APP Workshop Upper GI

4 stages of cellular respiration

Glycolysis Link reaction Krebs Cycle (citric acid cycle) Oxidative Phpshorylation (electron transport chain)

What are the characteristic symptoms of Peptic Ulcer Disease?

Pain: Epigastric burning pain (upper central abdomen), often occurring at night.

GI Dyspeptic Symptoms: Indigestion, heartburn, bloating, and early satiety.

Associated Symptoms: Nausea and vomiting.

Which PUD red flag symptoms require urgent GP referral vs. immediate A&E attendance?

Urgent GP Referral: Worsening pain, loss of appetite, feeling full early, unintentional weight loss, or pain on swallowing.

A&E Immediate Referral: Hematemesis (vomiting blood

How are amino acids transported into cells, and where does the energy for this transport come from?

Mechanism: Co-transport with sodium ions (Na+) via a shared cell surface receptor. Energy Source: Driven by the Na+ concentration gradient across the cell membrane. Gradient Maintenance: Na+

What key patient risk factors increase the likelihood of developing PUD?

Age: Over 65 years. Medications: High-dose

What are imino acids, and what key functional groups do they contain?

Chemical relatives of amino acids. (Containing mine and carboxyl functional groups.

Are alginates antacids? What chemical reaction occurs when alginic acid meets saliva in the mouth?

Nature: No, alginates are not antacids—alginate itself is an acid (alginic acid) and a naturally occurring carbohydrate. Reaction: On contact with saliva, alginic acid reacts with Sodium Bicarbonate to form Sodium Alginate.

How are peptides further digested in the duodenum, and how are the resulting amino acids absorbed?

Enzymatic Breakdown: Trypsin, elastase, and chymotrypsin reduce peptides into smaller units in the duodenum. Conversion: Peptidases break smaller peptides down into free amino acids (via a reduction reaction). Absorption: Co-transport across the small intestines into the bloodstream.

How does sodium alginate protect the oesophagus in Gastro-oesophageal Reflux Disease (GORD)?

Raft Formation: In contact with gastric acid, sodium alginate precipitates into a gel that floats on top of stomach contents. Protection: Creates a pH-neutral "raft" barrier that prevents acid from reaching the oesophagus.

How does the inhibition of prostaglandin synthesis relieve pain and inflammation, and what drug class performs this function?

NSAIDs block the COX-2 enzyme so it can no longer make prostaglandins—turning down the body's pain and swelling signals. NSAIDs (Non-Steroidal Anti-Inflammatory Drugs).

How does H. pylori survive the acidic environment of the stomach and attach to host cells?

Produces the enzyme urease, which converts urea into ammonia and CO2​. Ammonia neutralizes stomach acid around the bacteria. Motility: Flagella allow it to swim through the gastric mucus layer. Attachment: Adhesins (surface proteins) bind to receptors on gastric epithelial cells.

What are antacids, and what is their primary mechanism of action?

Definition: Over-the-counter medications used to relieve heartburn, indigestion, and acid reflux. Mechanism: Weak alkaline (basic) compounds that directly neutralize existing stomach acid (HCl), raising gastric pH toward neutral. Key Distinction: They do not stop acid production (unlike PPIs or H2​-blockers); they only neutralize acid that is already present.

What are eicosanoids, what receptor type do they act on, and what general biological processes do they regulate?

Definition: A large family of arachidonic acid oxidation products (e.g., Thromboxane A, Prostaglandins, Leukotrienes) that act as lipid mediators. Mechanism: Act on target cells via G-protein-coupled receptors (GPCRs). Biological Roles: Regulate vascular homeostasis, gastric mucosal protection, platelet aggregation, inflammation, tissue remodelling, asthma, arthritis, and cancer.

What are the distinct groups of amino acid cell surface receptors, and which specific amino acid has its own transporter?

Neutral amino acids Basic amino acids Acidic amino acids Imino acids Specific Transporter: Proline (and certain other amino acids) may have dedicated transporters.

What are the standard full-dose Proton Pump Inhibitors (PPIs) used for PUD treatment?

20-40mg of the -zoles

What is Peptic Ulcer Disease (PUD), its core pathophysiology, and its three primary triggers?

Definition: Ulcers in the gastric lining (gastric ulcer) or small intestine (duodenal ulcer). Pathophysiology: Imbalance where ulcerogenic factors (increased acid) outweigh protective mucosal defences. 3 Primary Triggers: H. pylori infection (bacterial damage + increased acid). NSAIDs (inhibit protective prostaglandins). Excessive gastric acid production.

What is an autacoid?

Locally produced modulating factors generated on demand that influence local cell

What type of bacterium is Helicobacter pylori, discovered it, and why was this discovery significant?

A spiral-shaped, Gram-negative bacterium that colonizes the human stomach. Proven that peptic ulcer disease is caused by bacterial infection, rather than stress or spicy foods.

Where does the majority of protein digestion begin, and what are proteins broken down into during this initial stage?

Location: Stomach Product: Peptides containing 4 to 9 amino acids

Bioavailability in IV vs oral administration

IV = 100% Oral is less because has to go through GI tract and liver first before reaching bloodstream

How do anabolic pathways (e.g., fatty acid

fat synthesis, gluconeogenesis) differ from catabolic pathways regarding their electron carrier requirements?

How do ibuprofen and NSAIDs produce ulcers

Inhibits to prostaglandins which reduces production of enzymes which protect the stomach lining

How does ATP Synthase generate ATP from the accumulated hydrogen ions?

ATP Synthase attempts to maintain chemiosmosis by transporting hydrogen ions back across the inner membrane into the matrix. It couples this movement to a phosphorylation reaction, forming ATP from ADP and inorganic phosphate (Pi).

How is the hydrogen ion gradient established in the intermembrane space?

As electrons move down energy levels in the transport chain, they release free energy. Proton pumps use this free energy to actively transport hydrogen ions across the inner mitochondrial membrane into the intermembrane space.

Main routes of administration of drug?

oral Buccal Rectal (large intestine rectum) Epithelial surfaces Inhalation Injection

Pharmacodynamics

what drugs do to the body

Pharmacokinetics

what the body does to the drug

Processes in the body ATP is used for?

Muscle contraction Neurotransmission Protein synthesis Cell signalling

What are the 3 forms of CoQ?

Ubiquinol: Fully reduced (2 extra electrons) Ubisemiquinone: Semi-reduced (1 extra electron) Ubiquinone: Fully oxidised (no extra electrons)

What happens to electron carriers during electron transport, and why is this process crucial for catabolic pathways?

During electron transport, reduced electron carriers (NADH and FADH₂) donate their electrons to the system and are oxidized to NAD⁺ and FAD, respectively. These oxidized carriers are necessary to keep catabolic pathways (such as glycolysis, the citric acid cycle, and fatty acid oxidation) running.

What happens to hydrogen atoms when electrons enter the electron transport chain?

heir hydrogen atoms dissociate into electrons and hydrogen ions as they are donated to the first and second electron complexes.

What is a drug?

a chemical substance of known structure which produces a biological effect when administered to a living organism

What is a medicine?

a Chemical preparation containing 1 o more drugs with the intention of producing a therapeutic effect

What is the final electron acceptor at the end of the electron transport chain, and what is formed?

Oxygen accepts the electrons from the last electron carrier to form H20

What role does Coenzyme Q (CoQ) play in the electron transport system?

CoQ provides a transition between moving electrons in pairs (first part of the system) and moving them one at a time (last part of the system).

Where are coenzymes delivered from and to during the start of oxidative phosphorylation?

Coenzymes are delivered from the mitochondrial matrix to the electron transport chain in the inner membrane.

aerobic meaning

with oxygen

carbohydrate disaccharides

maltose, sucrose and lactose

carbohydrate polysaccharide

starch and glycogen

cellular respiration

process in living organisms where carbon containing compounds are broken down to release energy in the form of adenosine triphopshate ATP

chemiosmosis

the movement of ions down their electrochemical gradient

oxidative phosphorylation generates...

the largest amount of ATP

starch and glycogen digestion

starch and glycogen (amylase) maltose (maltase) glucose

sucrose digestion

sucrose (sucrase) glucose and fructose

what are cytochromes?

specialised proteins containing a haem group (prosthetic) which act as proton pumps

what are the mitochondria

specialised organelles which are the site of aerobic respiration

what is ATP

adenosine triphosphate - a molecule which carries chemical energy in living organisms

what is the electron transport chain?

sequence of protein complexes including cytochromes, enzymes and coenzymes which are specialised to transport electrons

where does oxidative phosphorylation take place?

the mitochondrial matrix -> the inner mitochondrial membrane

which stages of cellular respiration are aerobic?

Link reaction Kreb's Cycle Oxidative Phosphorylation

Mouth Description and function

D - Entry point for food; chewing and mixing food with saliva 

F - Mechanical breakdown of food; initiation of digestion 

Salivary glands Description and function

D - Found in the mouth, produces saliva

F - Chemical: Releases digestive enzyme amylase which breaks down polysaccharides (starch) into maltose. Mechanical: provides moisture to food for easy swallowing

Oesophagus Description and function

D - Hollow shaped muscular tube which connects the mouth to the stomach 

F - Peristalsis to move boluses. 

Stomach Description and function

D - J shaped organ which produces gastric juices (acids and digestive enzymes) and has mucosal layer in stomach lining. 

F - Mechanical: churning food (gastric juices), food storage organ (holds food and slowly releases to duodenum) 

Chemical: digestion with enzymes and acids 

HCl kills bacteria. 

Duodenum Description and function

D - Section in the first part of the small intestine 

F - Neutralised highly acidic stomach acid. Bile gets released into here. 

Contains 3 digestive enzymes – proteases, lipases and amylase 

order of digestive material

Food

Bolus

Chyme

Feces

Label these GI regions

A - oesophagus

B - Liver

C - stomach

D - pancreas

E - large intestine

F - small intestine

G - mouth

H - rectum cavity (end of large intestine)/ Anus (muscle)

Lower Oesophageal Sphincter Location and Function

L - Where oesophagus meets the stomach

F - controls the rate the boluses enter the stomach from the oesophagus and vice versa —> prevents acid and gastric juices reflux

Pyloric Sphincter Location and Function

L - At the junction of the stomach to duodenum

F - Regulates the movement of chyme between the stomach and the small intestine. 

Ileocecal Sphincter Location and Function

L - Between end of small intestine and beginning of large intestine  

F - Regulates the movement of digested food from small intestine to large intestine. 

Anal Sphincters (Internal and External) Location and Function

L - Between last intestine and anus. 

F - Internal is involuntary, external is voluntary. 

Controls excretion of fecal matter. Controlling bowel movements. 

Polysaccharide enzyme and end product

amylase, disaccharide

protein enzyme and end product

proteases - tripsin, pepsin, chymotripsin, peptidases

amino acids

triglycerides/lipids enzyme and end product

lipase and bile

fatty acids and glycerol

roles of the enteric nervous system (ENS) in the process of digestion

outer myenteric plexus coordinated muscle contraction like peristalsis

submucosal plexus manages the releases of the gastric juices to help digest food

entero endocrine cells release hormones into the GI tract to regulate digestion and intestinal homeostasis

communicates to the CNS to process that you’re hungry, CNS communcates to the ENS the feeling of hunger

role of the ENS in combatting GI driven infection

myenteric plexus trigger contractions to clear out the contents of the large intestine causing diarrhoea and vomiting

gastrin where is it produced? function?

The stomach 

Stimulates the parietal cells to release highly acidic gastric juice (HCl), 

Stimulates the secretion of pepsinogen (peptides) 

Stimulates muscle contraction (gastric motility) 

secretin where is it produced? function?

The mucosa layer of the duodenum 

Controls digestion by neutralising stomach acid in the small intestine stimulates the pancreas the release pancreatic juice containing bicarbonate to neutralise stomach acid and also reduces gastric acid secretion. 

Cholecytokinin (CKK) where is it produced? function?

Enteroendrocrine I-cells in the small intestine and duodenum 

Gall bladder contraction (bile) and pancreatic enzyme secretion. Slows down gastric emptying  

Ghrelin where is it produced? function?

The fundus in the stomach  

Tells the brain you’re hungry 

Red flags which may indicate serious GI

Severe abdominal pain

Blood in stool, Sudden chest pain, vomiting blood (vomit which looks like coffee) - darker blood higher up GI tract more serious, fresh blood lower down GI tract less serious

Unintentional weight loss  

Vomiting, nausea, diarrhoea 

Dysphagia (difficulty swallowing)