gastroenterology Flashcards

1
Q

define posseting

A

describes the small amounts of milk that often accompany the return of swallowed air (wind), whereas regurgitation describes larger, more frequent losses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

infant causes of vomitting

A
  1. Gastro-oesophageal 2. reflux
  2. feeding problems
  3. infection
    - gastroeneteritis
    - OM
    - whooping cough
    - urinary tract
    - menigitis
  4. food allergy and food intolerance
  5. eosinophilic oesophagitis
  6. intestinal obstruction
    - pyloric stenosis
    - atresia - duodenal
    - intussusception
    - malrotation
    - volvulus
    - dupilication cysts
    - strangulated inguinal hernia
    - hirschsprung disease
  7. congenital adrenal hyperplasia
  8. renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

preschool children causes of vomiting

A
  1. gastroenteritis
  2. infection
    - gastroeneteritis
    - OM
    - whooping cough
    - urinary tract
    - menigitis
  3. intestinal obstruction
    - intussusception
    - malrotation
    - volvulus
  4. raised ICP
  5. coeliac disease
  6. renal failures
  7. torsion of testes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

school age and adolescents causes of vomiting

A
gastroenteritis
infection - pyelonephritis
peptic ulceration
appendicitis
migraine
raised ICP
coeliac
renal failure
DKA
alcohol drug ingestion
BN/AN
pregnancy 
torsion of testes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

red flag clinical features

A

Bile-stained vomit -Intestinal obstruction

Haematemesis - Oesophagitis, peptic ulceration, oral/nasal bleeding, and oesophageal variceal bleeding

Projectile vomiting, in first few weeks of life Pyloric stenosis

Vomiting at the end of paroxysmal coughing Whooping cough (pertussis)

Abdominal tenderness/abdominal pain on movement - Surgical abdomen

Abdominal distension Intestinal obstruction, including strangulated inguinal hernia

Hepatosplenomegaly Chronic liver disease, inborn error of metabolism

Blood in the stool Intussusception, bacterial gastroenteritis

Severe dehydration, shock - Severe gastroenteritis, systemic infection (urinary tract infection, meningitis), diabetic ketoacidosis

Bulging fontanelle or seizures- Raised intracranial pressure

Faltering growth - Gastro-oesophageal reflux disease, coeliac disease and other chronic gastrointestinal conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

factors contributing to the gastro-oesophageal reflux

A

relaxation of the lower oesophageal sphincter as a result of functional immaturity.

fluid diet
horizontal posture a short intra-abdominal length of oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is gastro-oesophageal reflux

CFs

A

recurrent regurgitation or vomittung but are putting on weight normally

hoarse cry
dehydration
weight loss
failure to thrive
aspiration pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

complications of gastro- reflux

A

faltering growth from severe vomiting

  • Oesophagitis – haematemesis, discomfort on feeding or heartburn, iron-deficiency anaemia
  • Recurrent pulmonary aspiration – recurrent pneumonia, cough or wheeze, apnoea in preterm infants
  • Dystonic neck posturing (Sandifer syndrome)
  • Apparent life-threatening events
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

who is more predisposed to gastro-oesophageal reflux

A
  • children with cerebral palsy or other neurodevelopmental disorders
  • preterm infants, especially in those with bronchopulmonary dysplasia
  • following surgery for oesophageal atresia or diaphragmatic hernia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Ix for gastro-oesophageal reflux

A

clinical diagnosis

  • 24-hour oesophageal pH monitoring to quantify the degree of acid reflux - pH should be ABOVE 4
  • 24-hour impedance monitoring which is available in some centres. Weakly acidic or nonacid reflux, which may cause disease, is also measured
  • endoscopy with oesophageal biopsies to identify oesophagitis and exclude other causes of vomiting.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mx of gastro oesophageal reflux

A

uncomplicated - parental reassurance, adding inert thickening agents to feeds (e.g. Carobel), and smaller, more frequent feeds.

trial of alginate therapy ie Gaviscon not the same time as thickening agents

  • unexplained feeding difficulties (for example, refusing feeds, gagging or choking)
  • distressed behaviour
  • faltering growth - acid suppression with proton-pump inhibitors (e.g. omeprazole)

reduce the volume of gastric contents and treat acid-related oesophagitis

domeperidone - enhance gastric emptying - SEs arryhtmias

ABOVE FAILS
- cows milk protein allergy ???

surgical Mx only for children with complications unresponsive to intensive medical treatment or oesophageal stricture - Nissen fundoplication - fundus of the stomach is wrapped around the intra-abdominal oesophagus, is performed either as an abdominal or as a laparoscopic procedure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is pyloric stenosis
presents at what age
more common in who

A

hypertrophy of the pyloric muscle causing gastric outlet obstruction.

  • > It presents at 2–8 weeks of age, irrespective of gestational age.
  • > More common in boys (4 : 1), particularly firstborn, and there may be a family history, especially on the maternal side.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

clinical features of pyloric stenosis

A
  • vomiting, which increases in frequency and forcefulness over time, ultimately becoming projectile
  • hunger after vomiting until dehydration leads to loss of interest in feeding
  • weight loss if presentation is delayed.

hypokalaemic hypochloraemic metabolic alkalosis with a low plasma sodium and potassium occurs as a result of vomiting stomach contents.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Diagnosis of pyloric stenosis

examination features

A

test feed is performed
-> The baby is given a milk feed, which will calm the hungry infant, allowing examination

when feeding peristalsis may be seen as a wave moving from left to right across the abdomen

palpable in the right upper quadrant

tomach is overdistended with air, it will need to be emptied by a nasogastric tube to allow palpation.

US helpful to confirm prior to surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mx of pyloric stenosis

A

correct any fluid and electrolyte disturbance with intravenous fluids

once everything is settled - PYLOROMYOTOMY -> division of the hypertrophied muscle down not mucosa

Postoperatively, the child can usually be fed within 6 hours and discharged within 2 days of surgery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

define colic

A

inconsolable crying or screaming often accompanied by drawing up of the knees and passage of excessive flatus takes place several times a day.

occurs in the first weeks of life

if its severe and persistent, protein hydrolysate formula (cow’s milk protein free) may be considered and continued if symptoms improve. If they do not, then a trial of gastro-oesophageal reflux treatment may be considered.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is meckel diverticulum

presentation

A

2% of individuals ileal remnant of the vitello-intestinal duct, a Meckel diverticulum, which contains ectopic gastric mucosa or pancreatic tissue.

severe rectal bleeding
acute reduction in Hb

A technetium scan will demonstrate increased uptake by ectopic gastric mucosa in 70% of cases

Mx - surgical resection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is malrotation

A

During rotation of the small bowel in fetal life, if the mesentery is not fixed at the duodenojejunal flexure or in the ileocaecal region, its base is shorter than normal, and is predisposed to volvulus. Ladd bands are peritoneal bands that may cross the duodenum, often anteriorly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

presentations of malrotation

Ix
Mx

A
  • high caecum at the midline
  • High caecum at the midline
  • Feature in exomphalos, congenital diaphragmatic hernia, intrinsic duodenal atresia
  • May be complicated by the development of volvulus, an infant with volvulus may have bile stained vomiting
  • Diagnosis is made by upper GI contrast study and USS
  • Treatment is by laparotomy, if volvulus is present (or at high risk of occurring then a Ladd’s procedure is performed
    Obstruction with bilious vomiting is the usual presentation in the first few days of life but can be seen at a later age

any child with dark green vomiting needs an urgent upper GI contrast study to assess intestinal rotation unless signs of vascular compromise are present, when an urgent laparotomy is needed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is recurrent abdominal pain

presentation

A

pain sufficient to interrupt normal activities and lasts for at least 3 months.

periumbilical pain
constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ix of recurrent abdominal pain

A

urine microsopy adn culture is mandatory to exclude UTIs

abdominal US - excluding gall stones and pelvi-ureteric junction obstruction.

coeliac
TFTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is abdominal migraine

presentation

A

abdominal pain in addition to headaches

midline abdo pain w vomiting and facial pallor

long periods w no pain and shorter period with non specific abdo pain and pallor w or wo vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is IBS

A

altered gastrointestinal motility and an abnormal sensation of intra-abdominal events. Symptoms may be precipitated by a gastro-intestinal infection

experience pain on inflation of balloons in the intestine at substantially lower volumes than do controls.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

presentation of IBS

A
  • non-specific abdominal pain, often peri-umbilical, may be worse before or relieved by defaecation
  • explosive, loose, or mucousy stools
  • bloating
  • feeling of incomplete defecation
  • constipation (often alternating with normal or loose stools).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
H.pylori causes what | Ix
antral gastritis, which may be associated with abdominal pain and nausea. It is usually identified in gastric antral biopsies. The organism produces urease, which forms the basis for a laboratory test on biopsies and the 13 C breath test following the administration of 13 C-labelled urea by mouth. Stool antigen for H. pylori may be positive in infected children
26
Mx of peptic ulceration
PPI - omeprazole if investigations suggest they have an H. pylori infection, eradication therapy should be given (amoxicillin and metronidazole or clarithromycin
27
what is functional dyspepsia Sx
Those who fail to respond to treatment or whose symptoms recur on stopping treatment should have an upper gastrointestinal endoscopy and, if this is normal Sx early satiety, bloating, and postprandial vomiting and may have delayed gastric emptying as a result of gastric dysmotility.
28
what is eosinophile oesophagitis presentation diagnosis Mx
inflammatory condition affecting the oesophagus caused by activation of eosinophils within the mucosa and submucosa. presentation vomiting, discomfort on swallowing or bolus dysphagia, when food “sticks in the upper chest”. Diagnosis endoscopy where macroscopically, linear furrows and trachealization of the oesophagus may be seen, and microscopically, eosinophilic infiltration is identified. swallowed corticosteroids in the form of fluticasone or viscous budesonide.
29
what is gastroenteritis common cause other causes and presentation
1. rotavirus infection under 2 esp during winter 2. others bacterial suggested by the presence of blood in the stools campylobacter jejuni Shigella and some salmonellae produce a dysenteric type of infection, with blood and pus in the stool, pain and tenesmus Cholera and enterotoxigenic Escherichia coli infection are associated with profuse, rapidly dehydrating diarrhoea. 3. protozoan - Giardia and Cryptosporidium . ``` severe abdo pain bilious vomit vom without diarrhoea temp >39 neck stiffness persistent diarrhoea >10 days blood or mucus in stool looks very unwell altered conscious state abdominal distension difficulty breathing ```
30
which children will be at an increased risk of rehydration
* infants, particularly those under 6 months of age or those born with low birthweight * if they have passed six or more diarrhoeal stools in the previous 24 hours * if they have vomited three or more times in the previous 24 hours * if they have been unable to tolerate (or not been offered) extra fluids * if they have malnutrition.
31
assessment of gastroenteritis
most accurate measure of dehydration is the degree of weight loss during the diarrhoeal illness * no clinically detectable dehydration (usually <5% loss of body weight) * clinical dehydration (usually 5% to 10% loss of body weight) * shock (usually >10% loss of body weight; Fig. 14.9 and Table 14.1 ). Shock must be identified without delay.
32
red flag signs of shock
general appearance -> appears unwell or deteriorating Altered responsiveness, e.g. irritable, lethargic sunken eyes tachycardia tachypnoea reduced skin turgor
33
what is isonatraemic and hyponatraemic dehydration
plasma sodium remains within normal range loss of sodium more than water -> hyponatraemic shift of water from extracellular to intracellular components increase in brain volume -> seizures extracellular depletion -> shock
34
what is hypernatraemic dehydration
plasma concetration increases causes high fever or hot, dry environment) or from profuse, low-sodium diarrhoea. ECF becomes hypertonic therefore water comes out of the Signs - jittery movements - increased muscle tone - hyperreflexia - convulsions - drowsiness or coma.
35
when is stool culture required for gastroenteritis
- septic - if there is blood or mucus in the stools, - immunocompromised - recent foreign travel - if the diarrhoea has not improved by day 7]- if the diagnosis is uncertain
36
Mx if clinical dehydration in gastroenteritis ORS mechanism shock safety net
- oral rehydration solution - 50ml/kg over 4 hours as well as maintenance fluid adjunct to normal fluids or breastfeeding - deterioration or persisitent vomitting - continue breastfeeding ORS contains sodium and glucose which allows cotransport of SGLT 1 to work. increases salt and water uptake in the small intestinal lumen Na moving into lumen also pulls water too. no skl for 48 hours Shock - Bolus therapy 20ml/kg - fluid deficit -> 100ml/kg/24hr maintenacne fluids - first 10kg -> 100ml/kg - second 10kg -> 50ml/kg - subsequent kg ->20ml/kg safety net  Wash your hands (and your child’s) with soap and water after going to the toilet, changing nappies and before eating  Regularly clean the toilet at home with disinfectant/bleach  Do not share towels, flannels etc with your child  Wash soiled clothes separately- soiled clothing and bedding should be washed at high temperatures (60°)  Keep children off school, playgroup etc until at least 48 hours after their last symptom  Your child should not use swimming pools for another two weeks after they are well.
37
Mx of hypernatraemic dehydration
you cant reduce sodium too quickly as it will lead to a shift of water into cerebral cells -> seizures and cerebral oedema aim to reduce at less than 0.5 mmol/l per hour.
38
DD for diarrhoea
``` Infection (gastroenteritis) Inflammatory bowel disease Lactose intolerance Coeliac disease Cystic fibrosis Toddler’s diarrhoea Irritable bowel syndrome Medications (e.g. antibiotics) ```
39
postgastroenteritis syndrome
Infrequently, following an episode of gastroenteritis, the introduction of a normal diet results in a return of watery diarrhoea. In such cases, oral rehydration therapy should be restarted.
40
post gastroenteritis complications
Lactose intolerance Irritable bowel syndrome Reactive arthritis Guillain–Barré syndrome
41
what is coeliac disease
exposure to gluten causes an immune reaction that creates inflammation in the small intestine. It usually develops in early childhood but can start at any age. In coeliac disease autoantibodies are created in response to exposure to gluten. These autoantibodies target the epithelial cells of the intestine and lead to inflammation. There are two antibodies to remember: anti-tissue transglutaminase (anti-TTG) and anti-endomysial (anti-EMA). These antibodies correlate with disease activity and will rise with more active disease and may disappear with effective treatment. Inflammation affects the small bowel, particularly the jejunum. It causes atrophy of the intestinal villi. The intestinal cells have villi on them that help with absorbing nutrients from the food passing through the intestine. The inflammation causes malabsorption of nutrients and disease related symptoms.
42
presentation of coeliac disease
faltering growth, abdominal distension and buttock wasting, abnormal stools, and general irritability Diarrhoea Fatigue Weight loss Mouth ulcers Anaemia secondary to iron, B12 or folate deficiency Dermatitis herpetiformis is an itchy blistering skin rash that typically appears on the abdomen peripjeral neuropathy cerebellar ataxia epilepsy HLA-DQ2
43
diagnosis of coeliac
increased intraepithelial lymphocytes - villous atrophy - crypt hypertrophy endoscopically followed by the resolution of symptoms and catch-up growth upon gluten withdrawal. Check total immunoglobulin A levels to exclude IgA deficiency before checking for coeliac disease specific antibodies: Raised anti-TTG antibodies (first choice) Raised anti-endomysial antibodies ass w type 1 diabetes mellitus, autoimmune thyroid disease, Down syndrome, primary scleorising cholangitis, primary biliary cirrhosis turner
44
causes of chronic diarrhoea
* In an infant with faltering growth, consider coeliac disease and cow's milk protein allergy. * Following bowel resection, cholestatic liver disease or exocrine pancreatic dysfunction, consider malabsorption. * In an otherwise well toddler with undigested vegetables in the stool, consider chronic non-specific diarrhoea.
45
clinical features of crohn's disease
classical presentation - abdominal pain - diarrhoea - weight loss growth failure puberty delayed general ill health - fever - lethargy - weight loss extra-intestinal manifestations - oral lesions or perianal skin tags - uveitis - arthralgia - erythema nodosum
46
diagnosis of crohn's
endoscopic and histological findings on biopsy. Upper gastrointestinal endo­scopy, ileocolonoscopy and small bowel imaging are required. The histological hallmark is the presence of non-caseating epithelioid cell granulomata Small bowel imaging may reveal narrowing, fissuring, mucosal irregularities and bowel wall thickening.
47
Mx of crohn's
remission is induced with nutritional therapy, when the normal diet is replaced by whole protein modular feeds (polymeric diet) for 6–8 weeks. azathioprine, mercaptopurine or methotrexate maintain remission if failed biologics infliximab or adalimumab
48
complications of crohns
obstruction, fistulae, abscess formation or severe localized disease unresponsive to medical treatment, often manifesting as growth failure
49
features of UC
ectal bleeding, diarrhoea and colicky pain. Weight loss and growth failure may occur eryhtema nodosum arthritis
50
diagnosis of UC
endoscopy (upper and ileocolonoscopy) mucosal inflammation, crypt damage (cryptitis, architectural distortion, abscesses and crypt loss), and ulceration. Small bowel imaging is required to check that extracolonic inflammation suggestive of Crohn’s disease is not present.
51
Mx of UC
mild disease - mesalazine induction and maintenance therapy aggresive or extensive - steroids acute exacerbations and immunomodulatory therapy, e.g. azathioprine alone to maintain remission or in combination with low-dose corticosteroid therapy. There is a role for biological therapies such as infliximab or ciclosporin in patients with resistant disease severe - IV fluids and steroids FAILS -> ciclosporin surgery colectomy w ileostomy/ileorectal pouch severe complicated by a toxic megacolon or chronic poorly controlled disease
52
red flag symptoms/signs
Failure to pass meconium within 24 hours of life - Hirschsprung disease Faltering growth/growth failure - Hypothyroidism, coeliac disease, other causes Gross abdominal distension Hirschsprung disease or other gastrointestinal dysmotility Abnormal lower limb neurology or deformity, e.g. talipes or secondary urinary incontinence Lumbosacral pathology Sacral dimple above natal cleft, over the spine – naevus, hairy patch, central pit, or discoloured skin Spina bifida occulta Abnormal appearance/position/patency of anus Abnormal anorectal anatomy Perianal bruising or multiple fissures Sexual abuse Perianal fistulae, abscesses, or fissures Perianal Crohn's disease
53
Mx of constipation faecal impaction
faecal impaction stool softener - polyethylene glycol 3350 + electrolytes disimpaction regimen (escalating dose over 1-2 weeks) after 2 weeks add stimulants Not tolerated Lactulose - osmotic laxative Maintenance therapy movicol first line add a stimulant laxative stools hard -> lactulose/docusate mild constipation same as above + stimualnt laxative ie sodium picosulphate min of 6 months to ensure regular stooling titrating the dose encouraged to sit on the toilet after mealtimes to utilise the physiological gastrocolic reflec
54
complciations of untreated coeliac disease
``` Vitamin deficiency Anaemia Osteoporosis Ulcerative jejunitis Enteropathy-associated T-cell lymphoma (EATL) of the intestine Non-Hodgkin lymphoma (NHL) Small bowel adenocarcinoma (rare) ```
55
what is biliary atresia
obliteration or discontinuity within the extrahepatic biliary system, which results in an obstruction in the flow of bile. perinatal form presents in the first two weeks of life, and the postnatal form presents within the first 2-8 weeks of life
56
Sx signs of biliary atresia Ix Mx complications
- Jaundice >14 days - Dark urine and pale stools - Appetite and growth disturbance, however, may be normal in some cases signs - Jaundice - Hepatomegaly with splenomegaly - Abnormal growth - Cardiac murmurs if associated cardiac abnormalities present CONJUGATED BILIRUBIN HIGH serum alpha-1 antritrypsin sweat chloride test US of biliary tree and liver - distension and tract abnormalities Mx surgical intervention - hepatoportoenterostomy also called urgent kasai procedure -> bile drainage blocked bile ducts are removed and replaced with a segment of the small intestine - ursedeoxycholic acid -> adjuvant hepatoprotective and facilitates bile flow and it can be initiated following urinary bile acids being sent for analysis and continued until the resolution of jaundice complications - Unsuccessful anastomosis formation - Progressive liver disease - Cirrhosis with eventual hepatocellular carcinoma
57
what is intussusception
- Telescoping bowel - Proximal to or at the level of, ileocaecal valve - 6-18 months of age features - paroxysmal abdominal colic pain - during paroxysm the infant will characteristically draw their knees up and turn pale - vomiting - bloodstained stool - 'red-currant jelly' - is a late sign - sausage-shaped mass in the right upper quadrant Ix US -Mx: reduction with air insufflation
58
what is meconium ileus
- Usually delayed passage of meconium and abdominal distension - The majority have cystic fibrosis - X-Rays will not show a fluid level as the meconium is viscid, PR contrast studies may dislodge meconium plugs and be therapeutic Infants who do not respond to PR contrast and NG N-acetyl cysteine will require surgery to remove the plugs
59
what is necrotising enterocolitis
- Prematurity is the main risk factor - Early features include abdominal distension and passage of bloody stools - X-Rays may show pneumatosis intestinalis and evidence of free air - Increased risk when empirical antibiotics are given to infants beyond 5 days - Treatment is with total gut rest and TPN, babies with perforations will require laparotomy
60
Sx of <1yr and >1 yrs constipation
< 1yr Distress on passing stool Bleeding associated with hard stool Straining >1 yr Poor appetite that improves with passage of large stool Waxing and waning of abdominal pain with passage of stool Evidence of retentive posturing: typical straight-legged, tiptoed, back arching posture Straining Anal pain
61
possibel causes of constipation in children
``` dehydration low-fibre diet medications: e.g. Opiates anal fissure over-enthusiastic potty training hypothyroidism Hirschsprung's disease hypercalcaemia learning disabilities ```
62
features of idiopathic constipation
precipitating factors starts after a few weeks of life Generally well, weight and height within normal limits, fit and active - no neuro problems in legs and normal locomotor dev changes in infant formula weaning, insufficient fluid intake poor diet
63
Red flag signs of constipation
reported from birth or few weeks of life >48 hrs ribbon stools faltering growth AMBER flag previously unknown or undiagnosed weakness in legs, locomotor delay distension
64
define failure to thrive
when current weight or rate of weight gain is lower than that of children of the same age and sex
65
signs of dehydration
``` pale or mottled skin hypotension cold extremities reduce urine output sudden weight loss reduced skin turgor tachycardia prolonged capillary refill time tachypnoea eyes sunken dry mucous membranes sunken fontanelle decreased LOC ```
66
whos at increased risk of dehydration
- children younger than 1 year, particularly those younger than 6 months - Low birth weight - children who have passed more than five diarrhoeal stools in the previous 24 hours - children who have vomited more than twice in the previous 24 hours - can't tolerate fluids - stopped breastfeeding during the illness - signs of malnutrition.
67
mesenteric adenitis
Aetiology: Inflammation of the mesenteric lymph nodes in response to infection, usually viral. Epidemiology: True incidence unknown as easily missed or mistaken. Up to 20% of patients undergoing appendicectomy found to have mesenteric adenitis. More common in people <15 years old. History: abdominal pain, fever, recent or current respiratory tract infection, diarrhoea, constipation, nausea, vomiting Examination: diffuse abdominal tenderness, cervical lymphadenopathy, signs of URTI Investigation: Abdominal USS
68
appendicitis
Aetiology: Inflammation of the appendix most commonly due to obstruction of the appendix lumen by faecolith, normal stool or lymphoid hyperplasia. Epidemiology: Most cases between 15 & 59Y. Majority present as medical emergencies History: Sharp abdominal pain, initially periumbilical moving to RIF, fever, loss of appetite (anorexia) nausea, vomiting Examination: Pain brought on by movement, pain on palpation along McBurney’s point, rebound tenderness, guarding. Note not always seen in early presentation – can be vary varied. Investigation: FBC, urinalysis, pregnancy test, abdominal USS