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IMMS session 4: introduction to the cardiorespiratory system > GI > Flashcards

GI Flashcards

1
Q

what are some key cells in the stomach?

A
  1. mucous cells
  2. parietal cells
  3. chief cells
  4. enteroendocrine cells
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2
Q

what are parietal cells?

A
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3
Q

what are chief cells?

A

produces pepsinogen

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4
Q

what are enteroendocrine cells?

A
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5
Q

what is gastric acid

A

HCl

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6
Q

how much gastric acid is made each day?

A

2L/day

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7
Q

what secretes gastric acid?

A

parietal cells

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8
Q

how is gastric acid produced?

A

H+ and Cl- ions must be moved into the parietal cell. in order to maintain electrical neutrally, K+ is pumped out; that and H+ are against a conc gradient therefore the process is active. carbonate ions are also pumped out

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9
Q

how does gastric acid get turned on?

A
  1. sight/smell/taste of food leads to acetyl choline release (parasympathetic) that acts on parietal cells turning them on. furthermore, ACh triggers the release of gastrin and histamine which also increases acid production
  2. Gastric distension, presence of peptides and amino acids
    Gastrin release
    Gastrin acts directly on parietal cells
    Gastrin triggers release of histamine
    Histamine acts directly on parietal cells
    Net effect = increased acid production
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10
Q

what are some uses for protein in the stomach?

A
  1. direct stimulus for gastrin release
    2.buffer in stomach lumen, mop up H+ raising pH
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11
Q

what is somatostatin?

A
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12
Q

what impact does increasing pH have on somatostatin and parietal cells?

A

decreased secretion of somatostatin more parietal cell activity (lack of inhibition)

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12
Q

by what mechanism is gastric acid secretion stopped?

A

negative feedback loop

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12
Q

how is gastric acid production stopped?

A

Low luminal pH (high [H+])
Directly inhibits gastrin secretion
Indirectly inhibits histamine release (via gastrin)
Stimulates somatostatin release which inhibits parietal cell activity

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12
Q

what are enterogastrones?

A

released when the deudenum inhibits gastric acid production

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13
Q

how does the duedoneum inhibit gastric acid production?

A

Duodenal distension
Low luminal pH
Hypertonic luminal contents
Presence of amino acids and fatty acids

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14
Q

what so enterogastrons do?

A

Secretin (inhibits gastrin release, promotes somatostatin release)
Cholecystokinin (CCK)

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15
Q

what happens to ACh when gastric acid production is reduced?

A

gets released less

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16
Q

what is an ulcer?

A

a breach in a mucosal surface. peptic ulcers occur due to the stomach and occurs in the stomach, duodenum and oesophagus

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17
Q

what are some causes of peptide ulcers?

A

Helicobacter pylori infection
Drugs – NSAIDS
Chemical irritants – alcohol, bile salts, ? Dietary factors
Gastrinoma

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18
Q

what is gastrinomas?

A

cancers of the cancer cells

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19
Q

how does the gastric mucosa protect itself?

A

secretes alkaline mucus
tight junctions between epithelial cells
replacement of damaged cells

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20
Q

how does Helicobacter pylori
contribute to peptide ulcers?

A

produces ammonium ions from urea, which is toxic to the gastric mucosa

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21
Q

how do NSAIDs Non-steroidal anti-inflammatory drugs contribute to peptide ulcers?

A

mucus secretion is stimulated by prostaglandins.
cyclo-oxygenase 1 needed for prostaglandin synthesis
NSAIDs inhibit cyclo-oxygenase 1 so less mucus is produced

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22
Q

how do bile salts contribute to peptide ulcers?

A

Duodeno-gastric reflux
Regurgitated bile strips away mucus layer
Reduced mucosal defence

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23
Q

how is peptic ulcer disease treated?

A

eradicate the organism!
triple therapy:
1 proton pump inhibitor
2 antibiotics

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24
Q

why is pepsinogen secreted in an inactive form?

A

to prevent cells from digesting themsevles

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25
Q

what us pepsinogen mediated by?

A

the enteric nervous system (stimulated by food smell. taste)

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26
Q

where is pepsinogen activated and by what?

A

in the lumen of the stomach
gastric acid (cleaves pepsinogen) and pepsin activate pepsinogen (postive feedback)

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27
Q

why is it important that pepsin is pH dependant and at what pH is it active?

A

pH <2
pepsin only active at low pH. Irreversible inactivation in small intestine by HCO3-

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28
Q

what is another function of pepsin aside from converting pepsinogen?

A

breaks down collagen in meat – helps shred meat into smaller pieces with greater surface area for digestion

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29
Q

what is the volume of the empty stomach?

A

~50mL

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30
Q

how much volume can the stomach accommodate?

A

can accommodate ~1.5L with little increase in luminal pressure

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31
Q

what is the relaxation of the stomach triggered by?

A

parasympathetic vagus nerve
Nitric oxide and serotonin released by enteric nerves mediate relaxation

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32
Q

what happens to the force of peristalsis down the stomach?

A

increases

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33
Q

how is the frequency of peristalsis determined?

A

determined by pacemaker cells in muscularis propria and is constant (3/minute). initiated by interstitial cells of Cajal

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34
Q

what increases the strength of peristaltic contractions?

A

gastrin

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35
Q

what is gastric emptying and the symptoms?

A

capacity of stomach > capacity of duodenum

overfilling of duodenum by a hypertonic solution causes dumping syndrome:
vomiting, bloating, cramps, diarrhoea, dizziness, fatigue
weakness, sweating, dizziness

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36
Q

what is gastroparesis?

A

delayed gastric emptying

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37
Q

what causes gastroparesis?

A

don’t know, but more common in diabetes mellitus, drugs, abdominal surgery, MS, being female

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38
Q

what are some symptoms of gastroparesis?

A

nausea
early satiety
vomiting undigested food
GORD
abdo pain/bloating
anorexia

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39
Q

what are the broad catagories of sal
viary galnds?

A

major and minor

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40
Q

what % of sal
via is produced by major sali
vary glands?

A

80%

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41
Q

what are the major salivary glands?

A

parotid, submandibular and sublingual

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42
Q

what are the two types of acini?

A

serous and mucous

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43
Q

how does serous acini appear?

A

dark staining, small central duct

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44
Q

how does mucous acini appear?

A

pale foamy staining, large central duct with a nucleus at base

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45
Q

what does serous acini secrete?

A

water and alpha amylase

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46
Q

what does mucous acini secrete?

A

mucous (water and glycoproteins)

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47
Q

what type of acini does the parotid gland secrete and where does it secrete this from?

A

serous acini, stenson duct

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48
Q

what type of acini does the submandibular glands secrete and where are the secretions secreted from?

A

mixed, Whartons duct

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49
Q

what type of acini does the sublingual glands secrete and from where?

A

mixed but more mucous, Whartons duct acini

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50
Q

what is the overall structure of salivary glands?

A

ducts with acinar cells surrounding. surrounded by channels and transporters which allow fluid and electrolytes in and out

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51
Q

how does salvia help us eat food?

A

acts as a lubricant for mastication, swallowing and speech

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52
Q

how does salvia have functions with immunity?

A

is antibacterial/antiviral/antifungal

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53
Q

what does the oral pH need to be maintained at and how does salvia help with that?

A

7.2
bicarbonate/carbonate buffer system for rapid neutralisation of acids

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54
Q

what enzyme is within the salvia?

A

salivary amylase

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55
Q

what salivary glands are continuously active?

A

submandibular, sublingual and minor glands

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56
Q

what happens to glucose in the liver?

A

gets converted to glycogen or acetyl CoA or con
verted into trigluceratides and transported as LDL

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57
Q

where is glucose stored as glycogen?

A

muscles and liver

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58
Q

does the brain store glucose?

A

no, therefore it needs a constant store of glucose

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59
Q

what happens to glucose in the brain?

A

converted to acetyl CoA and used in krebs

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60
Q

do RBCs store glucose?

A

no, needs a constant source

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61
Q

what happens to glucose in RBCs?

A

converted anaerobically to lactate and pyruvate

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62
Q

what happens to glucose in adipocytes?

A

stored as triglycerides or converted to ATP

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63
Q

what happens to amino acids/uses for them?

A

form proteins, various other compounds and can get fed into Krebs

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64
Q

what happens to triglycerides?

A

combine with proteins to be transported in the blood (to form for example a chylomicron) which travels in the lymphatic system

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65
Q

what processes happen during a short fast? what is this process called?

A

glycogen is broken down by glucagon into glucose. glycogenolysis

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66
Q

what processes happen during a long fast? what process is this called?

A

glycogen has been used up, so amino acids and lactate (from RBCs) and glycerol (stored in adipocytes as lipids have been used up) which call go to the liver to create glucose
gluconeogenesis

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67
Q

what happens to fats during a fast? what is this process and what promotes this process

A

triglycerides and broken down into glycerol and fatty acids. glycerol is taken to the liver to be con
verted to glucose. fatty acids are taken to the kidney and muscles (to be used by them). fatty acids are also taken to the liver to form ketone bodies.
lipolysis and glucagon

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68
Q

which out of RBCs and the brain will use the little glucose available?

A

RBCs, as they cannot use ketone bodies like the brain can

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69
Q

what is cortisol and where is it made?

A

a steroid stress hormone found

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70
Q

what are adrenaline and noradrenaline and where are they made?

A

fight and flight hormone found

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71
Q

what is thyroxine and where is it found?

A
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72
Q

what is growth hormone somatostatin and where is it found?

A
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73
Q

what does insulin promote?

A

glycogen storage, fat storage and protein sysntehsis

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74
Q

what does glycogen promote?

A

glycogenesis, gluconeogenesis and ketogenesis

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75
Q

what is DIT?

A

the energy required to break down food

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76
Q

what does leptin do to appetite, where is it produced and how does work?

A

produced in adipocytes and act on the brain which works to supress appetite

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77
Q

what does ghrelin do to appetite, where is it produced and how does work?

A

produced in stomach works on brain and stimulates appetite

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78
Q

what are the stages of midgut development?

A
  1. elongation (growth)
  2. physiological herniation (protrusion into the umbilical cord)
  3. rotation (around the superior mesenteric artery)
  4. retraction (back into the abdomen)
  5. fixation
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79
Q

what is the elongation stage of the midgut?

A

the tube rapidly grows in the midgut areas to form an intestinal loop. the is a connection to the yolk sac, which is called the vituline duct

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80
Q

what does the primary intestinal loop give rise to?

A

the cephalic limb gives rise to proximal parts such as the distil parts of the duodenum, jejunum and parts of the ileum. the caudal limb gives arise to more caudal, tail end structures like caecum, appendix ascending colon, proximal 2/3 trans
verse colon and distil parts of the ileum.

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81
Q

what is the physiological herniation stage of midgut development? and why?

A

the intestinal loops herniates into the umbilical chord in the 6th week because the abdominal cavity is too small for the gut loops and the liver, which are both rapidly growing

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82
Q

what is stage 3 rotation of the development of the midgut?

A

the tube rotates 90 degrees anticlockwise which brings the caudal limb more cranially. this happens the same time as herniation

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83
Q

how do the parts that are destines to be the small and large intestine differ in development?

A

elongation continues in the large intestine, but no coiling (caudal limb), but the part destined to be the small intestine starts to coil (cephalic limb)

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84
Q

what is the retraction stage of the midgut development?

A

around week 10 the gut loop returns into the abdomen. the gut loop also rotates 180 degrees anticlockwise

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85
Q

when and where does the jejunum and ileum return?

A

returns first to the upper left side followed by the ileum which settles towards the right

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86
Q

what is the fixation stage of midgut development?

A

some mesenteries come into close contact with the posterior abdominal wall and become fused to the posterior wall and are considered reteroperitoneal

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87
Q

how does the caecum move in embryological development?

A

when the gut returns t the abdomen it is firs tin the upper right quadrant before it moves to the rig iliac fossa as the ascending colon lengthens. during this process the appendix develops and is found around McBurney point

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88
Q

what is omphalocoele?

A

the midgut loop does not return too the abdomen in the 10th week and remains in the umbilical cord, and it becomes covered in a layer of amnion. this has a high mortality and is associated with other congenital and chromosomal anomalies

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89
Q

how does the hindgut develop?

A

the cloaca is what the last part of the hindgut comunicates with. the unorectal setpum…

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90
Q

how does the anorectal canal form?

A

the ectoderm invaginates to form the anal pit and the lower part of the anorectal canal. the anal membrane ruptures and the upper and lower parts of the anal canal become continuous with eachother

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91
Q

what stimulates parietal cells?

A

acetylcholine, gastrin and histamine

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92
Q

what are some dunctions of the li
ver?

A

carb, protein, hormone, drug/toxin metabolism and storage

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93
Q

what molecule is used to store ion? what is its structure

A

ferritin which is 23 linked subunits, and contains 5000 atoms of iron in its central core

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94
Q

how is the amount of iron in a person measured?

A

measure ferritin found in serum or cytoplasm

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95
Q

what are some excess iron storage disorders?

A

haemolytic anaemia
iron replacment therapy

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96
Q

what is non-iron overload? with examples

A

when the ferritin is in high levels but iron isn’t e.g. liver disease

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97
Q

what causes ferritin deficiency?

A

iron deficiency

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98
Q

what levels of ferritin indicates depletion?

A

less than 20 µg/L indicates depletion

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99
Q

what levels of ferritin indicates absence of stored iron?

A

less than 12 µg/L

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100
Q

what are water soluble
vitams and wwhat does this mean?

A

B and C, pass through the body more readuly and require more regular intake

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101
Q

what are fat soluble
vitams and wwhat does this mean?

A

A,D,E and K can be stored better

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102
Q

what is the function of vitamin A?

A

ingest retinal directly from meat or produce retinal from carotenes

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103
Q

what are sources of vitamin A?

A

retinols (eggs, cereal, liver) or carotenoids which are broken into retinols (carrots, tomatoes)

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104
Q

what are the functions of
vitamin A?

A

Vision:
Used to form rhodopsin in the rod cells in the retina.
Reproduction:
Spermatogenesis in male
Prevention of foetal resorption of female
Growth
Stabilisation of cellular membranes

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105
Q

what can cause
vitamin A defiicency?

A

fat malasorption

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106
Q

hat are symptoms of vitamin A deficiency?

A

night blindness, blindness, xeropthalmia

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107
Q

what are symptoms of
vitamin D excess?

A
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108
Q

what are some functions of
vitamin D?

A

Increased intestinal absorption of calcium
Resorption and formation of bone
Reduced renal excretion of calcium

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109
Q

what happens when there is
vitamin D deficiency?

A

demineralisation of bone (rickets in children, osteomalacia in adults)

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110
Q

where do we get vitamin D from?

A

sunlight

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111
Q

where is vitamin E stored?

A

in non-adipose cells such as liver and plasma as a labile and fixed pool and adipose cells as a fixed pool

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112
Q

what is the function of
vitamin E?

A

antioxidant

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113
Q

what causes vitamin E deficiency?

A

fat malabsorption (cystic fibrosis), premature infants

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114
Q

what are some symptoms of
vitamin E deficiency?

A

Haemolytic anaemia
Myopathy
Retinopathy
Ataxia
Neuropathy

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115
Q

how is vitamin K transported?

A

rapidly taken up by the liver but then is transferred to very low-density lipoproteins and low density lipoproteins which carry it into the plasma

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116
Q

where is vitamin K taken from?

A

green vegetables, synthesised from intestinal bacteria

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117
Q

why is vitamin K important?

A

responsible for the activation of some blood clotting factors

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118
Q

what causes vitamin K deficney?

A

warfarin, haemorrhagic disease of the new born

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119
Q

what can excess vitamin K cause?

A

red cell fragility

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120
Q

where is vitamin C found?

A

fresh fruit and
vegetables?

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121
Q

why is vitamin C important?

A

Collagen synthesis
Antioxidant
Iron absorption

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122
Q

what can vitamin C deficiency cause? what is the symptoms?

A

scurvy, hair loss, teeth and gum disease as well as easy bruising and bleeding

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123
Q

what are the active forms of vitamin B12?

A

Methylcobalamin
5-deoxyadenosylcobalamin

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124
Q

what are sources of
vitamin B12?

A

fish, eggs, milk

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125
Q

what causes vitamin B2 deficiency?

A

veganism, malabsorption (lack of stomach acid, pancreatic disease, small bowel disease)

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126
Q

what are symptoms of
vitamin B12 deficiency?

A

Macrocytic anaemia
Peripheral neuropathy in prolonged deficiency

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127
Q

what are functions of folate?

A

coenzyme in methylation reactions, DNA synthesis, synthesis of methionine from homocysteine

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128
Q

what causes folate deficiency?

A

Malabsorption
Drugs that interfere with folic acid metabolism (anticonvulsants, methotrexate)
Disease states that increase cell turnover (e.g. leukaemia, haemolytic anaemia, psoriasis)

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129
Q

what are symptoms of folate deficicmey?

A

foetus with a neural tube defect, macrocytic anaemia

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130
Q

what clotting factors are produced by the liver?

A

I (Fibrinogen)
II (Prothrombin)
IV
V
VI
VII

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131
Q

where is vitamin B12 stored?

A

liver

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132
Q

where is vitamin B12 released from?

A

acid and enzymes in the stomach

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133
Q

how is vitamin B12 protected from stomach acid?

A

by binding to R proteins

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134
Q

how is vitamin B12 released from R proteins?

A

by pancreatic polypeptide

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135
Q

what happens in phase 1 of biotransformation reaction?

A

oxidation non synthetic functional groups such as OH NH2 and COOH are added which leads to a small increase in hydrophilicity through microsomal CYP450

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136
Q

what happens in phase 2 biotransformation reactions?

A

glucuronidation. the addition of biosynthetic groups like glucuronic acid to a to a large increase in hydrophilicity non microsomal and required UGT enzyme

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137
Q

where does detoxification take place in the liver?

A

smooth endoplasmic reticulum

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138
Q

what is the function of cytochrome P450 enzymes?

A

oxidise substrates

139
Q

what are cytochromes?

A

cellular proteins containing one or more haem groups that are involved in electron transfer

140
Q

what induced cytochrome P450?

A

certain drugs, some dietary components, and some environmental toxins eg smoking

141
Q

what cytochromes are most responsible for drug metabolism?

A

CYP2D6 and CYP3A4

142
Q

how is alcohol metabolised in the liver?

A

PK450 (PK2E1) takes excess ethanol into acetylaldehyde, (by reducing NAD and using alcohol dehydrogenase) which releases reactive oxygen species that damage liver cells.

143
Q

what is the pathway for alcohol metabolism?

A

ethanol to acetaldehyde by alcohol dehydrogenase, which gets converted to acetate by acetaldehyde dehydrogenase. some gets changed to CO2 and H2O

144
Q

where does most of water reabsorption take place?

A

ascending colon and part of the transverse

145
Q

what is the mucosa of the colon composed of?

A

simple columnar epithelial cells that are interspersed with goblet cells(secretes mucin that lubricated bowel) as well as the lamina propria that contains lymph

146
Q

what does the muscular propria contain?

A

inner circular muscle, Auerbach nerve plexus and longitudinal muscle for segmental motility

147
Q

what does the submucosa of the colon contain?

A

nerves

148
Q

where does the Auerbach nerve plexus lie and what does it do?

A

between the circular and

149
Q

what does the submucosal plexus lie and what does it do?

A
150
Q

what innervates the anal sphincter?

A

tells the anal sphincter to relax to go to the toilet
via the pudendal nerve

151
Q

what is the anatomy of the anal sphincter?

A

the internal haemorrhoid tissue, muscle, internal anal sphincter, external anal sphincter and external haemorrhoid tissue

152
Q

what are the four phases of defecation?

A

basal, pre-expulsive, expulsive and termination

153
Q

what happens during the basal phase of defecation?

A

in the colon there are segmental contractions which leads to mixing. in the rectum the motor complexes to keep the rectum empty and the anal sphincter undergoes tonic contractions and the puborectalis is contracted at 90 degrees

154
Q

what happens during hte pre-expulsive phase during defecation?

A

in the colon there are high amplitude contractions which leads to the mass movement of stool 8 time a day. in the rectum the filling causes distension and the rectum undergoes rectal compliance. the external anal sphincter maintains contraction and puborectalis remains contracted

155
Q

what happens during the expulsive phase of defecation?

A

rectum contracts, iAS,EAS and Pr relaxes

156
Q

what happens during the termination phase of defecation?

A

traction loss causes contraction of the EAS and
valsalva ceases

157
Q

what is the colonic transit study?

A

making a person swallow markers; if the markers aggregate suggests blockage or moves slowly shows slow movement of stool

158
Q

what is defecating proctogram?

A
159
Q

examples of positive nitrogen balance?

A

pregnancy, lactation, bodybuilder/anabolic steroids

160
Q

examples of negative nitrogen balance?

A

protein malnutrition, trauma/sepsis/burns

161
Q

where do amino acids go once absorbed by the gut?

A

go to the portal circulation, where they may be used in protein formation, other nitrogen compounds or may have their amino group removed so the carbon backbone are used as metabolic substrates, helping to form carbohydrates like glucose from gluconeogenesis or fatty acids to form triacylglycerols

162
Q

what is a essential amino acid?

A

they cannot be synthesised de novo in vivo

163
Q

what is a conditionally essential amino acid?

A

under certain circumstances they will be essential, and others not e.g. tyrosine can be made from phenylalanine. if someone’s diet contains sufficient phenylalanine, they will not need tyrosine in their diet, but if not tyrosine becomes essential

164
Q

what is the purpose of albumin?

A

for maintaining the oncotic pressure in blood, and is an important carrier protein for a variety of things including sex hormones, magnesium and calcium and drugs

165
Q

what is the main source of nitrogen within the body?

A

amino acids

166
Q

what are some important uses of nitrogen within the body?

A

biosynthestic pathways be incorportated into non-peptide molecules as diverse as neurotransmitters, nitric oxide and the nucleotides that constitute RNA and DNA

167
Q

what is an alpha-ketoacid? what is the process by which it is formed called?

A

an amino acids with the amino group cleaved off
transamination

168
Q

what is ALT?

A

alanine aminotransferase that converts alanine and alpha-ketoglutarate to pyruvate and glutamate. glutamate can transfer the amine group away to reform a-ketogluterate

169
Q

how are amino acids degraded?

A

glutamate dehydrogenase converts glutamate to a-ketoglutarate (by the addition of water) which also gives off an ammonium ion. a bicarbonate joins with it to form carbamyl phosphate which enters the urea cycle to form urea

170
Q

what happens to amino acids in the fasting state?

A

protein broken to amino acids, amino group is cleaved off by amino transferases…

171
Q

what is ubiqutin?

A

forms ubiquitin chains on lysine residue leading to proteasome destroying the proteins

172
Q

what is lysosomal protein degradation?

A
173
Q

integrated metabolism: catabolic state

A
174
Q

what are regulators of amino acid catabolism?

A

alanine, cortisol, glucagon, glutamine

175
Q

what are the major proteins synthesised in the liver?

A

most plasma proteins (-immunoglobulins), ferritin, albumin, all the factors within the clotting cascade

176
Q

how much albumin is produced by the liver each day?

A

10-15g

177
Q

is albumin positively or negatively charged?

A

negative

178
Q

what are functions of albumin?

A

plasma oncotic pressure and a carrier protein for hormones vitamins, drugs and electrolytes

179
Q

what is hypoalbuminaema?

A

a lack of albumin

180
Q

what causes hypoalbuminaemia?

A

liver and renal disease, sepsis, malnutrition

181
Q

what are consequences of hypoalbuminaemia?

A

oedema, effusions, lack of carrying hormones, electrolytes etc

182
Q

why is the clotting cascade vitamin K dependant?

A

important for maintain the structure of the intermediates of the clotting cascade?

183
Q

why may someone with liver disease have slower/poorer blood clotting?

A

since vitamin K requires bile (lipid soluble) and those with liver dysfunction have bile disfunction

184
Q

what are some symptoms of liver disease?

A

reduced symptoms of clotting factors, reduced synthesis of inhibitors, development of
varices

185
Q

what is the glucose alanine cycle?

A

when alanine gets converted to pyruvate, pyruvate goes to the links reaction. when pyruvate gets con
verted to alanine, this pyruvate comes from the links and glutamate gets de-aminated (gives amine to pyruvate) to reform a-ketoglutarate

186
Q

krebs bicycle

A
187
Q

what are the different ways urea enters the urea cycle?

A
188
Q

what are symptoms/conditions with ammonia toxcity?

A

decerebrate posturing, doll’s eye movement

189
Q

how does ammonia lead to neurotoxicity?

A

can cross blood brain barrier, depleting a-ketoglutarate (affecting Krebs)

190
Q

what are some treatments of urea toxicity?

A

low protein diet, liver transplantation and haemofiltration

191
Q

what is the overall function of the GI system?

A

take relatively large solids and digest them into smaller molecules that can be absorbed as nutrients, while still serving as a barrier to toxins, bacteria, parasites, etc.

192
Q

how much water enters and leaves the body a day?

A

9L out and in

193
Q

how is water moved from the lumen into the blood?

A

glucose and sodium ions are co-transported from the lumen into the epithelial cells. sodium moves out of the epithelium out the blood. water then follows and potassium is pumped into the epithelial cell with the sodium co-transporter

194
Q

what impacts the absorption of substances in the GI tract?

A

nutrient intake, GI motility, number and structure of enterocytes

194
Q

how does interestinal secretion work?

A
194
Q

what impacts the secretions of substances in the GI tract?

A

bile, irritants and bacterial toxins

195
Q

what is gluten?

A

a protein found in bread and wheat

196
Q

why do people with celiac disease have diahrea?

A

since gluten damages their epithelium so less nutrients can be reabsorbed, which prevents water moving by osmosis making stool more watery

197
Q

how does cholera lead to diarrhoea?

A

cholera toxin released from bacteria binds to intestinal cells which stimulates adenylate cyclase to produce cAMP which leads to the efflux of ions and water

198
Q

where does carbohydrate digestion start and how?

A

in the mouth by salivary amylase into maltose

199
Q

how do enterocytes absorb glucose and galactose?

A

galactose through an Na-dependent secondary active transport process

200
Q

how do enterocytes absorb glucose and galactose?

A

fructose is absorbed by facilitated transport

201
Q

where does protein digestion start?

A

in the stomach from pepsinogen made from chief cells

202
Q

where is bile reabsorbed and where does it go?

A

in the ileum towards the liver

203
Q

how does bile work?

A

bile emulsifies fat as it has an affinity for both fat and water so it can bring the fat into the water, so fat digesting enzymes can have access to it

204
Q

where is fat transported?

A

in the lymphatic system

205
Q

where are amlyase and lipase produced and what do they target?

A
206
Q

where are pepsin and lipase ..

A
207
Q

where are amylase, lipase and colipase pohsoplipase, trysin and chmyotryslin

A
208
Q

enterokinase dsaccharise andpeptsidase

A
209
Q

what is intrinisc factor, where is it produced and why is it important?

A
210
Q

what are the relevant functions of the liver?

A

1) metabolic regulation
store absorbed nutrients, vitamins
release nutrients as needed
2) haematological regulation
plasma protein production
remove old RBCs
3) production of bile
Required for fat digestion and absorption

211
Q

how do amino acids enter the portal
vein?

A

on the enterocyte, there is a sodium potassium pump, which pumps potassium in and sodium out. therefore sodium and the amino acid move into the enterocyte
via a co-transporter, and then the amino acid diffuses into the portal vein, before moving into the liver

212
Q

what happens to excess amino acids?

A

they are deaminated to form keto acids, which are intermediates in the krebs cycle, pyruvate or acetyl coA

213
Q

what forms when alanine gets deaminated?

A

forms pyruvate

214
Q

what is the distinction between gluco- and ketogenic amino acids?

A
215
Q

what is the name of the enzyme involved in transaminationand is the process reversible?

A

amino transferase, yes

216
Q

how is urea formed?

A

glutamate is converted back to a-ketoglutarate by losing an ammonia. the ammonia combines with bicarbonate to form carbamyl phosphate which enters the urea cycle to form urea

217
Q

what are the two methods of protein degredation?

A

lysosome and proteasome

218
Q

what is lysosome protein degradation and where does it occur?

A

lysosome contains proteases; it fuses with the protein, degrades it and releases it out of the cell for recycling. in the liver as phagolysed by Kupffer cells

219
Q

what is the proteasome method of protein degradation and where does it occur?

A

ubiquitin attaches to a lysosome side chain of a protein (four tags are required) and is delivered to proteasome (a small protein) that removes the peptide bonds. in cell cytoplasm

220
Q

describe the urea cycle?

A

carbamoyl phosphate combines with ornithine to form citrulline. citrulline combines with aspartate to form arginosuccinate (catalysed by arginosuccinate synthetase). arginosuccinate is converted to arginine (catalysed by arginosuccinate lyase) which releases fumarate. arginine is converted to ornithine, releasing urea

221
Q

what are some symptoms of maldigestion?

A

weight loss, diarrheal, abdominal pain, bloating and steatorrhea

222
Q

what is steatorrhea?

A

an increase in fat excretion in the stools

223
Q

what are the causes of PEI?

A

parenchymal diseases (cystic fibrosis, pancreatic cancers, acute and chronic pancreatitis), extra-pancreatic diseases (coeliac disease, IBD) and postsurgical (gastric resection, short bowel syndrome)

224
Q

what causes chronic pancreatitis and what is it?

A

caused by recurrent clinical/subclinical pancreatic, induced by alcohol, genetics and smoking

225
Q

what are the stages of swallowing?

A

buccal phase, where food is chewed and pushed into the oropharynx (voluntary), pharyngeal phase, where the nasopharynx is closed, the hyoid bone is elevated, the epiglottis closes and the pharynx becomes shorter and wider due to longitudinal muscle (involuntary phase), oesophageal phase, where upper oesophageal sphincter opens to allow food into the oesophagus. peristaltic waves occur all the way to the lower oesophageal sphincter. the hyoid becomes depressed, the epiglottic opens and the nasopharynx is opened

226
Q

what is the importance of the lower oesophageal sphincter?

A

prevents oesophageal reflux of acid

227
Q

where is the LES?

A

at the junction between the cardia of the stomach and the oesophagus

228
Q

what can cause acid reflux?

A

pressure caused by pregnancy and big meds leads to stomach acid refluxing into the oesophagus leading to GORD gastro-oesophageal reflux disease if it occurs chronically

229
Q

what happens when somebody has GORD?

A

metaplasia where the epithelium changes from stratified squamous non keratinising epithelium to simple columnar, which means it cannot function properly causing heartburn and chest pain as the epithelium is no longer protective

230
Q

what are the components of a gag reflex?

A

tickling sensation detected by cranial nerve IX glossopharyngeal which sends a gagging motor down cranial nerve X vagus

231
Q

what does salvia contain?

A

water, mucus, antibodies, enzymes (amylase)

232
Q

does the parotid gland need to be stimulated?

A

yes

233
Q

what supplies the most salvia and how much?

A

parotid, 80%

234
Q

what nerve supplies the parotid gland, and what runs through it?

A

supplied by 9 (glossopharyngeal), nerve 7 (facial) passes through it as well as external carotid artery and retromandibular vein

235
Q

are submandibular glands stimulated or continuous?

A

continuous

236
Q

what are serous demilunes and where are they found?

A

serous acini form crescents around mucous

237
Q

what is the submandibular gland innervated by?

A

cranial nerve 7 facial

238
Q

which gland supplies the most salvia out of the continuous ones and why?

A

submandibular as it is larger

239
Q

what type of salvia do minor glands secrete?

A

mucous except von ebner

240
Q

what can cause salivary dysfunction?

A

xerostomia (dry mouth, found in CF) obstructive calculi (stones) and inflammation

241
Q

what are the four layers of the stomach?

A

mucosa, submucosa, muscularis externa and serosa

242
Q

what is contained within the submucosa of the stomach?

A

submucosal plexus, subdivision of the enteric nervous system

243
Q

what is contained within the muscularis externa?

A

(in GI) inner circular and outer longitudinal muscle layers (in stomach) inner oblique, intermediate circular and outer longitudinal
myenteric plexus in both

244
Q

what are foveolar cells and where are they found?

A

mucous secreting cells at the cardia of the stomach

245
Q

what cells are found at the fundus of the stomach?

A

parietal cells that secrete HCl and intrinsic factor, chief cells that secrete pepsinogen and enterochromaffin cells that secrete histamine

246
Q

what cells are found in the body and the pylorus of the stomach?

A

G cells which secrete gastrin

247
Q

what are mediators of gastric acid secretion?

A

histamine and gastrin (more potent)

248
Q

what do D cells produce and where are they found?

A

somatostatin, duodenum and pancreatic islets

249
Q

what do I cells produce and where are they found?

A

cholecystokinin, duodenum

250
Q

what does cholecystokinin do?

A

secrete bile

251
Q

what do s cells produce and where are they found?

A

somatostatin, duodenum

252
Q

what are functions of the stomach?

A

digests + stores food, activates enzymes, kills microbes, secretes intrinsic factor, protects and lubricates

253
Q

what are the phases to gastric acid regulation?

A
  1. cephalic phase = thought, smell, taste, sight of food (turns on secretion)
  2. gastric phase
  3. duodenal phase
254
Q

what happens during the cephalic phase?

A

acetyl choline transmitted down vagus nerve, increases production of gastrin from g cells and histamine from enterochromaffin cells which increases the number of H+/K+ pumps on the apical side

255
Q

what happens during the gastric phase?

A

food in the stomach causes it to distend/ or amino acids are detected which triggers gastrin and histamine release increasing the number of H+/K+ ATPase pumps

however, low luminal pH reduced gastrin and therefore histamine which increases the production of somatostatin by reducing the number of H+/K+ ATPase pumps

256
Q

what happens during the duodenal phase?

A

distention, hypertonicity, lowered pH, high fatty acid & amino acid content triggers enterogastrone release which releases secretin that regulates pH and CCK that stimulates bile (alkaline bile salts) reducing the number of H+/K+ ATPase pumps

257
Q

how is a h pylori infection treated?

A

proton pump inhibitor decreases pH making conditions inhospitable for h pylori. also treated by antibiotics

258
Q

how are gastric acid ulcers caused by NSAIDs treated?

A

treated with analogues as they mimic the prostaglandin effect

259
Q

what drugs decrease gastric acid secretion, and therefore can be used to treat peptic ulcers?

A

proton pump inhibitors e.g. omeprazole and lansoprazole as well as histamine receptor antagonists such as ranitidine

260
Q

what cleaves pepsinogen to pepsin?

A

HCl and positive feedback (pepsin itself)

261
Q

what does pepsin do?

A

digests protein into peptides and shreds meat to make digesting easier

262
Q

how can we live without a stomach?

A

eat smaller meals and take B12 supplements (as the stomach secretes IF)

263
Q

where are peristaltic waves harder in the stomach?

A

weak at the fundus and cardia, but harder at the pyloric antrum

264
Q

how much chyme enter the stomach at a time?

A

3ml, rest is pushed back

265
Q

what causes stomach contractions, what is the rate and what stimulates them?

A

interstitial cells of cajal (pacemakers), 3 per minute and stimulated by gastric acid

266
Q

what slow down emptying into the duodenum and why?

A

low pH (duodenum not made to cope with low pH), high fatty acid and amino acid content, distension (duodenum has low
volume), hypertonicity (could draw water into duodenum causing diarrhoea). this leads to the stimulation of the enteric nervous system for a smaller response or the CNS for a longer one

267
Q

what is gastroparesis?

A

too delayed duodenal emptying where food empties in the stomach, food looks like faeces

268
Q

what is the total water content that passes through the GI per day and where do these water sources come from?

A

9000ml, 2000ml ingested and 7000ml secreted (intestines 1000, saliva 1500ml, stomach 2500 ml, bile 500 ml, pancreas 1500ml)

269
Q

how much water is reabsorbed, and where is it reabsorbed?

A

98% ~8800 mL, 200mL in stool, 5500mL in jejunum, 2000mL in ileum and 1300 in colon

270
Q

what ion is the most abundant in chyme?

A

sodium

271
Q

where is iron absorbed?

A

duodenum

272
Q

where are water soluble
vitamins absorbed?

A

jejunum (apart from B12)

273
Q

where are fat soluble vitamins absorbed?

A

ileum, B12 also absorbed here

274
Q

how are carbohydrates digested?

A

by alpha amylase in the mouth (little starch broken), pancreatic amylase in the duodenum (95% starch broken down) breaks into oligo/disaccharides go through duodenum till they are broken down by membrane bound oligo/disaccharidases to monosaccharides

275
Q

how are carbohydrates absorbed?

A

glucose and galactose are taken in by secondary active transport with Na+ through the SGLT-1. fructose through facilitated diffusion via a GLUG 5 transporter. all three leave duodenum basolaterally by GLUT 2. they then diffuses into the blood through capillary pores through portal vein to the liver

276
Q

what happens to digested carbohydrates when they reach the liver?

A

if in the absorptive stat (eaten) glucose is stored as glycogen in liver and skeletal muscles. if in postabsorptive state (fasted) glycogen stores are broken down into glucose and consumed by skeletal muscle

277
Q

how are proteins digested?

A

in the stomach, pepsin cleaves some bonds and shreds proteins. in the duodenum, pancreatic endopeptidases cleaves bonds mid chain, such as trypsin and chymotrypsin. also in the duodenum pancreatic exopeptidases (carboxypeptidases and membrane bound aminopeptidases) cleave off carboxy groups and amino groups

278
Q

how are proteins absorbed?

A

secondary active transport with Na+ (or H+) if small fragments and go basolaterally into the interstitial fluid then capillaries then systemic circulation

279
Q

how are fats digested?

A

starts in the mouth. smashed in the stomach and emulsified in the duodenum by bile salts. bile salts are amphipathic, so aggregate around fat droplets preventing reaggregation. since bile salts impair lipase binding, colipase intermediate helps lipase bind, which breaks triglycerides to monoglycerides and fatty acids. these are packaged into miscellas that are transported around the GI. contents released at the intestinal brush border

280
Q

how are fats absorbed?

A

monoglycerides and fatty acids reform to triglycerides in SER at small intestine. the triglycerides are packaged into vesicles with cholesterol which are modified by the golgi to form chylomicrons. these are exocytosis basolaterally into lacteals and enter lymphatic circulation

281
Q

what is vitamin A also called and what is it important for?

A

retinol, carotenoids, rhodopsin

282
Q

where is vitamin A stored?

A

within the liver; ito cells and space of disse

283
Q

what is vitamin D also called and what is it dependant on? how is it activated?

A

calciferol (inactive form activated by UV), dependant on Ca2+ and phosphate intestinal absorption

284
Q

where is vitamin D stored?

A

liver

285
Q

what does vitamin D deficiency cause?

A

rickets and osteomalacia

286
Q

what is vitamin e?

A

antioxidant (helps to slow down ageing process)

287
Q

where is vitamin e found and where is it stored?

A

nuts and seeds, in the liver

288
Q

what is the purpose of vitamin K, where is it found?

A

activates clotting factors 10,9,7,2. found in plants, foods, synthetic form k3+4,

289
Q

what can vitamin K deficiencies cause?

A

bleeding disorders

290
Q

what is vitamin B12 used for?

A

cell metabolism and energy

291
Q

how is vitamin B12 absorbed?

A

B12 intrinsic factor complex

292
Q

how is vitamin B12 transported?

A

binds to R protein transamin-1 in stomach, cleaved at duodenum and then binds to intrinsic factor

293
Q

where is vitamin B12 found and what does its deficiency cause?

A

poultry and eggs, pernicious anaemia

294
Q

where is vitamin C found, what is it used for and what does its deficiency cause?

A

immune system, Fe absorption, antioxidant. found in fresh fruit and
veg, deficiency leads to scurvy

295
Q

how is iron transferred and stored?

A

transferred in blood as transferrin, stored in liver as ferritin

296
Q

where is copper stored?

A

liver

297
Q

what is a source of calcium and where is it used for?

A

from dairy, needed for muscle contraction and synaptic transmission

298
Q

what is iodine a key component of and where is it found?

A

thyroid hormone, seafood

299
Q

what is body mass index?

A

weight (kg)/ height (m2)

300
Q

what is basal metabolic rate measured in?

A

kcal/hr/m2

301
Q

what supplies, innervates the foregut and what are its mesenteries? what does it extend from?

A

coeliac axis blood supply T12, T5-9 greater splanchnic nerve,
ventral (lesser omenta) and dorsal (greater omenta) mesenteries. mouth to the major duodenal papilla

302
Q

what supplies, innervates the midgut and what are its mesenteries? what does it extend from?

A

super mesenteric artery L1, T10-11 lesser splanchnic nerve, dorsal mesentery. major duodenal papillary to 2/3 transverse colon

303
Q

what supplies, innervates the hindgut and what are its mesenteries? what does it extend from?

A

inferior mesenteric artery L3, T12 least splanchnic nerve, dorsal mesentery. distil 1/3 transverse colon to rectum

304
Q

what is mesentery? what does it allow?

A

double layered peritoneum blood vessels and nerves to supply abdominal viscera. allows mesentery

305
Q

what does the endoderm go to form?

A

epithelial layers and mucosa

306
Q

what does the mesoderm go to form?

A

connective tissue and muscle

307
Q

what does the ectoderm go to form?

A

skin and cns

308
Q

what happens in the fourth week of embryogenesis?

A

trilaminar disc folds medially horizontally and endoderm fuses to form primitive gut tube. oropharyngeal membrane forms at the cranial end of the primitive gut tube which forms the mouth

309
Q

what happens in the seventh week of embryogenesis?

A

cloach membrane at the caudal end of the primitive gut tube ruptures to form the anus and urogenital opening

310
Q

describe midgut tube and hindgut development

A

midgut elongates and herniates through abdominal cavity before rotating and retracting and finally fixating in its final position

311
Q

describe the foregut development

A

4th week, fusiform dilation. 7th week rotates 90 degrees clockwise longitudinal to create the lesser sac, and in the 8th week undergoes
ventrodorsal rotation

312
Q

what does the ventral mesentery become?

A

lesser omentum

313
Q

what are some functions of the liver?

A

digestion (produces bile salts), immune (Kupffer cells), synthetic (the production of proteins, e.g. most clotting factors), hormonal and storage (glycogen)

314
Q

what proteins are produced by the liver, and what are the functions of these proteins?

A
  1. albumin (oncotic pressure maintained and carrier protein for unconjugated bilirubin)
  2. clotting factors (all but factor 8)
  3. complement (proteins that mark pathogens for an immune response)
315
Q

why is the liver important in the clotting cascade?

A

produces clotting factors (all but factor 8) and bile salts that are required to absorb
vitamin K, which some clotting factors 10,9,7 and 2 are dependant on

316
Q

describe the urea cycle?

A

ammonia and carbon dioxide combine with ornithine to form citrulline, which combines with ammonia again to form arginine. arginine is converted by arginase to urea to form ornithine again. CITARGORN

317
Q

describe why the glucose alanine cycle takes place?

A

glut and pyruvate converted to alanine and a-ketoglutarate in the muscles. the alanine goes to liver via the blood, where it is transaminated and for the pyruvate undergoes gluconeogenesis to form glucose (and then glycolysis) meaning the muscles do not waste energy on gluconeogenesis and just contraction

318
Q

what is the function of very low density lipoproteins?

A

carry triglycerides to adipose tissue

319
Q

what is the function of intermediate density lipoproteins?

A

vldl intermediates, converted to LDL

320
Q

what are xenobiotics?

A

foreign substances absorbed but not metabolised

321
Q

what does the liver do to lipophilic substances and why?

A

modifies them to be less lipophilic and therefore more easily excreted

322
Q

what does bile contain?

A

bile salts, cholesterol, xenobiotics, electrolytes, phospholipids, billirubin

323
Q

how is bilirubin metabolised?

A

Hb con
verted to heme and globin (at splenic macrophage). globin -> biliverdin -> unconjugated bilirubin. then transported to the liver via albumin. then glucuronidase at liver to become conjugated. released in bile to the duodenum. released to urobilinogen in intestines by bacteria at the terminal ileum. 10% reabsorbed in portal vein to urobilin; urine excreted. 90% continues in colon to stercobilin in stool

324
Q

where is the gall bladder surface anatomy?

A

mid midclavicular line @ costal margin

325
Q

what is the function of the gall bladder and what controls it?

A

stores and concentrates bile. contractions caused by cholecystokinin

326
Q

what are gallstones made from?

A

cholesterol

327
Q

what are the exocrine components of the pancreas, and what is the functions?

A

acinar cells (synthesizes, stores, and secretes digestive enzymes), and duct cells (secrete bicarbonate ions that neutralise stomach acid)

328
Q

what are the endocrine components of the pancreas, and what is the functions?

A

alpha cells (produce glucagon), beta cells (produce insulin), delta cells (produce somatostatin) all above found in islets of longerons, pancreatic polypeptide

329
Q

what happens within duct cells?

A

HCO3- move into the duodenal lumen, Cl- moves into cells and down a conc. gradient w/ cystic fibrosis transmembrane conductance regulator.

330
Q

what is cystic fibrosis?

A

a mutation of the cystic fibrosis transmembrane conductance regulator

331
Q

what occurs at acinar cells?

A

releases inactive zymogens, activated at brush border by enterokinase e.g. trypsinogen to trypsin

332
Q

what does the liver store with examples?

A

minerals (copper and iron), glycogen, vitamins (ADEK + B12)

333
Q

in what form is iron circulated and stored?

A

circulated as transferrin and stored as ferritin in Kupffer cells

334
Q

how is vitamin A absorbed and where is it stored?

A

absorbed as a lipids, stored in ITO cells + space of Disse

335
Q

how is vitamin B-12 transported, absorbed and stored?

A

binds to transcobalamin I to reduce breakdown in stomach. cleaved in duodenum, and binds to intrinsic factor. absorbed as B-12-IF complex and stored in liver

336
Q

how are lipids transported?

A

goes to liver via the portal system. packed and sent in lipoprotein. a the adipose surface, free fatty acids are released, and in adipocytes they reform as triglycerides

337
Q

what happens to lipids when the demand for energy increases?

A

triglycerides release fatty acids into the blood under hormone sensitive lipase action (HCL). hepatic lipase allows uptake of fatty acids into the liver for beta oxidation, glycerol enters glycolysis

338
Q

what does insulin do to fatty acids and what does insulin resistance lead to?

A

promote storage of triglycerides in adipocytes, resistance increases ffa and glucose in blood. less fa used as immediate fuel and more glucose used therefore more fatty deposits ad less energy production

339
Q

what is jaundice?

A

bilirubin levels greater than 50mmol/L

340
Q

what are the three types of jaundice?

A

pre-hepatic, hepatic and post hepatic

341
Q

what occurs with prehepatic jaundice? give examples of conditions where this happens

A

increased rbc hydrolysis (more circulates in conjunction with bilirubin). sickle cell, newborn jaundice. urine and stool normal but enlarged spleen

342
Q

what occurs during hepatic jaundice?

A

liver damage leads to unconj bilirubin uptake unpaired and conj bilirubin secretion unpaired e.g. alcohol, cirrhosis. urine is dark as urobilinogen is normally reuptake by liver before excretion but not is not due to damage. stool normal, enlarged spleen

343
Q

what occurs during post-hepatic jaundice?

A

caused by damage to the biliary system, which decreases levels of unconjugated bilirubin in serum. gall stones, pancreatic cancer. urine dark as less conj bilirubin. stool pale, normal spleen

344
Q

what is mesentry?

A

double layered peritoneum attaching organs to abdominal wall

345
Q

what type of mesentery does the foregut have?

A

ventral and dorsal mesentery (ventral from the central tendon of the diaphragm)

346
Q

what type of mesentery does the mid/hindgut have?

A

dorsal

347
Q

how many people have an accessory pancreatic duct and what does it drain?

A

drains inferior and uncinate process. opens in minor duodenal papilla

IMMS session 4: introduction to the cardiorespiratory system (11 decks)

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