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A&P 2 > Gastrointestinal Tract Physiology > Flashcards

Gastrointestinal Tract Physiology Flashcards

1
Q

What are the 4 digestive processes?

A
  1. Motility
  2. Secretion
  3. Digestion
  4. Absorption
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2
Q

What is motility and what is the function?

A

Contraction of smooth muscle in the digestive tract
- Mixing: promote digestion & facilitate absorption
- Moving the contents in the GIT

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3
Q

Secretion (Basic digestive processes)

A

Both exocrine (enzymes, HCl) & endocrine (hormonal) secretions
Mucus: along entire digestive tract
Saliva, acid, enzymes, bile, bicarbonate, hormones, etc

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4
Q

What is digestion (basic digestive processes)?

A

Chemical break down of complex macromolecules into smaller absorbable molecules
- Food that we consume are large and X cross plasma mbn of the intestinal epithelial cells

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5
Q

What is absorption (basic digestive processes)?

A

Digested material transferred from GIT lumen into blood/lymph

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6
Q

Basic digestive processes (motility, secretion, digestion, absorption) in the oral cavity & oesophagus

A

M: Swallowing, chewing
S: Saliva (salivary glands), lipase
D: Carbs, fats (minimal)
A: None

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7
Q

Basic digestive processes (motility, secretion, digestion, absorption) in the stomach

A

M: Peristaltic mixing & propulsion
S: HCl (parietal cells), pepsinogen & gastric lipase (chief cells), mucus & HCO3- (surface mucous cells), gastrin (G cells), histamine (ECL cells)
D: Protein, fats
A: Lipid-soluble substances such as alcohol & aspirin

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8
Q

Basic digestive processes (motility, secretion, digestion, absorption) in the small intestine

A

M: Mixing & Propulsion primarily by segmentation
S: HCO3- & enzymes (pancreas), bile (liver), mucus (goblet cells), hormones: CCK, secretin, GIP, others
D: Carbs, fats, polypeptides, nucleic acids
A: Peptides → AT; amino acids, glucose & fructose → secondary AT; fats → simple diffusion; water → osmosis, ions; minerals & vitamins → AT

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9
Q

Basic digestive processes (motility, secretion, digestion, absorption) in the large intestine

A

M: Segmental mixing; mass movement for propulsion
S: Mucus (goblet cells)
D: None (except by bacteria)
A: ions, water, minerals, vitamins, small organic molecules prod. by bacteria

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10
Q

What regulates digestive function?

A
  1. Autonomous smooth muscle function
  2. Intrinsic nerve plexuses
  3. Extrinsic autonomic nerves
  4. GI hormones
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11
Q

Short reflex pathway in the regulation of digestive function

A

Local changes in digestive tract detected by receptors in digestive tract = short reflex to intrinsic nerve plexuses (submucosal plexus & myenteric plexus) =

  • smooth muscle (contraction for motility)
  • Exocrine gland cells (secrete digestive juices)
  • Endocrine gland cells (secrete gastrointestinal & pancreatic hormones
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12
Q

Hormonal pathway in the regulation of digestive function

A

Local changes in digestive tract detected by receptors in digestive tract = gastrointestinal hormones =

  • smooth muscle (contraction for motility)
  • Exocrine gland cells (secrete digestive juices)
  • Endocrine gland cells (secrete gastrointestinal & pancreatic hormones
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13
Q

Long reflex pathway in the regulation of digestive function

A
  • Local changes in digestive tract detected by receptors in digestive tract = stimulates extrinsic autonomic nerves
  • External infleunces act directly on extrinsic autonomic nerves

=

  • smooth muscle (contraction for motility)
  • Exocrine gland cells (secrete digestive juices)
  • Endocrine gland cells (secrete gastrointestinal & pancreatic hormones
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14
Q

What are the receptors in the digestive tract?

A
  • Chemoreceptors
  • Mechanoreceptors
  • Osmoreceptors
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15
Q

What is the oral cavity?

A

Entrance to digestive tract
- Muscular lips help procure, guide, contain food in mouth

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16
Q

What are the functions of the oral cavity?

A

Mastication
Initiation of swallowing (deglutition)
Salivary secretion
Taste

MIST

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17
Q

What is mastication?

A

Involves mechanical action of slicing, tearing, grinding, mixing of ingested food by teeth

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18
Q

What are the functions of mastication?

A
  • Breaks food into smaller pieces = facilitate swallowing & inc. SA of food particles
  • Mixes food with saliva
  • Expose food to taste buds (inc. secretions to prepare for arrival of food)
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19
Q

Composition of saliva

A

Water (99.5%)
Electrolytes, proteins, mucus (0.5%)

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20
Q

Functions of saliva

A
  1. Initiates digestion of dietary starch by salivary amylase
  2. Initiates digestion of some lipids by lingual lipase (activity in adults are vv MINIMAL)
  3. Some antibacterial effect (lysozyme & salivary IgA)
  4. Dissolving molecules (taste buds)
  5. Helps in swallowing, speech, oral health (contains bicarbonate buffer = neutralise acid released by bacteria)
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21
Q

Pharynx

A

Cavity at rear of throat
Common passageway for digestive & respiratory tract

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22
Q

Swallowing is an _____-or-______ reflex

A

Swallowing is an all-or-none reflex

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23
Q

Oropharyngeal stage of swallowing

A

Initiated by tongue voluntarily pushing bolus of food to pharynx

  • Food bolus voluntarily pressed by tongue against roof of mouth & backwards towards pharynx
  • Activation of pharyngeal pressure receptors = medulla (swallowing centre) initiates reflexes to prevent food entry into resp. passages
  • Uvula contracts = blocks nasal passages from pharynx
  • Laryngeal muscles contract = close glottis at top of trachea (tightly aligning vocal cords)
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24
Q

Oesophageal stage of swallowing

A

Primary peristaltic wave sweeps from the beginning to end of oesophagus, forcing the bolus ahead of it toward the stomach

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25
Q

Functions of the stomach

A
  1. Stores food (& releases contents into s. intestine at controlled rate)
  2. Begins protein digestion (HCl & enzymes)
  3. Mixing movement produces chyme

J-shaped chamber

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26
Q

Gastric storage

A
  • Body of stomach
  • Receptive relaxation (bc of rugae) = expansion of stomach cavity with little change in intragastric pressure
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27
Q

Gastric mixing

A
  • Mainly in pyloric antrum = peristaltic contractions are stronger & more vigorous
  • Retropulsion = churning action breaks the food into smaller pieces producing chyme
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28
Q

Gastric emptying

A

Controlled propulsion of chyme into the duodenum w each peristaltic wave

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29
Q

Steps in gastric emptying

A
  1. A peristaltic contraction originates in the upper fundus & sweeps down toward pyloric sphincter
  2. The contraction becomes more vigorous as it reaches the thick-muscled antrum (bc muscle walls thicker)
  3. Strong antral peristaltic contraction propels the chyme forward
  4. A small portion of chyme is pushed through the partially open sphincter into the duodenum. Stronger antral contraction = more chyme emptied with each contractile wave
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30
Q

What does the upper fundus usually contain?

A

air

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31
Q

Steps in gastric mixing

A
  1. When the peristaltic contraction reaches the pyloric sphincter, the sphincter is tightly closed & no further emptying takes place
  2. When chyme that was being propelled forward hits the closed sphincter, it is tossed back into the antrum. Mixing of chyme = when chyme is propelled forward & tossed back into the antrum with each peristaltic contraction (retropulsion)
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32
Q

What is gastric emptying largely controlled by?

A

Factors in the duodenum

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33
Q

What are the factors regulating gastric motility & emptying?

A

Within stomach
- Vol. of chyme
- Degree of fluidity

Within duodenum
- Presence of fat, acid, hypertonicity or distension

Outside the digestive system
- Emotion
- Intense Pain

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34
Q

What is the mode of regulation and effects of volume of chyme in the stomach?

(Factors regulating gastric motility & emptying)

A

Mode of regulation: Distension has direct effect on gastric smooth muscle excitability + acting through intrinsic plexuses, vagus nerve, gastrin

Effects on gastric motility & emptying:
Inc. vol. stimulates motility & emptying

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35
Q

What is the mode of regulation and effects of degree of fluidity within stomach?

(Factors regulating gastric motility & emptying)

A

Mode of regulation: Direct effect –> contents must be in fluid form to be evacuated

Effects on gastric motility & emptying: Inc. fluidity allows more rapid emptying

(less fluid = slower emptying bc food particles still big therefore dec. fluidity)

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36
Q

What is the mode of regulation and effects of presence of fat, acid, hypertonicity, or distension in duodenum?

(Factors regulating gastric motility & emptying)

A

Mode of regulation: Initiates enterogastric reflex/trigers the release of enterogastrones (secretin, cholecystokinin: CCK)

Effects on gastric motility & emptying: Inhibit further gastric motility & emptying until duodenum has coped with factors already present

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37
Q

What is the mode of regulation and effects of emotion?

(Factors regulating gastric motility & emptying)

A

Mode of regulation: Alters autonomic balance

Effects on gastric motility & emptying: stimulates/inhibits motility & emptying

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38
Q

What is the mode of regulation and effects of intense pain?

(Factors regulating gastric motility & emptying)

A

Mode of regulation: Inc. sympathetic activity

Effects on gastric motility & emptying: inhibits motility & emptying

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39
Q

What is vomiting?

A

AKA emesis

  • Contraction of respiratory muscles & abdominal muscles
  • Stomach, oesophagus & sphincters relaxed
  • NOT a function of retroperistalsis in stomach
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40
Q

Where is the vomiting center?

A

Medulla of brainstem

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41
Q

Causes of vomiting

A
  • Throat stimulation
  • Irritation of stomach
  • Elevated intracranial pressure
    etc
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42
Q

What do mucous cells secrete and what is the function of the secretory product?

(Gastric glands)

A

Secrete: Alkaline mucus

Function: protects mucosa against mechanical, pepsin, and acid injury

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43
Q

What is the stimuli for secretion of alkaline mucus by mucous cells?

A

Mechanical stimulation by contents

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44
Q

What do chief cells secrete and what is the function of the secretory product?

(Gastric glands)

A

Secrete: Pepsinogen

Function: When activated, begins protein digestion

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45
Q

What is the stimuli for secretion of pepsinogen by chief cells?

A

ACh, gastrin

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46
Q

What do parietal cells secrete and what is the function of the secretory product?

(Gastric glands)

A

Secrete:
- Hydrochloric acid
- Intrinsic factor

Functions:
- HCl: Activates pepsinogen, breaks down connective tissue, denature proteins, kills micoorgs.
- Intrinsic factor: facilitates absorption of Vit. B12

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47
Q

State the exocrine cells in the stomach

A
  • Mucous cells
  • Chief cells
  • Parietal cells
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48
Q

What is the stimuli for secretion of HCl and intrinsic factor by parietal cells?

A

ACh, gastrin, histamine

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49
Q

What do Enterochromaffin-like (ECL) cells secrete and what is the function of the secretory product?

(Gastric glands)

A

Secrete: Histamine

Function: Stimulates parietal cells (helps to inc. acid production by stimulating parietal cells)

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50
Q

What is the stimuli for secretion of histamine by ECL cells?

A

ACh, gastrin

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51
Q

What do G cells secrete and what is the function of the secretory product?

(Gastric glands)

A

Secrete: Gastrin

Function: Stimulates parietal, chief, and ECL cells

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52
Q

What is the stimuli for secretion of histamine by G cells?

A

Protein products, ACh

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53
Q

What do D cells secrete and what is the function of the secretory product?

(Gastric glands)

A

Secrete: Somatostatin

Function: Inhibits parietal, G, and ECL cells

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54
Q

What is the stimuli for secretion of histamine by G cells?

A

Acid

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55
Q

Steps for HCl production

A
  1. CO2 + H2O <-> HCO3- + H+
    - Catalyzed by carbonic anhydrase
  2. H+-K+ ATPase pump (proton pump)
    - Pumps H+ out of the cell by AT
    - For every H+ pumped out of cell, one K+ enters the cell
  3. Luminal K+ channel allows K+ to passively leak back
  4. Cl-HCO3- antiporter
    - Accumulation of HCO3 in cell drives tpt of Cl- into cell
    - For every HCO3- that exits cell, one Cl- is brought into the cell by secondary AT
  5. Cl- channel
    - Cl- diffuses out into lumen
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56
Q

How does HCl form pepsin?

A

HCl activates/cleaves pepsinogen into pepsin

  • Pepsin can result in activation of pepsinogen (once pepsin forms)
  • Pepsin breakdown/cleaves protein (polypeptide) into peptide fragments
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57
Q

What are the phases in gastric secretion control?

A
  1. Cephalic phase
  2. Gastric phase
  3. Intestinal phase
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58
Q

What happens in the cephalic phase of gastric secretion?

A

Prepares the stomach for arrival of food
- Short phase (minutes)
- Inc. production of gastric juice & release of gastrin

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59
Q

What happens in the gastric phase of gastric secretion?

A

Increased secretion (started in previous phase)
Initiates digestion of proteins
- Long phase (3-4 hr)
- Release of histamine + local effect
- Sustained inc. production of gastric juice & inc. motility (mixing)

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60
Q

What happens in the intestinal phase of gastric secretion?

A

Control rate of gastric emptying
- long duration

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61
Q

What is the cephalic phase directed by?

(Gastric secretion)

A

CNS
- via the viagus nerve & submucosal plexus

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62
Q

How is the cephalic phase initiated?

(Gastric secretion)

A
  1. Sight/smell/taste/thought of food stimulates the CNS
  2. Vagus nerve carries sensory info & synapses with the submucosal plexus
  3. Submucosal plexus stimulates mucous cells (= mucus), chief cells (= pepsinogen), parietal cells (= HCl), G cells (= gastrin)
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63
Q

How is the gastric phase initiated?

(Gastric secretion)

A
  1. Food in the stomach causes distension
  2. Stretch receptors & chemoreceptors detect and stimulate the submucosal & myenteric plexuses
  3. Submucosal & myenteric plexuses stimulates mucous cells (= mucus), chief cells (= pepsinogen), parietal cells (= HCl), G cells (= gastrin)

Note: G cells also stimulated to release gastrin by presence of partly digested peptides

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64
Q

How is the intestinal phase initiated?

(Gastric secretion)

A
  1. Distension of duodenum = detected by deuodenal stretch & chemoreceptors
  2. The receptors triggers enterogastric reflex which stimulates the myenteric plexus
  3. Signals to the stomach to dec. peristalsis (dec gastric contractions) + dec. gastrin production
  4. The presence of lipids & carbs in the duodenum stimulates CCK release + dec. pH stimulates secretin
  5. These GI hormones are carried by blood stream to the chief cells & parietal cells
  6. Inhibits the function of the stomach + also signals peristalsis to dec.
  7. Feedback inhibition of pepsinogen & HCl production & gastric motility
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65
Q

What is the effect of gastrin on gastric function?

A

Inc. HCl
Inc. Pepsinogen
Inc. gastric motility

Overall inc. gastric function

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66
Q

What is the effect of secretin, gastric inhibitory peptide (GIP) & Cholecystokinin (CCK)?

A

Dec. gastric motility & secretion

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67
Q

What are the functions of the liver?

A
  1. Detoxifying/Degrading (body waste, hormones, drugs)
  2. Produce proteins (Plasma proteins: clotting factor, carrier tpt proteins, etc)
  3. Process nutrients (metabolic processing)
  4. Store nutrients (glycogen, fats, vitamins, etc)
  5. Vitamin D (activates)
  6. Remove bacteria & worn-out RBCs
  7. Bile salts (secretion)
  8. Cholesterol bilirubin
  9. Hormone secretion (e.g. Thrombopoietin)

Dumb Poor People Store Valuable Rings in Blue Cardboard Houses

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68
Q

Where does the liver receive blood from?

A

Hepatic artery

Hepatic portal vein

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69
Q

What blood does the hepatic artery deliver to the liver?

A

Arterial blood
- Provides liver’s O2 supply
- Carries blood-borne metabolites for hepatic processing

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70
Q

What blood does the hepatic portal vein carry to the liver?

A

Venous blood draining from the digestive tract
- Carried to liver for processing (detox) & storage of newly absorbed nutrients

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71
Q

The blood leaves the liver via which vasculature?

A

Hepatic vein

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72
Q

What does bile contain?

A

Bile salts
Cholesterol
Lecithin
Bilirubin
etc

DOES NOT CONTAIN DIGESTIVE ENZYMES

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73
Q

Where is bile secreted from?

A

Continuously secreted by the liver (in the duodenum)
- diverted to the gallbladder b/w meals
- bile is concentrated in the gallbladder (therefore higher chance of formation of gallstones)

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74
Q

Bile salts are recycled through the _____________ _____________

A

Bile salts are recycled through the enterohepatic circulation

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75
Q

What are bile salts?

A

Derivatives of cholesterol

76
Q

What is enterohepatic circulation?

A

Recycling of bile salts b/w the small intestine & liver

77
Q

How is bile redirected to the gallbladder in between meals?

A
  • In between meals, the sphincter of Oddi (aka hepatopancreatic sphincter) is closed
  • Bile travelling down the common bile duct towards the duodenum is unable to enter the duodenum (bc sphincter is closed)
  • Bile is redirected back up to the gallbladder
78
Q

What percentage of bile salts are reabsorbed by the terminal ileum?

What percentage of bile salts are lost in faeces?

A

95% reabsorbed
(recycled by blood)

5% lost

79
Q

Secreted bile salts consist of ____ % of old, recycled bile salts and ____ % newly synthesized bile salts

A

Secreted bile salts consist of 95 % of old, recycled bile salts and 5 % newly synthesized bile salts

80
Q

What are the functions of bile?

A
  1. Aid fat digestion & absorption
  2. Excretion of water insoluble substances
81
Q

What is the detergent action of bile salts?

A

Bile salts can convert large fat globules –> lipid emulsion

Lipid emulsion: many small fat droplets (suspended in aqueous chyme)

82
Q

Formation of micelles by bile salts

A

Bile salts & lecithin aggregate in small clusters with their fat-soluble parts huddled tgt in the middle to form a hydrophobic (“water-fearing”) core

Basically, allows water & oil to mix tgt

83
Q

What water insoluble substances are excreted?

A

E.g. cholesterol & bilirubin

Bilirubin is a waste product & has no role in digestion

84
Q

Effect of cholecystokinin (CCK) on gallbladder

A
  1. CCK secretion is stimulated by presence of fats in the duodenum
  2. Inc in CCK secretion = inc in plasma CCK
  3. CCK promotes gallbladder contraction (= emptying) & relaxation of sphincter of Oddi (hepatopancreatic sphincter)
  4. Inc. bile flow into duodenum
85
Q

What are the most common liver disorders?

A

Hepatitis
Cirrhosis

86
Q

What is the pancreas?

A
  • Mixture of exocrine and endocrine tissue
  • Elongated gland –> lies behind & below stomach
87
Q

What is the exocrine function of the pancreas?

A
  • Acinar cells secrete pancreatic enzymes (works well in slightly alkaline pH)
  • Duct cells secrete aqueous alkaline solution (neutralises acidic chyme)
88
Q

What are the pancreatic enzymes?

A
  • Pancreatic amylase
  • Pancreatic lipase
  • Pancreatic proteolytic enzymes (Proteases)
89
Q

What does pancreatic amylase do?

A

Breaks down complex carbohydrates –> starch & glycogen
- Secreted in active form

90
Q

What does pancreatic lipase do?

A

Main enzyme for fat digestion in GIT
- Hydrolyses dietary triglycerides into monoglycerides & free fatty acids
- Secreted in active form

91
Q

What does pancreatic proteolytic enzymes (proteases) do?

A

Secreted as inactive form:
- trypsinogen
- chymotrypsinogen,
- procarboxypeptidase

Trypsinogen activated by enteropeptidase to trypsin
- Trypsin then activates other enzymes
Chymotrypsinogen –> Chymotrypsin
Procarboxypeptidase –> carboxypeptidase
- Trypsin is also autocatalytic (can activate trypsinogen)

92
Q

What are the pancreatic proteolytic enzymes (proteases)?

A

Trypsin
Chymotrypsin
Carboxypeptidase

93
Q

What is the aqueous alkaline solution secreted by the pancreas?

A
  • High conc. of bicarbonate (HCO3-) used to produce the secretion
  • Neutralizes acidic chyme (bc. pancreatic enzymes optimal in neutral/slightly alkaline env.)
94
Q

What is pancreatic insufficiency?

A
  • Deficient of pancreatic enzymes
  • Dietary fat digestion seriously impaired (bc. fats mostly digested by pancreatic enzymes)
95
Q

How is the pancreatic aqueous NaHCO3- secretion stimulated?

A
  1. Acid in duodenal lumen causes inc. in release of secretin from duodenal mucosa
  2. Secretin carried by blood to the pancreatic duct cells
  3. Stimulate the pancreatic duct cells to inc. secretion of aqueous NaHCO3 solution into duodenal lumen
  4. Aqueous NaHCO3 solution neutralizes the acid in duodenal lumen
96
Q

How is the pancreatic digestive enzymes secretion stimulated?

A
  1. Fat and protein products in duodenal lumen cause inc. CCK release from duodenal mucosa
  2. CCK carried by blood to the pancreatic acinar cells
  3. Stimulate the pancreatic acinar cells to inc. secretion of pancreatic digestive enzymes into duodenal lumen
  4. Pancreatic digestive enzymes digests fat & protein
97
Q

List all the functions of CCK

A
  1. Inhibits gastric motility & secretion
  2. Stimulates pancreatic enzyme secretion
  3. Stimulates contraction of gallbladder & relaxation of hepatopancreatic sphincter
  4. Inc. production of bile

(Stimulated by chyme in duodenum)

98
Q

List all the functions of gastrin

A
  1. Inc. secretion of HCl & pepsinogen
  2. Enhances gastric motility

(Stimulated by protein in stomach)

99
Q

List all the functions of secretin

A
  1. Inhibits gastric emptying & gastric secretion
  2. Stimulates pancreas to produce HCO3-
  3. Stimulates secretion of bile

(Stimulated by acid in duodenum)

100
Q

State the functions of gastric inhibitory peptide (GIP)

A
  1. Promotes metabolic processing of nutrients once they are absorbed
  2. Stimulates release of insulin from pancreas
101
Q

State the functions of vasoactive intestinal peptide (VIP)

A
  1. Stimulate secretion of intestinal glands
  2. Dilation of intestinal capillaries = facilitates nutrient absorption
  3. Inhibits acid production in stomach
102
Q

Motility of the small intestines

A
  1. Peristalsis
  2. Segmentation contractions
103
Q

What is peristalsis?

A
  • Waves of muscular contractions
  • Moves bolus along the length of digestive tract
  • Oral to anal direction
104
Q

What is essential for peristalsis?

A

Myenteric plexus

105
Q

Steps in peristalsis

A
  1. Contraction of circular muscles behind the bolus
  2. Contraction of longitudinal muscles ahead of bolus
  3. Contraction in circular muscle layer forces bolus forward
106
Q

What is the function of segmentation contraction?

A
  • Mixes chyme with digestive juices
  • Exposes chyme to all absorptive surfaces
107
Q

What is segmentation contraction?

A

Oscillating, ringlike contractions every few cm
(mixes & slow propels chyme)

108
Q

Which part of the small intestine has a higher rate of segmentation contraction?

A

Higher rate at the start of the small intestine
- 12 contractions/min

Lower rate at the end: terminal ileum
- 9 contractions/min

109
Q

Peristalsis vs segmentation contraction

A

Peristalsis:
- 1 ring contract & move a certain distance
- Moves along FAST
- Can occur simultaneously

Segmentation contraction
- Multiple rings (9-12) contract at the same time (alternates b/w contracting & relaxing BUT DOES NOT contract & move)
- Propels slowly
- Can occur simultaneously

110
Q

Where is the myenteric plexus located ?

A

B/w longitudinal & circular muscle layers
- Part of the enteric plexus

111
Q

What does the myenteric plexus control and what stimulates it?

A

Controls mainly gastrointestinal movements

Stimulated by receptors in digestive tract (stretch receptors, chemoreceptors)

112
Q

What is the migrating motility complex?

A

Peristaltic movement
- sweeps the intestine clean b/w meals

113
Q

What is the function of the ileocecal juncture?

A

Prevents contamination of the small intestine by bacteria in the colon (basically prevents the bacteria from entering the small intestine)
- consists of ileocecal valve & sphincter

114
Q

Where are enterocytes located?

A

they are localized at the brush border of the small intestines

115
Q

What enzymes do enterocytes secrete into the small intestines?

A
  1. Enteropeptidase
  2. Disaccharidases
  3. Aminopeptidases
116
Q

What is enteropeptidase?

A
  • small intestine brush border enzyme
  • needed for activation of trypsinogen –> trypsin
117
Q

What are disaccharidases?

A
  • Maltase
  • Lactase
  • Sucrose-isomaltase
  • Breaks down disaccharides –> monosaccharides
118
Q

What are aminopeptidases?

A

Breaks down peptide –> a.a.

119
Q

List the monosaccharides

A
  1. Fructose
  2. Glucose
  3. Galactose
120
Q

List the disaccharides

A
  1. Sucrose
  2. Maltose
  3. Lactose
121
Q

List the polysaccharides

A
  1. Starch (plant source)
  2. Glycogen (animal source)

Long chains of glucose
- Broken down by amylase

122
Q

What is protein?

A

1 (more than 50 aa.a.) or more polypeptide chain (with 3D folding)

123
Q

What are polypeptides?

A

Long chains of amino acids (>10)

124
Q

What are peptides?

A

Short chain of a.a. monomers linked by peptide bonds

125
Q

State the
1. Enzymes for digesting nutrient
2. Source of enzymes
3. Site of action of enzymes
4. Action of enzymes
5. Absorbable units of nutrients

For carbohydrate (amylase)

A
  1. Amylase
  2. Salivary glands; Exocrine pancreas
  3. Mouth & (mostly) body of stomach; Small-intestine lumen
  4. Hydrolyzes polysaccharides to disaccharides & α-limit dextrins
  5. Monosaccharides, esp. glucose
126
Q

State the
1. Enzymes for digesting nutrient
2. Source of enzymes
3. Site of action of enzymes
4. Action of enzymes
5. Absorbable units of nutrients

For carbohydrate (Disaccharidases: maltase, sucrase-isomaltase, lactase)

A
  1. Disaccharidases: maltase, sucrase-isomaltase, lactase
  2. Small intestine epithelial cells
  3. Small-intestine brush border
  4. Hydrolyze disaccharides to monosaccharides
  5. Monosaccharides, esp. glucose
127
Q

State the
1. Enzymes for digesting nutrient
2. Source of enzymes
3. Site of action of enzymes
4. Action of enzymes
5. Absorbable units of nutrients

For protein (pepsin)

A
  1. Pepsin
  2. Stomach chief cells
  3. Stomach antrum
  4. Hydrolyzes protein to peptide fragments
  5. Amino acids & a few small peptides
128
Q

State the
1. Enzymes for digesting nutrient
2. Source of enzymes
3. Site of action of enzymes
4. Action of enzymes
5. Absorbable units of nutrients

For protein (trypsin, chymotrypsin, carboxypeptidase)

A
  1. Trypsin, chymotrypsin, carboxypeptidase
  2. Exocrine pancreas
  3. Small-intestine lumen
  4. Attach different peptide fragments
  5. A.a. & a few small peptides
129
Q

State the
1. Enzymes for digesting nutrient
2. Source of enzymes
3. Site of action of enzymes
4. Action of enzymes
5. Absorbable units of nutrients

For protein (Aminopeptidases)

A
  1. Aminopeptidases
  2. Small-intestine epithelial cells
  3. Small-intestine brush border
  4. Hydrolyze peptide fragments to amino acids
  5. A.a. & a few small peptides
130
Q

State the
1. Enzymes for digesting nutrient
2. Source of enzymes
3. Site of action of enzymes
4. Action of enzymes
5. Absorbable units of nutrients

For fat (lipase)

A
  1. Lipase
  2. Exocrine pancreas
  3. Small-intestine lumen
  4. Hydrolyzes triglycerides to fatty acids & monoglycerides
  5. Fatty acids & monoglycerides
131
Q

State the
1. Enzymes for digesting nutrient
2. Source of enzymes
3. Site of action of enzymes
4. Action of enzymes
5. Absorbable units of nutrients

For fat (bile salts)

A
  1. Bile salts (not an enzyme!)
  2. Liver
  3. Small-intestine lumen
  4. Emulsify large fat globules for attack by pancreatic lipase
  5. Fatty acids & monoglycerides
132
Q

What is the adaptation for absorption of the small intestine?

A

Inc. SA of small intestine - Inc. rate of absorption

  • Circular fold in small intestine
  • Villus
  • Microvilli (brush border)
133
Q

Which nutrients are absorbed via simple diffusion?

A

Monoglycerides & fatty acids
etc

134
Q

Which nutrients are absorbed via facilitated diffusion?

A

Fructose, a.a.
Water-soluble vitamins
etc

135
Q

What is facilitated diffusion?

A

Requires carrier protein
but NOT energy dependent

136
Q

What nutrient is absorbed via active transport?

A

Sodium

137
Q

What nutrients are absorbed via secondary active transport?

A

Glucose, a.a. & peptides
etc

138
Q

What is secondary active transport?

A

When primary AT is working, it creates a differential concentration gradient of molecules
- uses this to pull another molecule in/out of cell
- secondary AT is dependent on energy of primary AT

139
Q

Steps in facilitated diffusion

A
  1. Carrier protein takes conformation in which solute binding site is exposed to region of higher conc. (basically conformation site on area with higher conc.)
  2. Solute molecule binds to carrier proteins
  3. Carrier protein changes conformation so that binding site is exposed to region of lower conc.
  4. Transported solute is released & carrier protein returns to conformation in step 1
140
Q

Steps in the sodium potassium pump

A
  1. Sodium-potassium pump has 3 high-affinity sites for Na+ & 2 low-affinity sites for K+ when exposed to ICF
  2. When 3 Na+ from ICF (where Na+ conc. is low) bind to pump, it splits ATP into ADP + phosphate; phosphate group binds to pump
  3. Phosphorylation causes pump to change conformation so the Na+ binding sites are exposed to opp. side of mbn and the 3Na+ are released to ECF (where Na+ conc. is high) + affinity of Na+ binding sites dec.
  4. Conformation change also exposes pump’s binding sites for K+ to ECF + infinity of K+ inc.
  5. When 2K+ from ECF (where K+ conc. is low) = binds to pump & releases phosphate group. Dephosphorylation causes pump to revert to original conformation
  6. Two K+ released to ICF (where K+ conc. is high) as affinity of K+ binding sites dec. during change in shape + affinity of Na+ binding sites inc.
141
Q

What is a symport?

A

Membrane protein that moves two or more different molecules across a cell mbn in the same direction

142
Q

What is an antiport?

A

Membrane protein that moves two or more different molecules across a cell mbn in the opposite direction

143
Q

What are the absorbable units of lactose?

A

Galactose + Glucose

  • Broken down by lactase
144
Q

What are the absorbable units of maltose?

A

Glucose + Glucose

  • Broken down by maltase
145
Q

What are the absorbable units of sucrose?

A

Glucose + Fructose

  • Broken down by sucrase-isomaltase
146
Q

What are the steps in carbohydrate absorption?

A
  1. Starch & glycogen converted into disaccharide maltose by salivary & pancreatic amylase
  2. Maltose & lactose & sucrose converted to their respective monosaccharides (by disaccharides located in brush borders)
  3. Glucose + galactose absorbed into epithelial cells by Na+ & secondary AT located in luminal mbn
  4. Fructose enters cell by facilitated diffusion via GLUT-5. Glucose, galactose, fructose exit cell at basal mbn by facilitated diffusion via GLUT-2
  5. Monosaccharides enter the blood by simple diffusion
147
Q

Steps in protein absorption

A
  1. Proteins hydrolyzed into a.a. & few small peptide fragments by gastric pepsin & pancreatic proteolytic enzymes
  2. Small peptide fragments converted into a.a. by aminopeptidases (in brush borders)
  3. a.a. are absorbed into epithelial cells by Na+/amino acid symport (secondary AT)
  4. Small peptides absorbed by H+/small peptides symport (tertiary AT)
  5. Most absorbed small peptides broken down into a.a. by intracellular peptidases
  6. a.a. exit cell at basal mbn via passive carriers
  7. a.a. enters blood by simple diffusion
148
Q

Steps in fat digestion

A
  1. Fat emulsified by bile salts into a suspension of smaller fat droplets
  2. Lipase hydrolyzes triglycerides into monoglycerides & free fatty acids
  3. Water-insoluble products carried to luminal surface of small-intestine epithelial cells within micelles
  4. When a micelle approaches the absorptive epithelial surface, monoglycerides & fatty acids leave the micelle & passively diffuse through the lipid bilayer of luminal mbns
149
Q

Steps in fat absorption

A
  1. Monoglycerides & fatty acids are resynthesized into triglycerides inside epithelial cells
  2. Triglycerides aggregate & are coated with a layer of lipoprotein from the endoplasmic reticulum = form water-soluble chylomicrons
  3. Chylomicrons extruded through the basal mbn of cells by exocytosis
  4. Chylomicrons unable to cross the basement mbn of capillaries so enter lymphatic vessels = central lacteals (will enter bld eventually through lymphatic system)
150
Q

How is water reabsorbed?

A

Passive absorption
- Active reabsorption of electrolytes & nutrients create osmotic gradient
- Na+ - K+ ATPase creates a localised concentrated area of high osmotic pressure

151
Q

What happens to water in the duodenum?

A

Flow into the lumen due to hyperosmotic chyme
- Chyme in duodenum is hypersomatic (a lot of solutes) = retains water well

152
Q

What happens to water in jejunum & ileum?

A

Water is absorbed
- Nutrient molecules get absorbed first, followed by water

153
Q

Which vitamins are water soluble?

A
  • Vitamin B complex (all vit B except B12)
  • Vitamin C
    etc

Mostly by carrier mediated mechanisms (transporters)

154
Q

Which vitamins are fat-soluble vitamins?

A

Vitamin A, D, E, K
etc

Carried in micelles & absorbed with other lipids by simple diffusion

155
Q

How is Vitamin B12 absorbed?

A
  • Needs receptor to bind with B12 and gastric intrinsic factor = forms a complex
  • Then absorbed by receptor-mediated endocytosis
156
Q

Which form of iron is absorbed best?

A
  1. Heme iron - absorbed best
  2. Fe2+ (ferrous iron)
  3. Fe3+ (ferric ion) - absorbed…
157
Q

How does vitamin C inc. iron absorption?

A

Vitamin C reduces Fe3+ to Fe2+

158
Q

What is required for effective absorption of calcium?

A

Activation of Vitamin D in the kidney/liver

159
Q

How much of daily ingested iron is absorbed?

A

Slightly <10%
women > men

160
Q

In the small intestine, what is _________ will be _________.

A

In the small intestine, what is secreted will be absorbed

E.g. secrete 9.5L, absorb around 9L

Extensive absorption by small intestine keeps pace with secretion

161
Q

Whatever that is absorbed into the digestive capillaries must pass through what first?

A

Must pass through the hepatic biochemical factory

Except lipid –> bypass this as they enter the lymphatic system

162
Q

What has to be maintained among the stomach, pancreas, small intestine?

A

Biochemical balance
- Body usually X experience a net gain/loss of acid/base during digestion

163
Q

What is diarrhoea?

A

Passage of a highly fluid faecal matter, often with inc. frequency of defaecation

164
Q

What does diarrhoea result in?

A
  1. Dehydraton
  2. Loss of nutrients (X time for absorption)
  3. Metabolic acidosis = lose a lot of alkaline fluids from intestine
165
Q

What are the causes of diarrhoea?

A
  1. Excessive small intestinal motility
  2. Excess osmotically active particle in lumen (hold onto water = too much fluid in intestine)
  3. Toxins from Vibrio cholera etc = food poisoning
166
Q

Which anal sphincter can be voluntarily controlled?

A

External anal sphincter

167
Q

Types of anal sphincter

A
  1. Internal anal sphincter = smooth muscle = X be voluntarily controlled
  2. External anal sphincter = skeletal muscle = Can be voluntarily controlled
168
Q

Main purpose of the large intestine

A

Primarily a drying & storage organ
- forms & store faeces

Receives indigestible food, unabsorbable & remaining fluid components

169
Q

What does the large intestine secrete?

A

Mucus & some ions

170
Q

What does the large intestine digest?

A

Nothing
BUT bacteria present digest food (that we can’t digest) & produce Vit K, Vit B12 & folate, etc

171
Q

What does the large intestine absorb?

A

Water & ions

172
Q

What does the haustra do (large intestine)?

A

Contractions of the haustra slowly shuffle the colonic contents back & forth

  • Initiated by the rhythmic contractions of the colonic smooth muscles
  • Slow & nonpropulsive
173
Q

How is faeces propelled long distances in the large intestine?

A

Mass movement propels into the distal part of the large intestines (to the signmoid colon & rectum)

  • Large segments of the asc. & transverse colon contract simult.
174
Q

What is the purpose of haustra contractions?

A

For absorptive & storage function
X propel forward

175
Q

What is the defecation reflex initiated by?

A

Distension of the rectum
- Stimulates stretch receptors in the rectal wall

176
Q

What is the defecation reflex?

A

Muscle contraction with relaxation of both the internal & external anal sphincter muscle

[can be blocked - e.g. you don’t go toilet; after some time urge to defecate subsides

177
Q

What helps defecation?

A

Voluntary straining movements increases intraabdominal pressure
- Contraction of abdominal muscles (bc cannot control large intestine muscles directly)
- Forcible expiration against closed glottis

178
Q

What are the two positive feedback loops in the defecation reflex?

A
  1. Short intrinsic myenteric defecation reflex
  2. Parasympathetic defecation reflex (long reflex)

Both works together

179
Q

What is the short intrinsic myenteric defecation reflex?

A

Stretch receptors stimulate the plexus to initiate inc. local peristaltic contractions in sigmoid colon & rectum
- mediated by myenteric plexus
- Impt for movement in rectum

180
Q

What is the parasympathetic defecation reflex (long reflex)?

A

Stimulate mass movements in descending and sigmoid colon
- Involves the spinal cord
- Impt for movement in desc. & sigmoid colon

181
Q

Steps in the defecation reflex

A
  1. Faeces move into rectum causing distension, stimulating stretch receptors
  2. The first loop = short reflex that triggers a series of peristaltic contractions in the rectum = moves faeces toward anus. Internal anal sphincter relaxes
  3. The long reflex = spinal reflex coordinated by sacral parasympathetic system = stimulates mass movements that push faeces towards rectum from desc. colon & sigmoid colon. Further relaxes internal anal sphincter
  4. Voluntary releaxation of the ext. anal sphincter allows defecation
182
Q

What is constipation?

A
  • When faeces become too dry
  • Abdominal discomfort, dull headache, loss of appetite, nausea, etc
183
Q

What causes constipation?

A
  • Ignoring urge to defecate = keep absorbing water
  • Decreased colonic motility
  • Obstruction (e.g. tumour)
  • Impairment of defecation reflex (neuro pathways)
184
Q

Causes of intestinal gases (flatus)?

A
  • Swallowed air
  • Bacterial fermentation (Contains beneficial bacteria = microbiota & microbiome)
185
Q

What does colonic secretion consist of?

A

Alkaline (NaHCO3) mucus solution = protective function

186
Q

How is water & salt absorbed by the large intestine?

A

Once salt & water are absorbed –> luminal contents converted to faeces
- Some absorption takes place within colon but majority in small intestine

187
Q

How are water and salts absorbed by the large intestine?

A
  • Na+ actively absorbed
  • Cl- follow down electrical gradient
  • Water follows osmotically

A&P 2 (4 decks)

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