GI Tract

Question 1

Describe the three phases of digestion and how secretion in the gastrointestinal
tract regulates these phases

Answer 1

1.Cephalic Phase
saliva( (Amylase, Lipase,
antibodies)

2.Gastric Phase
The release of gastrin and the secretion of gastric juices AND MUCUS
break down of foods into chyme

3.Intestinal Phase
Intestinal Secretions ( varius enzymes )
Bile Release
Absorbtion

Question 2

Describe the regulation of the movement pattern in the different parts of the
gastrointestinal tract and how they are generated.

Answer 2

Transport movementsPeristaltic reflex (oesophagus to rectum. Neuronal reflex, triggered by stretch-sensitive neurons in the ENS. Preparative and propulsive parts.
Mass peristalsis/mass movements: in colon, often triggered by gastrocolic reflex
Mixing movementsPendular movements (spontaneous, in longitudinal muscle layer)Segmentation movements (ditto, in cirkular muscle)Haustration movements (ditto, in haustrae in colon)Note that transport can be driven down a pressure-gradient and that the mixing movements can add to transport by creating a gradient in the distal direction (normal) or in the proximal direction (vomiting).
Intermediate formGastric motility after a meal, pacemaker-triggered (=slow-wave) peristaltic reflex with mixing-, chopping-, and emptying function (3 per min, max 5ml each)

Question 3

Around the mouth there are many glands that produce saliva. Which are the
biggest?

Answer 3

sublingual gland, parotid gland, submandigular gland

Question 4

What is the function of saliva?

Answer 4

Acinary
cells produce the volume saliva excreted
-
Cell
i the salivary duct influence saliva componsition

*
~
1 ,5 LL/day (30-400 ml/hr)
*
pH 6-7
*
H
2 O, e l ek t r o l y t ees ( m uc i n, a llpha a m y l asass, bicarbonate
*
F
ununcti o nns/relevant for:
*
Chewing
*
Swallowing
*
Taste
*
Breakdown of carbohydrates
*
p
H regregulatory
*
Protection of mucous membranes
*
Proteins inhibit demineralization + stimulate
remineralisation by attracting
calcium ions
*
Antimicrobial
*
IgA
*
Lysosomal enzymes
*
Tissue healing
*
Speech
Digestion

Question 5

Which substance that is important in carbohydrate digestion is released with the
saliva? How is saliva secretion regulated?

Answer 5

Acinary
cells produce the volume saliva excreted
-
Cell
i the salivary duct influence saliva composition

regulated by : sympathetic , parasympathetic system, sensory input , hormones and drugs that control these systems ( acetylcholine, epinephrine)

Question 6

How is food transported from the mouth down to the stomach? Does it work
to swallow food if you are standing upside-down?

Answer 6

wallowing involves a series of muscle contractions and movements that propel food through the esophagus and into the stomach regardles of the body’s position.
Oral Phase: chewing

Pharyngial phase :swallowing , soft palate and epiglotis close

Esophagial phase: peristaltic waves of muscular contractions in the esophagus push the bolus downward toward the stomach.

Question 7

At the end of the esophagus, we find the cardia. What is cardia and in which part of
the body does it exist?

Answer 7

the point where the esophagus meets the stomach( but belongs to the stomach )

it has the gastroesophageal sphincter.

Question 8

The stomach is divided into several different parts. What are these different parts
called and what function do they have? Is there any difference between these parts?

Answer 8

In summary, the different regions of the stomach, including the:

1.cardia contains the lower esophageal sphincter (LES), which acts as a valve to prevent the backflow of stomach contents into the esophagus.

2.fundus primarily serves as a reservoir for ingested food.,

3. body mixes food with gastric juices, including hydrochloric acid and digestive enzymes ,

4.antrum helps regulate the release of chyme into the small intestine,

5.pylorus(pyloric sphincter)

Question 9

How is gastric hydrochloric acid formed and in which cell type does this formation
take place? Which are the functions of hydrochloric acid in the stomach?

Answer 9

Parietal
cells ( gastric glands)

Produce H C l
*
Lowers pH
*
Bacteriostatitic f ununctio n
*
Produce intrinsic factor
*
Essential for absororption of vit B12
iin distal ileum)

Question 10

What is gastrin? Where is it formed and what effects does this substance have on
the stomach features?

Answer 10

G cells ( gastic glands)

Stimulation of Gastric Acid Secretion

Stimulation of Pepsinogen Secretion ( Chief cells)

Stimulation of Mucus Production

Stimulation of Gastric Motility

Question 11

Explain how peristaltic waves affect the breakdown of bolus in the stomach

Answer 11

Mixing the bolus with HCL acid and enzymes and moving it at the same time

Question 12

Which parts does the small intestine consist of?

Answer 12

Duodenum, Jejunum, Ileum

Question 13

There are a couple of other organs that are connected to the intestine. What are
these organs? What is their function? What part of the intestine are they connected
to?

Answer 13

Pancreas, liver, gal blader all connect to the small intestine duadenum

They contribute to the digestive process by providing enzymes and bile to aid in the breakdown of nutrients, particularly carbohydrates, proteins, and fats, as food passes through the small intestine

Question 14

Which hormones are released from the duodenum? What function do these have?

antisos

Answer 14

Motilin plays a role in regulating the motility (movement) of the gastrointestinal tract

Gastric Inhibitory Peptide (GIP) is released in response to the presence of carbohydrates and fats in the chyme. Its main functions include:
Stimulating the release of insulin from the pancreas, helping to regulate blood glucose levels.
Inhibiting gastric acid secretion and slowing down gastric emptying, which allows for more controlled digestion and absorption of nutrients.

Cholecystokinin CCK is released in response to the presence of fats and proteins in the chyme. It has several important functions:
Stimulates the gallbladder to contract and release bile into the small intestine. Bile aids in the emulsification and digestion of fats.
Stimulates the pancreas to release digestive enzymes, including lipases (for fats) and proteases (for proteins).
Inhibits gastric emptying, allowing for more thorough digestion and absorption of nutrients in the small intestine.
Acts on the brain to induce feelings of satiety (fullness), which can help regulate food intake.

Secretin is released in response to the acidic chyme entering the duodenum from the stomach. Its primary function is to stimulate the pancreas to release bicarbonate ions into the small intestine. This helps neutralize the acidic chyme, creating an optimal pH environment for the action of digestive enzymes. Secretin also inhibits gastric acid secretion and slows down gastric emptying, allowing more time for digestion.

Question 15

What characterizes the motility of the small intestine when it contains food and
when it running out of food?

Answer 15

In summary, the motility of the small intestine adapts to its content and physiological state. When the small intestine contains food, it primarily engages in segmentation and peristalsis to mix, digest, and absorb nutrients. In contrast, during the fasting phase or when the intestine is running out of food, the migrating motor complex takes over, serving a housekeeping role by clearing the small intestine of residual material and bacteria

Question 16

State three lifestyle factors that contribute to the passage of food residues through
the colon is facilitated and thus the risk of constipation is reduced.

Answer 16

Dietary Fiber Intake
Hydration
Regular Physical Activity

Question 17

What is the explanation for toddlers not being able to control when to go on the
toilet but that they learn with age?

Answer 17

Physiological Development: Toddlers are still developing both physically and neurologically. The ability to control the muscles responsible for bladder and bowel function, known as sphincter muscles, is not fully developed in very young children. This means that toddlers may not have the necessary muscle strength or coordination to control their bladder and bowels effectively.

Question 18

Describe the MMC (“Migrating Motor Complex”). What significance does it have in
digestion? How is MMC regulated?
antisos

Answer 18

its moving to clear the small intestine
when the digestive system is relatively empty of food
sends hunger signal
he MMC is regulated by a combination of hormonal, neural, and local factors

Question 19

Describe some factors that can affect peptic ulcers.

Answer 19

• Helicobacter pylori
• NSAID drugs (Non-steroidal anti-inflammatory drugs ) becasuse they are acids

Question 20

Describe the mechanism of action of antacids, acid secretion inhibitors and mucosal
protective drugs.

Answer 20

Antacids (alkalines)
perform a neutralization
reaction:
* increasing the pH to
reduce acidity in the
stomach
* inhibiting the activity
of peptic enzymes

Examples: Ranitidin (Stomacid®); Famotidin (Pepsin®)
Mechanism of action: Competitively inhibits H2 receptors of
the parietal cells
Pharmacological effects: Inhibition of gastric acid secretion
Decrease the amount of pepsin secretion
Antiulcer effects – heals gastric and duodenal ulcers
Incidence of serious side-effects is very low
Side effects: Diarrhoea, Dizziness, Muscle pain, Alopecia

Examples: Omeprazole (Losec®); Esopremazole (Nexium®)
Mechanism of action: Irreversibly blocks the H+/K+-ATPase of
the parietal cells
Pharmacological effects: Targeting the terminal step of acid
production and the irreversible blockage reduces gastric acid
secretion up to 99 %
Decrease amount of acid affects protein digestion and affect later
vitamin B12 and calcium absorption
Antiulcer effects – heals gastric and duodenal ulcers
\

Misoprostol
Cytoprotective drugs
Mechanism of action: Promote protective mucus
secretion from epithelial cells in the stomach and
inhibit gastric acid secretion for gastric parietal
cells. It also increases the secretion of bicarbonate,
blood flow and cell regeneration.
Pharmacological effects:
Peptic ulcers
Gastric ulcer formation with NSAIDs
Side effects: Diarrhea, Abdominal cramping,
Dysregulated menstruation, Teratogenic

Sucralfate
Cytoprotective drugs

Mechanism of action: Forms an ulcer-adherent
complex with the protein exudate at the ulcer site.
It is also thought to protect ulcers from pepsin.
Pharmacological effects:
Accelerate the healing of duodenal ulcers
Sucralfate is not absorbed and does not inhibit
acid secretion or neutralize acid.
Coats the ulcer
Inhibits pepsin
May increase prostaglandin production

Question 21

What drugs can be used for constipation and what are their mechanism of action?

Answer 21

Bulk laxatives
Mechanism of action: Volume increasing which in
its turn gives increased peristalsis.
The patient needs to drink more fluids when they
using bulking agents.
Consists of dietary fibre that cannot be broken
down into the human intestine;
Works within 12-24 h but max power 48-72 h
Ex: Isphagula – a plant extract
Side effects: Gases, causes blockage of the intestine

Osmotic laxatives
Mechanism of action: Preparations that are not
absorbed into the body and can therefore exert an
osmotic force in the intestine.
The effect is due to increased stool volume,
increased fluid content in the intestine and
increased peristalsis.
Works within 3-72 h
Ex: Lactulose, Makrogol, Sorbitol
Side effects: Gases, abdominal pain

Fecal softener
Mechanism of action: Surfactant which acts as a
cleanser and softens feces
Operates within 12-72 h
Not commonly used today.
Ex: Liquid Paraffin, Glycerin
Side effects: Decrease absorption of fat soluble
vitamins

Intestinal irritating laxatives

Mechanism of action: Stimulates sensory
nerves in the colon which provides increased
motor skills.
Can only be given temporarily
Works within 6-12 h
Ex: Senna glukosider, natriumpikosulfat
Side effects: Regular use may cause
irreversible damage and impair intestinal function.

Linaclotide – Guanylate cyclase agonist

Mechanism of action: Stimulates
guanylate cyclase receptors, leading to increased
water secretion in the intestine and improved
intestine emptying
Used primarily in constipated patients
med IBS, ”irritable bowel syndrome”
Side effects: Diarrhoea

Prucalopride – 5-HT4-agonist
Mechanism of action: Binds to 5HT4 receptors
(serotonin receptors) that stimulate neurons that
contains acetylcholine.
Release of Acetylcholine increases the contraction
of smooth muscle of the colon and leads to
forward movements.
Used primarily in constipated patients
med IBS, ”irritable bowel syndrome

Question 22

Which drugs can be used for diarrhea and what are their mechanism of action?

Answer 22

DIARHEA
Loperamide

Mechanism of action: bind to μ-opioid receptors
in the enteric nervous system of the intestine,
which inhibits the release of acetylcholine and
prostaglandins. This leads to reduced
peristalsis.
Synthetic morphine-like substance that cannot
penetrate blood-brain barrier.
Side effects: Constipation, flatulence, headache

Question 23

• name the two most common primary bile acids and conjugated bile salts as well as the two most
  common secondary bile acids

Answer 23

all made from cholesterol

*PRIMARY BILE ACIDS

cholic acid

chenodeoxicholic acid

*SECONDAARY BILE ACIDS

deoxicholic acid ( can conjugate with glycine)

lithocholic acid ( can conjugate with taurine)

The conjugated ones are called bile salts

Primary- by the liver
Secondary – by bacteria

Question 24

• describe for the formation, secretion and function of bile and gallbladder function and regulatory
  mechanisms for bile formation and secretion.

Answer 24

I.n summary, bile is produced in the liver, stored in the gallbladder, and released into the duodenum to aid in fat digestion and the absorption of fat-soluble vitamins. Its secretion is tightly regulated by hormonal and neural signals, ensuring that the digestive system efficiently processes dietary fats.

The primary site of bile production is the liver. Hepatocytes, specialized cells in the liver, synthesize bile from various components, including cholesterol, bilirubin (a waste product of hemoglobin breakdown), and bile salts

Question 25

name the different functions of the liver such as storage of carbohydrates, vitamins, trace elements
(especially iron); plasma protein synthesis; coagulation factors synthesis

Answer 25

Metabolism of Hormones

Immune Function

Regulation of Blood Volume

Storage of Glycogen and Lipids

Metabolism of Amino Acids

Regulation of Cholesterol Levels

Metabolism of Fats

Synthesis of Blood Clotting Factors

Detoxification and Metabolism of Toxins

Bile Production

Plasma Protein Synthesis like albumin

Vitamin and Mineral Storage particularly iron

Carbohydrate Metabolism

Question 26

explain the defecation process.

Answer 26

Defecation is the process by which solid waste materials, known as feces or stool, are eliminated from the body through the rectum and anus. This process involves several physiological and muscular actions to ensure the efficient expulsion of waste products. Here is an explanation of the defecation process:

ANS regulated’

Question 27

define the role of colipase, lipase, and bile salts in fat digestion

Answer 27

In summary, bile salts help emulsify dietary fats, creating smaller droplets for lipase to act on. Lipase, with the help of colipase, then breaks down these fats into fatty acids and glycerol, which can be absorbed by the body. This coordinated process ensures efficient digestion and absorption of dietary fats, which are essential for energy production and the uptake of fat-soluble vitamins.

Question 28

describe the regulatory mechanisms for pancreatic secretion between and after meal

Answer 28

Brain Stimulation: Sensory receptors in the mouth and digestive tract send signals to the brain when food is detected. These signals activate the vagus nerve.

Vagal Stimulation: The vagus nerve sends signals to the pancreas, stimulating the secretion of pancreatic enzymes, such as amylase and lipase, as well as bicarbonate ions. This prepares the digestive system for the incoming meal.

Stomach Distension: As food enters the stomach, it distends (expands), which stimulates stretch receptors in the stomach walls.

Neural Regulation: The stretch receptors activate the enteric nervous system and send signals to the brain. The brain, in turn, signals the pancreas via the vagus nerve to increase pancreatic enzyme secretion.

Hormonal Regulation: The presence of food in the small intestine triggers the release of hormones such as cholecystokinin (CCK) and secretin from the intestinal cells. These hormones have specific effects on the pancreas:

Cholecystokinin (CCK): CCK is released in response to the presence of fat and protein in the small intestine. It stimulates the pancreas to secrete digestive enzymes, including lipase and proteases.
Secretin: Secretin is released in response to the acidic chyme (partially digested food) entering the small intestine. It signals the pancreas to release bicarbonate ions, which help neutralize the acidic chyme, creating a suitable pH for enzyme activity.

Question 29

analyze the integrated effects of gastrin, secretin, histamine, and CCK for digestion, and describe
the principles of these hormones secretion and where they are formed

Answer 29

Function

Gastrin and histamine increase gastric acid secretion, creating an acidic environment suitable for protein digestion in the stomach.
Secretin and CCK act in the small intestine, where secretin neutralizes stomach acid with bicarbonate and CCK stimulates the release of bile and pancreatic enzymes for the digestion of fats and proteins.

Gastrin:

Formation: Gastrin is primarily produced by G cells in the gastric antrum of the stomach.

Secretin
Formation: Secretin is produced by the S cells in the duodenal and jejunal mucosa of the small intestine.

Histamine:

Formation: Histamine is synthesized and released by enterochromaffin-like (ECL) cells in the gastric mucosa and also by mast cells throughout the body.

Cholecystokinin (

Formation: CCK is primarily produced by the I cells in the duodenum and jejunum of the small intestine.

Question 30

interpret the hormonal and neuronal regulatory mechanisms for pepsin and acid secretion in the
stomach.

Answer 30

In summary, both hormonal and neuronal mechanisms play critical roles in the regulation of pepsin and acid secretion in the stomach. Gastrin, produced by G cells,( and histamin ) is the primary hormonal regulator, while the vagus nerve provides neural input, especially during the cephalic phase of digestion. Together, these mechanisms ensure that the stomach maintains an acidic pH, which is essential for the activation of pepsin and efficient protein digestion.

Question 31

describe the control of the stomach emptying and the factors that regulate it.

Answer 31

Neural Control: ANS and ENS

Hormonal Control like gastrin
Hormones play a crucial role in regulating stomach emptying. The release of gastrin, a hormone produced by the stomach lining, stimulates the secretion of gastric juices and promotes stomach contractions. In contrast, the release of cholecystokinin (CCK) and secretin from the small intestine inhibits stomach emptying and slows down the release of gastric juices. These hormones act as feedback mechanisms to ensure that food is processed at the appropriate rate.

sphyncter pylori

Question 32

explain the swallowing and transport of food through the esophagus and how these functions are
controlled including the function of the esophageal sphincters

Answer 32

Oral Phase:

The process of swallowing begins voluntarily as the tongue pushes chewed food and liquids to the back of the mouth.
The soft palate elevates to close off the nasal passages, preventing food or liquid from entering the nose.
The epiglottis, a flap-like structure, moves downward to cover the entrance to the windpipe (trachea), ensuring that food and liquids enter the esophagus and not the airway.

Question 33

describe the chewing of food and its importance in digestion

Answer 33

Chewing leaves food small enough for the gastric juices in the stomach to further degrade it and reduce it to microscopic size.

Question 34

describe the neuromuscular organization of the digestive tract (“Enteric nervous system”, ENS) and
be able to relate the different parts of this nervous system to various functions such as motor and
secretion regulation

Answer 34

ENS:
(ca 500 million neurons)
Plexus submucosa
Plexus myentericus
Controls secretion & motility
ANS:
Parasympathetic
Sympathetic
Controls activity in ENS

Question 35

what do you know about short and long reflex?

Answer 35

Local signal- short reflex- specific responses locally
Then we have long reflex- more or less activity signal

Question 36

• summarize the passage times through the gastrointestinal tract, the importance of the composition of the food and how dietary fiber affects passage time.

Answer 36

10min esophagus
1-3 h stomach
7-9 h small intestine
25-30 h large intestine
30-120 h rectum

The composition of the food plays a crucial role in determining the passage time through the gastrointestinal tract. Different nutrients, such as carbohydrates, proteins, and fats, are digested and absorbed at different rates. For example, simple carbohydrates are typically absorbed quickly in the small intestine, while complex carbohydrates and proteins may take longer to break down and absorb. Fats, on the other hand, require bile and enzymes for digestion and absorption and can slow down the passage of food.

High-fiber foods, such as fruits, vegetables, and whole grains, add bulk to the digestive contents and can accelerate the movement of food through the digestive system. This is beneficial for regular bowel movements and can help prevent constipation.

Dietary fiber, i.e.
cellulose,
hemicellulose, etc., is
partially digested by
the intestinal flora,
generating organic
acids, so-called SCFA,
which are taken up by
enterocytes in the
colon.

Question 37

• describe the role of the gastrointestinal tract in the absorption and secretion of fluid and electrolytes.

Answer 37

small intestine and colon reabsorb fluid

then we have: dietery input
saliva , gastric secrecions ,liver bile , pancreatic juice, intestinal secritions , colonic mucus secretions

The acidic environment of the stomach helps break down proteins and allows for the absorption of some electrolytes, such as calcium and magnesium

The duodenum, jejunum, and ileum, the three sections of the small intestine, have specialized cells and transporters for this purpose. Sodium, potassium, chloride, and bicarbonate ions are actively transported across the intestinal epithelial cells to regulate electrolyte balance and maintain proper hydration.

Large Intestine: In the colon, the absorption and secretion of electrolytes are finely tuned to regulate water and electrolyte balance. Sodium absorption in the colon is a key process, and it is often coupled with water absorption. The large intestine also secretes potassium and bicarbonate to help neutralize acid produced by gut bacteria. The balance of these processes is essential for forming solid stools and preventing diarrhea or constipation.

Ileum and Colon: These parts of the gastrointestinal tract play a vital role in the absorption of vitamin B12 and bile salts, which are necessary for the absorption of fats and fat-soluble vitamins, including A, D, E, and K.

Question 38

• describe the process for vitamin B12 and iron absorption in the gastrointestinal tract and the absorption

Answer 38

Absorption of vitamin B12
From food
Sometimes protein bound
Requires pepsin activity

Mucous cells
REM proteins (Haptocorrin Binding)
Binds B12 at low pH

Parietal cells
Intrinsic factor releases

Duodenum
pH rises, REM breaks
down. B12-IF complex
is formed.

Lower ileum
Absorption through the
B12-IF receptor: cubilin

Blood
Transcobalamin II is
the main transporter
to 50% to liver and
50% to other tissues.

Dietary Iron Types: There are two main forms of dietary iron: heme iron (found in animal products) and non-heme iron (found in plant and animal sources).

Stomach: In the stomach, gastric acid helps convert non-heme iron ( Fe3+)into a more absorbable form, ferrous iron (Fe2+), which can then be absorbed more efficiently.

Duodenum Absorption: Iron absorption primarily occurs in the duodenum, the first part of the small intestine. Here, both heme and non-heme iron can be absorbed. Heme iron is directly absorbed into intestinal cells via a heme transporter, while non-heme iron is transported through divalent metal transporter 1 (DMT1) into the enterocytes.

Iron Binding to Ferritin: Inside the enterocytes, iron can be stored as ferritin or transported into the bloodstream. Some iron is stored within the intestinal cells, serving as a reserve for the body’s needs.

Before it gets transoported iron is turned into Fe3+ with the help of hephaestin

Transferrin Transport: Iron is transported to the bloodstream via the protein transferrin. It is then carried to various body tissues, such as the bone marrow for red blood cell production, the liver for storage, and other organs for metabolic functions.

Question 39

• explain the digestion and absorption of carbohydrates and proteins as well as the participation of the different enzymes

Answer 39

Digestion and Absorption of Carbohydrates:

Mouth: The digestion of carbohydrates begins in the mouth with the enzyme amylase, which is present in saliva. Amylase breaks down complex carbohydrates, such as starches, into simpler sugars, primarily maltose.

Stomach: Carbohydrate digestion continues in the stomach for a short period, but the acidic environment generally halts this process.

Small Intestine: The majority of carbohydrate digestion and absorption occurs in the small intestine. The pancreas secretes pancreatic amylase into the duodenum. This enzyme further breaks down carbohydrates into maltose and other disaccharides. Additionally, the small intestine lining contains enzymes like maltase, sucrase, and lactase, which further break down disaccharides into monosaccharides. These monosaccharides, mainly glucose, fructose, and galactose, are then absorbed into the bloodstream through the intestinal epithelial cells.

saliva are produced either throught the simple refrex involving pressure receptors or chemoreceptors

or through the conditioned reflex - through seeing smellng or thinking about food ( cerebral cortex)

Absorption of carbohydrates
Absorption mainly in the upper jejunum, only as
monosaccharides:
* GLU + GAL through SGLT1: Sodium-Glucose
Linked Transporter, secondarily active.
* FRU and sugar alcohols through GLUT5:
facilitated transport.
to v. portae via GLUT2: insulin independent
Digestion and Absorption of Proteins:

Stomach: Protein digestion begins in the stomach with the help of the enzyme pepsin, which is activated by the acidic environment and breaks down proteins into smaller polypeptides.

Small Intestine: In the duodenum, the pancreas secretes various proteases, including trypsin, chymotrypsin, and carboxypeptidase, which further break down polypeptides into smaller peptides and individual amino acids. These enzymes are secreted as inactive zymogens and are activated in the duodenum.

Brush Border Enzymes: In the small intestine, the intestinal lining contains brush border enzymes, such as aminopeptidases and dipeptidases, which cleave the remaining peptides into single amino acids.

Absorption: The final products of protein digestion, the individual amino acids, are absorbed into the bloodstream through the intestinal epithelial cells. These amino acids are transported to the liver and are then distributed throughout the body for various metabolic processes, including the synthesis of new proteins.

Protein and lipid breakdown products
stimulate I cells in duodenum to secrete CCK, which then stimulates vagal afferents.

H+ stimulates
S cells in the
duodenum to
secrete secretin,
which acts on
receptors on duct
cells, stimulating
HCO3 secretion.

gastin and secretin both activate the production of pepsin ( protein digestion )
somatostatin stops gastrin

Question 40

• explain the digestion and absorption of lipids in the gastrointestinal tract

Answer 40

Emulsification in the Stomach: The process begins in the stomach, where dietary fats are exposed to gastric acid and gastric lipase. However, significant fat digestion occurs mainly in the small intestine. Stomach contractions help break down fat into small droplets, aiding in their later digestion.

Bile Secretion: The liver produces bile, which is stored in the gallbladder. When fatty food enters the duodenum (the first part of the small intestine), the gallbladder releases bile into the small intestine. Bile plays a crucial role in the digestion and absorption of fats by emulsifying them. Bile salts in bile surround fat droplets, breaking them down into smaller, more manageable micelles.

Pancreatic Enzymes: The pancreas secretes pancreatic lipase and colipase into the duodenum. Pancreatic lipase is the primary enzyme responsible for digesting triglycerides, the most common form of dietary fats. Colipase helps activate pancreatic lipase and stabilize its action in the presence of bile salts.

Emulsification and Hydrolysis: Bile salts from the gallbladder surround the fat droplets, creating micelles. This process increases the surface area for lipase to work on. Pancreatic lipase then hydrolyzes triglycerides into two free fatty acids and one 2-monoglyceride molecule.

Formation of Mixed Micelles: The products of fat digestion (free fatty acids and 2-monoglycerides) are absorbed into the mixed micelles. These micelles contain bile salts and the digested fat products. This facilitates the transport of fat digestion products to the surface of the intestinal cells.

Absorption into Enterocytes: The mixed micelles approach the absorptive cells (enterocytes) lining the small intestine. The fatty acids and monoglycerides can diffuse into the enterocytes’ cell membrane.

Re-synthesis of Triglycerides: Inside the enterocytes, the absorbed fatty acids and monoglycerides are re-synthesized into triglycerides. These newly formed triglycerides combine with proteins to create chylomicrons, which are large lipoprotein particles.

Chylomicron Secretion: Chylomicrons are released from the enterocytes into the lymphatic system via lacteals, specialized lymphatic vessels in the small intestine. This is because they are too large to enter the bloodstream directly. Eventually, they enter the bloodstream through the thoracic duct, a major lymphatic vessel. Once in the bloodstream, chylomicrons transport dietary fats to various tissues in the body, where they are either used for energy or stored.

*Salivary lipase (optimal pH=4.5-5.4) from secretory
cells on tongue papillae (active without co-lipase)
* 10-30% TG hydrolysis with gastric lipase (active
without co-lipase).
* Lipase from pancreas: Pancreatic lipase + co-lipase

taking in of lipids by an ebterocyte requires the acidic environement just outside of the cell so that the negative charge on the outside of the micele is neutralised

After absorption, re-esterification occurs to TAG and cholesteryl esters
(ER) and packaging in chylomicrons; secretion by exocytosis into lymph
lacteals.
* The chylomicron is built around apo B-48.
* In the blood, apo E and apo C-II are picked up (from HDL).
* Apo C-II binds lipoprotein lipase (LPL) which cleaves TAG to tissue cells
* goes to the liver via apo E.

Question 41

• explain the role of the central nervous system in regulating hunger and satiety.

Answer 41

Hypothalamus: The hypothalamus is a key brain region involved in the regulation of hunger and satiety. It contains specific nuclei that are responsible for monitoring and responding to signals related to food intake. Two critical nuclei in this process are the lateral hypothalamus (LH) and the ventromedial hypothalamus (VMH).

The LH is often referred to as the “hunger center.” When it is activated, it can stimulate appetite and food intake. Neurons in the LH release orexigenic (appetite-stimulating) signals, such as neuropeptide Y (NPY) and agouti-related peptide (AgRP).

The VMH is often considered the “satiety center.” When activated, it can promote feelings of fullness and reduce food intake. Neurons in the VMH release anorexigenic (appetite-suppressing) signals, such as pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART).

Hormones: The CNS receives signals from various hormones that are released from the gut, adipose tissue, and pancreas, which provide information about nutrient levels in the bloodstream. Leptin, produced by adipose tissue, is a hormone that plays a crucial role in signaling satiety. Insulin, released by the pancreas, also influences the CNS regarding glucose levels.

Gut-Brain Communication: The gut releases hormones like ghrelin (the “hunger hormone”) when the stomach is empty, signaling to the brain that it’s time to eat. Conversely, when the stomach is distended after a meal, stretch receptors and other signals are sent to the brain to indicate fullness.

Neurotransmitters: Neurotransmitters, such as serotonin, dopamine, and norepinephrine, are involved in mood regulation and can influence eating behavior. An imbalance in these neurotransmitters can impact hunger and satiety signals.

Reward Centers: The mesolimbic pathway, which includes the nucleus accumbens and ventral tegmental area, is associated with the reward and pleasure aspects of eating. These regions can influence food-seeking behavior and can override satiety signals in certain situations, leading to overeating.

Circadian Rhythms: The CNS also regulates hunger and satiety according to the body’s circadian rhythms. The body’s internal clock can influence when hunger occurs and when the body is naturally inclined to eat.

Traditional views on control of food intake
Glucostat-theory

Low blood sugar
stimulates food intake.
Lipostat-theory

Free fatty acids in the
plasma inhibit food intake.

Negative Feedback
from the
gastrointestinal tract

OGT-expressing neurons as nutrient sensors in hypothalamus and brainstem

UDP-GlcNAc is the donor for O-GlcNAc transferase (OGT)
and an ideal sensor of the metabolic status of the cell

Question 42

• describe the pre-absorptive, absorptive and post-absorptive appetite suppressants signals and saturation signals.

Answer 42

Pre-absorptive Appetite Suppressants:

Cholecystokinin (CCK): This hormone is released by the small intestine in response to the presence of fats and proteins in the digestive system. CCK signals to the brain that food has been consumed, contributing to a sense of satiety and reducing further food intake.

Peptide YY (PYY): PYY is released by the small and large intestine following a meal, especially in response to the presence of protein. It acts on the hypothalamus to reduce appetite and food intake.

Ghrelin Inhibition: Ghrelin is often referred to as the “hunger hormone” because its levels increase when the stomach is empty. Pre-absorptive signals, such as the presence of food in the stomach, can reduce ghrelin release, helping to suppress appetite.

Cortex inputs to hypothalamus

sight, smell , emotions and taste are also in this category

Absorptive Signals:

Blood Glucose Levels: The levels of glucose in the bloodstream are closely monitored by the body. When blood glucose levels rise after a meal, it signals to the brain that energy has been acquired. This can lead to a reduction in appetite.

Insulin: Insulin is released by the pancreas in response to elevated blood glucose levels. It helps transport glucose into cells for energy. As a result, insulin can lead to a feeling of satiety and reduce further food consumption.

Post-Absorptive Appetite Suppressants:

Leptin: Leptin is produced by adipose (fat) tissue and serves as a long-term regulator of energy balance. It signals to the brain about the body’s energy reserves. When fat stores are sufficient, leptin levels rise and can reduce appetite.

Glucagon-Like Peptide-1 (GLP-1): GLP-1 is released by the small intestine and colon in response to the presence of nutrients. It promotes feelings of fullness and can delay gastric emptying, which helps control food intake.

PYY: In addition to its role as a pre-absorptive signal, PYY is also released post-absorption, and its levels continue to rise for several hours after eating, contributing to prolonged feelings of fullness.

Satiation Signals:

Stretch Receptors: The stomach contains stretch receptors that are activated as it fills with food. These receptors signal to the brain that the stomach is distended, contributing to the feeling of fullness and reducing food intake.

Oral Sensory Input: The taste, texture, and temperature of food, as well as the act of chewing and swallowing, provide sensory input that can influence satiation. The brain responds to these sensory cues, and when they are satisfying, they can reduce appetite.

many of these effect are throught the vagus nerve

Adiponectin signaling
from adipose tissue

liver
Glucose output down

Fat accumulation down

Inflammation down

skeletal muscle
Glucose uptake up

Fat accumulation down

Energy expenditure up

heart
Inflammation down

Endothelial adhesion down

Foam cell formation down

Question 43

• describe the vomiting process with prodromal phase and emptying phase and explain stimuli and neurogenic control of vomiting, as well as the effects of vomiting on circulation and respiration.

Answer 43

Prodromal Phase:

This is the preparation phase that precedes actual vomiting.
Nausea: Nausea is a subjective feeling of discomfort that often precedes vomiting. It can be triggered by various factors, such as noxious odors, motion sickness, or illness.
Salivation: An increase in salivation may occur, which is thought to protect the oral mucosa from the acidic stomach contents during vomiting.
Autonomic Responses: During this phase, autonomic responses like increased heart rate and diaphoresis (sweating) may occur.
Emptying Phase:

This is the phase during which the stomach contents are expelled.
Retching: Retching involves deep, rhythmic contractions of the diaphragm and abdominal muscles. This action increases intragastric pressure, which is a necessary step to force the stomach contents into the esophagus.
Anti-peristalsis: During vomiting, peristalsis in the small intestine reverses, preventing the intestinal contents from moving into the stomach.
Opening of the Gastroesophageal Sphincter: The lower esophageal sphincter, or gastroesophageal sphincter, relaxes to allow the contents of the stomach to move into the esophagus.
Rising Vomitus: The stomach contents are expelled through the mouth and sometimes the nose in a forceful manner.
Stimuli and Neurogenic Control of Vomiting:

Chemoreceptor Trigger Zone (CTZ): The CTZ, located in the area postrema of the brainstem, is sensitive to various chemical stimuli. It can be activated by toxins, drugs, or metabolic disturbances. The CTZ then sends signals to the vomiting center in the brain.

Vomiting Center: The vomiting center is located in the medulla oblongata of the brainstem. It integrates sensory input from various sources, including the CTZ, the vestibular system (responsible for balance and motion sickness), and other regions of the brain. It coordinates the motor responses necessary for vomiting.

Sensory Input: Sensory input from the gastrointestinal tract, inner ear, and the higher centers of the brain can trigger vomiting. For example, noxious smells or sights, irritation or distension of the stomach, and vestibular disturbance can all stimulate the vomiting center.

Effects of Vomiting on Circulation and Respiration:

Vomiting can have several effects on the body’s circulation and respiration:

Bradycardia: Vomiting may lead to a temporary slowing of the heart rate (bradycardia) due to the activation of the vagus nerve, which can be stimulated during retching and vomiting.

Hypotension: The increase in abdominal pressure during retching can result in decreased venous return to the heart, potentially causing a drop in blood pressure.

Respiratory Effects: During vomiting, the glottis typically closes to protect the airway from the stomach contents. This can temporarily reduce airflow and increase intrathoracic pressure, which may affect respiration.

Risk of Aspiration: The risk of aspiration, where stomach contents enter the airway, can lead to respiratory distress and lung injury. This is why the body employs protective mechanisms like glottal closure.

Question 44

• explain the symptoms and mechanisms that lead to gastric-esophageal reflux disease (GERD), dyspepsia and peptic ulcer (ulcer pepticum) and their clinical consequences.

Answer 44

astroesophageal Reflux Disease (GERD):

Symptoms:

Heartburn: A burning sensation in the chest or throat.
Acid regurgitation: Sour-tasting fluid backing up into the mouth.
Regurgitation of food or a sour-tasting liquid.
Chest pain.
Difficulty swallowing.
Chronic cough.
Laryngitis or voice changes.
Dental problems.
Mechanisms:
GERD is caused by the weakening of the lower esophageal sphincter (LES), a ring of muscle that normally prevents stomach acid from flowing back into the esophagus. This weakening can be due to factors such as obesity, pregnancy, smoking, certain medications, and a hiatal hernia (where a portion of the stomach moves above the diaphragm).

Clinical Consequences:
Untreated GERD can lead to complications like esophagitis (inflammation of the esophagus), esophageal strictures (narrowing of the esophagus), Barrett’s esophagus (a condition that increases the risk of esophageal cancer), and chronic cough or asthma.

Dyspepsia (Indigestion):

Symptoms:

Abdominal pain or discomfort.
Bloating.
Early satiety (feeling full quickly after eating).
Nausea.
Belching.
Heartburn.
Mechanisms:
Dyspepsia is a non-specific condition often caused by various factors, including overeating, eating too quickly, excessive consumption of fatty or spicy foods, alcohol, stress, and medications. In some cases, it can be associated with underlying conditions like gastritis or peptic ulcers.

Clinical Consequences:
Dyspepsia is primarily a symptom, and its consequences depend on the underlying cause. In most cases, it is self-limiting and not associated with severe complications. However, if it is persistent and due to an underlying condition, it may require further investigation and management.

Peptic Ulcer (Ulcer Pepticum):

Symptoms:

Burning or gnawing abdominal pain, typically in the upper abdomen.
Pain that may worsen at night and when the stomach is empty.
Bloating and burping.
Nausea and vomiting.
Unintended weight loss.
Dark, tarry stools (indicative of gastrointestinal bleeding).
Mechanisms:
Peptic ulcers are open sores or erosions in the lining of the stomach or the first part of the small intestine (duodenum). They are primarily caused by the erosion of the protective mucus lining, allowing stomach acid and digestive enzymes to damage the underlying tissue. The main factors contributing to peptic ulcers are Helicobacter pylori infection, prolonged use of non-steroidal anti-inflammatory drugs (NSAIDs), and, less commonly, excessive alcohol consumption and smoking.

Clinical Consequences:
Peptic ulcers can lead to complications, including gastrointestinal bleeding, perforation (when the ulcer eats through the wall of the stomach or intestine), and gastric outlet obstruction (due to swelling or scarring that blocks the passage of food). If left untreated, these complications can be life-threatening.

Question 45

• predict the metabolic and clinical consequences of a gastric bypass.

Answer 45

Gastric Bypass

Gastric bypass surgery is a type of
bariatric, or weight loss, surgery.
* Roux-en-Y gastric bypass is considered
the ‘gold standard’ of weight loss
surgery.
* Restricts the amount of food that the
stomach holds
* Limits the amount of calories and
nutrients the body absorbs
* Changes the gut hormones, which help
feel fuller longer, contribute to appetite
suppression and the reversal of obesitycaused
metabolic syndrome.

Consequences of a gastric bypass
Metabolic Consequences:

Weight Loss: Gastric bypass typically leads to significant and sustained weight loss. This has numerous metabolic benefits, including improved insulin sensitivity and blood glucose control.

Improved Insulin Sensitivity: Patients often experience rapid improvements in insulin sensitivity, which can lead to better blood sugar control. Many individuals with type 2 diabetes experience remission or substantial reductions in their medication needs after surgery.

Resolution of Metabolic Syndrome: Metabolic syndrome, a cluster of risk factors for heart disease and diabetes, often improves or resolves after gastric bypass surgery.

Reduction in Inflammatory Markers: Gastric bypass can lead to reduced levels of inflammatory markers in the blood, which are associated with various chronic diseases.

Altered Gut Hormones: Changes in the anatomy of the digestive system affect the release of gut hormones like ghrelin, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY), which contribute to appetite regulation, satiety, and metabolic improvements.

Clinical Consequences:

Improved Type 2 Diabetes: Many individuals with type 2 diabetes experience significant improvements, and in some cases, remission of the condition after gastric bypass surgery. However, careful monitoring and management of diabetes is still necessary.

Resolution of Obstructive Sleep Apnea: Weight loss and reduced fat mass often lead to improved breathing and resolution of obstructive sleep apnea, a common condition in obese individuals.

Reduced Cardiovascular Risk: Weight loss and improved metabolic markers reduce the risk of cardiovascular diseases like heart attacks, high blood pressure, and high cholesterol.

Lower Risk of Certain Cancers: Obesity is a risk factor for several types of cancer. Weight loss following gastric bypass may reduce the risk of obesity-related cancers.

Psychological Benefits: Many patients experience improved mood, self-esteem, and quality of life after substantial weight loss.

nutritional deficiencies

Question 46

• explain the metabolic and clinical consequences of non-alcoholic fatty liver disease (NAFLD)

Answer 46

Insulin Resistance: NAFLD is closely associated with insulin resistance, a condition in which the body’s cells do not respond effectively to insulin. This leads to elevated blood sugar levels, which can contribute to the development of type 2 diabetes.

Dyslipidemia: Individuals with NAFLD often have abnormal lipid profiles, characterized by elevated triglycerides, low levels of high-density lipoprotein (HDL) cholesterol, and increased levels of low-density lipoprotein (LDL) cholesterol. These lipid abnormalities are risk factors for cardiovascular disease.

Obesity: NAFLD is strongly linked to obesity. Excess body fat, especially abdominal obesity, can contribute to the accumulation of fat in the liver.

Metabolic Syndrome: NAFLD is considered a hepatic manifestation of metabolic syndrome, a cluster of risk factors including obesity, insulin resistance, high blood pressure, and dyslipidemia. Metabolic syndrome is associated with an increased risk of cardiovascular disease and type 2 diabetes.

Hormonal Imbalance: NAFLD can lead to hormonal imbalances, including elevated levels of androgens (male hormones) in women, which can result in conditions like polycystic ovary syndrome (PCOS) and irregular menstruation.

Clinical Consequences of NAFLD:

Liver Inflammation (Non-Alcoholic Steatohepatitis, NASH): A subset of individuals with NAFLD develop NASH, which is characterized by liver inflammation and liver cell damage. NASH can progress to more severe liver conditions, such as fibrosis and cirrhosis.

Liver Fibrosis: In some cases, NASH can lead to liver fibrosis, where scar tissue accumulates in the liver. The severity of fibrosis can range from mild to advanced.

Cirrhosis: Advanced liver fibrosis can progress to cirrhosis, which is characterized by extensive scarring and loss of liver function. Cirrhosis is a serious, irreversible condition that can lead to liver failure.

Hepatocellular Carcinoma (Liver Cancer): Individuals with cirrhosis due to NAFLD/NASH have an increased risk of developing hepatocellular carcinoma, a form of liver cancer.

Cardiovascular Disease: NAFLD is associated with an increased risk of cardiovascular disease, as the metabolic abnormalities and inflammation associated with the condition can affect the blood vessels and increase the risk of heart attacks and strokes.

Psychological Impact: NAFLD can have psychological and emotional consequences due to the stress and anxiety associated with the diagnosis, as well as concerns about the long-term impact on liver health.

Question 47

• analyze the general effects of jaundice and identify if it is a prehepatic, hepatic or posthepatic jaundice

Answer 47

General Effects of Jaundice:

Yellowing of the Skin and Eyes: The most recognizable symptom of jaundice is the yellow discoloration of the skin and the whites of the eyes. This occurs due to the accumulation of bilirubin in the tissues.

Dark Urine: Jaundice can lead to the production of dark or brownish urine, a result of bilirubin being excreted in the urine.

Pale Stools: Jaundice may cause pale or clay-colored stools due to the reduced excretion of bilirubin into the digestive tract. Normal bilirubin gives stools their brown color.

Itchy Skin: Some individuals with jaundice may experience pruritus, or itching of the skin. This is often associated with elevated bilirubin levels.

Fatigue and Weakness: Jaundice may be accompanied by general symptoms of malaise, fatigue, and weakness.

Types of Jaundice:

Prehepatic Jaundice: This type of jaundice occurs before the liver. It is often caused by excessive breakdown of red blood cells, leading to an increased production of bilirubin. Common causes include hemolytic anemias, such as sickle cell anemia or thalassemia, as well as conditions like Gilbert’s syndrome. Prehepatic jaundice generally results in a higher concentration of unconjugated bilirubin in the bloodstream.

Hepatic Jaundice: Hepatic jaundice occurs within the liver itself and is often related to liver diseases or disorders that impair the liver’s ability to metabolize bilirubin. Causes may include viral hepatitis, alcoholic liver disease, cirrhosis, or drug-induced liver injury. Hepatic jaundice can result in a combination of unconjugated and conjugated bilirubin in the bloodstream.

Posthepatic Jaundice: Posthepatic jaundice occurs after the liver, often due to the obstruction of the bile ducts. Causes include gallstones, tumors, or strictures in the bile ducts. In posthepatic jaundice, there is a predominance of conjugated bilirubin in the bloodstream.

Question 48

• explain the symptoms, molecular mechanisms, and clinical consequences of different intolerances (gluten and lactose) as well as diarrhea and constipation.

Answer 48

Gluten Intolerance (Non-Celiac Gluten Sensitivity):

Symptoms:

Gastrointestinal symptoms: Bloating, abdominal pain, diarrhea, and sometimes constipation.
Extra-intestinal symptoms: Headaches, fatigue, joint pain, and mood disturbances.
Molecular Mechanisms:

Non-celiac gluten sensitivity is not well understood. It is different from celiac disease, an autoimmune condition, and wheat allergy.
Some proposed mechanisms include the involvement of innate immune responses and the gut microbiota, but these mechanisms are still a subject of ongoing research.
Clinical Consequences:

The symptoms of non-celiac gluten sensitivity can significantly impact a person’s quality of life but do not typically result in severe medical complications.
Treatment usually involves adopting a gluten-free diet, which can alleviate symptoms.
Lactose Intolerance:

Symptoms:

Gastrointestinal symptoms: Bloating, gas, diarrhea, and abdominal cramps after consuming lactose-containing foods or drinks.
Lactose intolerance does not typically cause extra-intestinal symptoms.
Molecular Mechanisms:

Lactose intolerance results from the deficiency of lactase, the enzyme needed to digest lactose (milk sugar).
In individuals with lactose intolerance, undigested lactose reaches the colon, where it ferments, causing gas and diarrhea.
Clinical Consequences:

Lactose intolerance is a common condition that, when managed with dietary modifications, does not lead to severe health issues.
Lactase supplements or lactose-reduced products can help individuals consume dairy products more comfortably.
Diarrhea:

Symptoms:

Frequent, loose, and watery stools.
May be accompanied by abdominal cramps, bloating, and urgency.
Molecular Mechanisms:

Diarrhea can have various causes, including infections (e.g., viral or bacterial gastroenteritis), food intolerances, malabsorption disorders (e.g., celiac disease), medications, and underlying medical conditions.
Clinical Consequences:

Acute diarrhea is often self-limiting and not usually severe. Chronic diarrhea, which lasts for more than a few weeks, may be a sign of an underlying medical condition and should be evaluated by a healthcare professional.
Severe or persistent diarrhea can lead to dehydration and malnutrition if not properly managed.
Constipation:

Symptoms:

Infrequent bowel movements (typically less than three times per week).
Difficulty passing stools, often accompanied by straining and discomfort.
Hard, dry stools.
Molecular Mechanisms:

Constipation can be caused by a variety of factors, including inadequate dietary fiber, dehydration, lack of physical activity, medications, and underlying medical conditions (e.g., irritable bowel syndrome or hypothyroidism).
Clinical Consequences:

Constipation can cause discomfort and is often a sign of an underlying issue.
Chronic constipation may lead to complications like hemorrhoids, anal fissures, or rectal prolapse if left untreated.

Question 49

• explain the symptoms, molecular mechanisms, and clinical consequences of irritable bowel syndrome as well as Crohn’s disease.

Answer 49

Inflammatory bowel disease
Inflammatory disease of the intestines. It primarily causes
ulcerations (breaks in the lining) of the small and large intestines, but
can affect the digestive system anywhere from the mouth to the anus
Symptoms:
* Chronic diarrhea (blood and mucous)
* Weight loss
* Rectal bleeding
* Fever
* Night sweats

Inflammatory Bowel Disease
Explain the symptoms, molecular mechanisms, and clinical consequences of irritable bowel syndrome as
well as Crohn’s disease.
Inflammatory Bowel Disease
* Irritable bowel disease
* Ulcerative colitis
* Crohn’s disease
Inflammatory Bowel Disease
Explain the symptoms, molecular mechanisms, and clinical consequences of irritable bowel syndrome as
well as Crohn’s disease.
Inflammatory Bowel Disease
* Irritable bowel disease
* Ulcerative colitis
* Crohn’s disease

Crohn’s disease - mechanisms
* Genetics: identified and confirmed 71
susceptibility loci for Crohn’s disease
on 17 chromosomes
* Lifestyle and environmental effects
* Previous infectious gastroenteritis
* Impaired interaction of the intestinal
commensal microbiota
* Mucin cover becomes insufficient
* The adaptive immune system in
Crohn’s disease is now thought to
mediate and perpetuate, but
probably not start, intestinal
inflammation.

Irritable bowel syndrome
* Functional bowel disorder characterised by chronic or recurrent abdominal
pain associated with either relief or exacerbation by defecation, or a change
in bowel habit.
* IBS is one of the most widely recognised functional bowel disorders, with
more than 10% of the global adult population reporting symptoms
compatible with the condition in population-based surveys

Genetic factors (most notably
an identified mutation
of SCN5A)
* Post-infectious changes
* Chronic infections and
disturbances in the intestinal
microbiota
* Low-grade mucosal
inflammation
* Immune activation, and
altered intestinal
permeability
* Disordered bile salt
metabolism
* Abnormalities in serotonin
metabolism
* Alterations in brain function

Question 50

• explain mechanisms of action of drug groups in the treatment of obesity as a lipase inhibitor, liraglutide, and bupropion/naltrexone.

Answer 50

1. Lipase Inhibitors (e.g., Orlistat):

Mechanism of Action:

Lipase inhibitors like Orlistat work by reducing the absorption of dietary fats in the small intestine.
Orlistat inhibits pancreatic lipase, an enzyme that breaks down dietary fats into smaller molecules that can be absorbed by the body.
By blocking this enzyme, Orlistat reduces the hydrolysis of fats, leading to the excretion of unabsorbed fats in the feces.
Clinical Consequences:

Reduced fat absorption leads to a decrease in caloric intake from dietary fats, which can result in weight loss.
Side effects may include oily stools, flatulence, and deficiencies of fat-soluble vitamins (A, D, E, and K). To mitigate these deficiencies, individuals taking Orlistat are often advised to take vitamin supplements.
2. Liraglutide (a GLP-1 Receptor Agonist):

Mechanism of Action:

Liraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist, a class of drugs used to treat type 2 diabetes and obesity.
GLP-1 is a hormone produced in the intestines that enhances insulin secretion and reduces appetite.
Liraglutide mimics the action of GLP-1 by binding to its receptors in the brain and pancreas.
It slows gastric emptying, promotes satiety, and reduces food intake, leading to decreased calorie consumption and weight loss.
Clinical Consequences:

Liraglutide helps individuals with obesity lose weight by reducing appetite and food intake.
It may also have positive effects on glucose metabolism and insulin sensitivity, which can be beneficial for individuals with obesity and insulin resistance.
Side effects may include nausea, vomiting, and diarrhea.
3. Bupropion/Naltrexone Combination:

Mechanism of Action:

Bupropion is an atypical antidepressant that is believed to work on the brain’s neurotransmitter systems, particularly norepinephrine and dopamine, to help reduce appetite and promote weight loss.
Naltrexone is an opioid receptor antagonist, which is thought to modulate the reward system in the brain and reduce the pleasurable sensations associated with food and overeating.
Clinical Consequences:

The combination of bupropion and naltrexone works synergistically to reduce food cravings and increase satiety.
This can result in decreased caloric intake and weight loss.
It is typically used for individuals with obesity who have not had success with other weight loss interventions.

Question 51

• describe the mechanism of action of drug groups in the treatment of vomiting such as H1-receptor antagonists, muscarinic receptor antagonists, 5-HT3 receptor antagonists, D2 receptor antagonists and NK1 antagonists.

Answer 51

Antihistamines - H1 receptor antagonist
Examples:
* Cinnarizine
Mechanism of action: Antagonist of histamine H1
receptors, and many also have antimuscarinic effects.
Promethazine also blocks some 5-HT receptor
subtypes.
Pharmacological effects:
* Antihistamines are effective against most causes of
vomiting but they are rarely treatments of choice.
Side effects:
* Sedation
* Headache.
* Antimuscarinic effects: dry mouth, urinary retention
and blurred vision.
Netter

Muscarinic antagonists
Examples:
* Hyoscine (scopolamine)
Mechanism of action: Competitive antagonist at
muscarinic M1 receptors.
Pharmacological effects:
* Muscarinic receptors are involved in the
visceral afferent input from the gut to the
vomiting centre
* Used for the treatment of motion sickness and
postoperative vomiting.
Side effects:
* Sedation.
* Antimuscarinic effects: dry mouth, urinary
retention and blurred vision.

5-HT3 receptor antagonists
Examples:
* Ondansetron
* Granisetron
* Palonosetron
Mechanism of action: block the 5-HT3
receptors in the chemoreceptor trigger
zone (CTZ) and in the gut.
Pharmacological effects:
* Reduce vomiting induced by drugs and
surgery.
Side effects:
* Headache is common.
* Constipation
* Flushing.
* Predisposes to arrhythmias.

D2 receptor antagonists
Examples:
* Domperidone
* Metoclopramide
Mechanism of action: Antagonists of dopamine
D2 receptors and inhibit dopaminergic stimulation
of the CTZ.
Pharmacological effects:
* Reduce vomiting induced by drugs and
surgery.
* Ineffective in motion sickness
Side effects:
* Dystonias (especially in children and young
adults)
* Parkinsonian-like syndrome

Aprepitant – NK1 Antagonists
Mechanism of action: Neurokinin-1-
receptor (substance P) antagonist that
blocks the action of neurokinin-1 in the
brain.
Pharmacological effects:
* They augment the effects of 5-HT3
receptor antagonists
* Used in chemotherapy-induced nausea
and vomiting
Side effects:
* Constipation
* Diarrhea
* Loss of appetite
* Anorexia
* Abdominal pain

Question 52

• give an overview of common side effects of drugs used in the treatment of diseases related to the digestive system.

Answer 52

1. Antacids and Acid Blockers (Proton Pump Inhibitors, H2 Blockers):

Common Side Effects: These drugs are often used to treat acid-related conditions such as gastroesophageal reflux disease (GERD) and peptic ulcers. Common side effects may include diarrhea, constipation, headache, and dizziness.
Long-Term Use Concerns: Prolonged use of proton pump inhibitors (PPIs) can be associated with potential risks such as vitamin and mineral deficiencies, increased risk of fractures, and an increased susceptibility to certain infections.
2. Laxatives:

Common Side Effects: Laxatives are used to relieve constipation. Common side effects include diarrhea, abdominal cramps, and electrolyte imbalances.
Overuse and Dependence: Overuse of laxatives can lead to dependence, where the bowel becomes reliant on laxatives to have a bowel movement. Long-term misuse can result in more severe health issues.
3. Antiemetics (Anti-Nausea Medications):

Common Side Effects: Antiemetics are used to alleviate nausea and vomiting. Side effects can include drowsiness, dizziness, and dry mouth.
Sedation: Some antiemetics, particularly older-generation medications, can cause sedation, which may not be suitable for all individuals.
4. Anti-Inflammatory Medications (e.g., NSAIDs):

Common Side Effects: Non-steroidal anti-inflammatory drugs (NSAIDs) can cause gastrointestinal side effects such as stomach irritation, ulcers, and gastrointestinal bleeding.
Cardiovascular and Renal Effects: In addition to gastrointestinal issues, NSAIDs can also affect the cardiovascular system and kidneys, which may pose risks in some individuals.
5. Antibiotics:

Common Side Effects: Antibiotics are used to treat bacterial infections in the gastrointestinal tract and other areas. Common side effects can include diarrhea, nausea, and abdominal discomfort. In some cases, they may disrupt the balance of gut bacteria (microbiota).
Clostridium difficile Infection (CDI): Prolonged or inappropriate use of antibiotics can increase the risk of developing Clostridium difficile-associated diarrhea or colitis.
6. Immunomodulators (e.g., Biologics for Inflammatory Bowel Disease):

Common Side Effects: These drugs, used to treat conditions like Crohn’s disease and ulcerative colitis, can lead to side effects such as increased susceptibility to infections and infusion reactions.
Monitoring: Regular monitoring is often required to manage potential risks associated with immunomodulators.

Question 53

• analyze the principal mechanisms for the occurrence of deficiency (intake, absorption, need, loss).

Answer 53

1. Inadequate Dietary Intake:

One of the most common causes of nutrient deficiencies is an insufficient intake of essential nutrients. This can result from an imbalanced or inadequate diet, restricted food choices, or poor dietary habits.
For example, not consuming enough fruits and vegetables can lead to a deficiency in vitamins and minerals like vitamin C, folate, and potassium.
2. Impaired Nutrient Absorption:

Even if an individual consumes an adequate amount of a nutrient, deficiencies can still occur if the body has difficulty absorbing it. Malabsorption can be caused by various factors, including digestive disorders (e.g., celiac disease, Crohn’s disease), surgical procedures (e.g., removal of part of the stomach or small intestine), or certain medications (e.g., proton pump inhibitors that reduce stomach acid, which is necessary for nutrient absorption).
In cases of malabsorption, even though nutrients are ingested, they are not properly absorbed and utilized by the body.
3. Increased Nutrient Requirements (Higher Needs):

Some conditions or life stages may increase the body’s demand for specific nutrients. For example, during pregnancy and lactation, women require higher amounts of certain nutrients like folic acid, iron, and calcium to support fetal development and breast milk production.
Increased physical activity, growth periods (e.g., adolescence), and certain medical conditions can also raise nutrient requirements.
4. Excessive Nutrient Loss:

Nutrient losses can occur through various means, including excessive sweating, frequent urination, diarrhea, and vomiting.
Certain medical conditions, such as kidney diseases or diabetes, can result in excessive excretion of nutrients, leading to deficiencies.
5. Genetic Factors (Inherited Disorders):

In some cases, nutrient deficiencies can be due to genetic factors. These are often rare genetic disorders that affect the metabolism, absorption, or utilization of specific nutrients. For example, hemochromatosis is a genetic condition that leads to excessive iron absorption, potentially causing iron overload and toxicity.
6. Poor Nutrient Storage and Utilization:

Some individuals may have difficulties storing and utilizing nutrients effectively, even when they are adequately absorbed from the diet. For instance, vitamin B12 deficiency can occur if the body is unable to effectively store or utilize the vitamin, even if it is consumed in sufficient quantities.
7. Dietary Restrictions and Lifestyle Choices:

Dietary restrictions, such as vegan or vegetarian diets, may lead to deficiencies in certain nutrients like vitamin B12, iron, and omega-3 fatty acids if not carefully planned.
Lifestyle choices, such as excessive alcohol consumption, smoking, or crash dieting, can also increase the risk of nutrient deficiencies.

Question 54

• give examples of and describe the connection between diet and disease (cancer, cardiovascular disease, saturated and unsaturated fatty acids, trans fats, fiber, phenylketonuria).

Answer 54

1. Cancer and Diet:

There is a strong connection between diet and cancer risk. For instance, diets high in red and processed meats have been linked to an increased risk of colorectal cancer. Conversely, diets rich in fruits, vegetables, and whole grains are associated with a reduced risk of various cancers. Phytochemicals in these foods can have protective effects. Additionally, some dietary factors, like alcohol consumption, are known to increase the risk of certain cancers, such as breast and liver cancer.
2. Cardiovascular Disease and Saturated Fatty Acids:

Saturated fatty acids, found in foods like red meat, butter, and full-fat dairy products, have been linked to an increased risk of cardiovascular disease. They can raise LDL cholesterol levels in the blood, contributing to the development of atherosclerosis and heart disease. Reducing saturated fat intake by choosing lean protein sources and low-fat dairy products can help lower cardiovascular disease risk.
3. Cardiovascular Disease and Unsaturated Fatty Acids:

Unsaturated fatty acids, including monounsaturated and polyunsaturated fats found in foods like olive oil, fatty fish, and nuts, have cardioprotective effects. These fats can help reduce LDL cholesterol and lower the risk of cardiovascular disease. The Mediterranean diet, which is rich in unsaturated fats, is associated with a lower risk of heart disease.
4. Cardiovascular Disease and Trans Fats:

Trans fats, often found in partially hydrogenated oils in processed and fried foods, are strongly associated with an increased risk of cardiovascular disease. They raise LDL cholesterol levels and lower HDL cholesterol. Many countries have implemented restrictions on trans fats in processed foods to reduce their negative impact on public health.
5. Dietary Fiber and Digestive Health:

Dietary fiber, found in whole grains, fruits, vegetables, and legumes, is essential for digestive health. It helps prevent constipation, diverticular disease, and hemorrhoids. Fiber can also reduce the risk of colorectal cancer by promoting regular bowel movements and acting as a prebiotic, supporting a healthy gut microbiome.
6. Phenylketonuria (PKU) and Diet:

Phenylketonuria is a genetic disorder that affects the metabolism of the amino acid phenylalanine. People with PKU must follow a strict low-phenylalanine diet to prevent the buildup of phenylalanine, which can lead to intellectual disabilities and other health issues. They rely on specially formulated medical foods and must strictly limit or avoid high-protein foods like meat, dairy, and certain grains.

Question 55

• describe the consequences of the most important nutritional problems globally and in Sweden such as protein deficiency, as well as established vitamin and mineral deficiencies.

Answer 55

Protein Deficiency:

Protein deficiency, often associated with a lack of access to high-quality protein sources, can lead to stunted growth, muscle wasting, weakened immune function, and impaired cognitive development, particularly in children.
In severe cases, protein-energy malnutrition can lead to conditions like kwashiorkor or marasmus, which can be life-threatening.
Vitamin A Deficiency:

Vitamin A deficiency is a significant global health problem, particularly in low-income countries. It can result in night blindness, increased susceptibility to infections, and xerophthalmia (dry eye), which can lead to blindness.
Fortification of foods and vitamin A supplementation programs have been effective in combating this deficiency.
Iron Deficiency Anemia:

Iron deficiency is a common nutritional problem worldwide, affecting both developed and developing countries. Iron deficiency anemia can lead to fatigue, weakness, and impaired cognitive function.
It is especially prevalent in women of childbearing age and young children. Iron-rich foods and iron supplementation are commonly used to address this issue.
Iodine Deficiency:

Iodine deficiency can result in thyroid disorders and intellectual disabilities, particularly in developing regions. It can cause a condition known as goiter.
Universal salt iodization has been a successful public health measure to address iodine deficiency.
Nutritional Problems in Sweden:

Vitamin D Deficiency:

Sweden, with its limited sunlight exposure during the winter months, faces a high prevalence of vitamin D deficiency. This can lead to weakened bones and an increased risk of fractures.
Supplementation and dietary strategies are commonly used to address this issue, especially in the form of vitamin D-fortified foods.
Iron Deficiency:

Iron deficiency anemia can also be a concern in Sweden, particularly among certain population groups, including pregnant women and young children.
Iron-rich foods and dietary supplements may be recommended to prevent or treat iron deficiency anemia.
Obesity and Diet-Related Diseases:

Like many developed countries, Sweden faces challenges related to obesity and associated health issues, such as type 2 diabetes, cardiovascular disease, and certain cancers.
Promoting healthier dietary habits and increasing physical activity are important strategies to address these concerns.

Question 56

• outline how the different diets can affect the nutritional needs

Answer 56

1. Vegetarian Diet:

Reduced Protein Intake: Vegetarian diets often include less animal-based protein. To meet protein needs, individuals may need to consume a variety of plant-based protein sources, such as legumes, nuts, and tofu.
Potential Vitamin and Mineral Deficiencies: Vegetarians should pay attention to nutrients like vitamin B12, iron, and calcium, which are commonly found in animal products. Supplementation or careful food choices may be necessary to prevent deficiencies.
Increased Fiber Intake: Vegetarian diets are typically high in fiber due to the consumption of fruits, vegetables, and whole grains. This can benefit digestive health.
2. Vegan Diet:

More Strict Nutrient Considerations: Vegan diets exclude all animal products, requiring careful attention to nutrient intake. Vitamin B12, vitamin D, calcium, iron, and omega-3 fatty acids are nutrients that may need special consideration.
Emphasis on Plant-Based Protein: Protein sources come exclusively from plants, so it’s important to incorporate a variety of legumes, grains, nuts, and seeds to meet protein needs.
Higher Fiber Intake: Like vegetarian diets, vegan diets are typically high in fiber, which can promote digestive health and satiety.
3. Ketogenic Diet:

Reduced Carbohydrate Intake: The ketogenic diet severely restricts carbohydrate consumption and promotes the consumption of fats and moderate protein. This shifts the body into a state of ketosis, where it primarily uses fat for energy.
Increased Fat Intake: The ketogenic diet emphasizes fats as the primary source of energy. This can affect lipid profiles and may require monitoring for those with specific health concerns.
Potential Micronutrient Deficiencies: Due to the restrictive nature of the diet, individuals may be at risk of deficiencies in certain vitamins and minerals. Careful planning and supplementation may be necessary.
4. Mediterranean Diet:

Balanced Macronutrient Intake: The Mediterranean diet is characterized by a balance of carbohydrates, fats, and protein. It encourages the consumption of healthy fats (olive oil, nuts, fatty fish), whole grains, and lean protein sources.
High in Antioxidants: The diet is rich in fruits, vegetables, and herbs, providing an abundance of antioxidants that can have various health benefits.
Emphasis on Omega-3 Fatty Acids: Frequent consumption of fatty fish provides omega-3 fatty acids, which can support heart and brain health.
5. Low-Carb Diet:

Carbohydrate Restriction: Low-carb diets limit the intake of carbohydrates, which can lead to changes in energy metabolism and weight loss.
Potential for Micronutrient Deficiencies: The reduction of carbohydrates can affect the intake of fiber, vitamins, and minerals found in carbohydrate-rich foods. Careful food choices and supplementation may be necessary.
Higher Fat and Protein Intake: Low-carb diets often include more fats and proteins, which can impact macronutrient balances and lipid profiles.

Question 57

• describe the mechanisms behind malnutrition with a focus on global prevalence and causes

Answer 57

Global Prevalence of Malnutrition:

Malnutrition is a global health issue that affects individuals in both high- and low-income countries.
Undernutrition is often more prevalent in low-income and developing regions, particularly in Sub-Saharan Africa and South Asia, where poverty, food insecurity, and limited access to healthcare are significant factors.
Overnutrition, leading to conditions like obesity and diet-related chronic diseases, is increasing worldwide, driven by urbanization, changing dietary patterns, and reduced physical activity.
Causes of Malnutrition:

Inadequate Dietary Intake:

Poverty and Food Insecurity: Many people in low-income regions lack access to a variety of nutritious foods. Poverty limits the ability to purchase essential nutrients, and food insecurity can lead to inconsistent access to adequate meals.
Limited Food Availability: In some areas, the availability of nutritious foods is scarce, leading to a reliance on low-quality diets.
Cultural Practices: Cultural practices and dietary restrictions may lead to inadequate nutrient intake, particularly for women and children.
Infections and Diseases:

Infectious Diseases: Diseases like diarrhea, malaria, and HIV/AIDS can increase nutrient requirements and decrease nutrient absorption, leading to malnutrition.
Chronic Diseases: Chronic diseases like Crohn’s disease or cancer can impair nutrient absorption and utilization.
Poor Sanitation and Hygiene:

Lack of access to clean water and sanitation facilities can result in frequent infections and diarrhea, which can lead to nutrient loss and malnutrition.

Question 58

• explain the basic dietary guidelines

Answer 58

1. Eat a Variety of Foods:

Consume a wide range of different foods to ensure you get a variety of essential nutrients.
Different foods provide different vitamins, minerals, and other nutrients that are essential for good health.
2. Balance Macronutrients:

Include a balanced mix of macronutrients:
Carbohydrates: Prefer complex carbohydrates like whole grains, fruits, and vegetables over simple sugars.
Protein: Choose lean sources of protein like poultry, fish, legumes, and nuts.
Fats: Opt for healthy fats from sources like avocados, nuts, and olive oil and limit saturated and trans fats.
3. Portion Control:

Be mindful of portion sizes to prevent overeating. Avoid large portions, particularly of calorie-dense and highly processed foods.
4. Consume Fruits and Vegetables:

Aim to fill half your plate with fruits and vegetables in a variety of colors. They are rich in vitamins, minerals, fiber, and antioxidants.
5. Whole Grains:

Choose whole grains like brown rice, whole wheat bread, and oats over refined grains to increase fiber intake and improve overall nutrition.
6. Lean Protein Sources:

Incorporate lean sources of protein like poultry, fish, tofu, legumes, and lean cuts of meat.
Limit red and processed meats.
7. Dairy or Dairy Alternatives:

Include dairy products or dairy alternatives in your diet to ensure adequate calcium intake. Choose low-fat or non-fat options when possible.
8. Healthy Fats:

Consume healthy fats from sources like avocados, nuts, seeds, and olive oil.
Limit saturated fats and avoid trans fats, commonly found in processed and fried foods.
9. Hydration:

Stay well-hydrated by drinking plenty of water throughout the day. Limit sugary and high-calorie beverages.
10. Limit Added Sugars:

Minimize the consumption of foods and drinks high in added sugars, including sugary snacks, sugary beverages, and desserts.
Check food labels for hidden sugars.
11. Sodium (Salt) Reduction:

Reduce sodium intake by avoiding highly processed and salty foods.
Season foods with herbs and spices instead of salt.
12. Moderation and Balance:

Practice moderation and balance in your diet. Enjoy occasional treats but make healthier choices the majority of the time.
13. Physical Activity:

Complement a healthy diet with regular physical activity. Aim for at least 150 minutes of moderate-intensity aerobic activity per week.
14. Special Dietary Considerations:

Tailor your diet to meet specific dietary needs if you have allergies, intolerances, or medical conditions like diabetes or celiac disease.

Question 59

• present the nutritional recommendations for macronutrients

Answer 59

. Carbohydrates:

Carbohydrates are a primary source of energy for the body. They should make up the largest portion of daily caloric intake.
Recommended Range: Approximately 45% to 65% of total daily calories should come from carbohydrates.
Sources: Whole grains, fruits, vegetables, legumes, and some dairy products.
2. Proteins:

Proteins are essential for tissue repair, growth, and immune function.
Recommended Range: About 10% to 35% of daily calories should come from protein.
Sources: Lean meats, poultry, fish, dairy products, legumes, nuts, and seeds.
3. Fats:

Dietary fats are essential for various bodily functions, including energy storage and the absorption of fat-soluble vitamins (A, D, E, and K).
Recommended Range: Approximately 20% to 35% of daily calories should come from fats.
Types of Fats:
Saturated Fats: Less than 10% of daily calories should come from saturated fats, which are found in animal products and some tropical oils.
Unsaturated Fats: The majority of fat intake should be from unsaturated fats, including monounsaturated and polyunsaturated fats. These are found in sources like olive oil, nuts, seeds, and fatty fish.
Trans Fats: Minimize or avoid trans fats, which are found in many processed and fried foods.
4. Fiber:

Dietary fiber is a type of carbohydrate that is not digested. It is important for digestive health and can help prevent chronic diseases.
Recommended Intake: The recommended daily intake of fiber varies by age and sex but is generally around 25 grams for adult women and 38 grams for adult men.