COTE Flashcards
Define delirium
An acute and fluctuating disturbance in consciousness
Describe the key features of delirium
-change in cognition: widespread memory impairment, disorientation, language disturbance, hallucinations
-acute onset/fluctuating: onset over hours or a few days with severity worsening throughout the day
-disturbance of consciousness: decreased ability to focus or sustain attention, distractibility, losing track of conversations
Other: sleep disturbance, emotional disturbance, delusions and restless or listless
What are the two main types of delirium?
Hyperactive: agitation, aggression, psychotic symptoms, oversensitive to stimuli, repeatedly getting out of bed/trying to wander
Hypoactive: lethargic, quiet, few psychotic symptoms, slower speech/not talking (less commonly diagnosed so worse prognosis)
can be mixed
What are the predisposing factors for someone developing delirium?
Old age <65 years old
Cognitive impairment eg dementia
Frailty/multiple comorbidities
Significant injuries eg hip fracture
Surgery
History of (or current) alcohol excess
Sensory impairment eg deaf or blind
Lack of stimulation
Terminal phase of illness
Surgery
Polypharmacy
What are the causes of delirium?
Infection: viral/bacterial eg UTI, pneumonia, biliary infection
Drugs: changes to medication/new medication OR illegal drugs eg in a younger person
Electrolyte/Fluid imbalance: dehydration, hypercalcaemia
Alcohol or drug withdrawal
Organ failure eg cardiac
Endocrine: hypo or hyperthyroid or low/high blood sugars
Epilepsy
Intercranial pathology: have they had recent head trauma?
Pain
CONSTIPATION (in elderly people)
Changes to environment eg home –> hospital, family/carers not around, overstimulation in hospital environment
Give the drug classes and examples of drugs that can cause delirium
Anticholinergics: atropine
Antipsychotics: chlorpromazine, thioridazine
Antidepressants: tricyclics
Opiates: codeine, tramadol
Corticosteroids: prednisolone
Investigations for delirium
Basic obs at bedside: are they in pain, BP, pulse ox, last time BO
Bloods:
-confusion screen= U&Es (dehydration/hypercalc), B12, TFTs, glucose
-FBC
-Coagulation eg intercranial bleed?
CXR- pneumonia?
Mid-stream urine/urinalysis- UTI
Management for delirium
Non-Medical: quiet environment, ensure patient gets enough sleep, presence of family/carers, use of clocks to orient to time, familiar objects, calm manner when dealing with the patients, keep routine as similar as possible
Medical: treat cause if possible eg
-antibiotics: pneumonia or UTI
-plenty of fluids and nutrition to avoid patient becoming dry
-laxatives for constipation
-pain relief if in pain
Drug management for delirium
-only if patient is threatening safety of themselves/others or interfering in medical treatment
-should be used as a last resort
-minimum effective dose
-dose PRN
-short acting benzodiazepines eg lorazepam
Differences between delirium and dementia
Delirium:
-acute/subacute
-often reversible
-fluctuation common throughout the day
-poor attention
-conscious level usually affected but may be subtle
-hallucinations and misinterpretations common
-agitation and aggression common
-disorganised thought and unreal ideas
-motor signs inc tremor or asterixis
-poor short AND long term memory
-dysgraphia
Dementia:
-chronic onset
-rarely reversible
-little diurnal variation
-poor attention in severe dementia
-normal conscious level
-hallucinations in later disease
-agitation and aggression uncommon in early disease
-disorganised thought in later disease
-motor signs only later
-speech normal
-dysgraphia present later
-long term memory often normal till later
Define dementia
Progressive and acquired decline in the memory and cognitive functioning of an alert person with daily life significantly affected
Describe the pathology of Alzheimer’s disease
Pathological changes:
-deposits of beta-amyloid plaques occur outside of neurons. Amyloid precursor protein (APP) helps neurones grown and repair. Normally broken down by alpha secretase and gamma secretase into a soluble peptide. If beta secretase breaks down APP, it creates a monomer called amyloid beta, which is sticky. They can bind together to form the beta amyloid plaques.
-Neurofibrillary tangles made of the protein tau which holds the tubules of the neuron cytoskeleton together. The beta amyloid plaque build up leads to the activation of kinase inside the neuron. This leads to phosphorylation of the tau protein, changing its shape and clumping with other tau proteins.
Neurones with tangles do not function as well and end up apoptosing and the brain begins to atrophy.
What are two most common types of dementia?
Vascular dementia and Alzheimer’s
Describe the symptoms and progression of Alzheimer’s
Insidious onset, with progressive but slow decline.
-poor memory
-language problems
-disorientation
-agitation
-sleep disturbance
-anxiety and depression
-withdrawal/apathy
-motor disturbance
-loss of independence
Early stages begin with profound short term memory loss and issues with high functioning eg finances leasing to later stages of broad cognitive dysfunction and behavioural changes
Describe the investigations and their findings in Alzheimer’s
Physical exam- normal
Neuroimaging- shows no other causes of dementia eg infarct with disproportionate medial temporal lobe atrophy
Cognitive assessment: MMSE assesses different areas of higher cortical functioning
Describe the pathology of vascular dementia
Vascular dementia is a progressive loss of brain function caused by long term poor blood flow to the brain usually because of a series of strokes
Atherosclerosis in arteries to the brain leads to plaques breaking off and blocking smaller arteries or small arteries can get completely blocked with plaque growing inside them
Once blood flow to parts of the brain is stopped, the tissue becomes damaged leading to necrosis and a loss of mental functions governed by that area
Describe the symptoms and progression of vascular dementia
Progression is often a sudden decline in function and appears stepwise, with cognitive impairment patchy vs the uniform impairments of Alzheimer’s
-front lobe symptoms: falls, depression, reduced creativity, impaired judgement
-extrapyramidal symptoms: parkinsonism, restlessness, involuntary muscle contractions
-pseudobulbar features: involuntary outbursts of emotion
-other features mimic Alzheimer’s eg memory issues, language problems etc
-depression and apathy also common symptoms
Urinary incontinence and falls without other explanation are often early features
Describe the investigations and their results in vascular dementia
Physical exam: focal neurology showing hyperreflexia, extensor plantars, abnormal gait
Neuroimaging: multiple large vessel infarcts OR a single critical infarct eg thalamus OR white matter infarcts or periventricular white matter changes OR microvascular disease that may be too fine to be seen on neuroimaging
Describe the general dementia management
General: modify reversible aggravating factors eg constipation, drug side effects, mild anaemia and treat depression with SSRIs. Carers for helping with ADLs, medications etc
Social: encouraging physical and mental activity, creating a safe and caring environment with a predictable routine PLUS respite and support for caregivers/family.
Practical: simple interventions eg alarms & calendars and simplifying medication eg with dosette boxes
Contraindications for starting anti-cholinesterase inhibitors?
QT prolongations, second or third degree heart block in an unpaced patient, sinus bradycardia of <50bpm
May make incontinence worse
Describe the medical management of Alzheimers & Lewy Body dementia
Acetylcholinesterase inhibitors: they work by blocking acetylcholinesterase which breaks down acetylcholine
-mostly useful in Alzheimer’s, Lewy body and Parkinson’s disease dementia as they have the greatest cholinergic deficits- rivastigamine, galantamine, donepezil
Memantine: blocker of NMDA receptors that may reduce glutamate mediated destruction of cholinergic neurons
What are the factors that influence fall frequency?
Intrinsic factors: maintaining balance is complex- requires good muscle strength, stable joints, multiple sensory modalities and a functional peripheral/central nervous system.
Extrinsic factors: environmental factors eg lighting, steps, shoes, floor surface, presence of rails
What are the factors that influence fall severity?
-multiple system impairments leading to less effective saving mechanisms
-osteoporosis and increased facture rates
-secondary injury due to post fall immobility eg bed sores, pneumonia and dehydration
-psychological adverse effects eg loss of confidence
List some possible causes of falls
cardiovascular: arrhythmias, orthostatic hypotension, bradycardia, valvular heart disease
Neurological: stroke, peripheral neuropathy
GU: UTI, incontinence
Endocrine: hypoglycaemia
MSK: arthritis, disuse atrophy
ENT: benign paroxysmal positional vertigo, ear wax
Polypharmacy
What drugs are associated with falls?
Drugs can be either directly psychoactive or may lead to systemic hypotension and cerebral hypoperfusion —>
-benzodiazepines
-antidepressants eg SSRIs
-Opiates
-diuretics
-anti HTN esp ACE-i and alpha blockers
-antiarrhythmics
-hypoglycaemics
Describe the investigations for falls
Bedside: vital signs
BP lying and standing: orthostatic hypotension
Urine dipstick: infection & rhabdomyolysis
ECG: bradycardia and arrhythmias
Cognitive screening eg AMT: cognitive impairment
Blood glucose: hypoglycaemia
FBC: anaemia/ raised WBC
U&Es: dehydration and electrolyte abnormalities eg hypocalc
LFT: alcohol use
Bone profile: calcium abnormalities
CXR: pneumonia
CT head: chronic or acute subdural, stroke
Echo: valvular heart disease
How is fall frequency reduced?
-Drug review
-Treatment of orthostatic hypotension
-Strength and balance training
-Walking aids
-Environmental assessment and modification eg by OT
-Vision
What is orthostatic hypotension?
When someone experiences a drop in BP of >20mmHg systolic or 10mmHg diastolic when going from lying/sitting to standing
What are the causes of orthostatic hypotension?
Drugs: vasodilators, diuretics, B blockers, CCB, opiates
Chronic hypertension
Volume depletion eg dehydration or haemorrhage
Sepsis leading to vasodilation
Autonomic failure eg diabetes, Parkinson’s, dementia
Prolonged bed rest
Adrenal insufficiency
Raised intrathoracic pressure
What is the first line investigation into orthostatic hypotension?
Posture Test
BP should be measure on sitting/lying and after standing for 3 minutes.
Multiple BP measurements should be taken
If the HR doesn’t raise as much as expected eg <15pbm cause of the hypotension is probably neurogenic eg peripheral neuropathy
What is the treatment for orthostatic hypotension?
-treat the cause eg changing/reducing drugs
-reduce consequences of falls eg pendant alarms
-modify behaviour eg getting up slowly, reduce dehydration
-consider starting drugs eg fludrocortisone to raise BP or desmopressin
What is syncope?
Sudden, transient loss of consciousness due to a reduced cerebral perfusion
What is presyncope?
A feeling of light-headedness that would lead to syncope if corrective measures were not taken
What are the causes of syncope?
Peripheral factors: eg orthostatic hypotension, low circulating volume eg dehydration
Vasovagal syncope: common in young and old people. Vagal stimulation eg pain, fright, emotion leads to hypotension. Prodrome eg pale, clammy and light headed followed by nausea and abdo pain and then syncope
Carotid sinus syndrome
Pump problem: myocardial infarction or ischaemia/arrhythmia
Outflow obstruction eg aortic stenosis
Pulmonary embolism
What are the investigations for syncope?
Bloods: check for anaemia, sepsis, kidney function
ECG: look at PR interval, QT interval, ischaemic changes, LVH
Holter monitor: if arrhythmias suspected
Lying and standing BP
Define Parkinson’s Disease
A neurodegenerative disorder characterised by loss of dopaminergic neurones within the substantia nigra pars compacta of the basal ganglia. There may also be Lewy Body formation in the substantia nigra as well.
What is the pathophysiology of Parkinson’s?
There is a progressive reduction of dopamine in the basal ganglia of the brain which leads to disorders of movement.
What are the motor signs and symptoms of Parkinson’s?
Bradykinesia: slowness in initiation of voluntary movement. Increased repetitive actions
OR hypokinesia: reduced facial expression/arm swing and difficulty with fine movements eg buttoning clothes and opening jars
-cogwheel rigidity
-rest tremor which improves on sleeping/moving/increased concentration
-balance problems
Describe some of the non-motor signs and symptoms of Parkinson’s?
-depression/anxiety/fatigue
-reduced sense of smell
-cognitive impairment
-sleep disturbance
-constipation
How is Parkinson’s diagnosed?
PD is mainly a clinical diagnosis –> should be suspected in patients with tremor, rigidity, postural instability and bradykinesia
What is the management of PD?
A dopamine agonist eg levodopa
OR a monoamine oxidase-B inhibitor eg rasagiline
PLUS physical and non-pharmacological therapies
Define osteoporosis
A bone disease characterised by low bone mass and structural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture. It is normally asymptomatic until a fragility fracture occurs. Older people who have had a fragility fracture almost certainly have osteoporosis
What is an osteoporotic fracture?
A fragility fracture occurring as a consequence of osteoporosis. Fractures usually occur in the wrist, spine and hip- can occur in ribs/pelvis
What is a fragility fracture?
A fractures following a fall from standing height or less as a result of routine activities eg bending or lifting
What are the risk factors for osteoporosis?
SHATTTERED
Steroid use
Hyperthyroidism, hyperparathyroidism
Alcohol use
Thin BMI <18.5
Testosterone decrease
Early menopause
Renal or live failure
Erosive/inflammatory bone disease eg rheumatoid arthritis
Dietary eg reduced Ca, malabsorption, DM
What are the investigations for osteoporosis?
Blood tests: normal (unless after a fracture)
DEXA scan- usually used in younger people and rarely used in older population
Secondary causes:
TSH for all
Testosterone levels in men
What is a DEXA scan and what scores does it produce?
Measures bone mineral density (BMD) by measuring how much radiation is absorbed by the bones. Reading at hip is key.
Two scores:
Z score - represents the number of standard deviations the patient’s bone density falls below the mean for their age
T score - represent the number of standard deviations below the mean for a healthy young adult their bone density is
What is the pathophysiology for osteoporosis?
The activity of osteoclasts increases and is not matched by the osteoblasts so bone mass decreases.
Glucocorticoids increase bone turnover
Oestrogen is protective
How is osteoporosis managed?
Not steroid induced : bisphosphonate eg alendronic acid or IV zol, calcium and vitamin D supplementation
Steroid induced: stop steroids, bisphosphonate and calcium/vitamin D supplementation
What is an advance decision?
It is a decision patients make when they still have capacity to refuse a specific type of treatment in the future. If it is binding, it takes precedence over decisions made in your best interest by other people.
What conditions need to be fulfilled to make an advance decision legally binding?
-written down
-signed by the patient
-signed by a witness
-patient needs to have capacity
-over 18
-circumstances in which the patient wishes to refuse treatment are explained clearly
-it must be the patient’s own decision and not made under duress
What can be included in an advance decision?
Life sustaining treatments can be refused however cannot refuse basic care eg washing or food or drink, cannot demand specific treatments or for something that is illegal or the refusal to treat a mental health condition
What is an advance statement?
A written statement that sets down our preferences, wishes, beliefs and values regarding your future care. It is not legally binding but carers should take it into account when looking after you
What does an advance statement include?
-how religious and spiritual beliefs should be reflected in your care
-where you would like to be cared for eg at home, hospital, hospice, care home
-how you like to do things eg shower vs bath, how you like to sleep and what you like to eat
-practical issues eg care of pets if you become ill
What is the Mental Capacity Act?
Legislation that protects people who lack capacity and allows them to make decisions about their care
What does the MCA say?
-assume someone has capacity unless proven otherwise
-wherever possible, help people make their own decisions
-someone does not lack capacity because they make an unwise decision
-decisions for someone without capacity must always be in their best interests
-treatment and care should always be least restrictive of their basic rights and freedom
How to decide if something is in someone’s best interests
-encourage participation
-identify all relevant circumstances: identify what that person would take into account when making a decision
-find out the person’s views/beliefs/wishes and values if possible
-avoid discrimination: do not make assumptions on basis of age, appearance, condition or behaviour
-assess whether the person may regain capacity, and if they might, whether the decision can be postponed
What is a DNACPR?
If a patient’s heart stops working, the healthcare team would not try to restart it. The decision is made by the patient and/or the doctor
Define stroke
Sudden onset of focal neurological deficit lasting more than 24hrs or leading to death caused by vascular problems
What are the two types of stroke?
Infarction: a clot caused by atherosclerosis blocking blood flow in a blood vessel or low flow of blood to the brain
Haemorrhage: bleed in the brain (spontaneous and not associated with trauma)
What are the symptoms of an anterior cerebral artery stroke?
contralateral hemiparesis and sensory loss with lower limbs>upper limbs
What are the symptoms of a middle cerebral artery stroke?
contralateral hemiparesis and sensory loss with upper limbs>lower limbs
homonymous hemianopia
aphasia
What are the symptoms of a posterior cerebral artery stroke?
Contralateral homonymous hemianopia with macular sparing
Contralateral loss of pain and temperature due to spinothalamic damage
What are the symptoms of a vertebrobasilar artery stroke?
Cerebellar signs
Reduced consciousness
Quadriplegia or hemiplegia
What are the symptoms of a midbrain infarct (Weber’s syndrome)?
Oculomotor palsy
Contralateral hemiplegia
What are the symptoms of a posterior inferior cerebellar artery occlusion
Ipsilateral facial loss of pain and temperature
Ipsilateral Horner’s syndrome –> miosis, ptosis and anhidrosis
Ipsilateral cerebellar signs
Contralateral loss of pain and temperature
What is a total anterior circulation stroke?
Affected blood vessel is anterior middle or cerebral artery and has the three following symptoms:
-Hemiplegia
-Homonymous hemianopia
-Higher cortical dysfunction eg dysphasia
What us a partial anterior circulation stroke?
Anterior or middle cerebral artery affected and two of:
-hemiplegia
-homonymous hemianopia
-higher cortical dysfunction eg dysphasia
What investigations should you do if you suspect stroke?
First line head imaging: non-contrast CT head
ECG: check for AF
Bloods: rule out hypoglycaemia and hyponatraemia, do blood clotting, lipids and Hba1c
CT angiogram: identifies arterial occlusion
What investigations should you do if you suspect stroke?
First line head imaging: non-contrast CT head
ECG: check for AF
Bloods: rule out hypoglycaemia and hyponatraemia, do blood clotting, lipids and Hba1c
CT angiogram: identifies arterial occlusion
How should an ischaemic stroke be managed?
Antiplatelets: 300mg aspirin immediately
BP: should not be lowered acutely as will affect reperfusion of brain
Thrombolysis: alteplase (tissue plasminogen activator) given <4.5hours of symptom onset and haemorrhage MUST be excluded
Thrombectomy: must score >5 on NIH stroke scale
Anticoagulation: if AF is the cause, anti-coag should be started 14 days post stroke
How should a haemorrhagic stroke be managed?
Admit to neurocritical care
IV mannitol to reduce raised intercranial pressure
Surgical intervention@ decompression may be needed
What is the prevention after an ischaemic stroke?
Clopidogrel (antiplatelet therapy)
High intensity statin therapy
Anti HTN eg CCB or ACE-i or thiazide diuretic
Antiplatelet eg people with AF
Exercise, quit smoking, control diabetes, reduce drinking, lose weight
What does constipation mean?
Either of the following:
-time between bowel evacuations is longer than normal
-the stool is harder than normal
-the total faecal mass present in the abdomen is increased
What are the 3 types of constipation?
-hard faeces present in the rectum
-the whole distal large bowel loaded with soft putty like faeces
-high impaction due to obstructing pathology
What are the causes of constipation?
-reduced motility of the bowel: due to drugs (opiates, antidepressants, antipsychotics, CCB), immobility, dehydration, hypothyroidism, hypercalcaemia
-failure to fully evacuate bowels: painful rectum, difficult access to toilet, lack of privacy, altered daily routine
-neuromuscular: Parkinson’s
-mechanical obstruction of bowel: diverticular disease, carcinoma of colon
What is the treatment of constipation?
Stimulant laxatives eg senna/bisacodyl as tablets or as suppositories
Stool softening (osmotic) laxatives eg lactulose or macrogol
What are pressure sores?
Areas of skin necrosis due to pressure induced ischaemia found on sacrum, heels, over greater trochanters, shoulders etc
What is the grading system for pressure sores?
0: skin hyperaemia
1: non-blanching erythema
2: broken skin or blistering
3: ulcer down to subcutaneous fat
4: ulcer down to bone, joint or tendon
How are pressure sores managed?
Prevention: assess patient risk of developing sores and regular assess
Turning & handling: regularly turning patients, encourage early mobilisation, avoid friction by using correct manual handling devices
Pressure relieving devices: appropriate mattresses
Healing environment: nutrition, manage incontinence, good glycaemic control in people with diabetes
Debridement: dead tissue should be removed
Dressings
Antibiotics
What are the age related causes of urinary incontinence?
-diminished total bladder capacity
-diminished bladder contractile function
-increased frequency of uninhibited bladder contractions
-reduced ability to postpone voiding
-atrophy of vagina and urethra in females
-loss of pelvic floor and urethral sphincter musculature
-hypertrophy of the prostate in males
What is benign paroxysmal positional vertigo?
The most common cause of vertigo. It is an inner ear disorder where there is rapid onset vertigo with certain head movements
Describe the pathology of BPPV?
Otoconia (bio-crystals present in the vestibular system and involved in balance) are displaced from the macula and become trapped in the posterior canal. They stimulate hair follicles even when the head is still leading to a sensation of vertigo.
What are the causes of BBPV?
Head injury
Vestibular neuronitis (viral illness)
Labrynthititis (age related)
Complications of mastoid surgery
What are the risk factors for BBPV?
Age: 40-60yo
Women
Meniere’s diseae
Patient’s with migraines/anxiety disorders
What are the signs and symptoms of BBPV?
-brief episodes of vertigo lasting 30secs-1min
-symptoms provoked by head movements eg bending forward or rolling over in bed
-nausea
-imbalance —> can cause falls, esp relevant in geriatrics
What is the gold standard investigation for BPPV?
Dix-Hallpike Test
A positive test will show:
-onset of nystagmus after 5-20 seconds
-vertigo
-rotatory and vertical nystagmus
BPPV is normally unilateral so will often be in one eye
What is the conservative management for BPPV and why?
BPPV is often self limiting and symptoms may subside after 6 months –> avoid positions that bring on vertigo and inform patients that symptoms recur in 36% of patients
What is the medical management for BPPV?
Vestibular rehabilitation
Epley manoeuvre: return the otoconial particles back into the utricle from the posterior canal
Anti-emetics: prochlorperazine or cyclizine
vestibular sedatives: cinnarizine
Surgical management: denervate the posterior semi circular canal
Define heart failure
A clinical syndrome involving reduced cardiac output because of impaired cardiac contraction
What is congestive heart failure?
A combination if left and right sided ventricular failure
What are the risk factors for HF?
-previous myocardial infarction
-male
-age
-IHD
-HTN
-diabetes
-valvular heart disease
-renal failure
-AF
What is systolic HF?
The heart can’t pump hard enough during systole and so can’t meet the body’s metabolic demands (there’s a low stroke volume eg the amount of blood being ejected from the heart)
What is diastolic HF?
The heart can’t fill with enough blood during diastole. (there’s a low total volume of blood in the heart which leads to a low stroke volume and low ejection volume)
What is the common cause of left sided HF?
LSHF is normally caused by systolic (pumping) dysfunction where the heart can’t pump out enough blood
How does HTN cause (systolic) left sided HF?
It becomes difficult for the LV to pump blood out into the hypertensive system, meaning the LV has to work harder. This leads to LV hypertrophy. Hypertrophy has a higher O2 demand and squeezes the coronary arteries so supply is reduced. This leads to weaker contractions.
How does HTN cause (diastolic) left sided HF?
Long standing HTN leads to hypertrophy which leads to the ventricle wall crowding into the LV, which means less room for filling.
What causes the fluid retention in HF?
When the heart pumps out less blood, there is decreased blood flow to the kidneys. The RAAS is activated leading to fluid retention which fills the heart a bit more during diastole. More fluid in the blood vessels means more fluid leaking into the tissues.
What causes the pulmonary oedema in HF?
Blood starts to back up into the lungs due to the heart not being able to pump enough blood into the body. A back up of blood in the pulmonary veins and capillary beds leads to an increase in pressure in the PA and lead to fluid moving from the blood vessels into the alveoli.
What causes the dyspnoea in HF?
Extra fluid in the alveoli means it takes longer for the O2 and CO2 exchange
Why does LSHF cause RSHF?
It causes an increased pressure in the pulmonary artery which makes it harder for the right ventricle to pump blood to the lungs.
How does chronic lung disease lead to RSHF?
Chronic lung disease leads to hypoxia in the lungs, making the pulmonary arterioles constrict. This raises the pulmonary blood pressure leading to right sided hypertrophy and failure. (cor pulmonale)
What causes the symptoms of RSHF?
In LSHF, blood gets backed up to the lungs but in RSHF blood gets backed up to the body. This means patients have congestion in the veins of the systemic circulation –> eg jugular venous distension, hepatosplenomegaly, ascites and pitting oedema in the legs.
What are the signs & symptoms of LSHF?
Signs: tachypnoea and tachycardia, cool peripheries, peripheral/central cyanosis, displaced apex beat, crackles on auscultation, third heart sound
Symptoms: dyspnoea (esp exertional), orthopnoea, fatigue and weakness, cough w/ pink frothy sputum
What are the signs & symptoms of RSHF?
Signs: raised JVP, peripheral pitting oedema, hepatosplenomegaly, ascites
Symptoms: fatigue and weakness, swelling in the legs, distended abdomen
What are the investigations for HF?
NT-proBNP: increased in chronic heart failure
ECG: broad QRS complexes
CXR:
-A= alveolar oedma
-B= Kerley B lines
-C= cardiomegaly
-D= dilated upper lobe vessels
-E= pleural effusion
What is the management for HF?
1st Line:
-beta blocker eg bisoprolol
-ACEi eg ramipril
(ARB eg losartan if ACEi not tolerated)
2nd Line:
-Aldosterone antagonist eg spironolactone
Define AKI
An acute drop in kidney function, diagnosed by measuring serum creatinine.
NICE criteria for AKI?
- Rise in creatinine of 25mm/L or more in 48 hours
- Rise in creatinine of 50 or more in 7 days
- urine output of <0.5ml/kg/hour for 6 hours
RF for AKI?
Age
Underlying kidney disease
Diabetes
Sepsis
Contrast
HF
Nephrotoxins eg NSAIDs, ACEi, cancer therapies, vancomycin, aminoglycosides.
Pre-renal causes of AKI
Heart failure
Hypotension
Dehydration
It is due to inadequate blood supply to the kidneys reducing the filtration of the blood
Renal causes of AKI?
Intrinsic disease of the kidneys
Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis
Post-renal causes of AKI?
Caused by obstruction to the outflow of urine form the kidney, causing back pressure into the kidney (obstructive uropathy)
kidney stones
masses eg cancer
ureter/uretral strictures
enlarged prostate or prostate cancer
Investigations for AKI?
Urinalysis: urine dipstick for leucocytes +/- nitrites (UTI), haematuria + leucocytes (glomerulonephritis)
Blood tests: U&Es particularly creatinine & K+ (hyperkalaemia is a common complication of AKI)
AKI staging? (inc. SCr and urine output)
Serum Cr:
see online diagrams.
Management of AKI?
Treat underlying cause.
Fluid rehydration with IV fluids
Stop nephrotoxins and avoid contrast
Relieve obstructions
Specialist renal input
Complications of AKI?
Hyperkalaemia
Fluid overload/HF/pulmonary oedema
Metabolic acidosis
Uraemia can lead to encephalopathy or pericarditis
Define TIA
A transient episode of neurological dysfunction caused by a focal brain, spinal cord or retinal ischaemia without acute infarction. Sudden onset with symptoms generally resolving within an hour
Management of TIA?
Start 300mg aspirin daily & secondary prevention measures for cardiovascular disease. Should be referred and seen within 24 hours by a stroke specialist
Describe specific features of frontotemporal dementia
Personality change & behavioural disturbance eg apathy, social/sexual disinhibition
Other cognitive functions may be relatively well preserved
Progressive self neglect and abandonment of work, activities and social contacts
Describe arterial ulcers?
Typically toes/shins/pressure points
Painful even without infection
Red, yellow or black sores
Deep wound
Tight and hairless skin
Affected area is cool to touch from minimal blood circulation
Leg reddens when dangling and turns pale when elevated
Mx is surgical
Describe venous ulcers?
Medial/lateral malleoli
Painless even in the presence of infection
Discharge
Inflammation
Swelling
Itchy/hardened skin
Scabbing or flaking
Brown/black stained skin
Mx: compression therapy
How is frontotemporal dementia classified?
Behaviour variant (previously Pick’s Disease due to association with Tau protein aggregations called Pick bodies)
Primary progressive apahasia:
- nonfluent variant
-semantic variant