• Carbohydrates are large macromolecules consisting of carbon, hydrogen and oxygen atoms. They have the empirical formula C_m(H₂O)_n, where m is different from n. Exceptions do exist though.
  • Four different forms exist, depending on their size: Polysaccharides, oligosaccharides, disaccharides, and monosaccharides.
• Most of our dietary carbohydrate is in the form of starch, with a small amount of sucrose and lactose.
• Polysaccharide hydrolysis begins in the oral cavity with salivary alpha-amylase, however most of the polysaccharide breakdown occurs in the upper intestines by pancreatic amylase. This converts polysaccharides into maltose, a disaccharide.
• The dietary carbohydrates are then presented to the small intestines in the form of disaccharides: Lactose (Galactase + Glucose), Maltose (Glucose + Glucose) & Sucrose (Glucose + Fructose)
• The brush-border membrane of the small intestine contains disaccharidases (Lactase, Maltase and Sucrase), which further reduce the disaccharides into monosaccharides which can be absorbed.
• Glucose and galactose are absorbed by secondary active transport, in which co-transport carriers (Sodium-glucose transporter proteins) on the luminal border transports both the monosaccharide and Na+ from the lumen into the interior of the intestinal cell. This therefore does not use energy, but instead depends on the sodium concentration gradient.
• When the glucose/galactose is in the cell, it is then able to move down its concentration gradient by means of a passive carrier (GLUT2 receptors) in the basolateral border to enter the blood within the villus.
• Fructose however is absorbed into the blood by facilitated diffusion via the GLUT5 transporter.

Protein absorption

• Proteins are macromolecules involving the polymerisation of amino acids (empirical formula: H₂N-HCR-COOH) linked together by peptide bonds. Note: R is a variable region.
• Protein absorption involves both exogenous (food sources) and endogenous proteins that have entered the digestive tract lumen, e.g. digestive enzymes, proteins within cells and small amounts of plasma protein that leak from the capillaries.
• Dietary protein digestion typically begins in the stomach when pepsinogen is converted to pepsin by the action of hydrochloric acid. This reduces the polypeptides into smaller peptide chains or amino acids.
• Digestion then continues via pancreatic proteolytic enzymes. The pancreas release pro-enzymes, trypsinogen and chymotrypsinogen.
• These become active within the lumen as trypsinogen is converted into trypsin by enterokinases, an enzyme present on the brush border of the small intestine. Trypsin then activates chymotrypsinogen; together these digest proteins into amino acids or into smaller oligopeptide fragments.
• The amino acids are then absorbed across the intestinal cells by secondary active transport, i.e. via the sodium concentration gradient. Small peptides however gain entry through a different carrier, and may be broken down by aminopeptidases within the brush border or intracellular peptidases.
• Once broken down within the cell, they are able to diffuse passively into the blood.

Fat absorption

• Since fat is not soluble in water, it must undergo a series of transformations in order to be digested and absorbed.
• Dietary fat in the form of large fat globules composed of triglycerides is first emulsified by the detergent action of bile salts (secreted in the liver; stored in the gallbladder) into a suspension of smaller fat droplets. This lipid emulsion prevents the fat droplets from coaelescing and thereby increases the surface area available for attack by pancreatic lipases.
• Lipase then hydrolyzes triglicerides into monoglycerides and free fatty acids.
• These water-insoluble products are then carrier into the interior of water-soluble micelles, which are formed by bile salts and other bile constituents, to the luminal surface of the small intestine epithelial cells
• When a micelle approaches the absorptive epithelial surface, the monoglycerides and fatty acids leave the micelle and passively diffuse through the lipid bilayer of the luminal membranes
• The monoglycerides and free fatty acids are then resynthesized into triglycerides inside the epithelial cells
• These triglycerides aggregate are are coated with a layer of lipoprotein to form water-soluble chylomicrons, which are extended through the basal membrane of the cells by exocytosis
• Chylomicrons however are unable to cross the basement membrane of blood capillaries, so instead enter the lymphatic vessels, the central lacteals.

Vitamin absorption

• There are two groups of vitamins
  • Water-soluble vitamins (primarily absorbed with water)
  • Fat-soluble vitamins (A, D, E, K)
    • These are vitamins carried in the micelles and absorbed passively with the end products of fat digestion.

References

Read more about our sources

The post Physiology of Absorption appeared first on almostadoctor.

Gastroenteritis (colloquially known by many names, including gastric flu, “gastro”, vomiting and diarrhoea, “food poisoning”, “the squits”) is a very common presentation to general practice and emergency departments, in people of all ages, but especially in children, or families with young children.

Gastroenteritis is a broad term, but usually used to refer to an infective illness which causes diarrhoea, vomiting and often abdominal pain. The majority of cases are viral, and a smaller percentage are true “food poisoning” (usually bacterial, occasionally parasitic) related to improper preparation or storage of food.

It typically occurs in outbreaks in winter (often rotavirus or norovirus – “winter vomiting virus”), and may cause hospital wards to be shut down during an outbreak.

In most patients with vomiting and diarrhoea together, gastroenteritis should be considered as the most likely diagnosis. In patients with vomiting only, or diarrhoea only, particularly in the presence of fever or abdominal pain, caution should be applied and a careful history and examination undertaken to look for other – often more serious – causes. In children in particular, vomiting alone can be a sign of a more serious underlying illness.

The cause is not usually identified – and most cases are self limiting and resolve in a few days. The treatment does not usually depend on the cause, and typically consists of managing nausea and vomiting and encouraging oral fluid intake. Severe cases of dehydration may require hospital admission for IV fluid administration.

In developing countries, gastroenteritis is a leading cause of death.

Epidemiology & Aetiology

• Affects about 20% of the population each year
• Viral infections cause 30-40% of cases in developed countries
  • In children, the proportion caused by viruses is much greater
• Risk factors
  • Poor sanitation / poor personal hygiene
  • Immunocompromised patients
  • Poor food preparation
    • Undercooked
    • Reheated – reheating food correctly will kill bacteria, but will not destroy any toxins they left behind
    • Left at room temperature for too long
    • Particularly at risk foods include seafood

Causes

Viral causes are by far the most common. In the UK, norovirus – the “winter vomiting virus” is renowned for causing outbreaks on hospital wards. 

Common organisms include:

• Viral causes
  • Norovirus
  • Rotavirus – very common in young children
  • Adenovirus – very common in young children
  • Enterovirus
  • Ebola – recent deadly outbreaks in Africa
  • Viral causes are usually person-to-person direct transmission, although infected food handlers may also cause outbreaks via food without direct contact.
• Bacterial Causes
  • Campylobacter ( most commonly from raw / undercooked chicken)
  • Escherichia Coli (undercooked mince or meat, raw milk, contaminated vegetables)
  • Salmonella (most commonly from raw eggs)
  • Shigella
  • Staphylococcus – usually the toxins from the bug rather than the bug itself
  • Bacterial causes are more likely to cause blood in the diarrhoea than viral causes. Bacterial causes are also usually commonly clustered around food outbreaks. 
• Parasites
  • Giardia
  • Entamoeba (amoebiasis)
  • Cryptosporidium (from contaminated water)
  • Parasitic causes may also cause bloody diarrhoea but tend to have longer incubation periods than bacterial infections

Presentation

• Diarrhoea – often watery – multiple episodes – up to 10x per day is not unusual
• Vomiting – again can be frequent – up to 10x daily
• Typical incubation periods:
  • Virus – 1 day
  • Bacterial – hours to days (up to 4 days)
  • Parasite – 7-10 days
• Bloody diarrhoea makes a bacterial presentation more likely – e.g. E. Coli O157 or salmonella or E. histolyica (not commonly seen in UK)
• Children are more likely to be febrile with an infective gastroenteritis
• In adults, fever may be indicative of a more serious cause

Examination

• Heart rate
• Blood pressure
• Temperature
• Abdominal examination – often non-specific tenderness
• Degree of dehydration
  • Less than 5% – MILD
    • Postural hypotension
    • Thirsty
    • Reduced urine output
    • Dry mucosa
    • Mild tachycardia
  • 5-10% – MODERATE
    • Any of the above, PLUS
    • Dizziness
    • Tiredness
    • Muscle cramps
    • Dry tongue . mucus membranes
    • Sunken eyes (+/- sunken fontanelle in young children)
    • Reduced skin turgor
    • Postural hypotension with systolic BP dropping to <90
    • Tachycardia
  • 10% or more – SEVERE
    • Any of the above, PLUS
    • Oligouria
    • Confusion
    • Weakness
    • In children – floppy / unresponsive
    • Tachycardia
    • Reduced capillary refill time
    • Systolic BP <90

Differential diagnoses

Almost anything that causes diarrhoea or vomiting can be considered as a differential diagnosis, and hence the potential list is extremely long. Below are some common examples

• Urinary tract infection
  • often causes nausea and vomiting. May also cause diarrhoea. Consider urine MC+S in patients who present with diarrhoea and vomiting
•  Appendicitis
  • Typically vomiting, no diarrhoea, with abdominal pain +/- fever
• Diverticulitis
  • In adults over 50, with diarrhoea only and abdominal pain (typically LLQ) +/- fever
• Pancreatitis
  • Profuse vomiting, usually with epigastric pain
• Inflammatory bowel disease
  • Diarrhoea, no vomiting, may be blood stained or with mucus, with abdominal pain
• Constipation with overflow diarrhoea
  • Usually elderly patients, often with a history of recent constipation
• Gastritis
  • e.g. due to alcohol, NSAIDs
• Addison’s disease
• Type 1 diabetes – may present with vomiting in children and adolescents

Investigations

Stool MC+S is not routinely performed, but should be considered if:

• Blood or mucus in the stool
• Patient known to be immunocompromised
• Symptoms not resolving after 7 days
• Recent overseas travel
• Any uncertainty about diagnosis

In patients who are severely unwell – e.g. severe dehydration, consider:

• FBC
• Urea + electrolytes
• Specific investigations to rule out other causes – e.g USS or CT abdomen

Management

Indications for hospital admission

• Signs of severe dehydration
• Consider if not yet severely dehydration, but unable to retain fluids orally
• Consider if social circumstances may not be amenable to safe care at home – e.g. elderly or isolated, underlying medical conditions

Outpatient Management

• Oral rehydration is the mainstay of treatment
  • In adults, there is no evidence that oral rehydration solutions (e.g. dioralyte, hydralyte) are any more effective than water, although they are frequently recommended
  • Titrate to urine output
  • In children, oral rehydration solutions should be used, or watered-down apple juice (5 parts water, one part apple juice) is an alternative. Children can be reluctant to drink solutions. If parents are struggling, use a syringe, with small amounts regularly – e.g. 1ml/Kg every 5 minutes). Continue to offer breast milk if the child is usually feeding via this method
  • Aim for 50ml/Kg every 4 hours
  • Aim to record the fluid intake on a fluid chart
  • Vomiting is NOT a contraindication to oral rehydration – contrary to popular belief, it doesn’t “all come back up again” and significant amounts are often still absorbed
  • Consider IV fluids if not responding to oral intake
  • NG tube is an alternative to IV fluid in children
• Food intake:
  • Guided by appetite
  • Small frequent meals
  • Avoid fatty and spicy foods
  • Plain starchy foods considered best
  • NO evidence for fasting or avoidance of solid food intake
  • In children – feed as directed by the child
• Reducing the spread of infection
  • Frequent hadn’t washing is effective at reducing the spread of infection
  • Do not share towels
  • Wash any soiled bed sheets, separately from other clothes and at the highest temperature recommended on washing label
  • Recommend cleaning bathroom surfaces – e.g. taps, door hands, toilet flush and toilet seat at least daily
  • Norovirus is partially resistant to alcohol hand gel, and C. difficile spores are not killed by alcohol. As such, hand washing with soap and water is recommended
• School / work exclusion
  • Exclude for 48 hours from the last episode of diarrhoea or vomiting
  • Some guidelines recommend 24 hours instead of 48 hours
• Anti-emetics
  • Patient.co.uk states “not usually necessary in primary care” – my personal experience in primary care and as an Emergency Department Registrar in Australia is that they are VERY frequently prescribed – especially in children – in primary care and emergency departments.
  • Often ondansetron (private prescription only for this indication in both UK and Australia, and previously prohibitively expensive but now retails for <£5GBP or <$20AUD for 4 tablets of 4mg) is the most effective – 4mg single dose (or 2mg TDS in children between 8-16kgs, not recommended in children <8kgs, but in emergency departments sometimes given as 0.15mg/Kg doses). Particularly useful as it comes in an orally dispersible “wafer” which dissolves on or underneath the tongue and thus doesn’t require the patient to swallow a tablet with water in severe cases of vomiting. Often a single dose only is required – symptoms are usually much improved by 8 hours when a second dose can be given if required.
  • Metoclopromide – 10mg TDS in adults is another option
  • Cyclizine – 50mg TDS – an antihistamine – frequently used for nausea and vomiting on the NHS – because it is cheap!
• Anti-diarrhoea drugs – e.g. loperamide (“Immodium” or “gastro-stop”)
  • Not usually recommended
  • Are available over the counter and often patients have tried these before presentation
  • Carry a rare risk of bowel obstruction
  • Anecdotally in my practice seem to be associated with a longer duration of abdominal pain and bloating
  • Should NEVER be used if fevers or blood or mucus in stool
  • I rarely prescribe them if someone has an event they really can’t miss (e.g. wedding, funeral, job interview – although generally they should be isolating themselves anyway), with full disclosure of the above risks
• Antibiotics are almost never indicated
  • Most cases are viral
  • Even in a bacterial cause, most cases will resolve in a few days without the use of antibiotics. In common bacterial causes – such as E Coli or shigella, antibiotics can react with toxins and cause haemolytic uraemia syndrome and thus should still be avoided
• Notifiable diseases
  • Be aware of the results of any stool MC+S samples – as many identifiable causes are notifiable diseases

Complications

• Dehydration and electrolyte disturbance are the main complications
• Haemolytic uraemia syndrome – rare. Features include acute kidney injury, haemolytic anaemia and thrombocytopenia. Usually occurs in very young children or frail elderly adults
• Bacterial causes may cause reactive symptoms which are sometimes delayed in presentation by several weeks. These can include:
  • Arthritis
  • Carditis
  • Urticaria
  • Conjunctivitis
  • See reactive arthritis
• Salmonella is associated with a risk of systemic and secondary organ infection
• Toxic megacolon – rare
• Guillian-Barre Syndrome associated with viral infection
• Lactose intolerance – often transient
• Be aware of reduced medication absorption – particularly important examples include oral contraceptives and anti-convulsants

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Gastroenteritis in Adults and Older Children – patient.info
• Gastroenteritis – RCH
• Gastroenteritis in Children – HealthPathways

Read more about our sources

The post Gastroenteritis appeared first on almostadoctor.

Enuresis (involuntary urination) in children often occurs at night, with or without daytime features.

It can be divided into primary enuresis (has always had enuresis) and secondary enuresis (was continent, and later developed incontinence due to a secondary cause).

• Common reversible causes: UTI, constipation, emotional stress.
• Diagnosis requires a full voiding and bowel history with examination to exclude neurological disorders.
• Treatment with oxybutynin, fluid restriction, bladder training and behavioural therapies may be effective
• In secondary enuresis, treating the underlying cause will typically resolve the problem
• Enuresis before the age of 5 is normal, and is only considered pathological after the age of 5

In about 1% of cases it persists into adulthood. Cases in older children and younger adults can be particularly emotionally distressing.

Aetiology

• More common in boys
• The frequency of the bedwetting determines the severity. More frequent cases typically take longer to resolve
• Often a family history
• Associated with sleep apnoea (30% of cases)
• More common on obese children – affects 30% of obese children
• Associated with global developmental delay
• Factors that contribute to secondary enuresis
  • Emotional stress – e.g. bullying, separation from mother, starting new school
  • Constipation (+/- anal fissure)
  • UTI

Pathology

1. Primary nocturnal enuresis (PNE)– this is where the child has never experienced a period of prolonged dryness and continues to wet the bed more than 2 nights a week after the age of 5.
   • May be a disorder of sleep arousal – whereby the child is not awakened by the sensation of a full bladder
   • May be due to an overactive bladder or small bladder volume
   • It can be further divided into:
     1. Those with daytime symptoms
     2. Those without daytime symptoms
2. Secondary nocturnal enuresis(SNE) – this occurs after the child has had a period of at least 6 months without bed wetting. It can be related to emotional stress, constipation (+/- anal fissure) and UTI.

Clinical features and history

Primary enuresis

• How many times a week?
• At what time does bedwetting occur?
  • Is there a pattern?
• Does the child wake after the wetting
• What is the daytime toilet use pattern?
  • If there are daytime symptoms – consider screening for UTI
• Any constipation?
• Fluid intake
• Any other developmental problems?
• Why have they presented at this particular time?
  • School trip
  • Sleepover
  • Family troubled by the problem

Secondary enuresis

• When did it start?
• Does this correlate with any other changes in the child’s life?
• Bedwetting pattern
  • How often?
  • How may nights per week
  • Any pattern?
  • Does the child wake after bedwetting

Examination

• Abdominal examination
  • May elicit an enlarged bladder (outflow obstruction), or a mass consistent with faecal loading (constipation)
• Spine – spina bifida
• Lower limb neurological examination – neurological cause
• Perineum
• Urine dipstick (UTI, diabetes)

Diagnosis

Ask the parents to keep a diary of:

• Times of enuresis (both daytime and night time)
• Time of bowels opening
• Bristol stool scale of the bowel motion

Indications for further investigation

• Primary enuresis with  daytime symptoms
  • Urine MC+S
  • Assessment of constipation
• Secondary enuresis
  • Urine MC+S
  • Assessment of constipation
  • Blood sugar for diabetes
  • Behaviours / emotional issues
  • Consider child abuse
  • Ask the child if they think it is a problem and what the cause is

Treatment

Most cases are managed in primary care.

Primary enuresis often suits a more conservative approach and tends to settle with time, whilst secondary enuresis is consider to be more serious, and and thorough history, examination and potentially investigations should be performed to seek an underlying diagnosis.

Educate parents about behavioural strategies to help bedwetting

• Reassure the parents it is a common problem and most children will grow out of it
• Encourage regular fluids throughout the day and before bed – don’t advise withholding of fluids
  • Avoid caffeinated drinks before bed
• Encourage regular toilet breaks throughout the day – e.g. during school break times, and at night before going to bed
• Avoid lifting or carrying the child to the toilet during the night – wake them up and encourage them to be independent
• Consider a dry bed training regimen
  • Night 1: The child is woken every hour until 1am and encouraged to go to the bathroom
  • Nights 2-6: The child is woken once, 3 hours after falling asleep, and encouraged to go to the toiler
  • Night 7: The child should wake on their own
  • Repeat if >3 consecutive nights of bed wetting

Primary enuresis

• Waiting – many parents get anxious when their child wets the bed, but often they will outgrow it if you give them long enough. Some research shows that punishing a child for bed wetting can make the situation worse, as the punishments results in lower self-esteem and a downward spiral of symptoms.
• Alarm – a moisture detecting pad can be placed in the bed, and an alarm goes off when it gets wet. This wakes up the child, and helps them to associate the feeling of a full bladder, with having to wake up. These alarms make children 13x more likely to stop bed wetting, however there is a high relapse rate (up to 50%) and treatment regimens often have to be repeated.
  • Suitable for well motivated children from the age of 6-7 onwards
  • The child should be “in charge” of the alarm – they should learn how to turn it off – and should be fully awake when getting up to go to the toilet when it goes off!
  • Typically takes about 6-8 weeks to work
  • Needs an emotionally supportive family. Often not useful in an emotionally distressed household.
  • Efficacy may be assisted by the use of positive reinforcement – such as a start chart. These should be used to reinforce the behaviours of getting up and going to the toilet, operating the alarm correctly – and not for dry nights alone
  • Typically available for hire from pharmacies or community health providers. Can also be purchased outright for about GBP£50 or AUD$100.
  • Discontinue if no benefit within 4 weeks
  • Once dry for >2 weeks – encourage fluid intake before bed time to reinforce the sensation and behaviour of getting up to go to the bathroom. This is sometimes called overlearning
  • Involving the child in the cleaning of the soiled bedsheets has been proven to make alarm therapy more effective

• Desmopressin
  • Available as a sublingual “melt” or a tablet
    • sublingual – 120-240mcg at night
    • Oral – 200-400mcg at night
    • Age 6+ only
    • Risk of hyponatraemia (low), but avoid concurrent use of NSIADs
  • Indicated if alarm therapy is not appropriate or has failed
  • High relapse rate – 60-70%
  • May be suitable for short-term use (e.g. for school trips and sleepovers)
  • Restrict fluid from one hour before dose until 8 hours after dose
  • Cease after 4 weeks if ineffective
  • Cease one week every 3 months to assess ongoing need for medication
• Studies have shown that alarm training is either slightly more effective or equally effective to desmopressin, but that desmopressin treatment has a higher relapse rate
• Tricyclics are no longer recommended – very high relapse rate, and inferior to alarms and desmopressin
• Oxybutynin may be used in cases with severe daytime symptoms. It is not effective (nor indicated) for nocturnal enuresis alone

Secondary Enuresis

• Treat any underlying constipation
  • High fibre diet
  • Osmotic laxative – such as movicol (dose depends on child’s age)
  • Encourage regular fluid intake
• Otherwise, the same measures as above – include:
  • Alarms
  • Behavioural therapies
  • Desmopressin

Indications for referral to paediatrics

• Persistent symptoms despite use of an alarm
• Day-time enuresis when secondary causes have been ruled out
• History of recurrent UTI
• Diabetes or developmental delay has been idnetified
• Significant emotional or psychosocial problems

Faecal incontinence

• Most commonly due to constipation in children with psychological predisposing factors.
• History and examination is required to rule out physical cause e.g. coeliac disease and Hirschsprung’s disease.
• Management involves explaining the physiology of the condition (remove blame from child); treatment of constipation (stimulant laxative); behavioural strategies (toilet-sitting times).
• 5 year cure is 75%

References

• Enuresis – bed wetting and Monosymptomatic Enuresis – RCH
• Behavioural interventions including alarms: bedwetting (enuresis) – RACGP
• Nocturnal enuresis in children – patient.info
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

The post Incontinence in Children and nocturnal enuresis appeared first on almostadoctor.

Gastro-intestinal reflux disease (GORD) is a condition characterised by retrosternal, and sometimes epigastric pain, as a result of reflux of the acidic contents of the stomach into the oesophagus.

In the acute presentation it may be difficult to differentiate GORD from the symptoms of MI and other symptoms of acute chest pain.
Occasional feelings of ‘heartburn’ (dyspepsia) are normal. Acid reflux will cause peristaltic contraction of the oesophagus and alkaline saliva secretion, and normally this will cause the symptoms to go away.
It is only when pathological changes have occurred that allow gastric contents to be in prolonged contact with the oesophagus that we would call it GORD.

In GORD acidic stomach contents will spill out of the stomach and back up the oesophagus. The presence of a hiatus hernia increases the risk, but not everyone with a hiatus hernia gets GORD.There will usually be a problem with the lower oesophageal sphincter (LOS) whereby it doesn’t contract normally. Certain foods make the sphincter less likely to contract. There is also often decreased gastric emptying.
The oesophagus may become inflamed, reddened and ulcerated, although the level of tissue damage is not related to the severity of symptoms. In some cases, the normal squamous epithelium may be replaced by a columnar epithelium, similar to that found in the stomach. This is known as Barrett’s oesophagus.

Treatment typically consists of lifestyle advice, ant-acids and proton pump inhibitors (PPIs). It is important in patients with persistent symptoms to investigate for an underlying cause (e.g. helicobacter pylori, stricture) – which usually involves h. pylori testing and / or endoscopy.

Epidemiology

• GORD resulting in heartburn affects about 30% of the population

Aetiology

• Hiatus hernia
• Eating certain foods – fat, chocolate, caffeine
• Smoking
• Obesity
• Dysfunction of the lower oesophageal sphincter (LOS)
• Alcohol
• Helicobacter Pylori
• “Stress”

Pathology

There are several mechanisms by which GORD can occur:

• Lower oesophageal sphincter (LOS) – This is formed by the bottom 4cm or oesophageal smooth muscle.Normally this is contracted at all times, except during swallowing. It is even capable of increasing its normal tone is response to increased intragastric and intra-abdominal pressures. Also, the action of the diaphragm contracting may help to close of the bottom of the oesophagus, and the folds of the stomach also offer some sort of protection. The natural angle between the cardia and the oesophagus will also prevent some reflux. Problems can occur when:
• The LOS relaxes when it shouldn’t
• LOS tone doesn’t increase when the patient is lying flat – as would normally happen
• Hiatus Hernia – this is present in around 40% of the general population and often causes no problems. It is a congenital defect, where part of the stomach extends above the level of the diaphragm. Almost all patients with oesophagitis or Barrett’s oesophagus will have a hiatus hernia. (see Barrett’s oesophagus for more information)
• Delayed oesophageal clearance – this is present in many people with oesophagitis, and often remains after treatment for the condition. It increases the amount of time that oesophageal muscoa will stay in contact with acid for. This effect can be exaggerated by a hiatus hernia, because gastric contents can become trapped within the hernial sac.
• Delayed gastric emptying – this is usually present, but the reason why it occurs is unknown.
• Increased intra-abdominal pressure – this means that obesity and even pregnancy are proven pre-disposing factors.
• Dietary factors – fat, chocolate, alcohol and coffee all relax the lower abdominal sphincter. Smoking can also have a similar effect.

Symptoms

• Dyspepsia – ‘Heartburn’ – retrosternal chest pain, particularly after eating. May be worse on lying down. The pain is usually relieved by antacids. This pain is caused by the sensitivity of oesophageal mucosa to acid, and by spasms of the oesophageal sphincter.The pain is aggravated by drinking alcohol and hot drinks, and by bending over.  The amount of pain is very poorly correlated to the amount of oesophagitis.
  • Some people may have severe oesophagitis, but no pain (these patients may present with iron deficiency anaemia as a result of blood loss), whilst others may have very severe pain but only mild oesophagitis.
  • The pain is relieved by antacids.
  • The pain often radiates to the jaw, back and arms, hence…
  • The differential diagnosis for the pain is very difficult. 20% of patients admitted to cardiac wards are actually suffering from GORD.
  • Basically, the patient will present with a burning pain after eating, particularly after eating the aforementioned foods.
• Regurgitation of food and acid into the mouth – this generally occurs when the patient is lying flat. Note that aspiration pneumonia is very rare.
• Waterbrash – salivation due to the presence of acid in the oesophagus.
• Weight gain – this is a pre-disposing factor – not a symptom. Often a patient will put on a bit of weight, and shortly afterwards, the dysphagia will first present.
• Choking at night – as gastric acid irritates the larynx
• Dysphagia – this may be present in those people with a stricture. The stricture could be a result of mucosal damage due to reflux
• Excess Belching

Diagnosis and Investigations

In patients under 65 with no red flag symptoms, diagnosis is usually clinical. In patients whose symptoms failed to respond to standard treatments (lifestyle changes, antacids, and PPIs) then further investigations should be performed to look for an underlying cause (e.g. H. pylori, peptic ulcer stricture). These might include:

• H. pylori testing
  • Urea breast test is most sensitive and specify (both about 90%), but requires 2 weeks off PPIs beforehand and specialist equipment and test centre.
  • Serology and stool testing also exist – they are less sensitive and specific but much easier to perform
• Endoscopy – this can asses the level of inflammation, biopsy for histology and can also be used therapeutically to dilate the stricture if present.
• Barium swallow – may shows the presence of a hiatus hernia, or strictures
• 24hr luminal pH + manometry – may be used to confirm GORD before surgery. It will show a good correlation between pH in the oesophagus, and symptoms, and will rule out the possibility of oesophageal dysmotility. In this procedure involves inserting a catheter with a pH probe at the end down the oesophagus to the oesophageal-gastro junction. If the pH is below 4 for 6-7% of the 24 hour period, then diagnosis is confirmed.
• Radio-labeled technetium – this can sometimes be used to show reflux.

Complications

Upon endoscopy, the oesophagus can appear anything from slightly reddened, to severely ulcerated. Remember however, that this poorly correlates to symptoms, and some people with severe symptoms may have perfectly normal endoscopy and histology.
 Exposure of the patient’s oesophagus to the contents of the stomach will usually lead to inflammation and desquamation. The reflux causes the loss of many of the mucosal cells. thus the mucosa contains a higher proportion of immature cells. this is known as basal cell hyperplasia. There is also invasion of the area by inflammatory cells.
o   When the reflux is severe, cell proliferation cannot keep up with the rate of desquamation, and ulceration will occur. These ulcers can be a source of blood loss, and in some cases they can even perforate.
The ulcer can heal by a process of fibrosis and epithelial regeneration, but in the area of fibrosis, a stricture may occur.
In many people, the epithelial regeneration will be that of normal squamous cells, but in some people, the regeneration of cells will result in a columnar epithelium replacing the squamous one. This is known as Barrett’s oesophagus.
Barrett’s Oesophagus is a major complication of GORD. Many GORD patient’s will suffer from some degree of it.
Anaemia – this can result from chronic bleeding due to long term oesophagitis. This is especially common in patients with hiatus hernia. However, it is very important to remember other causes of iron deficiency anaemia as a result of blood loss .You mustn’t diagnose GORD as the cause without also investigating the possibility of colorectal bleeding, even in the presence of a hiatus hernia and oesophagitis.
Benign oesophageal stricture – these develop as a consequence of fibrosis due to long standing oesophagitis. They present with dysphagia that is worse for solids than liquids. After eating meat, there may be a bolus obstruction that causes complete dysphagia.Heartburn may also be present although it isn’t always. This condition is diagnosed by endoscopy, and biopsies are normally taken to exclude malignancy. The patient should be put on PPI’s and be educated on the need to chew food thoroughly. As patients are often elderly, and examination of sufficient dentition should be carried out.
Gastric volvulus – this is rare, but can be dangerous. It occurs when a hiatus hernia turns in upon itself and causes complete oesophageal gastric blockage. Patients will present with chest pain, vomiting and dysphagia. Most cases will spontaneously resolve, but they tend to recur, and surgery is advisable.
Webs – these are an out growing of the mucosal lining of the oesophagus. They will grow inwards into the lumen, and they look a little bit like a hymen. They are a common cause of dysphagia high up the oesophagus. You can break through them with an endoscope, and this will pretty much heal them. It may look a bit scary on endoscopy because there is blood, but actually, your endoscopy has been therapeutic!

Treatment

• Treatment of symptoms with antacids
• Proton Pump Inhibitors (PPIs)
• Raising of the head at night time (e.g. with extra pillow, raise the head of the bed)
• Encourage loss of weight
• Encourage cessation of smoking
• Reduce alcohol consumption.
• Avoid wearing very tight clothes! This helps keep intra-abdominal pressure down.
• Avoid eating late in the evening.
• Adherence is generally poor

Simple antacids – these are readily available, and patients often use them themselves:

• Magnesium Tricilicate – This may cause diarrhoea.
• Aluminium Hydroxide – this may cause constipation

Alginate-containing antacids – these available OTC and often used by patients before they come to see their doctor. You take 10ml 3x a day, and they will form a ‘foam-raft’ in the stomach on top of the gastric contents, which help to prevent reflux.
PPI’s – these will reduce acid secretion by up to 90%. An example is omeprazole – 40mg daily. After about 2 months of use, they can result in rebound increased acid secretion, which may last for around 2 months. If patients intend on using these for many years, then a lower does (e.g. 10mg) may be sufficient for maintenance.
Prokinetic agents – these can be helpful in some patients. They are usually dopamine antagonists, and they will increase the rate of gastric emptying due to increased peristalsis. Examples include metocloperamide and domperidone.
H. Pylori eradication – this seems to have little effect on symptoms of GORD, but is usually advisable to prevent other conditions (i.e. gastric ulcer and gastric neoplasm)
Symptoms will nearly always recur when PPI / antacids treatments are stopped.
 

Surgery

Surgery for GORD is usually a last resort. This is only used if the above treatments are in-effective. After several years on the above treatments, their effect may become lessened, and so surgery may be considered at such time. It is quite rare for patients to have surgery because most patients symptoms aren’t severe enough; they may interfere with quality of life slightly, but can be readily controlled by drug treatment.

The most common type of surgery is a Nissen fundoplication. It is performed laproscopically, however, in 2% of cases, during the operation, a laparotomy may have to be performed due to issues arising during surgery.  In this procedure, the fundus of the stomach (i.e. the top part) is wrapped around the bottom of the oesophagus and sewn in place. This means that when the stomach contracts, the bottom of the oesophagus is sealed off, and reflux is prevented. This type of surgery will also prevent a hiatus hernia, as the part of the stomach that may cause one of these is now sewn in place. This treatment will be beneficial in about 80% of cases.

Complications (of Nissen)

• Dysphagia – due to the wrap being too tight.
• Dumping
• Excessive scarring
• Bloating – the fundoplication is such a good procedure at doing its job that it ends up holding gas inside the stomach as well.
• Para-oesophageal herniation – this occurs alongside the site of the fundoplication, often as a result of increased intra-gastric pressure.
• Achalasia – this is rare. It is an oesophageal motility disorder, whereby the bottom of the oesophagus may not relax properly during swallowing. It will cause dysphagia, regurgitation and chest pain. It is a condition that most commonly occurs spontaneously but can also occur after surgery and as a result of gastric carcinoma.
• In 15% of cases, the fundoplication may ‘split open’ over time. In such cases it is possible to perform the procedure again, but it is more tricky the second time round.
• Patients who have had the laparoscopic surgery only can eat again within 2-3 days. In laparotomy this is more like 8 days.
• Patients often feel so good after laprosocpy that they have to be advised to be careful! They shouldn’t do anything too strenuous for up to 8 weeks after as this increase the risk of para-oesophageal herniation.

 
Oesophagotomy – this is performed in cases with high grade dysplasia.

Other causes of oesophagitis

• Infection – candidasis is the most common form of this and will often occur in immunocompromised patients.
• Corrosive – for example in a suicide attempt by ingesting household bleach or battery acid. It may also cause perforation and strictures. Conservative management is the best option.
• Drugs – if a stricture is present in a patient, then NSAID’s and potassium supplements may cause ulceration. In such patients, then liquid preparations of these drugs should be used.

The post GORD – Gastro-oesophageal reflux disease appeared first on almostadoctor.

• Grade 1: Trivial lack of awareness. Impaired attention span. Altered sleep, euphoria or depression. Mild asterixis may be present.
• Grade 2: Lethargy or apathy. Disorientation. Inappropriate behavior. Slurred speech. Asterixis.
• Grade 3: Gross disorientation. Bizarre behavior. Semi-stupor. Asterixis absent.
• Grade 4: Coma (unresponsive to verbal or noxious stimuli)

The post Hepatic Encephelopathy appeared first on almostadoctor.

Dysphagia literally means ‘trouble swallowing’. It is not a condition in itself, but a symptom. There can be many causes varying from a muscular spasm or neurological cause, to oesophageal malignancy. As a result, any patient that presents with dysphagia needs to be thoroughly investigated for the possibility of malignancy.

Types of dysphagia

Pharyngeal / oesophageal

• Motor neuron disease
• Myasthenia gravis
• Upper oesophageal achalasia
• Polio
• Botulism
• Cerebrovascular accident resulting in damage to 9^th, 10^th and 12^th cranial nerves – this is the most common cause.

Oesophageal

• Achalasia
• Oesophageal spasm
• Luminal obstruction (e.g. due to stricture, bolus, carcinoma or perhaps trauma damage)

External

• Retrosternal goitre
• Lung cancer
• Pharyngeal diverticulum
• Vascular abnormalities – e.g. abdominal aortic aneurism, enlarged heart.
• Any type of mediastinal mass.
• Diabetes – can cause motility disorders in upper GI tract. Most commonly causes delayed gastric emptying,

Symptoms associated with dysphagia

• Chest pain due to oesophageal reflux
• Pain on swallowing – odynophagia – associated with oesophagitis
• Reflux of food or bile into the mouth – associated with severe GORD
• Coughing and aspiration of food – due to laryngeal or bulbar nerve palsy
• Palate incompetence – food goes into the nose when swallowing – associated with bulbar nerve palsy particularly after a cerebrovascular accident.
• Loss of weight / anorexia – suggests upper GI malignancy
• Hoarseness of voice – can be due to associated laryngeal malignancy, or as a result of laryngeal nerve palsy.

Diagnosis

• Progressively worse dysphagia – suggests malignancy
• Difficulty swallowing solids but not liquids – suggests muscular incoordination
• Dysphagia with retrosternal pain and regurgitation – suggests stricture or carcinoma
• Dysphagia with weight loss – suggests malignancy

Investigations

• Barium swallow – this gives very good views of the upper oesophagus, and thus will aid diagnosis of pharyngeal pouches and strictures, however often a negative result will be found, and this will require endoscopy. As a result, this test is rarely used, and endoscopy if the first investigation of choice.
• Endoscopy – this is actually quite risky compared to say endoscopy for gastric purposes, because things like pharyngeal pouches and strictures increase the risk of perforation. Strictures are often visible, and these can be diagnosed as benign or malignant. It may also be possible to diagnose achalasia if the oesophagus appears dilated in the presence of food residue.
• CT scan – this is rarely used as an investigation but may be regularly used to assess the level of malignancy.
• Endoscopic ultrasound – this is very useful at measuring things to do with the oesophageal wall. It cannot be performed if there is a narrowing at the top of the oesophagus because this prevents the passage of the instrument.
• 24Hr pH monitoring – this helps to see the amount of oesophagitis present and thus decided whether this may be a causing factor.

Pharyngeal Pouches

Achalasia

1. The oesophageal sphincter will not relax properly, and so food cannot pass into the stomach in the normal manner
2. The peristaltic contractions of the oesophagus do no propagate properly, and so the oesophagus will gradually become more and more dilated.

Complications

Diagnosis

Chest X-ray
Barium swallow – this will produce a characteristic ‘bird’s beak’ appearance (see below)
Manometry – this is where the pressure within the oesophagus is measured.

 

Treatment

Scleroderma

References

Read more about our sources

The post Dysphagia appeared first on almostadoctor.

Epstein-Barr virus (EBV) is a type of human herpes virus. It is extremely widespread, and is contracted by close person to person contact. It can cause a wide range of clinical consequences, and the most common clinical manifestation is Infectious Mononucleosis.

Many infections (up to 50%) are subclinical and asymptomatic. In (the other) 50% of people, primary infection with the virus will cause clinical symptoms, usually in the form of infectious mononucleosis.
In both subclinical, and clinical primary infections, the host will carry the virus asymptomatically for the rest of their life, after the initial presentation has resolved.

Long-term, it has been associated with an increased risk of B cell lymphoma, T cell lymphoma, Hodgkin’s lymphoma, and nasopharyngeal carcinoma.

Epidemiology

• Up to 95% of individuals carry the virus
• Approximately 50% of cases are symptomatic on primary infection, most commonly in the form of Infectious Mononucleosis
• Can present at any age. May be more common in teenagers, and occasionally referred to as ‘kissing disease’

Infectious Mononucleosis

Presentation and Diagnosis

• Headache
• Fever
• Tonsillitis / sore throat
• Cervical lymph node enlargement and tenderness (usually symmetrical)
• Malaise and severe fatigue
• May have tonsillar exudate
• Nausea / vomiting / GI symptoms. Up to 90% of patients also have a mild hepatitis
• Splenomegaly occurs in 50% of patients
• Jaundice and hepatomegaly are rare
• Occasionally patients may present with hepatitis with none of the other features

• Fever >38 degrees
• Tender cervical lympadenopathy
• Tonsillar Exudate
• No cough

Often in a bacterial cause, there is asymmetrical cervical lymphadenopathy also.

It is particularly important to differentiate EBV from bacterial causes because giving amoxicillin or ampicillin in EBV infection is contraindicated and can cause a rash (which is unrelated to any penicillin hypersentivity).

Treatment

• Avoid antibiotics
• Most cases resolve spontaneously within 1-2 weeks
• Fatigue can persist for several weeks or months

Other Infections

References

Read more about our sources

The post EBV – Epstein Barr Virus appeared first on almostadoctor.

Introduction

Pancreatic cancers are 95% exocrine, adenocarcinomas. These affect the duct or surround the duct. The remaining 5% are neuroendocrine tumours e.g. insulinomas, glucagonomas (the former being the more common). This article pertains to adenocarincoma, with the latter briefly mentioned at the end.

Typically, the more common adenocarcinoma occludes the pancreatic duct or branches of it. 70% occur at the head, causing (an initial) painless jaundice as the obstructed bile cannot flow through the sphincter of Oddi and refluxes back up through the biliary tree and into the blood. Tail tumours are more likely to be neuroendocrine than head tumours.

These tumours nearly always present late and nearly always have a terrible prognosis, with mean survival from diagnosis of 6-10 months depending on the presence or absence of metastases respectively. >80% have metastasised at diagnosis.

Epidemiology

• Increasing in incidence rising 4% per decade
• Nearly 9000 new diagnoses yearly in the UK
• 10^th most common cancer
• 5% of all cancer deaths but only 3% of all cancer diagnoses
• In excess of 8,000 annual deaths (2011 data, Cancer research UK)
• 5 year survival <2%

>90% have KRAS mutations, and many other mutations besides.

Risk factors

• Age (above 60s, very rare below 40)
• Smoking (RR 1.7)
• Diabetes mellitus
• Helicobacter pylori infection status (may be subclinical, often is)
• Partial gastrectomy
• Family history and genetics (<5% of cases)
• Obesity
• Male sex (RR 1.3)

Dubious but commonly asked by patients: red meat consumption, sugar intake, poor vegetation intake.

Note: whilst chronic pancreatitis is associated, alcohol and gallstones (a known proponent of chronic pancreatitis) per se are not associated with pancreatic cancer: contrary to the Oxford handbook of clinical medicine. Chronic pancreatitis is thought to be required for the dysplastic transformation (personal communication on wards).

Symptoms

• Pain is found in 70% of presentations (similar to that seen in pancreatitis – epigastric radiating to the back. Remember the pancreas is retroperitoneal apart from the tail, found in the splenorenal ligament)
• Anorexia and nausea
• Diarrhoea
• Cachexia
• Jaundice (obstructive picture with pale stools and dark urine)
• Itch (due to peripheral bilirubin)

Symptoms of advanced disease

• Pulmonary emboli – SOB, chest pain
• Diabetes mellitus – polyuria, polydipsia
• Ascites – abdominal fullness

Courvoisier’s law: in the presence of painless jaundice, a palpable gallbladder is unlikely to be due to gallstones. I.e potentially pancreatic cancer; it’s spread to the gallbladder already. Whilst pain is the most common presentation, painless jaundice is always sinister.

Thrombophelbitis/Trousseau’s sign: uncommon but can occur e.g. portal venous thrombosis.

On examination

• Typically: cachectic, jaundiced old patient presenting with abdominal pain/breathlessness/diarrhoea.
• Masses may be felt in the epigastric region – either hepatomegaly or gallbladder
• Ascites

Blood tests

• Obstructive jaundice picture (raised bilirubin and alkaline phosphatase, may have hepatocellular dysfunction too with raised ALT and AST)
• Hyperglycaemia
• Anaemia
• Hypokalaemia (if vomiting or diarrhoea)
• Hypercalcaemia (may be related to chronic pancreatitis or Trousseau’s sign of latent malignancy)
• CA19-9 is a tumour marker is 77% sensitive and 87% specific if significantly raised and is more likely to be raised if the cancer has metastasised.

Investigations

Typically

• US – sensitive to masses in the biliary tree and pancreatic ducts
• CXR – Can determine lung involvement
• Endoscopic US or biopsy
• If there is a suspicious mass on US, endoscopy can help confirm the diagnosis. Histology is not normally required for formal diagnosis.
• CT/PET staging

Treatment

The mainstay of treatment is palliative with significant analgesia required. Many patients ask for or are recommended palliative endoscopic stenting to help control their symptoms. Bilirubin itch is debilitating, but endoscopic stenting can provide a good remedy. Patients will often be on PCA (patient-controlled analgesia) and may attend hospital for symptomatic ascites drainage. <20% have an operative option available.

Surgery

• Whipple’s procedure (head) – a massive operation and rarely done, but potentially curative. A Pancreatoduodenectomy.
• Distal pancreatectomy (tail)

Chemotherapy

• Gemtacitabine (weekly IV infusion) prolongs median survival and improves QoL in some, but many do not wish for chemotherapy.

Radiotherapy

• Mostly reserved for adjuvant usage in potentially ‘curable’ tumours

Prevention

Low dose aspirin for 5 years has been shown to reduce the risk of pancreatic cancer by around 75%.
(Effect of aspirin on long-term risk of death due to pancreatic cancer: analysis of individual patient data from randomised trials. Rothwell et al 2011, Lancet)

Neuroen​docrine tumours

Glucagonomas and insulinomas are much rarer.

They can be watchfully waited upon, have RF ablation, surgically excised and so on. These can be associated with MEN-1, particularly insulinomas

References

Read more about our sources

The post Pancreatic Cancer appeared first on almostadoctor.

Pancreatitis is a condition involving inflammation of the pancreas. It can be acute or chronic; acute pancreatitis can return to normal after resolution of the episode, conversely chronic pancreatitis, is continuing inflammation, often with irreversible structural changes.

Acute Pancreatitis

Aetiology

Gallstones and alcohol account for the vast majority of episodes. The severity varies from mild self-limiting to extremely severe with extensive pancreatic and peripancreatic necrosis as well as haemorrhage. In its most severe form the mortality can be between 40-50%, as damage can result in the release of is lytic enzymes into the blood, contributing to severe shock and digestion of surrounding tissue. The causes of pancreatitis can be remembered with the acronym GET SMASHED:

• G – Gallstones
• E – Ethanol (alcohol!)
• T – Trauma

• S – Steroids
• M – Mumps
• A – Autoimmune – e.g. SLE
• S – Scorpion bites (rare!)
• H – Hypercalcaemia, hypothermia, hyperlipiaemia
• E – ERCP
• D – Drugs – e.g. azathiaprin

Pathogenesis

Necrosis >> Autolysis >> Infection >> Pseuodycyst
A theory suggests that the final common pathway has marked ↑ in intracellular calcium which → activation of intracellular proteases. There is evidence that alcohol interferes with calcium homeostasis in pancreatic acinar cells. In severe inflammation, it becomes swollen and haemorrhagic. Proteases digest the walls of blood vessel → blood extravasation; amylase is released into the blood (but is a non-specific diagnostic marker). Released lipases (better diagnostic marker) cause fat necrosis within abdomen and subcutaneous tissue, can → discolouration of skin (Grey Turner’s sign). The released fatty acids can bind Ca²⁺ can → hypocalcaemia.Concomitant destruction of adjacent islets can → hyperglycaemia and thus cause Type  II diabetes. Also, formation of abscesses and cysts within the pancreas or adjacent tissues can occur.Infection secondary to pancreatic tissue damage does not always occur. Not all cases of infection lead to cyst / pseudocyst formation.
Pulmonary failure in acute pancreatitis is believed to be caused by circulating activated digestion enzymes (e.g. trypsin, phospholipase A2, etc.) leading to a loss of surfactant, atelectasis and irritation eventually leading to ARDS and pleural effusion. Cardiac depression and breakdown of the blood brain barrier can also occur in severe AP and are possibly due to the same etiology.

Clinical features

Upper abdominal pain, normally beginning in the epigastrium accompanied by nausea and vomiting. As inflammation spreads in peritoneal cavity pain → more intense, involvement of the retroperitoneum frequently → back pain. In severe cases the patient may have tachycardia, hypotension and be oliguric. Abdominal examination may show widespread tenderness with guarding; also reduced/absent bowel sounds. Also periumbilical bruising (Cullen’s sign) and Grey Turner’ sign (flank bruising) if present show severe necrotising pancreatitis. Left sided pleural effusion, if present, is indicative of poor prognosis.

Diagnosis

• Blood tests will show raised serum amylase (may be many times norm level, important indication of pancreatic inflammation), lipase, also with raised urinary amylase. Amylase is not prognostic, nor is the level related to the degree of tissue damage Lipase levels are more specific and may relate to the level of tissue damage, but levels do not rise until up to 8 hours after the onset of symptoms.
• CXR to exclude gastroduodenal perforation, which also ↑ serum amylase. May show gallstones or pancreatic calcification.
• Ultrasound scan (USS) → find gallstones (biliary cause of pancreatitis), may also sow pancreatic swelling and necrosis.
• Contrast-enhanced spiral CT → assess extent of pancreatic necrosis + to detect complications such as abscess dev, fluid collection and pseudocyst formation.
• MRI (MRCP) assesses degree of pancreas damage and finds gallstones, can differentiate between fluid and solid inflammation.
• ERCP (Endoscopic Retrograde Cholangiopancreatography) used to look at pancreatic duct for inflammatory fibrosis or tumours, and pancreatic juice can be collected and biochemically examined.
• Operative biopsies or needle aspiration cytology under USS.
• APACHE (acute physiology and chronic health evaluation score) is a means of assessing the severity of a wide spectrum of illness, adjusted for age + obesity and other health problems, has a high sensitively as early as 24 hours after symptom onset. A score of >8 indicates severe disease
• The Glasgow scoring system can also be used to asses the severity and prognosis of pancreatitis. The modified version of the score can be remembered with the acronym PANCREAS:

• PO₂ Oxygen < 60mmHg or 7.9kPa
• Age > 55
• Neutrophilia White blood cells > 15
• Calcium < 2 mmol/L
• Renal Urea > 16 mmol/L
• Enzymes Lactate dehydrogenase (LDH) > 600iu/L Aspartate transaminase (AST) > 200iu/L
• Albumin < 32g/L
• Sugar Glucose > 10 mmol/L

Treatment

• Replace lost fluids (IV) and a urinary catheter might be necessary
• Nasogastric suction to prevent abdominal distension and vomitus and hence ↓ risk of aspiration pneumonia. Continuous oxygen administration may be necessary, depending on sats.
• Prophylactic antibiotics, broad spectrum e.g. cefuroxime or aztreonam ↓ infection complications
• Analgesia, pethidine and tramadol administered under patient control system
• Enteral nutrition, via nasojejunal tubes.
• In patients with multiorgan failure → ventilation and renal support, mortality rate >80%.
• Complications of acute pancreatitis:
  • Within the first week, the morbidity and mortality reflect the systemic inflammatory response, which in turn results in multiple organ failure. After this, the prognosis is related to the extent of pancreatic necrosis. Extensive necrosis (> 50%) is associated with high risk of further complications, which frequently need surgical intervention. Infection of the necrotic pancreas can lead to sepsis, resection of infected areas of pancreas may be needed. Some fluid collections will be surrounded by granulation tissue → pseudocyst, larger ones (> 6cm) may become infected or → intraperitoneal bleeding, thus need to be drained surgically.

Prognosis – The vast majority of patients with mild or moderate acute pancreatitis will make a full recovery. Severe acute pancreatitis patients may become pancreatically insufficient with respect to exocrine (malabsorption) and endocrine function (diabetes).

Chronic Pancreatitis

Aetiology

Pathogenesis

Possibly, due to inappropriate activation of enzymes within the pancreas, this has been demonstrated in the case of hereditary pancreatitis, where genetic abnormalities of cationic trypsinogen and its inhibitory proteins have led to unopposed trypsin activity within the pancreas. Chronic alcohol intake is also believed to ↑ the level of trypsinogen relative to its inhibitor, and human trypsinogen has a tendency to auto-activate → unopposed activity → damage pancreas.  It is believed that the intrapancreatic enzyme activity → precipitation of proteins within the pancreatic duct lumen in the form of plugs. These form a starting point for calcification and also → ductal hypertension → further pancreatic damage. Cytokine activation and oxygen stress → perpetuate this process, via inflammation.  Clinical features Pain: usually epigastric often radiating through into the back, it may be episodic. Exacerbations may follow further alcohol excess. During periods of abdominal pain, weight loss may be severe. Malabsorption and diabetes by develop due to exocrine and endocrine insufficiency respectively. Jaundice secondary to common bile duct obstruction, may be a feature in a small number of patients.

Diagnosis

• ERCP (Endoscopic Retrograde Cholangiopancreatography) often shows distorted pancreatic ducts due to scar tissue resulting from chronic inflammatory process.
• X-Ray of upper abdomen often reveals flecks of calcification due to previous fat necrosis.
• Serum amylase and lipase levels are elevated.
• Faecal elastase levels will be abnormal in the majority of patients.
• PABA and pancreolauryl tests
• USS and contrast enhanced spiral CT, MRI with MRCP (magnetic resonance Cholangiopancreatography), which has replaced ERCP are used as in diagnosis of acute pancreatitis
•  Endoscopic ultrasound

Treatment

Combination of NSAIDs and opiate (tramadol) for pain relief. Trycyclic antidepressants e.g. amitriptyline are used for chronic pain. Oral pancreatic enzyme supplements reduce pancreatic stimulation (by -ve feedback) and hence intensity of pain. Pain does improve over time, after 6 to 10 years, 60% of patients are pain free. For patients with debilitating pain, surgical intervention is an option, with duct drainage and limited resection which can relieve pain in 80% of patients, but mortality of 5%. Endoscopic techniques can be used to improve pancreatic drainage. An acid suppressor (H₂-receptor antagonist or PPI) is also given, to compensate for decreased bicarbonate secretion. Despite this, a proportion of patients continue to malabsorb, due to inadequate mixing of pancreatic supplements with the food as well as the low pH in the duodenum.

Pancreatic enzyme supplements – pancreatin

Pancreatin consists of protease, lipase and amylase, which are inactivated by gastric acid and by heat. Supplements, therefore, must be taken with food (but not mixed with very hot food), and either concurrently with gastric acid suppression therapy (e.g. with cimetidine, a H₂-receptor antagonist or a proton pump inhibitor) or as enteric-coated formulations. Pancreatin preparations in clinical use are of porcine origin. Dosage is adjusted according to the size, frequency and consistency of stools.

Unwanted effects include irritation of the mouth and perianal skin, nausea, vomiting and abdominal discomfort. Some higher-strength formulations should be avoided in children under 15 years of age with cystic fibrosis, since they have been associated with the formation of large-bowel strictures. Thus, the amount of pancreatin given has to be balanced with the side effects. For example, to reduce the side effects, the amount of pancreatin given has to be reduced; which in turn means the amount of total dietary fat consumed has to also be reduced, to avoid steatorrhoea.

Complications

Same as acute pancreatitis, pseudocyst formation etc. Also, formation of ascites, accumulation of serous fluid in the peritoneal cavity and occasionally pleural effusions.

Steatorrhoea

Passage of fat in large amounts in the faeces (up to 30 mmol per 24 hours), due to failure to digest and absorb it, is associated with pancreatic insufficiency. This will usually improve with pancreatic enzyme supplements, e.g. pancreatin, and a low fat diet.

References

Read more about our sources

The post Pancreatitis appeared first on almostadoctor.

Presentation

• Abdominal pain in the epigastric region. For DU’s, the pain is when you are hungry, and GU’s the pain is when you eat. This is because when you are hungry, you produce acid in anticipation of food (the cephalic phase), which is then washed straight into the duodenum and isn’t buffered. When you eat, the food buffers the acid, and so the pain is reduced. In GU, the pain is greater when you eat due to the physical pressure of food on the ulcer. DU pain is present at night as well as in the day.
• Nausea may accompany the pain, and although vomiting is infrequent, it will often relieve the pain.
• Weight loss may be present, particularly in gastric ulcers.
• Left untreated, the symptoms of DU follow a spontaneous relapse and remission course
• Examination is not always that helpful, as there is nearly always general tenderness in all dyspepsia’s.
• History of NSAID’s / alcohol / steroids

Investigations

• Urea breath test to test for presence of H. Pylori
  • Patients will swallow urea that is labelled with an uncommon isotope – i.e. carbon 13 or 14. Usually Carbon 113 is used as it is non-radioactive. Then 10-30 minutes later, a breath sample is taken to measure the amounts of exhaled carbon dioxide containing the labelling isotope. The sample is measured using a mass-spectrometer, which is expensive, but is highly sensitive (97%) and specific (96%). This indicates that the urea has been split up and the carbon absorbed by the body. The urea is split by the enzyme urease which is present in H. Pylori, and thus this indicates the presence of H. Pylori.
  • Often a baseline sample of carbon dioxide is taken before the labelling isotope is given and then the two results compared.
  • There are also urea splitting bacteria in the colon that will cause the labelled carbon to be present in exhaled air about 5 hours after ingesting the urea.
• Serological tests for IgG. These are useful for confirming the presence of H. Pylori, but not as accurate as the breath test. It is about 90% specific. It can take over a year for IgG levels to fall below 50% of their original value even after H. Pylori eradication, so this is not a useful test to see if the infection has been eradicated. Antibodies can also be found in the saliva, but these are nowhere near as accurate as serology.
• Stool test. This is a highly sensitive (96%) and specific (97%) immunoassay that will detect the presence of H Pylori, and can also be used to see if H Pylori has been eradicated. PPI’s must be stopped one week before the test for eradication. This is now often the first line test.

Invasive

• Endoscopy. (OGD) This will confirm the presence of an ulcer by sight, but a sample of gastric mucosa may also be taken. This can be tested in three ways:
  • Put in a urea solution containing Phenol red. If H. Pylori is present, then the urea will be rapidly split to release ammonia, and the solution will increase in pH and change colour. This is known as the rapid urease test.
  • Cultured and tests against various antibiotics
  • Looked at histologically.
• FBC – to check for anaemia
• U+E – rarely shows up Zollinger-Ellison syndrome
• Faecal occult blood
• Barium meal test – sometimes used in patients who are unable to tolerate endoscopy.

Causes

Pathology

• These are usually held responsible for the ulcers where H pylori infection is absent (about 25%). They inhibit cyclo-oxygenases (COX), which are enzymes that enable the production of prostanoids (prostaglandins and thromboxanes). There are 3 variants of COX, 1,,& 3. COX-1 is involved with protection of the gastric mucosa, and it is sometimes called the ‘housekeeping’ enzyme, due to its role in every day wear and tear repair.
• Ultimately, NSAID’s inhibit prostaglandin formation and so reduce the ability of the stomach to heal itself. Small abrasions to the lining of the stomach that occur all the time, and would normally heal are now less likely to heal. Pepsin may also act on these abrasions, and ulceration may possibly occur.
• The major repair pathways that prostaglandins affect are:
  • Bicarbonate secretion into the mucous layer
  • Tight junction maintenance between gastric cells to prevent lumen contents getting between the cells
  • Gastric bloodflow – delivering lots of bicarbonate ions to buffer to acid to the gastric cells.
• Taking long term aspirin makes you 3x as more likely to get an ulcer, and other NSAID’s have a similar effect. Take them both together and your risk is 10x greater!

Treatment

• The patient is under 55 and has tested positive for H. Pylori
• The patient is over 55 and testes have confirmed a gastric ulcer is responsible for their symptoms.
• The patient has no significant underlying pathologies (e.g. cancer) but H. Pylori is present. This is slightly controversial as it has been implicated in GORD, but it is still recommended.

• First line therapy – Triple therapy – patients will be treated with a proton pump inhibitor, and two antibiotics. An example would be:
• Omeprazole 20mg + metronidazole 400mg + clarithromycin 400mg  All twice daily.
• Omeprazole 20mg + metronidazole 400mg + amoxicillin 1g  All twice daily.
• There is very high resistance for metronidazole (25%) and that is why another antibiotic is taken.  This regimen should be followed for 7 days, and then a PPI taken for a further 3-4 weeks.

Complications

• Perforation
• Haemorrhage – this is a result of an ulcer being in an ‘unlucky’ place, and as it gets deeper, it comes across a blood vessel. This can be quite serious if it is a relatively major vessel, and result in anaemia.
• Penetration of adjacent organs
• Anaemia
• Malignancy

Perforation

• Sudden onset severe abdominal pain. At first pain may be localised to the upper abdomen, but it quickly spreads and becomes generalised.
• If the pain radiates to the back, then it is likely to be a posterior duodenal ulcer.
• Localised or generalised peritonitis. Very tender to the touch. You can tell if someone has peritonitis as opposed to a different cause of abdominal pain because if they have peritonitis they will want to lie very still, but with other causes of pain, they may ‘writhe’ around in pain.
• Signs of SIRS (systemic inflammatory response syndrome).
• Breathing will be shallow due to diaphragmatic pain and shock.
• The abdomen will be immobile with board like rigidity.
• Bowel sounds are absent, and the dullness over the liver may not be there due to the prescence of gas in the abdominal cavity
• After a few hours, the initial symptoms may die down, but there will still be the rigidity. Over a longer period of time, the patien’s condition will deteriorate due to peritonitis.
• Perforation has a mortality rate of 25% – this is dependent on the patient’s age and other factors.
• The main problem with a perforated ulcer is that it will cause peritonitis.

Investigations

• X-ray may show gas under the diaphragm (in about 50% of cases)– pneumoperitoneum – shown below by the distinctive lines underneath the diaphragm. Don’t get this confused with air in the stomach, which is perfectly normal and most commonly seen after a recent meal. It is important when taking an x-ray like this that the patient has been sat upright for at least 10 minutes beforehand and is sat upright when the x-ray is taken Otherwise you will not be able to see any air! Sitting like this may be uncomfortable for the patient.

Management

• After resuscitation then the perforation will be treated surgically – it will be closed by being sewn up, and then part of the greater omentum may also be sewn over the affected area – the omentum is still attached to the rest of itself! If this is not possible, then a pyloroplasty may be made from the perforation.
• A pyloroplasty is where the pyloric sphincter of the stomach is widened. It allows quicker emptying of the stomach in people at high risk of PUD and is sometimes performed before an ulcer has perforated. In this case it is performed because sealing up the perforation is too difficult, and it is a treatment that may have beneficial effects for the patient by reducing the risk of future ulcers.

Complications (of surgery)

• Peritonitis

• Chest infection from aspiration during intubation
• Wound infection

• Adhesions. These can occur years after surgery and will ofte4n cause obstruction of the bowel. They are much lea common with key hole surgery than with open surgery – probably due to the reduces physical moving of the bowel by this type of surgery.
• Keyloid scarring – this is where a big thick scar develops over the site of the incision and is virtually impossible to get rid of. You can get rid of it by cutting it off, but it is very likely to grow back again just the same.

Flashcard

References

Read more about our sources

The post Peptic Ulcer Disease appeared first on almostadoctor.