Gastro Flashcards

1
Q

CONSTIPATION
i) what are most cases due to? naame three secondary causes?
ii) name five features that maay suggest constipation
iii) what is encopresis? what causes it? what age does it become pathological? name three rare causes
iv) name three lifestyle factors that can contribute to constipation
v) what can desensitisation of the rectum lead to over time?

A

i) most are idiopathic
secondary - hirschprungs, CF, hypothyroid, sp cord lesions, intestinal obstruction, cows milk intolerance
iii) faecal incontinence - sign of chronic constipation where rectum becomes stretched and loses sensation > large hard stool stays in rectum and only loose stool can pass out
other caauses are spina bifida, hirschprungs, ceb palsy, learning disability, abuse
iv) habit, low fibre, poor fluid intake, sedentary lifestyle
v) desense can lead to faecal impaction > large stool block the rectum > stretching > further desensitisation

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2
Q

MANAGEMENT OF CONSTIPATION
i) name five red flags which may point to serious underlying conditions
ii) name three complications
iii) what is the first line laxative? how long should they be continued for?
iv) what may faecal impaction require?

A

i) not passing meconium within 48hrs of birth (CF or hirschprungs), neuro symptoms (ceb palsy), vomiting (intes obstruc or hirschprungs), ribbon stool (anal stenosis), failure to thrive (coeliac, hypothyoid, sfeguarding), acute severe abdo pain and bloating (obstruc or intussception)
iii) complicat - pain, reduced sensation, anal fissures, haemmorhoids, overflow and soiling
iii) movicol first line - continue long term and slowly wean off as child develops normal habits
iv) impacttion can require disimpaction regimen with high dose laxatives initiaally

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3
Q

GASTRO OESOPHAGEAL REFLUX
i) what happens? what sphincter is implicated? why does it happen more in babies? after what age does it usually stop?
ii) name five signs of problematic reflux in babies? name four signs in children over one year (similar to adults)
iii) name five abdo causes of vomiting
iv) name three practical solutions that can be given to manage? name three things that can be given in more problematic cases
v) what investigation may need to be done in severe cases?

A

i) contents of the stomach reflux through the lower oes sphincter > oes, throat, mouth
baabies have an immature LOS so reflux is easier - usually stops after age 1
ii) problematic - chronic cough, hoarse cry, distress post feed, reluctance to feed, pneumonia, poor weight gain
over 1 - heartburn, acid regurg, retrosternal/epigasatric pain, bloat, nocturnal cough
iii) vomiting - over feeding, GORD, pyloric stenosis (projectile), gastritis, appendicits, infections, intes obstruction
iv) small frequent meals, burping to help milk settle, not over feeding, keeping baby upright after feed
v) gaviscon mixed with feeds, thcikened milk/formula, PPIs eg omeprazole

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4
Q

GORD RED FLAGS
what may the following be a sign of:
1) not keeping any food down
2) projectile or foreceful vomiting
3) bile stained vomit
4) haematemesis or melanea
5) abdo distention
6) rerduced conc/bulging fontaanelle
7) blood in stool
8) rash/angioedema/signs of allergy

A

1) + 2) pyloric stenosis/intestinal obstruction
3) intestinal obstruction
4) peptic ulcer, oesophagitis, varives
5) intes obstruction
6) meningitis
7) gastroenteritis/cows milk protein allergy
8) cows milk protein allerrgy

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5
Q

PYLORIC STENOSIS
i) what is the pyloric sphincter? what happens to it to cause pyloric stenosis? what does this prevent?
ii) what type of vomiting is seen? when does it usually present? how may the baby appear? (3)
iii) what may been seen on examination of the abdo after feeding? what may be felt in the upper abdomen?
iv) what chloride level is seen on blood gas? what else does the blood gas show in relation to acid base balance?
v) which imaging test is done? what does it show? how is it treated?

A

i) ring of smooth muscle between the stomach and duodenum > thickening of the sphincter and narrowing of the pylorus causes PS (food cant get to duo as normal)
ii) see projectile vomiting presenting in first few weeks of life
baby may appear pale, thin, failing to thrive
iii) after feeding may see peristalsis
may feel a firm round mass in upper abdo (like a large olive) - hypertrophic muscle of the pylorus
iv) low chloride, metabolic alkalosis (baby vomiting up HCl)
v) do an abdo US > thickened pylorus
treaat with lap pylromyotomy (incision to widen the canal and allow food to pass to duo)

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6
Q

COELIAC DISEASE
i) what do autoantibodies to gluten target in the intestine? which three antibodies are associated with it?
ii) which area of the SI is particularly affected? name four ways it may present in a child? which skin condition can it px with? which type of symptoms can it sometimes present with?
iii) after presentation with which condition are all patients then tested for CD? name the two HLA associations

A

i) auto ABs target epithelial cells in the intestine
anti TTG, endomysial antibodies (EMA), deaminated gliadin peptide antibodies (anti DGPs)
ii) jejunum > atrophy of intestinal villi
px as failure to thrive, diarrhoea, weight loss, mouth ulcers, anaemia (malabs)
derm - dermatitis herpetiformis (itchy blistering rash on abdomen)
can also px with neurol symptoms eg periph neuropathy, cerebellar ataxia, epilepsy
iii) alwaays test for CD after dx with T1DM
HLA DQ2 (90%) and HLA DQ8

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7
Q

DIAGNOSIS AND TX OF COELIAC
i) which Ig levels should be checked? why? which auto AB is first checked?
ii) which two things may intestinal biopsy show?
iii) name four conditions CD may cluster with?
iv) name three complications of untreated CD
v) what is the treatment?

A

i) check IgA for deficiency aas auto ABs are IgA so if defic in IgA then ABs will be normal falsely
check anti TTG first then EMAs
ii) crypt hypertrophy and villous atrophy
iii) T1DM, thyroid disease, AI hepatitis, PBC, PSC, downs syndrome
iv) vitamin deficiency, anaemia, osteoporosis, ulcerative jejunitis, NHL
v) lifelong gluten free diet

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8
Q

BILIARY ATRESIA
i) what is it? what does it result in? what is there a build up of in the blood?
ii) when does it present? what feature does it most commonly present with? why? name two other px symptoms
iii) what is the initial investigation? what will the result be in BA?
iv) name two other tests that should be done to exclude other conditions
v) how is it managed? what may some patients need?

A

i) congential condition where a section of the bile duct is narrowed or absent > cholestasis (bile cant get from liver to bowel)
build ip of conjugated bili as it cant be excreted
ii) presents shortly after birth with significant jaundice (due to high conjugted bili)
suspect BA in persistent jaundice >14d in term babies and >21d in prem babies
may also px with dark urine/pale stool, appetite and growth disturbance
iii) intial investigation is conjugated and unconjugated bilirubin > see a high proportion of conjugated bili as liver is processing it but it cant get out
iv) serum alpha 1 anti trypsin (defic can cause cholestasis)
chloride sweat test to exclude CF
iv) manage with surgery (kasai portoenterostomy) > att SI to opening of liver
some patient may need a liver transplant to fully resolve the condition

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9
Q

INTESTINAL OBSTRUCTION
i) what type of constipation does it cause? name four causes
ii) name four presenting features? what type of vomiting maay be seen? are bowel sounds present?
iii) what is the initial imaging of choice? what may be seen? will there be air in the rectum?
iv) where do patients need to be referred to? name two things that are done in initial management
v) what else willl patients require? what ultimtely needs to be done?

A

i) causes absolute constipation
causes - meconium ileus, hirschprungs, oes atresia, intussception, malrotation of intestines with volvulus, strangulated hernia
ii) px with persistent vomiting that may be billous (bright green bile), abdo pain and disten, fail to pass stool or wind
bowel sounds abnormal - high pitched or tinkling early or absent later
iii) abdo xray is first line imaging - see dilated loops of bowel proximal to the obstruction and collapsed loops ditaal
absence of air in the rectum
iv) refer to surgical unit
initially mx with nil by mouth and NG tube to help drain stomach and stop vomiting
v) also need IV fluids to correct dehy/electro imbalance
need to find underlying cause

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10
Q

HIRSCHPRUNGS DISEASE
i) what is it? which nerve plexus is involved? what is the nerve plexus responsible for? which specific nerve cells are absent?
ii) what is total colonic agangliosis? what happens to the proximal and distal part of the affected segment?
iii) is there a strong family history? name three other syndromes it may be associated with?
iv) how may it present shortly after birth? name four other ways it may present?

A

i) congenital condition with absence of nerve cells of the myenteric plexus in distal bowel and rectum
ME plexus - forms the ENS, runs along the bowel wall > stim peristalsis in large bowel
absence of parasympathetic ganglion cells
(PSG cells start higher in the GI tract during dev and in HD they dont migrate down so leave the end portion of the colon not innervated)
ii) colonic agangliosis is where the entire colon is affected > the agang part can not relax and becomes constricted > lack of faeces movement and bowel obstruction
prox to obstruction is distended and distal is constricted
iii) strong FH
assoc with downs syndrome, NF1, wardenburg syndrome MEN II
iv) after birth can px with acute intestinal obstruction
other symptoms: delay in passing meconium (>24hrs), chronic constipation since birth, abdo pain/distention, vomiting, poor weight gain, fail to thrive

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11
Q

HIRSCHPRUNGS DISEASE MX AND COMPLICATIONS
i) which imaging is useful?
ii) what test is used to confirm the diagnosis? what will it show?
iii) what is hirschprungs associated enterocolitis? when does it usually present? name three features
iv) what can HAEC lead to? (2) how is it managed?
v) how is hirschprungs disease managed?

A

i) abdominal x-ray
ii) rectal biopsy > absence of aganglionic cells
iii) HAEC is inflammation and obstruction of the intestine
px 2-4 weeks postnataal with fever, abdo distention, bloody diarrhoea, sepsis
iv) can lead to toxic megacolon and perforation of the bowel
need urgent abx, fluid resus and decompression of the obstructed bowel
v) HD > definitive mx is surgical removal of aganglionic section of bowel (may be left with some incontinence)

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12
Q

INTUSSUSCEPTION
i) what happens? whaat does this lead to in relation to passage of faeces?
ii) what age group is it most common in? which sex?
iii) name three associated conditionss?
iv) name four presenting features? how may the stools look? what shaped mass may be felt in the abdomen?

A

i) bowel invaginates/telescopes into itself > thickens size of bowel and narrows lumen of folded area > palpable mass in abdo and obstruction of faeces
ii) occ in 6m to 2yrs and more common in boys
iii) most common presents with concurrent viral illness
henoch-schonlein purpura, CF, intestinal polyps, meckels diverticulum
iv) px with severe colicky abdo pain, pale/lethargic/unwell
redcurrant jelly stools
sausage shaped mass in RUQ on palpation

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13
Q

INTUSSCEPTION MX AND COMPLICATIONS
i) which imaging can be used to dx? what else can be done?
ii) how may a therapeutic eneema reduce it?
iii) what is done if enemas dont work?
iv) name three complications

A

i) ultrasound or contrast enema
ii) contrast, water or air are pumped into the coon to force the folded bowel out into the normal position
iii) surgical reduction
iv) obstruction, gangrenous bowel, perforation, death

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14
Q

APPENDICITIS
i) which part of the bowel does the appendix come from? how can it lead to peritonitis?
ii) what is peak age incidence? what is the key px featurer? where does it present? what is McBurneys point?
iii) name three other classic features? name two things that suggest peritonitis
iv) how is it diagnosed? which two imaging maay be done?

A

i) caecum
inflammation can proceed to rupture > peritonitis
ii) peak age 10-20yrs > abdominal pain
central aabdo pain > RIF
Mcburneys point is 1/3 distance from ASIS to umbilicus > on palpation of abdo there is. tenderness over mcb point
iii) loss of appetite, N+V, rovsings sign (palp of LIF causes pain in RIF), guarding, rebound yenderness, percussionn tenderness
peritonitis - rebound and percussion tenderness
iv) dx clinically with raised inflammatory markers
may do CT scan to exclude other dx or US in females to exclude gynae pathology

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15
Q

DIFFERENTIALS AND MANAGEMENT OF APPENDICITIS
i) what should be considered in all girls of childbearing age? name another gynae differential
ii) what is meckels diverticulum? name two things it can cause?
iii) what can px with abdo pain in younger children assoc with tonsilitis or URTI?
iv) what is definitive mx?
v) name three complications

A

i) ectopic pregnancy (serum or urine bHCG)
ovarian cysts
ii) meckels > malformtion of distal ileum > inflammed and rupture or cause volvulus
iii) mesenteric adenitis - inflamed abdo LNs (no spec tx required)
iv) definitive - removal of inflamed appendix
v) bleeding/infection/damage too bowel/anaes risks/VTE

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16
Q

INFLAMMATORY BOWEL DISEASE
i) features of crohns (NESTS)
ii) features of UC (CLOSEUP)
iii) name four presenting features to suspect for IBD
iv) name four extra intestinal manifestations

A

i) No blood /mucus
Entire GI tract
Skip lesions on endoscopy
Terminal ileum most aff/ transmural thickness
Smoking as a RF
ii) Continuous inflam
Limited to colon and rectum
Only superficial mucosa
Smoking protective
Excrete blood and mucus
Use aminisalicyclates
Primary sclerosing cholangitis
iii) perfuse diarrhoeaa, abdo pain, bleeding, weight loss, anaemia
iv) finger clubbing, erythema nodosum, pyoderma gangrenosum, episcleritis, inflam arthritis, PSC (UC)

17
Q

TESTING AND MX OF IBD
i) name four bloods that should be done? will CRP be raised? what speciaal blood test is done?
ii) which investigation is gold standard in dx of IBD? what can imaging look for?
iii). which two things need to be measured in children with IBD?

A

i) anaemia, infection, thyroid, kidney, liver
raised CRP due to active inflammtion
faecal calprotectin - rel by intestines when inflammed (90% spec for IBD)
ii) endoscopy (OGD and colonoscopy)
US/CT/MRRI look for complications eg fistulas, asbscesses, strictures
iii) measure growth and pubertal development espec when exac or on steroids

18
Q

GENERAL MX OF IBD
i) what drugs are first line to induce remission in CD? name three other things that can be added
ii) what two drrugs are first line to maint remission in CD? name an alternative? when may surgery be done for CD? (2)
iii) what is first line to induce remission in mild/mod UC? what is second line? what is first line in severe disease? what is second line?
iv) name the main drug class to maint remission in US?
v) what type of surgery may be done in UC? what will the patient be left with?

A

i) CD - first line are steroids (pred/IV hydrocortison)
if steroids dont work add immsupp - azathioprine/mercaaptoprrine/MTX/infliximab
ii) maint remission = azathioprine/mercaptoprine
can also use MTX, influx, adalimumab
can do surgery if disease only affects distal ileum/complications eg strictures or fistuls
iii) mild/mod UC > aminosalicyclate eg mesalazine (oral or rectal)
second line - CS eg prednisolone
severe UC > first line is IV CS eg hydrocortisone
second line IV ciclosporin
iv) maint remission - aminosalicyclaye eg mesalazine
v) usually only aff colon and rectum so removing it all (panproctocolectomy) will remove disease
pt left with ileostomy (J pouch)