can you differ them from a stroke

A
  • The main feature of hemiplegic migraines is hemiplegia (unilateral limb weakness). Other symptoms may include ataxia (loss of coordination) and impaired consciousness.
  • strokes have sudden hemiplegia
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7
Q

Rx for migraines

A

Patients may develop strategies for managing symptoms, often retreating to a dark, quiet room and sleeping.

Medical options for an acute attack are:

  • NSAIDs(e.g., ibuprofen or naproxen)
  • Paracetamol
  • Triptans(e.g., sumatriptan)
  • Antiemeticsif vomiting occurs (e.g., metoclopramide or prochlorperazine)

Opiatesarenotused to treat migraines and may make the condition worse.

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8
Q

Presentation of tension headaches

A

a mild ache or pressure in a band-like pattern around the head.

They develop and resolve gradually.

They do not produce visual changes.

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9
Q

Bell’s Palsy - What are the functions of the facial nerve - 3 parts?

A

Motor functionfor:

  • Facial expression
  • Stapediusmuscle in the inner ear
  • Posterior digastric,stylohyoidandplatysmamuscles - these are jaw and neck muscles, not throat!!

Sensory functionfortastefrom theanterior 2/3of the tongue.

Parasympatheticsupply to the:

  • Submandibularandsublingualsalivary glands
  • Lacrimal gland(stimulating tear production)
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10
Q

What is bells palsy and what causes it?

A

Facial nerve palsy - isolated dysfunction of the fascial nerve causing unilateral facial weakness

it is idiopathic - no apparent cause

recovery several weeks - 12 months, 1/3 patients have residual weakness

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11
Q

what is Ramsay-Hunt syndrome?

A

Ramsay-Hunt syndrome is caused by the varicella zoster virus (VZV). It presents as a unilateral lower motor neurone facial nerve palsy. Patients stereotypically have a painful and tender vesicular rash in the ear canal, pinna and around the ear on the affected side. This rash can extend to the anterior two-thirds of the tongue and hard palate.

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12
Q

Tx - Ramsay hunt-syndrome

A

Treatment is withaciclovirandprednisolone. Patients also requirelubricating eye drops.

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13
Q

What is Guillain-Barré syndrome

A

Guillain-Barré syndrome is an acute paralytic polyneuropathy that affects the peripheral nervous system. It causes acute, symmetrical, ascending weakness and can also cause sensory symptoms. It is usually triggered by an infection and is particularly associated with to Campylobacter jejuni, cytomegalovirus (CMV) and Epstein-Barr virus (EBV).

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14
Q

Presentation of Guillain-Barré syndrome

A

Symptoms usually start within four weeks of the triggering infection - campylobacter, EBV, CMV. They begin in the feet and progress upward. Symptoms peak within 2-4 weeks. Then, there is a recovery period that can last months to years.

The characteristic features are:

Symmetrical ascending weakness
Reduced reflexes

There may be peripheral loss of sensation or neuropathic pain. It may progress to the cranial nerves and cause facial weakness. Autonomic dysfunction can lead to urinary retention, ileus or heart arrhythmias.

Severe cases - respiratory failure.

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15
Q

Presentation of BPPV

A
  • A variety of head movements can trigger attacks of vertigo. A common trigger is turning over in bed.
  • Symptoms settle after around 20 – 60 seconds, and patients are asymptomatic between attacks.
  • Often episodes occur over several weeks and then resolve but can reoccur weeks or months later.
  • BPPV does not cause hearing loss or tinnitus.
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16
Q

What is otitis externa

A
  • inflammation of the skin in the external ear canal
  • it can spread to the pinna (external ear)
  • acute or chronic - +/- 3 weeks
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17
Q

what is the most common cause of hypothyroidism in the developed world? Explain what this is?

A
  • hashimoto’s thyroiditis is an autoimmune condition causing inflammation of the thyroid gland
    • don’t get confused with De Quervain’s (post-infectious) thyroiditis, both have initial goitre then hypothyroidism period i think
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18
Q

what antibodies are associated with Hashimoto’s thyroiditis?

A

It is anautoimmunecondition causinginflammationof the thyroid gland. It is associated withanti-thyroid peroxidase(anti-TPO)antibodiesandanti-thyroglobulin(anti-Tg)antibodies.

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19
Q

Other than Hashimoto’s disease, what are the causes of hypothyroidism (6)

A
    • Iodine deficiency - developing world
    • Hyperthyroidism Tx - LIST THESE?
    • other thyroiditis
      • Medications - lithium and amiodarone
      • De Quivinne’s Thyroiditis - post flu/mumps leads to inital thryotoxicosis followed by hypothyroidism followed by
      • past-partum thyroiditis
    Secondary Cause:
    • Hypopituitism (other pituitary hormones are also decreased )
      • pituitary adenomas
      • pituitary surgery
      • infection
      • Sheehan syndrome (postpartum haemorrhage → ischemia)
      • radiation
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20
Q

what are the causes of hyperthyroidism

A

The causes of hyperthyroidism can be remembered with the “GIST” mnemonic:

G – Graves’ disease
I – Inflammation (thyroiditis)
S – Solitary toxic thyroid nodule
T – Toxic multinodular goitre

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21
Q

What is thyroiditis? What causes it (4)

A

Thyroiditis(thyroid glandinflammation) often causes aninitial periodofhyperthyroidism, followed byunder-activityof the thyroid gland (hypothyroidism). The causes of thyroiditis include:

  • De Quervain’s thyroiditis
  • Hashimoto’s thyroiditis
  • Postpartum thyroiditis
  • Drug-induced thyroiditis
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22
Q

Rx for Hyperthyroidism - 5

A
  • 1st line - carbimazole (titrated or block and replace with levothyroxine) - sounds like an antifungal lol
    • propylthiouracile
    • radioactive iodine + levothyroxine
    • thyroidectomy + levothyroxine
    • Beta blockers for relief of adrenaline -ike symptoms
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23
Q

what is a thyrotoxic crisis? How does it present and how is it managed?

A

Thyroid storm is a rare presentation of hyperthyroidism. It is also known as thyrotoxic crisis. It is a rare and more severe presentation of hyperthyroidism with fever, tachycardia and delirium. It can be life-threatening and requires admission for monitoring. It is treated the same way as any other presentation of thyrotoxicosis, although they may need additional supportive care with fluid resuscitation, anti-arrhythmic medication and beta blockers.

Mx of normal thyrotoxicosis:
- carbimazole - 1st line
- propylthiouracil
- radioactive iodine
- surgery

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24
Q

Define allodynia

A

Allodyniarefers to when pain is experienced with sensory inputs that do not normally cause pain (e.g., light touch).

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25
Q

Physiology of pain - describe the anterolateral system?

A

For memory Z2F:

  • The signal from nociceptors travels in thecentral nervous system, up the spinal cord (mainly in thespinothalamic tractandspinoreticular tract) to the brain where it is interpreted as pain, mainly in thethalamusandcortex.

For understanding - Neuroscientifically challenged video:

  • nociceptors send signals to the spinal cord that then ascend to the brain on pathways known as the anterolateral system
  • there are 3 pathways that make up the antero lateral system: spinothalamic, spinoreticular and spinomesencephalic tracts
  • spinothalamic tract - the main pathway for transmitting pain to the cerebral cortex that is thought to allow for conscious sensation and localisation of pain. Decussates at the spinal level, ascends and synapses in the thalamus. Third order neurones ascends from the thalamus, through the in the internal capsule and terminate at the somatosensory cortex.
  • Spinoreticular - same pathway as the spinothalamic tract but also synapses in the reticular formation, neurone throughout the brainstem involved in attention and consciousness. This is thought to play in the emotional response to pain
  • Spinomesechephalic tract - same pathway as spinothalamic but synapses in the aqueductal grey in the midbrain that releases endogenous opioids and results in descending inhibition of pain signals in the spinal-cord.
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26
Q

Define neuropathic pain, what are the typical features of neuropathic pain (5) ?

A

Neuropathic painis caused by abnormal functioning or damage of the sensory nerves, resulting in pain signals being transmitted to the brain. Typical features suggestive of neuropathic pain are:

  • Burning
  • Tingling
  • Pins and needles
  • Electric shocks
  • Loss of sensation to touch of the affected area
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27
Q

What are the three steps of the analgesic ladder?

A

The World Health Organisation (WHO) analgesic ladder was originally to help manage cancer-related pain. It is also often used for acute and chronic painful conditions. The idea is that patients with mild pain start on the first step, and when pain is more severe or does not respond to the lower steps, higher steps on the ladder are used until the pain is adequately managed.

There are three steps to the analgesic ladder:

Step 1: Non-opioid medications such as paracetamol and NSAIDs
Step 2: Weak opioids such as codeine and tramadol (tramadol has multiple mechanisms of action, including being an SNRI and agonist of opioid receptors)
Step 3: Strong opioids such as morphine, oxycodone, fentanyl and buprenorphine

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28
Q

What are the ‘adjuvants’ to the analgesic ladder?

A

Other medications that can may be combined with the analgesic ladder for additional effect (calledadjuvants) or used separately to manage neuropathic pain. These are:

  • Amitriptyline– a tricyclic antidepressant
  • Duloxetine– an SNRI antidepressant
  • Gabapentin– an anticonvulsant
  • Pregabalin– an anticonvulsant
  • Capsaicin cream(topical) – from chilli peppers
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29
Q

what are the Key side effects of NSAIDs (6)

A

The key side effects ofNSAIDsare:

  • Gastritis with dyspepsia (indigestion)
  • Stomach ulcers
  • Exacerbation of asthma - prostaglandins inhibit leukotriene release (bronchospasm)
  • Hypertension
  • Renal impairment
  • Coronary artery disease, heart failure and strokes (rarely) - prostaglandins protect vascular endothelium
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30
Q

What are the 5 key side effects of opiods?

A

The key side effects ofopioidsare:

  • Constipation
  • Skin itching (pruritus)
  • Nausea
  • Altered mental state (sedation, cognitive impairment or confusion)
  • Respiratory depression (usually only with larger doses in opioid-naive patients)
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31
Q

How are opioids used in palliative care for pain management?

A

Using opioids to control pain in palliative patients is a specific scenario where the doses are titrated and optimised over time. This involves using a combination of:

Background opioids (e.g., 12-hourly modified-release oral morphine)
Rescue doses for breakthrough pain (e.g., immediate-release oral morphine solution)

The rescue dose is usually 1/6 of the background 24-hour dose. For example, if the patient is getting 30mg in 24 hours of modified-release morphine (15mg every 12 hours), each rescue dose will be 5mg, given every 2-4 hours as required.

If the patient requires regular rescue doses for breakthrough pain, the dose of the background opioid can be increased. The rescue doses will also need increasing so that they remain 1/6 of the background 24-hour dose.

TOM TIP: Remember that each rescue dose is 1/6 of the 24-hour background dose. This is a very common exam question and something that seniors will commonly ask to test your knowledge. The question may be something like, “this patient is on 30mg of modified-release morphine every 12 hours; what would be the correct breakthrough dose?” In this scenario, 10mg is the correct answer, as the patient is getting 60mg background morphine every 24 hours (30mg twice a day).

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32
Q

what is the difference between chronic primary and chronic secondary pain?

A

Chronic primary pain – where no underlying condition can adequately explain the pain

Chronic secondary pain – where an underlying condition can explain the pain

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33
Q

3 mechanisms of chronic pain

A
  • Sensitisation of the primary afferent nociceptors by frequent stimulation
  • Increased activity of the sympathetic nervous system
  • Increased muscle contraction in response to pain
  • Biological,psychologicalandsocialfactors contribute to the persistence of the pain.
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34
Q

KEY Management of chronic pain - 5 things

A
  • Supervised group exercise programs
  • Acceptance and commitment therapy (ACT)
  • Cognitive behavioural therapy (CBT)
  • Acupuncture
  • Antidepressants (e.g., amitriptyline, duloxetine or an SSRI)
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35
Q

What is the appropriate medical management of chronic primary pain (where no underlying condition can adequately explain the pain)?

A
  • Antidepressants (e.g., amitriptyline, duloxetine [SNRI] or an SSRI)

It is worth noting that the NICE guidelines (2021) advise that forchronic primary pain(where no underlying condition can adequately explain the pain), patients shouldnotbe started on:

  • Paracetamol
  • NSAIDs
  • Opiates
  • Pregabalin
  • Gabapentin

TOM TIP: Chronic pain is incredibly common. It is worth noting these recent guidelines that clearly state to avoid basically all forms of analgesia (other than antidepressants) in patients with chronic primary pain. These guidelines may come up in exams, potentially asking you the most appropriate medication for a patient with chronic primary pain (antidepressants). This is different to chronic secondary pain, where there is an underlying condition that explains the pain.

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36
Q

Management of Osteoathritis

A

Non-pharmacological management involves patient education and lifestyle changes, such as:

  • Therapeutic exercise to improve strength and function and reduce pain
  • Weight loss if overweight, to reduce the load on the joint
  • Occupational therapy to support activities and function (e.g., walking aids and adaptations to the home)

Pharmacological management recommended by the NICE guidelines (2022) are:

  1. Oralparacetamol(Short term) and topicalNSAIDs
  2. Add oralNSAIDs(consider co-prescribing aproton pump inhibitor, such asomeprazole, to protect the stomach)
  3. Consideropiatessuch ascodeine

They are best used intermittently, only for a short time during flares. Weak opiates and paracetamol are only recommended for short-term, infrequent use. NICE (2022) recommend against using any strong opiates for osteoarthritis.

Intra-articular steroid injections may temporarily improve symptoms (NICE say up to 10 weeks).

Joint replacement may be used in severe cases. The hips and knees are the most commonly replaced joints.

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37
Q

what tool is used to assess for neuropathic pain?

A

TheDN4 questionnairecan be used to assess the characteristics of the pain and the likelihood of neuropathic pain. Patients are scored out of 10. A score of 4 or more indicates neuropathic pain - hence the name

Douleur neuropathique en 4

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38
Q

What are the 4 first line treatments for neuropathic pain?

A

There are four first-line treatments for neuropathic pain:

  • Amitriptyline– a tricyclic antidepressant
  • Duloxetine– an SNRI antidepressant
  • Gabapentin– an anticonvulsant
  • Pregabalin– an anticonvulsant

NICE recommend using one of these four medications to control neuropathic pain. If it does not help, it can be slowly withdrawn, and an alternative can be tried. All four can be tried in turn. Only one neuropathic medication should be used at a time.

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39
Q

How is trigeminal neuralgia managed?

A

Trigeminal neuralgiais a type of neuropathic pain. However, NICE recommendcarbamazepineas the first-line medication for trigeminal neuralgia, and if that does not work to refer to a specialist.

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40
Q

classical triad of parkinson’s

A

There is aclassic triadof features in Parkinson’s disease:

  • Resting tremor(a tremor that is worse at rest)
  • Rigidity(resisting passive movement)
  • Bradykinesia(slowness of movement)
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41
Q

Pathophysiology of parkinson’s - what is the function of the basal ganglia?

A

Thebasal gangliaare a group of structures situated near the centre of the brain.** They are responsible for coordinating habitual movements such as walking, controlling voluntary movements and learning specific movement patterns**.

Dopamineplays an essential role in the basal ganglia function. Patients with Parkinson’s disease have a slow but progressive drop in dopamine production.

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42
Q

4 features of a parkinson’s tremor

A
  • asymmetrical
  • pill-rolling appearance
  • resting - worse at rest, improves with movement of that arm
  • worse when distracted - performing a task in the opposite hand makes it worse
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43
Q

Features of parkinson’s other than the triad

A
  • Depression
  • Sleep disturbance and insomnia
  • Loss of the sense of smell (anosmia)
  • Postural instability (increasing the risk of falls)
  • Cognitive impairment and memory problems
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44
Q

Define bradykinesia - list some examples

A

Bradykinesiadescribes the movements gettingslowerandsmallerand presents in several ways:

  • Handwriting gets smaller and smaller (micrographia)
  • Small steps when walking (“shuffling” gait)
  • Rapid frequency of steps to compensate for the small steps and avoid falling (“festinating” gait)
  • Difficulty initiating movement (e.g., going from standing still to walking)
  • Difficulty in turning around when standing and having to take lots of little steps to turn
  • Reduced facial movements and facial expressions (hypomimia)
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45
Q

4 Tx options for parkinson’s

A

The treatment options are:

  • Levodopa (synthetic dopamine)- combined withperipheral decarboxylase inhibitors
  • COMT inhibitors
  • Dopamine agonists
  • Monoamine oxidase-B inhibitors
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46
Q

Parkinsons - what is levodopa often combined with

A

Levodopaissynthetic dopaminetaken orally. It is usually combined with aperipheral decarboxylase inhibitor(e.g.,carbidopaandbenserazide), which stops it from being metabolised in the body before it reaches the brain.

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47
Q

Parkinson’s - what is the main adverse effect of Levodopa

A

The main side effect oflevodopaisdyskinesia. Dyskinesia refers to abnormal movements associated withexcessive motor activity. Examples are:

  • Dystonia(where excessive muscle contraction leads to abnormal postures or exaggerated movements)
  • Chorea(abnormal involuntary movements that can be jerking and random)
  • Athetosis(involuntary twisting or writhing movements, usually in the fingers, hands or feet)

Amantadineis aglutamate antagonistthat may be used to managedyskinesiaassociated withlevodopa.

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48
Q

Management for Dementia- each of the 4 types, and two aspects of treatment

A
  • Non-pharmacological interventions (promote cognition, independence, and wellbeing) - cognitive stimulation therapy, group reminiscence therapy

Alzheimer’s:
* Acetylcholinesterase (AChE) inhibitors (donepezil, galantamine, and rivastigmine)
* Memantine (a N-methyl-D-aspartic acid receptor antagonist)
Lewy Bodies:
* Donepezil or rivastigmine are recommended first line.
Vascular dementia:
* management of cardiovascular disease - stroke, heart disease, diabetes, HTN, high cholesterol, CKD
* If comorbid alzheimer’s, parkinson’s disease dementia or lewy body then AChE inhibitors or memantine are options, if no comorbid dementia then no!!
Fronto-temporal demmentia:
* People with frontotemporal dementia should not be offered AChE inhibitors or memantine.

**Drug treatments for non-cognitive symptoms (mood disturbance, personality change, agitation, psychosis) may include antipsychotics:
*** Risperidone and haloperidol are the only antipsychotics licensed for treating non-cognitive symptoms of dementia.

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49
Q

Management of behavioural and psychological symptoms of dementia

A

Antipsychotic medications:

Risperidone or Haloperidol)

These symptoms include agitation, anxiety, wandering, aggression, delusions and hallucinations
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50
Q

What is chronic fatigue syndrome?

A

Persistant, disabling fatigue lasting >6 months, affecting mental and physical function that significant impaired their ability to engage in usual activities and cannot be explained by another illness.

Plus 4 of:

  • myalgia (muscle pain)
  • polyarthragia (joint pain)
  • memory impairment/cogniftive difficulites
  • unrefreshing sleep/sleep disturabance
  • post-exertional malaise (slow recovery, low levels of exertion)
  • peristant sore throat, cervical/axillary lymph nodes
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51
Q

Management of chronic fatigue syndrome (5+)

A

Same as Fibryomalgia
- referral to specialist CFS service
- CBT (developing coping strategies)
- manage any underlying causes or contributory factors - stress, chronic conditions, insomnia,
- graded exercise programmes
- manage stress, depressiona dn anxiety
- advice on sleep hygeine - avoid daytime sleeping
- **pain managment **- anti-depressants.

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52
Q

Chronic Fatigue vs Fibromyalgia

A
  • both characterised by chronic symptoms of fatigue and widespread pain
  • They are both functional disorders - without a clear pathology, that are managed with support, CBT and graded exercise
  • difference is that in fibromyalgia widespread pain is the main feature, whereas in CFS there is persistent disabling fatigue as the main feature
  • Think of Iona vs CAS patient - really helpful
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53
Q

Ix for Fibromyalgia

A
  • the same as CFS - all normal, ruling out other causes of pain and fatigue
  • FBC, TFTs, CRP/ESR…
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54
Q

What is fibromyalgia and what are the key features? (7+)

A

A functional disorder where there is chronic (>3 months) and widespread (left and right sides, above and below the waist, and axial skeleton) pain. Basically it is primary chronic pain rather than secondary

  • profound fatigue is usually also present
  • post-exertional pain and fatigue (small amounts of exertion)
  • widespread myofascial trigger points - severe tender points
  • paresthesia
  • morning stiffness
  • poor concentration
  • sleep disturbance
  • low mood
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55
Q

Mx for Fibromyalgia (3)

A
    • graded group exercise programmes
    • CBT or Acceptance and commitment (ACT) - develop coping strategies
    • consider antidepressants - duloxetine (SNRI), amitriptyline for pain and sleep (not low mood)
      • Don’t use Gabapentine or pregabaline!!! NSAIDs, paracetamol or opioids - they don’t work
    others
    • lifestyle modification - pacing to avoid over exertion
    • some find acupuncture helpful
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56
Q

Ix for glandular fever

A

Heterophilic antibodies - most people (i think cheaper, takes up to 6 weeks)

  • monospot test
  • paul brunnel test

EBV serology - faster, used in kids

  • EBV viral caspid antigen antibodies - IgM (acute infection) and IgG (after the condition)
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57
Q

What drug can you not to give to someone with infectious mononucleosis

A

Amoxicillin - Mononucleosis causes an intensely itchy maculopapular rash in response to amoxicillin or cefalosporins.

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58
Q

Management of Infecitous mononucleiosis (lifestyle advice?)

A

Infectious mononucleosis is usually self limiting. The acute illness lasts around 2 – 3 weeks, however it can leave the patient with fatigue for several months once the infection is cleared.

Patients are advised to avoid alcohol, as EBV impacts the ability of the liver to process the alcohol. Patients are advised to avoid contact sports due to the risk of splenic rupture. Emergency surgery is usually required if splenic rupture occurs.

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59
Q

Name 4 causes of Otitis externa

A
  • Bacterial infection
  • Fungal infection - especially following topical antibiotics
  • Eczema
  • dermatitis - Seborrhoeic + Contact
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60
Q

What are the two most common bacterial causes of otitis externa?

A

Pseudomonas aeruginosa - aminoglycoside Rx (gentamicin)
Staphylococcus aureus

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61
Q

4 Sx of otitis externa

A

Ear pain
Discharge
Itchiness
Conductive hearing loss (if the ear becomes blocked)

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62
Q

Otitis externa - On examination what is found? Lastly, what about the tympanic membrane?

A

Examination can show:

Erythema and swelling in the ear canal
Tenderness of the ear canal
Pus or discharge in the ear canal
Lymphadenopathy (swollen lymph nodes) in the neck or around the ear

The tympanic membrane may be obstructed by wax or discharge. It may be red if the otitis externa extends to the tympanic membrane. If it is ruptured, the discharge in the ear canal might be from otitis media rather than otitis externa.

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63
Q

Management of Otitis Externa (4 categories)

A

Mild - Acetic acid 2% (antifungal and antibacterial effects)

Moderate - topical antibiotic (neomycin or gentamicin) + steroid (dexamethasone).

Topical antibiotics cannot be used if the tympanic membrane is perforated, why?

Severe pain or systemic symptoms (fever is abnormal) - oral flucloxacillin or ENT admission and IV antibiotics

Fungal Infection - clotrimazole

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64
Q

What is malignant Otitis Externa, how does it present and how is it managed?

A

Malignant otitis externa is a severe and potentially life-threatening form of otitis externa. The infection spreads to the bones surrounding the ear canal and skull. It progresses to osteomyelitis of the temporal bone of the skull.

Malignant otitis externa is usually related to underlying risk factors for severe infection, such as: Diabetes, Immunosuppressant medications (e.g., chemotherapy), HIV

Symptoms are generally more severe than otitis externa, with persistent headache, severe pain and fever.

Malignant otitis externa requires emergency management, with:

Admission to hospital under the ENT team
IV antibiotics
Imaging (e.g., CT or MRI head) to assess the extent of the infection

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65
Q

Neuro Key concept - What is ataxia, and what are the two main types?

A

Ataxia

Ataxia is a problem with coordinated movement. It can be sensory or cerebellar.

Sensory ataxia is due to loss of proprioception, which is the ability to sense the position of the joint (e.g., is the joint flexed or extended). This results in a positive Romberg’s test (they lose balance when standing with their eyes closed) and can cause pseudoathetosis (involuntary writhing movements). A lesion in the dorsal columns of the spine can cause sensory ataxia.

Cerebellar ataxia results from problems with the cerebellum coordinating movement, indicating a cerebellar lesion.

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66
Q

The most common bacterial cause of otitis media

A

The most common bacterial causes of otitis media, as well as other ENT infections such as rhino-sinusitis is streptococcus pneumonia. (It is also the most common alternative cause of bacterial tonsilitis to group A strep)

Other common causes include:

Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus

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67
Q

what are the most common causes of tonsilitis?

A

The most common cause of tonsillitis is a viral infection. Viral infections do not require or respond to antibiotics.

The most common cause of bacterial tonsillitis is group A streptococcus (Streptococcus pyogenes). This can be effectively treated with penicillin V (phenoxymethylpenicillin). The most common cause of otitis media, rhinosinusitis and the most common alternative bacterial cause of tonsillitis is Streptococcus pneumoniae.

Other causes:

Haemophilus influenzae
Morazella catarrhalis
Staphylococcus aureus

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68
Q

Management of Otitis media

A

Most cases of otitis media will resolve without antibiotics, and NICE guidelines from 2018 highlight the importance of not providing antibiotics for otitis media.

They state that most cases of otitis media will resolve within 3 days without antibiotics, but it can last for up to a week. Complications (mainly mastoiditis) are rare.

  • Give simple analgesia to help with pain and fever.
  • Antibiotics if given can be delayed prescription - amoxicillin 1st line
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69
Q

Management of Sinusitis - Acute and Chronic

A

NICE recommend for patients with symptoms that are not improving after 10 days, the options of:

High dose steroid nasal spray for 14 days (e.g., mometasone 200 mcg twice daily)
A delayed antibiotic prescription, used if worsening or not improving within 7 days (phenoxymethylpenicillin first-line)

Options for chronic sinusitis are:

Saline nasal irrigation
Steroid nasal sprays or drops (e.g., mometasone or fluticasone)
Functional endoscopic sinus surgery (FESS)

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70
Q

Everything you need to know about Croup

define it exactly - structure affected?

Age of patients?

Sx?

classic cause?

management?

A

Croup is an acute infective respiratory disease affecting young children. It typically affects children aged 6 months to 2 years, however they can be older.

It is an upper respiratory tract infection causing oedema in the larynx.

Sx:
Increased work of breathing
“Barking” cough, occurring in clusters of coughing episodes
Hoarse voice
Stridor
Low grade fever

The classic cause of croup that you need to spot in your exams, is parainfluenza virus.

It usually improves in less than 48 hours and responds well to treatment is steroids, particularly dexamethasone.

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71
Q

What are the symptoms of impacted ear wax

A

In most people, ear wax does not cause any problems.

Ear wax can build up and become impacted and stuck to the tympanic membrane. This can result in:

Conductive hearing loss
Discomfort in the ear
A feeling of fullness
Pain
Tinnitus

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72
Q

What is Presbycusis? Pathophysiology? Ix? Mx?

A

Presbycusis is described as age-related hearing loss. It is a type of sensorineural hearing loss that occurs as people get older. It tends to affect high-pitched sounds first and more notably than lower-pitched sounds. The hearing loss occurs gradually and symmetrically.

The causes of reduced hearing in presbycusis are complex. There are several different mechanisms, including loss of the hair cells in the cochlea, loss of neurones in the cochlea, atrophy of the stria vascularis and reduced endolymphatic potential.

Ix - audiometry

Rx - Presbycusis is Irreversible, Hearing aids, or for severe cases, cochlear implants

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73
Q

What scoring system can be used to assess if a sore throat (tonsilitis and pharyngitis) is likely to be bacterial/benefit from antibiotics? How does it affect the management?

A

The FeverPAIN scoring system can be used to estimate the probability that a sore throat is due to a bacterial infection (streptococcus) and will benefit from antibiotics. A score and 4 – 5 gives a 62 – 65% probability of bacterial tonsillitis. Antibiotics are considered for a score of more than 4. A point is awarded for each of the following.
* Fever during previous 24 hours
* P – Purulence (pus on tonsils)
* A – Attended within 3 days of the onset of symptoms
* I – Inflamed tonsils (severely inflamed)
* N – No cough or coryza (inflammation of the mucus membranes in the nose)

Management if not scoring high enough:
Advise simple analgesia with paracetamol and ibuprofen to control pain and fever. Safetynetting - contsider antibiotics if not settled after 3 days or the fever rises above 38.3ºC. Also, consider antibiotics if they are at risk of more severe infections, such as young infants, immunocompromised patients or those with significant co-morbidity, or a history of rheumatic fever.

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74
Q

GP - what does examination involve for tonsilitis (3)

A

Examination of the throat will reveal red, inflamed and enlarged tonsils, with or without exudates. Exudates are small white patches of pus on the tonsils.

There may be anterior cervical lymphadenopathy, which refers to swollen, tender lymph nodes in the anterior triangle of the neck (anterior to the sternocleidomastoid muscle and below the mandible). The tonsillar lymph nodes are just behind the angle of the mandible (jawbone).

Z2F doesn’t say this, but I’d also examine the ears for signs of otitis media.

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75
Q

What is quinsy, why does it occour and what are the symptoms?

A

Quinsy is the common name for a peritonsillar abscess. Peritonsillar abscess arises when there is a bacterial infection with trapped pus, forming an abscess in the region of the tonsils.

Peritonsillar abscesses are usually a complication of untreated or partially treated tonsillitis, although it can arise without tonsillitis.

Quinsy can occur just as frequently in teenagers and young adults as it does in children, unlike tonsillitis which is much more common in children.

Similar Sx to tonisilitus, additional symptoms that can indicate a peritonsillar abscess include:
- Trismus, which refers to when the patient is unable to open their mouth
- Change in voice due to the pharyngeal swelling, described in textbooks as a “hot potato voice”
- Swelling and erythema in the area beside the tonsils on examination

76
Q

Paeds - When is tonsillectomy appropriate for managing tonsillitis?

A

DON’T TRY TOO HARD TO LEARN THESE NUMBERS JUST ROUGHLY KNOW ITS VERY RECURRENT TONSILLITS

A common question you will get from patients and parents is whether a child needs a tonsillectomy for recurrent tonsillitis. The NICE clinical knowledge summaries give the number of episodes required for a tonsillectomy:

7 or more in 1 year
5 per year for 2 years
3 per year for 3 years

Other indications are:
- 2x episodes of quinsy (tonsillar abscesses)
- Enlarged tonsils causing difficulty breathing, swallowing or snoring

77
Q

Define Vertigo

A

A sensation that there is movement between the patient and their environment. Vertigo is often associated with nausea, vomiting, sweating and feeling generally unwell.

78
Q

What causes Meniere’s disease and how does it present?

A

Ménière’s disease is caused by an excessive buildup of endolymph in the semicircular canals, causing a higher pressure than normal, disrupting the sensory signals. It causes attacks of hearing loss, tinnitus, vertigo and a sensation of fullness in the ear. These attacks typically last several hours before settling. It most often occurs in middle-aged adults and is not associated with movement. The symptoms are not positional. Patients will have spontaneous nystagmus during attacks (nystagmus is discussed in more detail later). Over time, the patient’s hearing will gradually deteriorate.

79
Q

Pathophysiology of BPPV

A

BPPV is caused by crystals of calcium carbonate called otoconia that become displaced into the semicircular canals. This occurs most often in the posterior semicircular canal. They may be displaced by a viral infection, head trauma, ageing or without a clear cause.

The crystals disrupt the normal flow of endolymph through the canals, confusing the vestibular system. Head movement creates the flow of endolymph in the canals, triggering episodes of vertigo.

80
Q

Dx for BPPV

A

The Dix-Hallpike manoeuvre can be used to diagnose BPPV (Dix for Dx – diagnosis). It involves moving the patient’s head in a way that moves endolymph through the semicircular canals and triggers vertigo in patients with BPPV.

In patients with BPPV, the Dix-Hallpike manoeuvre will trigger rotational nystagmus and symptoms of vertigo. The eye will have rotational beats of nystagmus towards the affected ear (clockwise with left ear and anti-clockwise for right ear BPPV).

81
Q

Rx for BPPV

A

The Epley manoeuvre can be used to treat BPPV. The idea is to move the crystals in the semicircular canal into a position that does not disrupt endolymph flow.

Brandt-Daroff exercises can be performed by the patient at home to improve the symptoms of BPPV.

Read more about them on Z2F if you forget what they are.

82
Q

What is conjunctivitis and what causes it?

A

Conjunctivitis is inflammation of the conjunctiva.

The conjunctiva is a thin layer of tissue that covers the inside of the eyelids and the sclera. Conjunctivitis may be bacterial, viral or allergic. It may be unilateral or bilateral.

me - think of conjunctival pallor - the conjunctiva is the pink thing you can see when you pull back your lids. its not attached to the white bit but it covers them.

83
Q

How does conjunctivitis present - bacterial vs viral

A
  • PAINLESS Red, bloodshot eye
  • Itchy or gritty sensation
  • Discharge (Bacterial = purulent and sticky, viral =clear)
84
Q

When do you need to urgently (same-day) refer to ophthalmology?

A

Conditions that require emergency same-day referral to ophthalmology tend to cause pain or reduced visual acuity.

85
Q

Sx of B12 deficiency

A

In addition to the fatigue, breathlessness, headaches… of anaemia generally

Vitamin B12 deficiency can causeneurological symptoms:

  • Peripheral neuropathy, withnumbnessorparaesthesia(pins and needles)
  • Loss ofvibration sense
  • Loss ofproprioception
  • Visual changes
  • Mood and cognitive changes
86
Q

Tx for B12 deficiency

A

Intramuscular hydroxocobalamin - initially given to all patients with B12 deficiency

87
Q

Physiology - How is iron absorbed and what can affect this

A

Iron is mainly absorbed in the duodenum and jejunum. It requires the acid from the stomach to keep the iron in the soluble ferrous (Fe2+) form. When the stomach contents are less acidic, it changes to the insoluble ferric (Fe3+) form. Medications that reduce stomach acid, such as proton pump inhibitors (e.g., omeprazole), can interfere with iron absorption. Inflammation of the duodenum or jejunum (e.g., from coeliac disease or Crohn’s disease) can also reduce iron absorption.

88
Q

causes of Iron deficiency in Adults, Women specifically, Children (Sx)

A

Men and women who aren’t menstruating - Blood loss from the GI tract - unexplained iron deficiency required an ODG

Women - menstruation

children - dietary insufficiency of iron

Pregnancy

89
Q

Iron Studies- what is the transferrin, ferritin, tranferrin saturations, serum iron, what value is most important clinically

A

Transferrin - carrier protein that transports Iron in the blood

Ferritin - protein that stores Iron within cells, an acute phase reactant (inflammation)

Serum iron - free iron, varies significantly throughout the day

Transferrin saturations - indicates the total Iron in the body. THIS IS THE IMPORTANT ONE!!!!

90
Q

A male patient turns jaundiced and becomes anaemic after developing an infection or taking antimalarials. What MIGHT be the underlying diagnosis

A

The underlying diagnosis might be G6PD deficiency.

Aside from infections and drugs, another common trigger is fava beans (broad beans) but I know that you already knew that one

91
Q

Key symptoms in the presentation of Mumps, including 4 complications

A
  • prodrome - a few days of flu-like symtoms
  • Parotid gland swelling, either unilateral or bilateral, with associated pain is the key feature that should make you consider mumps.
  • It can also present with symptoms of the complications, such as:
    • Abdominal pain(pancreatitis)
    • Testicular painand swelling (orchitis)
    • Confusion, neck stiffness and headache (meningitisorencephalitis)
    • sensorineural hearing loss
92
Q

Management of Mumps? (including Ix)

A
  • The diagnosis can be confirmed usingPCR testingon a saliva swab. The blood or saliva can also be tested forantibodiesto the mumps virus.
  • Management issupportive, with rest, fluids and analgesia. Mumps is a self limiting condition. Management of complications is also mostly supportive.
  • notifiable disease
93
Q

What is eczema and how does it present

A

Eczema is a chronic atopic condition caused by defects in the normal continuity of theskin barrier, leading toinflammation in the skin. Eczema usually presents in infancy with dry, red, itchy and sore patches of skin over theflexor surfaces(the inside of elbows and knees) and on the face and neck.

94
Q

what are the two complications of eczema?

A
  • eczema herpeticum - viral skin infection caused by Herpes simplex virus entering the broken skin barrier
  • bacterial infection (usually staph.aureus) - breakdown in barrier allows an entry point. Rx - flucloxacillin
  • severe cases may require admission to hospital
95
Q

Pathophysiology of acne vulgaris

A
  • chronic inflammation (with or without infection) of pilosebaceous units (dimples in the skin containing hair follicles + sebaceous glands)
  • It results from the increased production of sebum (promoted by androgenic hormones in puberty), trapping of keratin (dead skin cells) and blockage of pilosebaceous units. This leads to swelling and inflammation of the pilosebaceous units.
  • excessive growth of Propionibacterium acnes is through to exacerbate acne
96
Q

Stepwise management of acne vulgaris (6 things - 3 topical, 3 oral), which antibiotics)

A
  • opical benzoyl peroxidereduces inflammation, helps unblock the skin and is toxic to theP. acnesbacteria
  • Topical retinoids(chemicals related tovitamin A) slow the production ofsebum(women of childbearing age need effective contraception)
  • Topicalclindamycin(prescribed withbenzoyl peroxideto reduce bacterial resistance)
  • Oral antibiotics**-lymecycline**
  • Oral contraceptive pill can help female patients stabilise their hormones and slow the production ofsebum - the combined contraceptive pill Dianette is most effective but not for longterm use (VTE risk)
  • SEVERE ACNE → ISOTRETINOIN - oral retinoid
97
Q

Define Shingles

A

Shingles (herpes zoster) is a viral infection (Varicella zoster) of an individual nerve and the skin surface that is served by the nerve (dermatome)

98
Q

presentation of shingles

A
  • prodromal phase of neuropathic pain in the affected dermatome. Headache, photophobia, malaise, and fever (less common) may also occur as part of the prodromal phase.
  • maculopapular rash forms that then develops into vesicles - very painful, itchy
  • Basically i think it fucking hurts!
99
Q

Bloods for someone with obesity (5)

A
  • HBA1c: Diabetes
  • Lipid profile: hyperlipidaemia
  • Liver function tests (LFTs): non-alcoholic fatty liver disease
  • Thyroid-stimulating hormone (TSH): hypothyroidism
  • Urea and electrolytes (U&Es):chronic kidney disease
  • Specific tests such as dexamethasone suppression test forcushing syndrome, TSH for hypothyroidism, and ultrasound forPCOS can be requested if an underlying disease process is suspected.
100
Q

complications of chickenpox (6)

A

Bacterial superinfection
Dehydration
Conjunctival lesions
Pneumonia
Encephalitis (presenting as ataxia)
After the infection the virus can lie dormant in the sensory dorsal root ganglion cells and cranial nerves reactivate later in life as shingles or Ramsay Hunt syndrome.

101
Q

Simplified pathophysiology of type 2 diabetes (5/6 key sentences)

A

Repeated exposure to glucose and insulin makes the cells in the body resistant to the effects of insulin. More and more insulin is required to stimulate the cells to take up and use glucose. Over time, the pancreas becomes fatigued and damaged by producing so much insulin, and the insulin output is reduced.

A high carbohydrate diet combined with insulin resistance and reduced pancreatic function leads to **chronic high blood glucose levels **(hyperglycaemia). Chronic hyperglycaemia leads to microvascular, macrovascular and infectious complications, as described in the type 1 diabetes section.

102
Q

What are the HbA1c treatment targets for type 2 diabetes?

A

48 mmol/mol for new type 2 diabetics

53 mmol/mol for patients requiring more than one antidiabetic medication

103
Q

Medical management of T2D- first, second, and third line?

A

First-line
- metformin.
- Once settled on metformin, add an SGLT-2 inhibitor (e.g., dapagliflozin) if the patient has existing cardiovascular disease or heart failure. NICE suggest considering an SGLT-2 inhibitor in patients with a QRISK score above 10%.

Second-line
- add a sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor.

Third-line options are:

  • Triple therapy with metformin and two of the second-line drugs
  • Insulin therapy (initiated by the specialist diabetic nurses)

Where triple therapy fails, and the patient’s BMI is above 35 kg/m2, there is the option of switching one of the drugs to a** GLP-1 mimetic (e.g., liraglutide)**.

TOM TIP: SGLT-2 inhibitors are increasingly being recommended. Older patients often have a QRISK score above 10%, making them fall into the “high risk” category for cardiovascular disease. NICE suggests considering SGLT-2 inhibitors alongside metformin as part of the first-line treatment in type 2 diabetics at high risk of cardiovascular disease. SGLT-2 inhibitors are recommended second-line as part of dual therapy in these patients. The significant potential side effect to remember is diabetic ketoacidosis.

104
Q

Hyperosmolar hyperglycemic state (HHS) - what are the key features? how can it be distinguished from diabetic ketoacidosis? what are the symptoms? how is it managed?

A

Hyperosmolar hyperglycemic state (HHS) is a rare but potentially fatal complication of type 2 diabetes. It is characterised byhyperosmolality(water loss leads to very concentrated blood), high sugar levels (hyperglycaemia) and theabsence of ketones, distinguishing it from ketoacidosis.

It presents with polyuria, polydipsia, weight loss, dehydration, tachycardia, hypotension and confusion.

It is a medical emergency with high mortality. Involve experienced seniors early. Treatment is withIV fluidsandcareful monitoring. YOU GOT THIS WRONG - INSULIN IS USED FOR HYPERKALEMIA NOT HHS - The fluids are the issue like with DKA

105
Q

key complications of type 2 diabetes - 8

A

Key complications of type 2 diabetes are:

Infections (e.g., periodontitis, thrush and infected ulcers)
Diabetic retinopathy
Peripheral neuropathy
Autonomic neuropathy
Chronic kidney disease - (i think this is nephropathy)
Diabetic foot
Gastroparesis (slow emptying of the stomach)
Hyperosmolar hyperglycemic state

106
Q

What are the 3 key features of DKA? Explain why they each occour

A
  • Ketoacidosis
    • Dehydration
    • Potassium imbalance

Ketoacidosis

Without insulin, the body’s cells cannot recognise glucose, even when there is plenty in the blood, so the liver starts producing ketones to use as fuel. Over time, there are higher and higher glucose and ketones levels. Initially, the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH. Over time, the ketone acids use up the bicarbonate, and the blood becomes acidic. This is called ketoacidosis.

Dehydration

High blood glucose levels (hyperglycaemia) overwhelm the kidneys, and glucose leaks into the urine. The glucose in the urine draws water out by osmotic diuresis. This causes increased urine production (polyuria) and results in severe dehydration. Dehydration results in excessive thirst (polydipsia).

Potassium Imbalance

Insulin normally drives potassium into cells. Without insulin, potassium is not added to and stored in cells. The serum potassium can be high or normal as the kidneys balance blood potassium with the potassium excreted in the urine. However, total body potassium is low because no potassium is stored in the cells. When treatment with insulin starts, patients can develop severe hypokalaemia (low serum potassium) very quickly, leading to fatal arrhythmias.

107
Q

How is DKA diagnosed?

A

A diagnosis requires all three of:

Hyperglycaemia (e.g., blood glucose above 11 mmol/L)
Ketosis (e.g., blood ketones above 3 mmol/L)
Acidosis (e.g., pH below 7.3)

108
Q

management of DKA

A

The most dangerous aspects of DKA are dehydration, potassium imbalance and acidosis. These are what will kill the patient. Therefore, the priority is fluid resuscitation to correct dehydration, electrolyte disturbance and acidosis. This is followed by an insulin infusion to get the cells to start taking up and using glucose and stop producing ketones.

The principles of management can be remembered with the “FIG-PICK” mnemonic:

F – Fluids – IV fluid resuscitation with normal saline (e.g., 1 litre in the first hour, followed by 1 litre every 2 hours)
I – Insulin – fixed rate insulin infusion (e.g., Actrapid at 0.1 units/kg/hour)
G – Glucose – closely monitor blood glucose and add a glucose infusion when it is less than 14 mmol/L
P – Potassium – add potassium to IV fluids and monitor closely (e.g., every hour initially)
**I – Infection – treat underlying triggers such as infection
**C – Chart fluid balance
K – Ketones – monitor blood ketones, pH and bicarbonate

109
Q

Causes of Haematuria (4)

A
  • infection
  • malignancy - bladder cancer
  • glomerulanephritis
  • kidney stones
110
Q

How is chronic kidney disease diagnosed?

A

A diagnosis can be made when there are consistent results over three months of either:

Estimated glomerular filtration rate (eGFR) is sustained below 60 mL/min/1.73 m2
Urine albumin:creatinine ratio (ACR) is sustained above 3 mg/mmol

111
Q

When is someone with CKD referred to a renal specialist

A

The NICE clinical knowledge summaries (May 2023) suggest referral to a renal specialist when:

eGFR less than 30 mL/min/1.73 m2
Urine ACR more than 70 mg/mmol
Accelerated progression (a decrease in eGFR of 25% or 15 mL/min/1.73 m2 within 12 months)
5-year risk of requiring dialysis over 5% (kidney failure risk equation)
Uncontrolled hypertension despite four or more antihypertensives

112
Q

Complications of CKD - What are the features of renal bone disease? What does this lead to? Key X-ray sign? Management?

A
    • High serum phosphate - reduced excretion
    • Low vitamin D activity - reduced Vitamin D metabolism
    • Low serum calcium - (low vitamin D)
    Theparathyroid glandsreact to thelow serum calciumandhigh serum phosphateby excretingmore parathyroid hormone, causingsecondary hyperparathyroidism. Parathyroid hormone stimulatesosteoclastactivity, increasing calcium absorption from bone.Osteomalaciaoccurs due to increased turnover of bones without adequate calcium supply.Osteosclerosisoccurs when the osteoblasts respond by increasing their activity to match the osteoclasts, creating new tissue in the bone. Due to the low calcium level, this new bone is not properly mineralised.Rugger jersey spineis a characteristic finding on aspinal x-ray. This involvessclerosisof both ends of each vertebral body (denser white) andosteomalaciain the centre of the vertebral body (less white). The name refers to the stripes found on a rugby shirt.Management of renal bone disease involves a combination of:
    • Low phosphate diet
    • Phosphate binders
    • Active forms of vitamin D (alfacalcidol and calcitriol)
    • Ensuring adequate calcium intake
113
Q

Management of CKD (5 things)

A

1 - Treat the underlying cause of CKD- diabetes, hypertension, glomurolonephritis

Medications that help slow the disease progression are:

2 - ACE inhibitors(orangiotensin II receptor blockers) - diabetes, hypertension or significant proteinuria
3 - SGLT-2 inhibitors(specificallydapagliflozin) - diabetes and proteinuria

Reducing the risk of cardiovascular complications:

4 - Exercise, maintain a healthy weight and avoid smoking
5 - Atorvastatin 20mgfor primary prevention of cardiovascular disease (in all patients with CKD)

Other stuff
Management of complications involves:

Oral sodium bicarbonate to treat metabolic acidosis
Iron and erythropoietin to treat anaemia
Vitamin D, low phosphate diet and phosphate binders to treat renal bone disease

Management of end-stage renal disease involves:

Special dietary advice
Dialysis
Renal transplant

114
Q

complications of CKD - 3 key ones

A
  • Anaemia
    • Renal bone disease
    • Cardiovascular disease
    • Peripheral neuropathy
    • End-stage kidney disease
    • Dialysis-related complications
115
Q

How do you determine if someone is obese

A
  • BMI calculation - 25+ overweight, 30+ obese
    • lower BMI thresholds for people who are not white - more prone to central adiposity and cardiometabolic risk occours at a lower BMI
    • also a waist-to height circumference should be measured to calculate the degree of central adipoisty (0.5 is point at which risk increases)
116
Q

Management of obesity: 3 steps, indications for each?

A
  • Objective of treatment is 5-10% reduction in body weight
  • I think the indications are key actually
  • First line- lifestyle modification - regular exercise, healthy eating, alcohol reduction
  • Drug treatment - drug treatment can be offered to individuals who cannotlose weight through dietary changes and have a BMI of 30kg/m2 or27kg/m2with co-morbidities.8.9
    • Orlistat - preventing absorbtion of diatery fats (inhibits gastric lipase release)
    • Liraglutide (GLP-1 mimetic) - delayed gastric emptying and induced early satiety
  • Bariatric Surgery - BMI of≥40 kg/m2or a BMI between35-40 kg/m2withco-morbiditiessuch as type 2 diabetes orhypertenion
    • Roux-en-Y bypass
    • sleeve gastrectomy
    • gastric bypass
117
Q

Management of BPH

A

you know this, mainly forgot that finnisteride takes up to 6 months

The medical options are:

Alpha-blockers (e.g., tamsulosin) relax smooth muscle, with rapid improvement in symptoms
5-alpha reductase inhibitors (e.g., finasteride) gradually reduce the size of the prostate

The general idea is that alpha-blockers are used to treat immediate symptoms, and 5-alpha reductase inhibitors are used to treat enlargement of the prostate. They may be used together where patients have significant symptoms and enlargement of the prostate.

5-alpha reductase converts testosterone to dihydrotestosterone (DHT), which is a more potent androgen hormone. Inhibitors of 5-alpha reductase (i.e. finasteride) reduce DHT in the tissues, including the prostate, leading to a reduction in prostate size. It takes up to 6 months of treatment for the effects to result in an improvement in symptoms.

The surgical options are:

Transurethral resection of the prostate (TURP)
Transurethral electrovaporisation of the prostate (TEVAP/TUVP)
Holmium laser enucleation of the prostate (HoLEP)
Open prostatectomy via an abdominal or perineal incision

118
Q

Pathophysiology - which zones of the prostate are affected by prostate cancer vs BPH

A

BPH originates in the transition zone, which surrounds the urethra

Prostate cancer can originate in any of the zones, but 80% originate in the peripheral zone (the part that can be directly felt on DRE)

119
Q

BPH - Ix for a man presenting with LUTs symptoms

A
    • Digital rectal examination(prostate exam) to assess the size, shape and characteristics of the prostate
    • Abdominal examinationto assess for a palpable bladder and other abnormalities
    • Urinary frequency volume chart, recording 3 days of fluid intake and output
    • Urine dipstickto assess for infection, haematuria (e.g., due to bladder cancer) and other pathology
    • Prostate-specific antigen(PSA) - to check for prostate cancer, although BPH also raises PSA, depending on patient preference, 75% false positive, 15% false negative
    YOU MISSED THE URINE DIPSTICK AND FREQUENCY CHART
120
Q

Management of Prostate cancer? (5) Key complications of each? A big boy

A
  • Management of Prostate cancer? (5) Key complications of each
    • Surveillanceorwatchful waitingin early prostate cancer
    • External beam radiotherapydirected at the prostate - key complication?
    • Brachytherapy
    • Hormone therapy
    • Surgery
    A key complication ofexternal beam radiotherapyisproctitis(inflammation in the rectum) caused by radiation affecting the rectum. Proctitis can cause pain, altered bowel habit, rectal bleeding and discharge. Prednisolone suppositories can help reduce inflammation.Brachytherapyinvolves implanting radioactive metal “seeds” into the prostate. This delivers continuous, targeted radiotherapy to the prostate. The radiation can cause inflammation in nearby organs, such as the bladder (cystitis) or rectum (proctitis). Other side effects include erectile dysfunction, incontinence and increased risk of bladder or rectal cancer.Hormone therapyaims to reduce the level of androgens (e.g., testosterone) that stimulate the cancer to grow. They are usually either used in combination with radiotherapy, or alone in advanced disease where cure is not possible. The options are:
    • Androgen-receptor blockerssuch as bicalutamide
    • GnRH agonistssuch as goserelin(Zoladex) orleuprorelin(Prostap)
    • Bilateral orchidectomyto remove the testicles (rarely used)
    Side effects of hormone therapy include:
    • Hot flushes
    • Sexual dysfunction
    • Gynaecomastia
    • Fatigue
    • Osteoporosis
    Radical prostatectomyinvolves a surgical operation to remove the entire prostate. The aim is to cure prostate cancer confined to the prostate. Key complications areerectile dysfunctionandurinary incontinence.
121
Q

Discuss prostate cancer prognosis in general. Where do advanced prostate cancer metastasis to? What promotes prostate cancer growth?

A

It varies in how aggressive it is, and many prostate cancers are very slow-growing and do not cause death. Advanced prostate cancer most commonly spreads to thelymph nodes and bones. Prostate cancer is almost always androgen-dependent, meaning they rely on androgen hormones (e.g.,testosterone) to grow.

There is a challenge with prostate cancer, as the ideal situation is to:

  • Find and treat clinically significant prostate cancers early
  • Avoid picking up cancers that would not turn out to be clinically significant (avoiding unnecessary stress, investigations and treatment)
122
Q

How do prostate cancers present?

A
  • Prostate cancer may beasymptomatic. THIS IS IMPORTANT AARON
  • It may also present withlower urinary tract symptoms(LUTS), similar to benign prostate hyperplasia. These symptoms include hesitancy, frequency, weak flow, terminal dribbling and nocturia.

Other symptoms include:

  • Haematuria
  • Erectile dysfunction
  • Symptoms of advanced disease or metastasis (e.g., weight loss, bone pain or cauda equina syndrome)
123
Q
  • What is the first and Second line investigation for suspected prostate cancer?
A

1st - Multiparametric MRI - results are reported on a Likert scale

2nd - Prostate biopsy, Likert Scale 3 and above (equivocal)
	
	Suspected being the key word- GP does a PSA and DRE and then refers for these tests based if they feel prostate cancer is likely
124
Q

Triad of presenting features in pyelonephritis that distinguish it from a lower UTI

A
  • fever
  • loin pain
  • nausea or vomitting

It is essential to distinguish between lower urinary tract infections and pyelonephritis. Pyelonephritis is a more severe condition with significant complications, including sepsis and kidney scarring

125
Q

Causative organisms of a lower UTI

A

KEEPS mnemonic

  • Klebsiella pneumoniae(gram-negative, anaerobic, rod-shaped bacteria)
  • Escherichia coli - the most common cause
  • Enterococcus
  • Pseudomonas aeruginosa
  • Staphylococcus saprophyticus
  • Candida albicans(fungal)
126
Q

Ix for lower UTI - what indicates a likely UTI on Urine dipstick

A
  • nitrites- best indication of infection, treat as a UTI
  • Leukocytes + red cells - likely a UTI
  • only leukocytes- send an MSU
127
Q

2 Rx for lower UTI in the community? duration?

A

Follow local guidelines. An appropriate initial antibiotic in the community would be:

  • Nitrofurantoin(avoided in patients with an eGFR <45)
  • Trimethoprim(often associated with high rates of bacterial resistance)

Alternatives:

  • Pivmecillinam
  • Amoxicillin
  • Cefalexin

The typical duration of antibiotics is:

  • 3 daysof antibiotics for simple lower urinary tract infections in women
  • 5-10 daysof antibiotics for immunosuppressed women, abnormal anatomy or impaired kidney function
  • 7 daysof antibiotics for men, pregnant women or catheter-related UTIs

It is worth noting that NICE recommend changing the catheter when someone is diagnosed with a catheter-related urinary tract infection.

128
Q

Management of Pyelonephritis

A
  • Management of PyelonephritisReferral to hospital is required if there are features of sepsis or if it is unsafe to manage them in the community.NICE guidelines (2018) recommend the following first-line antibiotics for 7-10 days when treating pyelonephritis in the community:
    • Cefalexin
    • Co-amoxiclav (if culture results are available)
    • Trimethoprim (if culture results are available)
    • Ciprofloxacin (keep tendon damage and lower seizure threshold in mind)
    Patients admitted to hospital with sepsis require thesepsis six, which includes a serum lactate, blood cultures, urine output monitoring, oxygen, empirical broad-spectrum antibiotics and IV fluids.Two things to keep in mind with patients that have significant symptoms or do not respond well to treatment are:
    • Renal abscess
    • Kidney stoneobstructing the ureter, causing pyelonephritis
129
Q
  • Management of UTI in pregnancy
A

Urinary tract infections in pregnancy increase the risk of pyelonephritis, premature rupture of membranes and pre-term labour.

    • Management of UTI in pregnancyUrinary tract infection in pregnancy requires7 daysof antibiotics. All women should have an MSU for microscopy, culture and sensitivity testing.The antibiotic options are:
      • Cefalexin(the typical choice)
      • Nitrofurantoin(avoided in the third trimester)
      • Amoxicillin(only after sensitivities are known)
      Nitrofurantoinshould be avoided in thethird trimesteras there is a risk ofneonatal haemolysis(destruction of the neonatal red blood cells).Trimethoprimshould be avoided in thefirst trimesteras it works as afolate antagonist. Folate is essential in early pregnancy for the normal development of the fetus. Trimethoprim in early pregnancy can causecongenital malformations, particularlyneural tube defects(e.g.,spina bifida). It is not known to be harmful later in pregnancy but is generally avoided unless necessary.
130
Q

What is overflow incontinence and what causes it?

A

Much rarer form of incontinence

Overflow incontinence can occur when there ischronic urinary retention due to anobstructionto theoutflowof urine. Chronic urinary retention results in an overflow of urine, and the incontinence occurs without the urge to pass urine. It can occur withanticholinergic medications,fibroids,pelvic tumoursandneurological conditionssuch asmultiple sclerosis,diabetic neuropathyandspinal cord injuries. Overflow incontinence is more common in men, and rare in women. Women with suspected overflow incontinence should be referred forurodynamic testingand specialist management.

131
Q
  • Ix for Urinary incontinence
A
  • Ix for Urinary incontinence
    • a bladder diary - 3+ days
    • Urine dipstick - infection, microscopic haematuria
    • post-void residual bladder volume - assess for incomplete emptying
    • Urodynamic testingcan be used to investigate patients with urge incontinence not responding to first-line medical treatments, difficulties urinating, urinary retention, previous surgery or an unclear diagnosis. It is not always required where the diagnosis is possible based on the history and examination.
132
Q

Management of Stress incontinence (3) vs Urge incontinence (4)

A

The first step is to distinguish between urge and stress incontinence, as this dictates the management. Patients are usually managed in primary care initially and referred to a specialist MDT for further management where there are concerning features or an inadequate response to first-line treatment.

Management of stress incontinence involves:

- Avoiding caffeine, diuretics and overfilling of the bladder
- Avoid excessive or restricted fluid intake
- Weight loss (if appropriate)
- ***Supervised pelvic floor exercises***for at least three months before considering surgery
- ***Surgery***- Tension-free vaginal tape, autologous sling
- ***Duloxetine***is an SNRI antidepressant used second line where surgery is less preferred

BASICALLY - PELVIC FLOOR EXERCISES → SURGERY

Management of urge incontinence and overactive bladder involves:

- ***1st line- Bladder retraining***(gradually increasing the time between voiding) for at least six weeks
- ***Anticholinergic medication***, for example, oxybutynin, tolterodine and solifenacin - side effects
- ***Mirabegron***is an alternative to anticholinergic medications - contraindicated in uncontrolled hypertension
- ***Invasive procedures***where medical treatment fails - botulinum injection….

BASICALLY BLADDER EXERCISES → MEDICATION → SURGERY
133
Q

Management of urge incontinence - side effects of anticholinergic medications

A

oxybutynin, tolterodine and solifenacin

Anticholinergic medicationsneed to be used carefully, as they haveanticholinergic side effects. These include dry mouth, dry eyes, urinary retention, constipation and postural hypotension. Importantly they can also lead to acognitive decline,memory problemsand worsening ofdementia, which can be very problematic in older, more frail patients.

134
Q
  • What Ix can be used to confirm anaphylaxis
A

Anaphylaxis can be confirmed by measuring theserummast cell tryptasewithin 6 hours of the event.Tryptaseis released during mast cell degranulation and stays in the blood for 6 hours before gradually disappearing.

135
Q

Presentation of anaphalaxis

A

Patients present with a history of exposure to an allergen (although it can be idiopathic).

There will be rapid onset of allergic symptoms:
Urticaria
Itching
Angio-oedema, with swelling around lips and eyes
Abdominal pain

Additional symptoms that indicate anaphylaxis are:
Shortness of breath
Wheeze
Swelling of the larynx, causing stridor
Tachycardia
Lightheadedness
Collapse

136
Q

Management of anaphylaxis (Immediate)

A

Initial assessment of acutely unwell child is with an ABCDE approach, assessing and treating:

  • look for sudden airway, breathing or circulation problems, and usually a skin change (itchy rash)

Once a diagnosis of anaphylaxis is established:

  • remove the trigger and lie the patient flat, elevating the legs
  • Intramuscular adrenalin, repeated after 5 minutes if required
  • give high flow oxygen
  • give IV fluids - crystalloid
  • if not responding after 5 minutes, repeat IM adrenaline, if still not responding → refractory anaphylaxis
  • steroids and antihistamines are not routinely used, can consider using an inhaler but above is the key stuff
137
Q

Management of Allergic Disorder

A
  • longterm is just lifestyle stuff- avoidance of food, cleaning and hoovering for dustmites, epipen for those at risk of anaphalaxis

FOLLOWING EXPOSURE - Treatment of allergic reactions are with:

  • Antihistamines(e.g.cetirizine)
  • Steroids(e.g. oralprednisolone, topicalhydrocortisoneor IVhydrocortisone)
  • Intramuscular adrenalinin anaphylaxis

Antihistaminesandsteroidswork by dampening the immune response to allergens. Close monitoring is essential after an allergic reaction to ensure it does not progress to anaphylaxis.

138
Q

What are the 3 Ix options for allergy

A
  • Skin prick testing
    • RAST testing, which involves blood tests for total and specificimmunoglobulin E(IgE)
    • Food challenge testing - the GOLD STANDARD but requries alot of time and resources in specialist centres
    Think carefully before performing an allergy test, particularly a RAST test. They often come back showing that the patient issensitisedto many of the things you have tested for, and it becomes very challenging to explain to the child or their parents that the positive test results do not mean it is unsafe for the child to eat those foods.
139
Q

Grab some paper- big boy. The different exanthema all present very similarly with fever, coryzal symptoms followed by a rash.
What features help distinguish between the following?
Key complication?
Cause of each?

  • Measles
  • Scarlet fever
  • Rubella
  • Parvovirus B19
  • Roseola
  • Kawasaki disease
A

Answer is in notion in a nice table

Measles
Koplik spots (pathognomonic). Others: conjunctivitis
Severe symptoms and compilations - pneumonia and encephalitis are the key complications
Measles virus

Scarlet fever
Strawberry tongue. Others: sandpaper rash, tonsilitis
Post-streptococcal glomerulonephritis,
Acute rheumatic fever
Group A step. - (strep pyogenes) - Rx w/ Penicillin V

Kawasaki disease
Strawberry tongue; Fever lasting more than 5 days! Others: conjunctivitis, rash
comp - elsewhere
VASCULITIS

Rubella
NOTHING UNIQUE - Milder rash and symptoms vs measles, lacks Koplik spots, fever.
Congenital Rubella Syndrome (triad of blindness, deafness, congenital heart disease)
rubella virus

Parvovirus B19
NOTHING UNIQUE- Slapped cheeks - differs from scarletfever - milder and lacks strawberry tongue
Aplastic anaemia
parvovirus B19

Roseola
Only affects Infants (<2), High fever that comes on and suddenly lasts 3-5 days, then suddenly resolves
febrile convulsion
Human Herpes 6 & 7

140
Q

Define an exanthem?

A

an eruptive widespread rash

Sidenote: It is usually caused by a virus (toxin or immune response) and accompanied by systemic symptoms including, fever, malaise and headache
141
Q

How does measles present? Name the pathognomonic sign for measles?

A

Pathognomonic sign - Kolpik spots - greyish spots on the buccal mucosa

Other Symptoms:

- fever
- coryzal symptoms (inflammation of nasal mucous membranes
- conjunctivitis
- exanthem (widespread eruptive rash) - appears a few days after the other symptoms
142
Q

Two causes of a strawberry tongue? how can you differentiate between the two causes?

A
  • scarlet fever
    • Kawasaki disease
    • Me: Both present in very similar ways (fever, rash, lymphadenopathy), the key feature of kawasaki disease is fever lasting more than five days. If you come across a child with a fever persisting for more than 5 days, think of Kawasaki disease! A rash, strawberry tongue, lymphadenopathy and conjunctivitis will seal the diagnosis in your exams.
143
Q

Name the 5 traditional causes of viral exanthemas

A
  • measels
    • scarlet fever
    • rubella (german measels)
    • parovirus b19
    • roseola infantum
    Ignore dukes disease- not a distinct disease, just non-specific viral exanthemaGP tip - differentiate them based on the other presenting features and not the rash.
144
Q

What are the two most common types of psoriasis, how do they present? Paediatric type - what triggers it? Prognosis?

A

Plaque psoriasis features the thickened erythematous plaques with silver scales, commonly seen on the extensor surfaces and scalp. The plaques are 1cm – 10cm in diameter. This is the most common form of psoriasis in adults.

Guttate psoriasis is the second most common form of psoriasis and commonly occurs in children. It presents with many small raised papules across the trunk and limbs. The papules are mildly erythematous and can be slightly scaly. Over time the papules in guttate psoriasis can turn into plaques. Guttate psoriasis is often triggered by a streptococcal throat infection, stress or medications. It often resolves spontaneously within 3 – 4 months, 25% go on to develop chronic psoriasis

145
Q

Management of Psoriasis (adults)

A

TOPICAL THERAPY

  • moisturising emollients as regular therapy
  • Topical steroids - most common
  • Calcipotriol - Topical vitamin D analogues(anti-proliferative effect on keratinocytes)
  • tar preparations - inflammatory and anti-pruritic

SYSTEMIC THERAPY - unresponsive psoriasis

  • methotrexate (DMARD)
  • acitretin (oral retinoid - antiinflammatory),
  • cyclosporin - (immunosupressant) lots of adverse effects
  • biologics infliximab (TNF-alpha)
146
Q

Upper vs Lower RTI? Which is flu?

A

The upper respiratory tract includes your nose, mouth, sinuses, pharynx, and larynx. Its primary role is to filter and transport oxygen-rich air into the lungs.

The lower respiratory tract includes everything below the larynx: the trachea, bronchial tubes, and lungs.

Acute bronchitis refers to infection and inflammation in the bronchi and bronchioles. Both pneumonia and acute bronchitis are classed as lower respiratory tract infections. Upper respiratory tract infections (e.g., a common cold) are usually viral. As a general rule, the lower down the respiratory tract, the higher the probability of bacterial infection, as opposed to viral. The upper respiratory tract includes your nose, mouth, sinuses, pharynx, and larynx. Its primary role is to filter and transport oxygen-rich air into the lungs. The lower respiratory tract includes everything below the larynx: the trachea, bronchial tubes, and lungs.

Flu can be both i think - uncomplicated is just cough, coryzal, fever, GI, complicated is dyspnoea, hypoxaemia, lung infiltrate

147
Q

How do you differentiate between the flu and a common cold (3 things)

A

TOM TIP: There is a lot of overlap between the common cold and flu, but some key features can help you differentiate them clinically.

- ***Onset - Flu tends to have an abrupt onset, whereas a common cold has a more gradual onset.***
- ***Fever - Fever is a typical feature of the flu but is rare with a common cold.***
- ***Fatigue/Wipe out -  people with the flu are “wiped out” with muscle aches and lethargy, whereas people with a cold can usually continue many activities.***
148
Q

Manangement of CA pneumonia

A

The NICE guidelines on pneumonia (updated 2022) recommend using the CRB-65 scoring system out of hospital and CURB-65 in hospital. They suggest considering hospital assessment when the CRB-65 score is more than 0.

C – Confusion (new disorientation in person, place or time)
U – Urea > 7 mmol/L
R – Respiratory rate ≥ 30
B – Blood pressure < 90 systolic or ≤ 60 diastolic.]
65 – Age ≥ 65

Mild community-acquired pneumonia is typically treated with 5 days of oral antibiotics, for example:

1ST LINE - Amoxicillin
Doxycycline
Clarithromycin

149
Q

Big Boy - What are the two types of chest infection in adults. For each of them, give their:

  • definition
  • cause
  • presentation
  • Ix
  • Management
A

Table is in GP list, acute bronchitits

Acute Bronchitis vs Pneumonia

Definition
LRTI which causes acute inflammation in the bronchial airways. It is a clinical diagnosis characterised by cough resulting from acute inflammation of the trachea and large airways with no evidence of pneumonia.

Pneumoniais aninfection of the lung tissue in whichthe air sacs in the lungs become filled with microorganisms, fluid and inflammatory cells, affecting the function of the lungs

Cause
Usually caused by a virus. The most common viruses associated with acute bronchitis include rhinovirus, enterovirus, influenza A and B, parainfluenza, coronavirus, human metapneumovirus, respiratory syncytial virus, and adenovirus

Community-acquired pneumoniais usually caused by bacterial infection. Streptococcus pneumoniae and Haemophillus influenza are the main causative pathogens of CAP, other include Staph Aureus, Group A streot, Moraxella catarhhalis and atypical bacteria (mycoplasma pneumoniae, Clamydia, Legionella Species. Rarely, viral pathogens can cause pneumonia - influenza, RSV, adenovirus and some corona viruses |

| Ix
|Pulse oximetry
| Pulse Oximetry, A point-of-care test for the CRP level can be used in primary care to help guide diagnosis and the use of antibiotics. On admission - CXR, FBC, Renal profile, CRP. Severe - sp[utum and blood cultures, pneumococcal and legionella urinary antigen tests |

| CXR
| normal
| Abnormal - infiltrate is definitive diagnosis |

| Management
| Self-limiting, cough usually lasts about 3-4 weeks. Reassurance. Antibiotics will not help.
| Use CRB-65 score to decide if the person required admission (more than 0!) TEST YOURSELF. Mild community-acquired pneumonia is typically treated with 5 days of oral antibiotics, for example:

1ST LINE - Amoxicillin
Doxycycline
Clarithromycin

Presentation | Hx - Cough is the predominant symptom in both acute bronchitis andcommunity-acquired pneumonia. May or may not have sputum, wheeze, or breathlessness. Sometimes mild constitutional symptoms. O/E - Mildly ill, Wheeze often presen
| Cough is the predominant symptom in both acute bronchitis andcommunity-acquired pneumonia. Dyspnoea, sputum production, pleural pain, sweating, fever, shivers, aches and pains. O/E- Moderately to severely ill - focal chest signs - crepitations, reduced air entry…. |

150
Q

Define Asthma

A

Asthma is a chronic inflammatory airway disease leading to variable airway obstruction. The smooth muscle in the airways is hypersensitive and responds to stimuli by constricting and causing airflow obstruction.

151
Q

define occupational asthma

A

Occupational asthma refers to asthma caused by environmental triggers in the workplace.

152
Q

Ix - asthma (4) adults vs chidlren? Results for each test?

A

Children:
A diagnosis is made clinically based on a typical history and examination. When there is an intermediate or high probability of asthma, a trial of treatment can be implemented and if the treatment improves symptoms a diagnosis can be made.

There are investigations that can be used where there is an intermediate probability of asthma or diagnostic doubt - same as adults.

Adults:
The NICE guidelines (2020) recommend initial investigations in patients with suspected asthma:

- Fractional exhaled nitric oxide (FeNO)
- Spirometry with bronchodilator reversibility

Where there is diagnostic uncertainty after initial investigations, the next step is testing the peak flow variability.

Where there is still uncertainty, the next step is a direct bronchial challenge test with histamine or methacholine.

Spirometry is the test used to establish objective measures of lung function. It involves different breathing exercises into a machine that measures volumes of air and flow rates and produces a report. A FEV1:FVC ratio of less than 70% suggests obstructive pathology (e.g., asthma or COPD).

Reversibility testing involves giving a bronchodilator (e.g., salbutamol) before repeating the spirometry to see if this impacts the results. NICE says a greater than 12% increase in FEV1 on reversibility testing supports a diagnosis of asthma.

Fractional exhaled nitric oxide (FeNO) measures the concentration of nitric oxide exhaled by the patient. Nitric oxide is a marker of airway inflammation. The test involves a steady exhale for around 10 seconds into a device that measures FeNO. NICE say a level above 40 ppb is a positive test result, supporting a diagnosis. Smoking can lower the FeNO, making the results unreliable.

Peak flow variability is measured by keeping a peak flow diary with readings at least twice daily over 2 to 4 weeks. NICE says a peak flow variability of more than 20% is a positive test result, supporting a diagnosis.

Direct bronchial challenge testing is the opposite of reversibility testing. Inhaled histamine or methacholine is used to stimulate bronchoconstriction, reducing the FEV1 in patients with asthma. NICE say a PC20 (provocation concentration of methacholine causing a 20% reduction in FEV1) of 8 mg/ml or less is a positive test result.

153
Q

What is an acute asthma exacerbation, what are the key symptoms?

A

An acute exacerbation of asthma involves a rapid deterioration in symptoms. Any typical asthma triggers, such as infection, exercise or cold weather, could set off an acute exacerbation.

Presenting features of an acute exacerbation are:

Progressively shortness of breath
Use of accessory muscles
Raised respiratory rate (tachypnoea)
Symmetrical expiratory wheeze on auscultation
The chest can sound “tight” on auscultation, with reduced air entry throughout

154
Q

How are acute asthma exacerbations graded?

A

these are just a few key features

Moderateexacerbationfeatures:

  • Peak flow 50 – 75% best or predicted

Severeexacerbationfeatures:

  • Peak flow 33-50% best or predicted
  • Respiratory rate above 25
  • unable to complete sentences

Life-threatening**exacerbationfeatures:

  • Peak flow less than 33%
  • Oxygen saturations less than 92%
  • PaOless than 8 kPa
155
Q

Sx suggestive of asthma in kids (3 key sx) vs alternative diagnosis

A
  • Asthma presents as a dry cough with wheeze and shortness of breath
  • Sx are episodic and there is often Diurnal variability
  • Other things such as FHx of atopy, bilateral polyphonic wheeze

Sx Suggestive of alternative diangosis
- Wheeze only related to coughs and colds, more suggestive ofviral induced wheeze
- Isolated cough (no SOB or wheeze) or productive cough (sputum)
- no repsonse to treatment
- unilateral wheeze

156
Q

Management of Asthma in kids and adults

A

Under Five: SABA (salbutamol) → + ICS OR leukotriene antagonist

5-12:  SABA (salbutamol) → + ICS → trial LABA (salmeterol) → increase ICS, consider  + leukotriene antagonist / + theophylline (bronchial smooth muscle relaxer)

children 12+/ Adults: SABA → +ICS → +LABA → Increase ICS, consider + leukotriene receptor antagonist / +LAMA (Tiotropium)/ oral theophylline

Basically tolders - dont use salmeterol or tiotropium, kids under 12 - dont use tiotropium
157
Q

Define chronic bronchitis and emphysema

A

Chronic bronchitisrefers to long-term symptoms of a cough and sputum production due to inflammation in the bronchi.

Emphysema involves damage and dilatation of thealveolar sacsandalveoli, decreasing the surface area for gas exchange.

158
Q

Is it typical for a patient with COPD to present with:
- productive cough?
- clubbing?
- haemotysis
- wheeze
- SOB?
- chest pain?

if not, what are these Sx suggestive of?

A

A typical presentation of COPD is a long-term smoker with persistent symptoms of:

Shortness of breath
Cough
Sputum production
Wheeze
Recurrent respiratory infections, particularly in winter

TOM TIP: COPD does NOT cause clubbing, haemoptysis (coughing up blood) or chest pain. These symptoms should be investigated for a different cause, such as lung cancer, pulmonary fibrosis or heart failure.

159
Q

Longterm manamgement of COPD

A

lifestyle - smoking cessation, flu and pneumococcal vaccine, pulmonary rehabilitation

Initial:

SABA + SAMA (Ipratropium bromide)

2nd Step - no asthmatic or steroid repsonsive features (raised eosinophils, FEV1 varaition)

LABA (salmeterol) + LAMA (tiotropium)

2nd Step - asthmatic or steroid repsosive:

LABA + ICS - (Fostair)

3rd step

LABA + LAMA + ICS - trelegy, trimbox, trixeo
160
Q

Acute exacerbation of COPD - first line management (3)

A

First-line medical treatment of an acute exacerbation of COPD involves:

Regular inhalers or nebulisers (e.g., salbutamol and ipratropium)
Steroids (e.g., prednisolone 30 mg once daily for 5 days)
Antibiotics if there is evidence of infection

2nd line:
IV aminophylline
NIV
intubation and ventilitation

161
Q

What is Seborrhoeic dermatitis? What causes it?

A

A form of eczema - Seborrhoeic dermatitis is an inflammatory skin condition that affects the sebaceous glands. The sebaceous glands are the oil producing glands in the skin. It affects areas that have a lot of these glands, such as the scalp, nasolabial folds and eyebrows. It causes erythema, dermatitis and crusted dry skin. In infants it causes a crusted dry flaky scalp, often called cradle cap. It is thought that Malassezia yeast colonisation has a role to play in the development of seborrhoeic dermatitis, and the condition improves with anti-fungal treatment (ketoconazole shampoo).

162
Q

Summary management of constipation - adults and children

A
  • Basically same in adults and kids:
    1. exclude secondary cause
    2. lifestyle advise (3 things)- dietary fibre intake, fluid intake and activity levels
    3. laxatives
      • children - 1st Movicol (osmotic)
      • Adults:Step 1: Start bulk-forming laxative (ispaghula)Step 2: Add or switch to an osmotic laxative (macrogol → lactulose)Step 3: Add stimulant laxative (senna, dulcolax)
      • adults opioid induced → osmotic + stimulant
    4. treat faecal impaction - disimpaction regime of laxatives (osmotic / stimulant) , enemas…
163
Q

Name the 4 types of laxatives and give an example of each

A
  • Bulk-forming laxatives - ispaghula husk (Fybogel), methylcellulose (Celevac)
    - Bulk-forming laxatives ‘bulk out’ the stool with soluble fibre. This increases faecal mass and stimulates peristalsis.
    - Their onset of action is up to 72 hours, and common adverse effects include flatulence, bloating and cramping.
    - Patients should be advised toincrease fluid intakewhen taking bulk-forming laxatives.
    • Osmotic laxatives - lactulose, macrogols (Movicol, Laxido)
      • Osmotic laxatives draw water via osmosis into the stool, making it softer and easier to pass. Adverse effects include abdominal cramps, diarrhoea, nausea and vomiting.
    • Stimulant laxatives- senna (Senokot), bisacodyl (Dulcolax), sodium picosulfate
      • Stimulant laxatives stimulate the nerves of the digestive tract to cause peristalsis.
    • Stool softening laxatives- docusate
      • Stool softening laxatives decrease the surface tension of faecal mass and increase intestinal fluid in the stool.
164
Q

Management of dyspepsia when someone presents for the first time.

A
  1. Exclude red flag symptoms → OGD
  2. address potential triggers (lifestyle advice)
  3. offer a one month trial of PPI
  4. consider H. pylori testing - (urea breath test or stool antigen test)

There are other steps after initial managment:
- H.pylori eradication
- antacids for short term
- H2 receptors antagonists (famotidine)
- surgery - laproscopic fundoplicaiton
- dont know when OGD is done otehr than red flag?

165
Q

GORD - What type of epithelium is found in oesophagus vs stomach, What is Barrets oesphagus and how is it managed?

A
  • GORD - What type of epithelium is found in oesophagus vs stomach, What is Barrets oesphagus and how is it managed?Theoesophagushas asquamous epithelial liningthat makes it more sensitive to the effects of stomach acid. The stomach has acolumnar epithelialliningthat is more protected against stomach acid.Barrett’s oesophagusrefers to when the lower oesophageal epithelium changes fromsquamoustocolumnar epithelium. This process is calledmetaplasia. It is caused by chronic acid reflux into the oesophagus. Patients may notice improved reflux symptoms after they develop Barrett’s oesophagus.Barrett’s oesophagusis apremalignant conditionand a significant risk factor for developingoesophageal adenocarcinoma(cancer of theepithelial cells). There can be a stepwise progression fromno dysplasiatolow-grade dysplasia,high-grade dysphasia, andadenocarcinoma.Treatment ofBarrett’s oesophagusis with:
    • Endoscopic monitoringfor progression to adenocarcinoma
    • Proton pump inhibitors
    • Endoscopic ablation(e.g.,radiofrequency ablation)
166
Q

What is GORD? What causes it?

A

Gastro-oesophageal reflux disease(GORD) is where acid from the stomach flows through thelower oesophageal sphincterand into the oesophagus, where it irritates the lining and causes symptoms.

Causes:
- greasy and spicy food
- caffeine
- alcohol - these top three are not just gastritis!
- stress
- smoking
- obesity
- hiatus hernia
- Not caused by H.pylori but the symptoms of gastritis are similar hence why i think tesitng is done?

167
Q

Management of hiatus hernia

A

Treatment is either:

- ***Conservative***(with medical treatment of gastro-oesophageal reflux)
- ***Surgery (laparoscopic fundoplication)***if there is a high risk of complications or symptoms are resistant to medical treatment
168
Q
  • What is a hiatus hernia?
A

A hiatus hernia refers to the herniation of the stomach up through thediaphragm. The diaphragm opening should be at thelower oesophageal sphincterlevel and fixed in place. A narrow opening helps to maintain the sphincter and stops acid and stomach contents fromrefluxinginto the oesophagus. When the opening of the diaphragm is wider, the stomach can enter through the diaphragm, and the contents of the stomach can reflux into the oesophagus.

Key risk factors are increasing age, obesity and pregnancy.
169
Q
  • what are the 4 types of hiatus hernia
A
  • Type 1: Sliding - where the stomach slides up through the diaphragm, with the gastro-oesophageal junction passing up into the thorax
    • Type 2: Rolling - where a separate portion of the stomach (i.e., the fundus), folds around and enters through the diaphragm opening, alongside the oesophagus.
    • Type 3: Combination of sliding and rolling
    • Type 4: Large opening with additional abdominal organs entering the thorax
170
Q
  • Presentation (3) and management of Diverticulosis
A
  • Presentation (3) and management of DiverticulosisMay be asymptomatic - incidental finding on colonoscopy or CT scan. Treatment is not necessary where the patient is asymptomatic. However, advice regarding a high fibre diet and weight loss is appropriate.Diverticulosis may cause lower left abdominal pain, constipation or rectal bleeding. Management is with increased fibre in the diet andbulk-forming laxatives(e.g., ispaghula husk).Stimulant laxatives(e.g., Senna) should beavoided. Surgery to remove the affected area may be required where there are significant symptoms.
171
Q
  • Presentation of Acute Diverticulitis
A
  • Presentation of Acute DiverticulitisDiverticulitis refers toinflammationin the diverticula.Acute diverticulitispresents with:
    • Pain and tenderness in the left iliac fossa / lower left abdomen
    • Fever
    • Diarrhoea
    • Nausea and vomiting
    • Rectal bleeding
    • Palpable abdominal mass (if an abscess has formed)
    • Raised inflammatory markers (e.g., CRP) and white blood cells
    It is a bit like appendicitis basically + diarhoea and rectal bleeding
172
Q
  • Management of Acute diverticulitis (uncomplicated vs severe pain)
A
  • Management of Acute diverticulitis (uncomplicated vs severe pain)The NICE clinical knowledge summaries (updated January 2021) suggest management of uncomplicated diverticulitis in primary care with:
    • Oral co-amoxiclav (at least 5 days)
    • Analgesia (avoiding NSAIDs and opiates, if possible)
    • Only taking clear liquids (avoiding solid food) until symptoms improve (usually 2-3 days)
    • Follow-up within 2 days to review symptoms
    Patients with severe pain or complications require admission to hospital. Hospital treatment involves management as with any patient with an acute abdomen or sepsis, including:
    • Nil by mouth or clear fluids only
    • IV antibiotics
    • IV fluids
    • Analgesia
    • Urgent investigations (e.g., CT scan)
    • Urgent surgery may be required for complications
173
Q

what are haemorrhoids? what are the two types of haemorrhoids? what are the symptoms of each of them?

A
  • what are haemorrhoids? what are the two types of haemorrhoids? what are the symptoms of each of them?Haemorrhoids are enlargedanal vascular cushions. It is not clear why they become enlarged and swollen, but they are often associated with constipation and straining.Internal Haemorrhoids - occour in the lower rectum (not innervated with pain fibres). In the anus, there are three vascular mucosal cushions which help maintain anal continence - at 3, 7 and 12 o’clock
    • painless, bright red bleeding
    • feeling a lump inside the anus
    • can prolapse - graded by this
    External Haemorrhoids - develop under the skin around the anus. The skin (anoderm) is richly innervated wiht pain fibres - very painful and itch:
    • bright red bleeding
    • painful and itchy
    • severe pain if a blood clot forms within them (thrombosed external haemorrhoids → surgery may be needed)
174
Q
  • management of haemorrhoids (GP - 3), When to refer Secondary Care?
A
  • management of haemorrhoids (GP - 3), When to refer Secondary Care?GP management:
    • Simple analgesia for pain relief
    • Topical treatmentscan be given for symptomatic relief and to help reduce swelling - astringents (shrink (anusol)) + hydrocortisone, lidocaine
    • ensure stools are soft and easy to pass - treat constipation with increased fibre, fluids, laxatives, avoid straining
    • Refer to secondary care when people do not respond to conservative treatment or there are recurrent symptoms.
    Secondary care:
    • Rubber band ligation (fitting a tight rubber band around the base of the haemorrhoid to cut off the blood supply)
    Just learn above the rest is useless…
    • Injection sclerotherapy (injection of phenol oil into the haemorrhoid to cause sclerosis and atrophy)
    • Infra-red coagulation (infra-red light is applied to damage the blood supply)
    • Bipolar diathermy (electrical current applied directly to the haemorrhoid to destroy it)
    • Surgery - haemorrdectomy, stapled haemorrhoidectomy, haemorrhoid artery ligation
175
Q

Management of an anal fissure?

A
  • Management of anal fissure
    • refer if secondary cause suspected- IBD…
    • ensure stool is soft and easy to pass - constipation management (lifestyle + laxatives)
    • hygiene - keep clean and dry to add healing
    • pain management - simple analgesia (paracetamol or ibuprofen), severe pain - short course of lidocaine ointment before passing stools
    • for adults with symptoms for more than 1 week - rectal GTN ointment to aid healing
    • if unhealed after 6-8 weeks of GTN ointment - refer to colorectal surgery
176
Q

4 Steps of the topical corticosteroid ladder

A

HEBD mnemonic
Hydrocortisone -> eumovate -> betnovate ->dermovate

177
Q

Compare what joints tend to be affected in psoriatic vs rheumatoid arthritis? What other signs does psoriatic athritis present with?

A

Psoriatic arthritis tends to affect the distal interphalangeal (DIP) joints and axial skeleton, whereas rheumatoid arthritis tends not to affect these joints.

Other signs
- Plaquesof psoriasis on the skin
- Nail psoriasis - pitting, Onycholysis,
- Dactylitis
- Enthesitis- inflammation of the entheses, which are the points of insertion of tendons into bone
- ME - DIPJ involvement and spondylitis (back stiffness and pain)

178
Q

Management of Psoriatic athritis?

A
  • Non-steroidal anti-inflammatory drugs(NSAIDs) - FOR PAIN
  • Steroids
  • 1ST LINE - DMARDs(e.g., methotrexate, leflunomide or sulfasalazine)
  • Anti-TNF medications (etanercept,infliximaboradalimumab)
  • Ustekinumab(anti-interleukin 12and23)
179
Q

Management of conjunctivitis, including in neonates and allergic?

A

Usually SELF RESOLVES, use hygiene measures to stop the spread and cleaning eye with cooled boiled water for discharge

If necessary for Bacterial → chloramphenicol or fusidic acid eye drops

Allergic → anti-histamines, for chronic seasonal symptoms - topical mast cell stabilisers

neonates → urgent referral for gonococcal infection (risk of permanent vision loss)

180
Q
  • KEY ILA - Identify the cause of vaginal discharge1) No itching of the vagina/vulva, fish-like smell, thin grey discharge2) Itching/burning of the vagina/vulva, fish-like smell, green/yellow discharge3) Offensive discharge, dysuria and painful sex, bleeding between periods and postcoital4) odourless purulent discharge, possibly green or yellow associated with dysuria and pelvic pain5) Thick white discharge associated with itch6) clear/off white discharge with no associate symptoms
A
    1. BV - itching or irritation are not common but are possible
    2. trichomonas - similar to clamydia and gonorhea with the pain but i think the itching is key
    3. chlamydia - only one with abnormal bleeding
    4. Gonorrhoea - pelvic pain, G + C don’t itch!!!
    5. Candidiasis/thrush
    6. Physiological
181
Q

Blepharitis refers toinflammationof theeyelid margins. How does it present and what is associated with? Management?

A

It causes a gritty, itchy, dry sensation in the eyes. It can be associated with dysfunction of theMeibomian glands, which are responsible for secretingmeibum(oil) onto the surface of the eye. It can lead tostyesandchalazions.

Management is with warm compresses and gentle cleaning of the eyelid margins to remove debris (e.g., using a cotton bud and baby shampoo) - basically the same for all begnign eyelid conditions

182
Q

Stye- what are the three types and how are they managed?

A

Hordeolum externumis an infection of theglands of Zeisorglands of Moll. The glands of Moll are sweat glands at the base of the eyelashes. The glands of Zeis are sebaceous glands at the base of the eyelashes. A stye causes a tender red lump along the eyelid that may contain pus.

Hordeolum internumis infection of theMeibomian glands. They are deeper, tend to be more painful and may point inwards towards the eyeball underneath the eyelid.

STYES ARE TENDER AND INFECTIONS

Styes are treated with hot compresses and analgesia. Topical antibiotics (e.g., chloramphenicol) may be considered if it is associated with conjunctivitis or if symptoms are persistent.

183
Q

What is a chalazion?

A

A chalazion occurs when aMeibomian glandbecomes blocked and swells. It is often called aMeibomian cyst. It presents with a swelling in the eyelid that is typically not tender

Sidenote:Hodeolum internum (stye) can be in meibomium gland but it is infected and tender

184
Q

Not Key - how is entropion vs ectropion managed? What is trichiasis

A

Entropion

  • Initial - taping the eyelid down to prevent it turning inwards and causing ulceration and corneal damage, + lubricating eyedrops
  • Definitive management - surgery

Ectropion - bottom lid outwards

  • Mild cases may not require treatment. Regular lubricating eye drops are used to protect the surface of the eye
  • More significant cases (exposure keratopathy risk) may require surgery to correct the defect. A same-day referral to ophthalmology is required if there is a risk to sight.

Trichiasis refers to inward growth of the eyelashes, rather than interterning lids. It results in pain and can causecorneal damageandulceration. Management is to remove the affect eyelashes

185
Q

a pateint presents with swollen, red, hot skin around the eyelid and eye.What are you worries about?

A

DONT NEED TO KNOW THIS JUST BE AWARE OF IT and the difference in presentation xx

Periorbital cellulitis (also known aspreseptal cellulitis) is an eyelid and skin infection in front of theorbital septum(in front of the eye). It presents with swollen, red, hot skin around the eyelid and eye.

It must be differentiated fromorbital cellulitis, a sight and life-threatening emergency. Patients are referred urgently to ophthalmology for assessment. A CT scan can help distinguish them. Treatment is withsystemic antibiotics(oral or IV). Preorbital cellulitis can develop into orbital cellulitis, so vulnerable patients (e.g., children) or severe cases may require admission for monitoring.

Orbital cellulitis is an infection around the eyeball involving the tissues behind theorbital septum. Symptoms include pain with eye movement, reduced eye movements, vision changes, abnormal pupil reactions, and proptosis (bulging forward of the eyeball). Orbital cellulitis requires emergency admission under ophthalmology and intravenous antibiotics. Surgical drainage may be needed if an abscess forms.