Quesmed wrong answers

Question 1

What are the Rome 4 criteria for constipation?

Answer 1

1. Fewer than three bowel movements per week
2. Hard stool in more than 25% of bowel movements
3. Tenesmus (sense of incomplete evacuation) in more than 25% of bowel movements
4. Excessive straining in more than 25% of bowel movements
5. A need for manual evacuation of bowel movements

Question 2

What are the two categories of constipation?

Answer 2

• Primary constipation: no organic cause, thought to be due to dysregulation of the function of the colon or anorectal muscles
• Secondary constipation: due to factors such as diet, medications, metabolic, endocrine or neurological disorders or obstruction

Question 3

What are the causes of constipation?

Answer 3

• Dietary factors, such as inadequate fibre or fluid intake
• Behavioural factors, like inactivity or avoidance of defecation
• Electrolyte disturbances, like hypercalcaemia
• Certain drugs, particularly opiates, calcium channel blockers and some antipsychotics
• Neurological disorders, like spinal cord lesions, Parkinson’s disease, and diabetic neuropathy
• Endocrine disorders, such as hypothyroidism
• Colon diseases, like strictures or malignancies
• Anal diseases, like anal fissures or proctitis

Question 4

How is constipation investigated?

Answer 4

• Full blood count
• Electrolytes
• Thyroid function tests
• Blood glucose
• Abdominal x-ray if suspicious of a secondary cause of constipation
• Barium enema if suspicious of impaction or rectal mass
• Colonoscopy if suspicious of lower GI malignancy

Question 5

How is constipation managed?

Answer 5

Management depends on the underlying cause and may include:
- Exclusion of underlying causes including colorectal cancer
- Lifestyle modifications such as dietary improvements and increased exercise

1. Bulk laxatives such as ispaghula husk or methylcellulose
2. Add Osmotic laxatives like lactulose or macrogol and/or Stimulant laxatives like senna or bisacodyl if fails to help with symptoms
3. Stool softeners like docusate sodium in chronic constipation

• Enemas (e.g., sodium citrate) if impaction is present
• Suppositories such as glycerol

If laxatives fail to resolve symptoms, referral to a specialist centre for evaluation of gut motility may be necessary.

Question 6

What is the action of trimethoprim and how does it affect renal function?

Answer 6

It works by inhibiting dihydrofolate reductase and interfering with folate metabolism. It is through this mechanism that can lead to megaloblastic anaemia as a SE.

Trimethoprim can lead to a transient rise in creatinine levels by reducing the creatinine excretion of the kidneys.

This does NOT reflect the actual GFR and therefore this phenomenon is not reflective of an Acute kidney injury but rather the calculated eGFR due to a transient rise in Creatinine.

Question 7

What is the MRI finding in vascular dementia?

Answer 7

White matter hyperintensities representing chronic small vessel ischaemic changes in the brain

Question 8

What is the treatment for delirium tremens?

Answer 8

Chlordiazepoxide (long acting benzodiazepine) or other benzos which reduces the chance of seizures

Question 9

What is deprivation of liberty?

Answer 9

Article 5 of the Human Rights Act states that ‘everyone has the right to liberty and security of person. No one shall be deprived of his or her liberty [unless] in accordance with a procedure prescribed in law’.

There is likely a deprivation of liberty if:
- The person is subject to continuous supervision and control and
- The person is not free to leave

Question 10

What is the deprivation of liberty safeguards and what are the criteria?

Answer 10

The Deprivation of Liberty Safeguards is the procedure in law used where it is necessary to deprive a patient or resident of their liberty as they lack capacity to consent to treatment or care to keep them safe from harm.

These procedures must be authorised by a supervisory authority e.g. local authority.

The following conditions must be met to allow a person to be deprived of their liberty under the safeguards:
- The person must be 18 or over.
- The person must be suffering from a mental disorder.
- The person must be a patient in hospital or a resident in a care home.
- The person lacks capacity to decide for themselves about the restrictions which are proposed so they can receive the necessary care and treatment.
- The proposed restrictions would deprive the person of their liberty.
- The proposed restrictions would be in the person’s best interests.
- Whether the person should instead be considered for detention under the Mental Health Act.
- There is no valid advance decision to refuse treatment or support that would be overridden by any DoLS process.

Question 11

What are advanced decisions?

Answer 11

An Advanced Decision, short for Advanced Decision to Refuse Treatment, is a legally binding document. Its purpose is to ensure that an individual can refuse a specific treatment(s) that they do not want to have in the future.

Question 12

What are the advanced decision criteria?

Answer 12

In order for an Advanced Decision to be legally binding, it must meet certain criteria:

​ 1. It must be valid (this means it must have been made at a time when the individual had capacity to make that decision).

​ 2. It must be applicable (this means the wording must be specific to the medical circumstances, and not vague or unclear).

​ 3. It must have been made when the individual was over 18, and fully informed about their decision.

​ 4. It must not have been made under the influence or duress of other people

​5. It must be written down, be signed and witnessed (if it concerns a refusal of life-saving treatment)

Question 13

What can advanced decisions cover?

Answer 13

Treatments that can be refused include life-sustaining treatments. It cannot refuse basic care (such as washing), food or drink by mouth, measures designed purely for comfort (e.g. painkillers), or treatment for a mental health condition if the individual is sectioned under the Mental Health Act. It can also not demand specific treatment or something that is illegal (e.g. assisted dying).

Question 14

What is an advanced statement?

Answer 14

An Advance Statement is sometimes called a “Statement of Wishes and Care Preferences”. It allows an individual to make general statements about their wishes, beliefs, feelings and values and how these influence their preferences for their future care and treatment.

An Advance Statement is not by itself legally binding, but legally must be taken into consideration when making a “best interests” decision on someone’s behalf under the Mental Capacity Act (MCA), 2005. This is because one of the criteria of the MCA is that a patient’s “wishes, feelings, beliefs and values” must be taken into consideration; an Advanced Statement provides evidence of this.

Question 15

What can an advanced statement cover?

Answer 15

Information that can be included in an Advanced Statement can be anything that is important to the individual. This might include:

​- Religious or spiritual views, and those that might relate to care

​- Food preferences

​- Information about your daily routine​ Where you would like to be cared for (in hospital, at home, in a care home etc.)

​ Any people who you would like to be consulted when best interests decisions are being made on your behalf (however this does not give the same legal power as creating a Lasting Power of Attorney)

An Advanced Statement can be made verbally, but it is better to write it down so there is clear documented evidence of an individual’s wishes and views. Copies of the Advanced Statement can be given to anyone the individual wishes to have a copy (e.g. their GP, carers and relatives)

Question 16

Which side effect is important to monitor for in dopamine agonist use (eg ropinirole)?

Answer 16

Impulsivity
Can lead to pathological gambling and hypersexuality

Question 17

What are the side effects of levodopa and how can they be avoided?

Answer 17

Levodopa is a medication used most commonly in the treatment of Parkinson’s disease and other movement disorders (e.g. dopa-responsive dystonia).

Side effects can be split into peripheral and central (depending on where the acting dopamine receptor is for the side effect).

Peripheral side effects include:
- Postural hypotension
- Nausea & vomiting
*Peripheral side effects are reduced by the co-administration of a peripheral dopa decarboxylase inhibitor, such as carbidopa (prevents conversion of levodopa to dopamine outside the CNS).
*Domperidone is an anti emetic that can be given for nausea. It acts as a peripheral dopamine antagonist.

Central side effects include:
- Hallucinations
- Confusion
- Dyskinesia
- Psychosis
With time, and as the underlying disease progresses, levodopa may become a less effective and patients may report end-of-dose effects, where motor activity progressively declines as the previous dose wears off, and on-off phenomena, which manifest as seemingly random fluctuations in drug effect.

One of the most disabling side effects are the drug-induced dyskinesia, writhing and uncoordinated movements of the limbs associated with poorly organised dopaminergic control of motor activity.

It typically takes 2-5 years to develop complete loss of response.

Question 18

Other than levodopa, which treatments can be given for Parkinson’s disease?

Answer 18

1. Dopamine agonists
   - Examples include: Ropinirole, rotigotine, Apomorphine. Previous ergot derived formulations (eg cabergoline) as now not widely used as are associated with lung fibrosis.
   - Have a longer half life than levodopa but are not as potent
   - Are often used in early disease in those without functional impairment, or late in disease when dyskinesias and motor fluctuations secondary to levodopa is a problem.
   - Side effect profile is as for levodopa - although there is a higher frequency of side effects than for levodopa.
   - Apomorphine is the most potent dopamine agonist and is typically given subcutaneously. It works well against motor fluctuations and dyskinesia. Often used late in disease. Beware autoimmune haemolytic anaemia in these patients & regular FBCs and DAT scans should be done.
2. MAO-B Inhibitors
   - Examples include: Selegiline, Rasagiline.
   - Reduce dopamine breakdown peripherally & thus increase central update of levodopa. Often used in combination with levodopa later in disease.
   - Can cause serotonin syndrome.
3. COMT Inhibitors
   - Include Entacapone and tolcapone.
   - Extend the use of levodopa. Useful in wearing off effect in levodopa use.
   - Tolcapone is more potent than entacapone and can result in hepatotoxicity.
4. Amantadine
   = NMDA receptor antagonist that has an unclear action in Parkinson’s.
   - Can be used in those suffering from dyskinesia.

Question 19

How is breakthrough pain medication dosage calculated?

Answer 19

Breakthrough pain medication is calculated as a sixth of the total daily dose

Question 20

Which medications are used for pain in end of life care?

Answer 20

1. Morphine
   - First line for pain management
   - Good for all types of pain
   - Monitor for constipation
   - Monitor for unwanted sedation
   - Please note that when coverting from oral morphine to subcutaneous morphine, you must divide the total dose by two
2. Diamorphine
3. Oxycodone
4. Alfentanyl
   - Useful for patients with renal failure who cannot take morphine

Question 21

In end of life care, which medications can be used for restlessness and confusion?

Answer 21

• Haloperidol
• Levomepromazine
• Midazolam

Question 22

What drop in systolic blood pressure is used to diagnose postural hypotension?

Answer 22

> = 20mmHg

(or a drop >=10mmHg in diastolic blood pressure)

Within 3 minutes of standing/

Question 23

What is anaemia?

Answer 23

Anaemia is defined by a reduction in the concentration of circulating haemoglobin in the peripheral blood to lower than is normal limit for age and sex.

Anaemia occurs when red blood cell (RBC) production is outstripped by RBC loss

The normal lifespan of RBCs in circulation is 120 days before they are destroyed

Question 24

What are the causes of anaemia?

Answer 24

Causes of anaemia include:

1. Bleeding (haemorrhage)
2. Breakdown of RBCs (haemolysis)
3. Ineffective RBC production (ineffective erythropoiesis)
   Anaemia should always be a trigger for further investigation and not an endpoint diagnosis in itself.

Question 25

What are the clinical features of anaemia?

Answer 25

• Shortness of breath
• Fatigue
• Pallor of the conjunctiva
• Increased cardiac output, palpitations, heart murmurs and cardiac failure

Question 26

How is anaemia classified?

Answer 26

Anaemia can be classified by the average size of the circulating RBCs, measured by the mean corpuscular volume (MCV), as:
1. Macrocytic
2. Normocytic
3. Microcytic
The normal range for MCV is lower in children compared with adults.

Question 27

What is megaoblastic anaemia and what are the causes?

Answer 27

Morphologically, macrocytic anaemia is usually typified by large RBCs due to abnormal RBC development, giant metamyelocytes and hypersegmented neutrophils (in the peripheral circulation).

Macrocytic anaemia may be megaloblastic or non-megaloblastic (non-megaloblastic does not have associated hypersegmented neutrophils)

1. Causes of megaloblastic anaemia (MCV >100 fl)
   - B12 deficiency from reduced intake (eg. dietary) or reduced absorption (eg. pernicious anaemia, inflammatory bowel disease, gastrectomy)
   - Folate deficiency
   - Drugs
   *hydroxycarbamide (previously called hydroxyurea). azathioprine, cytosine arabinoside. azidothymidine
2. Causes of non-megaloblastic macrocytic anaemia
   - Liver disease
   - Alcohol
   - Hypothyroidism
   - Myelodysplastic syndrome
   - Hypothyroidism
   - Pregnancy (usually a mild macrocytosis)

Question 28

What are the causes of normocytic anaemia?

Answer 28

Causes include:
- Recent bleeding
- Anaemia of chronic disease
- Combined iron & B12/folate deficiency
- Most non-haematinic-deficiency causes

Question 29

What is microcytic anaemia and what are the causes?

Answer 29

Microcytic anaemia is defined as the presence of small, often hypochromic, RBCs in a peripheral blood smear

It is usually characterized by a low MCV (<76 fl).

Causes include :
- Iron deficiency: IDA is the most common cause of microcytic anaemia. It results from insufficient iron intake, malabsorption, chronic blood loss (e.g. gastrointestinal bleeding), or increased iron requirements (e.g. pregnancy).
- α-thalassaemia, β-thalassaemia, HbE, HbC: Thalassaemias are a group of inherited haemoglobin disorders characterized by reduced production of normal globin chains, leading to microcytosis.
- Anaemia of chronic disease (this more often causes normochromic normocytic anaemia)
- Lead poisoning
- Sideroblastic anaemias (rare): Sideroblastic anaemias are a heterogeneous group of conditions characterized by defective haem synthesis and the accumulation of iron within the mitochondria of erythroid precursors.

Question 30

What are the causes of orthostatic hypotension?

Answer 30

• Medications, particularly vasodilators, diuretics, negative inotropes, antidepressants, and opiates
• Chronic hypertension due to the loss of baroreceptor reflexes
• Dehydration
• Sepsis
• Autonomic nervous system dysfunction, such as - Parkinson’s disease
• Adrenal insufficiency

Question 31

How is orthostatic hypotension managed?

Answer 31

• Ensuring adequate hydration
• Evaluating polypharmacy to identify medication-related causes
• Implementing strategies to reduce adverse outcomes from falls (e.g., fall alarm, soft flooring)
• Advising behavioral changes such as rising from sitting slowly, maintaining adequate hydration
• Recommending the use of compression stockings
• Employing pharmacotherapy, including fludrocortisone and midodrine, although the evidence base for fludrocortisone is weak

Question 32

What is the mechanism of action of midodrine for postural hypotension

Answer 32

Midodrine is an alpha-1-adrenergic receptor agonist. Activation of alpha-1-adrenergic receptors leads to an increase in vascular tone and an increase in blood pressure.

Question 33

How are primary neurodegenerative disorders classified?

Answer 33

1. Tauopathies WITH Beta-Amyloid: Alzheimer’s Disease
2. Tauopathies WITHOUT Beta-Amyloid:
   - Fronto-Temporal Dementia,
   - Corticobasal Degeneration,
   - Progressive Supranuclear Palsy
3. Alpha-Synocyclninopathies:
   - Lewy Body Dementia,
   - Parkinson’s Disease,
   - Multiple System’s Atrophy
4. Polyglutamine disorders: Huntington’s Disease
5. Vascular dementia: though not a primary neurodegenerative disorder, often grouped together with them as such

Question 34

How is lewy body dementia and parkinsons disease dementia differentiated?

Answer 34

If the dementia and movement disorder develop within a year of each other, it is referred to as Lewy Body Dementia; if they develop a year apart, it is referred to as Parkinson’s Disease Dementia.

It is thought that in Parkinson’s, the inclusions first affect the substantia nigra to cause the movement disorder before ascending to involve the paralimbic and neocortical areas to result in dementia; in Lewy body dementia, it starts at the top and eventually descends to the substantia nigra, hence the difference in the timing of these two closely inter-related conditions.

Question 35

What is pseudodementia?

Answer 35

Pseudodementia is a condition primarily associated with cognitive deficits in older patients suffering from depression. It is an important differential of dementia, characterised by cognitive and memory impairments that mimic those of dementia but with an underlying psychiatric cause.

While the exact cause of pseudodementia is unknown, it is primarily associated with depression in older adults. Other psychiatric conditions, such as anxiety disorders, can also contribute to its development.

Question 36

What are the features of pseudodementia?

Answer 36

• Short duration of symptoms mimicking dementia
• Equal impact on long-term and short-term memory
• Amnesia concerning specific, often emotionally charged, events
• Detailed complaints about memory disturbances
• Highlighted failures in responses to memory-related questions
• Early loss of social skills in the disease progression
• Common responses of “don’t know” to questions, rather than attempting to guess
• Minimal effort in task performance

Question 37

How is pseudodementia managed?

Answer 37

The management of pseudodementia primarily involves treating the underlying depressive disorder, often with a combination of antidepressant medication and cognitive-behavioural therapy. With appropriate treatment, cognitive symptoms usually improve or resolve. In contrast, dementia is a progressive condition with, to date, no curative treatment.

Question 38

what can be used instead of morphine in palliative care pain relief when there is poor renal function?

Answer 38

(morphine and codeine, NSAIDs are renally excreted and will result in a build up of toxic metabolites)

Oxycodone is an alternative

Question 39

Why are typical antipsychotics not used in Lewy body dementia/Parikinsonism?

Answer 39

Typical antipsychotics such as haloperidol often lead to worsening of confusion or Parkinsonism in patients with Lewy body dementia (they increase extrapyramidal side effects). These reactions can be severe and even life-threatening.

Question 40

Which cholinesterase inhibitors are used in alzheimer’s disease?

Answer 40

Rivastigmine
Galantamine
Donepezil

Question 41

Which drugs are associated with lower seizure thresholds?

Answer 41

1. Antibiotics: Imipenem, penicillins, quinolones (eg ciprofloxacin) cephalosporins, metronidazole, isoniazid
2. Antipsychotics
3. Antidepressents: Bupropion, Tricyclics, Venlafaxine
4. Tramadol
5. Fentanyl
6. Ketamine
7. Lidocaine
8. Lithium
9. Antihistamines

Question 42

What is Benserazide?

Answer 42

Benserazide is a decarboxylase inhibitor which prevents the peripheral breakdown of levodopa. This means that levodopa is decarboxylated into dopamine in the brain, enabling the full therapeutic dose to take effect.

Question 43

What is Charles Bonnet syndrome?

Answer 43

Charles Bonnet syndrome is a medical condition characterized by complex visual hallucinations in individuals who are partially sighted or visually impaired, but otherwise cognitively healthy.

The most common conditions leading to Charles Bonnet syndrome are age-related macular degeneration, followed by glaucoma and cataract.

Question 44

What are the features of Charles Bonnet syndrome?

Answer 44

The hallmark of Charles Bonnet syndrome is the occurrence of well-formed, vivid, elaborate, and often stereotyped visual hallucinations in a partially sighted person. The individual maintains insight into the unreality of what he or she is seeing. The imagery can be varied, including groups of people or children, animals, and panoramic countryside scenes.

Question 45

What are the causes and risk factors of subdural haematomas?

Answer 45

A subdural haematoma refers to the condition characterized by an accumulation of venous blood in the potential space between the dura mater and arachnoid mater of the brain.

Subdural haematomas typically occur in elderly individuals, particularly those over 65 years of age. It is often a consequence of minor trauma, leading to shearing forces that tear bridging veins between the cortex and dura mater. Risk factors include:
- Advancing age (>65 years old)
- Bleeding disorders or anticoagulant therapy
- Chronic alcohol use
- Recent trauma.

The haematoma results from shearing forces that tear the bridging veins between the cortex and dura mater. These forces commonly arise from minor head traumas, but can also occur spontaneously in patients with bleeding disorders, anticoagulant therapy, chronic alcohol use, and recent trauma.

Question 46

What are the clinical features of a subdural haematoma?

Answer 46

• Headache
• Nausea or vomiting
• Confusion
• Diminished eye, verbal, or motor response
• Focal neurological signs indicating the haematoma site.

The presentation is typically sub-acute (within 3 days to 3 weeks) or chronic (>3 weeks).

Question 47

How is subdural haematoma investigated?

Answer 47

Diagnosis of a subdural haematoma is primarily established through a CT scan. The appearance of the clot varies based on its age:
1. Hyperacute phase (<1 hour): The clot may appear isodense, with underlying cerebral oedema.
2. Acute phase (<3 days): The clot appears as a crescent-shaped hyperdense extra-axial collection over the affected hemisphere.
3. Sub-acute phase (3 days to 3 weeks): The clot appears more isodense compared to the adjacent cortex, making identification more difficult. Contrast-enhanced CT or MRI can aid identification. There may be associated mass effect causing midline shift and sulcal effacement.
4. Chronic phase (>3 weeks): The haematoma appears hypodense relative to the adjacent cortex.

Bilateral SDH occurs in 15% of adults and 80% of infants.

Question 48

How is subdural haematoma managed?

Answer 48

In patients with subdural haematoma, surgery is needed if there is any focal neurology, if the patient is deteriorating or if there is a large haematoma, raised intracranial pressure or midline shift. Conservative management is appropriate in patients with small, asymptomatic subdural haemorrhage, but these patients will still require close observation, regular examination and serial CT scanning.

The management of a subdural haematoma depends on its stage:

1. Acute haemorrhages: Craniotomy is the preferred method.
2. Chronic haemorrhages: Burr holes are typically recommended.

The overall goal is to relieve pressure on the brain and to treat or prevent any related neurological symptoms or complications.

Question 49

What are the 5 key principles of the mental capacity act?

Answer 49

Five key principles underpin the MCA.
1. Capacity is assumed; it needs to be proven otherwise
2. Enabling people to make their own decisions
3. Unwise decisions
4. Best interests
5. Less restrictive option

Question 50

What is Section 5(2)

Answer 50

Section 5(2) allows doctors to detain a patient with a mental health condition under the Mental Health Act for up to 72 hours whilst awaiting an assessment for consideration of further detention.

Question 51

What is section 2?

Answer 51

Patients can be detained for up to 28 days under Section 2. This may be used for patients who need assessment and possible treatment of a mental health disorder and are at risk of harm, either to themselves or to others.

Question 52

What is section 3?

Answer 52

Patients can be detained for up to 6 months under Section 3. This may be used for patients who need assessment and treatment of a mental health disorder and are at risk of harm, either to themselves or to others.

Question 53

Which scoring tool can assess for delirium?

Answer 53

4AT

A score of 4 or above is suggestive of possible delirium +/- cognitive impairment.

Question 54

What is the waterlow score?

Answer 54

The Waterlow score identifies the risk of a patient having a pressure ulcer.

Question 55

What is the MoCA score?

Answer 55

The MoCA is a sensitive screening tool used to detect cognitive impairment.

Question 56

What is the MUST score?

Answer 56

The MUST score helps identify adults who are malnourished or those who are at risk of malnutrition to ensure their needs are being adequately met.

Question 57

What are the clinical features of alzheimer’s?

Answer 57

• Memory Impairment: Early in the disease, individuals often experience difficulties in recalling recent events and conversations.
• Language Impairment: This may manifest as difficulty finding words, struggling to express oneself, and, in later stages, aphasia.
• Executive Dysfunction: Impaired ability to plan, organize, and carry out tasks, leading to difficulties in activities of daily living.
• Behavioural Changes: Individuals may exhibit agitation, aggression, or apathy, sometimes accompanied by mood swings and irritability.
• Psychological Symptoms: Hallucinations, delusions, and paranoia can occur, particularly in later stages of the disease.
• Disorientation: Affected individuals may become disoriented in familiar surroundings, unable to recognize places or people.
• Loss of Motor Skills: In advanced stages, motor skills decline, leading to difficulties with mobility and self-care.

Question 58

What is the mechanism of sildenafil (viagra) and what are the side effects?

Answer 58

Mechanism
It is a phosphodiesterase 5 (PDE5) inhibitor which enhances the effect of nitric oxide causing smooth muscle relaxation and subsequent penile erection due to inflow of blood.

Side effects
Sildenafil citrate is contra-indicated in patients taking organic nitrates due to risk of hypotension.

Side effects include flushing, headache, dyspepsia, nasal congestion, dizziness, diarrhoea, rashes and UTIs.

Question 59

Which medication is used for agitation in end of life care?

Answer 59

Midazolam is the standard benzodiazepine used for agitation towards the end of life. It may also help reduce the sensation of breathlessness.

Question 60

What are the causes of postural hypotension?

Answer 60

The causes of orthostatic hypotension include:
- Medications, particularly vasodilators, diuretics, negative inotropes, antidepressants, and opiates
- Chronic hypertension due to the loss of baroreceptor reflexes
- Dehydration
- Sepsis
- Autonomic nervous system dysfunction, such as Parkinson’s disease
- Adrenal insufficiency

Question 61

What are the clinical features of postural hypotension?

Answer 61

Patients with orthostatic hypotension may present with:
- Dizziness
- Syncope
- Falls
- Fractures
- More frequent occurrences after meals or exercise
- More frequent occurrences in warm environments
- Sometimes precipitated by coughing or defecating
- Symptoms can occur several minutes after standing up

Question 62

How is postural hypotension managed?

Answer 62

Management of orthostatic hypotension depends on the underlying cause and may include:
- Ensuring adequate hydration
- Evaluating polypharmacy to identify medication-related causes
- Implementing strategies to reduce adverse outcomes from falls (e.g., fall alarm, soft flooring)
- Advising behavioral changes such as rising from sitting slowly, maintaining adequate hydration
- Recommending the use of compression stockings

• Employing pharmacotherapy, including fludrocortisone and midodrine, although the evidence base for fludrocortisone is weak

Question 63

How is delirium managed?

Answer 63

Management of delirium primarily focuses on treating the underlying cause. Non-pharmacological strategies should be the first line, which include:

• Providing an environment with good lighting
• Maintaining a regular sleep-wake cycle
• Regular orientation and reassurance
• Ensuring the patient’s glasses and hearing aids are used if needed

For patients who are extremely agitated and potentially a danger to themselves or others, pharmacological interventions such as small doses of haloperidol or olanzapine may be considered. However, these should be used with caution, especially in the elderly, due to the risk of side effects.

Question 64

What is the pathophysiology of alzheimer’s disease?

Answer 64

Alzheimer’s disease is a complex and progressive neurodegenerative disorder characterized by distinct pathophysiological hallmarks. These hallmarks are responsible for the gradual decline in cognitive function and the characteristic clinical features observed in affected individuals.

• Amyloid Plaques: The accumulation of beta-amyloid protein fragments outside nerve cells in the form of plaques is a hallmark feature. These abnormal protein deposits are believed to disrupt neuronal communication, trigger inflammation, and ultimately lead to cell death.
• Tau Tangles: Inside nerve cells, abnormal tau protein accumulates, forming neurofibrillary tangles. These tangles interfere with the transport of essential nutrients within neurons, contributing to their dysfunction and eventual demise.
• Neuronal Loss and Brain Atrophy: As the disease progresses, significant neuronal loss occurs, particularly in brain regions responsible for memory and cognitive function, such as the hippocampus and the cerebral cortex. This loss is associated with brain atrophy, visible on imaging studies.
• Neurotransmitter Imbalance: Alzheimer’s disease disrupts the balance of neurotransmitters, particularly acetylcholine, which plays a crucial role in memory and learning. Reduced acetylcholine levels further contribute to cognitive decline.
• Inflammatory Response: Chronic neuroinflammation, characterized by the activation of microglia and astrocytes, is a prominent feature in Alzheimer’s disease. Inflammation may exacerbate neuronal damage and contribute to the progression of the disease.

Question 65

What tests are undertaken in a confusion screen?

Answer 65

FBC, U&E, LFTs, CRP/ESR, Ca2+, TFTs, B12, folate, syphilis, HIV.

Question 66

What are the presenting features of microcytic anaemia?

Answer 66

• Fatigue and Weakness
• Pallor
• Shortness of Breath
• Palpitations
• Cold intolerance
• Iron-deficiency anaemia specific:
  *Nail changes such as koilonychia (spoon-shaped nails)
  *Atrophic glossitis
  *Angular stomatitis
  *Pica: Iron-deficiency anaemia may manifest as pica, with cravings for non-food substances like ice (pagophagia) or clay (geophagia).

Question 67

How is anaemia investigated?

Answer 67

Investigations all patients should have include:
1. Full Blood Count (FBC): hemoglobin levels, red blood cell count, hematocrit, and mean corpuscular volume (MCV). In microcytic anaemia, the MCV is typically lower than the reference range.
2. Peripheral Blood Smear Examination: A peripheral blood smear allows visual examination of red blood cells. It can reveal microcytosis, hypochromia (reduced hemoglobin content), and, in certain cases, abnormal cell morphology.
3. Iron Studies: Iron studies consist of several key parameters:
- Serum Iron: Measures the concentration of iron in the blood. In microcytic anaemia, serum iron may be decreased.
- Ferritin: Ferritin is an intracellular protein that stores iron. Low ferritin levels are indicative of iron deficiency.
- Transferrin Saturation: This parameter assesses the percentage of transferrin (a protein that transports iron) saturated with iron. Reduced transferrin saturation is consistent with iron deficiency.

Specific tests to investigate for underlying causes include:
- Haemoglobin Electrophoresis: Helps distinguish thalassaemias from other causes of microcytic anaemia by identifying abnormal hemoglobin variants.
- Serum Lead Levels: When lead poisoning is suspected, measuring blood lead levels is essential for diagnosis.
- Bone Marrow Examination: In selected cases, particularly when there is diagnostic uncertainty or unusual clinical features, a bone marrow examination may be warranted. This invasive procedure allows a detailed assessment of the bone marrow, including cell morphology, iron stores, and other relevant findings.

Question 68

What are the adverse effects of iron supplementation?

Answer 68

• Side effects - diarrhoea, constipation, black stools, abdominal pain, nausea
• Iron supplements should be taken on an empty stomach (preferably one hour before a meal) with a drink containing vitamin C, such as a glass of orange juice or another juice drink with added vitamin C. This aids absorption.
• Oral iron decreases the absorption of oral Levothyroxine. Therefore if both are prescribed, advise patients to take at least 4 hours apart.