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MD3002 > Week 2 > Flashcards

Week 2 Flashcards

1
Q

What did the Panel convened by the WHO in August 2014 conclude regarding Ebola patients being treated with promising drugs which have not yet been evaluated for safety & efficacy in humans?

A

Concluded Ebola outbreak was exceptional and ethically acceptable to offer proven interventions but ethical standards (informed consent, fairness, autonomy) must be maintained

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2
Q

What do different countries in Britain classify as “Children & young people”?

A
  1. <18 in England, Wales & Northern Ireland

2. <16 in Scotland

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3
Q

What is the definition of “Children”?

A

People who are probably not mature enough to make important decisions themselves

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4
Q

For a child who lacks capacity who makes the decision?

A
  • Parents but decisions are constrained by best interests of the child
  • If they are NOT seen to be making decision that promotes welfare of the child, it can be overridden
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5
Q

What is the missing word regarding a child who lacks capacity:
“If ____ can be given, it should be sought”?

A

Assent

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6
Q

As well as a clinical best interest, what other 6 things should you consider?

A
  1. Views of child/young person, including previously expressed preferences
  2. Views of parents
  3. Views of others close to child
  4. Cultural, religious or other beliefs and values of the child/parent
  5. Other healthcare professional views
  6. Which choice will least restrict the child’s future options
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7
Q

Give an example of when doctors and parents disagree?

A

Parents were Jehovah’s Witnesses and their child had T cell leukaemia and refused to allow blood transfusing, refusal was overruled

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8
Q

What is the Gillick Competence?

A

A young person under 16 with capacity to make any relevant decisions is often referred to as being “Gillick competent”

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9
Q

Competence is determined if the person can do what 4 things?

A
  1. Understand
  2. Retain
  3. Use/weigh this information
  4. Communicate decision
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10
Q

What is the problem with determining competence regarding a child/young person?

A

A young person who has the capacity to consent to straightforward, relatively risk-free treatment may not necessarily have the capacity to consent to complex treatment involving high risks or serious consequences

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11
Q

Why is consent often more easily accepted than refusal in the mature minor?

A

Doctors only need 1 key to unlock “consent”. Potential keys:

  1. Mature minors
  2. Parents
  3. Courts
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12
Q

What is the age restriction to organ donation in Scotland?

A

Anyone under 16 (competent or not) CANNOT be a living donor

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13
Q

What is the age restriction to organ donation in England, Wales & Northern Ireland?

A

Solid organ donation by living children is permitted

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14
Q

What is the BMA’s opinion on children being organ donators?

A

The were opposed, now support so long as young person is competent to give valid consent & is not under coercion

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15
Q

What are the Netherlands legal rules for age restrictions in Euthanasia?

A

Legal for those over 12 (with permission of their parents)

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16
Q

What has the Dutch Paediatric Association recently (June 2015) called for?

A

Age limit for Euthanasia to be lifted all together

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17
Q

What is Belgium’s legal rules for age restrictions in Euthanasia?

A

Lifted all age restrictions in 2014

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18
Q

What did the Nuffield Council on Bioethics report published in May 2015 say about children and clinical research?

A
  • Its crutial if children themselves are to benefit from best possible treatment when ill.
  • Should parents allow young children to participate if it causes minor discomfort/distress?
  • Can be seen as the critically ill child’s “only hope”
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19
Q

What is bioequivalence?

A

Looking at the effectiveness of one agent compared to another, it specifically relates to generic or therapeutic substitution

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20
Q

What is Generic substitutions?

A
  • Different formulation of the same drug is substituted (branded vs unbranded)
  • They are all considered by licensing authority to be equivalent to each other & to the originator drug.
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21
Q

What is therapeutic substitution?

A
  • Replacement of the originally-prescribed drug with an alternative molecule with assumed equivalent therapeutic effect
  • Alternative drug may be in the same class / assumed therapeutic equivalence (different beta-blockers)
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22
Q

Why do oral drugs have a low bioavailability (4)?

A
  • Destroyed in gut
  • Not absorbed
  • Destroyed by gut wall
  • Destroyed by liver
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23
Q

What are the pros and cons of buccal/sublingual mucosa oral route?

A
  • Direct absorption into blood stream
  • Avoids first pass metabolism
  • Not ideal surface for absorption
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24
Q

What do you need the drug to have in order for it to reach the gastric mucosa?

A

Enteric coating

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25
Q

What are the pros and cons of small intestine oral route?

A
  • Main site of drug absorption

- Large surface area, more neutral pH

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26
Q

What are the cons of Large intestine/colon oral route?

A

Poor absorption, long transit times

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27
Q

What are the pros of rectal mucosa oral route

A

Direct to systemic circulation

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28
Q

What are the 4 ways small molecules cross cell membranes?

A
  1. Diffusing directly through the lipid
  2. Diffusing through aqueous pores
  3. Transmembrane carrier proteins
  4. Pinocytosis
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29
Q

What is the definition of a young person?

A

Those who are mature enough to make important decisions themselves

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30
Q

What percentage of bioavailability must generics have?

A

80-125% compared to reference product

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31
Q

What is an excipient?

A

Inactive substance put into drug to bulk it up

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32
Q

A weak base is _____ in acidic pH?

A

Ionised

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33
Q

A weak acid is _____ in acidic pH?

A

Unionised

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34
Q

What is the Henderson-Hasselbalch equation for a weak base?

A

pKa- pH = log10 [BH+]/[B]

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35
Q

What is the Henderson-Hasselbalch equation for a weak acid?

A

pKa- pH = log10 [AH]/[A-]

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36
Q

What do foods tend to do to the rate of gastric emptying in general?

A

Slows the rate

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37
Q

What is gastric emptying?

A

How quickly food leaves the stomach

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38
Q

What can cause decreased absorption of a drug?

A
  • Increased intestinal motility
  • Interactions with food, acids
  • Presystemic metabolism
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39
Q

What can cause delayed absorption of a drug?

A
  • Gastric emptying

- Cmax (plasma conc.) may be decreased

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40
Q

What can cause increased absorption of a drug?

A
  • Poorly water soluble drugs

- Decreased presystemic metabolism

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41
Q

What is Levodopa?

A
  • Prodrug
  • Treatment of Parkinson’s disease
  • Precursor of dopamine
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42
Q

Where is Levodopa rapidly taken up?

A

Stomach & Small intestine

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43
Q

What is the active transport system for Levodopa called?

A

Large neutral amino acid transport carrier (LNAA)

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44
Q

Where is DOPA decarboxylase (enzyme) present?

A

Gastric mucosa

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45
Q

What does Antacids and proton pump inhibitors do?

A

Changes gastric / intestinal pH

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46
Q

What does anticholinergics do?

A

Decrease GI motility

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47
Q

What does vasodilators do?

A

Changes GI perfusion

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48
Q

What does neomycin do?

A

Interference with mucosal function

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49
Q

What does Charcoal do?

A

Decreases absorption

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50
Q

What is Diabetic Gastroparesis?

A

Delayed gastric emptying, slows / stops movement of food from stomach to small intestine

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51
Q

Describe the appearance of Crohn’s disease (decreased drug absorption)?

A
  • Cobblestone appearance of mucosal surface due to linear ulceration
  • Abcess
  • Narrowed lumen
  • Thickened wall
  • Then back to normal intestine
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52
Q

What are the 6 factors that affect oral absorption?

A
  1. Particle size & formulation
  2. GI motility
  3. First pass metabolism
  4. Physicochemical factors
  5. Splanchnic blood flow
  6. Efflux pumps
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53
Q

Where is first pass metabolism?

A

By gut wall or hepatic enzymes

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54
Q

What are the 3 Physicochemical factors which affect oral drug absorption?

A
  1. Direct drug interactions
  2. Dietary factors
  3. Varying pH
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55
Q

What are the 2 Parenteral drug routes?

A
  1. Subcutaneous - slow

2. Intramuscular - lipophilic drugs rapid

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56
Q

What is the rate of onset of drugs administered parenterally affected by?

A
  • Extent of capillary perfusion
  • Drug vehicle
  • Affected by factors that alter perfusion
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57
Q

What are the systemic effects of inhalation of drugs?

A
  • Lipid-soluble drugs
  • Drugs of abuse
  • Accidental poisoning
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58
Q

What are the local effects of inhalation of drugs?

A
  • Modify structure
  • Particulate size
  • Selectivity for receptors
  • Rapid breakdown in circulation
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59
Q

What are the advantages of Intranasal drug administration?

A
  • Avoids hepatic first pass metabolism

- Ease, convenience, safety

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60
Q

What is the main limitation of Intranasal drug administration?

A

Limited drugs suitable as it required concentrated drug

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61
Q

What are the local effects of topical drug route?

A
  • Corticosteriods for eczema (hydrocortisone)
  • Antihistaines for insect bites (mepyramine)
  • Local anaesthetics (EMLA)
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62
Q

What are the systemic effects of topical drug route?

A
  • Transdermal patches (HRT, GNT, nicotine)”

- Accidental poisoning (AChEstrase insecticides)

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63
Q

Where does the foregut start and end?

A

Mouth to just distal to developing liver

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64
Q

What supplies the foregut?

Where does the referred pain go to?

A
  • Coeliac trunk

- Pain to epigastrium (T7 to 9)

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65
Q

What does the foregut give rise to?

A
  • Oesophagus
  • Stomach
  • Proximal duodenum
  • Liver & biliary system
  • Pancreas
  • Spleen
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66
Q

When does the development of the stomach appear?

A

4th week

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67
Q

What is the movement of the Stomach during development?

A
  • 90o clockwise around longitudinal axis so left side faces anteriorly & lesser curve to the right, while greater curve to the left (lies posterior)
  • AP axis so pyloric part comes to lie on right & oesophagi-gastric junction slightly left, so greater curve faces left & inferior
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68
Q

What is the movement of the Duodenum during development?

A
  • Initially in midline
  • Rotates & swings right due to stomach
  • “Falls” onto posterior abdominal wall & becomes retroperitoneal
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69
Q

What happens to the duodenum lumen during development?

A

Obliterated by proliferation of cells, then it is re-canalized

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70
Q

How is the liver developed?

A
  • From endodermal bud during 3rd week

- Penetrates ventral mesentery & septum transversum

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71
Q

What 2 things does the liver give rise to?

A
  • Hepatic ducts

- Gallbladder

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72
Q

How is the Pancreas developed?

A
  • From duodenum dorsal & ventral endodermal buds

- Rotation causes ventral bud to lie behind & fuse with dorsal bud

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73
Q

What do the fusion of dorsal & ventral buds form?

A

Main pancreatic duct

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74
Q

What is the accessory duct a remnant of?

A

Duct of dorsal bud

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75
Q

What does the ventral mesentery directly in contact with the liver become?

A

Liver’s Visceral peritoneum

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76
Q

What are the 2 examples of times the foregut development can go wrong?

A
  1. Part of the biliary system may duplicate

2. Ventral pancreas may form 2 lobes, forming an obstructive Annular Pancreas

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77
Q

What is in the free edge of the falciform ligament?

A

Umbilical vein

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78
Q

What is in the free edge of the lesser omentum?

A
  • Bile duct
  • Hepatic artery
  • Portal vein
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79
Q

What forms within the dorsal mesentery?

A

Spleen

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80
Q

What is another name for the dorsal mesentery?

And what will it become?

A
  • Mesogastrium

- Greater omentum

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81
Q

What lies posterior of the stomach and lesser omentum?

A

Lesser Sac

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82
Q

What is the opening into the lesser sac called?

A

Epiploic foramen

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83
Q

What are the boundaries of the Epiploic foramen?

A

ANTERIOR- free border of lesser omentum, with bile duct, hepatic artery proper & portal vein
POSTERIOR- IVC
SUPERIOR- caudate lobe of liver
INFERIOR- 1st part of duodenum

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84
Q

What are the boundaries of the Lesser Sac?

A

ANTERIOR- caudate lobe of liver, lesser omentum, stomach
POSTERIOR- pancreas
LATERAL LEFT- left kidney & adrenal gland
LATERAL RIGHT- epiploic foramen

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85
Q

How does the greater omentum end up handing off the greater curve?

A

Stomach rotates on AP axis & greater curve faces inferiorly, dorsal mesentery is dragged with it so the big double-layer fold (greater omentum) hangs

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86
Q

What does the the greater omentum lie in front of in the abdomen?

A

Lie over intestine and fuse with transverse colon

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87
Q

What is the lienorenal ligament?

A

The mesentery between spleen and posterior abdominal wall

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88
Q

What is the gastroleinal/gastrosplenic ligament?

A

The mesentery between spleen and stomach

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89
Q

What is often referred to as the “Policeman of the Abdomen”?

A

Greater Omentum

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90
Q

What is the start and end point of the midgut?

A

Starts distal to entrance of bile duct into duodenum, ends 2/3 along transverse colon

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91
Q

What supplies the midgut?

Where does the referred pain go to?

A
  • Superior Mesenteric Artery

- Peri-umbilical region (T10)

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92
Q

What happens to the midgut by the 5th week?

A

Suspended from dorsal abdominal wall as primary intestinal loop by mesentery

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93
Q

What connects the midgut to the yolk sac?

A

Vitelline duct

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94
Q

What happens to the primary intestinal loop?

A
  • Cranial limb of loop grows to become much of jejunum & ileum.
  • Loop rotates counter clockwise by 90o & 180o as loop drops back into abdomen at 70 days (10 weeks)
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95
Q

What is the position of caecum at 70days compared to the end?

A

As intestine drops back into abdomen caecum is up in right hypochondrium, then migrates with appendix inferiorly to right iliac fossa

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96
Q

What are the possible congenital abnormalities related to midgut development?

A
  • Partial/Abnormal rotation
  • Vitelline duct fistula/patent (faecal discharge at umbilicus)
  • Vitelline cyst
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97
Q

What can failure of recanalisation lead to?

A

Narrowing/complete obstruction of GI tract at any point

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98
Q

What does the hindgut give rise to?

A
  • Distal end of transverse colon (1/3)
  • Descending colon
  • Sigmoid colon
  • Rectum
  • Upper 2/3 anal canal
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99
Q

What supplies the hindgut?

Where does the referred pain go to?

A
  • Inferior mesenteric artery

- Suprapubic region (T12)

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100
Q

Where is the most inferior part of the hindgut developed from?

A

Cloaca

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101
Q

What does the Cloaca develop into?

A

ANTERIORLY- urogenital system

POSTERIORLY- anorectal canal

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102
Q

When does the distal membrane of the cloaca break down?

A

8 weeks

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103
Q

What does the pectinate line mark?

A

Lies between proximal 2/3 of anal canal derived from hindgut endoderm & distal 1/3 from ectoderm

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104
Q

What can the common origin of anal canal and urogenital organs mean?

A

Fistulae between can occur

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105
Q

What is it called when the anal membrane isn’t broken down?

A

Imperforate anus

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106
Q

What is Hirchsprung disease?

A

Problem with colon innervation leading to constricted, ganglionic segment of bowel with an expanded segment proximally (innervation normal)

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107
Q

What is the definition of Psychosomatic disorders?

A

Disorders where emotional / psychological factors can impact on the symptoms

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108
Q

Give 5 examples of psychosomatic disorders?

A
  1. Asthma
  2. Atopic dermatitis
  3. Tension-type headaches
  4. Chronic fatigue syndrome
  5. Irritable bowel syndrome
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109
Q

What is the definition of Irritable Bowel Syndrome (IBS)?

A

Common digestive condition, your GP may be able to identify IBS based on symptoms, although blood tests may be needed to rule out other conditions

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110
Q

List the many symptoms/signs of Irritable Bowel Syndrome?

A
  • Abdominal pain & cramping, may be relieved by defecation
  • Change in bowel habits (diarrhoea, constipation, both)
  • Bloating/swelling of stomach
  • Excessive wind
  • Occasionally experiencing an urgent need to go to the toilet
  • Feeling you haven’t emptied bowels after going
  • Passing mucus
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111
Q

What is the occurrence of irritable bowel syndrome?

A
  • 20-30yrs old
  • More common in women
  • 10-20% of population
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112
Q

What is the Rome III Criteria for diagnosing Irritable bowel syndrome?

A

Last 3 months, symptom onset at least 6months prior to diagnosis the individual experiences recurrent abdominal pain at least 3 days per month in last 3 months associated with 2/+ of:

  • Improvement with defecation
  • Change in frequency
  • Change in form
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113
Q

What is the criteria for diagnosis in the UK for Irritable bowel syndrome?

A

Rome III criteria & 2+ of the following:

  • Change in how you pass stools
  • Bloating, hardness/tension in abdomen
  • Symptoms worse after eating
  • Passing mucus from rectum
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114
Q

What conditions can blood tests rule out?

A
  • Coeliac

- Ulcerative Colitis

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115
Q

What conditions can stool samples rule out?

A

Calprotectin (IBD)

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116
Q

What does HRQoL stand for?

A

Health Related Quality of Life

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117
Q

What are the putative causes of Irritable bowel syndrome?

A
  • Emotional stress
  • Psychological disorders
  • Hyper-reactivity in the brain-gut interface
  • Infection
  • Food intolerance
  • Abnormal muscle contraction
  • Serotonin receptors
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118
Q

What are the health messages in the common sense model of IBS?

A

Abdominal pain, disturbed bowel habit affected by GI infections, food intolerance, abnormal gut physiology

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119
Q

What are emotional reactions in the common sense model of IBS affected by?

A
  • Life events
  • Chronic stressors
  • Psychological disorders
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120
Q

How can you manage IBS?

A
  • Diet/lifestyle (physical activity) changes
  • Drug treatments
  • Psychological approach
  • Complementary therapies approach
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121
Q

What are the 1st line drug treatments for IBS?

A
  • Antidiarrhoeal
  • Laxatives
  • Antispasmodics
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122
Q

What are the 2nd line drug treatments for IBS?

A
  • Laxatives
  • Antidepressants
  • Tricyclic antidepressants (TCA’s) if 1st line ineffective
  • Selective serotonin reuptake inhibitors (SSRI’s) if TCA’s ineffective
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123
Q

What are the complementary therapies for managing IBS?

A
  • Nutraceuticals
  • Chinese herbal medicine
  • Probiotics
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124
Q

What are the different psychological approaches (after 12 months) used to manage IBS?

A
  • Cognitive behavioural therapy
  • Hypnotherapy
  • Psychological therapy
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125
Q

What are the targets for a doctor trying to treat an IBS patient?

A
  • Reduce disability
  • Improve coping
  • Reduce dependence on healthcare
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126
Q

What are arthritic osteophytes?

A

Indent the oesophagus & cause pain on swallowing

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127
Q

Describe the superior 1/3 of the oesophagus?

A
  • Begins C6
  • Supplied by inferior thyroid arteries
  • Drainage to brachiocephalic veins
  • Supplied by branches of Vagus (recurrent laryngeal nerves)
  • Drain to deep cervical lymph nodes
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128
Q

Describe the middle (thoracic) 1/3 of the oesophagus?

A
  • Supplied by thoracic aorta & bronchial arteries
  • Drainage to azygos system
  • Supplied by oesophageal plexus (vagus & sympathetic)
  • Drain to tracheobronchial lymph nodes
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129
Q

Describe the inferior (abdominal) 1/3 of the oesophagus?

A
  • Supplied by gastric artery
  • Drainage to left gastric veins & portal vein
  • Supplied by branches of oesophageal plexus (vagus & sympathetic)
  • Drain to left gastric & coeliac lymph nodes
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130
Q

How can the oesophageal constrictions be shown?

A

Normal barium swallow through endoscope

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131
Q

What are the 4 oesophageal constrictions?

A
  1. Upper oesophageal sphincher 17cm
  2. Arch of aorta
  3. Left main bronchus 28cm
  4. Diaphragm (lower oesophageal sphincter) 43cm
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132
Q

What structure causes an indentation on the oesophagus?

A

Left atrium

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133
Q

What lies anterior to the oesophagus?

A
  • Trachea
  • Right pulmonary artery
  • Left main bronchus
  • Left atrium
  • Diaphragm
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134
Q

What lies posterior of the oesophagus?

A
  • Vertebral bodies (C6-T12)
  • Thoracic duct
  • Thoracic aorta
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135
Q

What is the epithelium and lining of the oesophagus?

A

Stratified squamous epithelium with submucosal mucous glands and has smooth muscle walls

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136
Q

Where does the oesophagus pass through to exit the thorax and enter the abdomen?

A

Right crus of diaphragm at T10 just left of the midline

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137
Q

How can Cirrhotic liver disease cause oesophageal varies?

A

Disease raises portal venous pressure (portal hypertension) & blood escapes via submucosal veins in oesophagus, veins become dilated & tortuous. Can cause fatal haemorrhage

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138
Q

What are the 3 components of the “physiological” cardiac sphincter which prevents gastric reflux?

A
  1. Contraction of right crus of diaphragm
  2. Tonic contraction of circular layer of smooth muscle in lower oesophagus
  3. “Valvular” effect of oblique entry of oesophagus into stomach, augmented by oblique muscle layer
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139
Q

What controls closure of the “physiological” cardiac sphincter?

A

Vagal control

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140
Q

What does the Z-line represent?

A

Transition from stratified squamous (oesophageal) to columnar (gastric) epithelium

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141
Q

What 3 regions of the abdomen does the stomach lie in?

A
  • Epigastric
  • Umbilical
  • Left hypogastric
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142
Q

What are the 4 parts of the stomach?

A
  1. Cardia
  2. Fundus (full of gas)
  3. Body
  4. Pyloric (antrum & canal)
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143
Q

What happens to the circular muscle coat at the pyloric region of the stomach?

A

Thickened to form pyloric sphincter that controls outflow of gastric contacts into duodenum

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144
Q

What are the mucosal fold of the stomach also called?

A

Rugae / “Magenstrasse”

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145
Q

Describe the left gastric artery and what it supplies?

A
  • Arises from coeliac artery
  • Passes upward & left to reach oesophagus
  • Descends along lesser curvature
  • Supplies lower 1/3 of oesophagus & proximal part of lesser curve & adjacent body of stomach
146
Q

Describe the right gastric artery and what it supplies?

A
  • Arises from hepatic artery at upper pylorus
  • Runs left along lesser curvature
  • Supplies distal part of lesser curve & adjacent body of stomach
147
Q

Where does the short gastric arteries arise from?

What does it supply?

A
  • Splenic artery at hilum of the spleen

- Fundus

148
Q

Where does the left gastro-epiploic (omental) artery arise from?
What does it supply?

A
  • Splenic artery at hilum of spleen

- Stomach

149
Q

Where does the right gastro-epiploic artery arise from?

What does it supply?

A
  • Gastroduodenal branch of hepatic artery

- Stomach

150
Q

Where does the gastroduodenal artery lie?

A

Posterior to 1st part of the duodenum

151
Q

What does the left & right gastric veins of the stomach drain into?

A

Portal veins

152
Q

What does the right gastroepiploic vein of the stomach drain into?

A

Superior mesenteric vein

153
Q

What does the short gastric veins & left gastroepiploic veins drain into?

A

Splenic vein

154
Q

What does all the lymph of the stomach eventually pass to?

A

Coeliac nodes

155
Q

What is the nerve supply of the stomach?

A
  • Sympathetic fibres (pain & vasomotor) T5-9 via greater splanchnic nerves & coeliac plexus
  • Parasympathetic fibres from right & left vagus nerves (secretion & motility)
156
Q

Where is referred pain of the stomach to?

A

Lower chest & epigastrium

157
Q

What is Vagotomy?

A
  • Surgical operation where 1/+ branches of vagus nerve are cut to reduce rate of gastric secretion (in treating peptic ulcers)
  • Motility is affected so cut after those going to pyloric sphincter
158
Q

What is Bariatric surgery for?

A

Obese patients

159
Q

What are the boundaries of the stomach bed?

A

POSTERIOR- lesser sac, retroperitoneal structures, post. ado wall
SUPERIOR- left crus of diaphragm, spleen, left suprarenal gland, upper pole of left kidney
INFERIORLY- body & tail of pancreas, transverse mesocolon, left colic flexure & splenic artery

160
Q

How long is the small intestine?

A

6-7m

161
Q

Where does the duodenum receive bile and pancreatic ducts?

A

Major papilla/ Ampulla of Vater

162
Q

Describe the 1st / superior part of the duodenum?

A
  • Begins at pylorus

- Runs up, backwards & right starting on transpyloric plane at level of L1

163
Q

Describe the 2nd / descending part of the duodenum?

A

Runs vertically down in front of hilum of right kidney on right side of L2 & L3

164
Q

Describe the 3rd / horizontal part of the duodenum?

A
  • Runs horizontally to left on subcostal plane

- Pass infant of L3 & following lower margin of head of pancreas

165
Q

Describe the 4th / ascending part of the duodenum?

A

Runs up & left to duodenojejunal flexure at L2

166
Q

What are the boundaries/relations of the 1st / superior part of the duodenum?

A

ANTERIOR- quadrate lobe of liver & gallbladder
POSTERIOR- lesser sac, gastroduodenal artery, bile duct & portal vein, IVC
SUPERIOR- entrance of lesser sac
INFERIOR- head of pancreas

167
Q

What are the boundaries/relations of the 2nd / descending part of the duodenum?

A

ANTERIOR- gallbladder, right lobe of liver, transverse colon, coils of small intestine
POSTERIOR- hilum of right kidney & right ureter
LATERALLY- ascending colon, right colic flexure, right lobe of liver
MEDIALLY- head of pancreas, bile duct, main pancreatic duct

168
Q

What are the boundaries/relations of the 3rd / horizontal part of the duodenum?

A

ANTERIOR- root of mesentery of small intestine, superior mesenteric vessels, coils of jejunum
POSTERIOR- right ureter, right psoas muscle, IVC, aorta
SUPERIOR- head of pancreas
INFERIOR- coils of jejunum

169
Q

What are the boundaries/relations of 4th / ascending part of the duodenum?

A

ANTERIOR- root of the mesentery, coils of jejunum

POSTERIOR- left margin of aorta, medial border of left psoas muscle

170
Q

What can be the rare problem of the duodenojejunal gaining a mesentery?

A

There may be small paraduodenal recesses into which bowel may herniate

171
Q

What is the upper 1/2 of the duodenum blood supply?

A

Gastroduodenal branches of common hepatic artery (Coeliac trunk, foregut)

172
Q

What is the lower 1/2 of the duodenum blood supply?

A

Superior mesenteric artery (midgut)

173
Q

What artery is at risk with posterior ulcers of the 1st part of the duodenum?

A

Gastroduodenal artery

174
Q

What veins drain the duodenum?

A
  • Superior pancreaticoduodenal vein drains into portal vein

- Inferior vein joins superior mesenteric vein

175
Q

What is the lymph drainage of the duodenum?

A

Coeliac & Superior mesenteric (SM) nodes

176
Q

What is the nerve supply of the duodenum?

A
  • Sympathetic greater (T5-9) & lesser splanchnic (T10-11)
  • Parasympathetic (vagus) via coeliac & superior mesenteric plexuses
177
Q

List the 3 different layers/types of muscle in the stomach?

A
  1. Outer- longitudinal
  2. Middle- circular
  3. Inner- oblique
178
Q

How does the muscle wall thickness change throughout the stomach?

A

Increases proximal to distal

179
Q

What is the extrinsic nerves supplying the stomach?

What do the different nerves do?

A
  1. Parasympathetic- stimulate gastric smooth muscle motility & secretions
  2. Sympathetic- inhibit motility & secretions
180
Q

What is the enteric nervous system supplying the stomach?

A

Myenteric plexus:

  • parasympathetic via vagus
  • sympathetic via coeliac ganglion
181
Q

What is the sensory afferent fibres supplying the stomach?

A

Between sensory receptors & the ENS (pressure, distention, pH, pain) & centrally via the vagal & splanchnic nerves

182
Q

What is the orad region?

A

Proximal part of the stomach

183
Q

What happens at the orad region of the stomach?

A
  • Distention of lower oesophagus induces relaxation of lower oesophageal spinchter
  • Reduces pressure & increases volume of stomach (1.5litres)
184
Q

In the vagovagal reflex what is the afferent information?

A

Mechanoreceptors associated with chewing, oesophageal & stomach distension relay information to CNS via sensory neurons

185
Q

In the vagovagal reflex what is the efferent information?

A

Neurotransmitter, VIP, released from postganglionic peptidergic vagal neurons is responsible for orad relaxation

186
Q

What is the purpose of thin muscle fibres in the fundus & body?

A

Weak contractions, contents settle into layers based on density

187
Q

What is the purpose of thick muscle fibres in caudad region?

A
  • For mixing

- Contraction waves begin in middle of body. move distally with increasing strength towards pylorus

188
Q

What are the 3 movement patterns in the stomach?

A
  1. Propulsion- bolus pushed toward the closed pylorus
  2. Grinding- antrum churns the trapped material
  3. Retropulsion- bolus pushed back into proximal stomach
189
Q

What increase action potential frequency of the muscle in stomach?

A

Parasympathetic stimulation, gastrin & motilin

190
Q

What decrease action potential frequency of the muscle in stomach?

A

Sympathetic stimulation & secretin

191
Q

What are Migrating myoelectic complexes (MMCs)?

A
  • Mediated by motilin, released from endocrine cells in the upper GI tract
  • 90min intervals to clear residual chyme
192
Q

What are the 3 steps to gastric emptying?

A
  1. After a meal stomach contains 1.5L of solids, liquids & gastric secretions
  2. Emptying of gastric contents takes approx. 3hrs
  3. Rate is regulated to ensure gastric H+ is neutralised in duodenum & there is adequate time for digestion & absorption of nutrients
193
Q

What are the 3 physical factors affecting gastric emptying?

A
  1. Liquids empty more rapidly that solids
  2. Isotonic fluids empty more rapidly than hypo- or hypertonic
  3. Solids must be reduced to particles <1mm3, retropulsion continues until this is achieved
194
Q

What 2 chemical factors inhibit gastric emptying when in duodenum?

A
  1. Fat

2. H+ ions

195
Q

What is the effect of fat on gastric emptying?

A

Mediated by cholecystokinin (secreted when fat reaches duodenum)

196
Q

What is the effect of H+ on gastric emptying?

A
  • Mediated by reflexes in enteric nervous system.
  • H+ receptors in duodenum detect low pH & relay information to gastric smooth muscle via interneurons in myenteric plexus
197
Q

What are the 3 purposes for motility in the small intestine?

A
  1. Mixes chyme with digestive enzymes & pancreatic secretions
  2. Exposes nutrients to intestinal mucosa for absorption
  3. Propels unabsorbed chyme into large intestine
198
Q

How frequent are the slow waves in the duodenum & ileum?

A
  • Duodenum 12 per min

- Ileum 9 per min

199
Q

What are segmental contractions for?

A

Mixing

200
Q

What 2 things stimulate orad contraction (peristalsis)?

A

ACh & Substance P

201
Q

What 2 things stimulate caudad relaxation (peristalsis)?

A

VIP & nitric oxide

202
Q

What is Taeniae (tenia) coli?

A

3 separate longitudinal bands of smooth muscle on the outside of the colon

203
Q

What is the parasympathetic innervation of the colon?

A
  • VAGUS: caecum, ascending colon, transverse colon

- PELVIC NERVES: descending & sigmoid colon, rectum & anal canal

204
Q

What does sympathetic innervation of the colon do?

A

Stops colonic movements

205
Q

Where can reverse peristalsis occur in the colon and why?

A
  • Towards the caecum

- Retention favours Na+ & water absorption

206
Q

What happens after the contents of the small intestine enters the caecum & proximal colon?

A

Ileocaecal sphincter contracts

207
Q

How much chyme does the colon receive per day?

A

500-1500ml

208
Q

What are haustra/haustrations?

A

Small pouches caused by sacculation which give the colon its segmented appearance

209
Q

What is the faeces like in the distal colon?

A

Semi-solid due to water being absorbed

210
Q

What 2 reflexes is the mass movements in the colon caused by?

A
  1. Gastrocolic reflex

2. Duodenocolic reflex

211
Q

What is the gastrocolic reflex?

A

Distension of stomach by food increases motility of colon & frequency of mass movements

212
Q

What is the afferent limb in the stomach mediated by?

A

Parasympathetic nervous system

213
Q

What is the efferent limb of the reflex increasing colon motility mediated by?

A

CCK & gastrin

214
Q

What happens to the rectosphincter reflex during defecation?

A

Smooth muscle of rectum contracts & internal anal sphincter relaxes

215
Q

What does the external anal sphincter do (striated muscle & voluntary control)?

A

Remains tonically contracted

216
Q

Where is the vomiting centre?

A

In medulla

217
Q

During vomiting what is the afferent information?

A
  • Vestibular system
  • Back of throat
  • GI tract
  • Chemoreceptor trigger zone in the 4th ventricle
218
Q

During vomiting what is the efferent response?

A
  • Reverse peristalsis in small intestine
  • Relaxation of the stomach and pylorus
  • Forces inspiration to increase abdominal pressure
  • Relaxation of lower oesophageal sphincter
  • Forceful expulsion of gastric & duodenal contents
219
Q

What are the host defences in the mouth (4)?

A
  • Flow of liquids
  • Saliva
  • Antimicrobials
  • Normal Microbiota
220
Q

What are the host defences in the oesophagus (2)?

A
  • Flow of liquids

- Peristalsis

221
Q

What are the host defences in the stomach (3)?

A
  • Acid pH
  • Antimicrobials
  • Mucus
222
Q

What are the host defences in the small intestine (7)?

A
  • Flow of gut contents
  • Peristalsis
  • Mucus
  • Bile
  • Secretory IgA
  • Antimicrobial peptides
  • Normal bacterial microbiota
223
Q

What are the host defences in the large intestine (4)?

A
  • Normal microbiota
  • Peristalsis
  • Mucus
  • Shedding & replication of epithelium
224
Q

What is the commensal bacteria and host’s relationship?

A

One population is benefited (bacteria) and the other is neither benefited / harmed (host)

225
Q

What is the symbiotic bacteria and host’s relationship?

A

Both host and bacteria have a cooperative / mutually dependent relationship

226
Q

What is a parasitic bacteria and host’s relationship?

A

Host is being killed off as bacteria is draining it and using up all its nutrients

227
Q

What are the 3 examples of probiotics?

A
  1. Lactobacillus spp.
  2. Bifidobacterium spp.
  3. Bacteroides spp.
228
Q

What is a Probiotic?

A
  • “Friendly” bacteria

- Live bacteria & yeasts that are good for digestive system

229
Q

What are Prebiotics?

A
  • Non-digestible food ingredients

- Stimulate growth/activity of gut microbiota

230
Q

What 6 things can Probiotics & Prebiotics do?

A
  1. Development of mucosal barrier
  2. Synthesis of vitamins
  3. Metabolism of bile acids
  4. Production of short-chain fatty acids
  5. Reduction in pH in large bowel
  6. Immune system activation
231
Q

Where is Lactobacillus spp. usually found in the GI tract?

A
  • Oesophagus
  • Stomach
  • Duodenum
    UPPER GI TRACT
232
Q

Where is Bacteroides spp. usually found in the GI tract?

A
  • Large bowel
  • Faecal material
    LOWER GI TRACT
233
Q

What are the 5 different roles of the gut microbiota?

A
  1. Prevent colonisation by pathogens
  2. Excrete useful metabolites
  3. Ferment unused energy substrates
  4. Synthesise & excrete vitamins
  5. Produce hormones
234
Q

What is Bacteriotherapy?

A
  • Also known as Fecal Transplantation
  • Transfer of stool from healthy donor into the GI tract of someone with devastated microbiota for the purpose of treating recurrent C. difficile colitis
235
Q

What are the different factors controlling gut microflora?

A
  • Physiological status
  • Underlying disease
  • Intestinal secretions
  • Intestinal motility
  • Immune mechanisms
  • Environmental factors
  • Use of antibiotics
236
Q

How many lymphocytes are there in the GI tract?

A

> 10 million per gram tissue

237
Q

What are the different pathogen recognition receptors in the GI tract?

A
  • PAMPs/MAMPs: pathogen/microbe associated molecular patterns
  • TLRs: toll-like receptors
  • NODs: nucleotide-binding oligomerization domain-containing proteins
  • NLRs: NOD-like receptors
238
Q

How are most GI infections acquired?

A

Via the faecal-oral route

239
Q

Why is infection not the same as colonisation?

A

Infection only occurs when micro-organism causes ill-health

240
Q

Commensals may become ______ if the circumstances are right?

A

Pathogenic

241
Q

What are the 3 different ways you can develop intestinal infection?

A
  1. Ingestion of infected food & water
  2. Ingestion of bacterial toxins
  3. Oral antibiotics
242
Q

Describe Gastroenteritis?

A
  • Inflammation of stomach & intestines
  • Resulting from bacterial toxins / viral infection
  • Causing vomiting & diarrhoea
243
Q

What is Enterocolitis?

A

Inflammation of mucosa of both small & large intestine

244
Q

What does diarrhoea cause?

A

Increased fluid and electrolyte loss

245
Q

Describe Dysentery?

A
  • Inflammation of GI tract
  • Large intestine usually
  • Blood & pus in faeces
  • Pain, fever, abdominal cramps
246
Q

What are the 7 possible clinical effects of pathogenic invasion of GI tract?

A
  1. Diarrhoea/dysentery
  2. Malaena (black stools)
  3. Blood in faeces
  4. Pus in faeces
  5. Abdominal cramps
  6. Fever
  7. Sepsis
247
Q

What are the 4 different secretory fluids, enzymes & mucous which go into the lumen of the GI tract?

A
  1. Salivary glands (saliva)
  2. Gastric mucosa (gastric secretion)
  3. Exocrine cells of pancreas (pancreatic secretion)
  4. Liver (bile)
248
Q

What are the characteristics of Saliva?

A
  • High HCO-3
  • High K+
  • Hypotonic
  • α-amylase & lingual lipase
249
Q

What are the factors which increase secretion of Saliva?

A
  • Parasympathetic (primarily)

- Sympathetic

250
Q

What are the facts which decrease secretion of Saliva?

A
  • Sleep
  • Dehydration
  • Atropine
251
Q

How much saliva is secreted per day?

A

1 litre per day

252
Q

What are the functions of Salivary secretion?

A
  • Initial digestion of starches and lipids
  • Dilution & buffering of ingested foods
  • Lubricaton of ingested foods with mucous (mucin)
253
Q

What is the structure of Parotid salivary gland?

A

Serous cells secreting an aqueous fluid composed of water, ions and enzymes

254
Q

What is the structure of Sublingual salivary gland?

A

Mostly mucous cells

255
Q

What is the structure of Submandibular salivary gland?

A

Mixed glands containing serous & mucous cells (mucin glycoprotein for lubrication)

256
Q

Describe Acinar cells?

A

Produce initial isotonic saliva composed of water, ions, enzymes and mucus

257
Q

Describe Myoepithelial cells?

A

In acini are stimulated by neural input to eject saliva

258
Q

Describe Ductal cells?

A

Modify initial saliva by altering electrolyte concentrations

259
Q

What is the combined action (4) for modification of salivary secretion?

A
  • Absorption of Na+ and Cl-
  • Secretion of K+ and HCO-3
  • Because more NaCl is absorbed than KHCO3 secreted there is net absorption of solute
  • Low water permeability of ductal cells means that the final saliva is hypotonic
260
Q

What are the 4 acinar cell secretions?

A
  1. α-amylase
  2. Lingual lipase
  3. Mucus
  4. Kallikrein
261
Q

What does Kallikrein do?

A

Enzymatic cleavage of kininogen to bradykinin (potent vasodilator)

262
Q

What does neural stimulation of salivary glands result in?

A
  • Increased saliva production
  • HCO-3 production
  • Enzyme secretion
  • Myoepithelial cell contraction
263
Q

What are the 4 different gastric secretions and what do they do?

A
  1. HCl: protein digestion
  2. Pepsinogen: Protein digestion
  3. Intrinsic factor: Vitamin B12 absorption (in ileum)
  4. Mucus: protects gastric mucosa & lubricates food
264
Q

What are the factors that increase gastric secretions?

A
  • Gastrin
  • Acetylcholine
  • Histamine
  • Parasympathetic
265
Q

What are the factors that decrease gastric secretion?

A
  • H+ in stomach
  • Chyme in duodenum
  • Somatostatin
  • Atropine
  • Cimetidine
  • Omeprazole
266
Q

Where are the Parietal/Oxyntic & Chief/Peptic cells located in the stomach?

A

Body

267
Q

Where are the G cells located in the stomach?

A

Antrum

268
Q

What do Parietal cells secrete?

A

HCl which acidifies gastric contents to pH 1-2

269
Q

What does low gastric pH do to inactive pepsinogen?

A

Inactive pepsinogen –> pepsin (active form)

270
Q

What secretion happens at the apical membrane of a gastric parietal cell?

A
  • H+ secreted into lumen via H+-K+ ATPase

- Cl- follows by diffusion through apical channel

271
Q

What secretion happens at the basolateral surface/membrane of a gastric parietal cell?

A
  • HCO-3 exchanged for Cl- via chloride-bicarbonate exchanger (alkaline tide)
  • Eventually HCO-3 secreted back into GI tract in pancreatic secretions
272
Q

What happens at the Celphalic phase of gastric HCl release?

A
  • 30% of HCl secretion
  • Direct stimulation of parietal cells by vagus
  • Indirect stimulation of parietal cells by gastrin
273
Q

What does GRP stand for?

What does it do?

A
  • Vagal Gastrin Releasing Peptide

- Stimulates gastrin release from G cells, gastrin hormone stimulates parietal cells to release HCl

274
Q

What happens at the Gastric phase of HCl release?

A
  • 60% of HCl secretion

- Distension of stomach & presence of breakdown products of proteins, amino acids and small peptides of stomach

275
Q

In the gastric phase what does Distention cause?

A
  • Direct vagal stimulation of parietal cells
  • Indirect stimulation via gastrin
  • Local reflexes in antrum that stimulate gastrin release
276
Q

What happens at the Intestinal phase of gastric HCl release?

A
  • 10% of HCl secretion

- Presence of breakdown products of proteins in the duodenum

277
Q

What is the origin, action and second messenger of neurocrine Acetylcholine?

A

ORIGIN: Vagus nerve
ACTION: binds to muscarinic (M3) receptors on parietal cells
SECOND MESSENGER: IP3/Ca2+

278
Q

What is the origin, action and second messenger of paracrine Histamine?

A

ORIGIN: vagus nerve
ACTION: diffuses to & binds to H2 receptors on parietal cells
SECOND MESSENGER: cAMP

279
Q

What is the origin, action and second messenger of hormone Gastrin?

A

ORIGIN: G cells in stomach antrum
ACTION: binds to CCKB receptors on parietal cells
SECOND MESSENGER: IP3/Ca2+

280
Q

When is HCl secretion inhibited?

A

After Chyme moves into small intestine and H+ buffering capacity of food is no longer a factor

281
Q

What is the direct and indirect pathway of Somatostatin produced from the small intestine?

A

DIRECT: binds to receptors on parietal cells & inhibits adenylate cyclase via Gi protein
INDIRECT: inhibits histamine release from ECL cells and gastrin release from G cells

282
Q

What are the 2 ways inactive pepsinogen is secreted?

A
  • Secreted by chief & mucous cells in oxyntic glands in response to vagal stimulation
  • H+ triggers local reflexes which stimulate chief cells to secrete pepsinogen
283
Q

What is required for Vitamin B12 absorption in the ileum?

A

Mucoprotein released from parietal cells

284
Q

What does a lack of intrinsic factor cause?

A

Pernicious anaemia

285
Q

What is given to patients following a gastrectomy?

A

Injections of Vitamine B12 to bypass the absorption defect and stop pernicious anaemia from occuring

286
Q

What is Zollinger-Ellison syndrome?

A
  • Rare condition in which tumours (Gastrinoma) form in small intestine or non-􏰀􏰀􏰀β cell of the pancreas
  • Secrete large amounts of hormone gastrin, which causes stomach to produce too much acid
287
Q

What does the high circulating levels of gastrin in Zollinger-Ellison syndrome cause?

A
  • Increased H+ secretion by parietal cells
  • Hypertrophy of the gastric mucosa
  • Duodenal ulcers (constant secretion of gastric H+)
  • Acidification of intestinal lumen (inactivation of pancreatic lipases)
288
Q

Where in the abdomen does the jejunum lie?

A

Upper left abdomen

289
Q

Where in the abdomen does the ileum lie?

A

Lower right abdomen

290
Q

What is the physical difference between jejunum and ileum?

A
  • Jejunum is wider, thicker walled and redder than ileum
291
Q

Why does the jejunum’s walls feel thicker than the ileum’s?

A

Permanent infolding of submucosa, the plicae circulares, are larger, more numerous and more closely set in the jejunum

292
Q

Describe the mesentery suspending the jejunum?

A
  • Attached to post. abdominal wall above & left of aorta at L2
  • Vessels form only 1/2 arcades, with long & infrequent branches
  • Fat deposited near root
293
Q

Describe the mesentery suspending the ileum?

A
  • Attached below & right of aorta at SI joint
  • Numerous short terminal vessels arising from 3/4+ arcades
  • Fat deposited throughout
294
Q

What is the ileocaecal valve?

A
  • 2 horizontal folds of mucous membrane that project around orifice of ileum
  • At junction of small & large intestine
295
Q

Where do the jejunal and ill arteries arise from?

A

Superior Mesenteric Artery (SMA) & its ileocolic branch

296
Q

Where do the veins corresponding to branches of SMA drain?

A

Superior Mesenteric vein, which forms portal vein

297
Q

What is the lymph drainage of jejunum and ileum?

A

Superior Mesenteric nodes

298
Q

What is the nerve supply of the jejunum & ileum?

A
  • Sympathetic, lesser splanchnic nerve T10 & 11

- Parasympathetic (vagus) nerves via superior mesenteric plexus

299
Q

Where does the referred pain of jejunum & ileum go to?

A

Peri-umbilical (T10)

300
Q

Where does the Superior mesenteric artery (SMA) arise from and what does it supply?

A
  • Aorta at L1
  • Carries sympathetic nerves from T10 & 11
  • Supplies Midgut
301
Q

What is the purpose of a lacteal in the centre of each villus on the mucous membrane of small intestine?

A

Absorption of digested fats & lipids (chyle)

302
Q

What is the route of passage of Chyle in the small intestine?

A

From lacteals into mesenteric lymph channels (NOT through lymph nodes), converge on the cistern chyli

303
Q

Where is the Peyer’s patches located?

A

Ileum

304
Q

What is the route of passage of Lymph in the small intestine?

A

Into mesenteric lymph channels, filter through mesenteric nodes, afferents from nodes converge on nodes at root of SMA then pass to cisterna chyli

305
Q

What/How is a Meckel’s Diverticulum formed?

A
  • Remnant of vitello-intestinal duct
  • End of ileum
  • 2% of people
306
Q

What parts of the colon are retroperitoneal?

A

Ascending & Descending

307
Q

What parts of the colon are intraperitoneal?

A

Transverse & Sigmoid

308
Q

What are omental appendices/appendices epiploicae?

A

Little sacs of fat projecting along serous coat of colon

309
Q

What are the 3 taeniae coli?

A

Condensations of the longitudinal muscle layer outside the colon

310
Q

What are the 3 internal differences that the large intestine lacks compared to the small intestine?

A
  • Lacks plicae circularis
  • Lacks villi
  • Lacks peyers patches
311
Q

Describe the caecum?

A
  • Covered by peritoneum
  • Not on a mesentery
  • In right iliac fossa
312
Q

Where is the root of the appendix at?

A

McBurney’s point

313
Q

Describe the appendix?

A
  • Narrow blind ended tube hanging from caecum
  • Submucosa packed of lymphoid tissue
  • Suspended on meso-appendix that transmits appendicular vessels
314
Q

What are the 5 different positions of the appendix?

from common to least common

A
  1. Retrocaecal
  2. Pelvic
  3. Subcaecal
  4. Pre-ileal
  5. Retro-ileal
315
Q

Due to the appendicular artery being close to appendix, what can happen during an inflamed appendix?

A

Artery can become obstructed causing gangrene and rupture of appendix

316
Q

Describe the appendicular artery?

A

From ileocolic branch of superior mesenteric, from aorta at L1

317
Q

What is the nerve supply of the appendix?

A

Derived from T10/11

318
Q

What is the referred pain of the appendix?

A

Early appendicitis refers pain to peri-umbilical region, then pain moves to right inguinal region

319
Q

What is the lymph drainage of the caecum and appendix?

A

Nodes on the SMA

320
Q

Where does the sigmoid colon lie in the abdomen?

A

In front of the pelvic brim, becomes continuous with rectum at S3

321
Q

What is Sigmoid volvulus?

A

When the sigmoid colon rotates upon itself

322
Q

What can a colonic diverticulae mimic when obstructed?

A

Left sided “appendicitis”

323
Q

What are the Superior Mesenteric Artery (SMA) branches?

What do they supply?

A
  • Ileocolic, right colic & middle colic branches

- Caecum, ascending colon, hepatic flexure & 2/3 transverse colon

324
Q

What are the Inferior Mesenteric Artery (IMA) branches?

What do they supply?

A
  • Left colic & sigmoid branches

- 1/3 of transverse colon, splenic flexure, descending colon & sigmoid colon

325
Q

What nerve supply does the Inferior Mesenteric Artery carry?

A

Sympathetic nerves derived from T12 (least splanchnic nerves) and parasympathetic from S2,3,4 (not vagus)

326
Q

What does the Inferior Mesenteric artery continue as?

A

Superior Rectal Artery supplying rectum & anal canal

327
Q

Is the rectum intra- or retroperitoneal?

A

Retroperitoneal

328
Q

What are the characteristics of pancreatic secretions?

A
  • High HCO-3 (isotonic)

- Pancreatic lipase, amylase & proteases

329
Q

What are the factors that increase pancreatic secretion?

A
  • Secretin
  • Cholecystokinin (CCK)
  • Parasympathetic supply
330
Q

How much fluid per day does the exocrine pancreas secrete?

A

1L

331
Q

What is the innervation of the pancreas?

A
  • Parasympathetic from vagus stimulates secretion

- Sympathetic inhibits secretion

332
Q

Where are the pancreatic enzymes stored?

A

In condensed zymogen granules until release

333
Q

Where is the aqueous component of pancreatic secretion released from?

A

Centroacinar cells & ductal cells

334
Q

What does modification of the pancreatic secretion by ductal cells result in?

A

Fluid secretion rich in HCO-3

335
Q

where is the enzymatic component of pancreatic secretion released from?

A

Acinar cells

336
Q

Where are pancreatic (inactive) proteases activated?

A

In duodenum (enterokinase)

337
Q

What are the 3 phases of regulation of pancreatic secretion?

A
  1. CEPHALIC phase initiated by taste, smell & conditioning mediated by vagus (mainly enzymatic)
  2. GASTRIC phase initiated by distension of stomach & mediated by vagus (mainly enzymatic)
  3. INTESTINAL phase (80%) both enzymatic & aqueous secretions
338
Q

What do duodenal I cells secrete?

A

CCK in response to presence of amino acids, small peptides & fatty acids in lumen

339
Q

What do vagal release?

A

ACh potentiates CCK action

340
Q

What do S cells of the duodenum release?

A

Secretin which is the major stimulus for aqueous rich HCO-3 secretion

341
Q

How is secretin release triggered?

A

Arrival of acidic chyme in duodenum

342
Q

What is ACh & CCK’s effect on secretin?

A

Increase action

343
Q

What is bile secretion a mixture of?

A
  • Bile salts (50%)
  • Bile pigments (2%)
  • Cholesterol (4%)
  • Phospholipids (40%)
344
Q

What is the purpose of bile salts?

A

Emulsify lipids to prepare them for digestion & solubilise products of digestion into “packets” called micelles

345
Q

What are the 3 functions of the gallbladder?

A
  1. Reservoir for bile
  2. Concentration of bile
  3. Ejection of bile
346
Q

How is bile ejected from the gall bladder?

A
  • Begins 30mins after a meal

- Stimulus is release of Cholecystokinin from I cells in duodenum & jejunum

347
Q

What is Cholecystokinin?

A

33 amino acid peptide hormone related to gastrin

348
Q

When is Cholecystokinin released from I cells of duodenal & jejunal mucosa?

A

In response to presence of monoglycerides, fatty acids, small peptides & amino acids

349
Q

What are the 5 hormonal actions of Cholecystokinin

A
  1. Contraction of gall bladder & relaxation of sphincter of Oddi to eject bile (emulsification & solubilisation of dietary fat)
  2. Secretion of pancreatic enzymes (lipase & proteases)
  3. Secretion of pancreatic HCO3
  4. Growth of exocrine pancreas & gallbladder
  5. Inhibition of gastric emptying
350
Q

What is the role of Hepatocytes?

A

Liver cells which synthesise & secrete constituents of bile

351
Q

What happens to bile salts when lipid absorption is complete?

A

They are recirculated to the liver by enterohepatic portal circulation

352
Q

What is the structure of a mixed micelles (core and surface)?

A
  • Core contains products of lipid digestion

- Surface coating of bile salts which are amphipathic

353
Q

What is the definition of absorption?

A

Movement of nutrients, water and electrolytes from lumen of intestine to blood

354
Q

What is the arrangement of the surface of small intestine?

A

Circular folds of Keckring

355
Q

What are the only carbohydrates that can be absorbed?

A

Monosaccharides

356
Q

What is the different mechanisms for carbohydrate digesting in the small intestine?

A
  • Na+ dependant cotransport

- Facilitated diffusion

357
Q

In Secondary Active Transport, what does SGLT1 stand for?

What does it do?

A
  • Sodium dependent glucose transporter 1

- Transports glucose & galactose across apical membrane

358
Q

In Facilitated Diffusion, what does GLUT 5 stand for?

What does it do?

A
  • Glucose Transporter 5

- Transports fructose across the apical membrane

359
Q

What is the difference between Endopeptidases & Exopeptidases?

A
  • Endopeptidase break peptide bonds of nonterminal amino acids (within the molecule)
  • Exopeptidases break peptide bonds from end-pieces of terminal amino acids
360
Q

What is the 3-step protein digestion in the small intestine?

A
  1. Pancreatic proteases secreted as inactive precursors
  2. Activation of trypsinogen to active form, trypsin, by brush-border enzyme enterokinase
  3. Trypsin catalyses conversion of other inactive precursors to active enzymes

MD3002 (15 decks)

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