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Phase 1 mine > GI better deck > Flashcards

GI better deck Flashcards

1
Q

what are the embryological boundaries of the foregut

A

mouth to common bile duct

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2
Q

what are the embryological boundaries of the midgut

A

common bile duct to 2/3rds transverse colon

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3
Q

what are the embryological boundaries of the hindgut

A

2/3rds transverse colon to anal canal

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4
Q

what develops from the endoderm

A

bowel epitheliumhepatocytes of liverendo/exocrine cells of pancreas

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5
Q

what develops from the visceral mesoderm

A

muscle wallconnective tissue of wall/pacreas/livervisceral peritoneum

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6
Q

what is the primitive gut derived from

A

endoderm + visceral mesoderm

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7
Q

what is the oropharyngeal membrane

A

at cranial end of embryo at head of foregut4th week = ruptures to form the mouth

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8
Q

what is the cloacal membrane

A

at end of hindgut at caudal end 7th week = ruptures to form the anus

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9
Q

what are the pharyngeal arches

A

extensions of foregut from oropharyngeal membrane to respiratory diverticulum = 5 arches (no no.4)

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10
Q

what are pharyngeal arches made of

A

mass of mesenchymal tissue invaded by cranial neural crest cellsexternally covered by endoderm = cleftsinternally covered by ectoderm = pouches

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11
Q

bones and innervation of 1st arch

A

maxilla/mandible/incus/malleus= mandibular nerve

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12
Q

bones and innervation of 2nd arch

A

stapes/styloid/lesser horn hyoid cartilage = facial nerve

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13
Q

bones and innervation of 3rd arch

A

body and greater horn of hyoid cartilage = glossopharyngeal nerve

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14
Q

bones and innervation of 4th arch

A

thyroid cartilage/epiglottic cartilage = superior laryngeal nerve of vagus

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15
Q

bones and innervation of 6th arch

A

cricoid cartilage/arytenoid cartilages/corniculate/cuneiform cartilage= recurrent laryngeal nerve of vagus

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16
Q

describe the development of the oesophagus

A
  1. 4th week = respiratory diverticulum form
  2. trancheosophageal septum develops = separates respiratory diverticulum form dorsal foregut = separated into respiratory primordium and dorsal oesophagus
  3. initially short oesophagus = lengthen with descent of heart and lungs
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17
Q

describe the development of the stomach at the 4th week

A
  1. appears as fusiform dilation of foregut2. attached to body wall by dorsal/ventral mesenteries3. L/R vagus on L/R side of stomach4. dorsal wall grows faster = greater curvature
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18
Q

describe the development of the stomach at the 7th week

A
  1. stomach rotates 90 degrees clockwise = produces lesser sac behind2. lesser curvature facing R greater facing L3. L vagus of anterior, R on posterior
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19
Q

describe the development of the stomach at the 8th week

A
  1. stomach/duodenum rotate upwards = C shaped duodenum 2. = thinning of dorsal mesentery = becomes greater omentum3. ventral mesentery attach to liver = lesser omentum= produce distinct spaces of peritoneal cavity = greater/lesser sac
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20
Q

how is the 4 layers of greater omentum formed

A

during foetal period anterior/posterior greater omentum fuse = one thick sheet of 4 layers

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21
Q

name the stages of midgut development

A
  1. elongation
  2. physiological herniation
  3. rotation
  4. retraction
  5. fixation
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22
Q

describe physiological herniation

A

during 6th week

  1. loop of midgut elongates rapidly
  2. liver enlargement = abdominal cavity too small
  3. = midgut pushed out into extraembryonic cavity
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23
Q

describe stage 3: rotation

A

loop of midgut rotates 270 anticlockwise around axis of superior mesenteric artery jejunum and ileum form a number of coiled loops

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24
Q

describe stage 4: retraction

A

during 10th weekherniated midgut return to abdominal cavityjejunum return first

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25
Q

describe stage 5: fixation

A

some of gut mesenteries lie against back of abdomen = parts of bowel fixed to wall with single anterior layer of peritoneum = retroperitoneal

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26
Q

what structures in the abdomen are fixed

A

duodenum except cap
ascending colon
descending colon
rectum

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27
Q

what structures in the abdomen are mobile

A 
stomach
jejunum/ileum
appendix
transverse colon
sigmoid colon
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28
Q

describe the formation of the anorectal canal

A

urorectal septum divides the cloacal membrane = into urogenital sinus and anorectal canal

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29
Q

what happens in stage 1 swallowing

A

= voluntary - food compressed against mouth roof and pushed towards oropharynx by tongue- buccinator/suprahyoid muscles manipulate food

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30
Q

what happens in stage 2 swallowing

A

= involuntary nasopharynx closed off by soft palate and pharynx shortened/widened by hyoid bone elevation

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31
Q

what happens in stage 3 swallowing

A

= involuntary - sequential contraction of constrictor muscle then depression of hyoid bone/pharynx- upper oesophageal sphincter relax- peristalsis until through lower oesophageal sphincter into stomach

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32
Q

describe peristalsis in the oesophagus

A

sequential contractions of constrictor muscles behind bolus

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33
Q

what is the gag reflex

A

reflex elevation of the pharynx often followed by vomiting caused by irritation of oropharynx/back of tongue

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34
Q

what is responsible for the gag reflex

A

reflex arc between glossopharyngeal (sensory/afferent nerve) and vagus (effector/efferent nerve)

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35
Q

name 3 functions of saliva

A
  1. lubricant for mastication
  2. maintaining oral pH (6.2-7.4)
  3. release digestive enzymes - salivary alpha amylase
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36
Q

what type of gland is the parotid gland

A

serous

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37
Q

what innervates the parotid gland

A

sympathetic = mandibular branch of trigeminalparasympathetic = glossopharyngeal

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38
Q

what type of gland is submandibular gland

A

mixed mucous and serous

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39
Q

what innervates the submandibular gland

A

parasympathetic = lingual nerve = chorda tympani branch of facial nerve

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40
Q

what type of gland is sublingual gland

A

mixed mucous and serous but mainly mucous

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41
Q

what innervates the sublingual gland

A

same as submandibular

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42
Q

what is the action of parasympathetic innervation of the salivary glands

A

stimulates saliva secretion

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43
Q

what is the action of sympathetic innervation of the salivary glands

A

inhibits saliva secretion

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44
Q

describe the structure of salivary glands

A
  1. acinar cells - serous and mucous

2. ducts

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45
Q

describe serous acinus

A

dark nucleus in basal thirdsmall central ductsecrete water and alpha amylase

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46
Q

describe mucous acinus

A

pale staining ‘foamy’nucleus at baselarge central ductsecrete mucous

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47
Q

describe the structure of intralobular ducts

A
  1. intercalated ducts

2. striated ducts

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48
Q

describe intercalated ducts

A

short narrow cuboidal cells = connect acini to larger striated ducts

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49
Q

describe striated ducts

A

= striated, basal membrane has microvillimajor site for reabsoprtion of NaCl

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50
Q

describe ion transport across the ducts

A

secrete = K+ and HCO3-reabsorb = Na+ and Cl- and H2O so saliva is hypotonic

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51
Q

what is BMR

A

basal metabolic rate = minimum amount of energy required to keep the body alive

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52
Q

how do you calculate BMI

A

weight/height squared

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53
Q

energy requirement at skeletal muscle and fuels used

A

40% body mass
22% BMR
triglycerides/glucose

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54
Q

energy requirement at liver and fuels used

A

2.6% body mass
21% BMR
triglycerides/amino acids

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55
Q

energy requirement at brain and fuels used

A

2% body mass
20% BMR
glucose

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56
Q

energy requirement at heart and fuels used

A

0.5% body mass
9% BMR
triglycerides/other lipids

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57
Q

energy requirement at kidneys and fuels used

A

0.4% body mass
8% BMR
glucose

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58
Q

how are fuels stored

A

amino acids/triglycerids/glucose to liver then converted
fat - adipose tissue
glucose - muscle

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59
Q

what fuels does muscle store

A

protein and glycogen

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60
Q

what fuels does adipose tissue store

A

triglycerides from glycerol and fatty acids

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61
Q

how much are excess glycogen stores and how long would they last

A

up to 15kg and up to 12 hours

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62
Q

how much are excess lipid stores and how long would they last

A

just 350g but last up to 3 months

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63
Q

how much are excess protein stores and how long would they last

A

only used in times of prolonged starvation about 6kg and last up to 10 days

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64
Q

what is glycogen

A

principle dietary polysaccharidealpha 1,4 glycosidic + 1,6 glycosidic links

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65
Q

what is starch

A

majority alpha 1,4 glycosidic, fewer 1,6 than glycogen

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66
Q

what is cellulose

A

only beta 1,4 glycosidic linkages

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67
Q

name 3 important fatty acids we absorb

A

palmitic acidstearic acidoleic acid

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68
Q

what are the 3 monosaccharides

A

glucosefructosegalactose

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69
Q

how many essential amino acids are there

A

8

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70
Q

what is vitamin A used for

A

cellular growth
vision
skin/mucous membranes

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71
Q

name 4 sources of vitamin A

A

liver
dairy
oily fish
fruit and veg

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72
Q

what occurs in vitamin A deficiency

A

night blindness
growth retardation
increase infection risk

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73
Q

what is vitamin C used for

A

collagen synthesis

antioxidant

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74
Q

name 2 sources of vitamin C

A

citrus fruit

green vegetables

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75
Q

what occurs in vitamin C deficiency

A

scurvy
bleeding gums
aching bones

76
Q

what is vitamin B12 used for

A

DNA synthesis

brain development

77
Q

name a source of vitamin B12

78
Q

what occurs in vitamin B12 deficiency

79
Q

what is vitamin D used for

A

calcium absorption in gutreabsorption in kidneys

80
Q

name 2 sources of vitamin D

81
Q

what occurs in vitamin D deficiency

A

frequent bone fractures
muscle weakness
bone pain

82
Q

what is vitamin E used for

A

antioxidant protects cell walls

83
Q

name a source of vitamin E

84
Q

what occurs in vitamin E deficiency

A

muscle weaknessretina degeneration

85
Q

what is vitamin K used for

A

blood clotting

86
Q

name a source of vitamin K

A

green vegetables

87
Q

what occurs in vitamin K deficiency

A

bleeding gumseasy bruising

88
Q

what are the functions of the stomach (6)

A
  1. store/mix food
  2. kill microbes
  3. secrete intrinsic factor
  4. secrete/activate proteases
  5. lubrication
  6. mucosal protection
89
Q

what are the 6 key cell types of the gastric mucosa

A
  1. mucous cell
  2. parietal cell
  3. chief cell
  4. enterochromaffin-like cell ECL
  5. G cell
  6. D cell
90
Q

what do parietal cells secrete and why

A
  1. HCl = activation of pepsinogen, host defence

2. intrinsic factor = absorption of B12 in terminal ileum

91
Q

what do chief cells secrete and why

A

pepsinogen = converted to pepsin by gastric acid

92
Q

what do G cells secrete and why

A

gastrin = upregulates acid secretion as binds to parietal + ECL cells

93
Q

what do D cells secrete and why

A

somatostatin = inhibits gastrin secretion

94
Q

what do ECL cells secrete and why

A

histamine = upregulates acid secretion from parietal cells

95
Q

describe the lining of the stomach

A

= epithelial layer invaginates into mucosa to form many tubular glands

96
Q

describe the lining of the upper portions of the body of the stomach

A

thinner wallparietal cells = HCl chief cells = pepsinogem

97
Q

describe the lining of the lower portion of the stomach

A

antrum has thicker smooth muscle layer

glands secrete little acid but contain G cells = gastrin

98
Q

describe gastric acid secretion

A
  1. H+ from bicarbonate reaction in parietal cell = transported into lumen by H+/K+ATPase
  2. Cl- enter parietal cell by exchange of HCO3- from bicarbonate reaction into capillary
  3. Cl- leave parietal cell via channels
  4. combine in stomach to form HCl
99
Q

turning on acid secretion: when is the cephalic phase

A

during a meal

100
Q

turning on acid secretion: what occurs in the cephalic phase

A

= stimulated by parasympathetic NS = sight/smell/taste/chewing- ACh released = trigger gastrin from G cells + histamine from ECL cells- increase HCl production

101
Q

what is the effect of histamine and gastrin release

A

increase number of H+/K+ATPase pumps on plasma membrane of parietal cells = more HCl

102
Q

turning on acid secretion: when is the gastric phase

A

once food has reached the stomach

103
Q

turning on acid secretion: what occurs in the gastric phase

A

= initiated by gastric distension + presence of peptides/aa from protein digestion - gastrin and histamine released = parietal cell increase HCl- net increase in acid production

104
Q

how does protein in the stomach turn on gastric acid secretion

A

= direct stimulus to G cells = positive feedback loop= acts as buffer to reduce H+ ions so pH rises = decrease somatostatin = more parietal cell activity

105
Q

turning off gastric acid secretion: what occurs in the gastric phase

A

low luminal pH =

  1. directly inhibits gastrin = indirectly inhibit histamine
  2. stimulates somatostatin = inhibit parietal cell
106
Q

turning off gastric acid secretion: what initiates the intestinal phase

A

duodenal distension
low pH
hypertonic solutions presence of aa/FA

107
Q

what occurs in the intestinal phase

A

= release of enteragastrones

  1. secretin
  2. cholycystokinin
  3. trigger neural pathways to reduce ACh
108
Q

what is secretin

A

produced by S cellsact on G cells to inhibit gastrin secretion + promotes somatostatin

109
Q

what is CCK

A

produced by I cells
act on parietal cells and pancreas to inhibit HCl secretion
promotes flow of digestive enzymes from pancreas/bile to gallbladder

110
Q

describe protease secretion

A
  1. pepsinogen secreted alongside HCl
  2. pepsinogen activated in lumen of stomach
  3. HCl cleaves pepsinogen to pepsin
  4. pepsin can cleave more pepsinogen in positive feedback loop
111
Q

what irreversibly inactivates pepsinogen

A

HCO3- released in duodenum

112
Q

what is the volume of the stomach when eating

A

1.5L = little increase in luminal pressure bc receptive relaxation

113
Q

what is responsible for receptive relaxation

A

smooth muscle in body and fundus

114
Q

what is receptive relaxation mediated by

A

parasympathetic NS acting on enteric nerve plexuses with coordination from afferent from stomach (vagus) and swallowing centre of brain

115
Q

what occurs in receptive relaxation

A

nitric oxide/seratonin released by enteric nerves = relaxationACh activates parietal/chief cells = initiates receptive relation

116
Q

where do peristaltic waves begin

A

body of the stomach

117
Q

describe peristalsis in the stomach (4)

A
  1. more powerful contractions in gastric antrum
  2. pyloric sphincter closes as peristaltic wave reaches
  3. little chime enters duodenum
  4. most rebound back to antrum for mixing again
118
Q

what determines the frequency of peristalsis in the stomach

A

pacemaker cells in longitudinal smooth muscle impulse to trigger contractions = 3 times per minute

119
Q

what do the interstitial cells of Cajal do

A

pacemaker cells of peristalsis

120
Q

describe the action of pacemaker cells

A

undergo slow depolarisation/repolarisation cycles
waves of depolarisation transmitted through gap junctions to adjacent smooth muscle cells = do not cause significant contraction in empty stomach

121
Q

how is the strength of peristaltic contractions varied

A

excitatory neurotransmitters and hormones further depolarise membranes
action potentials when threshold reached = threshold can be altered by enteric NS

122
Q

what increases the strength of gastric contractions

A

gastrin

gastric distension

123
Q

what decreases the strength of gastric contractions

A

duodenal distension
increase in duodenal fat/osmolarity
decrease in duodenal pH
increase sympathetic/decrease parasympathetic stimulation

124
Q

what is dumping syndrome

A

overfilling of duodenum by hypertonic solution

125
Q

what natural mechanisms delay gastric emptying

A

plasma enterogastronesneural receptors

126
Q

what is gastric reflux

A

lower oesophageal sphincter opens/doesnt close enough = acid moves up oesophagus

127
Q

what is gastroparesis

A

delayed gastric emptying

128
Q

name the 4 protective mechanisms of gastric mucosa

A
  1. alkaline mucus on luminal surface
  2. tight junctions between epithelial cells
  3. replacement of damaged cells as stem cells at base of pits
  4. feedback loops for gastric acid regulation
129
Q

what is GORD and what are the symptoms

A

gastro-oesophageal reflux disease - heartburn- regurgitation- acid reflux- dysphagia = swallowing problems

130
Q

where does the majority of water reabsorption occur

A

80% in small intestine

131
Q

what is chyme

A

= gastric juices/partially digested food
mostly water
Na+ = most abundant solute

132
Q

describe water transport in small intestine

A

epithelial membranes v permeable to water = net diffusion

133
Q

describe ion transport in small intestine

A

Na+ most of AT solutes = from lumen in cell membranes of jejunum/ileum membrane transport = variably coupled with glucose/amino acids/others

134
Q

describe water transport in the colon

A

contents = iso-osmotic so Na+ actively pumped out of lumen = water follows

135
Q

describe potassium reabsorption in the colon

A

by passive diffusion due to potential difference between lumen/capillaries

136
Q

describe chloride reabsorption in the colon

A

actively reabsorbed in exchange for bicarbonate = intestinal contents more alkaline

137
Q

which vitamins are at soluble

138
Q

where are fat soluble vitamins absorbed

A

in micelles

139
Q

which vitamins are water soluble

140
Q

where are water soluble vitamins absorbed

A

jejunum except B12

141
Q

name 2 important dietary disaccharides

A

lactosesucrose

142
Q

where is starch first digested

A

in the mouth by ptyalin (alpha amylase) with optimal pH 6.7

143
Q

where does the majority of starch digestion occur

A

95% in small intestine by pancreatic alpha amylase= produce maltose + mixture of others

144
Q

describe the digestion of starch in the small intestine

A

maltose = broken down into monosaccharides by oligosaccharide enzymes from luminal membrane of epithelial cells

145
Q

name 4 oligosaccharidases

A

maltase
lactase
sucrase
alpha-limit dextrinase

146
Q

what are alpha-limit dextrins

A

branched polymers of glucose consisting of around 8 units

147
Q

describe the absorption of hexoses/pentoses

A

rapidly absorbed across intestinal mucosa then enter the capillaries then to hepatic portal vein

148
Q

what is galactose

A

a D-isomer of glucose

149
Q

how is glucose/galactose absorbed

A

secondary active transport with Na+ through a sodium-glucose cotransporter = SGLT1 = requires high Na+ conc at mucosal surface

150
Q

how is fructose absorbed

A

facilitated diffusion via glucose transporter GLUT5 then exits via GLUT2

151
Q

how does glucose/galactose enter interstitial fluid

A

exit cell via GLUT2 receptors on basolateral membrane

152
Q

which amino acid optical isomers are found in proteins we utilise

153
Q

how are amino acid zwitterions formed

A

HN2 is a stronger base than COOH acid

NH2 picks up H+ from COOH to form zwitterion with +ve NH3 and -ve COO-

154
Q

what is pepsinogen 1

A

fragment only found in HCl secreting region of stomach

155
Q

what is pepsinogen 2

A

fragment found in pyloric region of stomach

156
Q

what is the optimum pH for pepsins

157
Q

describe the digestion of proteins in the duodenum

A

small peptides further fragmented by pancreatic enzymes = endopeptidases/exopeptidases

158
Q

name 3 endopeptidases

A

trypsin
chymotrypsin
elastase

159
Q

name 2 exopeptidases

A

carboxyl dipeptidase

amino peptidases of brush border= further digestion of peptide fragments to free amino acids

160
Q

where does final digestion of peptides occur

A

intestinal lumenbrush borderwithin cell

161
Q

how are free amino acids absorbed

A

via Na+ cotransporter on apical membrane then facilitated diffusion on basolateral membrane to portal blood

162
Q

how are di/tripeptides absorbed

A

H+ dependent cotransporters on apical membrane hydrolysed within cell to aa leave via facilitated diffusion to portal blood

163
Q

where does digestion of lipids occur

A

limited in mouth stomach by lingual/gastric lipases but mainly in small intestine

164
Q

what is lipase

A

digestive enzyme made in pancreas splits triglycerides to monoglyceride and 2 FA

165
Q

what is emulsification

A

lipid droplets converted into very small droplets

166
Q

what does emulsification require

A
  1. mechanical disruption = motility of GI tract

2. emulsifying agent = phospholipids from food/bile salts

167
Q

what are bile salts formed from

A

cholesterol in the liver

168
Q

describe the action of bile salts on lipids

A

non-polar parts associated = polar portions exposed to prevent aggregation of lipid droplets
HOWEVER lipase cannot access

169
Q

what is the action of colipase

A

binds to lipase and lipid droplet to hold them together

170
Q

what are micelles

A

lipid droplets converted into smaller = micelles
consist of bile salt
vitamins KADE
cholesterol
FA
monoglycerides and phospholipids clustered together= continuously breaking down/reforming

171
Q

describe absorption of lipids

A
  1. pancreatic lipase breakdown TG
  2. bile salts emulsify FA into micelles
  3. micelles taken up by mucosal membrane
  4. inside cell = re-esterified to form original lipids = maintain diffusion gradient
  5. lipids are packaged with cholesterol to form chylomicron
  6. chylomicron too large to enter circulation = lymphatic system via lacteals
172
Q

what are chylomicrons made up of

A

phospholipids
triglycerides
cholesterol
fat soluble vitamins

173
Q

what happens to chylomicrons after entering lymphatics

A
  1. lipase converts triglycerides in chylomicrons to glycerol + FA
  2. FA enter myocite/adipocyte and are oxidised as fuel/reesterified for storage
174
Q

what is malnutrition

A

deficiencies, excesses, imbalances of persons intake of energy/nutrients

175
Q

what is ‘MUST’

A

malnutrition universal screening tool

176
Q

what are the steps of MUST

A
  1. measure height/weight/BMI
  2. note percentage unplanned weight loss
  3. establish acute disease effect/score
  4. add scores from 1,2,3 = overall risk
  5. use management guidelines to develop care plan
177
Q

what epithelium are the lips

A

stratified squamos non-keratinising

178
Q

describe histology of lip skin

A

sub-mucosa = collagen/elastin
deeper layers = glands/striated
skeletal muscle
small blood vessels at sub-mucosa = moist

179
Q

describe the histology of the inner lips

A

small clumps salivary tissue

sebaceous glands = fordyce’s spots open to surface

180
Q

what type of epithelium is the tongue

A 
ventral/lower surface = SSNKE
dorsal/upper = SSKE
skeletal muscles insert to lower jaw + fibrous connective tissue underlying mucosa
mixed sero-mucous salivary glands
lymph nodules
181
Q

describe the histology of serous glands of the tongue

A

more pink staining
smallcluster of grapes
nucleus on base

182
Q

describe the histology of mucous glands of the tongue

A

small

michael palin = mucous pale

183
Q

name 3 types of taste buds

A

filiform papillae
fungiform papillae
circumvallate papillae

184
Q

describe filiform papillae

A

most common
tall
pointed at whole anterior 2/3

185
Q

describe fungiform papillae

A

mushroom-like
pale staining
spindle shaped
nerves

186
Q

describe circumvallate papillae

A

v shaped row

at margin of anterior 2/3 and post 1/3

187
Q

what 2 cell types are found in parotid glands

A

secretory cells = pyramidal, spherical nucleus, rich rER cytoplasm, prominent pink staining granulesstriated ducts = invaginations

Phase 1 mine (12 decks)

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