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Digestive System Module > Lecture 30 > Flashcards

Lecture 30 Flashcards

1
Q

Diarrhoea

A
  1. Normal: 200g/day
    Little clinical value (hard to practically measure)
  2. Consistency- loose
  3. Frequency- increased (for the individual)
    -what is normal for that patient. look for change in pattern of bowel habit
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2
Q

Bristol Stool Chart

A

Type1: separate hard lumps, like nuts. (hard to pass)
Type2: Sausage-shaped but lumpy
Type3: Sausage but with cracks on the surface
Type4: Sausage or Snake. Smooth and soft
Type5: Soft blocks, with clear but edges
Type6: Fluffy pieces with rugged edges, a mushy stool
Type7: Watery, no solid pieces. Entirely liquid
-easy to use for comparison, when seeing a person on a regular routine

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3
Q

What does stool consistency depend on?

A

Stool consistency depends on water

  • Constipation: not enough water
  • Diarrhoea: too much water
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4
Q

Acute vs Chronic diarrohea

A

Acute: up to 14 days
Chronic: over 14 days
Causes of acute and chronic diarrhoea are different
-important to know time frame of diarrhoea history

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5
Q

Causes of acute diarrhoea

A 
95% infectious
-Bacterial
-Viral
-Parasitic
Infectious causes of diarrhoea are excluded with stool samples to look for pathogens
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6
Q

Causes of chronic diarrohea

A

Many causes can be grouped according to underlying mechanism
some conditions will have a combination of mechanisms
-Inflammatory
-Osmotic
-Secretory
-Fatty
-helpful for pathology and classify causes

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7
Q

Inflammatory diarrohea pathophysiology

A

Damaged epithelium leads to (inflammatory) exudate

-commonest cause of inflammaotry chronic diarrohea : Inflammatory bowel disaese

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8
Q

Osmotic diarrohea pathophysiology

A

Osmotically active compounds in gut lumen draws fluid in

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9
Q

Secretory diarrohea pathophysiology

A

Colon/gut irritated byt something, causing stimulation of excessive fluid secretion

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10
Q

Fatty diarrohea pathophysiology

A

Fat malabsorption

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11
Q

Bacterial infective causes of Acute diarrohea

A 
-commonest causes
Salmonella
Escherichia coli
Campylobacter 
Shingella
Clostridium perfingens
Clostridium difficile
-following antibiotics
Yersinia
Staphylococcus areus
Bacillus cereus
Listeria monocytogenes
Vibrio (includes cholera)
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12
Q

Viral infective causes of Acute diarrohea

A 
Norovirus (common in resthomes/people in hospital)
Rotavirus
Adenvirus
-common community viral pathogens
Cytomegalovirus
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13
Q

Portozoa infective causes of Acute diarrohea

A

Cryptosporidium
Giardia
Entamoeba histolytica

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14
Q

What are the mechanisms of Infective causes relatively

A

Infective causes of acute diarrohea can have different mechanisms

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15
Q

Campylobacter mechanism of acute diarrohea

A

Inflammatory diarrohea

causes mucosal inflammation –> exudate

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16
Q

Giardia mechanism of acute diarrohea

A

Osmotic diarrhoea
Mild villous atrophy (mimics celiac disease)
–> carbohydrate malabsorption (stays and acts as osmotically active compound)
–> undigested sugars osmotically active
–> draws fluid in
Similar to lactose intolerance

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17
Q

Enterotoxigenic E. coli mechanism of acute diarrohea

A

Secretory diarrohea

releases a Toxin which is irritating to colon and stimulates excessive fluid secretion

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18
Q

Inflammatory diarrohea

A

Inflammatory bowel disease (most common cuase of inflammatory d - chrons diasease and ulcerativ colitis))
Diverticulitis (inflammation of diverticula/pockets in colon. can be consequence of constipation. Pockets can sometimes be impactr with stool/fibrous material, and can lead to inflammation)
Small Intestinal bacterial overgrowth
-not very common. many mechanisms leading to diarrohea
-overgrowth of bacteria causes direct inflammation of enterocytes (in SI and LI), causing direct inflammatory damage to enterocytes
Radiation colitis (consequence/complication of radtion treatment (e.g. for abdominal or pelvic cancers). colon in feild of radiation. Damage to mucosa)
Ischaemic colitis (decreased blood flow to colon, damaging mucosa-ischaemic- led to inflammation)
Colon cancer

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19
Q

Osmotic diarrohea

A
  1. Carbohydrate malabsorption
    a) lactose intolerance due to lactase deficiency
    - can be primary or secondary
    - Primary: deficiency of lactase enzyme
    - Secondary: to any condition that causes damage to the enterocytes–> loss of lactase
    b) Irritable bowel syndrome
  2. Coeliac disease
    - one of the most commonest cuases
    - villous abnormality
    - autoimmune condition, intolerance to gluten and gluten proteins. Damages villi. Leads to malabsorption things (carbs, nutrients, minerals) remains in gut
  3. Small intestinal bacterial overgrowth
    - malabsorption of proteins, carbohydrates, fats and other osmotically active by-products of bacterial metabolism (lots of biproducts released due to excessive overgrowth of bacteria)
  4. Laxative abuse
    - laxatives can be either osmotic in nature or stimulating
    - Stimulate: movements of colon
    - Osmotic: act as osmotically active compounds, not absorbed, causing diarrohea
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20
Q

Secretory diarrohea

A
  1. Terminal ileal resection
    - surgery to remove terminal ileum, bile acids not absorbed and enter colon, irritate colon, colon releases large amount of fluid and electrolyte
    - bile acid malabsorption
  2. Cholecystectomy
    - inflammatory and secretory
    - bile flow continuous into small intestine
  3. Microscopic colitis
    - the term includes lymphocytic colitis and collagenous colitis
  4. Inflammatory bowel disease
    - typically inflammatory but also has secretory component
  5. Diverticulitis
    - typically inflammatory but also has secretory component
  6. Neuroendocrine tumours
    - Rare: produce abnormal levels fo some endocrine hormones that can drive water secretion e.g. gastrinoma - excessive gastrin. carcinoid - excessive serotonin
  7. Small intestinal Bacterial overgrowth:
    - unabsorbed food products and bile acids can stimulate secretory cells in the colon
    - Addison’s disease
  8. Disordered motility
    - irritable bowel syndrome
    - post-vagotomy diarrhoea
    - diabetic autonomic neuropathy
    - hyperthyroidism
  9. Colon cancer
  10. Laxative abuse
21
Q

Fatty diarrhoea

A
  1. Pancreatic exocrine insufficiency
    -inadequate pancreatic enzymes
  2. Bile acid malabsorption
    -inadequate amount of bile acids
    -e.g. terminal ileum resection
    (also causes secretory diarrohea irritating colon)
  3. Small intestinal bacterial overgrowth
    -deconjugation of bile acids: impaired micelle formation - impaired fat digestion and absorption
  4. Coeliac disease
    -malabsorption of carb and fat
    -mucosal disease
  5. Short bowel syndrome
    -not enough mucosal surface
    -too much of SI removed surgically for conditions e.g. Crohns.
22
Q

Small Intestinal bacterial overgrowth

A

Not clinically that common
Excessive amounts of colonic bacteria in the small intestine
Colon has majority of bacteria- SI is relatively sterile
Bloating, flatulence, abdominal discomfort, diarrohea, steatorrhoea, malabsorption

23
Q

SIBO is predisposed by

A
  1. Impaired motility:
    - the migrating motor complex is a mechanism of preventing SIBO by cleansing the small bowel of debris that pools/sits too long in LI
    - this clearance isnt cleared
    - Scleroderma (CT disorder, abnormal fibrosis of organs including gut(impairing motility)), diabetes(autonomic neuropathy, which also impairs gut motility), opiate use (morphine- will slow down gut), radiation enteritis
  2. Anatomical disorders- stasis in the small intestine
    - adhesions (post surgery), strictures, small intestinal diverticula, blind loops (predisposed to bacteria growing in it) (bilroth) e.g. post surgical
  3. Metabolic/Systemic diseases
  4. Immune deficiency disorders
24
Q

SIBO Maldigestion

A
  1. Bacteria deconjugates bile acids leading to impaired micellular formation and fat digestion
    - bile acids broken down. w/o properly formed bile acids, cannot absorb fats well
  2. Bacterial degradation of carbohydrates in the intestinal lumen, which also produces osmotically active by-products
  3. Bacterial degradation of protein precursors in the intestinal lumen
25
Q

SIBO Malabsorption

A

Damages enterocytes by direct adherence, producing enterotoxins and enzymes
Malabsorption of:
-Bile acids
-Fats
-Carbs
-Proteins
-B12 (bacterial competes for B12 for nutrition)

26
Q

Fatty Diarrhoea in SIBO

A

(lack of bile acids) deconjugation of bile acids by bacteria
-impaired micelle formation
-impaired fat digestion and absorption
-different to most watery diarrhoea
-Thick, difficult to flush, sometimes apppears oily
Any of the 4 mechanism can be present, some can dominate

27
Q

Inflammatory Diarrhoea in SIBO

A

Bacteria causes direct dmaage and inflammation of enterocytes
Any of the 4 mechanism can be present, some can dominate

28
Q

Osmotic Diarrhoea in SIBO

A

Malabsorption of proteins, carbs, fats and other osmotically active by-products of bacteria metabolism
Deconjugated bile acids inhibits carb transporters
Any of the 4 mechanism can be present, some can dominate

29
Q

Secretory Diarrhoea in SIBO

A

Unabsorbed food products and bile acids can irritate colon and stimulate secretory cells in the colon
Any of the 4 mechanism can be present, some can dominate

30
Q 
Case 1
35 year old female
Epigastric pain2 weeks
-worse at night
-improved by eating food
Vomiting 3 hours after meals
Presents with passing black bowel motions for 2 days (melaena)
A

Epigastric pain typical of duodenal ulcer
-can cause narrowing of pyloris
Black bowel motions = melaena
-blood altered by acid
-sign of upper GI bleeding
Delayed vomiting suggests pyloric obstruction
Treatment options:
-Endoscopic balloon dilatation- treat stenosis itself as is potentially irreversible/temporary condition. Stretches pyloris and temporarily treat obstruction (still need to treat underlying problem of the ulcer)
-Gastro-jejunostomy and truncal vagotomy (uncommon nowadays)- if stenosis, may have to cut the area out . Billroth procedure
-now have better drugs to treat peptic ulcer disease: amaeprazol, proton pump inhibitors

31
Q

Melaena

A

Active bleeding from duodenal ulcer
black bowel motions
-blood becomes digested as enter SI
-if bleeding occurs beyond SI it comes out red or dark red

32
Q

Pre-pyloric ulcer

A

-distortion of normal anatomy by scarring
-effect gastric emptying
-can cause pain if ulcer is deep
-if left untreated to continue causing inflammation will lead to fibrosis and then will lead to scarring
-usually longer than 2 weeks. people may not have symptoms until last few weeks before present. Therefor normally ulcer has to be present for many months before causes stenosis
-Pyloric stenosis: cause of delayed vomiting
-stomach doesnt empty normally after eating
can cause vomiting after meal, esp. large meal
-if ulcer continues to work through stomach wall, will encounter artery and cause bleeding (melaena)

33
Q

Pyloric stenosis

A

cause of delayed vomiting
-stomach doesnt empty normally after eating
can cause vomiting after meal, esp. large meal
- if ulcer continues to work through stomach wall, will encounter artery and cause bleeding

34
Q

Billroth 1 and 2

A

Rare: done for peptic ulcer disease, gastric cancer (pyloris, duodenum)
Billroth 1: Distal part of stomach and duodenal bulb removed as segment. resect and join. Common bile duct still there- distal to anastomosis. No pyloris to control food exiting
Billroth 2: esp chosen if concern of recurrence in distal stomach (if cancer reoccurs will get stenosis in the same location). Take distal part of SI to make new anastomosis. Bile flows through to mix with food that leaves stomach. 2x loops: Afferent and Efferent Limbs, where food joins stomach and leaves.

35
Q

Case 1 cont:
Developed upper abdominal discomfort after meals
Diarrohea

A

-Developed upper abdominal discomfort after meals: (no pyloris), so Rapid gastric emptying of digested food particles into small bowel, distends prox SI causing pain
-high osmotic load draws large volume of fluid into jejunum (osmotic diarrohea)
Diarrhoea: Same reason as above: - Osmotic diarrhoea. Also vagotomy leads to increased small vowel motility

36
Q

Case 1 - 10 years later
Diarrohea gets a lot worse
-8-10 times/day with pain, bleeding and mucus (urgency)
Colonoscopy
-continuous inflammation from rectum to transverse colon
Diagnosis: ulcerative colitis

A

No melaena so not upper GI cause
Ulcerative colitis- one of the most common causes of inflammatory diarrhoea
Diarrhoea:
inflammatory exudate of fluid and electrolytes across damaged epithelium
(known due to bleeding and frequency)
-Inflammatory diarrhoea
Fails to respond to medications:
-Colectomy (colon removed) and ileostomy (terminal ileum taken to surface)

37
Q

Bleeding in stool

A

apart from inflammatory diarrhoea, other diarrhaea should not cause bleeding

38
Q

Colectomy

A

Colectomy for severe colitis
-for: difficult to treat colitis.
or refractory colitis - collitis that doesnt respond to medications
-medications are becoming more and more effective, so more able to avoid colectomy for Inflammatory bowel disease

39
Q

Ileostomy

A

Stoma
SI taken to the surface of the skin
contents drain into bag
mid portion of abdomen- right or left (usually right)
-Usually SI joined back to rectum
-but several cases this rejoining doesnt occur, - therefore can have either temporary or permanent ileostomy

40
Q

Usual ileostomy output

A

Volume: 600-1000mls
Consistency: thick liquid
Colour: dark green/brown (no bacteria) (bilus)
Odour: Nil (as no bacteria)
Content:
-similar electrolytes to plasma
Sodium loss 60-80 mmol per day - higher than normal state
-increased sodium reabsorption in kidneys
- require to counteract: High oral sodium intake usually enough
-over time is degree of adaptation, kidneys increase reabsorption of sodium
-therefore after ileostomy most people are able to manage this change in physiology by having a slightly high oral intake of sodium
-Sometimes requires elevated fluid intake as well

41
Q

Case 1 summary

A

Colectomy with formation of ileostomy
High output from ileostome- 2000ml/day
-as has had colectomy as well as gastric surgery. has excessive contents entering SI (as no pyloris of vagus nerve) + now no longer has colon to try compensate for increased fluid production. Due to osmotic diarrohea caused by intital gastric surgery, colon normally would undergo adaptation. But now burdern is too much
Due to previous gastric surgery
Management of high output:
By decreasing small bowel motility with medication
-allow for more time to stay in gut = increase reabsorption (e.g. anti-diarrhoea agents like loperamide) absorption can be increased
-reduce ileostomy output
-reduce sodium loss

42
Q

Case 2
65 year old female with Crohn’s disease
Previous resection of 150cm of terminal ileum
Since then, diarrhoea 3-4 times a day

A

Improved with cholestyramine (drug which binds bile acids) - colating agent (binds to bile reducing amount of diarrhoea)
-next few years:
several further operations for small bowel Chron’s disease
-more ileum resected
-remaining small bowel 1 metre
Severe diarrhoea with episodes of dehydration requiring hospital admissions
-secondary to short bowel syndrome - infrequent now as Chron’s treatment has improved

43
Q

Crohn’s disease

A

Chronic inflammatory condition
occur at any part of GI tract
typically likes terminal ileum and colon
If chronic inflammation is untreated, fibrosis –> narrowing –> strictures (common complication of Crohn’s disease)
-are medications to treat the inflammation. once fibrotic stricture the medications dont work, as they only really target the inflammation
-therefore those with strictures will require operation to resect
-Barum X-ray test

44
Q

B12 malabsorption due to Terminal Ileum resection

A

Removal of terminal ileum
–> loss of specialised receptors for B12/intrinsic factor
Malabsorption of B12

45
Q

Bile salt malabsorption due to Terminal Ileum resection

A

Portal circulation take bile into hepaticportal vein –> liver
Reduced re-uptake of bile salts via enterohepatic circulation
1. Bile acids lost through colon/feaces (white stool)
(excessive loss) Less bile acids –> fat malabsorption i.e. Fatty diarrhoea (steatorrhea)
2. Bile salts in colon, irritating –> stimulate water and electrolyte secretion i.e. Secretory diarrhoea
-usually one of the 2 will predominate, driving the diarrhoea. Will depend on diet

46
Q

Short bowel syndrome

A

Short bowel/gut syndrome
-complication of small bowel surgery
-not enough small intestine left
Malabsorption of:
Vitamins, minerals
Water(contributes to diarrohea), electrolytes
Proteins, fats, carbs
Bile acids
-Presence of colon and ileocaecal valve - do better
Colon resorbs water and ileocaecal valve acts as a “brake” to slow down transit into colon
-colon adapts and increased amount of water reabsorbed
-ileoceacal valve also acts as sphincter reducing amount of water entering the colon, allowing time for the colon to adjust to increased fluid load

47
Q

Short bowel syndrome

-Adaptive process

A

Ileal adaptation
-villi hypertrophy
Colon increases absorptive capacity
-sometimes these adaptive processes sometimes inadequate at controlling patient symptoms

48
Q

Short bowel syndrome - Management

A

Dietary (iso-osmolar diet- low osmotically active compounds)
Anti-motility drugs (anti-diarrohea medications/luperomide)
Acid suppressant medications (stomach 1-2L of gastric acid daily, contributing to fluid of the SI, suprress with proton pump inhibitors)
Cholestyramine (binds to excessive bile salts, causing fat malabsorption and secretory diarrhoea)
Total parenteral nutrition (TPN)
- if losing weight and nutrition
-intravenous nutrition in people who arent able to eat sufficiently

Digestive System Module (38 decks)

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