Case 13 Flashcards
(95 cards)
1
Q
What is the primary function of Secretin?
A
Inhibits gastric acid secretion and promotes bicarbonate release from the pancreas
Secretin is released by S-cells in the duodenum in response to the presence of acidic chyme.
2
Q
How does Secretin affect bile synthesis?
A
It acts on the liver to enhance bile acid synthesis
Secretin plays a role in the digestion process by promoting bile production.
3
Q
What type of cells release Secretin?
A
S-cells
S-cells are located in the duodenum and respond to acidic conditions.
4
Q
What is the role of I-cells in the digestive process?
A
I-cells release cholecystokinin (CCK) in response to fatty acids and amino acids
CCK is a hormone that plays a significant role in digestion.
5
Q
What does CCK do to gastric acid secretion?
A
Inhibits the release of HCl
CCK helps regulate digestive processes by modulating gastric secretions.
6
Q
What effect does CCK have on the gallbladder?
A
Stimulates contraction and release of concentrated bile
CCK is crucial for the digestion of fats by facilitating bile release.
7
Q
Fill in the blank: CCK binds to _______ in the liver to enhance secretin activity.
A
specific cells
This binding enhances the liver’s ability to produce bile.
8
Q
What is the relationship between CCK and the sphincter of Oddi?
A
CCK relaxes the sphincter of Oddi to allow bile to flow into the duodenum
This action is important for the digestive process when fats are present.
9
Q
True or False: Secretin promotes the release of HCl in the stomach.
A
False
Secretin primarily inhibits gastric acid secretion.
10
Q
What conditions trigger the release of Secretin?
A
Presence of acidic chyme in the duodenum
The release is a response to the pH of the intestinal contents.
11
Q
What hormone do I-cells release?
A
Cholecystokinin (CCK)
CCK is critical for digestion, particularly for fats and proteins.
12
Q
What type of cells can CCK bind to in the pancreas?
A
Acinar cells
CCK (cholecystokinin) can stimulate the release of digestive enzymes from these cells.
13
Q
What enzymes are released by acinar cells upon stimulation by CCK?
A
- Proteases (Trypsinogen, Chymotrypsinogen and Procarboxypeptidase)
- Pancreatic amylase
- Pancreatic lipases
- Pancreatic nucleases
These enzymes are involved in the digestion of proteins, carbohydrates, and fats.
14
Q
Where are K-cells located?
A
In the duodenum
K-cells respond to fatty acids and oligosaccharides and secrete GIP
15
Q
What hormone is released by K-cells when stimulated?
A
Gastric Inhibitory Peptide (GIP) or glucose-dependent insulinotropic polypeptide
GIP is involved in regulating gastric functions.
16
Q
What effect does GIP have on parietal cells?
A
Inhibits HCl release
GIP acts on receptors in the stomach to reduce gastric acid secretion.
17
Q
What additional effect does GIP have besides inhibiting gastric acid?
A
Stimulates the release of insulin from pancreatic beta cells
This action helps regulate blood sugar levels.
18
Q
Fill in the blank: CCK stimulates the release of digestive enzymes from _______.
A
acinar cells
19
Q
True or False: GIP only acts on the stomach to inhibit HCl release.
A
False
GIP also has effects on pancreatic beta cells.
20
Q
What are the primary functions of the enzymes released by acinar cells?
A
- Digestion of proteins
- Digestion of carbohydrates
- Digestion of fats
These enzymes play crucial roles in the digestive process.
21
Q
What do Acinar cells secrete and what activates them
A
Acinar cells are activated by CCK and secrete Proteases (Trypsinogen, Chymotrypsinogen and Procarboxypeptidase), Pancreatic Lipases, Pancreatic amylases and Pancreatic Nucleases
22
Q
What do ductal cells in the pancreas release and what activates them
A
Secretin can promote ductal cells in the pancreas to secrete bicarbonates
23
Q
What are the cells that give the pancreas its endocrine function
A
Islets of Langerhans
24
Q
What are the 5 primary cell types in the Islets of Langerhans and what do they secrete
A
- Beta cells (Insulin) (50-80%)
- Alpha cells (Glucagon) (20-25%)
- Delta cells (Somatostatin) (5-10%)
- PP/F cells (pancreatic peptides) (1-5%)
- Epsilon cells (ghrelin) (<1%)
25
What does insulin do (basic for now)
Lowers blood sugar by promoting glucose uptake into tissues
26
What does glucagon do
Increases blood sugar by stimulating hepatic glucose production and promoting glycogenolysis
27
What does somatostatin do (basic, released from delta cells)
Inhibits insulin and glucagon secretion and suppresses release of gastric secretion
28
What does pancreatic peptides do
Regulates pancreatic secretions by decreasing pancreatic secretions
29
What does ghrelin do
Acts on the hypothalamus to increase hunger / stimulate appetite and promotes energy storage
30
3 types of lipases
- TG lipase
- phospholipase A2
- carboxyl esterase**
31
How is glucose + galactose absorbed and what is its lumen carrier
Na+ dependent co-transport (secondary active transport) with SGLT1 carrier
32
How is fructose absorbed and what is its lumen carrier
Absorbed via facilitated diffusion by GLUT5 carrier
33
How is water absorbed and what is its lumen carrier
Moves via osmotic gradient and through junctional complexes, SGLT1 (same as glucose Na+ cotransport carrier) and amino acid transporters
34
How is amino acids absorbed and what is its lumen carrier
50% absorbed by PEPT1 as di/tri peptides via cotransport with H+ and other 50% by transporters through secondary active transport (BO transports alanine with Na+, XAG- transports glutamate in a Na/K pump with H+)
35
What does a mutation in SGLT1 cause and its treatment
No absorption of glucose or galactose which causes severe and potentially fatal diarrhea in infants.
Treatments is to not consume glucose and galactose lol
36
What does secondary active transport mean
Absorption against a concentration gradients using energy derived from Na+ gradient created by Na+ pump, so basically absorping something alongside Na+
37
How are free fatty acids absorbed
Simple diffusion
38
How is cholesterol absorbed
Receptor-mediated endocytosis via NPC1L1 protein (Excess cholesterol is pumped out of the cell into the lumen via ABCG5 and ABCG8
39
What does fat undergo for absorption
Fats must first be acted on by bile salts/acids which emulsify the fat droplets to increase its surface area for lipase to act on. Michelle’s are then formed so triglyceride products can be packaged and absorbed through the membrane. Remaining triglycerides are re-synthesised in the ER and packaged into chylomicrons and exocytosed for transport to the liver via the lymphatic system
40
What vitamins are fat soluble and how are they absorbed
- A, D, E, K (A don’t even know)
- absorbed by facilitated diffusion and endocytosis
41
What vitamins are water soluble and how are they absorbed (B12 especially)
- B & C ( BBC news)
- facilitated + active transport
- B12 is absorbed by endocytosis (intrinsic factor facilitates its transport and absorption into the blood)
42
What happens when you get incomplete digestion
Malabsorption
43
What happens when you get incomplete absorption
Diarrhoea
44
Explain iron absorption
Iron can either exist as heme or Fe3+
Reduction of Ferric Iron (Fe³⁺):
Duodenal cytochrome b (Dcytb) on the enterocyte surface reduces Fe³⁺ to Fe²⁺.
Ascorbic acid (Vitamin C) in the diet enhances this reduction.
Transport into Enterocytes:
Ferrous iron (Fe²⁺) enters enterocytes through the divalent metal transporter 1 (DMT1) on the apical membrane.
Intracellular Processing:
Inside the enterocyte, iron is either:
Stored as ferritin if not immediately needed.
Transported across the basolateral membrane to the bloodstream.
Export to the Bloodstream:
Iron exits enterocytes via ferroportin, the only known iron exporter.
Once in the bloodstream, ferrous iron is oxidized to ferric iron (Fe³⁺) by hephaestin or ceruloplasmin and bound to transferrin, the iron transport protein.
45
Explain iron regulation
Hepcidin – The Master Regulator:
Hepcidin, a hormone produced by the liver, controls systemic iron homeostasis by regulating ferroportin.
High hepcidin levels:
Bind to ferroportin and cause its degradation.
Block iron release from enterocytes, macrophages (iron recycling), and hepatocytes (iron stores).
Low hepcidin levels:
Allow ferroportin to transport iron into the bloodstream, increasing iron availability.
46
Explain calcium absorption in gut
Active Transcellular Absorption (Regulated; occurs primarily in the duodenum):
This energy-dependent process occurs when dietary calcium intake is low or when calcium demand is high (e.g., during growth, pregnancy, or lactation).
Steps:
Entry Across the Apical Membrane:
Calcium enters enterocytes through calcium channels called TRPV6 (Transient Receptor Potential Vanilloid 6).
Intracellular Transport:
Inside the enterocyte, calcium is bound to the protein calbindin-D to prevent toxicity and facilitate transport.
Exit at the Basolateral Membrane:
Calcium is actively transported out of the cell into the bloodstream via:
The PMCA1b (Plasma Membrane Calcium ATPase).
The NCX1 (Sodium-Calcium Exchanger).
47
What regulates calcium absorption
This pathway is tightly regulated by 1,25-dihydroxyvitamin D (calcitriol), the active form of Vitamin D, which increases the expression of TRPV6, calbindin-D, and PMCA1b.
48
3 digestion & absorption problems and what causes them
- Glucose-Galactose malabsorption syndrome (caused by mutation in SGLT1 protein)
- Inflammatory bowel disease (Crohn’s, ulcerative colitis and coeliac disease) causes damage to the mucosa therefore you have a loss of carrier proteins, surface area and transport etc
- Bacterial infections such as Shigella/Campylobacter can cause lumen wall destruction and blood in faeces
49
Ducts in the pancreas called
Intercalated ducts
50
What is the proportion of exocrine to endocrine function of pancreas
80% exocrine
20% endocrine
51
Acute pancreatitis causes (mneumonic)
I GET SMASHED
Idiopathic (20%), Gallstones (50%) and Ethanol (25%) main ones
52
What is the Pathophysiology or Pathogenesis of Acute Pancreatitis
Inappropriate intra-pancreatic activation of trypsin leading to Acinar auto-digestion and death
53
What does mild acute pancreatitis usually show
Pancreatic inflammation and oedema
54
What does severe pancreatitis usually shown
Pancreatic necrosis and multi-organ failure, death
55
3 different types of Acute Pancreatitis
Acute interstitial pancreatitis (mild)
Acute necrotising pancreatitis
Acute haemorrahagic pancreatitis
56
Theories on how AP happens and the common final pathway
- Pancreatic ductal obstruction
- Abnormal pancreatic secretion
- Ductal damage
- Direct toxin effect (alcohol, inflammation, membrane destruction, hypertriglyceridaemia and protein disposition$
All ultimately lead to increased intracellular calcium and inappropriate enzyme activation
57
Acute pancreatitis signs and symptoms
- Massive systemic inflammatory response
- Cullen’s sign which is superficial oedema with bruising in the subcutaneous fatty tissue around the peri-umbilical region
58
Acute pancreatitis diagnosis
- Lab tests to test for Amylase and Lipase in the bloodstream
- X-ray to exclude perforation
- CT to assess for pancreatic necrosis, abscess or fluid collection
59
Management of Acute pancreatitis
A - Airways
B- Breathing
C - Circulation
60
What classification do you use to assess Acute pancreatitis
Atlanta classification:
Mild: no organ failure, or complication
Moderate: transient organ failure OR complication
Severe: Persistent organ dysfunction lasting >48 hours
61
Acute pancreatitis complications
62
How to prevent recurrence of Acute pancreatitis
- remove gallstones
- reduce alcohol
- consider drug causes
- think autoimmune, familial, anatomical reasons for recurrence
63
What is chronic pancreatitis and how is it caused
Chronic, continuous inflammation, it begins as recurrent acute pancreatitis when then causes continuous inflammation which leads to pancreatic destruction and loss of exocrine and endocrine function. This leads to fibrotic changes and eventually Acinar to ducal metaplasia
64
Causes of chronic pancreatitis
Idiopathic (20-30%)
Alcohol (60-70%)
Genetic- e.g. Cystic Fibrosis (CFTR)
Autoimmune - e.g. IgG4
Hyperlipidaemia - Hypertriglyceriaemia
65
What is the pathophysiology/Pathogenesis of chronic pancreatitis
Increases Acinar protein secretion + reductions in NaHCO3 and fluids leads to increased viscosity and pancreatic duct plugging which leads to Acinar atrophy and fibrosis
66
chronic pancreatitis signs and symptoms
Pain:
- epigastric to back
- Episodic (relating to ongoing damage)
Malabsorption:
- Weight loss
- Steatorrhoea - fat malabsorption
Diabetes - type 3
Jaundice:
- due to bile duct obstruction because bilirubin is excreted via the bile duct, obstruction can lead to its buildup
67
chronic pancreatitis diagnosis
- Check faecal elastase (measure of fat in stool)
- Endoscopic ultrasound
- CT/MRI to check for atrophy or calcification etc.
68
chronic pancreatitis management
- Smoking cessation
- Alcohol cessation
- Pain control (NSAIDS, opiates, nerve blockers, decompression surgery etc)
- Treat malabsorption (replacement of pancreatic enzymes (CREON))
- Identify complications
69
Treatment for malabsorption
CREON/Pancreatin which is a combination of protease, lipase and amylase. Usually taken in capsules before or during meals/snacks to mimic normal secretion
70
What type of diabetes can chronic pancreatitis cause?
- Type 3/Type 3c diabetes
- Accounts for 5-10% of diabetes
- Difficult to manage
71
chronic pancreatitis can cause pancreatic cancer: true or false?
True
72
At what percentage of enzyme production does malabsorption occur
Less than 10% of max output
73
What is 1 unit of alcohol equivalent to in milliliters and grams?
1 unit = 10ml or 8g of alcohol
## Footnote
This is a standard measurement for alcohol consumption.
74
What enzyme metabolizes alcohol in the stomach?
alcohol dehydrogenase
## Footnote
This enzyme plays a key role in the initial metabolism of alcohol.
75
Where is alcohol primarily absorbed in the body and by what protein ?
duodenum/jejunum by cytochrome p450
## Footnote
These are parts of the small intestine where absorption occurs.
76
What is the progression of alcohol-related fatty liver disease?
alcoholic hepatitis (reversible) and then cirrhosis (irreversible)
## Footnote
This progression highlights the potential risks of excessive alcohol consumption.
77
What is delirium tremens?
A severe form of alcohol withdrawal that can cause hallucinations
## Footnote
It is characterized by confusion, agitation, and tremors.
78
What is the first-line treatment for alcohol withdrawal?
Benzodiazepine
## Footnote
Benzodiazepines enhance GABA, which helps alleviate withdrawal symptoms.
79
What medication can also be given for alcohol dependence?
Disulfiram
## Footnote
Normal Alcohol Metabolism:
Ethanol is metabolized in the liver in two main steps:
Ethanol → Acetaldehyde:
Catalyzed by alcohol dehydrogenase (ADH).
Acetaldehyde → Acetate:
Catalyzed by aldehyde dehydrogenase (ALDH).
Acetate is then further metabolized and excreted harmlessly.
Disulfiram’s Effect:
Disulfiram irreversibly inhibits aldehyde dehydrogenase (ALDH), the enzyme responsible for converting acetaldehyde to acetate.
As a result, acetaldehyde accumulates in the blood after alcohol consumption.
Acetaldehyde Accumulation:
Acetaldehyde is a toxic compound that causes unpleasant symptoms collectively known as the disulfiram-ethanol reaction (DER).
80
What is Korsakoff's syndrome caused by and how?
Chronic thiamine (vitamin B1) deficiency because alcohol leads to lumen lining to be damaged being thiamine can no longer be absorbed
## Footnote
It occurs when the lumen lining is damaged, preventing thiamine absorption.
81
What are the symptoms of Wernicke's encephalopathy?
Triad of ataxia (lack of/poor muscle coordination), ophthalmoplegia (paralysis of eye muscles), and confusion
## Footnote
This condition is also related to thiamine deficiency.
82
What deficiency leads to Wernicke's encephalopathy?
Thiamine (vitamin B1) deficiency
83
What is thiamine also known as
Vitamin B1
84
What is thiamine used for
Thiamine is a B vitamin that the body can’t produce, it is crucial for carbohydrate metabolism and energy production, especially in the brain. Thiamine is needed by some enzymes which, without it, can lead to toxic byproduct accumulation
85
What is diverticulitis?
Inflammation or infection of diverticula (small pouches) in the colon, often due to trapped fecal matter or bacteria.
86
What are the common symptoms of diverticulitis?
Left lower quadrant (LLQ) abdominal pain.
Fever.
Nausea and vomiting.
Altered bowel habits (diarrhea or constipation).
87
What is Cachexia
Cachexia is a syndrome of altered metabolic activity resulting in muscle protein loss that is present in up to two-thirds of patients with advanced cancer.
88
What is sarcopenia
The medical definition of sarcopenia is the gradual loss of muscle mass, strength and function. The condition commonly affects the elderly population and is thought to occur due to aging.
89
What is sarcopenic obesity
Sarcopenic obesity is a condition where an individual has both sarcopenia (muscle loss and weakness) and obesity (excessive fat accumulation)
90
What are the major conditions that can indicate the need for pancreatic surgery?
Acute or chronic pancreatitis, pancreatic cysts, and pancreatic cancers.
91
What does the Whipple procedure involve removing?
The head of the pancreas, part of the stomach (lower third), distal part of the bile duct and gallbladder, and some of the small intestine is removed
92
What is the pylorus-preserving Whipple procedure?
A variation where the stomach is left intact. (so The head of the pancreas, distal part of the bile duct and gallbladder, and some of the small intestine is removed)
93
What is removed during a distal pancreatectomy?
The body and tail of the pancreas and often the spleen.
94
What does a total pancreatectomy involve removing?
The entire pancreas, duodenum, gallbladder, part of the bile duct, and the spleen.
95
What are the parts of the pancreas
Uncinate process, Head, Neck, Body, Tail
