Exam revision Flashcards
What is a TIA?
TIA is defined as transient neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without evidence of acute infarction. It is a medical emergency
What is is risk of a patient developing stroke following a TIA?
within the first week following a TIA, the risk of stroke is up to 10%. The estimated incidence of TIA within the UK is 50 per 100,000 people per year.
What is the diagnostic criteria for TIA?
Traditionally, transient neurological dysfunction with resolution within 24 hours was diagnostic of TIA. However, up to a third of patients whose symptoms have resolved within 24 hours have evidence of infarction on imaging. Consequently, the definition is now ‘tissue-based’ rather than ‘time-based’ with the incoporation of the phrase ‘without evidence of acute infarction’. Thus, the end-point is biological tissue damage, not an arbitrary time cut-off.
What is the aetiology of TIA?
TIA is caused by temporary blockage to blood flow, which leads to ischaemia.
Ischaemia refers to the absence of blood flow to an organ, which deprives it of oxygen. Cerebral ischaemia may be due to in situ thrombosis, emboli, or rarely, dissection.
Thrombosis: local blockage of a vessel due to atherosclerosis. Precipitated by cardiovascular risk factors (e.g. hypertension, smoking) or small vessel disease (e.g. vasculitis, sickle cell). Listen for bruits
Emboli: propagation of a blood clot that leads to acute obstruction and ischaemia. Typically due to atrial fibrillation or carotid artery disease. valve disease prosthetic valves
Dissection: a rare cause of cerebral ischaemia from tearing of the intimal layer of an artery (typically carotid). This leads to an intramural haematoma that compromises cerebral blood flow. May be spontaneous or secondary to trauma.
Hyperviscosity-polycythemia,sickle cell,myeloma
Vasculitis-SLE,PAN,syphilis
During a TIA, there is a transient reduction in blood flow to an area of cerebral tissue that causes neurological symptoms. TIA commonly occurs secondary to embolisation from atrial fibrillation or carotid artery disease.
What are the risk factors for TIA?
TIA is a cardiovascular disease, and as such, it shares many common risk factors with conditions such as ischaemic heart disease and peripheral vascular disease.
Smoking Diabetes mellitus Hypertension Hypercholesterolaemia Obesity Atrial fibrillation Carotid artery disease Age Thrombophilic disorders (e.g. antiphospholipid syndrome) Sickle cell disease Family history
How does TIA present?
A TIA presents with sudden, focal neurological deficit that reflects the area of the brain devoid of blood flow.
A variety of neurological deficits can present in TIA, but the majority of symptoms will resolve within 1-2 hours.
Neurological deficit
Unilateral weakness or sensory loss
Dysphasia
Ataxia, vertigo, or incoordination
Amaurosis fugax: see below
Homonymous hemianopia: visual field loss on the same side of both eyes
Cranial nerve defects: particularly if associated with contralateral sensory/motor deficits
What are the differentials for amaurosis fugax
Amaurosis fugax
This is a classical syndrome of short-lived monocular blindness, which is often described as a black curtain coming across the vision. It is a term usually reserved for transient visual loss of ischaemic origin.
The principle cause of amaurosis fugax is transient obstruction of the ophthalmic artery, which is a branch of the internal carotid artery. However, other ischaemic causes to consider include giant cell arteritis (i.e. temporal arteritis) and central retinal artery occlusion. An important differential of transient visual loss, particularly in young patients, is migraine.
How can TIA be diagnosed?
Diagnosis
Any patient with ongoing symptoms requires urgent referral to a stroke unit.
TIA is a clinical diagnosis based on the history as the majority of patients will have complete resolution of symptoms. Any patient with ongoing symptoms needs to be treated as an acute stroke and urgently referred to a stroke unit.
Key aspects to making the diagnosis of TIA include:
Onset & duration of symptoms: collateral history may be needed
Associated symptoms (suggest alternative diagnosis): headache, vomiting, syncope, seizures
Neurological deficit: see clinical features
Cardiovascular risk factors: hypertension, diabetes, smoking, high cholesterol, family history
Co-morbidities: heart disease, atrial fibrillation, carotid disease, previous stroke/TIA
Anticoagulation history
Clinical examination: cardiovascular exam including BP, neurological examination, fundoscopy
NOTE: patients on anticoagulation with new neurological deficits require urgent admission and exclusion of intracerebral bleeding
The Face Arm Speech Time Test (FAST test)
A rapid diagnostic screen to assess for features of TIA/stroke used in the community. Anyone with a positive screen should be assessed urgently at a stroke unit. The test is positive if any of the following are met:
New facial weakness
New arm weakness
New speech difficulty
What are the differentials for TIA and
Numerous conditions can present similarly to TIA, which are collectively referred to as ‘stroke mimics’.
Toxic/metabolic: hypoglycaemia, drug and alcohol consumption
Neurological: seizure, migraine, Bell’s palsy
Space occupying lesion: tumour, haematoma
Infection: meningitis/encephalitis, systemic infection with ‘decompensation’ of old stroke
Syncope: extremely uncommon presentation of TIA, consider causes of syncope
When would you refer patient with TIA?
All patients with a suspected TIA should be referred to a specialist TIA clinic and be seen within 24 hours.
At the TIA clinic, patients should have a comprehensive medical assessment including blood tests, electrocardiogram (ECG) and imaging. If the episode occurred > 1 week ago, the assessment should be within 7 days.
The ABCD2 is a prognostic score that was traditionally used to identify people at high risk of stroke after a TIA score. It was originally used to triage the urgency of TIA referrals and treatment with aspirin. NICE no longer recommend its use.
What investigations are done for TIA?
Investigations
MRI is the key investigation in a patient with suspected TIA.
Bloods
Haematology: full blood count (FBC), HbA1c +/- haemoglobin electrophoresis
Routine biochemistry: Urea & electrolytes (U&Es), bone profile, liver function tests (LFTs), lipid profile
Coagulation: routine clotting
Special (as indicated): ‘young stroke screen’ (e.g. thrombophilia screen, Fabry’s)
Cardiac investigations
ECG: assessment for arrhythmias, especially atrial fibrillation
Echo: not routinely offered unless suspicion of heart disease or confirmed stroke
Imaging
MRI head with diffusion-weighted imaging (DWI): preferred to CT unless alternative diagnosis suspected that CT could detect. Enables detection of small infarcts.
Carotid dopplers: all patients who are candidates for carotid endarterectomy.
When is urgent admission warranted?
Certain features warrant urgent admission to hospital because of the high risk of stroke, bleeding or deterioration.
≥1 suspected TIA (crescendo TIA): typically within the last 7 days
Suspected cardioembolic source or severe carotid stenosis
Vulnerable patient: lack of reliable observer at home to monitor for worsening symptoms
Bleeding disorder or taking an anticoagulant
Any patient with ongoing symptoms needs to be treated as an acute stroke and urgently referred to a stroke unit.
ABCD2 SCORE 4 HIGH RISK,greater than 6 very high risk
How can TIA be managed?
Management
Any patient with a suspected TIA should be treated with 300 mg of aspirin unless contraindicated.
The management of TIA can be divided into acute treatment, secondary prevention and lifestyle measures.
Acute treatment
The principle management for TIA is 300 mg of aspirin that is usually continued for two weeks. This is followed by treatment with 75 mg of clopidogrel as long-term vascular prevention.
Patients with atrial fibrillation or significant carotid artery disease require a different treatment pathway.
Atrial fibrillation (AF): should be offered and counselled about starting an oral anticoagulant
Carotid artery disease (CAD): urgent referral for consideration of carotid endarterectomy if significant disease. Based on NASCET or ECST criteria for stenosis.
NASCET: 50-99% stenosis
ECST: 70-99% stenosis
Secondary prevention
Patients with a TIA should be offered secondary prevention treatments to optimise their cardiovascular risk
Anti-hypertensives: as per hypertension guidelines (tolerate higher if significant bilateral CAD)
Lipid modification: offer high-dose statin therapy unless contraindication.
Diabetic control: treat any new diagnosis of diabetes and optimise control of pre-existing disease
Obstructive sleep apnoea: referral to specialist sleep medicine/respiratory clinic if suspected
Pre-menopause: use of combined oral contraceptive pill contraindicated.
Lifestyle measures
Basic advice on physical activity, smoking cessation, diet optimisation and alcohol intake should be given to all patients
What is recommended for driving with TIA?
Driving
It is vital to advise all patients to stop driving if they have had a suspected, or confirmed, TIA.
Patients should always be advised to check the DVLA for the most up to date recommendations on driving.
Cars and motorcycles: stop driving one month, do not need to inform DVLA Larger vehicles (e.g. buses, lorries): stop driving, inform the DVLA
When should aspirin not be given?
Immediate antithrombotic therapy:
give aspirin 300 mg immediately, unless
1. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage)
2. the patient is already taking low-dose aspirin regularly: continue the current dose of aspirin until reviewed by a specialist
3. Aspirin is contraindicated: discuss management urgently with the specialist team
When should carotid endarterectomy be done in TIA?
With regards to carotid artery endarterectomy:
recommend if patient has suffered stroke or TIA in the carotid territory and are not severely disabled
should only be considered if carotid stenosis > 70% according ECST* criteria or > 50% according to NASCET** criteria
within 2 weeks
What is aspirin is contraindicated?
aspirin 75mg od with dipyridamole
What are the most common sites of crescendo attacks?
critical intracranial stenosis-superior division of MCA
What are the stroke mimics?
Differential diagnosis
M8S:
Migraine
Sugar: hypoglycaemia.
Seizures, especially Todd’s palsy.
Sepsis, encephalitis.
Syncope
SDH
Space occupying lesion.
OldStrokes with intercurrent illness.
Somatisation
Where is asbestos found?and how can it affect the lung?
Asbestos widely used to construct ceiling, walls and flooring of houses/ buildings
Provide insulation and fire protection
Latency period
Several years before pleural thickening develops
>20 years for fibrosis & plaque
Asbestos is a fibre-like material that was once used in buildings for insulation, flooring and roofing. Its use has been fully banned in the UK since 1999.
While asbestos can be dangerous, it’s not harmful if left alone. But if material containing asbestos is damaged, it can release a fine dust that contains asbestos fibres.
When the dust is breathed in, the asbestos fibres enter the lungs and can gradually damage them over time.
What are the different lung presentations of asbestos?
Asbestos can cause a variety of lung disease from benign pleural plaques to mesothelioma.
Pleural plaques
Pleural plaques are benign and do not undergo malignant change. They, therefore don’t require any follow-up. They are the most common form of asbestos-related lung disease and generally occur after a latent period of 20-40 years.
Pleural thickening
Asbestos exposure may cause diffuse pleural thickening in a similar pattern to that seen following an empyema or haemothorax. The underlying pathophysiology is not fully understood.
Asbestosis
The severity of asbestosis is related to the length of exposure. This is in contrast to mesothelioma where even very limited exposure can cause disease. The latent period is typically 15-30 years. Asbestosis typically causes lower lobe fibrosis. As with other forms of lung fibrosis the most common symptoms are shortness-of-breath and reduced exercise tolerance.
Mesothelioma
Mesothelioma is a malignant disease of the pleura. Crocidolite (blue) asbestos is the most dangerous form.
Possible features
progressive shortness-of-breath
chest pain
pleural effusion
Patients are usually offered palliative chemotherapy and there is also a limited role for surgery and radiotherapy. Unfortunately the prognosis is very poor, with a median survival from diagnosis of 8-14 months.
Lung cancer
Asbestos exposure is a risk factor for lung cancer and also has a synergistic effect with cigarette smoke.
What is asbestosis?
Asbestosis is a diffuse interstitial lung fibrosis that manifests in patients with pleural plaque disease ≥10 years following exposure to asbestos.
What are the CXR findings for asbestosis?
Takes >10 years for radiographic changes to develop
Small, irregular, oval opacities
Diffuse interstitial fibrosis
“Shaggy heart border” sign
Cardiac silhouette ill-defined on chest radiograph
Implies pleural disease on mediastinal interface
How can asbestosis be diagnosed?symptoms,signs,examination and investigation findings?
History of asbestos exposure, typically 20 or more years prior
Symptoms: dyspnoea, cough
Signs: crepitations on auscultation, finger clubbing, cyanosis, reduced chest expansion
Chest x-ray: linear interstitial fibrosis, pleural plaques, pleural thickening, atelectasis
Pulmonary function tests: may be normal or show a restrictive pattern (reduced forced vital capacity (FVC) and total lung capacity (TLC) with a normal FEV1/FVC ratio) or obstructive pattern (reduced FEV1).
High resolution CT: pleural thickening, pleural plaques
Bronchoscopy + biopsy: limited use as normally cannot sample enough tissue for a diagnosis
Open lung biopsy: for definitive diagnosis if cancer is suspected
How can asbestosis be managed?
Management
Smoking cessation Pulmonary rehabilitation Bronchodilators Oxygen therapy if SpO2 ≤89% Lung transplant If a death occurs due to asbestosis, this must be reported to the coroner Compensation
see a GP to have the flu vaccination and the pneumococcal vaccination – your lungs will be more vulnerable to infections like flu and pneumonia
How to get compensation?
Patients who develop asbestos related lung disease following occupational exposure may be eligible to claim compensation
If you’ve been diagnosed with asbestosis, you may be able to claim compensation through:
industrial injuries disablement benefit
a civil claim for compensation against previous employers
a claim for governmental compensation under the Pneumoconiosis etc. (Workers’ Compensation) Act 1979
Find out about industrial injuries disablement benefit on GOV.UK. You can also get advice on benefits and compensation on the British Lung Foundation website.
Support for people with asbestosis
Asbestosis can have a big impact on your life, but help is available. Support services include:
Asbestos Victims Support Groups Forum
British Lung Foundation – helpline 03000 030 555
Cancer Research UK: mesothelioma – helpline 0808 800 4040
Mesothelioma UK – helpline 0800 169 2409
What are the complications of asbestosis?
People with asbestosis also have a higher risk of developing other serious conditions, such as:
pleural disease – thickening of the lining covering the lungs (pleura)
mesothelioma – cancer that affects the lining of the lungs, tummy, heart or testicles
lung cancer
What are the different types of gall stones?
Bile is formed from cholesterol, phospholipids, and bile pigments (products of haemoglobin metabolism). It is stored in the gallbladder, before passing into the duodenum upon gallbladder stimulation.
Gallstones form as a result of supersaturation of the bile. There are three main types of gallstones:
Cholesterol stones – composed purely of cholesterol, from excess cholesterol production
There is a well recognised link between poor diet, obesity, and cholesterol stones
Pigment stones – composed purely of bile pigments, from excess bile pigments production
Commonly seen in those with known haemolytic anaemia
Mixed stones – comprised of both cholesterol and bile pigments
What are the risk factors for gall stones?
Classically the common risk factors for gallstone disease are colloquially described as the “5 F’s”: Fat, Female, Fertile, Forty, and Family history.
Other recognised risk factors include pregnancy and oral contraceptives*, haemolytic anaemia (specifically for pigment stones), and malabsorption (such as previous ileal resection or Crohn’s disease).
*Oestrogen causes more cholesterol to be secreted into bile
How to differentiate biliary colic and acute cholecystitis?
Biliary Colic
Biliary colic occurs when the gallbladder neck becomes impacted by a gallstone. There is no inflammatory response, yet the contraction of the gallbladder against the occluded neck will result in pain.
The pain is typically sudden, dull, and colicky in nature. It is often focused in the right upper quadrant although it may radiate to the epigastrium and/or back. The pain may be precipitated by the consumption of fatty foods* and the patient often complains of nausea / vomiting. In general, once pain relief has been started, symptoms often settle quickly.
*Fatty acids stimulate the duodenum endocrine cells to release cholecystokinin (CCK), which in turn stimulates contraction of the gallbladder.
Acute Cholecystitis
Patients with acute cholecystitis will report a constant pain in the RUQ or epigastrium, associated with signs of inflammation, such as fever or lethargy.
Patients with acute cholecystitis will be tender in the RUQ and may demonstrate a positive Murphy’s sign. Ensure to check for any guarding (may suggest a gallbladder perforation) and for features of sepsis.
What is Murphy’s sign?
Murphy’s Sign
Whilst applying pressure in the RUQ, ask the patient to inspire. Murphy’s sign is positive when there is a halt in inspiration due to pain, indicating an inflamed gallbladder. This can be achieved more accurately with an ultrasound, namely the sonographic Murphy sign.
What. are the differentials for RUQ pain?
There are a wide variety of pathologies that can present with RUQ pain. However, differentials to consider include gastro-oesophageal reflux disease, peptic ulcer disease, acute pancreatitis, or inflammatory bowel disease.
How can RUQ be investigated in suspected biliary colic?
Laboratory Test
Certain blood tests can help in the initial evaluation of suspected cases:
FBC and CRP – assess for the presence of any inflammatory response, which will be raised in cholecystitis
LFTs – biliary colic and acute cholecystitis are likely to show a raised ALP (indicating ductal occlusion), yet ALT and bilirubin should remain within normal limits (unless a Mirizzi syndrome, discussed below)
Amylase (or lipase) – to check for any evidence of pancreatitis
A urinalysis, including a pregnancy test if relevant, should be performed to exclude any renal or tubo-ovarian pathology.
What imaging techniques are used in biliary colic?
Imaging
A trans-abdominal ultrasound (Fig. 2) is one of the most sensitive modalities for visualising gallstone disease and is typically used first line to investigate suspected gallstone pathology.
Three specific areas are often visualised on US:
The presence of gallstones or sludge (the start of gallstone formation)
Gallbladder wall thickness (if thick walled, then inflammation is likely)
Bile duct dilatation (indicates a possible stone in the distal bile ducts)
If results from US scans are inconclusive, further imaging options are available. The gold standard investigation* for gallstones is Magnetic Resonance Cholangiopancreatography (MRCP), largely replacing ERCP for diagnostic purposes (Fig. 3). MRCP can show potential defects in the biliary tree caused by gallstone disease, with a sensitivity approaching 100%.
How can biliary colic be managed?
Biliary Colic
Patients with biliary colic should be prescribed analgesia (regular paracetamol +/- NSAIDs +/- opiates analgesia).
The patient should be advised about lifestyle factors that may help control symptoms (and help with future surgery), such as a low fat diet, weight loss, and increasing exercise.
Following first presentation of biliary colic, there is a high chance of symptom recurrence or the development of complications of gallstones, therefore an elective laparoscopic cholecystectomy* (Fig. 4) is warranted and should be offered within 6 weeks of first presentation.
*The laparoscopic route is preferred for cholecystectomy but is not always possible
By User:Pschemp [CC-BY-SA-3.0], via Wikimedia Commons
How can acute cholecystitis be managed?
Acute Cholecystitis
Patients with acute cholecystitis should be started on appropriate intravenous antibiotics (such as co-amoxiclav +/- metronidazole). Concurrent analgesia and antiemetics should also be prescribed.
A laparoscopic cholecystectomy is indicated within 1 week of presentation, as per NICE guidance, however this ideally should be done within 72hrs of presentation for a likely simpler procedure*.
For those not fit for surgery and not responding to antibiotics, a percutaneous cholecystostomy can be performed to drain the infection (although as the gallstones remain in-situ, the risk of recurring disease remains).
*A Cochrane review previously demonstrated that earlier cholecystectomies are safe and reduce overall hospital stay
Any patient readmitted with RUQ pain post-cholecystectomy, it is important to exclude a retained CBD stone post-operatively. US abdomen scan may be useful, yet if this is unremarkable, then further investigation via MRCP imaging is warranted.
What are the complications of gallstones?
Mirizzi Syndrome
A stone located in Hartmanns pouch (an out-pouching of the gallbladder wall at the junction with the cystic duct) or in the cystic duct itself can cause compression on the adjacent common hepatic duct.
This results in an obstructive jaundice, even without stones being present within the lumen of the common hepatic or common bile ducts. Diagnosis is confirmed by MRCP and management is usually with laparoscopic cholecystectomy.
Gallbladder Empyema
A gallbladder empyema is when the gallbladder becomes filled with pus (Fig. 6). Patients will become unwell, often septic, presenting with a similar clinical picture to acute cholecystitis. They are associated with significant morbidity and mortality.
The condition is diagnosed by either US scan or CT scan. Treatment is via laparoscopic cholecystectomy* (may require intra-operative drainage if tense gallbladder) or percutaneous cholecystostomy (if unsuitable for surgery).
*There is a higher rate of conversion to open cholecystectomy with emypema than with uncomplicated acute cholecystitis
Chronic Cholecystitis
Patients with chronic cholecystitis will typically have a history of recurrent or untreated cholecystitis, which has led to a persistent inflammation of the gallbladder wall. Patients present with ongoing RUQ or epigastric pain with associated nausea and vomiting.
It can be diagnosed typically by CT imaging (or often noted on histology post-cholecystectomy). Management in uncomplicated cases is via elective cholecystectomy. Its main complications are gallbladder carcinoma and biliary-enteric fistula.
Bouveret’s Syndrome and Gallstone Ileus
Inflammation of the gallbladder (typically if recurrent) can cause a fistula to form between the gallbladder wall and the small bowel (Fig. 7), termed a cholecystoduodenal fistula, allowing gallstones to pass directly into the small bowel (typically at the duodenum)
As a consequence, bowel obstruction can occur:
Bouveret’s Syndrome – a stone impacts in the proximal duodenum, causing a gastric outlet obstruction
Gallstone Ileus*– a stone impacts at the terminal ileum (the narrowest part of the small bowel), causing a small bowel obstruction
*The term ileus is misleading, as it is actually a bowel obstruction
By Thomas Newman, TeachMeSurgery [CC-BY-NC-ND 4.0]
How does fatty food trigger biliary colic?
*Fatty acids stimulate the duodenum endocrine cells to release cholecystokinin (CCK), which in turn stimulates contraction of the gallbladder.
What is Cholangitis and what are the causes?
Cholangitis refers to infection of the biliary tract. It is associated with high morbidity and mortality when left untreated, and therefore is an important condition to recognise and manage.
It is caused by a combination of biliary outflow obstruction* and biliary infection. During an obstruction, stasis of fluid combined with elevated intraluminal pressure allows the bacterial colonisation of the biliary tree to become pathological.
*In patients without outflow obstruction, a bacterial colonisation is unlikely to cause cholangitis
Causes
Any condition which causes occlusion of the biliary tree has the potential to cause cholangitis.
The most common causes are gallstones, ERCP (iatrogenic), and cholangiocarcinoma. Rarer causes include pancreatitis, primary sclerosing cholangitis, ischaemic cholangiopathy, and parasitic infections.
The most common infective organisms implicated in cholangitis are Escherichia Coli (27%), Klebsiella species (16%), and Enterococcus (15%).
What are the clinical features of cholangitis?
The common presenting symptoms of cholangitis are right upper quadrant pain, fever,and jaundice (when bilirubin >50 μmol/L). The patient may also complain of pruritus (itching), as a result of bile accumulation, and pale stool with dark urine, from the obstructive jaundice.
The patient’s past medical history may include gallstones, recent biliary tract instrumentation (i.e. ERCP/cholecystectomy), or previous cholangitis. Medication including oral contraceptive pill and fibrates can increase the risk, and a lipid-rich diet may be indicative of gallstones (as a potential underlying cause).
On examination, patients may have pyrexia (in 90% of cases), rigors, jaundice, right upper quadrant tenderness, confusion, hypotension, and tachycardia may be present.
Two common eponymous syndromes associated with cholangitis are:
Charcots Triad: Jaundice, Fever, and RUQ Pain
Reynold’s Pentad: Jaundice, Fever, and RUQ Pain, Hypotension, and Confusion
How is cholangitis investigated?
Laboratory Tests
Routine bloods should be taken, especially FBC (leucocytosis is found in the vast majority of patients) and LFTs (showing a raised ALP ± GGT with a raised bilirubin).
Blood cultures should always be taken in suspected cases, despite only being positive in 20% of cases. The best opportunity to obtain a positive blood culture is early, before the start of broad spectrum antibiotics.
Imaging
An ultrasound scan of the biliary tract will show bile duct dilation. The common bile duct is usually less than 6mm in size (it may be greater in the elderly and those who have had previous cholecystectomy), so any diameter larger than this suggests dilatation. Ultrasound imaging may also demonstrate the presence an underlying cause (e.g. gallstones).
The gold standard investigation for cholangitis is ERCP, as it is both diagnostic and therapeutic. Many endoscopists may require an MRCP prior to intervention, however to obtain detailed imaging of the biliary system prior to scoping.
How is cholangitis managed?
Management
Immediate Management
Patients with cholangitis may present with sepsis, so should be managed promptly, appropriately and often in a higher level of care. Ensure IV access is gained with sufficient fluid resuscitation, routine bloods, and blood cultures taken early, with broad spectrum IV antibiotic therapy instigated (e.g. co-amoxiclav + metronidazole), as per local guidelines.
Definitive Management
The definitive management of cholangitis is via endoscopic biliary decompression, removing the cause of the blocked biliary tree. For patients who are deteriorating, this may need to be done earlier than those who are responding well to antibiotic therapy.
ERCP, with or without a sphincterotomy and stenting, should clear any obstruction. In patients who may be too sick to tolerate ERCP, percutaneous transhepatic cholangiograpy (PTC) is the second line intervention.
In the long-term, patients may require a cholecystectomy if gallstones were the underlying cause. Any other cause for the cholangitis identified should also be managed as appropriate.
It is important to remember that there are significant complications of ERCP, including repeated cholangitis, pancreatitis (in 3-5% of patients), bleeding (more common when a sphincterotomy is performed), and perforation (a rare complication yet requires urgent surgical intervention if present)
What is the prognosis of cholangitis and what factors determine this?
The mortality of cholangitis is around 5-10% in those who are given antibiotic therapy. Early ERCP and early antibiotic therapy have both been found to improve patient outcomes.
Factors which increase the mortality rate include delayed diagnosis, liver failure, cirrhosis, CKD, hypotension, female gender, and >50yrs.
What causes acute pancreatitis?
Aetiology
The majority of acute pancreatitis cases occur secondary to gallstone disease or excess alcohol consumption. However, causes are wide ranging and a popular mnemonic is ‘GET SMASHED’:
Gallstones
Ethanol (Alcohol)
Trauma
Steroids
Mumps
Autoimmune disease, such as SLE
Scorpion venom (a rare and unlikely cause in most countries)
Hypercalcaemia
Endoscopic retrograde cholangio-pancreatography (ERCP)
Drugs, such as Azathioprine, NSAIDs, or Diuretics
Unfortunately, no evident cause will be found in 10-20% of patients with acute pancreatitis
What is acute pancreatitis and pathophysiology?how is it different to chronic?
Acute pancreatitis refers to inflammation of the pancreas. Its incidence is increasing, with around 30 per 100,000 cases each year in the UK. Mortality figures can range between 5-30%, depending on severity.
It can be distinguished from chronic pancreatitis by its limited damage to the secretory function of the gland, with no gross structural damage developing. Repeated episodes of acute pancreatitis can eventually lead to chronic pancreatitis.
Pathogenesis
Each cause described above will trigger a premature and exaggerated activation of the digestive enzymes within the pancreas. The resulting pancreatic inflammatory response causes an increase in vascular permeability and subsequent fluid shifts (often termed “third spacing”).
Enzymes are released from the pancreas into the systemic circulation, causing autodigestion of fats (resulting in a ‘fat necrosis’) and blood vessels (sometimes leading to haemorrhage in the retroperitoneal space). Fat necrosis can cause the release of free fatty acids, reacting with serum calcium to form chalky deposits in fatty tissue, resulting in hypocalcaemia.
Severe end-stage pancreatitis will eventually result in partial or complete necrosis of the pancreas.
What are the clinical features of acute pancreatitis?
Patients will classically present with a sudden onset of severe epigastric pain, which can radiate through to the back, with nausea and vomiting.
On examination, there is often epigastric tenderness, with or without guarding. In severe cases, there may be haemodynamically instability, due to the inflammatory response occurring.
Less common signs that are often described are Cullen’s sign (bruising around the umbilicus, FIg. 2A) and Grey Turner’s sign (bruising in the flanks, Fig. 2B) , representing retroperitoneal haemorrhage. Tetany may occur from hypocalcaemia (secondary to fat necrosis) and, in select cases, gallstone aetiology may also cause a concurrent obstructive jaundice.
What are the differentials for acute pancreatitis?
There are a wide variety of causes of an acutely painful abdomen, as discussed elsewhere. However causes specifically resulting in abdominal pain that radiates through to the back include abdominal aortic aneurysm, renal calculi, chronic pancreatitis, aortic dissection, or peptic ulcer disease.
What investigations are done for acute pancreatitis?
Laboratory Tests
Routine blood tests, as per investigation of any acute abdomen, are required. Specifically for acute pancreatitis, it is important to consider:
Serum amylase – diagnostic of acute pancreatitis if 3x the upper limit of normal*
Amylase can also be marginally raised in pathologies such as bowel perforation, ectopic pregnancy, or diabetic ketoacidosis
LFTs – assess for any concurrent cholestatic element to the clinical picture
Patients with acute pancreatitis noted that an alanine transaminase (ALT) level >150U/L has a positive predictive value of 85% for gallstones as the underlying cause
Serum lipase – A raised serum lipase is more accurate for acute pancreatitis (as it remains elevated longer than amylase), yet it is not available or routinely performed in every hospital
*Serum amylase levels do not directly correlate with disease severity
Imaging
An abdominal ultrasound scan may be requested if the underlying cause is unknown; it is typically used to identify any gallstones (as a potential underlying cause) and any evidence of duct dilatation
Whilst not routinely performed for acute pancreatitis, an AXR can show a ‘sentinal loop sign’. This is a dilated proximal bowel loop adjacent to the pancreas, which occurs secondary to localised inflammation. A CXR should be undertaken to look for pleural effusion or signs of ARDS.
A contrast-enhanced CT scan (Fig. 3) may be required if the initial assessment and investigations prove inconclusive. If performed after 48hrs from initial presentation, it will often show areas of pancreatic oedema and swelling, or any non-enhancing areas suggestive of pancreatic necrosis.
Current UK guidelines state that any CT scan used to assess for severity of disease should only be performed 6-10 days after admission in patients with features of persistent inflammatory response or organ failure*.
*Prior to this time frame, CT-based severity scoring systems have been shown to be equivocal to clinical scoring systems in predicting severity, whilst increasing length of hospital stay with no improvement in clinical outcome
By Hellerhoff (Own work) [CC BY-SA 3.0], via Wikimedia Commons
What scoring systems can be used for acute pancreatitis?
The modified Glasgow criteria is used to assess the severity of acute pancreatitis within the first 48 hours of admission. Any patient scoring with ≥3 positive factors within the first 48hrs should be considered to have severe pancreatitis and a high-dependency care referral is warranted.
Helpfully, the mneumonic to remember the score is PANCREAS: pO2 <8kPa, Age >55yrs, Neutrophils (/WCC) >15×109/L, Calcium <2mmol/L, Renal function (Urea) >16mmol/L, Enzymes LDH>600U/L or AST>200U/L, Albumin <32g/L, Sugar (blood glucose) >10mmol/L
Other risk stratification scores that can be used scoring severity of acute pancreatitis include the APACHE II score, the Ranson Criteria, and Balthazar score (CT scoring system).
What is the management of acute pancreatitis?
Management
There is no curative management for acute pancreatitis, so supportive measures are the mainstay of treatment. Treat any underlying cause as necessary (e.g. urgent ERCP and sphincterotomy for gallstones) where appropriate.
Supportive treatment includes:
Intravenous fluid resuscitation, and oxygen therapy as required
A balanced crystalloid should be used
Nasogastric tube if the patient is vomiting profusely
If the patient is able to eat, oral intake can be encouraged as tolerated
Catheterisation to accurately monitor urine output and start a fluid balance chart (due to the potential for rapid third space losses)
Aim for a urine output of at least >0.5ml/kg/hr
Opioid analgesia*
Current UK guidelines state that all patients with severe acute pancreatitis should be managed in a high dependency unit or intensive therapy unit (although this is often impractical).
A broad-spectrum antibiotic, such as imipenem, should be considered for prophylaxis against infection in cases of confirmed pancreatic necrosis.
Treating the underlying cause should be addressed, once the patient has been stabilised. For those caused by gallstones, early laparoscopic cholecystectomy is advised, whilst those secondary to alcohol excess should ensure they have access to the appropriate services made.
*A Cochrane review stated there is no current evidence that suggests opioid analgesia should be avoided due to increased risk of pancreatitis complications or other adverse events when compared to other analgesia
what are complications of acute pancreatitis?
Complications
Systemic Complications
The systemic complications of acute pancreatitis tend to occur within days of the initial onset:
Disseminated Intravascular Coagulation (DIC)
Acute Respiratory Distress Syndrome (ARDS)
Hypocalcaemia
Fat necrosis from released lipases, results in the release of free fatty acids, which react with serum calcium to form chalky deposits in fatty tissue
Hyperglycaemia
Secondary to destruction of islets of Langerhans and subsequent disturbances to insulin metabolism
Local Complications
Pancreatic Necrosis
Ongoing inflammation eventually leads to ischaemic infarction of the pancreatic tissue, hence such progression should be suspected in patients with evidence of persistent systemic inflammation for more than 7-10 days after the onset of pancreatitis.
Any suspected pancreatic necrosis should be confirmed by CT imaging and treatment will often warrant pancreatic necrosectomy (open or endoscopic)*.
Pancreatic necrosis is prone to infection and should be suspected if there is a clinical deterioration in the patient associated with raised infection markers (or from positive blood culture or changes of low density within the pancreas on CT). Definitive diagnosis of infected pancreatic necrosis can be confirmed by a fine needle aspiration of the necrosis.
*General consensus for intervention in cases of confirmed pancreatic necrosis is to be delayed until walled-off necrosis has developed, typically 3-5 weeks after the onset of symptoms
Pancreatic Pseudocyst
A pancreatic pseudocyst is a collection of fluid containing pancreatic enzymes, blood, and necrotic tissue; they can occur anywhere within or adjacent to the pancreas, however are usually seen in the lesser sac obstructing the gastro-epiploic foramen by inflammatory adhesions..
They are typically formed weeks after the initial acute pancreatitis episode. They lack an epithelial lining, therefore termed pseudocyst, and instead have a vascular and fibrotic wall surrounding the collection.
Pseudocysts may be found incidentally on imaging or can present with symptoms of mass effect, such as biliary obstruction or gastric outlet obstruction. They are prone to haemorrhage or rupture, and can become infected.
About 50% will spontaneously resolve, hence conservative management is usually the initial treatment of choice. Cysts which have been present for longer than 6 weeks are unlikely to resolve spontaneously. Treatment options include surgical debridement or endoscopic drainage (often into the stomach).
What is chronic pancreatitis ?how common is it?
Chronic pancreatitis is a chronic fibro-inflammatory disease of the pancreas, resulting in progressive and irreversible damage to the pancreatic parenchyma.
The incidence of chronic pancreatitis is quoted between 2-10 new cases per 100,000 people per year in Western countries. It has a male to female ratio of 4:1 and an average age of onset of 40 years.
Whan are the causes of chronic pancreatitis?
Aetiology
The main causes of chronic pancreatitis are either chronic alcohol abuse (60%) and idiopathic (30%).
Less common causes include metabolic (hyperlipidaemia, hypercalcaemia), infection (both viral (e.g. HIV, mumps, coxsackie) and bacterial (e.g. Echinococcus), hereditary (e.g. cystic fibrosis), autoimmune (e.g. autoimmune pancreatitis (AIP) or SLE), anatomical (malignancy or stricture formation), or congenital anomalies (e.g. Pancreas divisum or Annular pancreas).
Chronic pancreatitis can also be categorised as either
By TeachMeSeries Ltd (2021)
How does chronic pancreatitis present?
The major symptom in chronic pancreatitis is chronic pain, which may be complicated by recurring attacks of acute pancreatitis (often termed “acute-on-chronic” pancreatitis). The pain is typically in the epigastrium and back, often associated with nausea and vomiting.
Due to the damage that has occurred to the pancreatic parenchyma, patients may also present with:
Endocrine insufficiency – secondary to damage to the endocrine tissue of the pancreatic gland (islets of Langerhans), there is subsequent failure to produce insulin, resulting in impaired glucose regulation or eventual diabetes mellitus*
Exocrine insufficiency – secondary to damage to the acinar cells, resulting in failure to produce digestive enzymes, causing malabsorption, presenting with weight loss, diarrhoea, or steatorrhoea
On examination, the abdomen will be soft, however the patient may be tender in the epigastrium. There may also be signs of cachexia and malabsorption.
Often concurrent pseudocysts are present, due to previous recurrent attacks of acute pancreatitis. Patients with pseudocysts may present with symptoms of mass effect, such as biliary obstruction or gastric outlet obstruction.
*Type 3c (pancreatogenic) diabetes is the term given to diabetes mellitus secondary to pancreatic disease resulting in endocrine dysfunction.
What investigations are done for chronic pancreatitis?and what can be seen on imaging?
Investigations
Most patients presenting with abdominal pain should have a urine dip and routine bloods, including FBC and CRP. Serum amylase or lipase levels are often not raised in established disease.
In suspected cases of chronic pancreatitis, ensure to also check blood glucose (secondary to endocrine dysfunction) and LFTs (to ensure no concurrent obstructive jaundice)
A faecal elastase level will be low in most cases of chronic pancreatitis with exocrine insufficiency, often can aid the diagnosis.*
*The elastase enzyme is produced by the pancreas, being excreted into the bowel to aid with digestion, and importantly does not undergo any significant degradation during intestinal transit; as such, any exocrine dysfunction in chronic pancreatitis will present with low faecal elastase levels
Imaging
CT imaging can often show pancreatic atrophy or calcification, as well as any pseudocysts present (Fig. 2). Any overt causes for chronic pancreatitis, such as malignancy or congenital anomalies, may also be seen
The anatomy of the pancreas and the biliary tree can be determined using both ultrasound imaging or MRI imaging (specifically MRCP). However, a normal appearance of the pancreas on imaging does not necessarily exclude chronic pancreatitis.
Additional specialist tests, such as the secretin stimulation test or endoscopic ultrasound (EUS), may also be employed in cases of diagnostic uncertainty.
Adapted from work by Hellerhoff and James Heilman [CC BY-SA 3.0], via Wikimedia Commons
How can chronic pancreatitis be managed?
Chronic pancreatitis can only be managed definitively by treating any reversible underlying cause. This can include alcohol cessation or statin therapy for hyperlipidaemia.
However, analgesia becomes the mainstay of management for most cases of chronic pancreatitis. Whilst the WHO analgesic ladder should be followed in acute cases, for those with long-term pain, opioid analgesia might be replaced with neuropathic analgesics instead.
Patients with malabsorption secondary to exocrine dysfunction may benefit from enzyme replacement (including lipases), such as Creon®, that can be taken with meals to good effect. Patients are also at risk of becoming deficient in fat-soluble vitamins (A, D, E and K), therefore ensure adequate vitamin supplementation and check bone density routinely.
Those with pancreatogenic diabetes may benefit insulin regimes, along with annual surveillance with HbA1c.
Endoscopic Management
Endoscopic management is performed only in a select few patients where there is a targetable underlying cause. Surgical intervention is now rarely performed in cases of chronic pancreatitis, due to high morbidity and mortality, with limited symptomatic improvement.
Endoscopic retrograde cholangiopancreatography (ERCP) can be used for diagnostic and therapeutic purposes, including stone removal, stent placement, or sphincterotomy (especially in large duct pancreatitis).
Endosonography-guided celiac plexus blockade or thoracoscopic splanchnicectomy are interventions that be be performed purely for analgesic purposes.
Steroids
Steroids are effective at reducing symptoms in chronic pancreatitis with an autoimmune aetiology only. A high dose of prednisolone is used initially to bring symptoms under control; a low dose maintenance regime is then used.
What is the prognosis of chronic pancreatitis?
Chronic pancreatitis is associated with significant morbidity and reduced quality of life, as it can be a challenging condition to manage effectively.
In some patients, the disease may eventually ‘burn out’ after many years of pain, leaving residual endocrine and exocrine insufficiencies.
Pancreatic malignancy is a risk in those who have had the disease for 20 years or more; new or evolving symptoms should therefore undergo investigation.
What is Cauda Equina Syndrome?
Cauda equina syndrome (CES) is a surgical emergency caused by a compression of the cauda equina. If untreated, patients can develop debilitating complications, hence a high level of suspicion and rapid intervention is required.
The condition has peak onset between 40-50 years of age. Approximately 4 in every 10,000 patients presenting with lower back pain are ultimately diagnosed with the syndrome.
The cauda equina is a bundle of nerves situated inferior to the spinal cord.
The spinal cord tapers to an end (known as the conus medullaris), approximately at the first lumbar vertebra, with nerve roots L1-S5 leaving from at this region to pass down the spinal canal (as the cauda equina) to exit at their respective formaina.
Consequently, the cauda equina is formed by lower motor neurones, containing motor and sensory impulses to the lower limbs, motor innervation to the anal sphincters, and parasympathetic innervation for the bladder.
What are the causes Cauda Equina Syndrome?
Pathophysiology
Cauda equina syndrome is caused by compression of the cauda equina:
Disc herniation – most common at L5/S1 and L4/L5 level
Trauma – including vertebral fracture and subluxation
Neoplasm – either primary or metastatic
The most common cancers that spread to spinal vertebrae are thyroid, breast, lung, renal and prostate
Infection – e.g. discitis or Potts disease
Chronic spinal inflammation – e.g. ankylosing spondylitis
Iatrogenic – e.g. haematoma secondary to spinal anaesthesia
How does cauda equina present?
Cauda equina syndrome results in lower motor neurone signs and symptoms.
Symptoms include reduced lower limb sensation (often bilateral), bladder or bowel dysfunction, lower limb motor weakness, severe back pain, and impotence.
By Lesion [CC BY-SA 3.0], from Wikimedia Commons
Figure 2 – The distribution of saddle anaesthesia
An important feature to assess is bladder dysfunction, specifically the presence of retention. Confirmed retention or reduced ability to void (loss of desire, reduced urinary sensation) suggests complete or incomplete CES respectively.
On examination, features include perianal (the lower sacral dermatomes, termed “saddle” anaesthesia) or lower limb anaesthesia, loss of anal tone, urinary retention, and lower limb weakness and hypoflexia.
If no obvious cause is evident, a thorough history and examination may reveal the pathophysiology, such as weight loss as a sign of metastatic disease or living in an area of endemic tuberculosis.
As part of the examination for suspected CES, regardless of symptoms, patients will require a PR examination and a post-void bladder scan.
How can cauda equina be classified?
Classification
Cauda Equina Syndrome can be classified into 3 groups:
Cauda Equina Syndrome with retention (CESR) – Presents as back pain with unilateral or bilateral sciatica, lower limb motor weakness, sensory disturbance in the saddle region, loss of anal tone, and loss of urinary control
Incomplete Cauda Equina Syndrome (CESI) – As above, however only altered urinary sensation (e.g. loss of desire to void, diminished sensation, poor stream, and need to strain); painful retention may precede painless retention in some cases
Suspected Cauda Equina Syndrome (CESS) – Cases of severe back and leg pains with variable neurological symptoms and signs, and a suggestion of sphincter disturbance
Most cases will be progressive in nature and will not immediately cause complete compression on the cauda equina. This is important for the management, as incomplete cauda equina syndrome has a greater potential for neurological recovery.
What are differentials for cauda equina?
Differential Diagnosis
Radiculopathy – presents with radiating back pain, however there will be no faecal, urinary, or sexual dysfunction in these patients
Cord compression – a surgical emergency with a similar pathophysiology to CES, however is characterised by upper motor neurone signs
How can cauda equina be investigated?
Investigations
For suspected cases of cauda equina syndrome, an emergency whole spine MRI is the gold standard investigation. However, only 60% of patients suspected to have CES from clinical assessment have an abnormality found on MRI.
Further imaging may be required dependent on the underlying cause, however if CES is confirmed, then urgent surgical intervention is the priority.
What is the prognosis of cauda equina?
Prognosis
The prognosis of cauda equina syndrome is variable depending on both aetiology and the time taken from symptom onset to surgery.
Indeed, a retrospective study examined the case for early surgery and found that patients who were in theatre within 24 hours from onset of autonomic dysfunction had reduced bladder problems at long-term follow up.
What is the screening process for breast cancer
As the risk of breast cancer increases with age, breast screening in the UK is offered to all women at the age of 50 who are registered with a GP. They are invited for screening every three years until their 71st birthday. They can choose to continue with the programme after this time period at their own request. The procedure is a bilateral mammogram, taken in a horizontal and vertical plane.
Most women will have the same lifetime risk as the general population of developing breast cancer (around 11%) and so will follow the screening schedule as above. Some groups, however, are classified as high-risk and have a more frequent screening schedule: women who have a genetic mutation (BRCA and TP53), and women with a significant family history. Women with a BRCA mutation (both 1 & 2) start screening at the age of 30 with a yearly MRI and possibly a mammogram. Those with a TP53 mutation start screening at the age of 20 with a yearly MRI. More detailed information on breast screening in high-risk groups is available on the NICE website.
How can patients with breast cancer be risk categorised
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What are the different causes of gastroenteritis?
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What are the extra intestinal manifestations of Chron’s?
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What scoring system is used for UC?
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What are the complications for UC?
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How can Chron’s be managed?
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How can UC be managed?
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What is the duke’s criteria for staging bowel cancer?
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What are the signs of dying?
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What is the difference between palliative and hospice care?
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What anticipatory medicine can be given to patients who are dying
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What document can you used in deciding future care of patient if they lose capacity?
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How can capacity be assessed?
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Who can make decisions on behalf of a patient?
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What services are available for carers looking after terminal ill patients?
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What housing options are available for patients who are ill?What are the signs of gastric cancer?
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What is the prognosis of gastric cancer?
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What is the difference between invasive and noninvasive ventilation?
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What is the difference between Cipap and bipap?
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How urgent is an MRI in cauda equina?
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What advice would you give to someone on anti epileptics trying to get pregnant?
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What are the drug causes of pulmonary fibrosis?
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What are the side effects of steroids?
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What are the side effects of Methotrexate?
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What are the side effects of biologic treatment?
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What.are complications of seizures
Potential complications of epilepsy include:
- Sudden Unexpected Death in Epilepsy (SUDEP): Occurs in approximately 1:1000 patient years with epilepsy. Patients with a diagnosis of epilepsy need to be counselled about this risk.
- Status epilepticus: defined as a seizure that persists for more than 30 minutes. This is associated with a mortality of 15-20% - due to hypoxia and metabolic disturbances occurring during the seizure.
- Injuries sustained during a seizure or in the post-seizure period. Accidental injuries of some degree are estimated to occur in 6.5% of patients with epilepsy over 2 years. Injuries are partly culturally determined; e.g. severe injuries from burns sustained when falling into an open fire are particularly common in cultures where open fires are used for cooking and heating.
- Mood disorders and anxiety are common – occurring in a third to a half of patients with epilepsy.
- Cognitive impairment is common, and usually due either to the underlying brain disease of which seizures are a manifestation, or drug side effects.
- Cardiovascular and respiratory disease are more common in patients with epilepsy.
What are different types of seizures?
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What is status epileptics and how is that managed
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What are some side effects of anti-epileptics?
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What is recommendation for driving with a history of seizure?
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What is recommendation for driving with a history of epilepsy?
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What is and EEG?
- The brain normally produces tiny electrical signals that come from the brain cells and nerves which send messages to each other. These electrical signals can be detected and recorded by the electroencephalograph (EEG) machine
- During EEG – Patient may be asked to blink lots of times, or to breathe deeply. These can sometimes trigger patterns of electrical activity in the brain which are associated with certain types of epilepsy.
- Photic stimulation and hyperventilation should remain part of standard EEG assessment. The patient and carer should be inform that such activation procedures may induce a seizure and they have a right to refuse.
- Some specialised types of EEG : strobe lighting, Sleep EEG, Sleep-deprived EEG, Ambulatory EEG with video
When is an MRI warranted in seizures?
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How and when are anti-epileptics stopped?
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How is epilepsy managed and when can antiepilepticss be started after 1st seizure?
NICE: start antiepileptics if
(1) Neurological deficit
(2) Brain imaging shows structural abnormality
(3) the EEG shows unequivocal epileptic activity
(4) the patient or their family or carers consider the risk of having
a further seizure unacceptable
Generalised tonic-clonic seizures
● sodium valproate
● second line: lamotrigine, carbamazepine
Absence seizures (Petit mal)
● sodium valproate or ethosuximide
● sodium valproate particularly effective if co-existent
tonic-clonic seizures in primary generalised epilepsy
Myoclonic seizures
● sodium valproate
● second line: clonazepam, lamotrigine
Focal seizures (with or without secondary generalisation)
● carbamazepine or lamotrigine
● second line: levetiracetam, oxcarbazepine or sodium
valproate
*carbamazepine may exacerbate absence seizures and
myoclonic seizure
How can itch and jaundice in palliative care be managed?
Post- op chemotherapy
● Palliation of jaundice- endoscopic or percutaneous stent insertion
What is the tumour marker for pancreatic cancer and how can this be managed?
Ca-19-9
● Surgery- pancreaticoduodenectomy/ whipple’s
● Post- op chemotherapy
● Palliation of jaundice- endoscopic or percutaneous
stent insertion
● Palliative care for advance stage
How is the Septic arthritis management
Urgent joint aspiration
● Start empirical antibiotics flucloxacillin
What classification system is used to treat cellulitis?
NICE Clinical Knowledge Summaries recommend we use the Eron classification to guide how we manage patients with cellulitis:
Class Features
I There are no signs of systemic toxicity and the person has no uncontrolled co-morbidities
II The person is either systemically unwell or systemically well but with a co-morbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection
III The person has significant systemic upset such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable co-morbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromize
IV The person has sepsis syndrome or a severe life-threatening infection such as necrotizing fasciitis
They recommend the following that we admit for intravenous antibiotics the following patients:
Has Eron Class III or Class IV cellulitis.
Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
Is very young (under 1 year of age) or frail.
Is immunocompromized.
Has significant lymphoedema.
Has facial cellulitis (unless very mild) or periorbital cellulitis.
The following is recommend regarding Eron Class II cellulitis:
Admission may not be necessary if the facilities and expertise are available in the community to give intravenous antibiotics and monitor the person - check local guidelines.
Other patients can be treated with oral antibiotics.
Management
The BNF recommends flucloxacillin as first-line treatment for mild/moderate cellulitis. Clarithromycin, erythromycin (in pregnancy) or doxycyline is recommended in patients allergic to penicillin.
NICE recommend that patients severe cellulitis should be offered co-amoxiclav, cefuroxime, clindamycin or ceftriaxone.
How is HIV testing done?
Diagnosis
antibodies to HIV may not be present
HIV PCR and p24 antigen tests can confirm diagnosis
testing for HIV in asymptomatic patients should be done at 4 weeks after possible exposure
after an initial negative result when testing for HIV in an asymptomatic patient, offer a repeat test at 12 weeks
HIV antibody test
most common and accurate test
usually consists of both a screening ELISA (Enzyme Linked Immuno-Sorbent Assay) test and a confirmatory Western Blot Assay
most people develop antibodies to HIV at 4-6 weeks but 99% do by 3 months
p24 antigen test
usually positive from about 1 week to 3 - 4 weeks after infection with HIV
sometimes used as an additional screening test in blood banks
what are types and causes of delirium?
Acute confusional state is also known as delirium or acute organic brain syndrome. It affects up to 30% of elderly patients admitted to hospital.
Predisposing factors include: age > 65 years background of dementia significant injury e.g. hip fracture frailty or multimorbidity polypharmacy
The precipitating events are often multifactorial and may include:
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
Features - a wide variety of presentations memory disturbances (loss of short term > long term) may be very agitated or withdrawn disorientation mood change visual hallucinations disturbed sleep cycle poor attention
Common causes of delirium can be remembered using the mnemonic DELIRIUMS:
D - Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)
E - Eyes, ears and emotional
L - Low Output state (MI, ARDS, PE, CHF, COPD)
I - Infection
R - Retention (of urine or stool)
I - Ictal
U - Under-hydration/Under-nutrition
M - Metabolic (Electrolyte imbalance, thyroid, wernickes
(S) - Subdural, Sleep deprivation
Management
treatment of the underlying cause
modification of the environment
the 2006 Royal College of Physicians publication ‘The prevention, diagnosis and management of delirium in older people: concise guidelines’ recommended haloperidol 0.5 mg as the first-line sedative
the 2010 NICE delirium guidelines advocate the use of haloperidol or olanzapine
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 delirium different to dementia?
Factors favouring delirium over dementia
impairment of consciousness
fluctuation of symptoms: worse at night, periods of normality
abnormal perception (e.g. illusions and hallucinations)
agitation, fear
delusions
How is dementia investigated?
Dementia is thought to affect over 700,000 people in the UK and accounts for a large amount of health and social care spending. The most common cause of dementia in the UK is Alzheimer’s disease followed by vascular and Lewy body dementia. These conditions may coexist.
Features
diagnosis can be difficult and is often delayed
assessment tools recommended by NICE for the non-specialist setting include: 10-point cognitive screener (10-CS), 6-Item cognitive impairment test (6CIT)
assessment tools not recommended by NICE for the non-specialist setting include the abbreviated mental test score (AMTS), General practitioner assessment of cognition (GPCOG) and the mini-mental state examination (MMSE) have been widely used. A MMSE score of 24 or less out of 30 suggests dementia
Management
in primary care, a blood screen is usually sent to exclude reversible causes (e.g. Hypothyroidism). NICE recommend the following tests: FBC, U&E, LFTs, calcium, glucose, TFTs, vitamin B12 and folate levels. Patients are now commonly referred on to old-age psychiatrists (sometimes working in ‘memory clinics’).
in secondary care, neuroimaging is performed* to exclude other reversible conditions (e.g. Subdural haematoma, normal pressure hydrocephalus) and help provide information on aetiology to guide prognosis and management
What is the refferal criteria for cystoscopy?
NICE recommend urgent referral for Urology review (and usually cystoscopy) for patients who are
- aged 45 and over and have:
- unexplainedvisible haematuria without urinary tract infectionor
- visible haematuria that persists or recurs after successful treatment of urinary tract infection,or
- aged 60 and over and have unexplained non‑visible haematuriaandeither dysuria or a raised white cell count on a blood test.**
- Considernon-urgentreferral for bladder cancer in people aged 60 and over with recurrent orpersistentunexplained urinary tract infection
How can renal stones be managed?
Initial management of renal colic
Medication
the BAUS recommend an NSAID as the analgesia of choice for renal colic
whilst diclofenac has been traditionally used the increased risk of cardiovascular events with certain NSAIDs (e.g. diclofenac, ibuprofen) should be considered when prescribing
the CKS guidelines suggest for patients who require admission: ‘Administer a parenteral analgesic (such as intramuscular diclofenac) for rapid relief of severe pain’
BAUS no longer endorse the use of alpha-adrenergic blockers to aid ureteric stone passage routinely. They do however acknowledge a recently published meta-analysis advocates the use of α-blockers for patients amenable to conservative management, with greatest benefit amongst those with larger stones
Initial investigations
urine dipstick and culture
serum creatinine and electrolytes: check renal function
FBC / CRP: look for associated infection
calcium/urate: look for underlying causes
also: clotting if percutaneous intervention planned and blood cultures if pyrexial or other signs of sepsis
Imaging
BAUS now recommend that non-contrast CT KUB should be performed on all patients, within 14 hours of admission
if a patient has a fever, a solitary kidney or when the diagnosis is uncertain an immediate CT KUB should be performed. In the case of an uncertain diagnosis, this is to exclude other diagnoses such as ruptured abdominal aortic aneurysm
CT KUB has a sensitivity of 97% for ureteric stones and a specificity of 95%
ultrasound still has a role but given the wider availability of CT now and greater accurary it is no longer recommend first-line. The sensitivity of ultrasound for stones is around 45% and specificity is around 90%
Management of renal stones
Stones < 5 mm will usually pass spontaneously. Lithotripsy and nephrolithotomy may be for severe cases.
Most renal stones measuring less than 5mm in maximum diameter will typically pass within 4 weeks of symptom onset. More intensive and urgent treatment is indicated in the presence of ureteric obstruction, renal developmental abnormality such as horseshoe kidney and previous renal transplant. Ureteric obstruction due to stones together with infection is a surgical emergency and the system must be decompressed. Options include nephrostomy tube placement, insertion of ureteric catheters and ureteric stent placement.
In the non-emergency setting, the preferred options for treatment of stone disease include extra corporeal shock wave lithotripsy, percutaneous nephrolithotomy, ureteroscopy, open surgery remains an option for selected cases. However, minimally invasive options are the most popular first-line treatment.
Shockwave lithotripsy
A shock wave is generated external to the patient, internally cavitation bubbles and mechanical stress lead to stone fragmentation. The passage of shock waves can result in the development of solid organ injury. Fragmentation of larger stones may result in the development of ureteric obstruction. The procedure is uncomfortable for patients and analgesia is required during the procedure and afterwards.
Ureteroscopy
A ureteroscope is passed retrograde through the ureter and into the renal pelvis. It is indicated in individuals (e.g. pregnant females) where lithotripsy is contraindicated and in complex stone disease. In most cases a stent is left in situ for 4 weeks after the procedure.
Percutaneous nephrolithotomy
In this procedure, access is gained to the renal collecting system. Once access is achieved, intra corporeal lithotripsy or stone fragmentation is performed and stone fragments removed.
Therapeutic selection
Disease Option
Stone burden of less than 2cm in aggregate Lithotripsy
Stone burden of less than 2cm in pregnant females Ureteroscopy
Complex renal calculi and staghorn calculi Percutaneous nephrolithotomy
Ureteric calculi less than 5mm Manage expectantly
Prevention of renal stones
Calcium stones may be due to hypercalciuria, which is found in up to 5-10% of the general population.
high fluid intake
low animal protein, low salt diet (a low calcium diet has not been shown to be superior to a normocalcaemic diet)
thiazides diuretics (increase distal tubular calcium resorption)
Oxalate stones
cholestyramine reduces urinary oxalate secretion
pyridoxine reduces urinary oxalate secretion
Uric acid stones
allopurinol
urinary alkalinization e.g. oral bicarbonate
What are the risk factors for renal cell carcinoma and how does it present?
Renal cell cancer is also known as hypernephroma and accounts for 85% of primary renal neoplasms. It arises from proximal renal tubular epithelium. The most common histological subtype is clear cell (75 to 85 percent of tumours).
Associations* more common in middle-aged men smoking von Hippel-Lindau syndrome tuberous sclerosis
Features
classical triad: haematuria, loin pain, abdominal mass
pyrexia of unknown origin
left varicocele (due to occlusion of left testicular vein)
endocrine effects: may secrete erythropoietin (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH
25% have metastases at presentation
paraneoplastic hepatic dysfunction syndrome. Also known as Stauffer syndrome. Typically presents as cholestasis/hepatosplenomegaly. It is thought to be secondary to increased levels of IL-6
How can renal cell carcinoma present?
Management
for confined disease a partial or total nephrectomy depending on the tumour size
alpha-interferon and interleukin-2 have been used to reduce tumour size and also treat patients with metatases
receptor tyrosine kinase inhibitors (e.g. sorafenib, sunitinib) have been shown to have superior efficacy compared to interferon-alpha
Whats von hip Lindau syndrome?
Von Hippel-Lindau (VHL) syndrome is an autosomal dominant condition predisposing to neoplasia. It is due to an abnormality in the VHL gene located on short arm of chromosome 3
Features
cerebellar haemangiomas: these can cause subarachnoid haemorrhages
retinal haemangiomas: vitreous haemorrhage
renal cysts (premalignant)
phaeochromocytoma
extra-renal cysts: epididymal, pancreatic, hepatic
endolymphatic sac tumours
clear-cell renal cell carcinoma
What can cause a raised PSA?
PSA levels may also be raised by**:
benign prostatic hyperplasia (BPH)
prostatitis and urinary tract infection (NICE recommend to postpone the PSA test for at least 1 month after treatment)
ejaculation (ideally not in the previous 48 hours)
vigorous exercise (ideally not in the previous 48 hours)
urinary retention
instrumentation of the urinary tract
How can prostate cancer be investigated?
The traditional investigation for suspected prostate cancer was a transrectal ultrasound-guided (TRUS) biopsy. However, recent guidelines from NICE have now advocated the increasing use of multiparametric MRI as a first-line investigation.
Complications of TRUS biopsy: sepsis: 1% of cases pain: lasting >= 2 weeks in 15% and severe in 7% fever: 5% haematuria and rectal bleeding
Multiparametric MRI is now the first-line investigation for people with suspected clinically localised prostate cancer.
the results are reported using a 5‑point Likert scale
If the Likert scale is >=3 a multiparametric MRI-influenced prostate biopsy is offered
If the Likert scale is 1-2 then NICE recommend discussing with the patient the pros and cons of having a biopsy.
How can prostate cancer be treated?
Treatment depends on life expectancy and patient choice. Options include:
conservative: active monitoring & watchful waiting
radical prostatectomy
radiotherapy: external beam and brachytherapy
Localised advanced prostate cancer (T3/T4)
Options include:
hormonal therapy: see below
radical prostatectomy: erectile dysfunction is a common complication
radiotherapy: external beam and brachytherapy. Patients are at increased risk of bladder, colon, and rectal cancer following radiotherapy for prostate cancer
Metastatic prostate cancer disease - hormonal therapy
Synthetic GnRH agonist
e.g. Goserelin (Zoladex)
cover initially with anti-androgen to prevent rise in testosterone
Anti-androgen
cyproterone acetate prevents DHT binding from intracytoplasmic protein complexes
What are the pro and cons of psa testing?
Pros:
it may reassure you if the test result is normal
it can find early signs of cancer, meaning you can get treated early
PSA testing may reduce your risk of dying if you do have cancer
Cons:
it can miss cancer and provide false reassurance
it may lead to unnecessary worry and medical tests when there’s no cancer
it cannot tell the difference between slow-growing and fast-growing cancers
it may make you worry by finding a slow-growing cancer that may never cause any problems
What are markers of bone formation?
ALP
Osteocalcin
N terminal propeptide of type 1 collagen
What are the markers of bone resoption?
N terminal telopeptide of type 1 collagen
C terminal telopeptide of type 1 collagen
Hydroxyproline
How can thyroid eye disease be managed?
Prevention
smoking is the most important modifiable risk factor for the development of thyroid eye disease
radioiodine treatment may increase the inflammatory symptoms seen in thyroid eye disease. In a recent study of patients with Graves’ disease around 15% developed, or had worsening of, eye disease. Prednisolone may help reduce the risk
Features
the patient may be eu-, hypo- or hyperthyroid at the time of presentation
exophthalmos
conjunctival oedema
optic disc swelling
ophthalmoplegia
inability to close the eyelids may lead to sore, dry eyes. If severe and untreated patients can be at risk of exposure keratopathy
Management topical lubricants may be needed to help prevent corneal inflammation caused by exposure steroids radiotherapy surgery
Monitoring patients with established thyroid eye disease
For patients with established thyroid eye disease the following symptoms/signs should indicate the need for urgent review by an ophthalmologist (see EUGOGO guidelines):
unexplained deterioration in vision
awareness of change in intensity or quality of colour vision in one or both eyes
history of eye suddenly ‘popping out’ (globe subluxation)
obvious corneal opacity
cornea still visible when the eyelids are closed
disc swelling
Improve these notes
How can thyroid storm be managed?
IV propranolol
IV digoxin
Propylthiouracil through NG tube followed by Lugol’s iodine 6 hours later
Prednisolone/hydrocortisone
What are the different types of thyroid cancer?How can it be managed?
Features of hyperthyroidism or hypothyroidism are not commonly seen in patients with thyroid malignancies as they rarely secrete thyroid hormones
Main points
Type Percentage
Papillary 70% Often young females - excellent prognosis
Follicular 20%
Medullary 5% Cancer of parafollicular (C) cells, secrete calcitonin, part of MEN-2
Anaplastic 1% Not responsive to treatment, can cause pressure symptoms
Lymphoma Rare Associated with Hashimoto’s thyroiditis
Management of papillary and follicular cancer
total thyroidectomy
followed by radioiodine (I-131) to kill residual cells
yearly thyroglobulin levels to detect early recurrent disease
Further information
Type Notes
Papillary carcinoma
Usually contain a mixture of papillary and colloidal filled follicles
Histologically tumour has papillary projections and pale empty nuclei
Seldom encapsulated
Lymph node metastasis predominate
Haematogenous metastasis rare
Follicular adenoma
Usually present as a solitary thyroid nodule
Malignancy can only be excluded on formal histological assessment
Follicular carcinoma
May appear macroscopically encapsulated, microscopically capsular invasion is seen. Without this finding the lesion is a follicular adenoma.
Vascular invasion predominates
Multifocal disease raree
Medullary carcinoma
C cells derived from neural crest and not thyroid tissue
Serum calcitonin levels often raised
Familial genetic disease accounts for up to 20% cases
Both lymphatic and haematogenous metastasis are recognised, nodal disease is associated with a very poor prognosis.
Anaplastic carcinoma
Most common in elderly females
Local invasion is a common feature
Treatment is by resection where possible, palliation may be achieved through isthmusectomy and radiotherapy. Chemotherapy is ineffective.
What are the causes of neck lumps?
Standing behind the person, palpate the different areas of the neck to assess the position of the neck lump(s) and possible cause.
Anterior triangle (borders: midline, anterior border of sternocleidomastoid muscle, and the body of the mandible) — thyroid swellings (lobe), pharyngeal pouch, submandibular gland swelling, branchial cyst, lymph nodes (reactive, infective, or malignant), parotid swelling.
Posterior triangle (borders: posterior border of sternocleidomastoid muscle, trapezius, and the clavicle) — lymph nodes (reactive or malignant), carotid artery aneurysm, carotid body tumour, cervical rib, lipoma.
Midline — thyroid swellings (isthmus), thyroglossal cyst, laryngeal swellings, submental lymph nodes, dermoid cysts.
