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1: conversion of free fatty acids to ketones
2: conversion of ammonia to urea
3: synthesis of very low density lipoproteins
4: synthesis of somatomedin-C (IGF-I)
Ganong 13th Ed. Chapter: 17 Page: 243, 248, 251 Ch. 22 P. 337
1: storage of glucose as glycogen
2: processing of chylomicron remnants from the blood
3: gluconeogenesis to maintain blood glucose concentration
4: chemical modification and excretion of thyroxine
Guyton Page: 837
1: porto-systemic shunting of blood
2: reduced capacity for urea synthesis in the liver
3: bacterial production of ammonia in the gut
4: decreased hydrogen ion excretion by the kidney
Guyton 7th Edition CHAPTER: 70 PAGE: 837
1: may be formed from glutamine in the kidney
2: is taken up by glutamic acid in the brain
3: is converted to urea in the liver
4: is a substrate for urea production in the kidney
Ganong 13th Ed. Ch. 32 P. 514 Ch. 38 P. 599
1: about 85% of bilirubin is formed from haemoglobin released by destruction of mature red blood cells which normally have a life-span of 74 days
2: unconjugated bilirubin in plasma is filtered into the proximal convoluted tubules
3: about 20% of bilirubin in the small intestine recirculates to the liver in the enterohepatic circulation
4: unconjugated bilirubin rises in the plasma when there is excessive destruction of red blood cells
Ganong, 19th ed, Ch 26
1: they are absorbed largely from the ileum
2: the primary bile salts are cholate and chenodeoxycholate and are conjugated with glycine or taurine in the liver
3: they are synthesised from cholesterol and are concentrated in the gall bladder
4: about 90% of cholate and chenodeoxycholate which enter the small intestine are absorbed from the jejunum and recirculate to the liver
Ganong CHAPTER: 26 PAGE: 403
1: normally transported in the blood bound to albumin
2: normally converted to urobilinogen in the small intestine
3: conjugated in the liver with glucuronic acid
4: formed in the reticuloendothelial system and bone marrow
Haemoglobin is broken down in the reticuloendothelial system and bone marrow (D true). The 'haem' portion is subsequently transported to the liver bound to albumin (A true) where it is conjugated with glucuronic acid (C true). After secretion in the bile, it is converted in the small intestine to urobilinogen (B true) of which 10-20% is reabsorbed.
Guyton 7th Ed./Ganong 13th Ed./Walter & Israel 6th Ed. CHAPTER: 70/26/47 PAGE: 838-839/419/5
3: bile salts
Ganong 13th Edition CHAPTER: 26 PAGE: 420 (Fig.26-23)
A. bile salts
C. fatty acids
E. bile pigments
Hepatic bile is made up of bile salts (0.7%), bile pigments (0.2%), cholesterol (0.06%), and other substances (fatty acids 0.15%, fat 0.1%) dissolved in an alkaline electrolyte solution resembling pancreatic juice (A true).
1: reabsorption of bile salts from the intestine leads to further secretion of bile
2: active transport of NaCl out of the gall bladder is the mechanism by which the bile is concentrated
3: a certain concentration of bile salt is required for the formation of micelles
4: bile salts are derived from waste products of haemoglobin breakdown
Refer to Ganong, 19th Ed, Ch 26, page 479-482. This question is currently under review by the Physiology Sub Committee. 28 June 2002. This question has been updated. 9 Dec 2002.
Ganong 13th Edition CHAPTER: 26 PAGE: 418. The liver secretes about 500ml of bile daily, containing 0.7% bile salts. These are sodium and potassium salts of conjugated bile acids synthesised from cholesterol. The two principal bile acids formed in the liver are cholic acid and chenodeoxycholic acids. The normal rate of bile salt synthesis is only 0.2 to 0.4 gram daily (R false). The total bile salt pool of approximately 3.5 gram recycles repeatedly via the enterohepatic circulation with minimal faecal loss. Obstructive jaundice associated with complete obstruction of the bile duct can cause intense skin itching mainly contributed to by bile salt retention (S true). Five hundred ml of bile are secreted daily. Bile salts are secreted into the bowel lumen. Ninety to ninety-five per cent of these are absorbed in the terminal ileum, and returned to the liver via the enterohepatic circulation, and then re-excreted. In complete obstruction of the common bile duct bile salts accumulate in the serum and itching occurs (S true). Cholic acid is formed in the liver. This represents 50% of total bile salt production which amounts to 0.2-0.4 gm/day (R false). This is recycled, so effectively that 3.5 gm are recycled daily as the bile salt pool
1: chenodeoxycholic acid
2: deoxycholic acid
3: cholic acid
4: taurocholic acid
Ganong 15th ed Chapter:26 Page:466
Refer to Gangong, 19th Ed, Ch 26, page 480-481
Kyle CHAPTER: 18 PAGE: 408
A. relaxed, and open at both ends
B. closed at the stomach end only
C. closed at the oral end only
D. contracted throughout its length
E. closed at both ends
Ganong 13th Edition CHAPTER: 26 PAGE: 408
1: it has a resting pressure of 5mm of Hg above gastric pressure
2: exhibits tonic muscular activity unlike the body of the oesophagus
3: in achalasia absence of ganglion cells results in failure of adequate contraction in this region
4: reflex relaxation of the sphincter is integrated in the tractus solitarius and the nucleus ambiguous
Refer to Ganong, 19th Ed, Ch 26, page 469. Review July 2004 re: option should be true.
1: receptive relaxation
2: control of the rate of access of food to the small intestine
3: secretion of a lipase
4: secretion of a factor contributing to erythrocyte formation
Guyton 7th Edition Chapter: 63 & 64 Page: 761, 774-775. Receptive relaxation of the stomach takes place as oesophageal peristaltic waves pass towards the stomach, transmitted by myenteric inhibitory nerves (A true). The gastro-oesophageal sphincter relaxes ahead of time ready to receive food being propelled down the oesophagus during the act of swallowing. Stomach emptying is regulated by signs from both the stomach and duodenum. Signals from the stomach are twofold: (i) nervous signals, caused by distention by food; (ii) gastrin released by antral mucosa in response to certain types of food within the stomach (B true). The stomach secretes a number of minor enzymes, such as lipase (C true) amylase and gelatinase. These are of little quantitative significance in digestion. The stomach secretes intrinsic factor which is essential for vitamin B12 absorption (D true).
Removal of the part of the stomach nearest the pylorus would be expected to reduce gastric acid secretion; this operation would remove the antrum, and with it the hormonal stimulus to acid secretion. The response is incorrect. The antrum does not secrete most of the hydrochloric acid the body and fundus do this.
Ganong 11th Edition CHAPTER: 19 PAGE: 284
1: vagal stimulation increases the secretion of acid and pepsin.
2: resection of large segments of small intestine is associated with hypersecretion of acid.
3: vagotomy abolishes acid production.
4: vagotomy abolishes gastric motility.
The cells of the gastric glands secrete 2.5 litres of gastric juice daily. Regulation is by neural and humoral mechanisms. Vagal stimulation increases gastrin secretion by release of gastrin-releasing-peptide and acetylcholine. It is convenient to break up the physiological regulation of gastric secretion into cephalic, gastric and intestinal influences. Cephalic influences are vagally-mediated responses induced by activity in the CNS. The gastric influences are primarily local reflex responses and responses to gastrin. The intestinal influences are the reflex and hormonal feedback effects on gastric secretion initiated from the small intestine. Resection of large segments of small intestine is associated with hypersecretion of acid (2 true). Vagal stimulation increases the secretion of acid and pepsin (1 true). Vagotomy affects only the cephalic phase of secretion, and diminishes (but does not abolish) acid secretion. Gastrin is produced by G cells in the gastric antral mucosa and stimulates gastric acid and pepsin secretion. Acid in the antrum inhibits gastric secretion by a feedback mechanism involving somatostatin. Gastric motility is also reduced (but not abolished) after vagotomy (3 & 4 false). Gastric drainage procedures are required if total truncal vagotomy is performed, but not with highly selective vagotomy. All these operations are now relatively rare for peptic ulcer disease due to the effectiveness of H2 receptor blockers and proton pump inhibitors; and by control of infection from the bacterium Helicobacter pylori which disrupts the mucus barrier (as does aspirin and other NSAIDs).
1: vagal stimulation increases the secretion of acid and pepsin but not mucus
2: after the operation of high gastro-jejunostomy (gastric bypass) for obesity the level of plasma gastrin may rise following a meal
3: vagotomy abolishes acid production
4: vagotomy abolishes gastric motility
Ganong 13th Edition CHAPTER: 26 PAGE: 409-413, 403-404
1: the posterior vagus gives rise to hepatic branches which enter the liver via the lesser omentum and the porta hepatis
2: the main terminal branch of the anterior vagus nerve crosses the stomach distal to the incisura angularis about 5-6 cm from the pylorus
3: most of the fibres of the posterior vagus nerve terminate in the stomach
4: some vagal fibres travelling to the parietal cell mass may sink into the muscular wall at the oesophagus some distance above the cardia
Last (8) PAGE: 336
1: inhibits the release of gastrin
2: occurs due to the synergistic action of histamine, gastrin and acetyl choline
3: reflexly inhibits gastric secretion
4: promotes activity in inhibitory afferent fibres of the vagus
Ganong 11th Ed. CHAPTER: 26 PAGE: 396-397
Ganong 11th Edition CHAPTER: 26 PAGE: 397-398
1: intracellular protein breakdown
2: loss of potassium into gastric juice
3: decreased insulin production
4: increased renal loss of potassium
Guyton 7th Edition CHAPTER: 64, 77 PAGE: 774-775, 911
1: metabolic alkalosis
2: low pH of the urine
3: high serum sodium
4: low serum potassium
1: an increase in alveolar ventilation
2: a rise in plasma Cl-concentration
3: an increase in CSF pressure
4: a rise in plasma HCO-3 concentration
Ganong 13th Edition Chapter: 39 Page: 608-611
1: Low serum potassium.
2: Low pH of the blood.
3: Low pH of the urine.
4: Extracellular metabolic acidosis.
"Pyloric" stenosis occurs when the gastric outlet is obstructed by a benign duodenal or prepyloric ulcer or by a stomach cancer. Loss of gastric acid from prolonged vomiting can cause extracellular metabolic alkalosis (4 false), particularly when the cause of the obstruction is a peptic ulcer associated with hypersecretion of acid. Serum bicarbonate rises and serum chloride falls, with a rise in blood pH (2 false). The renal response of urinary bicarbonate excretion is initially associated with an alkaline urine containing sodium, potassium and bicarbonate. Subsequently the urine can become acid ("paradoxical aciduria") (3 true) after prolonged vomiting with continuing combined gastrointestinal and urinary losses of water and electrolytes, associated with gross deficiencies in water, sodium, chloride and potassium with low serum potassium (1 true). The late aciduria is associated with hydrogen ion excretion by renal tubular cells in the face of severe depletion of the cations sodium and potassium.
Correction requires intravenous administration of isotonic saline with added potassium, which almost always suffices to restore acid-base balance provided that continuing losses are avoided by correcting the obstruction.,
A. gastrin-releasing peptide
C. intrinsic factor
Secretin is released from the duodenum in response to duodenal acidification. It significantly increases pancreatic water and bicarbonate secretion and inhibits gastric acid output. Thus it leads to increased pH of duodenal contents (B true). Gastrin and gastrin-releasing peptide increase gastric acid output which would lower duodenal pH (A and E false). Cholecystokinin stimulates pancreatic enzyme secretion and contraction of the gallbladder (D false). Intrinsic factor is released from the oxyntic cells along with the secretion of acid and is essential for Vitamin B12 absorption in the ileum. It has no effect on duodenal pH (C false).
1: the most significant single factor that increases the luminal surface area is the presence of villi
2: mucosal cells are formed from undifferentiated cells in the crypts of Lieberkuhn
3: peristalsis is the only type of movement demonstrated
4: the frequency of slow waves decreases from the jejunum to the ileum
Ganong 20th Ed, Chapter 26, p490. It is the microvilli that make the greater contribution to increase in surface area. Reviewed March 2003.
1: about 8-9 litres of water are absorbed by the small and large intestine daily.
2: potassium is absorbed by the small intestine and secreted by the large intestine.
3: the absorptive surface of the small intestine is increased 600 fold by the valvulae conniventes, villi and microvilli.
4: diarrhoea can cause hypokalaemia.
The endogenous secretions (salivary glands 1500ml, stomach 2500ml, bile 500ml, pancreas 1500ml and small intestine 1000ml) total around 7 litres; to which is added 2 litres of ingested water in food and fluid. Of this total intestinal input of 9 litres almost all is absorbed (1 true), leaving 100 to 200ml as output in the stool. Of the reabsorption, approximately 8 litres occurs in the small intestine (6 litres in the jejunum and 2 litres in the ileum); and one litre in the colon. The absorptive surface of the small intestine is increased about 600 fold by the valvulae conniventes and villi (3 true). Potassium is absorbed from the small intestine and can be actively secreted into the large intestine (2 true). There is normally a nett secretion of potassium and bicarbonate into the colon. Active absorption of sodium from the colon is accompanied by water absorption. Diarrhoea can cause significant loss of electrolytes, including potassium (4 true). Reviewed Dec 2002.
4: isotonic intestinal secretion
Ganong 11th Edition CHAPTER: 26 PAGE: 390, 408. The intestinal glands of the jejunum produce secretin, cholecystokinin and mucus (A, B and C true) in an isotonic secretion (D true) as do glands in the duodenum.
1: vitamin B12
3: bile salts
Ganong 13th Edition CHAPTER: 25 PAGE: 399-400
Ganong 13th Edition CHAPTER: 26 PAGE: 402-405
Gastrin secreted by the stomach is inactivated primarily in the kidney and in the small intestine. Thus if this inhibitory effect is removed in part, more gastrin is present to stimulate gastric acid production (R true and is a valid explanation) and peptic ulcer may develop (S true).
A. intractable diarrhoea
B. increased likelihood of renal stone
D. increased serum calcium
E. lowered serum protein
1: bile salts
2: vitamin B12
3: fat-soluble vitamins
4: ferrous iron
Ganong, 19th ed, Ch 26
Guyton 7th Edition, Ganong 13th Edition CHAPTER: 66 & 26 PAGE: 799 & 414
Ganong 13th Ed. CHAPTER: 26 PAGE: 425
Ganong 13th Edition CHAPTER: 26 PAGE: 425-426
1: the harmful effects are caused by bacterial invasion of the small intestine
2: steatorrhoea is a clinical feature
3: bacterial overgrowth may contribute to the development of macrocytic anaemia
4: jaundice is a clinical feature
Ganong 13th Edition CHAPTER: 26 PAGE: 425-426
This question will be submitted at the March 2004 meeting regarding option 1(15/03/2004)
Ganong 13th ed. Chapter: 26 Page: 418
1: excess volume of feed
2: hyperosmolarity of feed
4: short bowel syndrome
Burnett - C. S. S. CHAPTER: 18.22.4 PAGE: 347
1: constancy of faecal content despite variation in diet
2: active transport of Na+ out of the colonic mucosa
3: sterile contents at birth
4: secretion of K+ and HCO3- into lumen
Refer to Ganong, 19th Ed, Ch 26, page 486 and following
Approximately 1000-2000 ml of isotonic chyme enter the colon each day from the ileum. As it passes through the colon, 90% of the water is absorbed by the colon until 200-250 ml of semi-solid faeces are found at the distal colon. Semi-solid or fluid faeces passes more easily through a constriction than solid faeces. Thus a proximal tumour will not stop fluid and semi-solid colonic contents and will be quiescent.
1: gastrin stimulates gastric mucosal growth
2: cholecystokinin secretion by cells of the upper small intestine is enhanced by amino acids and fatty acids
3: secretin augments the action of cholecystokinin in producing pancreatic secretion of digestive enzymes
4: gastric inhibitory peptide (GIP) increases the sensitivity of insulin response to raised blood glucose
Ganong 16th Edition CHAPTER: 26 PAGE: 452-54 Guyton CHAPTER: 78 PAGE: 977-78
1: lipolytic activity
2: present in the nerves of the gastrointestinal tract
3: release by vagal stimulation
4: portions of similar amino acid sequence
Ganong 13th Edition CHAPTER: 26 PAGE: 442-44
D. gastrin - releasing peptide
Ganong 19th ed, Ch 26
1: is a powerful stimulant of pancreatic enzyme
2: inhibits gastric motility
3: is produced in the upper small intestine
4: inhibits gastric acid secretion
Secretin is produced by cells in the mucosal glands of the duodenum and jejunum (C true). Its main action is to stimulate the pancreas to secrete watery, alkaline pancreatic juice augmenting CCK (A false). Secretin decreases gastric acid secretion (D true) by a feedback loop via gastrin by increasing the pH of the duodenum. Secretin has a mild inhibitory effect on the motility of most of the gastro-intestinal tract (B true). Ganong 13th Edition & Guyton 7th Edition CHAPTER: 26/63 & 64 (Guyton) PAGE: 405/764 -778 (Guyton)
1: released by acid in the duodenum
2: released by vagal stimulation
3: a stimulant of secretion from biliary and pancreatic duct cells
4: responsible for a high chloride ion concentration in external pancreatic secretion
Ganong, 19th ed, Ch 26
1: is secreted by cells in the mucosa of the duodenum
2: increases HCO3- secretion from the exocrine pancreas
3: decreases gastric acid secretion
4: augments the action of CCK on the pancreas
Ganong 13th ed. Chapter: 26 Page: 405
Ganong 13th ed. Chapter: 26 Page: 405
Refer to Ganong, 19th Ed, Ch 26, page 465-466
1: stimulates luminal gastrin release
2: stimulates gastric inhibitory peptide release
3: inhibits gastrin release into the blood stream
4: inhibits parietal cell function
Ganong 11th Edition CHAPTER: 26 PAGE: 391
1: secretion is increased by fatty acids in the duodenum
2: has a more marked effect on the ducts than on the acini of the pancreas
3: exerts a trophic effect on the pancreas
4: inhibits the action of secretin in producing secretion of an alkaline pancreatic juice
Ganong 16th Ed. Chapter 26 Page:442-443
1: is decreased by products of protein digestion in the stomach
2: is increased by hypercalcaemia
3: is low in pernicious anaemia
4: is increased after massive small bowel resection
Ganong 14th ed. Chapter: 26 Page: 411
A. is produced in the gastric antrum, stimulates HC1 secretion and is inhibited by secretin
B. is produced in the gastric body, stimulates secretin production and is inhibited by HC1 secretion
C. is produced in the gastric fundus, stimulates HC1 production and stimulates secretin production
D. stimulates secretin production
E. is produced in the gastric antrum, suppresses HC1 secretion and stimulates secretin production
Gastrin is formed in the G cells principally in the gastric antrum (B and C false), and is present in the duodenum in one-tenth the concentration released into the blood stream. It has two principal actions - one of increased HC1 secretion (E false) by the parietal cells of the fundus, the other a trophic effect on gastric an intestinal mucosa. An acid pH in the antrum is the powerful shut-off mechanism for acid, acting mainly through inhibition of gastric release. This is complete at pH 1.2. Gastrin and cholecystokinin (CCK) are partial agonists, but gastrin and secretin are antagonists. Secretin inhibits gastrin release after a meal. Acidification of the duodenum is the principal stimulus for secretin release (D false). Thus gastrin is formed principally in the gastric antrum, stimulates HC1 secretion and is inhibited by secretin (A true).
1: is functionally and structurally related to cholecystokinin
2: is secreted by the antral mucosa
3: is liberated by distension of the antrum
4: stimulates the secretion of both acid and pepsin
Gastrin, which is secreted by the antral mucosa under stimulus of antral distension is functionally and structurally related to cholecystokinin; and stimulates secretion of both acid and pepsin (1, 2, 3 and 4 true). The C-terminal pentapeptide of gastrin is identical to that of cholecystokinin (A true). Both peptides are released by a protein meal and both stimulate glucagon secretion. Gastrin is produced by G cells in the antral mucosa (B true). Receptors in the wall of the stomach and in the gastric mucosa respond to stretch (C true). Gastrin stimulates both the oxyntic and peptic cells to secrete acid and pepsin (D true).
1: Zollinger-Ellison syndrome
2: pernicious anaemia
3: secretory tumours of the pancreatic delta cells
4: most patients with duodenal ulcer
Ganong 13th Edition CHAPTER: 26 PAGE: 403-404, 413
Refer to Ganong, 19th Ed, Ch 26, page 462 and following
1: gastric antrum
2: gastric fundus
3: first part of duodenum
4: renal parenchyma
Refer to Ganong, 19th Ed, Ch 26, page 470 and following. To be reviewed at March 04 meeting re: option 2 "gastric fundus". (16/02/04).
1: potentiates action of acetylcholine in salivary glands
2: is formed from prepro-VIP
3: inhibits gastric acid secretion
4: causes vasoconstriction of peripheral blood vessels
Guyton 13th Edition CHAPTER: 26 PAGE: 405
A. Stimulation of an enzyme-rich pancreatic juice.
B. Relaxation of the sphincter of Oddi.
C. Stimulation of hepatic flow of bile.
D. Contraction of the gallbladder.
E. Stimulation of pancreatic juice rich in bicarbonate
Secretin, not cholecystokinin, stimulates a pancreatic juice rich in bicarbonate. The response is false and E is accordingly the correct answer.
A. suppress the release of gastrin.
B. bind with the gastrin molecule to prevent its action.
C. stimulate the secretion of bicarbonate.
D. stimulate the parietal cell.
E. stimulate the release of gastrin.
1: it is greatest in the upper small intestine
2: it occurs through active absorption of micelles
3: 95% of dietary fat is normally absorbed in adults
4: only 75% of dietary fat is absorbed in infants
Ganong 20th Edition, p459. Active absorption does not occur. Ganong refers to some "carrier" transport which is not neccessarily "active" and does not refer to evidence for "active" transport. Reviewed March 2003.
1: small amounts of medium and larger chain fatty acids are absorbed directly into the portal blood
2: chylomicra are small droplets of fat combined with apoproteins which aid diffusion through enterocyte membrane
3: without bile acids, less than 15% of fat is normally absorbed
4: between 80 - 90% of all fat absorbed from the gut is transported to the blood via the thoracic duct as chylomicrons
Refer to Guyton, 9th Ed, Ch 65, page 842-843; Ganong, 19th Ed, Ch 25, page 452 and following
1: bile salts combine with fatty acids and monoglycerides to form micelles
2: in the absence of bile salts fatty acids are not absorbed
3: fatty acids containing more than 10-12 carbon atoms are re-esterified to triglycerides in the mucosal cells
4: pancreatic lipase produces fatty acids and monoglycerides from dietary triglycerides
Ganong 19 Edition CHAPTER: 25 PAGE: 452-453 (also fig. 25.4)
A. Can constitute up to 70% of the total energy administered per day.
B. There is a specific requirement for short-chain fatty acids in order to generate ketone bodies for metabolism by colonocytes.
C. Omega-6 polyunsaturated fatty acid triglycerides should be provided in doses adequate to prevent essential fatty acid deficiency.
D. There is a specific requirement for medium-chain triglycerides to maintain the fluidity of membranes.
E. Omega-3 polyunsaturated fatty acids may modulate the immune response by inhibiting the induction of free-radical lipid peroxides.
Between 15% to 30% of the total calories administered per day can be provided as fat. There is no specific requirement for short-chain fatty acids. Medium-chain triglycerides can be used as a source of calories. Omega-6 polyunsaturated fatty acid triglycerides should be provided in doses adequate to prevent essential fatty acid deficiency ie. at least 7.0% of total calories. Omega-3 polyunsaturated fatty acids are sometimes referred to as 'Fish Oils'. Whilst they have no established requirement in critically ill patients, they are under clinical investigation as immune - modulating and anti-inflammatory agents. They may regulate the immune response in at least three ways: (1) by increasing membrane fluidity, (2) inducing free-radical lipid peroxides, and (3) by providing precursors for eicosanoid metabolism.
A. muscle protein
B. visceral protein
C. extracellular protein
D. liver glycogen
E. muscle glycogen
BURNETT. C.S.S. CHAPTER: 14.2.2 PAGE: 208
A. as free fatty acids in the portal vein blood.
B. as emulsified particles in the lymph.
C. as monoglycerides in the portal vein blood.
D. as triglyceride in the portal vein blood.
E. attached to plasma albumin carrier molecules.
Refer to Ganong, 19th Ed, Ch 25, page 453-454, Figure 25.5. Fats are emulsified in the small intestine by the detergent action of bile salts, lecithin, and mono-glycerides. After a fatty meal 95% or more of the ingested fat is absorbed. Fatty acids containing more than 10 to 12 carbon atoms are re-esterified to triglycerides in the mucosal cells; and are coated with protein, cholesterol and phospholipid to form chylomicrons which leave the mucosal cells and pass into the lymphatics as emulsified particles, accounting for most of the fat transport (B true). Only fatty acids containing less than 10 to 12 carbon atoms pass from mucosal cells directly into the portal blood. Absorption of long chain fatty acid begins in the duodenum and is greatest in the upper parts of the small intestine, although appreciable amounts are also absorbed from the ileum. Short chain fatty acids are produced by bacterial action on undigested complex carbohydrates from fruits and vegetables in the colon, and are probably trophic to colonic mucosa.
Refer to Ganong, 19th Ed, Ch 26, page 474-475
4: growth hormone
Ganong 16th ed. CHAPTER: 17 PAGE: 279. This question is currently under review by the sub committee. 4 June 2002. This question has been reviewed and has not been altered. 9 Dec 2002
1: transported primarily as very low density lipoprotein
2: increased by carbohydrate excess in the diet
3: removed from the circulation by both muscle and adipose tissue
4: increased when plasma cholesterol levels rise
Ganong 13th ed. Chapter 17 Page: 251-254
A. low density lipoproteins (LDL) contain more cholesterol than high density lipoproteins (HDL)
B. low density lipoproteins (LDL) contain more triglyceride than high density lipoproteins (HDL)
C. individuals with elevated LDL have a higher than normal incidence of atherosclerosis
D. individuals with elevated HDL have a higher than normal incidence of atherosclerosis
E. the primary function of HDL is in cholesterol exchange and esterification
Ganong 11th ed. CHAPTER: 17 PAGE: 243-245
1: facilitated by pancreatic juice
2: inhibited by cereal products
3: increased by adding ascorbic acid to the diet
4: predominantly in the duodenum
Refer to Ganong, 19th Ed, Ch 25, page 456 and following
1: is increased by low pH of gastric secretions
2: is increased in states of iron overload
3: requires the presence of transferrin
4: occurs in terminal ileum
Refer to Ganong, 19th Ed, Ch 25, page 456-458
1: pH of pancreatic juice
2: phytic acid
3: ascorbic acid
The absorption of non-haem iron is inhibited by its binding to dietary phytates in cereals (B true) and phosphates (D true). Alkaline conditions reduce iron absorption (A true). Ascorbic acid forms a highly soluble iron chelate which facilitates intestinal mucosal attachment. Ascorbate also acts as a reducing agent to maintain iron in the ferrous form which is more soluble than ferric iron in alkaline conditions and thereby more readily absorbed (C false).
1: absorption is mainly in the ferrous form
2: adult males require absorption of 0.5-1.0 mg. per day
3: absorption occurs mainly in the upper small intestine
4: haemosiderin is the principal storage form of iron in the tissues
Ganong 19th Edition CHAPTER: 25 PAGE: 456-458
1: his blood will show an iron deficiency anaemia
2: his absorption of iron from a full normal diet will be affected by arthritis
3: his plasma iron binding capacity will be decreased
4: there will be no suspicion of melaena on macroscopic examination of his stools
This man has lost 900 mg of iron which, under normal conditions, would have been his reserve iron store. As he has a past history of duodenal ulcer with probable iron loss and a history of active rheumatoid arthritis which will affect iron absorption and mobilisation, he is most likely to have iron deficiency anaemia (A true). Consequent to this iron deficiency, his plasma iron binding capacity may be increased (C false) although chronic inflammation may reduce the expected rise (B true). His iron absorption will thus tend to increase. Melaena will not be seen on macroscopic examination until more than 100 ml of blood are lost daily into the large intestine (D true).
ron is readily absorbed as ferrous (Fe++) iron. Most dietary iron, however is in the Fe+++ form. Gastric secretions are necessary to convert Fe+++ to Fe++ forms. Absorption takes place mainly in the duodenum and upper jejunum. Following radical gastrectomy iron deficiency anaemia is a relatively frequent complication (S true, R true and is a valid explanation of S).
Ganong, 19th ed, Ch 35
Ganong 15th Edition CHAPTER: 25, 26 PAGE: 446-47; 461-62. July 2004 review re: trainee suggests question should be true/false format.
Ganong CHAPTER:25 PAGE: 399
1: gastric acidity is required for absorption of haem-iron
2: achlorhydria leads to a significant reduction in absorption of non-haem-iron
3: iron absorption does not increase after haemolysis
4: iron absorption is increased after haemorrhage
Ganong, 19th ed, Ch 26; Guyton, 9th ed, Ch 32; Robbins, 6th ed, Ch 14. This question is currently under review by the sub committee. 4 June 2002. This question has been reviewed and has not been altered. 9 Dec 2002. Comments: Gastric acidity and secretions enhance iron absorption and patients without a stomach can become iron deficient but may still absorb some iron. (Hence can be treated with iron tablets.) Thus gastric acidity is not required.
Ganong 11th Edition & W & I 5th Edition CHAPTER: 26 PAGE: 390 609
1: a reduced packed cell volume
2: megaloblastic marrow
3: gastric atrophy
Anaemia is typically associated with a reduced packed cell volume (A true). Even though the red cells are larger than normal in pernicious anaemia, their numbers are considerably reduced, and the PCV is, therefore, low. Gastric atrophy is the most important cause of pernicious anaemia and results from an auto-immune reaction (C true). The megaloblastic marrow reflects a deficiency of Vitamin B12 and folate (B true). Pernicious anaemia is typically associated with a thrombocytopenia (D true).
1: insulin, in increased quantity following a-adrenergic stimulation
3: glucagon, in decreased quantity following administration of somatostatin
4: inactive precursors of trypsin and lipase
Ganong, 19th ed, Ch 19 and 26
1: phospholipase A
2: ribonuclease and deoxyribonuclease which split nucleotides from nucleic acids
3: chloride at about 130 mmol/l concentration
4: prolipase from nucleic acids
Pancreatic juice is alkaline and about 2 litres are secreted daily. Pancreatic juice contains phospholipase A, ribonuclease and deoxyribonuclease and prolipase (A,B,D true). The main anions are HCO3- and chloride. The concentration of bicarbonate is about 80 mmol/l rising to 150 mmol/l on stimulation by secretin. The concentration of chloride, by contrast, is about 55 mmol/l and falls when the pancreas is stimulated by secretin (C false). Question to be reviewed at March 04 meeting re: option a being true - proenzymes. (16/02/04). Question to be reviewed at March 04 meeting re: option D. (23/02/04)
1: phospholipase A
2: chloride at about 130 mmol/l concentration
3: ribonuclease and deoxyribonuclease which split nucleotides from nucleic acids
4: a bile salt activated lipase capable of hydrolysing cholesterol esters
Ganong, 20th ed, Ch 26 Pages 483, 458. Question updated 2 Dec 2002.
2: vagal stimulation
Ganong 13th Edition CHAPTER: 26 PAGE: 452-454. This question was referred to the Physiology Sub Committee for review on 1 Feb 2002.
1: secretin acts on the pancreas.
2: cholecystokinin (CCK) acts on the pancreas.
3: the vagus stimulates the pancreas.
4: the sympathetic nerves stimulate the pancreas.
Ganong 13th Edition Chapter: 26 Page: 415-416. The pancreatic juice of the exocrine pancreas contains enzymes of major importance in digestion. Their secretion is controlled by the gastrointestinal hormones secretin and CCK, and by reflex mechanisms. The active enzymes secreted include pancreatic amylase, trypsin and chymotrypsins, pancreatic lipase and carboxypeptidases. The juice is alkaline with a high bicarbonate content. About 1500ml is secreted daily. Secretion is primarily under hormonal control. Secretin acts on the pancreatic ducts to cause a copious secretion of a very alkaline pancreatic juice which is rich in bicarbonate and poor in enzymes (1 false). CCK acts on the acinar cells to cause production of pancreatic juice rich in enzymes (2 true). Stimulation of the vagi with release of acetylcholine causes discharge of zymogen granules and secretion of a small amount of juice rich in enzymes (3 true). A vagally-mediated conditioned reflex secretion of pancreatic juice occurs in response the sight or smell of food. The sympathetic nerve supply of the pancreas is vasoconstrictive, and has minimal effect on exocrine secretion (4 false).
Secretin stimulates pancreatic secretion, but this is poor in enzymes. Stimulation of the vagus causes secretion of a small amount of pancreatic juice rich in enzymes. This effect is blocked by atropine and by denervation of the pancreas, whereas the effects of cholecystokinin-pancreozymin are not. There is evidence for a vagally mediated conditioned reflex secretion of pancreatic juice. Sympathetic stimulation in the gastro-intestinal tract can inhibit peristalsis and increase the tone of the sphincters but does not affect pancreatic secretion. Cholecystokinin-pancreozymin causes contraction of the gall bladder and stimulates the pancreas to secrete pancreatic juice rich in enzymes. Furthermore, CCK augments the action of secretin in producing an alkaline-rich pancreatic juice.
1: acute renal insufficiency
2: administration of morphine
3: acute perforation of a duodenal ulcer
A. there is little enteric lipase in the epithelial cells of the small intestine
B. pancreatic enzymes are necessary for adequate emulsification of fat
C. lack of pancreatic bicarbonate reduces the efficiency of succus entericus enzymes
D. proteolytic enzymes in pancreatic secretion are essential for the release of fat from the forms in which it is ingested
E. pancreatic secretion is necessary to stimulate bile production
Ganong 19th ed, Ch 26
Answer: S is false and R is true
Ganong 13th. ed. Chapter: 26 Page: 419
Ganong 15th ed. Page: 262
A. absorption is inhibited by metabolic poisons
B. glucose in the lumen strongly reduces fructose absorption from the lumen
C. there is a maximum rate of absorption for glucose from the intestinal lumen
D. absorption rate can be different for sugars of similar molecular weight
E. carbohydrates must be broken down to disaccharides or monosaccharides before they can be absorbed in any quantity
Guyton 7th Edition Chapter: 65 PAGE: 787-788. Transport of most monosaccharides is an active process. This is demonstrated by the following: (i) Transport of most monosaccharides can be blocked by metabolic inhibitors such as iodoacetic acid, cyanides and phlorizin (A false). (ii) Transport is selective for the different monosaccharides (D false). (iii) There is a maximum rate of transport for each monosaccharide the most rapid being for galactose (C false). (iv) There is competition between certain sugars for respective carrier systems (B false). This question has been reviewed by the sub committee and remains unchanged.
A. Patients require 15 kcal/kg/day.
B. Patients require 25 kcal/kg/day.
C. Patients require 35 - 40 kcal/kg/day.
D. Patients require 50 kcal/kg/day and the blood glucose levels should be maintained less than 225 mg/dL (12.5 mmol/L).
E. Patients require 50 kcal/kg/day and the blood glucose level should be maintained more than 225 mg/dL (12.5 mmol/L).
Administering 25 kcal/kg usual body weight/day appears to be adequate for most patients. From 30% to 70% of the total calories administered per day can be given as glucose. The dose should be adjusted to maintain a blood glucose level <225 mg/dL - it may be desirable to administer insulin in patients with higher levels of glucose in the blood. The calorie-to-nitrogen ratio should be 150 kcal per gm of nitrogen (about 6.25 gm of protein contains 1 gm of nitrogen). In trying to adapt nutritional supply to needs, most dieticians and nutritionists will estimate energy expenditure from standard formulas like those of Harris and Benedict, which are derived from sex, weight, height, and age.
A. Butyrate, an endogenous product of fibre fermentation, is an important fuel for colonocytes.
B. It is desirable to consume > 250 gm of fibre each day.
C. A deficient fibre intake can lead to secretory diarrhoea.
D. The long-term consumption of a diet that is low in fibre increases the risk of bacterial translocation across the wall of the proximal colon.E. An inadequate fibre intake can impair the entero-hepatic circulation of bile salts and thereby lead to the diminished absorption of fat soluble vitamins
Endogenous products of fibre fermentation are important for colonocyte integrity and function. However, the provision of fibre has not been clearly demonstrated to be of any clinical advantage. Bacterial translocation, as well as other aspects of the gut barrier, will be covered later on in this module.
Answer: S is true, R is true and a valid explanation of S
Ganong 13th Edition CHAPTER: 25 PAGE: 395. In infants, moderate amounts of undigested protein are absorbed (R true and is a valid explanation of S). Maternal protein from colostrum is absorbed, affording passive immunity against infection. Absorption is via the small intestine by endocytosis and subsequent exocytosis. Foreign proteins entering the circulation, provoke the formation of antibodies (S true) leading to possible allergic symptoms.
A. Glycine should constitute at least 50% of the amino acids.
B. Dosing should ensure that the blood urea nitrogen level remains > 200 mg/dL.
C. Hepatic encephalopathy is not influenced by the amount of protein that is administered parenterally.
D. Solutions should contain > 0.25 g/kg/day of nucleotides to maintain the proliferative ability of bone marrow.
E. The protein requirement is about 1.2 to 1.5 g/kg/day.
The protein requirement is about 1.2 to 1.5 g/kg/day. Considerations for a decrease in dosing include a rising blood urea nitrogen level that exceeds 100 mg/dL or a rising blood ammonia level that is associated with clinical encephalopathy. A nutritional requirement for nucleic acids has not been established, but they are being investigated as beneficial nutrients for proliferation of intestinal crypt cells, lymphocyte proliferation, and cellular DNA and RNA synthesis. Glycine is the simplest of the amino acids as it is based only one carbon molecule. Its administration has no defined biological or clinical advantages, but it is often included in commercial solutions as a 'stuffer' amino acid ie. a convenient source of nitrogen. Incidentally, as opposed to chronic renal failure, there is no need to alter the amount of protein administered to patients with acute renal insufficiency. There is also no demonstrable advantage to be gained by administering just essential amino acids. Haemodialysis and haemofiltration remove amino acids in the range of 3 to 5 g/h. These losses need consideration when adjusting the amount of protein to be administered.
1: iron deficiency may cause anaemia
2: cobalt deficiency may cause megaloblastic anaemia
3: iodine deficiency may cause goitre formation
4: chromium deficiency may cause insulin resistance
Ganong 18th ed. Page: 293
BURNETT. C.S.S. CHAPTER: 14.7 PAGE: 213
A. less than 5% of the protein in the small intestine escapes digestion and absorption
B. absorption of amino acids is rapid throughout the whole of the small intestine
C. over 90% of the digested protein is dietary
D. the protein in the stools is largely undigested dietary protein
E. amino acids are actively transported from the mucosal cells into the blood stream
Ganong 13th Ed. CHAPTER: 25/26 PAGE: 394-395/424-425. Quesiton to be reviewed at the March 04 meeting re: options A & E (20/02/04).
A. BCAA administration to catabolic surgical patients enhances the quality and number of polyribosomes in skeletal muscle.
B. BCAA administration improves patient outcome after major hepatic surgery.
C. BCAA are mainly metabolised in the liver.
D. There is no role for parenteral BCAA therapy in patients with hepatic encephalopathy.
E. When used clinically, BCAA should be administered at a dose of 0.1 to 0.3 g/kg/d.
The BCAA - leucine, isoleucine, and valine - are essential amino acids required for protein synthetic functions. BCAA are primarily metabolised by skeletal muscle, rather than the liver. When given in a balanced amino acid formulation at a dose of 0.5 to 1.2 g/kg/d BCAA can improve nitrogen retention and increase protein synthetic functions relative to standard amino acids formulations e.g. the number and quality of polyribosomes in skeletal muscle. As illustrated, BCAA can be consumed in muscle to generate glutamine. Nevertheless, their exact role in promoting improved patient outcomes in surgical patients remains to be defined. But it is clear that, in patients who are protein-intolerant because of chronic or latent hepatic encephalopathy, BCAA-enriched parenteral nutrition permit greater protein intake without inducing encephalopathy than do standard protein formulas.
1: is probably the mediator responsible for direct inhibition in the spinal cord
2: when directly applied to the membranes of neurones causes hyperpolarization
3: with arginine and methionine is responsible for the synthesis of creatine in muscle
4: has an inhibitory function in the cord antagonized by atropine
Ganong 7th Ed. Ch. 4 P. 74 126 243. Pending review. May 2003
A. When administered in pharmacological doses arginine may act as a neuotransmitter.
B. Alanine is the main precursor of arginine.
C. Critically ill patients require 30 g/day of arginine.
D. Arginine is a unique substrate for the production of nitric oxide.
E. Arginine is the preferred nutrient for immunocytes.
Arginine is now considered to be a conditionally essential amino acid. Arginine is synthesised endogenously in the kidney from gut-derived citrulline (the small intestine converts dietary amino acids, including glutamine, to citrulline). Arginine participates in a variety of metabolic functions, including urea synthesis, lymphocyte proliferation, and wound healing. In addition, arginine is a unique substrate for the production of the biologic effector molecule, nitric oxide. This important pathway has been shown to be present in many tissues and cells including endothelium and inflammatory cells. The role of arginine in critically ill patients remain to be defined but doses of up to 30 g/day have been used in evaluative studies. Combinations of nutrients with immune function activity - arginine, fish oil, and nucleic acids - are being evaluated as enteral nutrients in critically ill patients: although they are sometimes referred to as 'immunonutrients', their clinical efficacy has yet to be confirmed by independent clinical trials.
A. Glutamine is the only amino acid that contains three nitrogen molecules.
B. Glutamine constitutes about 25% of the amino acid content of standard solutions of parenteral nutrients.
C. Critically ill patients require 20 g/day of glutamine.
D. Glutamine is the principal fuel used by rapidly proliferating cells.
E. The kidney consumes glutamine during periods of metabolic alkalosis.
We discussed the metabolism of glutamine in Topic 1. It is the main fuel consumed by rapidly dividing cells such as the gut mucosa, immunocytes, and some tumours. Glutamine is not included in standard solutions of parenteral nutrients because it is unstable in solution and breaks down to form toxic amounts of pyroglutamate and ammonia. It remains to be determined whether administering glutamine to catabolic patients results in an improved outcome. As mentioned in Topic 1, the kidney consumes glutamine during periods of metabolic acidosis.
1: intrinsic factor binding with vitamin B12 in the small intestine
3: trypsin which facilitates efficient absorption
4: a high oral intake of vitamin B12
Ganong 13th ed. PAGE: 414
Ganong 13th Ed. CHAPTER: 17 PAGE: 259
Refer to Burnett, 2nd Ed, Ch 6, page 104; STEM Module: Metabolism/Nutrition
1: Na+ transport across enterocyte membrane
3: carrier molecules
4: brush border disaccharidases
Ganong 16th Edition CHAPTER: 25 PAGE: 430
1: visceral distension
2: surgical diathermy
3: visceral ischaemia
4: cutting with a sharp instrument
Guyton, 9th ed, Ch 48; Ganong, 19th ed, Ch 17
1: is formed from breakdown of purines
2: reabsorption in renal tubules can be inhibited by probenecid (Benemid)
3: level in plasma is normally 0.2 - 0.4 mmol/l
4: urinary excretion is increased by allopurinol
Ganong 13th ed. Chapter 17 Page: 246
A. Serum concentrations < 30 g/L strongly correlate with a poor clinical outcome.
B. It is a useful marker of nutritional status because it has a relatively short half-life.
C. Synthesis is markedly inhibited during the early stages of undernutrition.
D. It has a low exchange rate between the intra- and extra-vascular compartments.
E. Serum concentrations are increased during sepsis.
Hepatic secretory proteins such as albumin, transferrin, retinol binding protein, and prealbumin are markers of visceral protein stores and are used as indicators of nutritional status. Numerous studies have demonstrated that a low serum albumin concentration ( < 30 g/L) strongly correlates with a high incidence of mortality and morbidity. However, albumin has a half-life of about 28 days and acute changes in serum albumin concentration cannot be ascribed to poor nutrition. For example, serum albumin concentrations are usually not affected by nutritional intake during starvation until starvation has reached an advanced stage and there is a marked reduction in body weight accompanied by overt muscle wasting. On the other hand, the low serum albumin concentrations that are observed in stressed patients persist until the parts start to recover and there is an absence of inflammatory foci. The exchange rate between intravascular and extravascular albumin is large and even small variations in the percentage of exchange can cause significant changes in serum albumin concentration. Levels of regulatory hormones, acute-phase reactants, and the measurement of the circulating levels of a number of cytokines have also been proposed as 'nutritional markers'. For example, C-reactive protein has the attraction of being present in very low concentrations in the serum of normal subjects, but rising exponentially within four hours of the onset of infection. However, such measurements reflect metabolic stress rather than nutritional status
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