Gastrointestinal Week 4 Flashcards

1
Q

Describe the gross anatomy of the large intestine (including caecum, appendix, colon and rectum):

A

Features of LI:

  • right colic (hepatic) flexure
  • left colic (splenic) flexure
  • haustra = sacculations that contract to churn the food. (one haustra will gradually expand as it fills with chyme until it reaches maximum capacity and then contracts to move food into the next haustra)
  • taenia coli = 3 longitudinal bands of muscle that contract to produce the haustra, thickening of muscularis externa
  • appendices epiploicae/epiploic appendices (fatty tags covering the LI surface)

Parts of LI:
CAECUM
- lies in R iliac fossa
- the ileocaecal valve has 2 lips which protrude into the caecum and an increase in pressure in the caecum squeezes the two lips together to prevent the reflux of contents into the ileum

APPENDIX

  • thin windy tube that opens off caecum
  • ~8cm long (varies from 2-20)

COLON:

  • retroperitoneal parts = ascending and descending colons
  • transverse colon suspended from transverse mesocolon (a peritoneal fold) from lower pancreatic border
  • ascending colon and proximal 2/3 of transverse = midgut derived, the remaining portion is hindgut
  • arterial supply from branches of SMA and IMA: middle and right colic and left colic
  • venous supply similar to arterial but from branches of SMV and IMV which drain into the hepatic portal system
  • SMV branches are ileocolic and right colic veins
  • IMV branches are left colic vein and sigmoid veins

RECTUM

  • ~15cm long
  • angle of 120 degrees at anorectal junction is maintained by puborectalis pt of levator ani muscles and is important to maintain rectal continence
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2
Q

Describe the anatomy of the anal canal:

A
  • last 4cm of alimentary canal
  • mucosal folds are present called COLUMNS
  • anal canal contains veins which can form haemorrhoids if pressure increases
  • internal anal sphincter surrounds upper 2/3 of canal, circular bands of involuntary smooth muscle
  • external sphincter surrounds lower 2/3 of anal canal, voluntary muscle
  • anorectal ring (a band of muscle) is at the junction of the rectum and anal canal, formed by fusion of internal and external sphincters and puborectalis muscle, palpable on DRE
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3
Q

Describe the histology of the LI:

A
  • colon and rectum lined by simple columnar epithelium
  • above pectinate line of anal canal = simple columnar epithelium
  • below pectinate line of anal canal = non-keratinised stratified squamous epithelium
  • pectinate line divides upper 2/3 anal canal from lower 1/3
  • above pectinate line = superior rectal artery/vein, visceral innervation sensitive to stretch
  • below pectinate line = inferior rectal artery/vein, somatic innervation sensitive to pain/touch/temperature/pressure
  • lots of absorptive cells in colon
  • many goblet cells to secrete mucous to lubricate the passage for the movement of colonic contents
  • thick mucous layer prevents irritation of mucosa by faeces/fermentation products
  • no circular folds or villi
  • MICROVILLI ARE PRESENT (IN LARGE AND SMALL INTESTINES)
  • mucosa thicker with deeper crypts and more goblet cells than the SI
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4
Q

Describe motility in the LI:

A
  • slow movement from caecum -> transverse colon, allows time for absorption to occur and faeces to be produced

1) normal peristalsis = 3-12 contractions per minute
2) mass movements = few times a day, where large proportion of proximal colon is emptied as faeces is forced into the rectum producing the urge to defecate, triggered by distension of the stomach/duodenum
3) segmentation/haustral churning = main movement type in caecum and proximal colon, one haustra relaxes and fully fills and distends, once at certain distension the haustral walls contract and squeeze contents into the next haustra

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5
Q

How does the defecation reflex work?

A

1 - distension of rectal walls activates stretch receptors and signals are sent to spinal cord neurons
2 - spinal reflex initiated and parasympathetic motor fibres cause relaxation of internal anal sphincter and rectal wall contraction
3 - IF CONVENIENT to defecate, voluntary motor neurons that keep the external sphincter contracted are inhibited, so external sphincter relaxes and faeces can pass
4 - IF INCONVENIENT to defecate, rectal wall contractions end and voluntary motor neurons are NOT INHIBITED and defecation is delayed
5 - rise in abdominal pressure by closing the glottis an contracting the abdominal muscles aids defecation

  • urge to defecate occurs when rectal pressures reach >15mmHg
  • external sphincter involuntarily relaxes when rectal pressures >55mmHg (this occurs in babies, elderly and people with spinal cord injuries)
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6
Q

How is water absorbed in the GI tract and describe electrolyte transport?

A
  • Na and Cl are pumped into intercellular spaces and water always follows
  • absorbed amino acids and sugar increase the osmotic absorption of water
  • 90% of water from colon contents is absorbed by the colon
  • XS urea is secreted into the colon to get metabolised and broken down by bacteria
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7
Q

Describe the normal gut flora of the GI system:

A
  • upper gut has few flora due to pancreatic enzymes and gastric activity
  • large and complex bacterial ecosystem can develop in the colon due to the HCO3- ions which buffer the pH
  • ~1000 different bacterial species in the colon and the majority (99%) are anaerobes
  • when we are infants the gut is colonised by commensal bacteria developing the gut-associated immune system
  • tolerance to this immune system is developed, preventing an immune response to colonic flora
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8
Q

What is the function (including benefits) of gut flora?

A
  • enables colon to salvage energy and nutrients that escape absorption in the small intestine
  • commensal bacteria keep pathogenic bacteria under control by competing with them for nutrients and space
  • gut flora converts urobilinogen -> stercobilin
  • bacteria degrade cholesterol and some drugs
  • gut flora ferments indigestible carbohydrates into short chain fatty acids
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9
Q

Name some short chain fatty acids produced by bacteria in the gut and their benefits:

A

Acetic acid

  • energy source
  • substrate for fat synthesis in the liver

Propionic acid

  • energy source
  • reduces cholesterol synthesis

Butyric acid

  • stimulates cell differentiation
  • involved in programmed death of cancer cells

In general, SCFA’s inhibit pathogenic bacteria growth and increase cell proliferation throughout the whole gut

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10
Q

What dangerous effect can antibiotics have on the gut flora and commensal bacteria?

A

Broad spectrum antibiotics can inhibit the growth and metabolism of normal colonic flora
- this puts individuals at risk of diarrhoea, infections etc.

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11
Q

What are the different toxins that bacteria in the gut can produce and how do they exert their effect?

A

ENTEROTOXINS:

  • produced by bacteria and adhere to the intestinal epithelium
  • cause XS fluid to be secreted into bowel lumen = dehydration
  • > activate cAMP
  • > PKA phosphorylated
  • > excretory Na channels activated
  • > Cl- released from enterocytes and water follows
  • some enterotoxins are preformed in food and cause vomiting

CYTOTOXINS:

  • damage the intestinal mucosa
  • may damage vascular endothelium also
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12
Q

What are the routes of transmission of enteric infection?

A

1) endogenous -> body’s own endogenous flora can cause infection
2) air borne -> spread from person to person by aerosol/droplet transmission
3) faecal-oral route -> by direct transfer of food and water with faeces
4) vector -> spread by an animal e.g. malaria
5) direct person to person transmission -> breast milk, blood transfusions, STI’s

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13
Q

What is an enteric infection?

A
  • affects nutrient absorption and digestion and GI tract

- characterised by diarrhoea, abdominal discomfort, nausea, vomiting and anorexia

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14
Q

What measures should be put in place to prevent and control spread of infection?

A
  • education of staff in healthcare environments and public
  • use proper sanitation equipment
  • isolation (automatic doors, air conditioning)
  • appropriate disposal of healthcare waste
  • use of PPE
  • hand decontamination
  • antibiotic stewardship
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15
Q

Briefly describe the anatomy of the spleen:

A
  • Fist sized organ
  • At the posterior of the abdomen at the level of ribs 9-11
  • Is posterior to the mid-auxillary line
  • In the greater sac of the peritoneal cavity
  • Attached to the gastrosplenic ligament: part of the greater omentum attaching the greater curvature of the stomach to the hilum of the spleen
  • Histology: has white pulp (lymphoid tissue) and red pulp (which filters the blood)
  • Has special vessels called sinusoids which take up old RBC’s and the red pulp contains macrophages to destroy them
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16
Q

What are the large fluid movements in the GI tract and describe the potential for large losses in diarrhoea?

A
  • massive water reabsorption occurs daily and only 100ml is excreted per day
  • fluid INTAKE - 2000ml
  • fluid TURNOVER - 9000ml
  • fluid excretion - 100ml

Due to this huge fluid turnover, it means that there can be a massive fluid loss if something goes wrong with the system

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17
Q

What are the 4 important membrane transporters found in the GI tract cells and describe their movements?

A
  • Na/K ATP pump drives the whole process by removing Na from the cell in exchange for K. This creates a concentration gradient which means Na can then passively move back into the cell. Various pumps transport different ions using Na.
  • When Na is removed by the Na/K ATP pump, water follows and can move out through the permeable tight junctions between enterocytes

4 main membrane transporters:

1) Na ion channel
2) Na co-transporter/symporter (moves Na into cell with amino acids, peptides, bile salts and vitamins)
3) Na antiporter/exchange carrier (moves Na into cell and H+ out)
4) Another antiporter which moves Cl- into cell and HCO3- out

Na is taken in from the gut lumen side with the other co-transported molecules, and then when it is released by the ATP pump, Na and H2O are released into the bloodstream side (basolateral side)

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18
Q

What was the breakthrough discovery that made oral rehydration therapy possible?

A

In cholera epidemic it was discovered that NaCl cannot be absorbed alone and glucose must be present.
Glucose enhances Na absorption.
This is why you give solutions like saline and dextrose, or water with sugar and salt in it.

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19
Q

What is the importance of children’s diarrhoea worldwide and how is it treated and prevented?

A

Diarrhoea is a major cause of children’s death worldwide

88% of worldwide deaths from diarrhoea are due to unsafe water/poor sanitation/poor hygiene

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20
Q

How can infectious diarrhoea be prevented?

A
  • vaccines against infections that cause diarrhoea
  • early breast feeding and vitamin A supplementation
  • handwashing with soap
  • improved water quality
  • community wide sanitation promotion
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21
Q

How can you treat infectious diarrhoea?

A
  • fluid replacement (ORT)
  • zinc supplements (decrease severity and duration of diarrhoea)
  • use of appropriate fluids
  • generally, increase fluid intake
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22
Q

Describe the body water compartments and what different osmolarities mean:

A
  • 3 water compartments are
  • intracellular fluid
  • extracellular fluid
  • intravascular fluid

High osmolarity = cellular dehydration
Low osmolarity = cellular over-hydration and oedema

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23
Q

How does osmotic pressure control fluid movement between body compartments?

A
  • body always tries to equalise osmolarity
  • too many osmotically active molecules in the blood = water leaves cells
  • when plasma has low osmolarity (i.e. lots of water) water will move into cells and could result in oedema
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24
Q

What are the main categories of intravascular fluids used and give examples?

Why are IV fluids used?

A

1) COLLOIDS
- large molecular weight substances
- e.g. albumin, hydroxy-ethyl-starch (HES), haemacel

2) CRYSTALLOIDS
- water and electrolyte solution e.g. salt solution
- e.g. saline, dextrose, Hartmann’s ringer lactate

Are used to prevent hypovolaemic shock and maintain intravascular volume if a patients BP is low

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25
Q

What are the main uses of the different IV fluids?

A
  • Normal post operative regime = 2 saline : 1 dextrose
  • Hartmann’s ringer lactate solution is used when someone’s bicarbonate levels are low (e.g. acidosis) as a substantial amount of bicarbonate is produced in lactate metabolism
  • Dextrose is used if a patient is dehydrates and needs water as dextrose is isomotic (contains glucose and water) and the glucose in dextrose is metabolised leaving only water
  • After IV infusion, some remains in the blood and some is metabolised

100% colloids remain in blood
25% saline remains in blood
10% dextrose remains in blood

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26
Q

What are the different types of infusion bags and when are they used?

A
  • standard bag is 500ml
  • > 2hrly bag: 6L in 24hrs = for emergency rehydration
  • > 4hrly bag: 3L in 24hrs = for emergency rehydration
  • > 6hrly bag: 2L in 24hrs = standard regime
  • > 8hrly bag: 1.5L in 24hrs = slow rehydration
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27
Q

What is the normal reference range of K in the body?

A

3.5 - 5 mmol/l

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28
Q

Describe potassium balance, why it is important to maintain values within the reference range and important rules when it is prescribed:

A
  • K normally intracellular (95% intracellular and 5% extracellular)
  • relatively small shifts in K can cause hypo/hypervolaemia which can cause ARRHYTHMIAS and CARDIAC ISSUES

When prescribing:
- always state desired concentration
- always state delivery period
- always dilute K solution with saline before use
MAX CONCENTRATION = 40mmol/l
MAXIMUM RATE = 10mmol/hr (or 20 if cardiac monitoring and a central line are available)

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29
Q

What must be assessed and considered when planning fluid replacement?

A
  • assess clinical state and how ill the person is
  • assess fluid intake and output
  • look for electrolyte shifts
  • decide on replacement, considering
  • > age
  • > renal function
  • > cardiovascular status
  • consider:
  • > daily need
  • > anticipated loss
  • > previous deficiy
30
Q

Describe hepatitis A:

A
  • RNA virus
  • faecal-oral transmission
  • no chronic carriage
  • travel related and rare in the UK
  • 1 month incubation period
  • no treatment available
  • EXCELLENT VACCINE AVAILABLE
  • > an inactivated vaccine with 95% efficacy
  • > used before exposure for prevention or 7 days after exposure
31
Q

Describe hepatitis E:

A
  • RNA virus
  • some people have no immunity and get chronic carriage
  • no treatment available
  • high mortality (especially in pregnant women)
  • NO VACCINE AVAILABLE
32
Q

What are the blood borne hepatitis viruses?

A

B, C and D

33
Q

Describe hepatitis B:

A
  • hepna DNA virus
  • can be transmitted vertically (mother to child) or horizontally (child to child, cuts when playing etc)
  • low prevalence in UK
  • vaccine available but not in UK (low prevalence)
34
Q

How does age determine the severity of a hep B infection?

A

Infection at birth/young:

  • asymptomatic as immune system is not developed enough to mount an immune response
  • this can lead to chronic infection

Infection as adult:

  • symptomatic but can be cleared by immune system so not always chronic carriage
  • chronic hep B develops in 25% cases and causes:
  • > cirrhosis -> hepatocellular carcinoma -> death
35
Q

What is the treatment for acute/chronic hep B?

A
Acute = no treatment
Chronic = treatment is available to try and suppress viral replication
36
Q

Describe hepatitis D:

A
  • ssRNA virus
  • REQUIRES HEP B TO SURVIVE
  • hep B + D increases the risk of chronic liver disease
  • treated using interferon (an anti-viral cytokine that the body produces naturally if you are ill and it increases the immune system responses but has many side effects)
37
Q

Describe hepatitis C:

A

MOST COMMON IN UK

  • ssa flavavirus
  • infection normally asymptomatic and not noticed
  • 6-7 week incubation period
  • no vaccine and no reliable immunity after injection
  • 70% individuals get chronic infection and risk of cirrhosis
38
Q

How can hep C be treated?

A

1) pegylated interferon - medication that encourages immune system to attack the virus
2) ribavirin - antiviral to stop the virus reproducing

3) direct acting antivirals: simeprevir and sofosbuvir
- they target specific points in the lifecycle of a virus to prevent replication

39
Q

What is the natural history (life course) of a hepatitis virus?

A

1) immune tolerance - where the body cannot rid the virus but puts up with it
2) immune clearance - immune system is developed enough and starts attacking the virus. It attacks the liver where the virus hides = levels of ALT increase
3) low replicative state - levels of the virus drop as it has been destroyed and ALT levels return to normal
4) re-activation (if the virus infects again)

40
Q

What does sAg +ve mean?

A

surface antigen - marker of infection

41
Q

What does sAb +ve mean?

A

surface antibody - marker of immunity

  • they have either had the infection in the past or have had the immunisation
42
Q

What does eAg +ve mean?

A

e-antigen - marker of high infectivity

43
Q

What does eAb +ve mean?

A

e-antibody - marker of low infectivity

44
Q

What does hep DNA +ve mean?

A

marker of infection

45
Q

What does core IgM +ve mean?

A

current infection present

46
Q

What does core IgG +ve mean?

A

not currently infected but has had the infection in the past

47
Q

What two factors have to be present for an infection to be diagnosed?

A

sAg +ve and hep DNA +ve

48
Q

Describe the two classifications of hep B carriers:

A

e. Ag +ve:
- high viral load
- highly infectious
- high risk of chronic carriage = HCC (hepatocellular cancer)

e. Ag -ve:
- low viral load
- les infectious
- low risk of chronic carriage = low risk of developing HCC

49
Q

Describe the fluid-circuit hypothesis:

A
  • absorption of fluid at villi tips normally exceeds excretion of fluid from the crypts = net absorption
  • diarrhoea arises when there is net secretion instead
    VILLOUS CRYPTS:
    -> Cl- actively transported out of enterocyte crypts
    -> Na+ follows and water also follows
    -> lumen of intestine then hyperosmolar

AT VILLI TIPS:

  • > Na+ actively transported into enterocytes
  • > Cl- follows
  • > as the internal enterocyte environment is then hyperosmolar water follows and enters
50
Q

What are the biochemical effects of sustained diarrhoea?

A
  • loss of K+ in stool (as RAAS activated)
  • acidosis of blood
  • loss of HCO3- in stool
  • reduced plasma [HCO3-]
  • reduced plasma [K+]
  • less Na and H2O
  • Loss of Mg
51
Q

Describe the differences in function between the proximal and distal colons:

A

PROXIMAL:

  • 95% absorption occurs
  • contents are liquid
  • pH 5-7
  • most bacterial activity
  • carbohydrate fermentation and H2 production

DISTAL:

  • 5% absorption
  • semi-solid contents
  • pH >7
  • less bacterial activity
  • amino acid fermentation and CH4 production
52
Q

What are the benefits of SCFA’s in the gut and how are they produced?

A

Microflora convert carbohydrate into acetic/butyric/propionic acid

Benefits:

  • increase cell proliferation throughout the whole gut
  • promote H2O reabsorption preventing osmotic diarrhoea
  • inhibit the growth of pathogenic bacteria
53
Q

Which factors control microflora composition of the gut?

A
  • physiochemical factors: pH, O2 supply, nutrient supply
  • host-bacteria interactions: saliva, bile, immune system
  • microbial interactions: toxic metabolites, bacteriophages
54
Q

What are the non-specific defence mechanisms in the gut?

A

1st line of defence:

  • intact skin
  • mucous membranes and their secretions
  • normal microflora balance

2nd line of defence:

  • phagocytic WBC’s
  • fever
  • inflammation
  • anti-microbial substances like lysosyme
55
Q

What are the specific defence mechanisms in the gut?

A
  • specialised lymphocytes (B and T cells)

- antibodies

56
Q

How can micro-organisms overcome gut defence mechanisms?

A
  • produce toxins which disable host immune cells
  • C.diff produced enterotoxins, damaging epithelial barrier and fluid loss can occur
  • E.coli stops fluid absorption by enterocytes
  • Vibrio cholera produces an enterotoxin that loosens tight junctions between enterocytes causing intestinal vasodilation
57
Q

What are the 4 main categories of diarrhoea and describe each of them:

A

1) Malabsorptive/osmotic
- laxatives
- antacids
- orlistat (lipase inhibitor for fat loss)
- inflammatory disease
= consume non-digestible food -> hyperosmolar state in the LI lumen -> H2O enters to try to dilute -> XS fluid and diarrhoea

2) Motility
- increased gut motility and less time for fluid-reabsorption to occur
- fluid passes straight out into the colon

3) Secretory
- acute infections
- failure of bile salt reabsorption
- laxative abuse
= there is reduced intestinal water absorption and net secretion so a high volume of diarrhoea produced

3) Inflammatory/infectious
- IBD
- infectious diseases
- irritable bowel
- infections and pathogens releasing endotoxins
= wherever the mucosa is infected the rate is secretion increases and propulsive activity of the bowel increases
-> increased motility and secretion
-> reduced absorption

58
Q

What is significant about the bacterial infection ‘shigella’?

A
  • causes dysentery (bloody diarrhoea)
59
Q

Name some neurotoxin secreting bacteria:

A
  • staphylococcus aureus

- clostridium botulinum

60
Q

Name some enterotoxin secreting bacteria:

A
  • E.coli

- salmonella

61
Q

Name some cytotoxin secreting bacteria:

A
  • shigella
  • staphylococcus aureus
  • helicobacter pylori
62
Q

What is a neurotoxin?

A

A toxin that is destructive to nerve tissue

63
Q

What is a cytotoxin?

A

Compound that destructive or toxic effects on cells in the body, especially in a particular organ area

64
Q

Describe salmonella:

A

gram -ve, non-sporing, motile

65
Q

Describe shigella:

A

gram -ve, non-sporing, motile

66
Q

Describe campylobacter:

A

gram -ve, sporing, aerobic

67
Q

Describe clostridium difficile:

A

gram +ve, aerobic, produces endotoxin and cytotoxin

68
Q

What are measured losses?

A
  • urine, vomit, diarrhoea, blood…
  • are measured by a nurse on a fluid chart
  • measured losses from the previous day are used to estimate the next day’s losses
69
Q

What are insensible losses?

A
  • sweat and respiratory losses
  • cannot be routinely measured
  • these losses increase in:
  • > hot hospital
  • > sweating
  • > patient has sepsis
  • > patient has fever
  • > patient is ventilated
70
Q

How do you calculate previous day deficit?

A

PDD = (previous day ML + IL) - previous days intake (oral and IV)

71
Q

What formula do you use to calculate how much fluid to give to someone over 24hrs?

A

ML + IL + PDD

72
Q

Describe 0.9% saline:

A
  • physiological saline has 9g Na/Cl per litre
  • it provides the body with the most important extracellular ions in near physiological concentration
  • is administered when there are Na and H2O losses (DEXTROSE GIVEN WHEN THERE ARE NO ELECTROLYTE LOSSES AND IS MAINLY FOR H2O REPLACEMENT)