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Alimentary System > Alimentary - Miscellaneous > Flashcards

Alimentary - Miscellaneous Flashcards

1
Q

Why are there differences in bacterial communities through the GIT?

A
  • due to differences in O2 conc.
  • > increasingly more anaerobic as u go through the GIT
  • due to differences in pH
  • > ie. mouth is more neutral, duodenum is more alkaline and stomach is more acidic
  • due to differences in transit times
  • > ie. transit times increase from mouth to colon -> larger amount of bacteria in the colon

… throughout the GIT

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2
Q

What are facultative anaerobic bacteria?

A

Bacteria which grow in the presence AND absence of oxygen, but grow poorly when oxygen is present

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3
Q

What are obligate anaerobic bacteria?

A

Bacteria which cannot grow in the presence of oxygen

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4
Q

Why is there typically more disease in the colon compared to the small intestine?

A
  • Lower substrate concentrations
  • > low fermentation rates
  • > low SCFA production
  • > low SCFA absorption
  • Higher pH (6.5)
  • > less pathogen exclusion (optimal pH for pathogen growth)
  • > more protein fermentation
  • Slower transit
  • > higher exposure to harmful chemicals
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5
Q

Why are resident bacteria essential for a healthy gut?

A

1 - Modification of host secretions
-> (mucin, bile, gut receptors)

2 - Defence against pathogens

  • > competition
  • > barrier function
  • > pH inhibition (they reduce the pH so pathogens can’t grow)

3 - Metabolism of dietary components
-> breakdown of dietary fibre

4 - Production of essential metabolites to maintain health

5 - Development of immune system
-> immune priming

6 - Host signalling
-> Gut-Brain axis

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6
Q

What are the health benefits of dietary fibre fermentation by bacteria?

A
  • Releases additional phytochemicals
  • Maintains a slightly acidic pH
  • Increases commensal bacteria population

(both of the above improves resistance to pathogens)

  • Essential supply of SCFAs (gut-brain axis)
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7
Q

What are the 3 main SCFAs produced by gut bacteria? In what ratio are they released?

A

1 : 1 : 3

butyrate : propionate : acetate

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8
Q

Why is widespread abx use harmful for the gut microbiome?

A
  • Decline in commensals (“good” bacteria)
  • Lack of diversity of bacteria (too much of one thing produced and less of another thing!)
  • Overgrowth of pathogenic bacteria
  • Spread of abx resistance
    (killing off of sensitive bacteria, overgrowth of resistant bacteria -> pass on their resistance genes)
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9
Q

What are the methods of bacterial gene transfer?

A

1 - Conjugation

2 - Transformation

3 - Transduction

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10
Q

What is the difference between a probiotic and a prebiotic?

A
  • Probiotic = live microorganisms which confer a health benefit to the host, when administered in adequate amounts (added live bacteria ie. to yoghurts, food, in tablets, etc)
  • Prebiotic = a substrate which is utilised by the host microorganisms conferring a health benefit (food for resident bacteria ie. naturally found in plant foods, supplements)
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11
Q

What is the difference between correlation and causation with respect to gut microbes and disease?

A

Changes in gut microbiota composition may be associated with diseases, but this does not always mean that they CAUSE the disease

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12
Q

Give some examples of diseases that correlate with microbial dysbiosis

A
  • IBS
  • IBD
  • CVD
  • Allergies
  • Obesity
  • Bone health
  • Brain health
  • RA
  • Diabetes
  • CRC
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13
Q

When are prebiotics useful?

A
  • food for the resident bacteria!!*
  • Improved gut function: stool bulking and faster gut transit
  • ?Management of IBD
  • > reduces inflammatory markers
  • May reduce risk of CRC
  • Supplementation of infant formula
  • Increases Ca2+ absorption and bone health (due to reducing pH)
  • Lowers glycaemic index (when consumed in place of sugars)
  • > lower blood glucose rise after meals
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14
Q

Which diseases can be potentially treated and prevented by the use of probiotics?

A
  • Abx.-Associated Diarrhoea
  • CDAD
  • H. Pylori
  • IBS
  • Infectious Diarrhoea
  • Necrotising Enterocolitis
  • Pouchitis
  • Traveller’s Diarrhoea
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15
Q

Why are probiotics beneficial? What is their mechanism of action?

A
  • note: the brand of probiotic and the bacterial species present matters*
  • Competition
  • Bioconversion (diet)
  • Production of vitamins
  • Direct antagonism (pathogens)
  • Competitive exclusion
  • Barrier function
  • Reduce inflammation
  • Immune stimulation
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16
Q

Why is FMT more effective in treating recurrent difficile infection (CDAD) than other GI diseases?

A
  • CDAD = C. Diff-associated disease*
  • FMT = Faecal Microbial Transplantation*
  • C. Diff tends to occupy empty niches following abx. therapy
  • Overgrowth of C. Diff results in toxin production, abdominal pain, fever
  • C. Diff spores are abx. resistant -> results in recurring C. Diff infection
  • Probiotics in ICU can reduce the incidence of CDAD
  • The most effective treatment for recurrent CDAD = FMT

(not suitable for conditions other than CDAD -> probs due to the extent to which the existing microbiota is present/absent)

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17
Q

How is BMR calculated?

A
  • By direct calorimetry
  • Depends on lean body mass
  • Schofield or Harris Benedict, Henry equations
  • Various adjustment factors for activity and illness
  • Easy to overestimate requirements
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18
Q

What are the clinical consequences of malnutrition?

A
  • Impaired immune response
  • Reduced muscle strength
  • Impaired wound healing
  • Impaired psycho-social function
  • Impaired recovery from illness and surgery
  • Poorer clinical outcomes
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19
Q

What BMI is overweight and obese?

A
  • Overweight = BMI >25

- Obese = BMI >30

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20
Q

What BMI is underweight?

A
  • BMI <20
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21
Q

How do you screen for undernutrition?

A

Malnutrition Universal Screening Tool (MUST)

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22
Q

What are the main causes of undernutrition?

A

Appetite Failure

  • Anorexia Nervosa
  • Disease-related

Access Failure

  • Teeth
  • Stroke
  • Cancer of H+N
  • Head injury

Intestinal Failure
-ie. Short Bowel syndrome -> reduction in the functioning gut mass below the minimal amount necessary for adequate digestion and absorption of nutrients

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23
Q

How to identify a pt. presenting with acute abdominal problems?

A
  • Someone who becomes acutely ill and in whom symptoms + signs are chiefly related to the abdomen
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24
Q

What clinical syndromes of Acute Abdomen usually require a Laparotomy?

A

1 - Rupture of an organ -> ie. spleen, aorta, ectopic pregnancy)

2 - Peritonitis -> ie. perforation of PU/DU, diverticulum, appendix, bowel or GB

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25
Q

What clinical syndromes of Acute Abdomen do not require Laparotomy?

A
  • Local peritonitis: ie. diverticulitis, cholecystitis, pancreatitis, appendicitis (latter requires laporoscopy)
  • Colic: muscular spasm in a hollow viscus (ie. gut, ureter, uterus, bile duct, GB)
  • Bowel obstruction
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26
Q

What are the investigations for Peritonitis?

A
  • Diagnostic Paracentesis
  • > sent for urgent MC+S -> neutrophils >250mm3 = SBP
  • Blood + urine cultures
  • Imaging -> if clinical suspicion of perforated viscus (AXR, CT)
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27
Q

What are the routes of infection for Peritonitis?

A
  • Perforation of GI/ biliary tract
  • Female genital tract
  • Penetration of abdominal wall
  • Haematogenous spread
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28
Q

What are the cardinal symptoms of Bowel obstruction?

A
  • Pain
  • Vomiting
  • Distension
  • Constipation
  • > full constipation (unable to open bowels or pass wind for a certain period of time)
  • Boborygmi
  • > rumbling sounds caused by gas moving through the intestines
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29
Q

What are the investigations of Bowel Obstruction?

A
  • Urgent Bloods: FBC, CRP, U+Es, LFTs
  • Imaging:
  • > CT w IV contrast (1st line)
  • > XR (used in some places as 1st line) -> AXR, CXR
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30
Q

What are the investigations for acute Pancreatitis?

A
  • Serum Amylase - levels fall within 24 hours (may be normal when severe)
  • Serum Lipase - rises earlier and falls later
  • ABG - oxygenation, acid-base status
  • CRP

Imaging:

  • AXR = “sentinel loop” of proximal jejunum
  • erect CXR = helps to exclude other causes ie. perforation
  • CT = standard choice of imaging (!!!) -> rules out complications
  • US (if gallstones and increased AST), ERCP (if LFTs worsen)
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31
Q

What are the XR findings for Bowel obstruction?

A
  • AXR: concurrent large and small bowel obstruction (?incompetent ileocaecal valve)
  • erect CXR: free air under the diaphragm (?bowel perforation)
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32
Q

What are the clinical features of Mesenteric Ischaemia?

A

1 - Acute severe abdominal pain (pain = constant, central or around RIF)

2 - No/minimal abdominal signs

3 - Rapid Hypovolaemia - Shock!
-> mesenteric ischaemia may be due to low-flow states, caused by poor CO

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33
Q

What are the investigations for Mesenteric Ischaemia?

A
  • Bloods
  • > FBC (raised Hb, WCC), CRP, U+Es
  • ABG
  • > oxygenation, acid-base status
  • Imaging
  • > AXR (“gas-less” abdomen early on -> filled w fluid!)
  • > CT Angio/w IV contrast = gold standard
  • Laparotomy - (chronic -> diagnosis often made at laparotomy)
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34
Q

What are the investigations for Acute Abdomen?

A
  • Bloods: U+Es, FBC, serum amylase, LFTs, CRP, Lactate, Urinalysis

Imaging: (?perforation)

  • erect CXR -> air under the diaphragm
  • AXR -> Rigler’s sign
  • CT - if readily provided + causes no delay
  • US - may identify perforation or free fluid
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35
Q

What is the treatment of acute abdomen?

A
  • Resuscitation!!!
  • > IV fluids, Sepsis (give 3, take 3), Decompress gut, ensure adequate pain relief, enhance tissue perfusion, ensure adequate oxygenation
  • active Observation!!!
  • > check if pt. deteriorates
  • > useful if diagnosis is uncertain and risk of alternative intervention is greater
  • Treatment!!!
  • > pain relief
  • > abx.
  • > definitive interventions ie. laparotomy (for ie. rupture of an organ, advanced peritonitis due to perforation), laparoscopy (gallstones -> cholecystectomy)
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36
Q

What are the clinical features of upper GI bleeding?

A
  • Haematemesis
  • Melaena
  • Elevated Urea
  • > due to partially digested blood -> haem -> urea
  • Associated w Dyspepsia (epigastric pain associated w eating) and Reflux
  • NSAID use
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37
Q

What are the clinical features of lower GI bleeding?

A
  • Fresh blood/clots
  • Magenta stools
  • Normal urea
  • > in contrast to elevated urea in upper GI bleeding
  • Typically painless
  • More common in advanced age
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38
Q

List some causes of upper GI bleeding

A

Oesophagus:

  • Oesophageal ulcer
  • Oeosphagitis (3)
  • Oesophageal varices (5)
  • Mallory-Weiss Tear (8)
  • Oesophageal malignancy (7)

Stomach:

  • Gastric ulcer (1)
  • Gastritis (2)
  • Gastric varices (5)
  • Gastric malignancy (7)
  • Dieulafoy (9)
  • Angiodysplasia (9)

Duodenum:

  • Duodenal ulcer (1)
  • Duodenitis (4)
  • Angiodysplasia (9)

Also can be no cause found!!

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39
Q

What are the most common causes of Oesopagitis?

A
  • Reflux Oesophagitis
  • Hiatus Hernia
  • Alcohol
  • Bisphosphonates
  • Systemic illness
  • bleeding typically occurs when pt. is also on anti-platelets or anti-coagulation*
40
Q

In which context do you typically get Oesophagela varices?

A
  • Secondary to portal HT (usually due to Liver Cirrhosis)
41
Q

In which context do you typically get a Mallory-Weiss tear?

A
  • Linear tear at GOJ
  • Follows period of retching/vomiting
  • > blood found in the vomitus!!
  • > alcohol or gastroenteritis history
42
Q

In which context do you typically get an Oesophageal malignancy?

A
  • Dysphagia or weight-loss history
  • Typically “oozes”
  • > blood doesn’t “gush” out
43
Q

In which context do you typically get an Angiodysplasia?

A

Chronic conditions ie. heart valve replacement, CKD

44
Q

What are the risk factors for DUs?

A
  • more common than GUs*
  • H. Pylori
  • NSAIDs/Aspirin
  • Alcohol XS
  • Systemic illness - “stress” ulcers
  • Zollinger-Ellison syndrome
45
Q

List some causes of lower GI bleeding

A
  • Diverticular disease
  • Haemorrhoids
  • Vascular malformations (Angiodysplasia, AVMs)
  • Neoplasia (carcinoma or polyps)
  • Ischaemic Colitis
  • Radiation Enteropathy/Proctitis
  • IBD (UC or Crohn’s involving the colon)
  • Small Bowel cause (5%)
  • > less common so only consider if colonic cause excluded
  • > ie. Meckel’s Diverticulum
46
Q

What is Meckel’s Diverticulum? What are its key features?

How do you diagnose it?

A
  • Gastric-remnant mucosa
  • Rule of 2’s:
  • > 2% population
  • > 2ft from ileocaecal valve
  • > 2 inches long
  • > 2 types of heterotopic mucosa (making it liable to bleeding…)
  • Diagnosis via Nuclear Scintigraphy
47
Q

What are the investigations for lower GI bleeding?

A

Large bowel cause

  • Flexible sigmoidoscopy
  • Full colonoscopy

Small bowel cause

  • CT Angio
  • Meckel’s scan Scintigraphy
  • Capsule endoscopy
  • Double balloon enteroscopy
48
Q

What are the risk stratification scoring systems included in the investigation of upper GI bleeding?

A
  • Rockall Score: >5 = high risk, ≤5 = low risk
  • Glasgow-Blatchford Score : <2 = discharge + outpatient management, ≥6 = high risk
  • Stratifies pts to find out who needs endoscopy or not + can be discharged from the ER*
49
Q

What is the management of acute GI bleeding?

A

1 - Resuscitation

  • ABCDE
  • Shock

2 - Risk stratification - ?critical care placement

  • UGIB = Rockall, Glasgow-Blatchford
  • LGIB = none (go by age, presence of co-morbidities, inpatient, initial shock, drugs ie. aspirin, NSAIDs)

3 - Diagnosis + Treatment

  • UGIB = Endo once stable (within 24hrs)
  • LGIB = Colonoscopy or CT angio (depending on severity)

4 - Withhold/reverse contributory meds as able

  • ie. anti-platelets, anti-coagulants
  • GIVE VIT K +/- Beriplex
  • recommence medsonce haemostasis achieved

5 - Specific meds

  • PPIs
  • Tranexamic acid

6 - Consider CT Angio/interventional radiography/surgical interventions as appropriate

50
Q

What is the management of an acutely bleeding peptic ulcer?

A
  • Endoscopy (!!!)
  • PPIs (!!!) - via infusion
  • Angio + embolisation -> if bleeding ongoing and uncontrollable
  • Laparotomy -> worse case scenario
51
Q

What is the management of acutely bleeding varices?

A
  • Endoscopy with endotherapy (!!!)
  • Terlipressin (!!!)
  • Abx -> often systemic
  • Reverse abnormal coagulation -> frozen platelets (as liver cirrhosis/disease is usually present so can’t make normal platelets)
  • Sengsten-Blakemore tube (if uncontrolled)
  • TIPSS (if uncontrolled)
52
Q

What is the treatment of Haemorrhoids?

A
  • Increasing fluid + fibre intake
  • Creams -> to ease the pain
  • Rubber band ligation
  • Elective surgical intervention (excisional haemorrhoidectomy)
53
Q

What is the treatment of Vascular malformations? (Angiodysplasia, AVMs)

A

Argon Phototherapy (APC)

54
Q

What is the treatment of Radiation Enteropathy/ Proctitis?

A
  • APC (Argon Phototherapy)
  • Sulcrafate Enemas
  • Hyperbaric oxygen
55
Q

What are the main drug classes used in the treatment of alimentary disease?

A
  • Acid suppression
  • Drugs affecting GI motility
  • Laxatives
  • Drugs for IBD
  • Drugs affecting intestinal secretions
56
Q

What are the different types of acid suppressant drugs?

A
  • Antacids
  • H2-Receptor Antagonists
  • PPIs
57
Q

What are the different drugs affecting GI motility?

A
  • Pro-kinetics/anti-emetics
  • Anti-motility (ie. Loperamide (Immodium), Opioids)
  • Anti-muscarinics/other anti-spasmodics
58
Q

What are the different drugs used for IBD?

A
  • Aminosalicylates
  • Corticosteroids
  • Immunosuppressants
  • Biologics
59
Q

Which drugs affect intestinal secretions?

A
  • Bile acid sequestrants

- Ursodeoxycholic acid

60
Q

What is the mechanism of action of antacids?

A
  • ie. Maalox
  • contain Magnesium or Aluminium
  • work to neutralise stomach acid by the active ingredient (base) reacting with stomach acid.
61
Q

What are the indications for Antacids?

A

Taken when symptoms occur

62
Q

What is the mechanism of action of alginates?

A
  • ie. Gaviscon

- Forms a viscous gel that floats on stomach contents and reduces reflux

63
Q

What are the indications for Alginates?

A
  • Taken when symptoms occur
64
Q

What is the mechanism of action of H2-receptor Antagonists?

A

Block histamine receptor thereby reducing acid secretion

65
Q

What are the indications for H2-receptor Antagonists?

A
  • ie. Ranitidine
  • Indicated in GORD/Peptic ulcer disease
  • Given orally/IV
66
Q

What is the mechanism of action of PPIs?

A
  • Blocks the proton pump and thereby reduces acid secretion
67
Q

What are the indications for PPIs?

A
  • Indicated in GORD/peptic ulcer disease
  • Oral or IV administration
  • Widely used
  • Triple therapy for treatment of PU/DU associated with H pylori
68
Q

What are the adverse reactions of PPIs?

A
  • GI upset
  • Predisposition to C. diff infections
  • Hypomagnesaemia
  • B12-deficiency
69
Q

What is the mechanism of action of Pro-kinetic/Anti-emetics?

A
  • Metoclopramide, Domperidone

- Increase gut motility and gastric emptying

70
Q

What are the indications for Pro-kinetic/Anti-emetics?

A
  • Gastroparesis

- GORD

71
Q

What is the mechanism of action of Anti-muscarinics/other anti-spasmodics?

A
  • Loperamide (Immodium), Opioids
  • Stimulates opiate receptors in GI tract to decrease ACh release -> decreases smooth muscle contraction + increases anal sphincter tone
72
Q

What are the indications for Anti-muscarinics/other anti-spasmodics? (GI)

A
  • Anti-diarrhoeals

also have unwanted effects ie. constipation

73
Q

What are the contraindications for Anti-muscarinics/other anti-spasmodics? (GI)

A
  • Constipation!

reduces motility in the gut

74
Q

What is the mechanism of action of Anti-motility drugs?

A

3 mechanisms

  • Anti-cholinergic muscarinic antagonists
  • Direct smooth muscle relaxants
  • CCBs (peppermint oil) -> reduce calcium required for smooth muscle contraction
75
Q

What are the indications for Anti-motility drugs?

A
  • Reduce symptoms of IBS + Renal Colic
76
Q

What are the contraindications for Anti-motility drugs?

A
  • Constipation
77
Q

What is the mechanism of action of Laxatives?

A

1 - Bulk (ie. Isphagula)

2 - Osmotic (ie. Lactulose)

3 - Stimulant (ie. Senna)

4 - Softeners (ie. Arachis oil)

78
Q

What are the indications for Laxatives?

A
  • Constipation!
79
Q

What are the different types of Aminosalicylates (5- ASAs) in IBD?

A
  • Mesalazine
  • Olsalazine
  • Sulfasalazine
80
Q

What are the indications for Aminosalicylates (5- ASAs) in IBD?

A
  • Mild-Moderate UC to induce and maintain remission
81
Q

What are the contraindications for Aminosalicylates (5-ASAs) in IBD?

A
  • Avoid if allergic to salicylates

- Caution in renal impairment

82
Q

What are the adverse effects of Aminosalicylates (5-ASAs) in IBD?

A
  • GI upset
  • Blood dyscrasias
  • Renal impairment
83
Q

What are the indications for Corticosteroids in IBD?

A

To induce remission in UC + CD

84
Q

What are the adverse effects of Corticosteroids?

A
  • Osteoporosis
  • Cushingoid features: ie weight gain, DM, HT
  • Increased susceptibility to infection (nb. watch out in the immunosuppressed!)
  • Addisonian crisis with abrupt withdrawal
85
Q

What are the indications for Biologics?

A
  • Moderate-severe CD or UC when other treatments have failed

- also used in Psoriasis and RA

86
Q

What are the contraindications for Infliximab? (Biologic)

A
  • Current TB or other serious infection
  • Multiple Sclerosis
  • Pregnancy/breast-feeding
87
Q

What are the adverse effects of Infliximab?

A

Basically a lot of the problems are to do w severe immunosuppression

  • Risk of infection, particularly TB so all patients should be screened
  • Infusion reaction (fever, itch)
  • Anaemia, thrombocytopenia, neutropenia
  • ?Demyelination (MS)
  • Malignancy
88
Q

What is the mechanism of action of Bile Acid sequestrants?

A
  • ie. Cholestyramine

- Reduces bile salts by binding with them in the gut and then secreting them as an insoluble complex

89
Q

What are the indications for Bile Acid sequestrants?

A
  • ie. Cholestyramine

- symptomatic relief from Pruritus (biliary cause)

90
Q

What are the cautions of Bile Acid sequestrants?

A
  • May affect the absorption of other drugs so should be taken separately
  • May affect fat-soluble vitamin absorption so may decrease Vitamin K levels
  • > affects clotting and warfarin
91
Q

What is the mechanism of action of Ursodeoxycholic acid?

A
  • Inhibits an enzyme involved in the formation of cholesterol
  • Alters the amount of cholesterol in bile and slowly dissolves cholesterol stones
92
Q

What are the indications for Ursodeoxycholic acid?

A
  • Gallstones

- PBC

93
Q

What classification scale can be used to consider the severity of Liver disease?

A

Child-Pugh classification

94
Q

Which drugs should you avoid in Liver disease?

A
  • Warfarin/anti-coagulants
  • Aspirin//NSAIDs
  • Opiates/Benzodiazepines
95
Q

What are the mechanisms by which major GI adverse effects of medication occur?

A
  • GI upset (!!!) = most common
  • Diarrhoea/constipation
  • > Cholinergics, NSAIDs, Antimicrobials (diarrhoea)
  • > Opioids, Anticholinergics (constipation)
  • GI bleeds/ulceration
  • > low-dose Aspirin/NSAIDs
  • Changes to gut bacteria
  • > loss of OCP activity
  • > reduced vit K absorption (increased PT time)
  • > overgrowth of pathogenic bacteria (ie. C. Diff)
  • Drug-induced Liver injury

Alimentary System (11 decks)

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