GI+HG Flashcards

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1
Q

What is the function of the GI tract

A
  • Mastication (mouth)
  • Ingestion (mouth)
  • Propulsion (Waves of peristalsis from cardiac sphincter to pylorus about 3 times a minute)
  • Mechanical and chemical digestion (begins in stomach completed in small intestine)
  • Absorption (some in stomach rest in small intestine)
  • Elimination of non-usable residues as faeces (large intestine)
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2
Q

What are the different GI disorders?

A
  • Nausea, vomiting, hyperemesis gravidarum
  • Coeliac disease
  • Constipation
  • Irritable bowel syndrome
  • Inflammatory bowel disease
    o Crohn’s disease
    o Ulcerative colitis
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3
Q

Problems involving the small intestines

What is coeliac disease?

A
  • Coeliac disease is not an allergy or an intolerance like some people believe, but a lifelong autoimmune disease where the body’s immune system damages the lining of the small bowel when gluten, a protein found in wheat, barley and rye, is eaten.
  • More common in those with other autoimmune disorders
  • Inflammatory condition of the small bowel (duodenum, jejunum, ileum) caused by an inability to digest GLUTEN (wheat protein)
  • Gluten = mixture of 2 proteins (gliadin, glutenin)
  • Lining of small intestine damaged on exposure to gluten; gut villi become inflamed and flattened, eventually undergoing atrophy
  • Results in malabsorption, malnutrition, systemic illness
  • Aetiology unknown but is related to a combination of genetic predisposition and environmental factors- the amount of gluten ingested, stress of a pregnancy or a GI infection.
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4
Q

What are the signs and symptoms of coeliac disease?

A
  • (Adults) General lassitude; diarrhoea; iron/folate deficiency; vitamin D/vitamin K deficiency; weight loss
  • Adults may experience less acute symptoms than children
  • (Children) Usually present at age 9 months to 3 years when cereals introduced into diet: Pale, bulky and foul-smelling stools; steatorrhoea- fat in the stools; malabsorption and failure to thrive; weight loss; abdominal distension; diarrhoea
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5
Q

Investigations and management of coeliac disease

A
  • Blood tests to detect auto-antibodies
  • Stool sample, to exclude infection
  • FBC (exclude anaemia; check WBC); CRP-inflammatory marker
  • Small bowel biopsy (via endoscopy)
  • Serological tests
  • Women first presenting in pregnancy – need to consider the desirability, practicability and safety of the more invasive investigations
  • Health education/advice; help with accessing information about Coeliac Disease; support breastfeeding; delay weaning in the infant
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6
Q

What are the complications of coeliac disease?

A
  • Anaemia
  • Osteoporosis
  • Short statures
  • Reproductive problems
  • Malignant disease
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7
Q

What are the pregnancy issues related to coeliac disease?

A
  • Can experience an aggravated response during pregnancy
  • Haematological disorders: iron-deficiency anaemia
  • Some studies have showed that if left untreated can increase risk of miscarriage, fetal growth restrictions and LBW.
  • Further vitamins and mineral supplementations need to be given- folic acid.
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8
Q

What is constipation?

A
  • Definitions of constipation vary:
    o fewer than 2 bowel motions per week
    o feeling of incomplete defecation
    o hard, lumpy stools
    o straining to move bowels
    o less frequent bowel motions than is customary
    o nausea; bloated feeling
  • Related to fluid intake, dietary fibre content, activity levels, effectiveness of gastro-colic reflex, psychological factors, hormone levels
  • Nausea & vomiting may cause reduced food/fluid intake
  • Pregnancy: progesterone and prostaglandins slow GI tract motility; gravid uterus exerts pressure on the sigmoid colon and rectum –> constipation
  • May have GI upset with iron supplementation
  • May be exacerbated by presence of haemorrhoids or anal fissure, or increase the risk of developing them
  • Impact: physical, emotional, behavioural effects; abdominal pain/discomfort; rectal bleeding; depression
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9
Q

What are the interventions for constipation?

A
  • Dietary advice: adequate fluid intake (at least 2 litres/day); increased fibre content - aim for gradual increase in fibre, to avoid bloating/discomfort
  • Reduce caffeine – diuretic effects will increase water loss
  • Consider temporarily stopping or changing iron tablets
  • Increased physical activity/exercise will promote gut peristalsis
  • Retraining the bowel – relaxation exercises; modify environment to facilitate comfort/privacy
  • Laxatives, stool softeners, suppositories, enema, bulking agents; should be a last resort, short-term measure only
  • Professional awareness of possibility of enforced immobility and changed environment (bed-rest, hospital in-patient stay) on normal bowel function
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10
Q

What is IBS

A
  • Functional disorder of the intestines
  • Appears to be the results of motor disturbances in the intestine that respond to certain stimuli.
  • Similar symptoms to other bowel functional disorders
  • Recurrent abdominal pain, discomfort, distension, bloating (relieved on defecation); more frequent, looser stools; passage of mucus per rectum; feeling of incomplete evacuation of bowel; bouts of constipation
  • May be linked with hormonal cycles (esp female); stress, genetic predisposition, food allergies and sensitivities, bacterial overgrowth in the intestines
  • Symptoms exacerbated by certain antibiotics and non-steroidal anti-inflammatory drugs (noxious stimuli to gut)
  • Symptoms may be exacerbated by pregnancy (especially if already experiencing constipation)
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11
Q

Management of IBS

A
  • Aetiology is unknown
  • Thorough assessment of progress and impact of the condition; nature, timing and severity of symptoms
  • Dietary review – reduce caffeine; avoid triggers; eliminate fructose and sorbitol sources; modify fibre content; avoid foods that ferment in the gut
  • Assess and aim to reduce emotional stressors
  • Provide environment that promotes relaxation, privacy, hygiene (may be difficult in hospital wards)
  • Pharmacological treatments – symptom relief
  • No evidence of malabsorption of nutrients
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12
Q

Drug treatment in IBS

A
  • Anticholinergic drugs (antispasmodics)
    o Smooth muscle relaxants; clients with IBS have increased gut motility after eating, resulting in cramps, bloating and diarrhoea; e.g. hyoscine (Buscopan), dicyclomine (Merbentyl)
  • Peppermint oil
  • Opioid derivatives (anti-diarrhoeal effect)
    o Slow gut peristalsis; long-term use may worsen constipation
  • Antidepressants (including SSRIs)
    o Have been used in clients unresponsive to conventional treatment; can reduce bowel’s response to distension/stimulation
  • Antibiotics and probiotics
    o May help if there is overgrowth of gut bacteria
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13
Q

Inflammatory Bowel Disease

Chron’s disease

A
  • Chronic inflammatory disease affecting ANY part of GI tract
  • Get granulomatous changes through whole thickness of bowel wall
  • Unknown cause but thought to be some genetic predisposition. It is considered that the condition is in response to environmental triggers, such as infection and drugs.
  • Less common than U.C: affects up to 5:10,000 people
  • More common in smokers (compared with non-smokers); both sexes are equally affected
  • Can lead to bowel perforation; stricture formation; fistulae; abscess formation
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14
Q

Complications of chron’s disease

A
  • Poor self esteem
  • Fissures in the anal canal
  • Abscesses in the pelvis
  • Arthritis
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15
Q

What is Ulcerative colitis?

A
  • Inflammatory disorder affecting large bowel mucosa
  • May involve rectum only, or part/whole of colon.
  • Never involves the small intestine
  • Unknown aetiology, but some evidence for genetic susceptibility
  • Twice as common in non-smokers
  • Affects women more frequently than men
  • Can result in colonic dilatation; malignancy
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16
Q

Signs and symptoms of IBD

A
  • Watery diarrhoea (with blood & mucus)
  • Lower abdominal pain/cramps
  • Change in frequency of bowel motions; urgency
  • Weight loss/malnutrition
  • Abdominal tenderness
  • Perianal abscesses, fistulae, skin tags (in C.D.)
  • Anal/rectal strictures (in C.D.)
  • R.I.F. mass (in C.D.)
  • Fever
  • Malaise
  • Anorexia
  • Tachycardia
  • Ulcers in mouth
  • Clubbing of fingers (proliferation of soft tissue)
  • Arthritis symptoms
  • Liver and kidney impairment
17
Q

Investigations of IBD

A
  • Thorough history-taking, examination, record-keeping and referral to appropriate specialists
  • Care should be offered by gastroenterologist who specialises in IBD.
  • Bloods: FBC, ESR, CRP, U&Es, LFTs, blood cultures, serum iron, B12, red cell folate
  • Stool sample for infection screening
  • Abdominal X-ray (?during pregnancy)
  • Colonoscopy; biopsy (rectum or colon)
  • Barium enema (not during pregnancy or during an acute attack)
18
Q

Management of IBD in pregnancy

A
  • Pregnancy does not usually affect the course of IBD; symptoms generally remain stable
  • Most symptom changes occur in early pregnancy or postnatally
  • Pregnancy outcome not affected by ‘quiescent’ IBD but may be adverse effects if active disease present
  • Women may already have a stoma (ileostomy, colostomy), with or without a stoma bag (some may have a conduit for administration of medication only)
  • Investigations: FBC, stool culture, serum albumin, sigmoidoscopy/proctoscopy
  • LSCS only for obstetric indications, or if have severe perianal Crohn’s disease
  • Anti-inflammatory drugs, such as sulfasalazine or mesalazine are safe to use during pregnancy and when breastfeeding
    o Sulfasalazine interferes with folate metabolism, so these women should be advised to take folic acid supplements (high dose)
    o Oral/rectal steroids safe to use in pregnancy
    o Avoid immunosuppressive agents such as 6-mercaptopurine; azathioprine (use the latter with caution)
    o Avoid NSAID’s as they may cause inflammations and bleeding in the small intestines.
19
Q

What is hyperemesis gravidarum?

A
  • Very severe NVP
  • May begin very early, even before a positive test
  • Symptoms peak at 9-13 weeks, improve around 16-24 weeks but may continue throughout the pregnancy
  • Weight loss is severe and rapid and dehydration is common
  • If not managed appropriately complications can ensue
  • Medical treatment is necessary
  • Psychological support is beneficial
20
Q

Impacts of HG?

A
  • Physical complications and risks for mum
    o Hypokaleamia and hypocalcaemia
    o Wernicke’s encephalopathy: brain condition
    o Re-feeding syndrome
    o Death
    o Also: Oesophageal damage, ongoing gastrointestinal problems, burst blood vessels, torn stomach muscles, VTE, pressure sores.
  • Risks and complications for baby if poorly managed:
  • Termination! IUGR, miscarriage, placental abruption, pre-term labour, intrauterine death. Malnutrition in early pregnancy linked with cardiometabolic disorders behavioural and development problems in childhood.
  • Psychological complications
    o Peri-natal depression, PTSD, flashbacks, PND
    o Caused by hyperemesis not a cause of it!!
    o Loss of hope of “normal pregnancy”
- Social impact
o Unable to work and maintain household, loss of identity 
o Isolation
o Financial hardship
o Relationship difficulties
o Concerns over care of other children
21
Q

HG is more likely in?

A
  • Young primips
  • Non-smokers
  • Non-caucasian
  • Multiple pregnancy
  • Previous history of HG (risk of admission 29 times higher)
  • Current or previous molar pregnancy
  • Pre-existing diabetes
  • Depression or psychiatric illness
  • Hyperthyroid disorder
  • Peptic ulceration or other gastrointestinal disorders
  • Asthma
22
Q

Aetiology of HG

A
  • Not entirely known, likely multifactorial
  • Genetic factor – 86% recurrence in subsequent pregnancy vs 0.7% for non-sufferers. 30-35% risk if mother/sister suffered.
  • Reduced risk of recurrence with a different partner – difficult to explain without genetics of foetus being involved!
  • Various theories around thyroid function, H.Pylori- bug in the stomach, oestrogen and hCG, Prostaglandin E2: None stand up in robust studies
  • New theories emerging around the hCG molecule, Growth and Differentiation Factor 15 (GDF15) and intracellular calcium release channel (RYR2) [1,2]
23
Q

Clinical indicators of HG

A
  • Constant nausea and/or vomiting >5 x a day for >5 days
    o or more severe but for less time? >10 times a day for 2-3 days is surely HG?
    o Nausea so constant and severe that she can’t eat/drink for 3+ days?
  • Weight loss >5% pre-pregnancy weight
  • Dehydration and malnutrition
  • Metabolic disturbances
  • Psychosocial morbidity, QoL affected – often the nausea is more impacting
  • Ptyalism – excessive salivation
  • Heightened/warped sense of smell
  • Acid reflux (in addition to vomiting)
  • Oesophagitis
  • Lethargy and fatigue (symptom of hypocalcaemia)
  • Headaches
  • Sensitivity to sensory stimulation, lights/noise/movement etc
  • Depression, effect not cause!
  • Constipation
  • Hair loss
  • Loss of bladder control
24
Q

Diagnosing HG

A
-	Differential diagnosis
o Gastrointestinal
o Neurological
o UTI
o ENT disease
o Drugs
o Metabolic and endocrine disorders
o Psychological disorders ie. Eating disorders

Assessing symptoms

  • History
  • Severity of symptoms
  • Impact of symptoms, physical/emotional/social/financial, be holistic
  • Treatment to date
25
Q

Treatments of HG

A

Principles of treatment

  • Rehydrate
  • Sort out the electrolytes/vitamins
  • Maintain with anti-emetics
  • Give realistic goals, it’s about managing rather than curing in the short term
  • None of the treatments are miracle cures and some have unpleasant side effects – be honest
  • Aim to work as a team with the patient to manage their condition

IV therapy
- Rehydration
o Rapid IV Fluid replacement
o Get 2 litres in them over 4 hours
o ie. 1 litre Hartman’s over 2 hours then 1 litre Normal Saline over 2 hours (with 20mmol potassium)
- Longer regimes never achieve full rehydration and they spiral down on discharge
- Avoid dextrose containing IV Fluids

  • Vitamins Electrolytes

o Vitamin B1
 Oral Thimine or IV Pabrinex
 Risk of Wernike’s encephalophathy
 Educate to need for tablet on discharge if vomiting is severe

o Potassium
 10mmol KCL over 1 hour
 Give in second bag of fluid

26
Q

Types of HG

A

Spectrum within a spectrum

  • “Mild HG” managed with cyclizine and perhaps second-line antiemetic, may need a round of rehydration. Symptoms improve significantly during second trimester
  • “Moderate HG” managed with ondansetron or steroids. Rehydration required at least once. Symptoms likely to last for most of pregnancy but hopefully improvement in second trimester
  • “Severe HG” is unresponsive to antiemetic therapy. Requires regular rehydration, possibly via a PICC line. Symptoms usually last until birth and complications can be ongoing for years. TOP may be necessary.