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ACEM Primary Written > Gastrointestinal: Physiology - Digestion and absorption > Flashcards

Gastrointestinal: Physiology - Digestion and absorption Flashcards

1
Q

What are the only types of polysaccharides digested in the human GI tract?

A

Starches

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2
Q

What is the most common type of dietary starch? What % of dietary starch does it constitute?

A

Amylopectin
Constitutes ~75% of dietary starch

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3
Q

Optimal pH for salivary a-amylase

A

6.7

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4
Q

Is salivary a-amylase active in the stomach?

A

Partially (despite the optimal pH being 6.7), due to active site being protected when in the presence of substrate

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5
Q

What enzymes act on ingested polysaccharides in the small intestine?

A

Salivary and pancreatic a-amylase

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6
Q

Three end-products of polysaccharide digestion by amylase

A
  1. Maltose (disaccharide: glucose + glucose)
  2. Maltotriose (trisaccharide: glucose + glucose + glucose)
  3. a-limit dextrins (glucose polymers with 8x glucose molecules on average)
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7
Q

How do amylases act on polysaccharides?

A

Hydrolyse internal 1:4a linkages
Spare 1:6a linkages and terminal 1:4a linkages

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8
Q

How are the oligosaccharide products of polysaccharide digestion further broken down in the small intestine?

A

By oligosaccharidases in the brush border of small intestinal epithelial cells

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9
Q

Three enzymes response for breakdown of maltotriose and maltose

A
  1. Maltase
  2. Sucrase
  3. Isomaltase
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10
Q

What types of linkages are hydrolysed by isomaltase?

A

1:6a

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11
Q

What enzymes hydrolyse the single glycoprotein chain into sucrase and isomaltase within the brush border of small intestine epithelial cells?

A

Pancreatic proteases

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12
Q

Structure of sucrose

A

Fructose + glucose

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13
Q

Structure of lactose

A

Galactose + glucose

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14
Q

Describe the pathophysiology of lactose intolerance

A

Intestinal lactase activity declines to low levels during childhood and adulthood
Inability to digest oligosaccharides (including lactose) causes bloating, diarrhoea and flatulence
The increased number of osmotically active oligosaccharide molecules within the intestinal lumen causes the volume of intestinal contents to increase -> bacteria break down oligosaccharides in the colon, further increasing the number of osmotically active particles -> CO2 and H2 gas are produced from disaccharide residues in the lower small intestine and colon

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15
Q

How common is lactose intolerance in northern and western Europeans vs other populations?

A

15% (70-100% in blacks, Native Americans, Asians and Mediterranean populations)

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16
Q

Where is the location of maximum absorption of hexoses in the human GI tract?

A

Proximal small intestine (all are removed before the remains of a meal reach the terminal ileum)

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17
Q

How are glucose and galactose absorbed from the intestinal lumen?

A

Via sodium-dependent glucose transport (SGLT-1)

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18
Q

What is the effect of Na+ concentration on glucose and galactose absorption in the small intestine?

A

Increased Na+ facilitates sugar influx, decreased Na+ inhibits

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19
Q

What is the difference in role/distribution of SGLT-1 vs SGLT-2?

A

SGLT-1: secondary active transport of glucose in GIT
SGLT-2: secondary active transport of glucose in renal tubules

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20
Q

How is glucose transported into the interstitium following its absorption from intestinal lumen into intestinal epithelial cells?

A

Via GLUT2

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21
Q

What is glucose/galactose malabsorption?

A

Syndrome caused by congenital defect in SGLT-1
Results in severe diarrhoea which may be fatal if glucose/galactose are not removed from the diet

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22
Q

Describe how fructose is absorbed

A

From intestinal lumen into epithelial cells via facilitated diffusion by GLUT5
Some fructose is converted to glucose within mucosal cells
Otherwise fructose is transported from epithelial cells into interstitium via GLUT2 (as for glucose and galactose)

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23
Q

What is the effect of phlorizin on glucose absorption in the small intestine (and reabsorption in the renal tubules)?

A

Depresses (acts as an inhibitor of SGLT-1 and SGLT-2)

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24
Q

What is the effect of insulin on intestinal transport of carbohydrates?

A

Little effect

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25
Q

Maximal rate of glucose absorption from the intestine

A

~120g/h

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26
Q

Where does protein ingestion begin?

A

In the stomach

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27
Q

Describe the formation, release and activity of pepsins

A

Secreted as inactivated precursors pepsinogens
Pepsinogens activated by gastric acid
Hydrolyse bonds between aromatic amino acids and a second amino acid to produce polypeptides of varying sizes
Activity terminated when gastric contents mixes with alkaline pancreatic juice in the duodenum and jejunum (optimal pH for pepsins is 1.6-3.2)

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28
Q

What is the difference between pepsinogens I and II?

A

Pepsinogen I: found only in acid-secreting regions
Pepsinogen II: found in acid-secreting regions and the pyloric region

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29
Q

What do pepsinogen I levels correlate with?

A

Maximal acid secretion

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30
Q

Optimal pH of pepsins

A

1.6-3.2

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31
Q

Describe the process of protein digestion

A

Begins in stomach with pepsins hydrolysing bonds between aromatic amino acid and a second amino acid to produce polypeptides of varying size
Polypeptides further digested by endopeptidases (trypsin, chymotrypsins, and elastase) in the small intestine
Final digestion to amino acids occurs in three locations:
- 1) Within the lumen
- 2) At the mucosal cell surface by aminopeptidases, carboxypeptidases, endopeptidases, and dipeptidases in the brush border
- 3) Some dipeptides and tripeptides are actively transported into intestinal cells and hydrolysed by intracellular peptidases

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32
Q

Name three types of endopeptidases

A
  1. Trypsin
  2. Chymotrypsins
  3. Elastase
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33
Q

Describe how pancreatic processes are released and activated

A

Secreted as inactivated proenzymes
Trypsinogen is converted to trypsin by enterokinase, a brush border hydrolase, when the pancreatic juice enters the duodenum
Enterokinase contains 41% polysaccharide which prevents it from being digested before it can exert its effect
Trypsin then converts proenzymes* into active enzymes (including trypsinogen, producing an auto-catalytic chain reaction)

  • proenzymes include chymotrypsinogen, proelastase, and procarboxypeptidases A and B
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34
Q

What is the result of congenital enterokinase deficiency?

A

Protein malnutrition

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35
Q

What is the difference in activity of endopeptidases vs exopeptidases?

A

Endopeptidases: act at interior peptide bonds
Exopeptidases: hydrolyse amino acids at carboxyl ends of polypeptides

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36
Q

Four aromatic amino acids

A
  1. Phenylaladine
  2. Histidine
  3. Tryptophan
  4. Tyrosine
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37
Q

How many different transport systems transport amino acids into enterocytes? How many of these are Na+ or Cl- dependent? How many are independent? How many transport systems move amino acids from enterocytes to the interstitium?

A

7 total transporting into enterocytes
5 involve co-transport with Na+, and 2 of these 5 also require Cl-
2 are independent

5 transporting from enterocytes to interstitium -> portal blood

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38
Q

How are dipeptides and tripeptides transported into enterocytes?

A

Via PepT1 (peptide transporter 1), H+ dependent

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39
Q

Where does the majority of amino acid absorption occur?

A

Duodenum and jejunum

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40
Q

What % of digested protein comes from ingested food? Where does the remaining % come from?

A

50% from ingested food
25% from proteins in digestive juices
25% from desquamated mucosal cells

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41
Q

What % of protein in the small intestine escapes digestion and absorption?

A

2-5% (some of this is eventually digested by bacterial action in the colon)

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42
Q

Where does the protein present in stool come from?

A

Almost all is from bacteria and cellular debris (not dietary)

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43
Q

What happens to peptidase activity in the setting of ileal resection?

A

Increased peptidase activity

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44
Q

Describe the pathophysiology of Hartnup disease

A

Congenital defect in the mechanism of transport of neutral amino acids in the intestine and renal tubules
Results in cystinuria but not nutritional deficiency of these amino acids, because peptide transport compensates

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45
Q

How is IgA absorbed by infants from maternal colostrum?

A

Absorption is by endocytosis from intestinal lumen to mucosa and subsequent exocytosis from mucosa to circulation

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46
Q

Describe the difference in protein digestion/absorption between infants and adults?

A

Infants absorb moderate amounts of undigested proteins (including IgA)
Absorption of intact proteins declines sharply after weaning

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47
Q

What is the % incidence of food allergy in children?

A

8%

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48
Q

Where are protein antigens (particularly bacterial and viral proteins) absorbed? What is the significance of this?

A

In large M (microfold) cells, specialised intestinal epithelial cells overlying aggregates of lymphoid tissue called Peyer patches
Antigens activate lymphocytes which enter the circulation but later return to intestinal mucosa and other epithelia where they secrete IgA in response to subsequent exposures (“secretory immunity”)

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49
Q

Describe the process of nucleic acid digestion and absorption

A

Nucleic acids split into nucleotides in the intestine by pancreatic nucleases
Nucleotides split into nucleosides and phosphoric acid by enzymes on luminal surfaces of mucosal cells
Nucleosides are then split into their constituent sugars and purine and pyrimidine bases
Bases absorbed by active transport

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50
Q

Where does most fat digestion begin?

A

Duodenum

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51
Q

Describe the activity of pancreatic lipase

A

Hydrolyses 1- and 3-bonds of triglycerides, producing free fatty acids and 2-monoglycerides

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52
Q

Describe the activity of pancreatic colipase

A

Secreted in inactivated proform, activated by trypsin in the intestinal lumen, and binds to bile acids on the surface of triglyceride droplet to anchor lipase and allow for its lipolytic activity

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53
Q

Describe the activity of cholesterol esterase

A

Catalyses hydrolysis of cholesterol esters, esters of fat-soluble vitamins, phospholipids, and triglycerides

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54
Q

What causes fat emulsification in the small intestine?

A

Detergent action of bile acids, phosphatidylcholine, and monoglycerides

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55
Q

What are micelles? How are they formed and what is their role?

A

Cylindrical aggregates with hydrophobic centres containing cholesterol, and amphipathic phospholipids and monoglycerides oriented with hydrophilic heads facing out and hydrophobic tails in the centre
Formed from interaction of bile acids and lipids
Help keep lipids in solution and transport them to intestinal brush border for absorption

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56
Q

Describe the process of fat digestion and absorption

A

Pancreatic lipase (with activity enhanced by colipase) liberates fatty acids from triglycerides
Cholesterol esterase hydrolyses cholesterol esters, esters of fat-soluble vitamins, phospholipids and triglycerides
Fats are emulsified by the detergent action of bile acids, phosphatidylcholine, and monoglycerides in the small intestine
Micelles are formed (composed of cholesterol, fatty acids, phospholipids and monoglycerides with hydrophobic core and hydrophilic outer), providing a mechanism for transport through the unstirred layer to the mucosal brush border
Lipids are then absorbed mostly by passive diffusion
Within enterocytes, absorbed fatty acids and monoglycerides are re-esterified to form triglyceride
Apoproteins synthesised in rough ER are coated around lipid cores to produce chylomicrons, which are secreted from the basolateral membrane via exocytosis and enter the lymphatics (too large to pass through junctions between capillary endothelial cells)

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57
Q

What % of dietary fat is absorbed with a moderate fat intake? Is this true for both adults and infants?

A

95% or more
Processes involved in fat absorption are not fully mature at birth and so infants fail to absorb 10-15% of ingested fat

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58
Q

Where is absorption of LCFAs the greatest? How does this differ from SCFAs?

A

LCFAs: proximal small intestine (but appreciable amounts also absorbed in ileum)
SCFAs: produced in and absorbed from the colon

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59
Q

Three causes of steatorrhoea

A
  1. Destruction or deficiency of exocrine pancreas (reduced lipase secretion)
  2. Hypersecretion of gastric acid (inhibits lipase)
  3. Defective reabsorption of bile acids in distal ileum (e.g. due to terminal ileum resection or disease)
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60
Q

What % of ingested fat appears in faeces when bile is excluded from the intestine?

A

Up to 50%

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61
Q

Why does the amount of fat in stools increase with failure of bile acid reabsorption in the distal ileum?

A

Liver cannot increase rate of bile acid production to sufficient degree to compensate for loss

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62
Q

How are SCFAs produced in the colon? How are they absorbed?

A

By the action of colonic bacteria on complex carbohydrates, resistant starches, and other components of dietary fibre

Absorbed by specific transporters

63
Q

Three SCFAs produced in the colon

A
  1. Acetate (60%)
  2. Propionate (25%)
  3. Butyrate (15%)
64
Q

5 roles of SCFAs

A
  1. Contribute to total caloric intake
  2. Trophic effect on colonic epithelial cells
  3. Anti-inflammatory
  4. Maintain acid-base equilibrium (absorbed in part by H+ exchange)
  5. Promote Na+ absorption
65
Q

Define vitamins

A

Small molecules that play vital roles in bodily biochemical reactions and cannot be synthesised endogenously (so must be obtained from the diet)

66
Q

Four fat-soluble vitamins

A

A, D, E, K

67
Q

Describe the process of fat-soluble vitamin digestion and absorption

A

Ingested as esters
Digested by cholesteral esterase
Highly insoluble, must be incorporated into micelles for absorption

68
Q

Where are most vitamins absorbed? What is the exception?

A

Proximal small intestine
Vitamin B12 is absorbed in the ileum in complex with intrinsic factor

69
Q

Which cells secrete intrinsic factor?

A

Gastric parietal cells

70
Q

Is water-soluble vitamin absorption Na+ dependent or independent?

A

Vitamin B12 absorption is Na+ independent
All other water-soluble vitamins are absorbed via Na+ cotransporters

71
Q

8 water-soluble vitamins

A

Thiamine (vitamin B1)
Riboflavin (vitamin B2)
Niacin (vitamin B3)
Pantothenate (vitamin B5)
Pyridoxine (vitamin B6)
Biotin (vitamin B7)
Cobalamin (vitamin B12)
Ascorbic acid (vitamin C)

72
Q

What % of ingested calcium is absorbed?

A

30-80%

73
Q

What two factors facilitate calcium absorption?

A
  1. Calcitriol (1,25-dihydroxycholecalciferol
  2. Protein
74
Q

What two factors inhibit calcium absorption?

A

Phosphates and oxalates (form insoluble salts with Ca2+)

75
Q

What is the effect of protein on magnesium absorption?

A

Protein facilitates magnesium absorption

76
Q

How much iron is lost by men vs premenopausal women daily?

A

Men: 0.6mg/day
Premenopausal women: variable but larger (~2x men on average)

77
Q

What is the average daily iron intake in the US and Europe? What % of this is absorbed?

A

20mg ingested daily
Amount absorbed is equal only to losses: so ~3-6%

78
Q

Three factors inhibiting dietary iron absorption

A
  1. Phytic acid in cereals
  2. Phosphates
  3. Oxalates

(all react with iron to form insoluble compounds in the intestine)

79
Q

In what form is most dietary iron found? In what form is it absorbed? How is it converted from its dietary form to the form required for absorption?

A

Most dietary iron is in ferric (Fe3+) form
Absorbed in its ferrous (Fe2+) form
Fe3+ converted to Fe2+ via action of Fe3+ reductase associated with iron transporter on the brush border of enterocytes

80
Q

What is the role of gastric secretions in iron absorption? What is the clinical significance of this?

A

Gastric secretions dissolve the iron and permit it to form soluble complexes with ascorbic acid and other substances that aid its reduction to Fe2+ form

Iron deficiency anaemia is a common complication of partial gastrectomy

81
Q

Where does iron absorption occur?

A

In the duodenum

82
Q

Describe the process of iron absorption

A

Fe3+ converted to Fe2+ by Fe3+ reductase on brush border
Fe2+ transported into enterocytes via DMT1 (divalent metal transporter 1)
Some is stored as ferritin
Remainder transported via ferroportin 1 on basolateral membrane (with assistance from associated hephaestin protein)
Fe2+ converted back to Fe3+ and bound to transferrin for transport in bloodstream

83
Q

How many iron-binding sites does transferrin have?

A

2

84
Q

Normal transferrin saturation

A

~35%

85
Q

Normal plasma iron level in men vs women

A

Men: 130ug/dL
Women: 110ug/dL

86
Q

How is heme absorbed?

A

Via apical transport protein in enterocytes
In the cytoplasm, HO-2 (heme oxygenase 2) removes Fe2+ from porphyrin

87
Q

Where is iron found in the body?

A

Haemoglobin (75%)
Myoglobin (3%)
Ferritin (remainder)

88
Q

What is haemosiderin?

A

Ferritin molecules in lysosomal membranes which aggregate in deposits containing up to 50% iron

89
Q

Three factors regulating iron absorption

A
  1. Recent dietary intake
  2. State of iron stores
  3. State of bone marrow erythropoiesis
90
Q

Four features of haemochromatosis

A
  1. Pigmentation of the skin
  2. Pancreatic damage with diabetes (“bronze diabetes”)
  3. Hepatic cirrhosis with high incidence of HCC
  4. Gonadal atrophy
91
Q

Most commonly affected gene in hereditary haemochromatosis and its role

A

HFE
Normally inhibits expression of duodenal transporters participating in iron uptake

92
Q

Summarise the mechanisms controlling food intake

A
93
Q

Where is CCK released and what is its effect?

A

Anorexin or satiety factor
Released by I cells in intestine or nerve endings in the brain

94
Q

Where is leptin produced and what is its effect?

A

Produced by adipose tissue: increased adipocyte size results in increased leptin release, which reduces food intake (in part by increasing expression of other anorexigenic factors in the hypothalamus e.g. POMC, CART, neurotensin, CRH) and stimulates metabolic rate
May inhibit ghrelin secretion

95
Q

Where is ghrelin produced and what is its effect?

A

Produced mainly by stomach (also by pancreas and adrenals)
Levels increase preprandially and decrease postprandially
Involved in meal initiation by increasing synthesis and release of central orexins in the hypothalamus (e.g. neuropeptide Y, cannabinoids), and by suppressing leptin

96
Q

Define metabolic rate

A

Amount of energy liberated per unit time

97
Q

Define calorie (cal)

A

Amount of heat energy necessary to raise the temperature of 1g of water 1°C (from 15° to 16°C)

98
Q

Define Calorie (kcal)

A

1000 cal

99
Q

kcal/g of carbohydrate

A

4.1kcal/g of carbohydrate

100
Q

kcal/g of fat

A

9.3kcal/g of fat

101
Q

kcal/g of protein

A

4.1kcal/g of protein (higher outside the body; endogenous oxidation of protein is incomplete, with end-products being urea and related nitrogenous compounds in addition to CO2 and H2O)

102
Q

Define respiratory quotient

A

Ratio in the steady state of the volume of CO2 produced to the volume of O2 consumed per unit of time

103
Q

Define respiratory exchange ratio

A

Ratio of CO2 to O2 at any given time, whether or not equilibrium has been reached

104
Q

RQ of carbohydrate

A

1.00

105
Q

RQ of fat

A

0.70

106
Q

RQ of protein

A

0.82

107
Q

How can O2 consumption and CO2 production (and therefore RQ) of an organ be calculated?

A

By multiplying blood flow per unit time by arteriovenous differences for O2 and CO2

108
Q

RQ of the brain

A

0.97-0.99

109
Q

13 factors affecting metabolic rate

A
  1. Muscular exertion during or just before measurement
  2. Recent food ingestion
  3. High or low environmental temperature
  4. Height, weight, BSA
  5. Sex
  6. Age
  7. Growth
  8. Reproduction
  9. Lactation
  10. Emotional state
  11. Body temperature
  12. Circulating levels of thyroid hormones
  13. Circulating epinephrine and norepinephrine levels
110
Q

What is the most important factor affecting metabolic rate?

A

Muscular exertion

111
Q

What is SDA? How long does it last? What is the mechanism?

A

Specific dynamic action: the obligatory energy expenditure that occurs during a food’s assimilation into the body (hence why metabolic rate is increased by recent ingestion of food)
Lasts up to 6hrs
Mechanism uncertain

112
Q

What is the effect of environmental temperature on metabolic rate?

A

Increases metabolic rate when environmental temperature lower or higher than body temperature
When lower than body temp: activates heat-producing mechanisms and metabolic rate rises
When higher than body temp: metabolic processes accelerate and metabolic rate increases 14% for every 1°C

113
Q

Define basal metabolic rate

A

Metabolic rate determined at rest in a room at a comfortable temperature in the thermoneutral zone 12-14hrs after last meal

114
Q

What happens to the BMR during sleep?

A

Falls 10%

115
Q

What happens to the BMR during prolonged starvation?

A

Falls up to 40%

116
Q

What is the maximal metabolic rate reached during exercise vs the BMR?

A

~10x BMR (may be up to 20x in trained athletes)

117
Q

BMR of man of average size

A

2000kcal/day

118
Q

What anthropomorphic value correlates well with BMR?

A

BSA (BMR = 3.52 x W^0.75)

119
Q

How many additional calories are needed per day in sedentary vs very active person?

A

Sedentary: additional 500kcal/day
Active: additional 3000kcal/day

120
Q

What compensatory changes occur in the intestine with removal of short segments of jejunum or ileum?

A

Compensatory hypertrophy and hyperplasia of remaining mucosa

121
Q

Describe short gut syndrome

A

Occurs when >50% of small intestine is resected or bypassed
Absorption of nutrients and vitamins is compromised (including fat if terminal ileum is resected, resulting in deficient bile acid reabsorption) -> malabsorption syndrome

122
Q

Three features of malabsorption syndrome

A

Body wasting
Hypoproteinaemia
Oedema

123
Q

MHC class II antigens implicated in coeliac disease

A

HLA-DQ2 or DQ8

124
Q

Briefly describe the pathogenesis of coeliac disease

A

Gluten and closely related proteins cause intestinal T cells to mount an inappropriate immune response, damaging intestinal epithelial cells and resulting in loss of villi and flattening of mucosa
Bowel function restores to normal with removal of grains containing gluten (including wheat, rye, barley and oats)

125
Q

How can the diarrhoea caused by bile acid malabsorption be managed?

A

With resin (cholestyramine) which binds bile acids in lumen and prevents secretatory effect on colonocytes

126
Q

Recommended daily protein intake

A

1g/kg of body weight/day

127
Q

How much protein should be eaten by a 65kg man who is moderately active (daily caloric need of 2800kcal)? How much fat and carbohydrate?

A

65g protein/day, which will supply 267kcal (65 x 4.1)
Reasonable fat intake would be 50-60g (465kcal)
Remainder can be carbohydrate

128
Q

14 essential trace elements

A
  1. Arsenic
  2. Chromium
  3. Cobalt
  4. Copper
  5. Fluorine
  6. Iodine
  7. Iron
  8. Manganese
  9. Molybdenum
  10. Nickel
  11. Selenium
  12. Silicon
  13. Vanadium
  14. Zinc
129
Q

What does cobalt deficiency cause?

A

Megaloblastic anaemia (cobalt is part of B12)

130
Q

What does iodine deficiency cause?

A

Thyroid disorders

131
Q

What does zine deficiency cause?

A

Skin ulcers
Depressed immune responses
Hypogonadal dwarfism

132
Q

What does copper deficiency cause?

A

Anaemia
Changes in ossification

133
Q

What does chromium deficiency cause?

A

Insulin resistance

134
Q

How are vitamins A and D transported in circulation?

A

Protein-bound

135
Q

How is vitamin E transported in the circulation?

A

Bound to chylomicrons
Transferred to VLDL in the liver

136
Q

8 features of hypervitaminosis A

A

Anorexia
Headache
Hepatosplenomegaly
Irritability
Scaly dermatitis
Patchy loss of hair
Bone pain
Hyperostosis

137
Q

3 features of hypervitaminosis D

A

Weight loss
Calcification of soft tissues
AKI

138
Q

2 features of hypervitaminosis K

A

GI upset
Anaemia

139
Q

What pathology can be caused by ingestion of megadoses of pyridoxine (vitamin B6)?

A

Peripheral neuropathy

140
Q

Actions, sources and deficiency symptoms of vitamin A (retinol)

A

Actions: visual pigments, foetal development, cell development
Sources: yellow vegetables and fruit
Deficiency symptoms: night blindness, dry skin

141
Q

Actions, sources and deficiency symptoms of thiamine (vitamin B1)

A

Actions: cofactor in decarboxylations
Sources: liver, unrefined cereal grains
Deficiency symptoms: Beriberi, neuritis

142
Q

Actions, sources and deficiency symptoms of riboflavin (vitamin B2)

A

Actions: constituents of flavoproteins
Sources: liver, milk
Deficiency symptoms: glossitis, cheilosis

143
Q

Actions, sources and deficiency symptoms of niacin (vitamin B3)

A

Actions: constituent of NAD+ and NADP+
Sources: yeast, lean meat, liver
Deficiency symptoms: pellagra

144
Q

Actions, sources and deficiency symptoms of pyridoxine (vitamin B6)

A

Actions: forms prosthetic group of certain decarboxylases and transaminases
Sources: yeast, wheat, corn, liver
Deficiency symptoms: convulsions, hyperirritability

145
Q

Actions, sources and deficiency symptoms of pantothenate (vitamin B5)

A

Actions: constituent of CoA
Sources: eggs, liver, yeast
Deficiency symptoms: dermatitis, enteritis, alopecia, adrenal insufficiency

146
Q

Actions, sources and deficiency symptoms of biotin (vitamin B7)

A

Actions: catalyses CO2 “fixation”
Sources: egg yolk, liver, tomatoes
Deficiency symptoms: dermatitis, enteritis

147
Q

Actions, sources and deficiency symptoms of folate (vitamin B9)

A

Actions: coenzymes for “1-carbon” transfer, involved in methylating reactions
Sources: leafy green vegetables
Deficiency symptoms: sprue, anaemia, NTDs in children born to folate-deficient women

148
Q

Actions, sources and deficiency symptoms of cobalamin (vitamin B12)

A

Actions: coenzyme in amino acid metabolism, stimulates erythropoiesis
Sources: liver, meat, eggs, milk
Deficiency symptoms: pernicious anaemia

149
Q

Actions, sources and deficiency symptoms of ascorbic acid (vitamin C)

A

Actions: maintains prosthetic metal ions in their reduced form, scavenges free radicals
Sources: citrus fruits, leafy green vegetables
Deficiency symptoms: scurvy

150
Q

Actions, sources and deficiency symptoms of D-group vitamins

A

Actions: increase intestinal absorption of Ca2+ and PO4-
Sources: fish liver
Deficiency symptoms: rickets

151
Q

Actions, sources and deficiency symptoms of E-group vitamins

A

Actions: antioxidants
Sources: milk, eggs, meat, leafy vegetables
Deficiency symptoms: ataxia and other symptoms and signs of spinocerebellar dysfunction

152
Q

Actions, sources and deficiency symptoms of K-group vitamins

A

Actions: catalyse y carboxylation of glutamic acid residues on various proteins concerned with blood clotting
Sources: leafy green vegetables
Deficiency symptoms: haemorrhagic phenomena

153
Q

Essential amino acids

A

PVT TIM HALL:
Phenylalanine
Valine
Threonine

Tryptophan
Isoleucine
Methionine

Histidine*
Arginine*
Leucine
Lysine

*Conditionally essential

154
Q

Where is the majority of water absorbed?

A

Jejunum

ACEM Primary Written (160 decks)

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