Gastrointestinal Flashcards
(114 cards)
1
Q
What are the layers of the intestinal wall?
A
○ serosa
○ longitudinal muscle layer
○ circular smooth muscle layer
○ submucosa
○ mucosa
2
Q
Slow waves in the gastrointestinal smooth muscle are caused by which cell acting as a pacemaker
A
Interstitial cells of Cajal
3
Q
What are slow waves in the gastrointestinal smooth muscle
A
rhythmic, undulating changes in resting membrane potential
4
Q
What are spike potentials in gastrointestinal smooth muscle
A
True action potentials which occur when membrane potential exceeds -40mv
5
Q
Entry of what ion into the smooth GI muscle causes contraction (action potential)
A
Calcium
6
Q
What are the two major plexuses of the enteric autonomic nervous system
A
Myenteric plexus: between longitudinal and circular muscle layers
Submucosal plexus: in the submucosa
7
Q
What are the functions of the myenteric and submucosal plexus
A
Myenteric - controls muscle activity along the length of the gut (contraction rate and rhythm)
Submucosal - controls function in each segment of intestine (local hormonal secretion, local muscle contraction)
8
Q
What is the effect of these neurotransmitters on gastrointestinal activity:
Norepinephrine (SNS)
Acetylcholine (PSNS)
A
Acetylcholine: mostly excites gastrointestinal activity
Norepinephrine: almost always inhibits gastrointestinal activity
9
Q
Gastrin:
- Stimuli for secretion:
- Site of secretion
- Actions:
A
- Stimuli for secretion: proteins, distension, nervous stimulation
- Site of secretion: G cells in antrum, duodenum and jejunum
- Actions: Stimulates gastric acid secretion and mucosal growth
10
Q
Cholecystokinin (CCK)
- Stimuli for secretion:
- Site of secretion
- Actions:
A
- Stimuli for secretion: Proteins, fats and acid
- Site of secretion: I cells of duodenum, jejunum, ileum
- Actions:
- Stimulates pancreatic enzyme secretion, pancreatic bicarbonate secretion, gallbladder contraction,
- Inhibits gastric emptying
11
Q
Secretin
- Stimuli for secretion:
- Site of secretion
- Actions:
A
- Stimuli for secretion: Acid and fat
- Site of secretion: S cells of duodenum, jejunum, ileum
- Actions:
- Stimulates pepsin secretion, pancreatic bicarbonate secretion, biliary bicarbonate secretion,
- Inhibits gastrin release and gastric acid secretion
12
Q
Gastric inhibitory peptide (GIP)
- Stimuli for secretion:
- Site of secretion
- Actions:
A
- Stimuli for secretion: Protein, Fat, Carbohydrate
- Site of secretion: K cells of duodenum and jejunum
- Actions:
- Stimulates insulin release;
- Inhibits gastric acid secretion
13
Q
Motilin
- Stimuli for secretion:
- Site of secretion
- Actions:
A
- Stimuli for secretion: Fat, Acid, Nervous
- Site of secretion M cells of duodenum and jejunum
- Actions: Stimulates gastric motility and intestinal motility
14
Q
Pepsinogen
- Stimuli for secretion:
- Site of secretion
- Actions:
A
- Stimuli for secretion: ACH from vagus nerves/enteric plexus and stomach acid
- Site of secretion: Peptic (chief cells) in gastric mucosa secrete pepsinogen
- Actions:
When activated by HCL causes proteolysis
15
Q
What do the parietal (oxyntic) cells secrete
A
HCl and intrinsic factor
16
Q
What do the enterochromaffin-like (ECL) cells secrete
A
Histamine
17
Q
What hormones are involved in gastric acid secretion
A
Histamine, Gastrin and Pepsinogen
18
Q
Somatostatin:
- stimulus
- site of secretion
- action
A
- nutirents (lipid and protein) and bile
- D cells in the GIT, Delta cells in pancreas, hypothalamus
- Inhibits acid and pepsinogen secretion, inhibits gall bladder contraction, inhibits pancreastic secretion, inhibits insulin secretion, inhibits intestinal motility and absorption
19
Q
Which gastric factors promote gastric emptying
A
- Gastric volume
- Gastrin
20
Q
Which gastric factors inhibit gastric emptying
A
- CCK (stimuated bu fat)
- Secretin (stimulated by acid)
- GIP (stimualted by carbohydrate and fat
21
Q
What is the gastroileal reflex
A
intensified peristalsis when next meal is eaten forces chyme into ICCJ
22
Q
What neurological compontents regulate defecation
A
- internal (smooth muscle) and external anal spincter (striated muscle)
- Local enteric nervous system peristalsis
- Parasymathetic defecation reflex intensifies peristaltic waves and relaxes internal sphincter
- External spincter under voluntary control of pudendal nerve
23
Q
What are the two main protein secretions in saliva
A
- serous secretion with α-amylase for starch digestion
- mucous secretion with mucin for lubrication
24
Q
Saliva contains high concentrations of which ions
A
K+ and HCO3-
25
Oxyntic glands
- location
- secretions
- body and fundus (proximal 80% stomach)
- Mucous neck cells - secrete mucous
- Peptic (chief) cells - secrete pepsinogen
- Parietal (oxyntic) cells - secrete HCL and intirinsic factor
- Enterochromaffin cells - secrete histamine
26
Pyloric glands
- location
- secretions
- Antrum (distal 20% stomach)
- secrete mainly mucous and gastrin
27
Pepsinogen is activated by what
Activated by HCl to form pepsin
28
What is the purpose of intrinsic factor
It is essential for vitamin B12 absorption in the ileum
in dogs secreted mainly from pancreas (not parietal cells)
29
What are the phases of gastric secretion
- Cephalic phase - beofre food enters stomach (30%)
- gastric phase (60%)
- Intestinal phase (10% )
30
Which factors inhibit gastric secretion
- intestinal distension, acid and protein
- Secretin, GIP, VIP, somatostatin
31
What do the pancreatic acini secrete
- protin digesting enzymens (trypsin, chymotrypsin, carboxypolypeptidase)
- Carbohydrate digesting enzymes (pancreatic amylase)
- Fat digesting enzymes (pancreatic lipase, cholesterol esterase, phospholipase)
- trypsin inhibitor (prevents activation within pancreas)
- intrinsic factor
32
What do the pancreatic ductules secrete
bicarbonate solution
33
What stimulates pancreatic secretion
- ACH from vagus and enteric nervous system
- CCK (stimulates maunly digestive enzyme secretion)
- Secretin (stimulates mainly bicarbonate secretion)
34
What are the two main functions of bile
* Bile acids: aid fat absorption through emulsification and absorption of fat end products by micelle formation
* Excretion of waste (bilirubin and excess cholesterol)
35
What are the main components of bile
bile salts, bilirubin, cholesterol, lecithin, electrolytes
36
Which hormones stimulates
gall bladder emptying
- CCK (in response to fat)
- ACH from vagal and enterinc nervous system
37
How does the liver synthesise bile salts
- Cholesterol converted to cholic acid and chenodexoycholic acid
- combine with glycine (and taurine) to form conjugated bile acids
- Sodium salts of these are excreted into bile
38
Outline enterohepatic circulation of bile salts
- 94% bile salts are reabsorbed from SI and recycled in liver
- diffusion in easly SI, active transport in distal ileum
- Enter portal blood and transported to liver
- during first passage through venous sinusoids almost entirely reabsorbed
39
Which glands secrete mucous in the duodenum
- where are they
- what is the purpose
- what inhibits secretion
- Brunner's glands
- first few cm of duodenum
- alkaline mucous protects duodenal wall and neutralises stomach acid
- sympathetic stimuation inhibits secretion
40
What do the crypts of Lieberkuhn secrete and where are they
- entire SI surface between villi
- goblet cells secrete mucous
- enterocytes secrete water and electrolytes at crypt and absorb nutient at villi
- Watery secretion provide vehicle for nutrient absorption
41
What enzymes are located in the small intestinal enterocytes
- Peptidases - split small peptides into AA
- Disaccharidases - spilt disaccharides into monosaccharides
- Intestinal lipases - spilt neutral fats into glycerol and FA
42
What is the life cycle of an intestinal epithelial cell
5 days
43
What is the primary secretion from the large intestine
- Alkaline mucous from the Crypts of Lieberkuhn, but no villi
44
Digestion of carbohydrates
- mouth + stomach
- small intestine
- Epithelium
- alpha almylase in mouth
- Acid inactivates in stomach
- pancreatic amylase in small intestine
- enterocyte brush border enzymes (lactase, sucrase, maltase)
- final products are monosaccharides (80% glucose)
45
Digestion of proteins
- Stomach
- Small intestine
- Epithelium
- Pepsin in stomach
- pancreatic enzymes (trypsin, chymotrypsin, carboxypolypeptidase)
- Brush border enzymes aminopeptidase
- 99% are reabsorbed as amino acids
46
Digestion of fats
- <10% lingual lipase in stomach
- primarily in small intestine
- Bile salt and lecitin emulsification
- pancreatic lipase triglyceride digestion
- bile salt micelles transport monoglycerides and FA to intestinal cells
- Cholesterol ester hydrolase breaks down cholesterol and phospholipase A" breaks dow PL - transported by bile micelles
47
Which transporters help with absorbing glucose, galactose and fructose
Glucose SGLT1
Galactose SGLT1 + GLUT2
Fructose GLUT5 and GLUT2
48
What is the mechanism for fat absorption
- monglycerides and FA move from micelles into epithelial cells
- re-converted into triglycerides in SER
- released as chylomicrons into lymphatics
- Bile micelles recycled
- some short chain + medium chain FA absorbed direclty into portal blood
49
what do bacteria in the colon produce
- Vitamin K, B12, thiamine (B1), riboflavin (B2)
- Gases
50
What are the central components of the vomiting pathway
- Vomiting centre - in medulla oblongata, coordinates
- Chemoreceptor trigger zone (CTZ) - area postrema of medulla, outside BBB, detects circulating toxins
- Nucleus tractus solitarius (NTS) - vagal afferent inputs from GIT
51
What are the peripheral components of the vomiting pathway
- Vagal afferents - sensory fibres from GIT detect mechanical and chemical stimuli - transmit to NTS
- vestibular system - transmit to vomiting centre via vestibular nuclei
- cortex and limbic centre
52
What are the major pathways for vomiting
* Peripheral Pathway: GI tract → Vagal afferents → NTS → Vomiting centre (5HT3 in dogs)
* Central Pathway: Circulating toxins → CTZ → Vomiting centre
* Vestibular Pathway: Inner ear → Vestibular nuclei → Vomiting centre
* Cortical Pathway: Higher brain centres → Vomiting centre
53
What is the role of Glucose 6 phosphatase and where is it found
- Liver cells
- breaks down flucose-6-phosphate to glucose and phosphate allowing transport of glucose in blood
54
Glucose transport is via which carriers
- which are active
GLUT - facilitated
SGLT - active
55
What happens to glucose when it enters cells
- it is phosphorylated by glucokinase or hexokinase to prevent diffusion back out the cell
56
* What is glycogen
* where is it stored
* how is it formed
- glycogen is a large polymer of glucose
- stored mainly in liver and muscle cells in granules
- allows storage without affecting osmotic pressure
- Glucose --> glucose 6 phosphate --> glucose 1 phosphate --> uridine diphosphate glucose --> glycogen
- other components (lactic acid, glycerol, pyruvic acid, some AA ) can also be converted to glycogen
57
What is the process of glycogenolysis and what stimulates it
- glucose melecules split from glycogen by phosphorylase
- activated by Epinephrine (SNS) and Glucagon (alpha cells in liver when BG drops)
58
Whyat is the process of splitting glucose to create pyruvic acid and what is the equation and net ATP gain
- Glycolysis
- End product of glycolysis then used for oxidation to produce ATP
- Glucose + 2ADP + 2PO43- --> 2 Pyruvic acid + 2ATP + 4H
- net gain of 2 ATP
59
What is the equation for conversion of pyruuvic acid to Acetly Co-A
* Pyruvic acid + Coenzyme A --> Acetyl CoA + 2CO2 +4H
60
* What is the citric acid cycle
* What is the purpose
* Where does it occur
* what is the equation
- chemical reaction where acetly portion of Acetly CoA is degrated to release H+ for later oxidation
- mitochondria
- Acetyl CoA + oxaloacetate --> citric acid --> oxaloacetic acid
- net result per glucose: 2 Acetyl CoA + 6H2O + 2ADP --> 4CO2 +16H +2CoA +2ATP
61
- What is oxidative phosphorylation
- where does it occur
- what is the mechanism
- ATP (90%) production from glucose
- mitochondria
- chemiosmotic mechanism
- Split hydrogen into ions + electrons - electrons enter the electron transport chain and creates ATP
- For every 2 electrons 3 ATP molecules made
62
What is the net ATP gain from breakdown of one glucose molecule to CO2 and H2O
- 38 ATP
- Glycolysis - 2 ATP
- Citric acid cycle 2 ATP
- ETC 34 ATP
63
What is anaerobic glycolysis and what is the equation
- provides energy when there is insufficient oxygen for oxidative phosphorlyation
- glucose can still be split to pyruvic acid
- lactic acid is produced to allow glycolysis to continue
- Pyruvic acid + NADH + H+ --> (lactate dehydrogenase) ---> Lactic acid + NAD+
- when oxygen available again lactic acid can be converted back to glucose or oxidised.
64
What is the pentose phosphate pathway
- alternative pathway for glucose metabolism
- responsible for 30% glycolysis in liver/fat
- independent of citric acid enzymes
- Helps convert glucose into fatty acids
65
What is Gluconeogenesis
- hormonal stimuation
- formation of glucose from amino acids and glycerol portions of fats
- Liver produces 25% of its glucose through gluconeogenesis
- increased ACTH secretion --> cortisol --> mobilises proteins --> gluconeogenesis
66
Chylomicrons
- formation and composition
- transport
- removal
- fromed in intestinal epithelial cells
- 90% triglycerides, 9% phospholipid, 3% cholesterol
- formed in intestinal lymph - thoracic duct - blood
- Lipoprotein lipase - releases FA + glycerol
- chylomicrons cleared from plasma by liver endothelium
67
How are free fatty acids transported
- bound to albumin in blood
- chylomicrons
- lipoproteins
68
Which stimulates triglyceride hydrolysis in adipose tissue
- insufficient glucose (leading to inadequate alpha-glycerophosphate)
- Hormone sensitive lipase activation
69
What are the 4 main types of lipoprotein and their features
- VLDL - high TAG content, mainly transport liver synthesised TAG to adipose
- IDL - reduced triglycerides
- LDL - high cholesterol
- HDL - high protein, lower cholesterol and phospholipids
70
How are triglycerides utilised for energy
- what is the net ATP gain
- hydrolysis into FA and glycerol
- glycerol --> glucose -6 - pjosphater --> glycolytic pathway
- FA --> beta oxidation to produce Acetly CoA and enter citric acid cycle
- One sterol molecule can have a net gain for 146 ATP
71
Acetoacetic acid
- formation
- purpose
- fatty acid breakdown in liver --> Acetyl CoA --> condensed to form acetocaetic acid
- transported in blood to other tissues
- converted to B hydroxybutyric acid and acteone for diffusion
- can be reconverted to AcetlyCoA for oxidation
72
What is ketosis
- when does it happen
- ketone bodies (acetoacetic acid, β-hydroxybutyric acid, and acetone) rise to abnormally high levels in blood and tissues
- when carbohydrates aren't metabolised
- fatty acid metabolism increases (increased glucaogon, cortisol and decreased insulin)
- body has limited capacity to oxidise ketone bodies as oxaloacetate required for cirtic acid cycle (is produced by carbohydrate metabolism)
73
What hormone is essential for fat synthesis from carbohydrates
- insulin
74
What stimulates fat mobilisation
- reduced carbohydrates
- reduced insulin
- increase in symathetic stimulation increases hormone sensitive lipase
- ACTH and glucocorticoid relase have ketogenic effects
- increased thyroid hormone
75
Where are plasma proteins formed
- Liver produces all albumin, all fibrinogen, 50-80% globulins
- remaining globulins formed in lymphoid tissue
76
How are proteins used for energy
- deamination (mainly transamination)
- to form keto acids --> oxidised in citric acid cycle
- Ammonia released durin deamination converted to urea in liver
77
What hormones are required to regulate protein metabolism and synthesis
- GH: increases tissue proteins
- Insulin: required for protein synthesis
- glucocorticoids: increase tissue breakdown of protein
- testosterone: increases tissue protein deposition
- thyroxine: increases protein metabolism
78
What are hepatic macrophages called
Kupffer cells
79
What are the main liver metabolic functions
- Carbohydrate metabolism (stores glycogen, gluconeogenesis)
- Fat metabolism (oxidation of FA, cholesterol and phospholipid synthesis, conversion of protein and carbohydrates to fat)
- Protein metabolism (deamination of amino acids, forms urea to remove ammonia, produces plasma proteins, synthesis non-essential AA)
- Storage (Vit A, D, B12, iron as ferritin,)
- forms cogluation substances (fibrinogen, prothrombin (II), factor VII, IX and X)
- drug metabolism and excretion (in bile)
80
Bilirubin formation and excretion
- haemoglobin --> globin + haem in macrophages --> free iron transported by transferrin --> forms biliverdin --> unconjugated bilirubin --> transported bound to albumin
- Liver conjugates bilirubin with glucaronic acid --> excretion onto bile
- bacteria convert bilirubin to urobilinogen, some reabsorbed and recycled
81
Name some orexigenic and anorexigenic substances
* Orexigenic (stimulate feeding): NPY, AGRP, ghrelin,
* Anorexigenic (inhibit feeding): α-MSH, leptin, insulin, CCK, Peptide YY
82
Which vitamin is essential for carbohydrate metabolism
Thiamine (B1)
83
Which vitamins are important for DNA synthesis and RBC formation
B12 (cobalamin) and B9 (folic acid)
84
Which vitamin is essential for amino acid metabolism
Pyroxidine (B6)
85
Which vitamin is essential for blood clotting, which factors require it
Vitamin K
* Factor II (prothrombin)
* Factor VII
* Factor IX
* Factor X
86
Which clotting factors does the liver not produce
* Factor VIII (produced by endothelial cells)
* von Willebrand factor (produced by endothelial cells and megakaryocytes)
87
Which vitamin K dependent clotting factor becomes depleted first and which coagulation measure increases
Factor VII
PT
88
What is the storage form of iron found in haem groups
Ferrous iron (Fe2+)
89
What is the transportable form of iron bound to apotransferrin in blood
Ferric iron (Fe3+)
90
What is Hepcidin
- protein produced by liver in reponse to increased iron stores and inflammation
- prevents iron absorption release from macrophages and hepatocytes
91
what protein transports iron in blood
* apotransferrin
* when bound to iron - called transferrin
92
What is the iron storage protein
Apoferritin
B1 globulin produced by liver
93
What is ferritin
- apoferritin + iron
- Available for rapid iron release
94
What is haemosiderin
- iron + phosphate/hydroxide
- Storage compound under excess iron conditions
95
What is hephaestin
* copper dependnet enzyme in enterocytes
* converts Fe2+ to Fe3+ for transport
96
What is ceruloplasmin
- copper dependnet enzyme location on cellular membranes (macrophages)
- converts Fe2+ to Fe3+ for transport
97
Outline B12 processing
- B12 bound to haptocorrin in stomach
- in duodenum binds to intrinsic factor (produced by pancreas)
- B12-IF complex recognised by cubam receptors in distal ileum + endocytosis
- B12 binds to transcobalamin II in blood
- stored in liver
98
What is Methylmalonic acid (MMA)
- intermediate metabolite in the breakdown of amino acids
- Requires vitamin B12 (cobalamin) as a cofactor
- if B12 deficieny MMA accumulates
99
Maropitant
- mechanism
- site of action
- NK1 antagonist
- CRTZ and emetic centre
100
Onsansetron
- mechanism
- site of action
- 5HT3 antagonist
- CRTZ, vaga afferents
101
Metoclopramide
- mechanism
- site of action
- Dopamine (D2) antagonist
- CRTZ, GI smooth muscle
102
Chlorpromazine
- mechanism
- site of action
- Alpha 2 antagonistm M1 agonist, H1 antagonist
- CRTZ, emetic centre
103
Diphenhydramine
- mechanism
- site of action
- H1 antagonist
- CRTZ
104
Butorphanol
- mechanism
- site of action
- ENKμ,δ
- CRTZ
105
What is the most common vascular ring anomaly in dogs and cats
- which breeds have a hereditary basis
- Persistent right aortic arch (PRAA)
- GSD and irish setters
106
What is protein C
- what disease are implicated
Anticoagulant protein
- reduced in dogs with cPSS
- reduced in dogs with acute hepatopathies
107
What are common serum biochemical changes with PSS
- hypoalbuminemia
- low BUN
- Hypocholesterolemia
- Hypoglycemia
- mild/moderate increases in ALP/ALT
108
RER calculation
70xBW^0.75
109
MER
- inactive dogs
- active dogs
- Inactive = RER x1.36
- Active = RER x 1.85
110
Cat dietary requirements
- Vitamin D
- Vitmain A
- Vitamin B3 (niacin)
- Taurine and arginine
111
Refeeding syndrome results in which metabolic derangements
- Hypophosphatemia
- Hypokalemia
- Hypomagnesemia
- Hyponatremia
- Hypocalcemia
- hyperglycemia
- thiamine deficiency
112
What is the half life of ALP in dogs and cats
- Dog - 2-3d
- Cat - 6hrs
113
What are the ALP iso-enzymes, which do cats not have
- Intestinal
- Liver
- Bone
- Kidney
- Glucocorticoid induced (dogs only)
114
What is the half life of ALT in dogs and cats
- Dogs: 40-60hrs
- Cats: 3-4hrs
