Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pre-Reg Clinical > 1. Gastro-intestinal system (conditions) > Flashcards

1. Gastro-intestinal system (conditions) Flashcards

1
Q

What is coeliac disease? (3)

A
  1. Autoimmune condition
  2. Chronic inflammation of the SMALL intestine
  3. Dietary proteins (gluten) activate an abnormal immune response in the intestinal mucosa, which can lead to malabsorption of nutrients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Symptoms of coeliac disease include…(3)

A
  1. Diarrhoea
  2. Bloating
  3. Abdominal pain
    +indigestion, constipation, fatigue, unintentional weigh loss, itchy rash, infertility, nerve damage, ataxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Management of coeliac disease

A
  1. The only effective treatment is a strict, life long gluten free diet.
  2. Management of risk of osteoporosis and and active treatment of bone disease (patients at risk of malabsorption of key nutrients). Advise NOT to self medicate with OTC vitamins/ minerals.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is diverticulosis? (3)

A
  1. An asymptomatic condition
  2. Characterised by the presence of diverticula
  3. Age dependent (majority of patients> 40y)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define diverticula

A

Small pouches protruding from the walls of the LARGE intestine

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

What is diverticular disease? (3)

A
  1. Symptomatic
  2. Condition where diverticula are present
  3. Which may lead to acute diverticulitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is acute diverticulitis? (1)

A

When diverticula suddenly become inflamed/ infected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Symptoms of diverticular disease include…

A
  1. Abdominal tenderness
  2. Mild/ intermittent lower abdominal pain (usually in lower left side). This tends to come and go and gets worse during or shortly after eating. Farting/ pooing should ease.
  3. Constpation
  4. Diarrhoea
  5. Occaisional large rectal bleeds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is complicated acute diverticulitis?

A

Diverticulitis (inflamed/ infected diverticula) associated with complications usch as abscess, bowel perforatoin and peritonitis, haemorrhage or sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is peritonitis?

A

Inflammation of the peritoneum, the tissue that lines the inner wall of the abdomen that covers and supports most of the abdominal organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Management of diverticular disease (10)

A
  1. Advice to eat a healthy, balanced diet
  2. Gradual increase of dietary fibre + drnk adequate fluid
  3. Exercize weight loss
  4. Smoking cessation
  5. Antibiotics NOT recommended
  6. Consider bulk forming laxatives
  7. Simple analgesia
  8. Antispasmodics
  9. NO NSAIDs. May increase risk of diverticular perforation
  10. If no response to treatment, consider alternative diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Management of diverticulosis

A

As asymptomatic, specific treatments not recommended. Bulk forming laxatives can be considered for constipation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Management of acute diverticulitis (5)

A
  1. Simple analgesia if systemically well
  2. Potential antibacterial management
  3. If persistent/ worsening symptoms reassess in primary care + consider referral
  4. Refer if complicated + uncontrolled for 1d assessment
  5. DO NOT recommend aminosalicylates/ prophylatic abx for prevention of recurrence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is coeliac disease? (3)

A
  1. Autoimmune condition
  2. Chronic inflammation of the SMALL intestine
  3. Dietary proteins (gluten) activate an abnormal immune response in the intestinal mucosa, which can lead to malabsorption of nutrients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is IBD? (2)

A
  1. Crohn’s

2. Ulcerative colitis

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

What is Crohn’s? (4)

A
  1. Chronic inflammatory bowel disease that affects the GI TRACT
  2. Characterised by:
    - thickened areas of the GI wall
    - with inflammation extending through all layers
    - deep ulceration+fissuring of the muscosa
    - presence of granulomas
  3. Affected areas may occur in any part of the GI tract, interspersed with areas of relatively normal tissue
  4. May present as recurrent attacks, with acute exacerbations combined with periods of remission or less active disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are granulomas?

A

Small lumps of immune cells that form in the body in areas where there is infection or inflamation

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

Symptoms of Crohn’s disease (9)

A

Depend on the site of disease but may include:

  1. Intestinal strictures
  2. Abcesses in the wall of the intestine
  3. Fistulae
  4. Anaemia
  5. Malnutrition
  6. CRC+ small bowel cancer
  7. Growth failure
  8. Delayed puberty
  9. Extra-intestinal manifestation (arthritis, joints, eyes, liver, skin, 2’ osteoporosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is fistulating Crohn’s? (3)

A
  1. Complication that involves the formatio of a fistula between the intestine and adjacent structures.
  2. Occurs in 1/4 of patients.
  3. May not need treatment if simple. May need surgery, abx, azothioprine, mercaptopurine, infliximab.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Define fistula

A

An abnormal/ /surgically made passage between a hollow organ and the body surface/ between 2 hollow/ tubular organs

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

Management of Crohn’s disease

A
  1. Non drug (smoking cessation, nutrition, surgery in some cases)
  2. Prednisolone/ methylprednisolone monotherapy if 1st presentation/ singe exacerbation in 12months
  3. Budesonide monotherapy if distal ileal/ ileocaecal/ right sided or pred CId. Less effective.
  4. Aminosalicylates alternative option. Less effective than both and so not appropriate for severe. But less s/es.
  5. Add on treatment (azathioprine/ mercaptopurine/ mtx) if 2 or more inflammatory exacerbations in a 12mth period/ cannot reduce steroid dose.
  6. Tumor necrosis factor alpha inhibitors options for the treatment of severe, active crohns disease if insufficient response.
  7. Maintaining remission: may not need therapy. May use azothioprine/ mercaptopurine (unlicensed). May use mtx if already used to induce remission. DO NOT use corticosteroids.
  8. If to maintain remission following srgery: azathioprine+ up to 3mth metronidazole. DO NOT use biologics/ budesonide.
  9. Loperamide/ codeine for diarrhoea if no colitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is ulcerative colitis? (7)

A
  1. Chronic inflammatory condition
  2. Characterised by diffuse mucosal inflammation
  3. Relapsing-remitting pattern
  4. Life-long
  5. Significant morbidity
  6. Most commonly presents 15-25y
  7. Pattern of inflammation is CONTINUOUS, EXTENDING FROM THE RECTUM UPWARDS to a varying degree
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Symptoms of active ulcerative colitis (3)

A
  1. Recurring diarrhoea, which may contain blood, mucus, pus
  2. Abdominal pain
  3. Urgent need to defacate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Management of ulcerative colitis

A
  1. Consider extent and severity using Truelove and Witts’ severity index
  2. Surgery may be necessary as emergency treatment
  3. If acute mild-moderate: 1st line is a topical aminosalicylate
    - can give corticosteroid for 4-8wks if contraindicated/ response insufficient
  4. acute moderate-severe: biological drugs following inadqueate response to conventional treatment (these can be continued into maintenance if effective+tolerated)
  5. if severe: immediate hospital admission. IV corticosteroids+ assess need for surgeyr. If IV corticosteroids not possible, IV ciclosporin/ surgery. Infliximab can be used if this is CId.
  6. To avoid relapse, mainteannce therapy with aminosalicylate is recommended. NO steroids due to s/es. Can consider azothioprine/ mercaptopurine. No evidence for mtx to induce/ maintain remission in UC although use in clinical practise is common.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Define toxic megacolon (2)

A
  1. Acute form of colonic distention

2. Very dilated colon accompanied by abdominal distention, sometimes fever, abdominal pain, or shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Purpura

A

Red/ purple discolored spots on the skin that do not blanch on applying pressure. To be watched out for with aminosalicylates (mesazalazine/ sulfasalazine) as may be a sign of blood dyscrasias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Blood dyscrasia

A

Morbid general state resulting from the presence of abnormal material in the blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is IBS? (4)

A
  1. A common chronic relapsing and often life long condition
  2. Mainly affects those between 20-30 years
  3. More common in women
  4. Symptoms usually relieved by defaecation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Symptoms of IBS (4)

A
  1. Abdominal pain/ discomfort
  2. Disordered defaecation
  3. Passage of mucus
  4. Bloating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Management of IBS (8)

A
  1. Diet+lifestyle changes (no more than 3 fresh fruit per day, increase fluid to at least 8 cups a day, avoid sorbitol if diarrhoea)
  2. Antispasmodic drugs
  3. Laxative
  4. Linaclotide (constella) if have not responded to laxatives from the different classes + have had constipation >12mths
  5. Loperamide 1st line for relief of diarrhoea
  6. Low dose TCA (unlicensed) for abdo pain/ dscomfort as 2nd line if no response
  7. SSRI if no response to TCA
  8. Psychological intervention if no relief of IBS>12mths
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is short bowel syndrome? (3)

A
  1. Shortened bowel due to large surgical resection (with or without stoma formation)
  2. May require medical management to ensure adequate absorption of nutrients and fluid
  3. Absorption of oral medication is also often impaired
  4. Oral intake influences the volume of stool passed so reducing food intake will lessen diarrhoea, but will also exacerbate the problems of undernurtition.
  5. Many drugs incompletely absorbed by patients with SBS and need to be prescribed in much higher doses than usual (levothyroxine, warfarin, oral contraceptives)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Management of SBS (11)

A
  1. May require replacement of vitamins+ minerals depending on the extent and position of the bowel resection (A, B12, D, E, K, essential fatty acids, zinc, selenium). May need PN.
  2. Magnesium deficiency is common and is treated with supplemention
  3. Oral rehydration salts as diarrhoea common. Again, may need PN to allow them to eat less if extent of diarrhoea unacceptable.
  4. Antimotility drugs (loperamide+codeine). Loperamide preferred as ot sedative+ does not cause dependence/ fat malabsorption. Could also use co-phenotrope (but this crosses BBB).
  5. Colestyramine- can be used in patients with an intact colon+ <100cm ileum resected. Used to bind to unabsorbed bile salts+reduce diarrhoea. Monitor for evidence of fat malabsorptoin/ fat soluble vitamin deficiencies.
  6. Omeprazole to reduce gastric acid secretion» reduce jejunostomy output. If less than 50cm of jejunum, give IV.
  7. Octreotide reduces ileostomy diarrhoea+large volume jejunostomy output by inhibiting pro-secretory substances. Unlicensed+not much evidence.
  8. Growth factors eg teduglutide. Can be used to facilitate intestinal adaptation after surgery in patients with short bowel syndrome,enhancing fluid, electrolyte and micronutrinet absorption.
  9. Enteric coated+ M/R preparations unsuitable for patients with SBS, particularly if ileostomy
  10. Do not use soluble tablets/ uncoated tablets/ liquid formulations
  11. Before prescribing liquid, prescriber should consider osmolarity, excipient content+ voume required. Hyperosmolar liquids some excipients can result in fluid loss.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Factors affecting absorption of drugs taken by mouth in patients with compromised GI systems (3)

A
  1. Length of small intestine available for drug absorption
  2. Small intestine has high area+ blood flow and so most important site for drug absorption
  3. Gastric emptying+ gastric transit time also affect drug handling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is constipation?

A
  1. Defacation that is unsatisfactory because of infrequent stools, difficult stool passage, or seemingly incomplete deecation
  2. Commonly seen in women, elderly + during pregnancy
    3.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Management of constipation

A
  1. New onset, especially in patients over 50, or accompanying anaemia, abdominal pain, weight loss or overt or occult blood in stool should provoke URGENT investigation because of the risk of maligancy/ other serious bowel disorder
  2. Increase in dietary fibre, adequate fluid intake, exercise. Increase fibre intake gradually to prevent flatulence and boating. May take as long as 4 weeks to see effects of high fibre. Sorbitol can help treat.
  3. Start with bulk forming laxative, ensuring adequate fluid intake
  4. If stools remain hard, add or switch to osmotic axative
  5. If stools soft/ difficult to pass/ person complains of inadequate emptying - add stimulant laxative
  6. If opioid induced recommend osmotic/ docusate + stimulant. AVOID BULK FORMING.
  7. If faecal impactation: depends on stoo lconsistency. If hard - high dose of oral macrogol. If this doesn’t work/ stool is soft - oral stimulant drug.
  8. If response inadequate, bisacodyl (or glycerol if stools hard)
  9. Alternatively docusate/ sodium citrate enema
  10. If response still insufficient, a sodium acid phosphate with sodium phosphate or arachis oil retention enema may be necessary
  11. If chronic consitaopn and 2 laxatives from different classes have been tried at the highest tolerated dose for at least 6 months, use of prucalopride in WOMEN only should be considered
  12. Advise gradually reducing+stopping laxatives once patient producing soft, formed stool without straining at least 3 times/ week
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Why avoid bulk laxatives in opioid induced constipation?

A

These laxatives increase the bulk of the stools, distend the colon, and augment peristalsis. Opioids prevent peristalsis of the increased bulk which worsens abdominal pain and can contribute to bowel obstruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is diarrhoea?

A
  1. The abnmormal passing of loose/ liquid stools with increased frequency/ volume/ both.
  2. Acute if <14 days
38
Q

Management of diarrhoea

A
  1. Prompt investigation if any red flags: unexplained weight loss, rectal bleeding, persistent, systemic illness, recent hospital treatment, antibiotics, foreign travel (other than to Western Europe/ North America/ Australia/ New Zealand)
  2. Aim is to prevent/ reverse fluid+ electrolyte depletion
  3. Most eisodes will settle without need for any treatment
  4. ORT is the mainstay of treatment
  5. If unable to drink/ severe dehdration - IV fluids
  6. Loperamide = 1st line treatment for patients when rapid control of symptoms is needed. It can be used for travellers diarrhoea, but should be avoided in bloody/ suspected inflammatory diarrhoea+ significant abdominal pain.
  7. Ciprofloxacin is occaisionally used for prophylaxis against travellers diarrhoea but routine use is NOT recommended.
39
Q

What is dyspepsia? (2)

A
  1. Describes a range of upper GI symptoms which are typically prsent for 4 or more weeks
  2. Symptoms can be attributed to an underlying cause e.g GORD but the majority of patients are likely to have functional dyspepsia, where an underlying cause cannot be identfiied ad endoscopy findings are normal
  3. Dyspepsia symptoms in pregnancy are commonly due to GORD
40
Q

Symptoms of dyspepsia include… (5)

A
  1. Upper abdominal pain/ discomfort
  2. Heartburn
  3. Gastric reflux
  4. Bloating
  5. Nasuea and/ or vomiting
41
Q

Management of dyspepsia (6)

A
  1. URGENT endoscopic investigation if patient has dysphagia, significant GI bleed, over 55+ unexplained weight loss+ symptoms of upper abdominal pain, reflux or dyspepsia
  2. Lifestyle measures: healthy eating, weight loss, trigger food avoidance, smaller meal, evening meal 3-4h before bed, smoking cessation, alcohol consumption
  3. Review drugs that can cause dyspepsia (alpha blockers, antimuscarinics, aspirin, benzodiazepines, beta blockers, bisphosphonates, CCBs, corticosteroids, nitrates, NSAIDs, theophyllines, TCAs)
  4. Antacids and/ or alginates may be used for short term symptom control but long term continuous use is not recommended
  5. When univestigated - take PPI for 4wk+ test for H.pylori
  6. When functional (no cause) - test for Hpylori infection and treat if positive. If not not infected with Hpylori, PPI/ H2RA should be taken for 4 weeks.
42
Q

What is peptic ulcer disease? (5)

A
  1. Gastric or duodenal ulceration
  2. Which is a breach in the epithelium of the gastric or duodenal mucosa
  3. Most commonly caused by NSAID use and Hpylori infection
  4. Smoking, alcohol consumption and stress may also contribute to the development of peptic ulcer disease
  5. Complications of peptic ulcer disease = gastric outlet obstruction and potentially life threatening GI perforation and haemorrhage
43
Q

Symptoms of peptic ulcer disease (2)

A
  1. Upper abdominal pain = the main symptom

May also experience..nausea, indigestion, heartburn, loss of appetite, weight loss and bloated feeling

44
Q

Patients at high risk of developing GI complications wit an NSAID - those with a history of complicated peptic ulcer, or those with 2 or more of the following risk factors (8)

A
  1. > 65
  2. High dose NSAID
  3. Other drugs that increase risk of GI s/es e.g aticoags, corticosteroids, SSRIs
  4. Serious comorbidity
  5. Heavy smoker
  6. Excessive alcohol consumption
    7, Previous adverse reactions to NSAIDs
  7. Prolonged requirement for NSAIDs
45
Q

Management of peptic ulcer disease (10)

A
  1. URGENT endoscopic investigation if dysphagia, significant acute GI bleeding or those aged 55 and over with unexplained weight loss and symptoms of abdo pain/reflux/ dyspepsia
  2. Lifestyle: healthy eating, weight loss, avoid trigger food, raising head of bed, smoking cessation, eating evening meal 3-4h before bed, reducing alcohol consumption
  3. Review drugs that induce peptic ulcers e.g. NSAIDs, aspirin, bisphosphonates, immunosuppressive agents, KCl, SSRIs + recreational drugs
  4. Test for Hpylori
  5. If positive for Hpylori and no NSAID use, eradicate the Hpylori infection
  6. If related to NSAID use, use PPI/ H2 receptor antagonist for 8 weeks, followed by eradication if patient is +ve for Hpylori
  7. If negative for Hpylori and no history of NHSAID use, use a PPI/ H2 receptor antagonist for 4-8 weeks
  8. If +ve for Hypylori, review patient 6-8 weeks after starting eradication treatment+retest
  9. If ulcer healed, need to r/v NSAID. use. Gastroprotection should always be co-prescribed and PPI is the preferred option.
    10 . Patients with peptic ulcer disease who are on long term treatment should receive an annyal review of their symptoms and treatment, encourage stepdown if apporpriate.
46
Q

Drugs that induce peptic ulcers (7)

A
  1. NSAIDS
  2. Aspirin
  3. Bisphosphonates
  4. Immunosuppressive agents
  5. Potassium chloride
  6. SSRIs
  7. Recreational drugs e.g. crack cocaine
47
Q

Define Zollinger-Ellison syndrome

A

Disease in which tumours cause the stomach to produce too much acid, resulting in peptic ulcers

48
Q

What is GORD? (6)

A
  1. A chronic conditions
  2. Where there is reflux of gastric contents (acid, bile, pepsin) back into the oesophagus
  3. Causing symptoms of heartburn and acid regurgitation
  4. May be erosive/ non erosive
  5. Risk factors: consumption of trigger foods, pregnancy, hiatus hernia, family hx, stress, anxiety, obesity, drugs, smoking, alcohol, straining
  6. Complications: oesophagitis, ulceration, haemorraheg, stricture formation, anaemia, aspiration pneumonia, Barrett’s oesophagus
49
Q

Symptoms of GORD (2)

A
  1. Heartburn
  2. Acid regurgitation
    Less commonly: chest pain, hoarseness, cough, wheezing, asthma, dental erosions
50
Q

Management of GORD (8)

A
  1. URGENT endoscopic investigation if ALARM
  2. Lifestyle
  3. Review drugs that may cause GORD
  4. Long term continuous use of antacids not recommended
  5. If endoscopy confirmation of GORD = PPI for 4-8 weeks
  6. If no response to PPI, offer H2 receptor antagonist
  7. Severe oesphagitis - PPI for 8 weeks
  8. If patient pregnant: lifestye advice, antacid/ alginate. If ineffective -omeprazole/ ranitidine
51
Q

Drugs that may cause GORD (11)

A
  1. Alpha blockers
  2. Anticholinergics
  3. Benzos
  4. Beta blockers
  5. Bisphosphonates
  6. CCBs
  7. Corticosteroids
  8. NSAIDs
  9. Nitrates
  10. Theophyllines
  11. TCAs
52
Q

What is Hpylori? (4)

A
  1. One of the most common causes of peptic ulcer disease
  2. 95% of duodenal and 70-80% of gastric ulcers associated with it
  3. Associated with acute and chronic gastritis, gastric cancer and gastric mucosa associated lymphoid tissue lymphoma
  4. Bacteria colonise only in the mucus layer of the stomach. Weakens the protective mucus coating of the stomach and duodenum. This allows acid to go through to the sensitive lining beneath.
53
Q

Symptoms of Hyplori (3)

A
  1. Infection doesn’t usually cause symptoms.
  2. The most common symptom is abdominla pain. 3.Usually dull, gnawing aching, comes and goes for several days/ weeks. Can occur 2-3h after meals. Wakes you up in the night. Relieved by eating and antacid medications.
54
Q

Management of Hpylori (6)

A
  1. Must confirm presence before starting eradication treatment (test and treat)
  2. PHE guidance on when to test
  3. Treatyment: triple therapy
  4. PPI+ 2 antibacterials
  5. If no pen allergy: PO 1st line for 7 days - PPI+ amoxilciin and either clarithromycin/ metronidazole
  6. If pen allergy: PO 1st line for 7 days - PPI+ clarithromycin and metronidazole
55
Q

What is food allergy? (5)

A
  1. An adverse IMMUNE response to a food
  2. Commonly cutaneous and GI reactions
  3. Less frequently: respiratory reactions+anaphylaxis
  4. Distinct from intolerance as this is not immunological
  5. Common allergens: cow’s milk, hen’s eggs, soy, weheat, peanuts, tree nuts, fish, shellfish
56
Q

Management of food allergy (4)

A
  1. Strict avoidance
  2. Sodium cromoglicate licensed as an adjunct to dietary avoidance in patients with a food allergy
  3. Chlorphenamine maleate is licnesed for the symptmomatic control of food allergt
  4. Igf food induced - adrenaline/ epinephrine is 1st line immediate treatment
57
Q

Gastro-intestinal smooth muscle spasm

A

The intestinal smooth muscle relaxant properties of antimuscarinic and other antispasmodic drugs may be useful in IBS
Alverine citrate, mebeverine Hcl and peppermint oil are believed to be direct relaxants of intestinal smooth muscle+may relieve pain in IBS

58
Q

Define ileus

A

Lack of movement somewhere in the intestines that leads to a buildup and potential blockage of food material. May lead to intestinal obstrutcion. May happen after surgery.

59
Q

What is cholestasis? (1)

A
  1. Impairment of bile formation and/ or bile flow
60
Q

Symptoms of cholestasis (6)

A
  1. Fatigue
  2. Pruritis
  3. Dark urine
  4. Pale stools
  5. Jaundice
  6. Signs of fat soluble vitamin deficiencies
61
Q

Management of cholestasis (5)

A
  1. Colestyramine for pruritis
  2. Ursodeoxycholic acid for pruritis
  3. Rifampicin (unlicensed) for pruritis
  4. If previous therapy ineffective/ not tolerated- sertraline/ for prurtitis
  5. Ursodeoxycholic acid is effective for the treatment of pruritis associated with intrahepatic cholestasis in pregnancy
62
Q

Define intrahepatic cholestasis

A

Usually occurs in late preganncy and associated with adverse fetal outcomes
No evidence that ursodeoxycholic acid used in late prgenancy affects birth weight in infant/ risk of preterm delivery. There is limited data about the effect of fetal exposure during the 1st trimester.

63
Q

What are gallstones? (4)

A
  1. Cholelithiases
  2. Occur when hard mineral or fatty deposits form in the gallbladder
  3. Majority of patients = asymptomatic
  4. Symptoms occur when stones irritate the gallbladder and block part of the biliary system
  5. When stones irritate the gallbaldder/ block part of the biliary system, if left untreated, can lead to biliary colic, acute cholecystits, cholangitis, pancreatitis and obstructive jaundice
64
Q

Symptoms of gallstones (2)

A
  1. Usually asymptomatic
  2. When the stones irritate the gallblader/ block part f the bilirary system…
    - pain
    - infection
    - inflammation
65
Q

Management of gallstones

A
  1. Asymptomatic need o treatment
  2. Treatment of symptomatic: surgical removal by laparoscopic cholecystectomy
  3. Analgesia to control pain - IM diclofenac if severe/ intramuscular opioid
  4. No evidence to support use of ursodeoxycholic acid use in this way
66
Q

Types of biliary disorders (3)

A
  1. Gallstones
  2. Inborn errors of primary bile acid synthesis
  3. Primary biliary cholangitis
67
Q

What are inborn errors of primary bile acid synthesis? (2)

A
  1. A group of dieases in which the liver does not produce enough primary bile acids due to enzyme deficiencies.
  2. These acids are the main components of the bile and include cholic acid and chenodeoxycholic acid
68
Q

Function of bile? (7)

A
  1. Helps emulsify lipids in food - charge prevets fat droplets coated with bile from reaggregating into larger fat particles
  2. Dispersion of fat into micelles provides a greater increased surface area for pancreatic lipase which actually digests the triglycerides and is able to reach the fatty core through gaps between the bile salt
  3. Triglyceride broken down into 2 ftty acids + monoglyceride, which are absorbed
  4. Since bile increases the absorption of fats, it is an oimproitant part of the absorption of fat soluble substances
  5. Is also a route of excretion for bilirubin, a byproduct of RBCs recycled by the liver
  6. Alkali - neutralizes excess stomach acid before it enters the duodenum
  7. Bile salts also act as bactericides
69
Q

Symptoms of inborn errors of primary bile acid synthesis (7)

A 
May present with 
1. Cholestasis  (interruption or suppression of the flow of bile from the liver) > pruritis, fatigue, jaundice
2. Fat-solube vitamin malabsorption
3. Liver disease
4. Progressive neurological disease
5. Rickets
6. Susceptibility to bleeding
7. Night blindness
Exact presentation depends on the specific enzyme deficiency
70
Q

Management of inborn errors of primary bile acid synthesis (3)

A
  1. Cholic acid licensed for treatment if due to inborn deficiency of 2 specific liver enzymes. Acts by replacing some of the missing bile acids, therefore relieving some of the symptoms of the disease
  2. Chenodeoxcholic acid licensed if due to a deificency of one specific enzyme in the bile acid synthesis pathwaywhen presenting as cerebrotendinous xanthomatosis.
  3. Ursodeoxycholic acid (unlicensed) has been used but absence of evidence.
71
Q

What is primary biliary cholangitis? (2)

A
  1. Chronic cholestatic disease which develops due to progressive destruction of small and intermediate bile ducts within the liver
  2. Subsequently evolving to fibrosis+cirrhosis
    “In primary biliary cholangitis the immune system mistakenly attacks the bile ducts. It’s not clear why this happens. The bile ducts become damaged and injured.”
72
Q

Symptoms of primary biliary cholangitis (6)

A
  1. Does not always cause symptoms
  2. Bone and joint aches
  3. Fatigue
  4. Pruritis
  5. Dry eyes and mouth
  6. Pain and discomfort in the UPPER RIGHT SIDE of the tummy
73
Q

Management of primary biliary cholangitis (2)

A
  1. Ursodeoxycgholic acid is recommended, including for those with asymptomatic disease. It slows disease progression but the effect on overall survival is unceratin.
  2. Liver transplantation can be considered in patients with advanced primary biliary cholangitis.
74
Q

What are oesophageal varices? (4)

A
  1. Varcies = swollen veins in oesophagus/ stomach
  2. Formed when blood flow through the liver is compromised
  3. Veins can bleed
  4. Because the lower third of the oesophagus is drained eventually into the portal vein. These become distended in associated with portal HTN. At high gradients, blood flowing through the hepatic portal system is redirected from the liver into areas with lower venous pressures.
75
Q

Management of oesophageal varices (2)

A
  1. Banding

2. Vasopressin analogue for bleeding

76
Q

What is obesity?

A
  1. A BMI>30kg/m2, but shoul dbe interpreted with caution
  2. Men with a waist circumference>/= to94cm (90 for Asian)+ Women with WC >/= 80cm - at increased risk of obesity related health problems. If >102cm(M) or 88cm (F) very high risk.
77
Q

Management of obesity (12)

A
  1. Consider underlying causes e.g. hypothyroidism
  2. Review meds that may cause weight gaine.g atypical antipsychotics, sulfonylureas, TCAs
  3. Engage in a sustainable weight management programme which includes strategies to change behaviour, increase physical activity and improve diet and eating behaviour
  4. Drug treatment should NEVER be used as the sole element of treatment
  5. Only consider drug for those with a BMI>30kg/m2 in whom diet, exercise and behaviour changes fails to achieve a realistic reduction in weight
  6. Consider prescribing a vitamin and mineral supplement if concern about inadequate micronutrient intake
  7. Orlistat is the only drug currently available in the UK that is recommended specifically for the management of obesity - acts by reducing the absoprtion of dietary fat
  8. Treatment with orlistat may be used to maintain weight loss rather than to continue to lose weight
  9. Consider discontinuation after 12 weeks if weight loss has not exceeded 5% since the start of treatment
  10. Drugs which produce a feeling of satiety e.g methylcellulose and streculia have been used (unlicensed_ in an attempt to control appetite, but little evidence for their efficacy
  11. Various centrally acting appetite suppressants have been used in the management but have been withdrawn/ no longer recommended due to serious safety concerns/ addictive potential
  12. Bariatric surgery if BMI>40kg/m2 or betwene 35-39.9kg/m2 +significant disease
78
Q

Meds that may cause weight gain (8)

A
  1. Atypical antipsychotics
  2. Beta adrenoceptor blocking drugs
  3. Insulin (T2DM)
  4. Lithium carbonate/ citrate
  5. Sodium valproate
  6. Sulfonylureas
  7. Thiazolidinediones
  8. TCAs
79
Q

Drugs which can cause dyspepsia (12)

A
  1. Alpha blockers
  2. Antimuscarinics
  3. Aspirin
  4. Benzodiazepines
  5. Beta blockers
  6. Bisphosphonates
  7. CCBs
  8. Corticosteroids
  9. Nitrates
  10. NSAIDs
  11. Theophyllines
  12. TCAs
80
Q

What are anal fissures? (1)

A
  1. An anal fissure is a tear/ ulcer in the lining of the anal canal, immediately within the anal margin
81
Q

Symptoms of anal fissures (3)

A
  1. Bleeding on defacation
  2. Peristent pain on defacation
  3. Linear split in the anal mucosa
82
Q

Management of anal fissures (8)

A
  1. If acute, present for <6 weeks: focus on ensuring that stools are soft and easily passed
  2. Bulk forming laxatives recommended (osmotic as an alternative) if acute <6 wks
  3. Short term use of a topical preparation containing a local anaesthetic e.g lidocaine or simple analgesia may be offeredfor prolonged burning pain following defecation.
  4. If inadequate, refer to hospital
  5. If chronic (>6 weeks) and associated pain - gve GTN ointment (unlicensed). Limited evidence suggests strnegth used does not influence effectiveness but that higher strength potentially increases the incidence of side effects. Healing effects good but headache incidence high. Recurrence of fissure after treatment common.
  6. Alternative to GTN is diltiazem or nifedipine which have lower incidence of ADRs than topical.
  7. If no response, may refer to specialist for local injection of botulinum toxin type A (unlicensed indication)
  8. Surgery an effective option for the management of chronic, but reserved for those who do not respond
83
Q

What are haemorrhoids? (6)

A
  1. Haemorrhoids (piles) are abnormal swellings of the vascular mucosal anal cushions around the anus
  2. Internal haemarrhoids arise above the dentate line a
  3. Usually pianless unless they become strangulated
  4. External haemorrhoids originate below the dentate line
  5. External can be itchy or painful
  6. Women are predisposed to developing haemorrhoids during pregnancy
84
Q

Symptoms of haemorrhoids (6)

A
  1. Bright red blood after pooing
  2. Itchy anus
  3. Feeling like you still need a poo after going to th etoilet
  4. Slimy mucus in underwear after wiping bottom
  5. Lumps around anus
  6. Pain around anus
85
Q

Management of haemorrhoids (11)

A
  1. Lifestyle: increase fibre and fluid intake to keep stools soft and easy to pass (minimise straining) - advice about perianal hygiene is helpful to aid healing and reduce irritation and itching
  2. Treat constipation with bulk forming laxative
  3. Simple analgesic for pain relief
  4. Avoid opioids as constipating
  5. Avoid NSAIDs if active bleeding
  6. Topical preparations (combinations) offer symptomatic relief of local pain and itching but evidence does not suggest that any preparation is more effective than any other
  7. If topical preparation contains local anaesthetic may only be used for a few days as may cause sensitization to the anal skin. Local anaesthetics can be absorbed through the rectal mucosa and very rarely may cause increased irritation - excessive application should be avoided
  8. Topical preparations containing corticosteroids may improve local inflammation but no data suggesting they reduce haemorrhoidal swelling, bleeding or protrusion
  9. Topical corticosteroids are suitable for occaisional short term use (no more than 7 days) after exclusion of infections. Long term use can cuase ulceration/ permanent damage.
  10. Treatments from specialists include various non drug procedures e.g rubber band ligation
  11. Pregnancy: Bulk forming laxatives are not absorbed and are therefore safe in pregnancy. If topical, give soothing. DO NOT GIVE local anaesthetics or corticosteroids.
86
Q

What is a reduced exocrine pancreatic insufficiency? (2)

A
  1. Characterized by reduced secretion of pancreatic enzymes into the duodenum (1st part of the small intestine)
  2. Can result from chronic pancreatitis, CF, obstructive pancreatic tumours, coeliac disease, Zollinger-Ellison syndrome+ GI/ pancreatic surgical resection
87
Q

Symptoms of exocrine pancreatic insufficiency (4)

A
  1. Maldigestion
  2. Malnutrition
  3. Low circulating levels of micronutrients, fat soluble vitamins and lipoproteins
  4. GI symptoms e.g diarrhoea, abdo cramps and steatorrhea
88
Q

Define steatorrhoea

A

Excess fat in faeces. Bulky, difficult to flush. Pale and oily appearance. Foul smelling.

89
Q

Management of exocrine pancreatic insufficiency (14)

A
  1. Pancreatic enzyme replacement therapy with pancreatin is the maintsay of treatment for exocrine pancreatic insufficiency
  2. Pancreatin contains 3 main groups of digestive enzymes: lipase, amylase and protease
  3. These enzymes respectively digest fats, carbohydrates and proteins into their basic components so that they can be absorbed and utilised by the body
  4. Pancreatin should be administered with meals and snacks
  5. Dose should be adjusted to lowest effective dose according to symptoms of maldigestion and malabsorption
  6. Fibrosing colonopathy has been reported in patients with CF taking high dose pancreatic enzyme replacemen therapy (>10,000 units/ kg/ day). Peak age for development = between 2-8 years
  7. Manufacturers advise that total dose in CF patients should not >10,000 units/kg/day of lipase
  8. Advise that if patient taking pancreatin develops new abdo symptoms patient should be reviewed to exclude the possibility of colonic damage
  9. Limited evidence that acid suppression may improve the effectiveness of pancreatin. PPIs or H2RAs may be trialled in patients who continue to experience symptoms despite high doses of pancreatin.
  10. Levels of fat soluble vitamins and micronutrients should be routinely assessed and supplementation advised whenever necessary
  11. Dietary advice should be provided
  12. Food intake should be distributed between 3 main meals per day and 2 or 3 snacks.
  13. Avoid foods hard to digest eg legumes and high fibre food. Avoid alcohol completely. Reduced fat diets not recommended.
  14. MCT enriched preparations offer no advantage over a normal balanced diet.
90
Q

Define fibrosing colonopathy

A

A form of long segment colonic disease. Gradual fusiform stenosis of the lumen resulting from submucosal widening due to the deposition of mature collagen.

91
Q

What is a stoma? (5)

A
  1. A stoma is an artificial opening on the abdomen
  2. To divert the flow of faeces/ urine into an exterrnal pouch located outside of the body
  3. May be temporary or permanent
  4. Colostomy/ ileostomy most common
  5. Gastrostomy, jejunostomy, duodenostomy or caecostomy may also be perfomed
92
Q

Management of a stoma (15)

A
  1. Enteric coated and M/R drugs UNSUITABLE, especially in patients with an ileostomy as there may not be sufficient release of active ingredient
  2. Soluble tablets, liquids, capsules or uncoated tablets are more suitabe due to their quicker dissolution
  3. If solid dose form given, contents should be checked for any remnants
  4. Avoid drugs with sorbitol as an excipient as laxative
  5. Avoid opioid analgesics due to constipation
  6. Avoid NSAIDs due to risk of gastric irritation and bleeding>monitor output for blood
  7. Tendency for diarrhoea (mg) or constipation (calcium) with antacids may be increased
  8. PPIs and somatostatin analogues (e.g. ocretotide) often used to reduce the risk of increased stoma output due to increased gastric acid secretion
  9. Loperamide+ codeine reduce intestinal motility and decrease water and sodium output from an ileostomy.
  10. Loperamide circulates through the enterohepatic circulation which is disrupted in patients with SBS so high doses may be required.
  11. Patients with a stoma are particularly susceptible to hypokalemia if taking digoxin. Potassium supplements/ K+ sparing diuretic may be advisable with monitoring for early signs of toxicity.
  12. Diuretics should be used in caution in patients with an ileostomy or urostomy as they may become excessively dehydrated and potassium depletion may occur.
  13. Usually advisable to to use a K sparing diuretic
  14. Iron preparations may cause loose stools and sore skin in stoma patients. Use IM iron if this is an issue. Avoid M/R preps.
  15. Avoid laxatives in patients with an ileostomy. Colostomy patients may suffer constipation and should be treated with dietary advice. Bulk forming drugs can be tried and if insufficient can give stimulant used with caution.
  16. For K supplements, liquid formulations are preferred to M/R formulations. The daily dose should be split to avoid diarrhoea.

Pre-Reg Clinical (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions