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
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
3
Q
What are obligate anaerobic bacteria?
A
Bacteria which cannot grow in the presence of oxygen
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
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
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)
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
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)
9
Q
What are the methods of bacterial gene transfer?
A
1 - Conjugation
2 - Transformation
3 - Transduction
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)
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
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
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
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
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
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)
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
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
19
Q
What BMI is overweight and obese?
A
- Overweight = BMI >25
- Obese = BMI >30
20
Q
What BMI is underweight?
A
- BMI <20
21
Q
How do you screen for undernutrition?
A
Malnutrition Universal Screening Tool (MUST)
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
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
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
25
What clinical syndromes of Acute Abdomen do not require Laparotomy?
- 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
26
What are the investigations for Peritonitis?
- Diagnostic Paracentesis
- > sent for urgent MC+S -> neutrophils >250mm3 = SBP
- Blood + urine cultures
- Imaging -> if clinical suspicion of perforated viscus (AXR, CT)
27
What are the routes of infection for Peritonitis?
* Perforation of GI/ biliary tract
* Female genital tract
* Penetration of abdominal wall
* Haematogenous spread
28
What are the cardinal symptoms of Bowel obstruction?
- 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
29
What are the investigations of Bowel Obstruction?
- Urgent Bloods: FBC, CRP, U+Es, LFTs
- Imaging:
- > CT w IV contrast (1st line)
- > XR (used in some places as 1st line) -> AXR, CXR
30
What are the investigations for acute Pancreatitis?
- 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)
31
What are the XR findings for Bowel obstruction?
- AXR: concurrent large and small bowel obstruction (?incompetent ileocaecal valve)
- erect CXR: free air under the diaphragm (?bowel perforation)
32
What are the clinical features of Mesenteric Ischaemia?
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
33
What are the investigations for Mesenteric Ischaemia?
- 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)
34
What are the investigations for Acute Abdomen?
- 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
35
What is the treatment of acute abdomen?
- 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)
36
What are the clinical features of upper GI bleeding?
- Haematemesis
- Melaena
- Elevated Urea
- > due to partially digested blood -> haem -> urea
- Associated w Dyspepsia (epigastric pain associated w eating) and Reflux
- NSAID use
37
What are the clinical features of lower GI bleeding?
- Fresh blood/clots
- Magenta stools
- Normal urea
- > in contrast to elevated urea in upper GI bleeding
- Typically painless
- More common in advanced age
38
List some causes of upper GI bleeding
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!!*
39
What are the most common causes of Oesopagitis?
- Reflux Oesophagitis
- Hiatus Hernia
- Alcohol
- Bisphosphonates
- Systemic illness
* bleeding typically occurs when pt. is also on anti-platelets or anti-coagulation*
40
In which context do you typically get Oesophagela varices?
- Secondary to portal HT (usually due to Liver Cirrhosis)
41
In which context do you typically get a Mallory-Weiss tear?
- Linear tear at GOJ
- Follows period of retching/vomiting
- > blood found in the vomitus!!
- > alcohol or gastroenteritis history
42
In which context do you typically get an Oesophageal malignancy?
- Dysphagia or weight-loss history
- Typically "oozes"
- > blood doesn't "gush" out
43
In which context do you typically get an Angiodysplasia?
Chronic conditions ie. heart valve replacement, CKD
44
What are the risk factors for DUs?
* more common than GUs*
- H. Pylori
- NSAIDs/Aspirin
- Alcohol XS
- Systemic illness - "stress" ulcers
- Zollinger-Ellison syndrome
45
List some causes of lower GI bleeding
- 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
What is Meckel's Diverticulum? What are its key features?
| How do you diagnose it?
- 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
What are the investigations for lower GI bleeding?
Large bowel cause
- Flexible sigmoidoscopy
- Full colonoscopy
Small bowel cause
- CT Angio
- Meckel's scan Scintigraphy
- Capsule endoscopy
- Double balloon enteroscopy
48
What are the risk stratification scoring systems included in the investigation of upper GI bleeding?
- 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
What is the management of acute GI bleeding?
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
What is the management of an acutely bleeding peptic ulcer?
- Endoscopy (!!!)
- PPIs (!!!) - via infusion
- Angio + embolisation -> if bleeding ongoing and uncontrollable
- Laparotomy -> worse case scenario
51
What is the management of acutely bleeding varices?
- 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
What is the treatment of Haemorrhoids?
- Increasing fluid + fibre intake
- Creams -> to ease the pain
- Rubber band ligation
- Elective surgical intervention (excisional haemorrhoidectomy)
53
What is the treatment of Vascular malformations? (Angiodysplasia, AVMs)
Argon Phototherapy (APC)
54
What is the treatment of Radiation Enteropathy/ Proctitis?
- APC (Argon Phototherapy)
- Sulcrafate Enemas
- Hyperbaric oxygen
55
What are the main drug classes used in the treatment of alimentary disease?
- Acid suppression
- Drugs affecting GI motility
- Laxatives
- Drugs for IBD
- Drugs affecting intestinal secretions
56
What are the different types of acid suppressant drugs?
- Antacids
- H2-Receptor Antagonists
- PPIs
57
What are the different drugs affecting GI motility?
- Pro-kinetics/anti-emetics
- Anti-motility (ie. Loperamide (Immodium), Opioids)
- Anti-muscarinics/other anti-spasmodics
58
What are the different drugs used for IBD?
- Aminosalicylates
- Corticosteroids
- Immunosuppressants
- Biologics
59
Which drugs affect intestinal secretions?
- Bile acid sequestrants
| - Ursodeoxycholic acid
60
What is the mechanism of action of antacids?
- ie. Maalox
- contain Magnesium or Aluminium
- work to neutralise stomach acid by the active ingredient (base) reacting with stomach acid.
61
What are the indications for Antacids?
Taken when symptoms occur
62
What is the mechanism of action of alginates?
- ie. Gaviscon
| - Forms a viscous gel that floats on stomach contents and reduces reflux
63
What are the indications for Alginates?
- Taken when symptoms occur
64
What is the mechanism of action of H2-receptor Antagonists?
Block histamine receptor thereby reducing acid secretion
65
What are the indications for H2-receptor Antagonists?
- ie. Ranitidine
- Indicated in GORD/Peptic ulcer disease
- Given orally/IV
66
What is the mechanism of action of PPIs?
- Blocks the proton pump and thereby reduces acid secretion
67
What are the indications for PPIs?
* Indicated in GORD/peptic ulcer disease
* Oral or IV administration
* Widely used
* Triple therapy for treatment of PU/DU associated with H pylori
68
What are the adverse reactions of PPIs?
- GI upset
- Predisposition to C. diff infections
- Hypomagnesaemia
- B12-deficiency
69
What is the mechanism of action of Pro-kinetic/Anti-emetics?
- Metoclopramide, Domperidone
| - Increase gut motility and gastric emptying
70
What are the indications for Pro-kinetic/Anti-emetics?
- Gastroparesis
| - GORD
71
What is the mechanism of action of Anti-muscarinics/other anti-spasmodics?
- Loperamide (Immodium), Opioids
- Stimulates opiate receptors in GI tract to decrease ACh release -> decreases smooth muscle contraction + increases anal sphincter tone
72
What are the indications for Anti-muscarinics/other anti-spasmodics? (GI)
- Anti-diarrhoeals
| also have unwanted effects ie. constipation
73
What are the contraindications for Anti-muscarinics/other anti-spasmodics? (GI)
- Constipation!
| reduces motility in the gut
74
What is the mechanism of action of Anti-motility drugs?
3 mechanisms
- Anti-cholinergic muscarinic antagonists
- Direct smooth muscle relaxants
- CCBs (peppermint oil) -> reduce calcium required for smooth muscle contraction
75
What are the indications for Anti-motility drugs?
- Reduce symptoms of IBS + Renal Colic
76
What are the contraindications for Anti-motility drugs?
- Constipation
77
What is the mechanism of action of Laxatives?
1 - Bulk (ie. Isphagula)
2 - Osmotic (ie. Lactulose)
3 - Stimulant (ie. Senna)
4 - Softeners (ie. Arachis oil)
78
What are the indications for Laxatives?
- Constipation!
79
What are the different types of Aminosalicylates (5- ASAs) in IBD?
- Mesalazine
- Olsalazine
- Sulfasalazine
80
What are the indications for Aminosalicylates (5- ASAs) in IBD?
- Mild-Moderate UC to induce and maintain remission
81
What are the contraindications for Aminosalicylates (5-ASAs) in IBD?
- Avoid if allergic to salicylates
| - Caution in renal impairment
82
What are the adverse effects of Aminosalicylates (5-ASAs) in IBD?
- GI upset
- Blood dyscrasias
- Renal impairment
83
What are the indications for Corticosteroids in IBD?
To induce remission in UC + CD
84
What are the adverse effects of Corticosteroids?
- Osteoporosis
- Cushingoid features: ie weight gain, DM, HT
- Increased susceptibility to infection (nb. watch out in the immunosuppressed!)
- Addisonian crisis with abrupt withdrawal
85
What are the indications for Biologics?
- Moderate-severe CD or UC when other treatments have failed
| - also used in Psoriasis and RA
86
What are the contraindications for Infliximab? (Biologic)
- Current TB or other serious infection
- Multiple Sclerosis
- Pregnancy/breast-feeding
87
What are the adverse effects of Infliximab?
*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
What is the mechanism of action of Bile Acid sequestrants?
- ie. Cholestyramine
| - Reduces bile salts by binding with them in the gut and then secreting them as an insoluble complex
89
What are the indications for Bile Acid sequestrants?
- ie. Cholestyramine
| - symptomatic relief from Pruritus (biliary cause)
90
What are the cautions of Bile Acid sequestrants?
- 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
What is the mechanism of action of Ursodeoxycholic acid?
- Inhibits an enzyme involved in the formation of cholesterol
- Alters the amount of cholesterol in bile and slowly dissolves cholesterol stones
92
What are the indications for Ursodeoxycholic acid?
- Gallstones
| - PBC
93
What classification scale can be used to consider the severity of Liver disease?
Child-Pugh classification
94
Which drugs should you avoid in Liver disease?
- Warfarin/anti-coagulants
- Aspirin//NSAIDs
- Opiates/Benzodiazepines
95
What are the mechanisms by which major GI adverse effects of medication occur?
- 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
