Conditions List Flashcards
What are the causes of Stroke?
-Vessel occlusion or thrombosis in situ
-Cardiac emboli (AF, endocarditis)
-Atherothromboembolism (eg from carotids)
-CNS bleeds (HTN, trauma, aneurysm rupture, anticoagulation, thrombolysis)
-Sudden BP drop
-Carotid artery dissection
-Vasculitis
-SAH
-Venous sinus thrombosis
-Antiphospholipid syndrome
-Thrombophilia
-Fabry disease
What are the risk factors for developing a stroke?
-HTN
-Smoking
-DM
-CV disease (valvular, IHD, AF)
-Increased clotting
-Increased homocysteine
-Syphilis
How do you manage an acute stroke?
- Protect the airway
- Maintain homeostasis: blood glucose (check signs are not due to hypoglycaemia), BP (only treat if hypertensive emergency such as encephalopathy or aortic dissection because lowering BP may affect cerebral perfusion
- CT/MRI immediately: diffusion-weighted MRI is gold standard, CT helps to rule out primary intracerebral haemorrhage
ONLY IF HAEMORRHAGE IS EXCLUDED:
4. Antiplatelet - give aspirin 300mg stat and continue for 2 weeks
5. Thrombolysis - If onset of symptoms was <4.5 hours ago, give alteplase (tissue plasminogen activator) with close monitoring (incl repeated CT 24 hours post lysis to check for bleeds)
6. Thrombectomy - if the area of infarction is confirmed and depending on the location of the infarct and the time since stroke (not used >24 hours after event). For those with large artery occlusion in the proximal anterior circulation
What are the contraindications to thrombolysis treatment of acute stroke?
-Major infarct or haemorrhage on CT
-Mild/non-disabling deficit
-Recent surgery, trauma, or artery or vein puncture at uncompressible site
-Previous CNS bleed
-AVM/aneurysm
-Severe liver disease, varices or portal hypertension
-Seizures at presentation
-Very low or very high blood glucose
-Stroke or serious head injury in last 3 months
-GI or urinary tract haemorrhage in last 21 days
-Known clotting disorder
-On anticoagulants or INR>1.7
-Low platelets
-History of intracranial neoplasm
-Rapidly improving symptoms
-BP> 180/105
What secondary preventative measures should be started after the acute management of a stroke?
-Control risk factors: eg lowering BP, most patients should be started on atorvastatin 80mg
-Start Antiplatelets: After 2 weeks of 300mg aspirin, switch patients to clopidogrel 75mg monotherapy. If this is CI or not tolerated, give low dose aspirin and slow release dipyridamole
What tests should be carried out following a stroke (post-acute phase)?
- Check BP: look for retinopathy, nephropathy or cardiomegaly on CXR
- Cardiac sources of emboli: 24hr ECG to check for AF. CXR may show large left atrium. Echo may show mural thrombosis due to AF or hypokinetic segment of cardiac muscle post-MI, valvular lesions in infective endocarditis or rheumatic heart disease. TOE more sensitive than TTO
- Carotid artery stenosis: Do carotid doppler ultrasound +/- CT?MRI angiography. (Carotid endarterectomy may be indicated)
- Check for hyper/hypoglycaemia, dyslipidaemia or hyperhomocysteinaemia
-Vasculitis: increased ESR, ANCA, check for active untreated syphilis
-Prothrombotic states: thrombophilia, antiphospholipid syndrome
-Hyperviscosity: polycythaemia, sickle-cell disease
-Thrombocytopaenia and other bleeding disorders
-Genetic tests eg CADASIL and Fabry disease
What treatment should be given to a stroke patient found to have AF?
Anticoagulation with a DOAC or Warfarin from 2 weeks (or from 7-10 days if clinically and radiologically small embolus).
What is the mechanism of action of aspirin?
Inhibits cox-1, suppressing prostaglandin and thromboxane synthesis
What is the mechanism of action of clopidogrel?
A thienopyridine that inhibits platelet aggregation by modifying platelet adenosine diphosphate (ADP) receptors
What is the mechanism of action of dipyridamole?
Increases cAMP and decreases thromboxane A2
What is vertigo?
Vertigo is a descriptive term for a sensation that there is movement between the patient and their environment. They may feel they are moving or that the room is moving. Often this is a horizontal spinning sensation, similar to how you feel after turning in circles then stopping abruptly.
Vertigo is often associated with nausea, vomiting, sweating and feeling generally unwell. There may be decreased balance, hearing loss, tinnitus and nystagmus.
What is the pathophysiology of vertigo?
The sensory inputs that are responsible for maintaining balance and posture are:
1. Vision
2. Proprioception
3. Signals from the vestibular system
Vertigo is caused by a mismatch between these sensory inputs.
The vestibular system is the most important sensory system to understand when learning about vertigo. The vestibular apparatus is located in the inner ear. It consists of three loops called the semicircular canals that are filled with a fluid called endolymph. These semicircular canals are oriented in different directions to detect various movements of the head. As the head turns, the fluid shifts inside the canals. This fluid shift is detected by tiny hairs called stereocilia found in a section of the canal called the ampulla. This sensory input of shifting fluid is transmitted to the brain by the vestibular nerve and lets the brain know that the head is moving in a particular direction.
The vestibular nerve carries signals from the vestibular apparatus to the vestibular nucleus in the brainstem and the cerebellum. The vestibular nucleus then sends signals to the oculomotor, trochlear and abducens nuclei that control eye movements and the thalamus, spinal cord and cerebellum. The cerebellum is responsible for coordinating movement throughout the body. Therefore, the vestibular signals help the central nervous system coordinate eye movements and other movements throughout the body.
Vertigo can be caused by either a:
-Peripheral problem, usually affecting the vestibular system
-Central problem, usually involving the brainstem or the cerebellum
What are the four common types of peripheral (vestibular) vertigo? What other causes may be possible?
- Benign paroxysmal positional vertigo
- Ménière’s disease
- Vestibular neuronitis
- Labyrinthitis
There are several other peripheral causes of vertigo. These are:
-Trauma to the vestibular nerve
-Vestibular nerve tumours (acoustic neuromas)
-Otosclerosis
-Hyperviscosity syndromes
-Varicella zoster infection (often with facial nerve weakness and vesicles around the ear – Ramsay Hunt syndrome)
What is benign paroxysmal positional vertigo?
Benign paroxysmal positional vertigo (BPPV) is caused by crystals of calcium carbonate called otoconia that become displaced into the semicircular canals. They may be displaced by a viral infection, head trauma, ageing or without a clear cause. The crystals disrupt the normal flow through the canals and therefore disrupt the function of the system. The symptoms are usually positional, because movement is required to confuse the system. Therefore, attacks of vertigo are triggered by movement and can last around a minute before the symptoms settle. Often symptoms occur over several weeks and then resolve, then can reoccur weeks or months later. A special test called the Dix-Hallpike manoeuvre can be used to diagnose BPPV.
What is Meniere’s disease?
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.
What is acute vestibular neuronitis?
Acute vestibular neuronitis describes inflammation of the vestibular nerve. This is usually attributed to a viral infection. Typically, the history is of acute onset of vertigo that improves within a few weeks.
What is Labrynthitis?
Labyrinthitis describes inflammation of the structures of the inner ear. This is usually attributed to a viral infection. Usually the history is of acute onset of vertigo that improves within a few weeks. Labyrinthitis can cause hearing loss, which distinguishes it from vestibular neuronitis.
What are the common causes of central vertigo?
Pathology that affects the cerebellum or the brainstem disrupt the signals from the vestibular system and cause vertigo. The most common pathology that results in a central cause of vertigo are:
- Posterior circulation infarction (stroke): will have a sudden onset and may be associated with other symptoms, such as ataxia, diplopia, cranial nerve defects or limb symptoms.
- Tumour: in the cerebellum or brainstem will have a gradual onset with associated symptoms of cerebellar or brainstem dysfunction.
- Multiple sclerosis: may cause relapsing and remitting symptoms, with other associated features of multiple sclerosis, such as optic neuritis or transverse myelitis.
- Vestibular migraine: will cause symptoms lasting minutes to hours, often associated with visual aura and headache. Attacks may be triggered by stress, bright lights, strong smells, certain foods (e.g. chocolate, cheese and caffeine), dehydration, menstruation, abnormal sleep patterns
All the central causes of vertigo will cause sustained, non-positional vertigo.
What key features in a history might point to the cause of vertigo?
When a patient presents with “dizziness’, it is important to first distinguish between vertigo and light-headedness. Ask whether the “room is moving” (vertigo) or whether they feel more of a light-headedness.
Ask about symptoms that will help you differentiate between central and peripheral vertigo:
1. Onset: Sudden onset (P), Gradual onset (C - except stroke)
2. Duration: Short (seconds or minutes -P), Persistent (C)
3. Hearing loss or tinnitus: Often present (P - except BPPV), Usually not (C)
4. Coordination: Intact (P), Impaired (C)
5. Nausea: More severe (P), Mild (C)
Key features that may point to a specific cause are:
-Recent viral illness (labyrinthitis or vestibular neuronitis)
-Headache (vestibular migraine, cerebrovascular accident or brain tumour)
-Typical triggers (vestibular migraine)
-Ear symptoms, such as pain or discharge (infection)
-Acute onset neurological symptoms (stroke)
What are the 4 things to examine when assessing a patient presenting with vertigo?
- Ear examination to look for signs of infection or other pathology
- Neurological examination to assess for central causes of vertigo (e.g., stroke or multiple sclerosis).
Cerebellar examination is an important part of a full neurological examination in patients with vertigo. The components can be remembered with the DANISH mnemonic:
D – Dysdiadochokinesia
A – Ataxic gait (ask the patient to walk heel-to-toe)
N – Nystagmus (see below for more detail)
I – Intention tremor
S – Speech (slurred)
H – Heel-shin test
- Cardiovascular examination to assess for cardiovascular causes of dizziness (e.g., arrhythmias or valve disease)
- Special tests
-Romberg’s test (screens for problems with proprioception or vestibular function)
-Dix-Hallpike manoeuvre (to diagnose BPPV)
-HINTS examination (to distinguish between central and peripheral vertigo). It stands for:
HI – Head Impulse
N – Nystagmus
TS – Test of Skew
Head Impulse Test
The head impulse test involves the patient sitting upright and fixing their gaze on the examiner’s nose. The examiner holds the patient’s head and rapidly jerks it 10-20 degrees in one direction while the patient continues looking at the examiner’s nose. The head is moved slowly back to the centre before repeating in the opposite direction. Ensure they have no neck pain or pathology before performing the test.
A patient with a normally functioning vestibular system will keep their eyes fixed on the examiner’s nose.
In a patient with an abnormally functioning vestibular system (e.g., vestibular neuronitis or labyrinthitis), the eyes will saccade (rapidly move back and forth) as they eventually fix back on the examiner.
The head impulse test helps diagnose a peripheral cause of vertigo but will be normal if the patient has no current symptoms or a central cause of vertigo.
Nystagmus
Nystagmus can be demonstrated by having the patient look left and right. The eyes rapidly saccade or oscillate, meaning they shake side to side as they try to settle into place. A few beats can be normal. Unilateral horizontal nystagmus is more likely to be a peripheral cause. Bilateral or vertical nystagmus suggests a central cause.
Test of Skew
The test of skew (also called the alternate cover test) involves the patient sitting upright and fixing their gaze on the examiner’s nose. The examiner covers one eye at a time, alternating between covering either eye. The eyes should remain fixed on the examiner’s nose with no deviation. If there is a vertical correction when an eye is uncovered (the eye has drifted up or down and needs to move vertically to fix on the nose when uncovered), this indicates a central cause of vertigo.
How is vertigo due to peripheral causes managed?
For peripheral vertigo, short-term options for managing symptoms include:
-Prochlorperazine/Buccastem (A vestibular suppressant)
-Antihistamines (e.g., cyclizine, cinnarizine and promethazine)
What can be used as prophylaxis in Meniere’s disease?
Betahistine
Vestibular suppressants do not stop the vertigo in BPPV. How can this condition be managed?
- Epley manoeuvre
How is vestibular migraine managed?
Usually managed by avoiding triggers and lifestyle changes (e.g., getting enough sleep and staying hydrated).
Medical management is similar to migraines, with triptans for the acute symptoms and propranolol, topiramate or amitriptyline to prevent attacks.
What is polypharmacy?
The concurrent use of multiple medications in an individual
What are 7 helpful steps to appropriate polypharmacy?
1: What matters to the patient
- Patient understanding objectives of drug therapy, management of existing health conditions and prevention of future health problems
2: Identify essential drug therapy
- Drugs that have essential replacement functions (eg levothyroxine) and drugs to prevent rapid symptomatic decline (eg drugs for Parkinson’s disease, heart failure)
3: Does the patient take unnecessary drug therapy?
- Review drugs with temporary indications, higher than usual maintenance doses and those with limited benefit
- For remaining drugs verify that each has a function that matters to the patient, review preventative treatment to ensure the pt is able to continue taking the medication for the required time to benefit, see if any lifestyle changes can replace unnecessary drug therapy
4: Are therapeutic objectives being achieved?
- Symptom control, biochemical/clinical targets, preventing disease/ exacerbation
- Check adherence
5: Are there ADRs?
- Check interactions, correct monitoring and dosage
- Check side effects and lab markers, cumulative adverse drug effects and drugs that may be used to treat ADRs from other drugs
- Is the drug therapy cost-effective
- Consider more cost effective alternatives
7: is the patient willing and able to take the drug therapy as intended?
- Correct form, dosing schedule, assistance if needed
What is appropriate polypharmacy?
Prescribing for an individual for complex conditions or for multiple conditions in circumstances where medicines use has been optimised and where the medicines are prescribed according to best evidence
It is present when:
(a) all drugs are prescribed for the purpose of achieving specific therapeutic objectives that have been agreed with the patient;
(b) therapeutic objectives are actually being achieved or there is a reasonable chance they will be achieved in the future;
(c) drug therapy has been optimized to minimize the risk of ADRs and
(d) the patient is motivated and able to take all medicines as intended.
What is inappropriate polypharmacy?
Present, when one or more drugs are prescribed that are not or no longer needed, either because:
(a) there is no evidence based indication, the indication has expired or the dose is unnecessarily high;
(b) one or more medicines fail to achieve the therapeutic objectives they are intended to achieve;
(c) one, or the combination of several drugs cause inacceptable adverse drug reactions (ADRs), or put the patient at an unacceptably high risk of such ADRs, or because
(d) the patient is not willing or able to take one or more medicines as intended.
What is frailty?
Frailty is well defined as a ‘reduced ability to withstand illness without loss of function’. The Gold Standards Framework defines this further as:
- Multiple co-morbidities with signs of impairment in day to day functioning
- Combination of at least three of:
- Weakness
- Slow walking speed
- Low physical activity
- Weight loss
- Self-reported exhaustion
What is the Number needed to treat?
The number needed to treat (NNT) is a measure used in assessing the effectiveness of a particular intervention. The NNT is the average number of patients who require to be treated for one to benefit compared with a control in a clinical trial. It can be expressed as the reciprocal of the absolute risk reduction.
The ideal NNT is 1, where everyone improves with treatment: the higher the NNT, the less effective is the treatment in terms of the trial outcome and timescale.
So if treatment with a medicine reduces the death rate over 5 years from 5% to 1% (very effective), the absolute risk reduction is 4% (5 minus 1), and the NNT is 100/4, (25).
What is multimorbidity?
Be aware that multimorbidity refers to the presence of 2 or more long-term health conditions, which can include:
- defined physical and mental health conditions such as diabetes or schizophrenia
- ongoing conditions such as learning disability
- symptom complexes such as frailty or chronic pain
- sensory impairment such as sight or hearing loss
- alcohol and substance misuse.
How should frailty be assessed in the community and in hospital outpatient settings?
- Consider assessing frailty in people with multimorbidity.
- Be cautious about assessing frailty in a person who is acutely unwell.
- Do not use a physical performance tool to assess frailty in a person who is acutely unwell.
Primary care and community care settings
When assessing frailty in primary and community care settings, consider using 1 of the following:
- an informal assessment of gait speed (for example, time taken to answer the door, time taken to walk from the waiting room)
- self-reported health status (that is, ‘how would you rate your health status on a scale from 0 to 10?’, with scores of 6 or less indicating frailty)
- a formal assessment of gait speed, with more than 5 seconds to walk 4 metres indicating frailty
- the PRISMA-7 questionnaire, with scores of 3 and above indicating frailty.
Hospital outpatient settings
When assessing frailty in hospital outpatient settings, consider using 1 of the following:
0 self-reported health status (that is, ‘how would you rate your health status on a scale from 0 to 10?’, with scores of 6 or less indicating frailty)
- the ‘Timed Up and Go’ test, with times of more than 12 seconds indicating frailty
- a formal assessment of gait speed, with more than 5 seconds to walk 4 metres indicating frailty
- the PRISMA‑7 questionnaire, with scores of 3 and above indicating frailty
- self-reported physical activity, with frailty indicated by scores of 56 or less for men and 59 or less for women using the Physical Activity Scale for the Elderly.
What are the complications of multimorbidity?
- Decreased quality of life and life expectancy
- Increased treatment burden: Difficulties in understanding and self-managing condition as well as adherence to lifestyle changes
- Mental health issues: Those with cognitive impairment are particularly vulnerable
- Polypharmacy: Adverse drug events increase in prevalence as the number of chronic conditions increases
- Negative impact on carers welfare
How should multimorbidity be assessed?
- Identify those who may benefit from the recognition of multimorbidity, opportunistically in routine care or through healthcare records
- Patients may require a multimorbidity approach if they: Have difficulties with daily activities, are frail, are prescribed over 10 medications, or frequently seek emergency care services
- Establish the extent of disease burden: Discuss mental health issues, wellbeing and the interaction between their health and quality of life
- Investigate how their treatment burden affects their daily activities
- Ask about social circumstances and assess their health literacy
- Assess the adequacy of pain management particularly in chronic pain conditions
- Frailty should be specifically assessed through the evaluation of gait speed, self-reported health status, or the PRISMA-7 questionnaire: The PRISMA-7 involves questions considering the age, sex, health problems, assistance required and walking aid use of the patient
What are some strategies to manage multimorbidity?
- Reducing treatment burden and optimising care is the goal in managing comorbidity
- Maximise the benefits of existing treatments
- Offer alternative follow-up arrangements if they are struggling to meet them
- Reduce the number of high risk medications being prescribed and consider the use of non-pharmacological treatments
- Consider a ‘bisphosphonate holiday’ in those taking bisphosphonates for longer than three years as there is no consistent evidence of continued benefits after this point. Discuss stopping bisphosphonates after 3 years and include patient choice, fracture risk and life expectancy in the discussion.
- Consider the use of screening tools such as STOPP/ START in older people to recognise medicine safety concerns: STOPP identifies medications where the risk outweighs the therapeutic benefits in certain conditions and START suggests medications that may provide additional benefits ie proton pump inhibitors for gastroprotection in patients on medications increasing bleeding risk
- Especially consider stopping the use of medications such as NSAIDS, warfarin and aspirin in patients with peptic ulcer disease, and pay particular attention to the prescription of reno-toxic or renally cleared drugs in reduced renal function
- Ask patients about the benefits and harms of their individual treatments, considering the overall prognostic benefit
- Promote self-management through education and engagement strategies
- Support carers and families of patients
- Use the action plan to follow up with the patient at agreed points: NHS England recommends a yearly review of all medications for people aged over 65, however, medications should be reviewed periodically to ensure that patients are being informed, given adequate laboratory tests and that treatments are optimised
What are the risk factors for multimorbidity?
Increasing age
Female sex
Low socioeconomic status
Tobacco and alcohol usage
Lack of physical activity
Poor nutrition and obesity
What are the parts to the PRISMA-7 questionnaire?
1 - Are you older than 85 years?
2 - Are you male?
3 - In general, do you have any health problems that require you to limit your activities?
4 - Do you need someone to help you regularly?
5 - In general, do you have any health problems that require you to stay at home?
6 - If you need help, can you count on someone close to you?
7 - Do you regularly use a cane, a walker or a wheelchair to move about?
What factors might precipitate delirium?
- infection: particularly urinary tract infections
- metabolic: e.g. hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration
- change of environment
- any significant cardiovascular, respiratory, neurological or endocrine condition
- severe pain
- alcohol withdrawal
- constipation
What are the features of delirium?
- memory disturbances (loss of short term > long term)
- may be very agitated or withdrawn
- disorientation
- mood change
- visual hallucinations
- disturbed sleep cycle
- poor attention
How is delirium managed?
- treatment of the underlying cause
- modification of the environment
- haloperidol 0.5 mg as the first-line sedative
- management can be challenging in patients with Parkinson’s disease, as antipsychotics can often worsen Parkinsonian symptoms
*careful reduction of the Parkinson medication may be helpful
*if symptoms require urgent treatment then the atypical antipsychotics quetiapine and clozapine are preferred
How is alzheimer’s disease managed?
- Non-pharmacological management
NICE recommend offering ‘a range of activities to promote wellbeing that are tailored to the person’s preference’
NICE recommend offering group cognitive stimulation therapy for patients with mild and moderate dementia
other options to consider include group reminiscence therapy and cognitive rehabilitation - Pharmacological management
- the three acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) as options for managing mild to moderate Alzheimer’s disease
- memantine (an NMDA receptor antagonist) is in simple terms the ‘second-line’ treatment for Alzheimer’s, NICE recommend it is used in the following situation reserved for patients with
*moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
*as an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
*monotherapy in severe Alzheimer’s - Managing non-cognitive symptoms
- NICE does not recommend antidepressants for mild to moderate depression in patients with dementia
- antipsychotics should only be used for patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress
When is donepezil contraindicated?
is relatively contraindicated in patients with bradycardia
adverse effects include insomnia
What are the risk factors for alzheimer’s disease?
- increasing age
- family history of Alzheimer’s disease
5% of cases are inherited as an autosomal dominant trait
mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form - apoprotein E allele E4 - encodes a cholesterol transport protein
- Caucasian ethnicity
- Down’s syndrome
What are the pathological changes in alzheimer’s disease?
Pathological changes
1. macroscopic:
- widespread cerebral atrophy, particularly involving the cortex and hippocampus
2. microscopic:
- cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
- hyperphosphorylation of the tau protein has been linked to AD
3. biochemical
- there is a deficit of acetylcholine from damage to an ascending forebrain projection
Neurofibrillary tangles
- paired helical filaments are partly made from a protein called tau
tau is a protein that interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules
- in AD are tau proteins are excessively phosphorylated, impairing its function
What is needed for a normal gait and how can impairment lead to falls?
Normal gait involves:
- The neurological system - basal ganglia and cortical basal ganglia loop.
- The musculoskeletal system (which must have appropriate tone and strength).
- Effective processing of the senses such as sight, sound, and sensation (fine touch and proprioception).
As individuals get older they are more likely to experience medical problems affecting these systems, which leads to gait abnormalities and increases the risk of falls.
What are the risk factors for falling?
Falls often occur due to a range of factors and individuals who have fallen previously are at a significantly higher risk of falling again. Other risk factors include:
- Lower limb muscle weakness
- Vision problems
- Balance/gait disturbances (diabetes, rheumatoid arthritis and parkinson’s disease etc)
- Polypharmacy (4+ medications)
- Incontinence
- >65
- Have a fear of falling
- Depression
- Postural hypotension
- Arthritis in lower limbs
- Psychoactive drugs
- Cognitive impairment
Some studies have shown that individuals with 4 or more risk factors have up to a 78% chance of falling It is not possible to remove all risk factors but it is important to limit these where possible.
What risk assessment should be made following a fall?
It is important to establish the following from the history:
- Where was the patient when they fell?
- When did they fall?
- Did anyone else see the patient fall? (collateral history)
- What happened? Were there any associated features before/during/after
- Why do they think they fell?
- Have they fallen before?
- Systems review
- Past medical history (especially issues related to balance/sight/gait)
- Social history
Which medications can cause postural hypotension?
Nitrates
Diuretics
Anticholinergic medications
Antidepressants
Beta-blockers
L-Dopa
Angiotensin-converting enzyme inhibitors - (ACE) inhibitors
