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Phase 1 Med (Liv) > GI (summary sheets) > Flashcards

GI (summary sheets) Flashcards

1
Q

What is the foregut?

A

Starts at the mouth and goes to the common bile duct (proximal half of duodenum)

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2
Q

What is the midgut?

A

Starts at the distal half of the duodenum (common bile duct) and goes to 2/3rds of transverse colon

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3
Q

What is the hindgut?

A

Starts from 2/3rds of the transverse colon to anal canal

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4
Q

What is the blood supply of the foregut?

A

Celiac artery

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5
Q

What are the components of the foregut?

A
  • Pharynx
  • Oesophagus
  • Stomach
  • Proximal half of duodenum and the derivative (liver, biliary apparatus and the pancreas)
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6
Q

What is the blood supply of the midgut?

A

Superior mesenteric artery

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7
Q

What are the components of the midgut?

A
  • Distal half of the duodenum
  • Jejunum
  • Ileum
  • Caecum
  • Appendix
  • Ascending colon
  • Right 2/3rds of the transverse colon
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8
Q

What is the blood supply of the hindgut?

A

Inferior mesenteric artery

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9
Q

What are the components of the hindgut?

A
  • Left 1/3 of the transverse colon
  • Descending colon
  • Sigmoid colon
  • Rectum
  • Anal canal
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10
Q

What is embryonic folding?

A

During the 4th week of development when the embryo fold and change shape to form a trilaminar disc into a cylinder

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11
Q

Why does embryonic folding happen in two planes?

A
  • Due to differing rates of growth of embryonic structures

- These happen simultaneously

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12
Q

What is the result of embryonic folding in the horizontal plane?

A

Two lateral body folds

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13
Q

What is the result of embryonic folding in the medial plane?

A

Formation of the cranial and caudal folds

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14
Q

Which part of the embryo is mainly responsible for the development of the GI tract?

A

The endoderm

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15
Q

What happens to the endoderm throughout embryonic folding?

A

The endoderm moves towards the midline and fuses - incorporating the dorsal part of the yolk sac to form the primitive gut tube

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16
Q

What is the primitive gut derived from?

A

The endoderm and the visceral mesoderm

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17
Q

In terms of GI, what does the endoderm give rise to?

A
  • Epithelial lining of digestive tract
  • Hepatocytes of the liver
  • Endocrine and exocrine cells of the pancreas
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18
Q

In terms of GI, what does the visceral mesoderm give rise to?

A
  • Muscle, connective tissue and peritoneal components of the wall of the gut
  • Connective tissue for the glands
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19
Q

How does the foregut develop embryologically?

A
  • On the cranial end of the embryo
  • Temporarily closed by the oropharyngeal membrane
  • At the end of the 4th week of development, it ruptures to form the mouth
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20
Q

How does the midgut develop embryologically?

A
  • Remains connective to the yolk sac until the 5th week of development
  • As embryonic folding continues, the connection to the yolk sac narrows into a stalk called the vitelline duct
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21
Q

How does the hindgut develop embryologically?

A
  • Lies at the caudal end of the embryo
  • Temporarily closed by the cloacal membrane
  • Ruptures during 7th week of development to form the anus
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22
Q

Where is the length of the pharyngeal arches?

A

Extends from the oropharyngeal membrane to the respiratory diverticulum

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23
Q

When do the pharyngeal arches form?

A

In the 4th & 5th week of foetal life

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24
Q

What are the 5 pharyngeal arches?

A

1, 2, 3, 4 & 6

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25
Q

What do the pharyngeal arches contribute to?

A

The external appearance of the embryo

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26
Q

What are the pharyngeal arches formed from?

A
  • Masses of mesenchymal tissue (connective tissue derived from mesoderm) which are invaded by crania neural crest cells
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27
Q

What are each of the pharyngeal arches covered by?

A
  • Externally by endoderm (forming the pharyngeal clefts)

- Internally by ectoderm (forming the pharyngeal pouches)

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28
Q

What does each pharyngeal arch have and what does it give rise to?

A
  • Has a nerve supply, arterial supply and venous supply

- Each gives rise to various structure of the pharynx and larynx

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29
Q

What is the innervation of the 1st pharyngeal arch?

A

Mandibular nerve (V3 - 3rd branch of trigeminal nerve (CN5))

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30
Q

What is the innervation of the 2nd pharyngeal arch?

A

Facial nerve (CN7)

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31
Q

What is the innervation of the 3rd pharyngeal arch?

A

Glossopharyngeal nerve (CN9)

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32
Q

What is the innervation of the 4th pharyngeal arch?

A

Superior laryngeal nerve of vagus nerve (CN10)

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33
Q

What is the innervation of the 6th pharyngeal arch?

A

Recurrent laryngeal nerve of vagus nerve (CN10)

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34
Q

Which muscles form from the 1st pharyngeal arch and what are their functions?

A
  • Mastication (function)
  • Tensor tympani
  • Diagastric
  • Myolohyoid
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35
Q

Which muscles form from the 2nd pharyngeal arch and what are their functions?

A
  • Facial expression (function)
  • Stapedius
  • Stylohyoid
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36
Q

Which muscles form from the 3rd pharyngeal arch?

A

Stylopharygeus of the pharynx

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37
Q

Which muscles form from the 4th pharyngeal arch?

A

Cricothyroid

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38
Q

Which muscles form from the 6th pharyngeal arch?

A

All muscles of the larynx except the cricothyroid

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39
Q

Which bones are formed from the 1st pharyngeal arch?

A
  • Maxilla
  • Mandible
  • Incus
  • Malleus
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40
Q

Which bones are formed from the 2nd pharyngeal arch?

A
  • Stapes
  • Styloid
  • Lesser horn of hyoid cartilage
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41
Q

Which bones are formed from the 3rd pharyngeal arch?

A
  • Body and greater horn of hyoid cartilage
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42
Q

Which bones are formed from the 4th pharyngeal arch?

A
  • Thyroid cartilage

- Epiglottic cartilage

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43
Q

Which bones are formed from the 6th pharyngeal arch?

A
  • Cricoid cartilage
  • Arytenoid cartilages
  • Corniculate
  • Cuneiform cartilage
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44
Q

Describe the development of the oesophagus

A
  • At 4th week, at end of pharynx and start of oesophagus, at ventral wall of foregut - respiratory diverticulum (lung buds) appear
  • The tracheoesophageal septum develops and separates the lung buds from the dorsal part of the foregut
  • Foregut is now divided into the ventral respiratory primordial and the dorsal oesophagus
  • Oesophagus lengthens rapidly with descent of heart and lungs
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45
Q

What is the function of mesenteries?

A

Parts of the gut tube are suspended from the dorsal and ventral body walls by it

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46
Q

What are mesenteries?

A

Double layers or peritoneum that surround an organ and connect it to the body wall.

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47
Q

What is intraperitoneal?

A

When peritoneum surrounds an organ and connects it to the body wall

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48
Q

What is a retroperitoneal organ?

A

When an organ is sitting directly on the posterior abdominal wall and covered by peritoneum on its anterior surface only

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49
Q

What are ligaments?

A

Double layers of peritoneum which pass from one organ to another or from one organ the body wall

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50
Q

What is the function of mesenteries and ligaments?

A

Provide pathways for blood vessels, lymphatics and nerves to go to and come from the abdominal viscera

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51
Q

What is the embryological formation of the dorsal mesentery?

A

By the 5th week the lower part of the foregut, midgut and major part of the hindgut are suspended from the posterior abdominal wall by mesentery

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52
Q

Where does the dorsal mesentery extend from?

A

The lower part of the oesophagus to the cloacal region

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53
Q

Where is the ventral mesentery present?

A

Only in the region of the foregut - terminal part of the oesophagus, the stomach and the upper part of the duodenum

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54
Q

What mesenteries does the foregut have?

A

Ventral and dorsal

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55
Q

What mesenteries does the midgut have?

A

Dorsal

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56
Q

What mesenteries does the hindgut have?

A

Dorsal

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57
Q

What is the ventral mesentery derived from?

A

The septum transversum

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58
Q

What does the free lower margin contain?

A

The hepatic artery, portal vein and bile duct

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59
Q

Where does the liver develops

A
  • In the ventral mesentery

- Divides it into the lesser momentum and the falciform ligament

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60
Q

What is the embryological development of the stomach?

A
  • A spiral dilation in foregut at 4th week
  • Developing stomach is attached to body walls by dorsal and ventral mesenteries
  • Left & right vagus flank the sides of the stomach respectively
  • Dorsal wall grows faster, giving the greater & lesser curvatures of stomach
  • During 7th week, stomach rotates 90 degrees clockwise - produces a space behind stomach (lesser sac)
  • Greater curvature (embryo. dorsal) faces left & lesser curvature (embryo. ventral) faces right
  • In the 8th week, the stomach and duodenum rotate, pulling the end of the stomach upwards, to pull into a C-shape
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61
Q

Where is the left vagus positioned?

A

The anterior side of the stomach

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62
Q

Where is the right vagus positioned?

A

The posterior side of the stomach

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63
Q

What is the space posterior to the stomach?

A

The lesser sac

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64
Q

What is the space anterior to the stomach?

A

The greater sac

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65
Q

How do the greater and lesser sacs of the stomach communicate?

A

The epiploic foramen, near the hilium of the liver

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66
Q

How is swallowing initiated?

A

When pressure receptors in the walls of the pharynx are stimulated by food or drink, forced into the rear of the mouth by the tongue

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67
Q

How many segments does the pharynx have?

A

3 continuous segments shared between the gastro-intestinal and respiratory tracts

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68
Q

Which nerve innervates the nasopharynx?

A

Maxillary nerve (V2 - second branch of trigeminal nerve (CN5))

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69
Q

Which nerve innervates the oropharynx?

A

Glossopharyngeal nerve (CN9)

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70
Q

Which nerve innervates the laryngopharynx?

A

Vagus nerve (CN10)

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71
Q

What is the purpose of swallowing?

A

Food leaves the oral cavity and passes through the pharynx on its way to the oesophagus & stomach

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72
Q

What happens in stage I (voluntary) of swallowing?

A
  • Food is compressed against the roof of the mouth and pushed towards the oropharynx by the action of the tongue
  • The buccinator and supra hyoid muscles manipulate food during chewing. They also elevate the hyoid bone and flatten the floor of the mouth
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73
Q

What happens in stage II (involuntary) of swallowing?

A
  • Nasopharynx is closed off by soft palate by the palate muscles tensing and elevating it
  • Pharynx is shortened and widened (by longitudinal muscles) by elevation of hyoid bones by actions of muscles of the floor of the palate which lower mandible if hyoid is fixed or elevate hyoid bone & larynx is mandible is fixed
  • Impulses from swallowing centre inhibit respiration, raise larynx and close glottis - prevents food entering trachea
  • Tongue forces food further back into pharynx, food tilts the epiglottis backward to cover closed glottis (prevents aspiration)
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74
Q

What happens in stage III (involuntary) of swallowing?

A
  • Sequential contraction of constrictor muscle followed by depression of hyoid bone and pharynx
  • Pharyngeal constrictor muscles contract sequentially from above down to drive food into oesophagus
  • Depression of hyoid & pharynx caused by infra hyoid muscle of the neck, fix the hyoid bone enabling opening of mouth. Also depress hyoid bone and larynx
  • Luminal pressure in pharynx @ opening of oesophagus = atmospheric pressure
  • Upper oesophageal sphincter relaxes
  • Peristalsis occurs
  • The lower oesophageal sphincter opens and relaxes throughout swallowing
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75
Q

What is the muscular structure of the oesophagus?

A
  • Skeletal muscle in upper 1/3

- Smooth muscle in lower 2/3

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76
Q

What is the structure of the pharyngeal constrictor muscles?

A
  • 3 overlapping
  • Form posterior and lateral sides of pharynx
  • Innervated by vagus
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77
Q

What is the upper oesophageal sphincter?

A

Ring of skeletal muscle surrounds oesophagus below pharynx

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78
Q

What is the lower oesophageal sphincter?

A

A ring of smooth muscle surrounding the oesophagus in the last portion of the oesophagus

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79
Q

What is a gag reflex?

A

The reflex elevation of the pharynx - often followed by vomiting caused by irritation of the oropharynx (back of tongue)

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80
Q

What causes the gag reflex?

A

Reflex arc between glossopharyngeal (CN9) and the vagus (CN10) nerves

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81
Q

What are the functions of saliva?

A
  • Lubricant for mastication
  • Maintaining oral pH
  • Release digestive enzymes
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82
Q

What is the required oral pH and how is this maintained?

A
  • About 7.4

- Achieved by bicarbonate/carbonate buffer system

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83
Q

Where is salivary amylase release from and what for?

A
  • Parotid gland

- Starch digestion

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84
Q

What does serous secretion provide?

A

Alpha amylase for starch digestion

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85
Q

What does mucous secretion provide?

A

Mucins for lubrication of mucosal surfaces

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86
Q

What secretion does the parotid gland give?

A

Serous

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87
Q

What secretion does the submandibular gland give?

A

Mucous and serous

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88
Q

What secretion does the sublingual glands give?

A

Mucous and serous - mainly mucous

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89
Q

What secretion go minor glands give?

A

Predominantly mucous but some are serous

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90
Q

Give 5 factors affecting the composition & amount of saliva produced

A
  • Flow rate
  • Sleep cycle
  • Type and size of gland
  • Duration and type of stimulus
  • Usual e.g. diet, age drugs etc.
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91
Q

How does the mucosa act as a defence of the oral cavity?

A

Physical barrier

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92
Q

How does the salivary glands act as a defence of the oral cavity?

A

Saliva washes away food particles which bacteria or viruses may use as metabolic support

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93
Q

How does the palatine tonsils act as a defence of the oral cavity?

A

Acts as the ‘surveillance system’ for the immune system

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94
Q

How do glands act as a defence of the oral cavity?

A
  • Salivary glands surrounded by lymphatic system - has functional immune cells
  • Submandibular, sublingual & minor glands are always active
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95
Q

What are the two morphologically and distinct epithelial tissues of the salivary glands?

A
  • Acinar cells

- Ducts

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96
Q

What are acinar cells?

A

Functional unit of a salivary gland

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97
Q

What are the functions of ducts of the salivary glands?

A

Collect to form the large cut entering the mouth. equipped with channels and transporters in the apical and basolateral membrane enabling transport of fluid and electrolytes

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98
Q

What are the two types of acini?

A

Serous and mucous

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99
Q

What is the appearance of serous acini?

A
  • Dark staining nucleus
  • Nucleus in basal third
  • Small central duct
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100
Q

What does the serous acini secrete?

A

Water and alpha amylase

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101
Q

Where is serous acini mainly found?

A

Parotid gland

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102
Q

What is the appearance of mucous acini?

A
  • Pale staining ‘foamy’
  • Nucleus at base
  • Large central duct
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103
Q

What does the mucous acini secrete?

A

Mucous (water and glycoproteins)

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104
Q

Where is mucous acini found?

A

In submandibular & sublingual glands

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105
Q

How are interlobular ducts divided?

A

Into intercalated and striated

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106
Q

What is the structure of intercalated interlobular ducts?

A

Short narrow duct segments with cuboidal cells that connect acini to larger striated ducts

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107
Q

What is the structure of striated interlobular ducts?

A
  • Striated like a thick lawn
  • Major site for reabsorption of NaCl
  • Appear striated at basal end
  • Basal membrane is highly folded into microvilli (giving striated appearance) for active transport of bicarbonate against conc. gradient
  • Microvilli are filled with mitochondria to facilitate the active transport
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108
Q

What is significant about the excretory ducts of salivary glands?

A

Not just a plumbing system, they modify the electrolyte composition of the saliva

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109
Q

What do the excretory ducts of salivary glands secrete and reabsorb?

A
  • Secrete potassium and bicarbonate

- Reabsorb sodium and chloride

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110
Q

What do epithelium of ducts of the salivary glands do?

A

Reabsorb water so final saliva is hypotonic (has less water so have a higher conc. of solutes)

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111
Q

What are the three major pairs of salivary glands?

A

Parotid, submandibular and sublingual

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112
Q

What percentage of salivary flow do the three major pairs of salivary glands contribute to?

A

80%

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113
Q

Minor salivary glands contribute what percent of salivary flow?

A

20%

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114
Q

Where are minor salivary glands found?

A

In submucosa or the oral mucosa of the lips, cheeks, hard and soft palate and the tongue

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115
Q

What is the structure of the parotid gland?

A
  • Superficial triangular outline between: zygomatic arch, sternocleidomastoid & ramus of mandible
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116
Q

What is the structure of the parotid duct?

A
  • Crosser masseter muscle and pierces through the buccinator muscle where it enters the oral cavity near the second upper molar
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117
Q

What is the innervation of the parotid gland?

A
  • Sympathetic sensory innervation (inhibits secretion) is provided by auriculo-temporal nerve (branch of mandibular nerve - division of trigeminal nerve (CN5))
  • Parasympathetic innervation supplied by glossopharyngeal nerve (CN9) - stimulates secretion
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118
Q

What structures pass through the parotid gland?

A
  • External carotid artery
  • Retromandibular vein
  • Facial nerve (CN7)
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119
Q

What is significant about the parotid capsule?

A

Is very tough

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120
Q

What is the structure of submandibular glands?

A

Two lobes separated by mylohyoid muscle - larger superficial lobe and a smaller deep lobe in the floor of the mouth

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121
Q

What is the pathway of the submandibular duct?

A

Begins in the superficial lobe, wraps around the free posterior border of the mylohyoid, then runs along the floor of the mouth and empties into the oral cavity at the sublingual papillae - located more posterior than the sublingual gland

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122
Q

What is the structure of the submandibular gland?

A
  • Mixed gland with serous and mucous acini
  • Some serous acini are arranged in crescent shaped groups of glandular cells at the bases of mucous acini refereed to as serious demilunes
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123
Q

What is the innervation of the submandibular gland?

A
  • Parasympathetic innervation is supplied by the chorda tympani branch of the facial nerve (CN7)
  • Sympathetic innervation is supplied via the lingual nerve which is derived from the facial nerve (CN7)
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124
Q

Where are the sublingual glands located?

A
  • More anteriorly than the submandibular glands
  • Located in the floor of the mouth between mylohyoid muscles and oral mucosa of floor of mouth
  • Very close to submandibular gland
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125
Q

How is saliva transmitted from the sublingual gland?

A

Via the submandibular duct and/or small ducts that pierce oral mucosa floor of mouth

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126
Q

How big is the sublingual gland?

A

Much smaller than submandibular - but size is variable

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127
Q

What is the innervation of the sublingual gland?

A
  • Parasympathetic innervation is supplied by the chorda tympani branch of facial nerve (CN7)
  • Sympathetic innervation is supplied via the lingual nerve which is derived from the facial nerve (CN7)
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128
Q

Where are the minor salivary glands found?

A
  • Buccal labial, palatal & lingual regions
  • Superior pole of tonsils (Weber’s glands)
  • Tonsillar pillars & at the base of the tongue (von Ebner’s glands - underlying circumvallate papillae)
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129
Q

Are minor salivary glands mucous or serous?

A

All mucous except serous glands of von Ebner

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130
Q

What is the duct system of minor salivary glands?

A

Lack a branching network of draining ducts so each salivary unit has its own simple duct

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131
Q

What is the stimulation patterns of the minor salivary glands?

A
  • Parasympathetic = stimulates salivary secretion

- Sympathetic = inhibits salivary secretion

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132
Q

What are the most common causes of xerostomia (dry mouth)?

A

Medication and irradiation for head and neck cancers

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133
Q

What causes obstructions of salivary ducts and where is it most common?

A
  • Saliva contains calcium and phosphate ions that can form salivary calculi (stones)
  • Most common in submandibular gland - block duct at the bend around the round mylohyoid or at exit of sublingual papillae
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134
Q

What causes infection of salivary ducts?

A
  • Secondary to obstruction

- Mumps

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135
Q

What causes degeneration of salivary ducts?

A

Complication of radiotherapy to head and neck for cancer treatment

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136
Q

What are the effects of salivary gland dysfunction?

A
  • Salivary output falls below 50% = xerostomia
  • Low lubrication - oral function becomes difficult
  • Low natural oral hygiene - poor pH control = accumulation of plaque = dental caries or increases incidence of opportunistic infections (especially fungal)
137
Q

What are the 6 main functions of the stomach?

A
  • Dissolve and continue digestion
  • Kill microbes
  • Secrete intrinsic factor
  • Activate proteases
  • Lubrication
  • Mucosal protection
138
Q

What are the key cell types of the stomach?

A

Mucous, parietal, chief, ECL, G and D

139
Q

What is the function of mucous cells of the stomach?

A
  • Produce mucous

- At entrance to gland

140
Q

What is the function of parietal cells of the stomach?

A
  • Produce gastric acid

- Produce intrinsic factor

141
Q

What is the function of chief cells of the stomach?

A

Produce pepsinogen

142
Q

What is the function of the enterochromaffin-like (ECL) cells of the stomach?

A

Releases histamine

143
Q

What is the function of G cells of the stomach?

A

Release gastrin

144
Q

What is the function of D cells of the stomach?

A

Release somatostatin

145
Q

What does the epithelial layer of the stomach invaginate into?

A

The mucosa, forming many tubular glands

146
Q

What do glands in the thin walled upper portions of the body of the stomach secrete?

A
  • Mucous
  • Hydrochloric acid (parietal cells)
  • Enzyme precursor pepsinogen (chief cells)
147
Q

What is the structure of the lower portion of the stomach (antrum)?

A

Has a much thicker layer of smooth muscle

148
Q

What is the function of the lower portion of the stomach (antrum)?

A

Responsible for mixing and grinding the stomach contents

149
Q

What do the glands of the lower portion of the stomach (antrum) secrete?

A
  • Little amounts of acid

- Contain the endocrine cells that secrete the hormone gastrin (G cells)

150
Q

Where does gastric acid secretion happen from?

A

Occurs from parietal cells

151
Q

What is gastric acid secretion dependent on?

A
  • Energy dependent

- Neurohormonal regualtion

152
Q

Briefly describe the process of gastric acid secretion

A
  • Water in the parietal cell breaks down into OH- and H+
  • CO2 & H2O from resp. is converted into bicarbonate by carbonic anhydrase
  • Rapidly dissociates
  • H ions are pumped into stomach lumen by H/K ATPase pumps
  • The K ions pumped into parietal cells can diffuse back into stomach by K channels on parietal cells
  • HCO3- is secreted into capillary for exchange of Cl- ions
  • Cl- ions enter stomach by diffusing through Cl- channels in parietal cell
  • In stomach, H+ and Cl- react to make HCl
153
Q

When does the cephalic phase of gastric acid secretion occur?

A

During a meal

154
Q

What nervous system is the cephalic phase of gastric acid secretion initiated by and what external factors is it initiated by?

A
  • Parasympathetic nervous system

- Sight, smell, taste of food and chewing

155
Q

What happens in the cephalic phase of gastric acid secretion?

A
  • Acetyl choline released
  • ACh acts indirectly on parietal cells, releasing gastrin and histamine
  • Both increase number of H/K ATPase pumps on parietal cells
  • Increased acid production
156
Q

What happens in the gastric phase of gastric acid secretion?

A
  • Initiated by: gastric distension & presence of peptides/AAs
  • Gastrin released - acts directly on parietal cells
  • Gastric triggers release of histamine - acts directly on parietal cells
  • Gastrin and histamine increase number of H/K ATPase pumps on parietal cell
157
Q

When does the gastric phase of gastric acid secretion begin?

A

Once food has reached the stomach

158
Q

What is the significance of protein in the stomach?

A
  • Direct stimulus for gastrin release
  • Act as a buffer thereby reducing the amount of H ions = increase pH, resulting in decreased secretion of somatostatin
  • More parietal cell activity
  • More acid production
159
Q

What is the gastric phase of turning OFF gastric acid secretion?

A
  • Low luminal pH directly inhibits gastrin, so indirectly inhibits histamine release
  • Low pH stimulates somatostatin release which inhibits parietal cell activity
160
Q

What is the intestinal phase of turning OFF gastric acid secretion?

A
  • Initiated by duodenal distension, low pH, hypertonic solutions, presence of AA & FA
  • All trigger release of enterogastrones such as a secretin (inhibits gastrin release & promotes somatostatin release) & cholecystokinin
  • Also trigger short and long neural pathways which reduce ACh release
161
Q

What is regulation of gastric acid secretion controlled by?

A

Brain, stomach and duodenum

162
Q

What are the substances involved in gastric acid secretion?

A
  • 1 parasympathetic neurotransmitter - ACh (+)
  • 1 hormones - gastrin (+)
  • 2 paracrine (produced in stomach) - histamine (+) & somatostatin (+)
  • 2 key enterogastrones - secretin (-) & CCK (-)
163
Q

What is an ulcer?

A

A breach in a mucosal surface

164
Q

Give 4 causes of peptic ulcers

A
  • Helicobacter pylori infection
  • Drugs e.g. NSAIDS e.g. aspirin and ibuprofen
  • Chemical irritants
  • Gastrinoma
165
Q

Explain how Helicobacter pylori infection can cause a peptic ulcer

A
  • Lives in gastric mucus
  • Secretes urease, splitting urea into CO2 and ammonia
  • Ammonium forms from ammonia and H+
  • Ammonium is toxic to gastric mucosa, resulting in less mucous produced
  • Secreted proteases, phospholipase begin attacking the gastric epithelium further reducing mucous production
  • Results in inflammatory response and less mucosal defence
166
Q

How can a Helicobacter pylori infection be treated?

A
  • Proton pump inhibitor

- Antibiotics

167
Q

Explain how certain drugs can cause a peptic ulcer

A
  • Mucous secretion is stimulated by prostaglandins
  • Cyclo-oxygenase 1 needed for synthesis
  • NSAIDs inhibit cycle-oxygenase 1
  • Thus reduced mucosal defence
168
Q

How can a peptic ulcer caused by drugs be treated?

A

Use prostaglandin analogues (mimic the effect of prostaglandins)

169
Q

Explain how chemical irritants can cause a peptic ulcer

A

Duodenal-gastric reflux causes bile to enter stomach, alkaline bile strips away gastric mucous layer of stomach resulting in reduced mucosal defence

170
Q

Explain how gastrinomas can cause a peptic ulcer

A
  • Rare tumours of parietal cells
  • Excessive gastrin release
  • Increase in gastric acid
  • Increased attack on gastric mucosa = ulcer
171
Q

What are the synthetic ways to reduce gastric acid secretion?

A
  • Proton pump inhibitors

- H2 receptor agonists

172
Q

How do proton pump inhibitors work?

A

Inhibits pumps pumping hydrogen ions into stomach lumen, they only block pumps, not the activators e.g. gastrin

173
Q

How do H2 receptor agonists work?

A

Block receptors for histamine thereby reducing acid secretion

174
Q

What are the 4 protective mechanism of the gastric mucosa?

A
  • Alkaline mucus on luminal surface
  • Tight junctions between epithelial cells
  • Replacement of damaged cells - stem cells at the base of pits to produce new cells
  • Feedback loops
175
Q

Why is pepsin secrete as the inactive pepsinogen?

A

To prevent it digesting the chief cells and the rest of the body?

176
Q

How is pepsinogen is mediated?

A

By input from the enteric nervous system via neurotransmitter ACh (parasympathetic)

177
Q

What does secretion of pepsinogen parallel with?

A

HCl secretion

178
Q

What happens when pepsinogen is released into the stomach lumen?

A

The low pH (generated by HCl) of the stomach activates a rapid autocatalytic process in which pepsin is produced from pepsinogen

179
Q

How is more pepsin produced after the initial batch?

A

It can aid the cleavage of pepsinogen (positive feedback)

180
Q

What can irreversible inactive pepsin?

A

The release of bicarbonate into the duodenum

181
Q

What is the role of pepsin in protein digestion?

A
  • Accelerates protein digestion
  • Breaks down collagen in meat, thereby helping shred meat resulting in smaller pieces with greater surface area for digestion
  • Normally accounts for 20% of total protein digestion
182
Q

What would happen if the stomach is removed in terms of vitamin B12?

A
  • No vitamin B12 absorption in the small intestine

- Since stomach parietal cells produce intrinsic factor (essential for B12 absorption in small intestine)

183
Q

What is the volume of the stomach in its various states?

A
  • Empty stomach has volume of around 50ml

- When eating it can accommodate roughly 1.5 with little increase in luminal pressure

184
Q

How can the volume of the stomach increase with only little increase in luminal pressure?

A

By the smooth muscles in the body and fundus receptive relaxation

185
Q

Describe the process of receptive relaxation

A
  • Mediated by parasympathetic nervous system acting on enteric nerve plexuses with coordination by afferent input from the stomach via the vagus nerve and by the swallowing centre in brain
  • Nitric oxide and serotonin released by the enteric nerves mediate relaxation
  • Acetyl choline activates parietal & chief cells & initiates receptive relaxation
186
Q

How does peristalsis occur in the stomach?

A
  • Each wave begins in the body of the stomach, producing a ripple as it goes towards the antrum
  • The initial contraction in the body is too weak to mix contents with acid and pepsin
  • There is more powerful contractions in the antrum which enables better mixing
  • The pyloric sphincter closes as peristaltic waves reaches it
  • Every time the wave reaches the sphincter, little chyme enters the duodenum
  • The antral contents are forced back towards meaning more mixing and digestion
187
Q

Where is the pyloric sphincter found and what is its structure?

A

A ring of smooth muscle and connective tissue between the atrium and duodenum

188
Q

What is chyme and what is it the end result of?

A
  • Smooth, orange coloured liquid

- The end result of stomach digestion and peristalsis

189
Q

What determines the frequency of peristaltic waves of the stomach?

A

Pacemaker cells (interstitial cells of Cajal) in the muscular propria (longitudinal smooth muscle layer)

190
Q

How frequent are the peristaltic waves of the stomach?

A

3 per minute

191
Q

How do the pacemaker cells control the rate of peristalsis of the stomach?

A
  • The depolarisation waves are transmitted through gap junctions to adjacent
  • These cells don’t cause significant contraction in the empty stomach
192
Q

When does the strength of peristaltic contraction vary?

A
  • Excitatory neurotransmitters and hormones further depolarise membranes
  • Action potentials are generated when the threshold is reached
  • The interstitial cells of Cajal are active all the time, but the action potential threshold for muscle contraction can be altered by the enteric nervous system
193
Q

What factors increase the strength of peristaltic contractions?

A
  • Gastrin

- Gastric distension (mediated by mechanoreceptors)

194
Q

What factors decrease the strength of peristaltic contractions?

A
  • Duodenal distension
  • Increase in duodenal fat
  • Increase in duodenal osmolarity
  • Decrease in duodenal pH
  • Increase in sympathetic nervous system stimulation
  • Decrease in parasympathetic nervous system stimulation
195
Q

What causes dumping syndrome?

A
  • Due to the capacity of the stomach being greater than that of the duodenum
  • Overfilling of the duodenum by a hypertonic solution
196
Q

What happens as gastric contents enter the duodenum?

A

Duodenal pH falls

197
Q

What regulates gastric emptying?

A

The same things which regulates parietal and chief cells

198
Q

What is gastroparesis?

A

Delayed gastric emptying - causes matter in the stomach to rot and smell and become a similar appearance to faeces

199
Q

What can cause gastroparesis?

A
  • Not known (idiopathic)
  • Autonomic neuropathies
  • Abdominal surgery
  • Parkinson’s
  • MS
200
Q

What are the symptoms of gastroparesis?

A
  • Nausea
  • Early satiety
  • Vomiting undigested food
  • GORD
  • Abdominal pain/bloating
  • Anorexia
201
Q

Give 3 examples of drugs which can cause gastroparesis

A
  • H2 receptor antagonists
  • Proton pump inhibitors
  • Opioid analgesics
202
Q

What is the most abundant substance in chyme?

A

Water

203
Q

Where does the majority of water reabsorption occur?

A

In the small intestine

204
Q

Which part of the small intestine reabsorbs the most water?

A

The jejunum

205
Q

Why is less water reabsorbed in the stomach?

A
  • Has a much smaller surface area available for diffusion

- Lacks the solute-absorbing mechanisms the create the osmotic-gradient

206
Q

What is the main characteristic of the epithelial membranes of the small intestine?

A
  • Very permeable to water

- Net water diffusion occurs whenever a water conc. difference is established by the active transport of solutes

207
Q

What is the most abundant solute in chyme and why is this relevant?

A
  • Na - accounts for most of the actively transported solutes because it constitutes the most abundant solute in chyme
  • Actively transported into the lumen in cell membranes of ileum and jejunum
208
Q

What is luminal membrane transport of sodium in the ileum/jejunum coupled with?

A

Glucose, amino acids or other substances

209
Q

What are the contents of the colon like in terms of water?

A

Iso-osmotic (conc. in lumen = blood)

210
Q

How is potassium reabsorbed in the colon?

A
  • By passive diffusion

- Determined by the potential difference between the lumen and intestinal capillaries

211
Q

How is chloride reabsorbed in the colon?

A
  • Actively reabsorbed in exchange for bicarbonate

- Results in intestinal contents becoming more alkaline

212
Q

What is the absorptive state (when the body undergoes in providing energy for cellular activities)?

A
  • During which ingested nutrients enter the blood from the GI tract
  • During this state, some of the ingested nutrients provide the energy requirements of the body and the rest is added to the body’s energy stores
213
Q

What is the post-absorptive state (when the body undergoes in providing energy for cellular activities)?

A
  • During which the GI tract is empty of nutrients and the body’s own stores must supply energy
214
Q

What is the average daily intake of lipids and in what form?

A
  • 70-100 grams per day

- In the form of triglycerides

215
Q

What are the 3 main important fatty acids we absorb?

A
  • Palmitic
  • Stearic
  • Oleic acid
216
Q

What is a triglyceride?

A

A glycerol molecule with 3 fatty acids attached

217
Q

Where does fat digestion mainly occur?

A
  • To a limited extent in the mouth and stomach

- Predominantly occurs in the small intestine

218
Q

Where is lipase synthesised?

A

Pancreas

219
Q

How does the enzyme lipase work?

A

Catalyses the splitting of bond linking fatty acids, producing two free fatty acids and monoglyceride

220
Q

How do the lipids in ingested food sit in the stomach?

A
  • Insoluble in water

- Aggregate into large lipid droplets in upper portion of the stomach

221
Q

How are large lipid droplets in the stomach converted into smaller droplets?

A

By the process of emulsification

222
Q

What are the two things which emulsification requires?

A
  • Mechanical disruption

- An emulsifying agent

223
Q

How does mechanical disruption aid emulsification?

A
  • Provided by the motility of the GI tract
  • In the lower portion of stomach and small intestine
  • Grinds and mixes luminal contents
224
Q

How does an emulsifying agent aid emulsification?

A
  • Due to phospholipids being both hydrophilic & phobic (amphipathic)
  • Bile salts are also amphipathic (formed from cholesterol in the liver)
  • Non-polar portion of the phospholipids & bile salts associated with non-polar interior of lipid droplet
  • Polar portions are exposed at water surface
  • They repel other lipid droplets - prevents formation of large droplets
225
Q

What impact does the emulsifying agent have for lipase and how is this overcome?

A
  • Impairs the accessibility of the droplet for lipase
  • Pancreas secretes collapse which binds to the droplet and lipase
  • The small droplets are further converted into micelles (with fat-soluble vitamins, bile salts, and fats)
226
Q

What happens with the fatty acids and monoglycerides which are soluble in water?

A

Able to diffuse across the lipid portion of the luminal plasma membranes of epithelial cells of the small. intestine

227
Q

What causes the continuous breaking down and reforming of micelles?

A

Due to them being in equilibrium with the free fatty acids and monoglycerides

228
Q

What can micelles also be known as?

A

The ‘holding station’ for lipids

229
Q

What happens to the fatty acids and monoglycerides in the small intestine?

A
  • Resynthesized into triglycerides in the sER where the enzymes are located
  • This decreases cytosolic conc. of free fatty acids & monoglycerides
  • Maintains a diffusion gradient into the cell from intestinal lumen
230
Q

What happens to the triglycerides once they are in the cells of the small intestine?

A
  • Aggregates into small droplets coated by proteins
  • Fat droplets pinch off the ER in vesicles, where they are process through the Golgi and modified into chylomicrons, fuse with the plasma membrane and enter the interstitial fluid via exocytosis
  • Chylomicrons then enter the lacteals
  • The lymph from the small intestines (where chylomicrons entered) empties into he systematic veins
231
Q

What do chylomicrons have?

A

Triglycerides, phospholipids, cholesterol and fat-soluble vitamins

232
Q

What are lacteals?

A

Lymphatic vessels in the intestinal villi

233
Q

Why do chylomicrons enter the lacteals instead of the bloodstream?

A
  • Can’t enter the capillaries due to the basement membrane providing a barrier to diffusion
  • Lacteals have large pores between their endothelial cells which enable the chylomicrons to pass through
234
Q

What happens to the chylomicrons once they have entered circulation?

A
  • Has a similar process to that of VLDL’s in the liver
  • The fatty acids are release, mainly within adipose, by the action of endothelial lipoprotein lipase
  • They diffuse into adipocytes and combine with alpha-glycerol phosphate to form triglycerides
235
Q

Why is glucose essential for triglyceride synthesis in adipocytes?

A
  • Adipocytes don’t have the enzyme for phosphorylation of glycerol to alpha glycerol
  • Glycerol can only be produced by reduction from glycolysis
236
Q

What are the three main sources of fatty acids for triglyceride synthesis?

A
  • Glucose that enters adipose tissue and is broken down to provide building blocks for the synthesis of fatty acids
  • Glucose that is used in the liver to form VLDL triglycerides, which are transported in the blood and taken up by adipocytes
  • Ingested triglycerides transported in the blood by chylomicrons and taken up by adipocytes
  • 2&3 require lipoprotein lipase
237
Q

How are fat-soluble vitamins (A, D, E & K) absorbed?

A

They follow the pathway for fat absorption in the ileum

238
Q

How are water-soluble vitamins (B & C - not B12) absorbed?

A
  • By diffusion or mediated transport in the jejunum
239
Q

How is vitamin B12 absorbed?

A
  • Binds to intrinsic factor (secreted by the parietal cells of stomach)
  • Binds to specific sites on epithelial cells in the lower portion of the ileum where B12 is absorbed via endocytosis
240
Q

What is vitamin B12 needed for?

A

Erythrocytes formation

241
Q

Where does the digestion and absorption of protein mainly happen?

A

The duodenum

242
Q

How many of the 20 amino acids can’t we manufacture?

A

8 (these are the essential amino acids)

243
Q

How do amino acids exist in terms of isomers?

A
  • Optical isomers

- Only the L-forms are found in the proteins we use

244
Q

What does the eventual amino acid structure end up being?

A

Zwitterion - Having both positive and negative groups on the same molecule

245
Q

What is the basic building block of a protein?

A

The peptide bond - CONH (HN-C=O)

246
Q

What is the primary structure of the amino acids?

A
  • Starts with a sequence of amino acids

- Various stages of folding occur initiated by the electrostatic forces present on different parts of the protein

247
Q

Where does digestion of proteins begin?

A

In the stomach, where the enzyme pepsin (chief cells release pepsinogen which is rapidly activated by the low luminal pH) cleaves some of the peptide linkages - forming peptide fragments

248
Q

Where is pepsinogen I found?

A

Only in the HCl secreting region (mainly the body) of the stomach

249
Q

Where is pepsinogen II found?

A

The pyloric region

250
Q

What is the function of pepsins?

A

Hydrolyses the bonds between an aromatic amino acid and a second amino acid

251
Q

Why does the action of pepsins end in the stomach?

A

Due to their optimum pH being around 1.6 - 3.2, which is too low outside the stomach

252
Q

What is the pH of the duodenal cap?

A

Around 2-4

253
Q

What is the pH in the majority of the duodenum?

A

Around 6.5

254
Q

What happens in the small intestine in regards to protein digestion?

A
  • The smaller peptides are further fragmented by enzymes produced in the pancreas (endopeptidases and exopeptidases)
  • Some di and tripeptides are absorbed and broken down by intracellular peptidases meaning final digestion happens in the intestinal lumen, brush border and within the cell
255
Q

Name the 3 locations where the final digestion of peptides occurs

A
  • The intestinal lumen
  • The brush border
  • Within the cells
256
Q

Name 3 examples of endopeptidases

A
  • Trypsin
  • Chymotrypsin
  • Elastase
257
Q

Give 2 examples of exopeptidases

A
  • Carboxyl dipeptidases

- The amino peptidases of the brush border

258
Q

Where does the digestion and absorption of carbohydrates occur?

A

Digested and absorbed in the first 20% of small intestine (the duodenum)

259
Q

What is a monosaccharide and name some examples

A
  • Single sugars

- Glucose, fructose and galactose

260
Q

What is a oligosaccharide and give 2 examples

A
  • Several sugar molecules

- Lactose and sucrose (also both disaccharides)

261
Q

What is the structure of lactose?

A
  • Forms beta linkages since the OH groups lies above the place of the molecules
  • Requires a different enzyme than sucrose to be broke down
  • Lactose intolerance - not enough beta enzymes
262
Q

What is a polysaccharide and give 2 examples

A
  • Many sugar containing molecules

- Starch and glycogen

263
Q

How do sugar molecules exist in terms of digestion?

A
  • Optical isomers

- Only the D-isomers are utilised in metabolism

264
Q

What is the structure of glycogen?

A
  • The principle dietary polysaccharide from animal sources
  • Polymer of glucose molecules which are joined by alpha 1-4 glycosidic linkages & some chain branching by alpha 1-6 glycosidic linkages
265
Q

What is the structure of starch?

A
  • Majority alpha 1-4 glycosidic linkages

- Some chain branching by alpha 1-6 linkages but less than glycogen

266
Q

What is the structure of cellulose?

A

Only beta 1-4 glycosidic linkages

267
Q

What is starch first degraded into and what by in digestion?

A
  • By ptyalin (the alpha amylase of saliva)

- In the mouth - only a small fraction of digestion happens here

268
Q

What is the optimum pH of saliva digestion in the mouth and what terminates it?

A
  • pH 6.7

- Terminated by gastric acidity of the stomach

269
Q

What happens to the digestion of starch once in the small intestine?

A
  • Pancreatic alpha amylase catalyses alpha 1-4 linkages
  • End products of this digestion: maltose, maltotriose, large polymers of glucose with alpha 1-4 linkages, branched polymers (alpha-limit dextrin)
  • These are further digested by the oligosaccharidases located at the outer portion of the membrane of the microvilli
  • They are broken down into monosaccharides
270
Q

Name 4 oligosaccharidases

A
  • Maltase
  • Lactase
  • Sucrase
  • Alpha-limit dextrinase
271
Q

How are hexoses and pentoses absorbed in the body?

A

Rapidly absorbed across the intestinal mucosa, enter the capillaries which drain into the hepatic portal vein

272
Q

How is glucose specifically absorbed in the body?

A
  • By symport with Na ions

- A high Na conc. at the mucosal surface facilitates glucose absorption

273
Q

How is galactose specifically absorbed in the body?

A
  • By symport with Na ions

- A high Na conc. at the mucosal surface facilitates glucose absorption

274
Q

How is fructose specifically absorbed in the body?

A

Absorbed by facilitated diffusion via a glucose transporter

275
Q

What happens to monosaccharides once they have been absorbed into the epithelial cells of the duodenum?

A
  • Leave the epithelial cells and enter the interstitial fluid by facilitated diffusion
  • Done by a glucose transporter protein in the basolateral membrane of the epithelial cell
  • The monosaccharide diffuses into the blood by the capillary pores
276
Q

What happens to the monosaccharides after they have entered the hepatic portal vein and thus the liver?

A
  • Liver converts them into glucose
  • Skeletal muscle breaks down glucose in the absorptive phase and converts glucose to glycogen for future
  • The liver converts glucose into glycogen for future
  • Can also convert into alpha-glycerol phosphate and FA to synthesise triglycerides
277
Q

What is the main consumer of glucose?

A

Skeletal muscle

278
Q

What component makes up most of the body?

A

Skeletal muscle

279
Q

What is the uptake of glucose in the absorptive state?

A

There is a net uptake of glucose by the liver

280
Q

What happens to most of the fat synthesise from glucose in the liver?

A
  • Packaged along with specific proteins into molecular aggregates of lipids and proteins (lipoproteins)
  • Secreted by hepatocytes and enter blood
281
Q

Why are very-low-density lipoprotein’s called so?

A
  • Contain more fat than protein

- Fat is less dense than protein

282
Q

What is the process of synthesis of VLDL’s in hepatocytes?

A

By a similar process of that of chylomicrons by intestinal mucosa cells

283
Q

How do VLDL’s enter the bloodstream?

A
  • Due to their large size, they don’t penetrate capillary walls
  • Their triglycerides are hydrolysed to monoglycerides and fattyacids by lipoprotein lipase
284
Q

Where is lipoprotein lipase located?

A

On the blood-facing surface of capillary endothelial cells, especially in adipose tissues

285
Q

What happens to the fatty acids which are generated by the action of lipoprotein lipase?

A
  • In adipose-tissue capillaries, they diffuse from the capillaries to adipocytes
  • They combine with alpha-glycerol phosphate to from triglycerides again
286
Q

What happens to most of the fatty acids in VLDL triglycerides from glucose in the liver?

A

End up being stored in triglyceride in adipose tissue

287
Q

What could happen to the monoglycerides produced by the breakdown of triglycerides by lipoprotein lipase in the blood?

A
  • Taken up by adipocytes where enzymes can reattach fatty acids to form a triglyceride
  • Travel via the blood to the liver to be metabolised
288
Q

Where can amino acids, triglycerides and glucose be converted into storage molecules?

A

The liver, then go to the respective storage areas:

  • Adipose tissue for fats
  • Muscle for glycogen
289
Q

What does BMI stand for?

A

Body Mass Index

290
Q

What is the equation to calculate BMI?

A

Weight (kg)/height^2 (m)

291
Q

What is the result of a BMI >30?

A

Obese

292
Q

What is the result of a BMI <18.5?

A

Underweight

293
Q

What is the result of a BMI >25?

A

Overweight

294
Q

What is the result of a BMI 18.5-25?

A

Normal

295
Q

How long can glycogen stores be sufficient for?

A

For 12 hours in an adult male

296
Q

How long can lipid stores be sufficient for?

A

3 months

297
Q

When does tissue protein become a viable source of energy?

A

In times of prolonged starvation

298
Q

Do different tissue have different energy requirements?

A

Yes

299
Q

What fuels are used by the brain?

A

Glucose and ketone bodies

300
Q

What fuels are used by muscle?

A
  • Glucose
  • Ketone bodies (in starvation)
  • Triacyglycerol
  • Branched-chain amino acids
301
Q

What fuels are used by the liver?

A
  • Amino acids
  • Fatty acids (including short chain acids)
  • Glucose
  • Alcohol
302
Q

Where are ketone bodies produced?

A

The liver

303
Q

Why can’t the liver use ketone bodies as a fuel source?

A

As they don’t have the enzyme thiolase

304
Q

What fuels are used by the kidney?

A
  • Glucose and ketone bodies (cortex)

- Only glucose (medulla0

305
Q

What fuels are used by the small intestine?

A

Ketone bodies (mainly in starvation) and glutamine (amino acid)

306
Q

What fuels are used by the large intestine?

A

Short chain fatty acids and glutamine

307
Q

What is basal metabolic rate (BMR)?

A

The minimum amount of energy require to keep the body alive

308
Q

How is BMR measured?

A

By O2 consumption is a person who is awake, restful and fasting for 12 hours

309
Q

What happens to BMR with age?

A

Decreases

310
Q

What are the measurements for BMR?

A

kcal expended/hr/m^2

311
Q

What are the functions of vitamin A?

A
  • Cellular growth & differentiation
  • Process of vision (retinal pigments)
  • Healthy skin
  • Reproduction
  • Embryonic development
  • Maintenance of bodies mucus membranes
  • Used in lymphocyte production - immune system
312
Q

Is vitamin A fat or water soluble?

A

Fat

313
Q

Where is vitamin A stored?

A

In Ito cells in the space of Disse of the liver

314
Q

What are the sources of vitamin A?

A
  • Liver
  • Dairy products
  • Oily fish
  • Margarine
315
Q

What may a deficiency of vitamin A cause?

A
  • Night blindness
  • Xerophthalmia (eye fails to produce tears)
  • Growth retardation
  • Keratinisation of epithelia
  • Impaired hearing, taste & smell
  • Increased susceptibility to infection
316
Q

Is vitamin C fat or water soluble?

A

Water

317
Q

What are the functions of vitamin C?

A
  • Synthesis of collagen, neurotransmitters & carnitine (used in beta-oxidation)
  • Antioxidant ability - can donate electrons to radical O2 compounds
  • Absorption of non-haem (plant based) iron
318
Q

What are the sources of vitamin C?

A
  • Citrus fruits
  • Green leafy vegetables
  • Potatoes
  • Kidney
319
Q

What may a deficiency in vitamin C cause?

A
  • Initial signs are non-specific
  • Weakness
  • Bleeding gums
  • Hyperkeratosis (thickening of outer layer of skin)
  • 50 - 100 days without Vitamin C = signs of scurvy
320
Q

Is vitamin B fat or water soluble?

A

Water

321
Q

What is the function of vitamin B?

A

Important in cell metabolism and energy production

322
Q

What is the main B vitamin and where is it found?

A

Fish, poultry, meat and eggs

323
Q

What does B12 deficiency result in?

A

Less erythrocyte formation - pernicious anaemia

324
Q

Where is vitamin B12 absorbed?

A

The terminal ileum

325
Q

What is required for vitamin B12 absorption?

A

Intrinsic factor - produced by the parietal cells of the stomach

326
Q

Is vitamin D fat or water soluble?

A

Fat

327
Q

How long would it take to become deficient in vitamin D?

A

3-4 months

328
Q

How is vitamin D3 formed?

A

By the action of ultra-violet (UV) radiation from sunlight on a cholesterol derivative in the skin

329
Q

How is vitamin D2 formed?

A

Derived from plants

330
Q

How does vitamin D become activated?

A
  • Its metabolised by the addition of hydroxyl groups
  • First in the liver and then in certain kidney cells
  • The end result is 1,25-dihydroxyvitamin D (1,25-(OH)2D) - the active hormonal form of vitamin D
331
Q

What is the function of 1,25-(OH)2D?

A

To stimulate intestinal absorption of Ca and phosphate

332
Q

What is a major consequence of vitamin D deficiency?

A
  • Decrease intestinal Ca absorption resulting in decreased plasma Ca
  • This is detected via a plasma membrane Ca receptor in parathyroid glands
  • Results in the release of parathyroid hormone to increase Ca
333
Q

What are the effects of the release of parathyroid hormone?

A
  1. It directly increases the resorption of BONE by osteoclasts, which causes Ca2+ & phosphate ions to move from bone into the extracellular fluid - this can lead to a decrease in bone mass
  2. It directly stimulates the formation of 1,25-dihydroxyvitamin D which then increases intestinal absorption of Ca2+ & phosphate ions
  3. It directly increases Ca2+ reabsorption in the kidneys, thereby decreasing urinary Ca2+ excretion
  4. It directly decreases the reabsorption of phosphate ions in the kidneys thereby increasing its excretion in the urine - this keeps plasma phosphate ions from increasing when PTH causes an increased release of both Ca2+ & phosphate ions from the bone
334
Q

What is the main function of vitamin E?

A

As an antioxidant

335
Q

Is vitamin E fat or water soluble?

A

Fat

336
Q

Is vitamin K fat or water soluble?

A

Fat

337
Q

What is the main function of vitamin K?

A

The production of clotting factors in the liver

338
Q

What is malabsorption?

A
  • The inadequate absorption of nutrients from the intestines
  • Failure to absorb certain vitamins, minerals, carbohydrates, proteins or fats
339
Q

What usually causes malabsorption?

A

Disease of the small bowel

Phase 1 Med (Liv) (13 decks)

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