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Year 1 LSS > Alimentary System > Flashcards

Alimentary System Flashcards

1
Q

How can vitamins be absorbed into the body?

A
  • Passive diffusion predominant mechanism
  • Fat soluble vitamins (A, D, E, K) transported to brush border in micelles. K taken up by active transport.
  • Specific transport mechanisms for vitamin C (ascorbic acid), folic acid, vitamin B1(thiamine), vitamin B12
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2
Q

How is mucus production in the large intestine triggerd?

A

By ACh –> PNS

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3
Q

What is the most common type of cancer in the GI tract?

Which tissue type does it originate from?

A

It is an Adenocarcinoma (every epithelial cancer from lower esophagus downwards)

It is derive from “glandular epithelium”

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4
Q

When and why is gastrin secretion inhibited?

A

It is inhibited when pH drops below 3 to protect the duodenal mucosa

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5
Q
A
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6
Q

What is the effect of Trypsin activation?

A

Active enzyme –> can break down proteins

Also can activate different pro-enzymes:

  • Auto-activation of Trypsinogen
  • Activation of Protease zymogens to Protease
  • Activation of procolipase to give rise to lipase
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7
Q

What are the symptoms of gilberts syndrome?

A

Asymptomatic

Jaundice might occur when fasting, dehydration, and in viral ilness

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8
Q

What are the main tasks of the submucosal plexus?

A

It intrinsically controls:

  • endocrine function
  • gastrointestinal secretions
  • blood flow
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9
Q

What is a portal triad?

A

The portal triad consists of

  1. Hepatic portal vein
  2. Hepatic artery
  3. Bile duct

It is situated at each corner of a hepatic lobule (hexagon)

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10
Q

How are cells in the large intestine differently organised than cells from the small intestine?

A

No nutrient absorption takes place —> less surface area needed:

  • No villi
  • Enterocytes have small, irregular microvilli
  • Enterocytes are organised to absorb ions (and drag water passively with it)
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11
Q

What are the advantages and disadvantages of an abdominal X-Ray, a CT scan and a barium enema for investigation of Cholorectal cancer?

A

X-Ray

  • not very specific, can’t detect anything
  • but cheap

CT:

  • Cheap, quick, good for big tumors
  • Not tissue sampling, small leasions might not be seen

Barium enema:

  • Unpleasant for patient, no tissue sampling
  • But more can be seen than on CT alone
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12
Q

Which role do genetics play in obesity?

A

Only can explain 5% of obesity

Can influence e.g.:

  • appetite regulation
    *
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13
Q

What are the three main functions of motility of the small intestine?

A
  1. To mix ingested food with digestive secretions and enzymes
  2. To facilitate the contact between contents and mucosal surface
  3. To move the contents along the small intestine
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14
Q

By which cell type are the colonic cryps dominated and why?

A

By goblet cells which produce mucus to:

  • to facilitate the passage of increasingly dry luminal contents (as more and more water is reabsorbed)
  • ‘covers’ bacteria and particulate matter, to protect the luminal surface from infect and/or abrasion.
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15
Q

Which parts of the oesophagus are supplied by which type of muscle?`

A
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16
Q

How much water could the large intestine absorbe a day?

A

Up to 4500ml a day

–> Everything that exceeds that –> Diarrhea

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17
Q

Summarise the circulation of an activated lymphocyte in the GALT

A
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18
Q

Which role does the liver play in Fat metabolism?

A

Triglycerides get transformed into fatty acids –> acetyl CoA or Ketones (acetoacetyl CoA)

lipoprotein synthesis (lipogenesis) from glucose/acetyl CoA) and glycerol

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19
Q

Why is trypsinogen and not trypsin secreted?

How is Trypsinogen activated?

A

By Enterokinase in the duodenum

–> otherwise it would break down all the pancreatic cells (breaks down proteins)

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20
Q

Name 5 signs of liver failure

A
  • Jaundice –> bilirubin

Also the liver has a role in oestrogen metabolism which can cause

  • Loss of body hair
  • gynaecomastia
  • testicular atrophy
  • palmar erythema: “liver palms’ - reddening of palms at the thenar and hypothenar eminences
  • Spider naevi : central arteriole with radiating small vessels
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21
Q

What are the symptoms of Ulcerative colitis?

A

Pain in left lower quadrant due to ulcers along the inner surface of large intestine, including the colon and rectum.

Severe and frequent diarrhea (sometimes blood in the stool).

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22
Q
A
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23
Q

What is distinctive about an activated/inactivated parietal cell?

A

They have tubulovesicles in inactivated parietal inactivated state with many proton pumps

When activated: the tubulovesicles fuse and secrete HCl

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24
Q

How are the exocrine cells in the pancreas called?

A

Exocrine acini cells

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25
Q

How much faeces does a normal adult produce per day?

What does it mainly consist of?

A

Normally 150g/ day

  • 2/3 water
  • Cellulose
  • Bacteria
  • cell leftovers (cell debris)
  • Some bile pigments/salts (colour)
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26
Q

Explain the processing and absorption of Sucrose

A

Sucrose is broken down by Sucrase into Glucose and Fructose

Glucose up: SGLT-1, out: GLUT-2

Fructose up: GLUT-5, out GLUT-2)

Sodium-Glucose linked transporter

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27
Q

Explain the movements happening (inkl. sensation + innervation) during defecation

A

(1) Distension of the rectal wall detected by mechanoreceptors (2) Waves of contraction to sigmoid colon and to relax internal anal sphincter (via sacral spinal cord)
(3) Conscious control to relax external anal sphincter

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28
Q

What are the abilities of the “social part” of the rectum?

A

Social part = last part of rectum

It can distinguish between solids, liquids and gas

BUT: Has difficulties distinguishing between gas and fat

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29
Q

Which two types of neurons are there in the Arcuate nucleus?

What are their effects?

A

1. Neuropeptide Y/ Agouti-related peptide (NPY/Agrp)

  • Stimulate food intake
  • Located laterally

2. POMC

  • Inhibit food intake
  • located more medially
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30
Q

How do you manage short bowel syndrome?

A

Three aims:

  • To provide adequate nutrition for patients
  • To ensure adequate water and electrolytes to maintain homeostasis
  • Correction and prevention of acid base imbalance
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31
Q

Which factors might cause a dysfunction in the enteric nervous system?

Which chronic conditions are associated with it?

A
  • Inflammatory diseases (Crohn’s/ Ulcerative bowel disease)
  • Irritatable Bowel syndrome
  • Aging
  • Post-operative injury
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32
Q

Name the five different regions of the pancreas

A
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33
Q

What are the 6 signs and symptoms of acute liver failure?

Explain each underlying reason

A

Sepsis

  • infection (90% with bacterial, 30% with fungal) normally within 3 days after hospital admission and without clinical signs like fever and leukocytosis

Cardiovascular

  • Decreased peripheral resistance induces hard work for heart to do–> sometimes fails

Metabolic

  • Hypoglycaemia, Hypoxia

Central Nervous system

  • Hepatic encephalopathy
  • Accumulation of toxins causes cerebral oedema

Renal

  • Hepatorenal syndrome
  • Likely because of accumulation of vasoconstrictive substance in cortex causing decreased blood supply

Coagulopathy

  • Liver does not synthesises coagulation factors anymore: bleeding
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34
Q

Explain the organisation of the biliary tree (which vessels drain into what etc.?) From smallest unit to gall bladder

A

From small to bigger:

  • millions of bile canaliculi adjacent to the hepatocytes (bile producing cells) –> drain into
  • small ductules, which in turn drain into
  • small bile ducts. Small bile ducts coalesce into
  • larger bile ducts for each liver segment (e.g. 2, 4a). These merge together to form
  • the right and left hepatic ducts, which converge to form the
  • common hepatic duct. Connected to this duct is the cystic duct, which connects the gall bladder
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35
Q

What are the advantages and disadvantages of a Colonoscopy and a CT-virtual colonoscopy?

A

Colonoscopy

  • safe, quick, high sensitivity, obatining tissue sample
  • But 2-day diarrhea preparation (–> dehydration?) + risk of bowel perforation

Virtual colonoscopy

  • No tissue sampling, removal but
  • less preparation, safe, quick easy
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36
Q

Which cells are predominantly present in the large intestine?

A

Very similar organisation to small intestine :

Ab undant Enterocytes + goblet cells (+ stem cells at bottom of crypts)

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37
Q

Identify major hepatocyte organelles and link them to the hepatocyte function.

A
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38
Q

What happens to bile in the intestine?

A

95% of bile is reabsorbed, the rest is being excreted in feces

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39
Q

What is the advantage and disadvantage of bile recirculation?

A

95% of bile gets reabsorbed in the gut and transported to the liver via the hepatic portal vein

Good: recycling, less energy required to produce new bile

Bad: toxins and drugs can also be reabsorbed –> can increases half-life of some drugs significantly

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40
Q

What is the characteristic change at the gastro-oesophageal junction?

A

Change from non-keratinising epithelium to columnar epithelium

Called Z-line

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41
Q

Which cells type is not present in the colon which can be seen in the small intestine and why?

A

The colon does not have paneth cells because of the mycobacteria in the gut

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42
Q

What is required for lymphocytes to be recruited into the gut mucosa?

What is Lymphocyte Homing?

A
  • tissue-sepecificendothelial adhesion molecules at the site of inflammation

which permit transmigration of the lymphocytes into the gut mucosa.

  • requires specialised post-capillary microvascular endothelial cells, e.g.high endothelial venules (HEVs) of lymphoid tissue.

–> This is called lymphocyte homing

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43
Q

From which to which spinal levels does the oesophasgus run and how long is ist?

A

It runs from C5-T10

Length: 25cm

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44
Q

How much bile is produced per day and by which cells?

A

500ml/day

  • 60% hepatocytes: primary secretion –> refelct conposition of blood, secrete proteins, bile saltes etc.
  • 40% billary endothelial cells (Cholangiocytes) –>secondary secretion: modification of bile (reabsorbtion of sugar and acids, secretion of IgA, alteration of pH, secretion of Cl- ions etc.)
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45
Q

Explain the arrangement of acinar cells in the pancreas

A

Acincar cells = terminal end of the duct –> secrete enzyme rich, viscous fluid

Centroacinar cells= at the junction of acinar cells and duct cells, characteristics of both acinar and duct cells, act more like duct cells

Duct cells: Modify secreted fluid by duct cells, produce bicarbonate-rich, aqueous mucus

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46
Q

What do G-cells in the stomach do?

What are the consequences?

A

Secrete gastrin into the bloodstream (endocrine hormone)

–> activates histamine release stimmulating acid production

Also effects on pancreas

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47
Q

What is leptin secreted by?

Where does it bind to?

What is its effect?

A

It is secreted by white adipose tissue

It binds to hypothalamic circuit

It decreases appetite

–> (a lot of fatty tissue = reduced appetite)

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48
Q

Is obesity a disease or a complication?

A

It has a own disease and a underlying cause of many diseases

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49
Q

What are the symptoms of Chron’s disease?

A

Pain in the affected area, most commonly in the right lower quadrant.

Diarrhea and blood in the stool.

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50
Q

Which anatomical parts of the stomach secrete HCL?

A

Body and Fundus

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51
Q

How long is the oesophagus in a typical adult male?

A

25cm

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52
Q

Which stomach cells produce HCL and the intrinsic factor?

A

Parietal cells

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53
Q

How is calcium transported into the bloodstream from the enterocyte?

A

Calcium in cell dissociates from calbindin and gets pumped through the basolateral membrane via

  • Plasma Membrane Ca2+ ATPase (high affinity but low capacity)
  • Na+/Ca2+ exchanger (low affinity but high capactiy)
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54
Q

Which cells are the immunological cells of the liver?

A

Kupffer cells

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55
Q

Explain the overall concept of water reabsorbtion in the GI tract

A

Na+ and other ions (Cl-/ HCO3-) get reabsorbed into enterocytes and transcellular transported into the extracellular fluid

Water comes (para and transcellular) with it

–> Increased pressure on basement membrane lets water and ions move into the capillaries

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56
Q

How are Fe3+/Fe2+ taken up into the blood via an enterocyte?

A

Fe3+ is being reduced by duodenal cytochrome B to Fe2+

  • Uptake via Divalent metal transporter 1 (DMT-1) (H+ coupled receptor)
  • Binds to unknown factors
  • Moves to Basolateral membrane and leaves via Ferroportin ion channel
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57
Q

What are the two plexi in the gut wall?

A
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58
Q

Which main type of muscle controlls the oesophagus at the upper oesophagal sphincter?

A

Skeletal muscle

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59
Q

Explain the mechanism of Crohn’s disease

A

It is an unregulated immune-response to a foreign pathogen

It can cause symptoms in the whole GI tract, from mouth to Anus

Normally thought to also have a genetic component–> very common: Frameshift mutation in the NOD2 gene

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60
Q

What is the inheritance pattern for Gilbert`s syndrome?

What percentage of the population does it affect?

A

It is autosomal dominant

Affects 2-7% of the population

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61
Q

What is the mechanism by which POMC influences food intake?

A
  1. POMC is converted into alpha Melanocyte-stimulating Hormone (a-MSH)
  2. a-MSH stimulates MC4R receptor in paraventricular nuclei
  3. Stimulation causes sending out of satieting signal –> reduction in food intake
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62
Q

What are the three phases of pancreatic secretion?

Name the stimulus, proportion, key mediator and the target cells of each phase

A
  1. Cephalic phase (20%)
    * –> sight, smell taste –> vagus nerve on acinar cells
  2. Gastric phase (10%)
    * Mechanoreceptors in the stomach (stretch) –> input from vagus on acinar cells
  3. Intestinal phase (70%)
    * low pH + presence of peptides by I and S cells in small intestine —> Hormone production
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63
Q

Explain the concept of the pancreas in carbohydrate metabolism

A

Secreted amylase breaks down polysaccharides into disaccharides in the duodenum

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64
Q

Summarise the way bild takes from production to secretion

A
  1. Small bile canaliculi adjacent to hepatocytes
  2. Drain into small bile ductules
  3. Drain into small ducts
  4. Drain into larger bile ducts (for each liver segment)
  5. Merge to right and left the hepatic duct
  6. common hepatic duct
  7. common hepatic duct + cystic duct from gall bladder form common bile duct until the duodenum
  8. Fuses with pancreatic duct to the ampulla of Vater
  9. Drains into the duodenum at duodenal papilla
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65
Q

How are Aminoacids/ Di-/Tri-peptides taken up and transported?

A

All three can be taken up by AA/Na+ symporter (secondary active transport)

Cytoplasmic peptidases break down di/tri-peptides

At basolateral: AA via facilitated diffusion into blood

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66
Q

By which mechanisms is water reabsorbed in the jejunum and ileum?

A

By

  • Na+, H+ ATPase
  • Cotransport with Glucose + AA
  • Cotransport with Chlorine ions
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67
Q

What it the universal inhibitor in the gut? Why is it called like that?

A

It is somatostatin:

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68
Q

Which cells in the small intestine produce secretin?

A

S cells

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69
Q

What is chronic pancreatitis?

A

Chronic pancreatitis is a progressive fibroinflammatory process of the pancreas that results in permanent structural damage, which leads to impairment of exocrine and endocrine function

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70
Q

How does oesophageal cancer processes from reflux to cancer?

A
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71
Q

Where in the GI tract is calcium absorbed?

A

In the Ileum and Duodenum

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72
Q

How can you diagnose Gilberts syndrome?

A
  • Raised unconjugated hyperbilirubin .
  • Otherwise normal liver biochemistry.
  • Normal full blood count, smear and reticulocyte count (thus excluding haemolysis)
  • Absence of signs of liver disease
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73
Q

What do the enteroendocrine cells in the small intestine do and how are they organised?

A

Endocrine cells–> Hormones into the bloodstream

Apical region: sensory part

Basolateral region: vesicles to excrete hormones

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74
Q

Where are the enzymes that break down disaccharides and medium chain saccharides in the small intestine located?

A

Are located in brush border —> membrane-bound

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75
Q

What is the distinguishing feature of the duodenum`?

A

It has submucosal glands which secrete a bicarbonate-rich alkaline solution into crypts to neutralize gastric acid

–> protection and optimal pH for enzymes

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76
Q

How are the crypts in the large intestine called?

A

They are called colonic crypts

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77
Q

What is/ are glycocalyx?

A

A network of carbohydrates on the apical membrane of enterocytes

helps to trap a layer of water, mucus and enzymes on the surface of the cell –> protect it from the luminal contents (especially enzymes ), and to regulate digestion and absorption

–> Layer called unstirred layer

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78
Q

Which hormone is being produced by G-cells in the small intestine?

A

Gastrin

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79
Q

Hwo is the toxic accumulation of Ion in the blood prevented?

A
  • Irreversible binding of iron to ferritin in the epithelial cells.
  • Iron/Ferritin is not available for transport into plasma.
  • Iron/Ferritin is lost in the intestinal lumen and excreted in the faeces.
  • Increase in iron concentration in the cytosol increases ferritin synthesis.
  • •(Hepcidin, the major iron regulating protein, suppresses ferroportinfunction to decreases iron absorption).
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80
Q

Explain the physiology of gastric acid production/secretion)

A

The principal of gastric acid secretion:

  1. Co2 it took up from the blood and reacts with water (catalyzed by carbonic anhydrase) to form H2CO3 which dissociates into H+ and HCo3-
  2. HCo3- gets exchanged for CL- at the basolateral membrane
  3. Cl- diffuses down its concentration gradient via Cl- channel into the lumen of the stomach
  4. K+ enters cells via K+ Na+ ATPase
  5. K+ goes into the lumen via K+ channels
  6. H+ is exchanged for K+

–> H+ and Cl- in lumen combine to give gastric acid, K+ diffuses through the pore into lumen again

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81
Q

What are the three main functions of bile?

A
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82
Q

How does colorectal cancer progress from normal to cancer?

What type of cancer is it?

A

It is also normally Adenocarcinoma

Note: though there is some genetical component, it is sequence of pattern and normally does not have a single gene defect

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83
Q

Which structures are present in the small intestine to increase its surface area (500 fold?)

A

The mucosa is arranged into folds

On folds, there are villi (1mm high)

Each enterocyte has microvilli

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84
Q

What are the function of the endocrine part of the GI tract?

A
  1. To regulate digestion and food processing
  2. Also influences development (some signals are required for development)
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85
Q

What is intrahepatic cholestasis?

A

An obstruction of bileflow/ no bile production due to

e.g. a hepatocellular swelling or abnormalities at cellular lever of bile excretion.

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86
Q

Compare the risk, complications, effects on the GI tract and requirements of enternal nutrition and parenternal nutrition

A
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87
Q

What is the main function of the chief cell in the stomach?

Where are they located?

A

To secrete

  • Pspsinogen (activated by acid) –> breaks down proteins into smaller peptide chains
  • Gastric lipase –> removed fatty acid from triglyceride

Located in gastric glands

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88
Q

Which types of motility can be seen in the small intestine?

A

Peristalsis (move down food)

Segmentation (mixing and surface area)

Migrating motor complex (prevent colonic flora from entering the small intestine, to clean everything out)

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89
Q

Explain the role of the pancreas in fatty acid metabolism

A

pancreatic Lipase together with Prolipase break down triglycerides to monoglycerides and fatty acids

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90
Q

Which enzymes are being secreted by the pancreas?

A

Active Enzymes:

  • Amylase
  • Lipase

Inactivated enzymes:

  • Trypsinogen
  • Procolipase
  • Protease zymogen

+ Trypsin inhibitor –> once trypsin gets activated everything else will go very quickly

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91
Q

Explain the role of the gall bladder

A
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92
Q

What are the symptoms of pancreatic cancer?

A

“Silent Killer” –> Non specific symptoms

Depression +

Virchow’s triad

  • Pain – 70%
  • Anorexia – 10%
  • Weight loss – 10%

Later:

  • Jaundice
  • weight loss
  • obstruction of gall bladder
  • ascites
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93
Q

How is Gilberts syndrome treated?

A

Patients need no treatment

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94
Q

Name examples of the paracrine function of the GI tract

A

E.g.

  1. Histamine –> tirggers HCl production
  2. Somatostatin –> can inbit HCl secretion
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95
Q

What is the characteristic of short bowel syndrome?

A

Significant removal of the bowl which leaves a max of 100cm of functional FI tract

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96
Q

How is alcohol metabolised?

A
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97
Q

What is Haemoptysis?

A

Coughing up blood

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98
Q

What is the role and function of goblet cells in the small intestine?

A

Secret Mucin –> together with water= mucus

Most abundant cell type

Important in lubrication of small intestine

–> more mucus required down the small intestine because water is constantly reabsorbed: more goblet cells

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99
Q

How would you investigate the patient if you suspect an acute pancreatitis?

A
  • History
  • Examination
  • Tests
  1. •SIMPLE
  2. •BLOOD TESTS
  3. •COMPLEX BLOOD TEST
  4. •SIMPLE IMAGING
  5. •CROSS SECTIONAL IMAGING
  6. •INVASIVE TEST
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100
Q

What is cholestasis?

A

Bile cannot drain into duodenum

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101
Q

What are the symptoms of chronic pancreatitis?

A
  • •Malabsorption
  • •Loss of 90% exocrine function
  • •Fat soluble vitamin malabsorption
  • •(A, D, E, K)
  • Steatorrhea
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102
Q

What is the function of the lower oesophageal sphincter?

A

It is (almost) the connection from oesophagus to stomach) –> it should prevent reflux

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103
Q

Which cells of the small intestine secrete Cholecystokinin?

A

I-cells

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104
Q

Explain the processing and absorbance of maltose.

A

Broken down by Maltase to give two glucose molecules

Glucose is taken up into enterocytes by Sodium Glucose Linked Transporter 1 (SGLT-1)

Excreted by GLUT-2 into the bloodstream

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105
Q

At which factors would you look to determine how severe an acute pancreatitis is?

A

How severe is the inflammation:

  • Necrosis vs non necrosis
  • •Organ failure
  • •Age
  • •Co morbidities
  • •Alcohol
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106
Q

Which stomach cells secrete pepsinogen and gastric lipase?

A

Chief cells

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107
Q

How is irritable bowel syndrome treated?

A
  • Diet modification - Avoiding certain foods such as apples, beans, cauliflowers.
  • Treatment of constipation - soluble fiber, stool softeners and osmotic laxatives
  • Treatment of spasms and pain - anti-diarrheals, anti-muscarinic
  • Management of stress, anxiety, depression
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108
Q
A
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109
Q

What is the effect of glocose-dependant insuliotropic peptide (Gastric inhibitory peptide) ?

A
  • upregulation of insulin secretion in response to glucose concentration in the small intestine.
  • In high concentrations, it does have inhibitory effects on stomach function.
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110
Q

To which stimulus does the pancreas secrete Bicarbonate?

Explain the physiological concept

A

pH low –> activates S-cells in small intestine –> secrete secretin

Secretin binds to basolateral receptors of duct cells. This leads to an increase in cAMP. Increased cAMP activates Cl- channel in the apical membrane.

This allows the chemical gradient for Cl- to occur and start Anionic exchangers –> HCO3- excreted

This rises pH in the small intestine

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111
Q

What are the main function fo hepatocytes?

A

80% of hepatic cells

They receive nutrients and building blocks from the sinusoid

Built and metabolize many things: e.g. albumin, clotting factors, bile salts, drug metabolism, etc.

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112
Q

Which two ways can ion take once it is being absorbed into the enterocyte?

A
  1. Into blood and furter transported via TF
  2. Storage in intracellular micelle
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113
Q

What is the significance of the microbiome in fibre break down in the gut?

A

Gut bacteria can break down some fibre and produce short-chain fatty acids which might help to regulate digestion (let body/ brain deal differently with digestion)

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114
Q

How does pepsinogen get activated and what is its name and function of the activated form?

A

Activated by HCl into Pepsin

Breaks down proteins into smaller peptide chains

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115
Q

What are the most common causes of an acute pancreatitis?

A
  • •Gallstones
  • •Ethanol
  • •Trauma
  • (Above most important)

But also different drugs /other signs

  • •Steroids
  • •Mumps
  • •Autoimmune
  • •Scorpion Bite
  • •Hyperlipidaemia/ Hypercalcaemia/Hypothermia
  • •ERCP
  • •Drugs (azathioprine, valproate)
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116
Q

What happens during the gastric phase of gastric secretion?

A

Food is in the stomach –> stretch and chemoreceptors activate vagus (again: ACh–> histamine–< activation of parietal cells–> HCl and pepsin (and lipase) + g cells

3-4 hours

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117
Q

What are mass movents in the large intestine?

A

Happen 1-3 times a day and propel chyme up to 3/4 of the way in a few seconds

This is promoted by indigestible high-fibre food

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118
Q

What is the function of M cells?

A

Uptake and tranport of antigens from lumen into payerspatch

  • Via Phagocytosis
  • Can tranport Proteins, Bacteria, Virus, and non-pathogenic particles

Production of ILI (pro-inflammatory)

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119
Q

What is the small functional unit of the liver?

A

Acini (Singular Acinus)

Consisting of two portal triads, and tow adjacent sides of a two hexagons which reach as far into the lobule as the central vein

It is seperated into zones

Zone 1-3

Zone 1: Oxygen + pathogen rich, zone 3 other way around

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120
Q

Describe the structure of a M-Cell

A

Apical surface:

  • M cells have fewer micorvilli But therefore: Microfolds
  • Form tight junctions
  • No glycocylax of hydrolytic enzymes to not alter antigens

Basolateral

  • Invaginations + formation of “pockets” to keep Antigen way as short as possible
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121
Q

Where does blood in the hepatic portal vein come from?

A

From the digestive tract and spleen

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122
Q

Which diseases can cause haemolytic jaundice?

A

Every diesease with increase break down of red blood cells

–> E.g. sickle cell anaemia, other haemolytic anaemias

123
Q

What do defects/mutations in the melanocortin system lead to?

A

They can lead to obesity via altering appetite regulation (often also ginger with melanocytes etc.)

E.g.

  1. POMC-deficiency /Melanocortin-4- receptor mutations
124
Q

Which molecule is responsible for jaundice?

At which serum concentration is jaundice detectable?

A

Bilirubin causes jaundice

It is detectable when bilirubin >40µmol/l

125
Q

How do you call the process of partial of complete whitening of the nails?

A

Leuconychia

126
Q

What is Dupuytren’s contracture

A
  • deformity of the hand
  • usually develops over years.
  • caused by the layer of tissue that lies under the skin of your palm in which thickened cords of tissue develop that can pull one or more fingers into a bent position
  • associated with persistent uncontrolled diabetes and excess alcohol consumption.
127
Q

Explain the underlying mechanism of haemolytic jaundice

A

Increased break down of red blood cells leading to increased production in bilirubin

–> Jaundice

Note: Can’t be excreted into the urine because unconjugated bilirubin is not water-soluble

128
Q

What is the function of the aqueous, bicarbonate-rich fluid secreted by the duct cells in the pancreas?

A

Helps to mobilise enzyme-rich fluid –> easier to move into duodenum

Bicarbonate helps to neutralise gastric acid

129
Q

By which mechanisms is water reabsorbed in the colon?

A
  • Ion channels
  • Cl-/ HCO3- Exchanger
130
Q

Which parasympathetic nerves innervate which part of the Colon?

A

Midgut: ascending colon + proximal 2/3 of transverse colon —> Vagus

Hindgut: Pelvic nerves

131
Q

What happens during the Intestinal phase of gastric secretion?

A

downregulation –> food leaves stomach

  • Centrally: nerve detects low pH or lipid/proteins in the duodenum
  • Gastro-Intestinal: I-cells secrete cholecystokinin (CCK) and S-cells secrete secretin into the blood
132
Q

How do you treat ulcerative bowel disease?

A

Depends on the severity of symptoms:

  1. Anti-inflammatory medication
  2. If more severe: immunosuppressants
  3. Las thing: removal of colon –> can cure disease but has many disadvantages aswell
133
Q

The lower oesophageal sphincter consists of two components.

Which ones are they?

A
  1. Internal component = built into SM of oesophagus
  2. External = diaphragm (voluntary control)
134
Q

Through which mechanism is Calcium absorbed into the enterocyte?

A

It is absorbed via

  • Ion channels
  • Intestinal calcium binding protein (IMCal) faciliated diffuseion
135
Q

What can be early symptoms of liver failure?

A
  • Lethargy
  • Anorexia
  • Malaise
  • Pruritus – itchy skin
  • Right upper quadrant pain
136
Q

What is an adenocarcinoma in the oesophagus associate with/ what are its characteristics?

A
  • It occursin the lower 1/3 of the oesophagus
  • Columnar epithelium
  • it is associated with reflux
  • Often seen in developed world–> Obesity increases intrabdominal Pressure leading to reflux
137
Q

In how many small anatomically independent segments can the liver be separated?

What makes them independent?

A

In eight segments (I-VII) with distinct anatomical borders

They each have their own blood supply and bile drainage

Each subsection drains into its own vein, with those subsequently draining into the left, middle and right hepatic veins before joining the vena cava

138
Q

What is the role of paneth cells in the small intestine?

Where are they located?

A

Immunological cells–> Secrete granules and engulf bacteria

Location in the crypts, near the stem cells

–> protect the stem cells

139
Q

Which substance do mucus cells in the stomach secrete?

A

Mucus–> bicarbonate-rich (to protect stomach epithelia)

140
Q

What do payers patches consist of?

A
  • They consist of aggregated lymphoid tissue covered whith follicle associated epitheilum (FAE)
  • It is richt in B-cells, T-cells macrophages and dendritic cells
141
Q

How much bile salts does the liver reproduce every day?

How do you call the newly synthesised bile salts?

A

About 0.1 - 0.5 mg/ day of primary bile salts are produced

142
Q

What could happen to the pancreas when there would be an obstruction of the pancreatic duct?

A

This could lead to an accumulation of enzymes

If trypsin inhibitor fails to inhibit trypsinogen

—> trypsin would be activated in the absence of enterokinase

This would lead to pancreatic auto-digestion and pancreatitis

143
Q

What is the most prevalent species of microbiota in the large intestine and what are their characteristics?

A

bacteriodetes

  • gram negative
  • anaerobic
  • non-spore forming bacteria
144
Q

What is the effect of PYY on the GI tract /(not in appetite regulation)?

A

It decreases digestive function, motility and secretion

145
Q

What is the distinctive feature of the ileum?

A

Peyer’s patches –> aggregation of specialized lymphoid tissue

146
Q

Explain the concept of secretion of a pancreatic duct cell

A
  1. HCO3- production (by CO2 via carbonic anhydrase)
  2. Na+ moves into the lumen of the duct via tight junctions ant pulls water with it
  3. CFTR channels activated to excrete Cl- –> produces chemical gradient for Cl- ions
  4. HCO3 exchange with Chloride (secondary active transport) —> HCO3 into lumen
  5. H+/Na+ exchanger to prevent acidification of cell –> blood will be more acid coming from the pancreas
  6. Na+ pumped outside Na+/K+ ATPase
147
Q

Explain the role of hepatic stellate cells

A

Most of the time inactive –> storage of Vit A

When activated: produce ECM (e.g. by cytokines released from Kupffer cells) –> can lead to fibrosis (pathological)

When acitvated= fibroblasts

148
Q

Explain the role and need of stem cells in the small intestine

A

Cells in villi have to be constantly replaced by stem cells

–> lost because of high risk for toxins and drugs/bacterial agents etc.

Lesions will be short lived and quickly repaired

149
Q

Which symptoms are associated with oesophageal cancer?

A
  • Dysphagia
  • unspecific symptoms (e.g. weight loss)
  • vomiting/coughing up blood
  • risk factos( reflux, smoking, alcohol)
150
Q

What is the main Immunoglobulin in the Gut and what is its structure?

A

It is IgA –> secreted as dimer, connected vie J chain

Secreted with Secretory component as SIgA

151
Q

How dos the control of the enteric nervous system correlates with the ANS?

A

The enteric nervous system is mainly independent but watched by the ANS:

152
Q

Which effect does alcohol have on other organ systems than the liver?

A
  • CNS – Wernickes encephalopathy, Cerebral atrophy, Cerebellar syndrome, Optic Atrophy, Peripheral neuropathy
  • CVS – Hypertension, Alcoholic cardiomyopathy, Stroke
  • GIT – Oesophagitis, Gastritis, Oesophageal and Gastric cancer, Pancreatitis, Pancreatic cancer, Alcoholic Hepatitis, Cirrhosis, Liver Cancer
  • GUT – Glomerulonephritis, Renal failure
  • LMS – Gout, Fractures, Myopathies,
  • Endocrine & Reproduction – Pseudocushings, Impotence, Subfertility, Breast Cancer, Fetal Alcohol Syndrome
153
Q

What is extrahepatic cholestasis?

A

resultss from the obstruction of bile flow at any point distal to the bile canaliculi

154
Q

What happens to bile salts in the small intestine?

A

95% are actively transported and reabsorbed into blood and returned to liver via hepatic portal vein

5% are lost into feces

155
Q

What is the distinctive feature or the duodenum?

A

Submucosal glands which secrete bicarbonate-rich alkaline mucus into crypts to neutralize gastric acid

–> protect epithelium and restore good pH for enzymes

156
Q

What does bile do?

When is bile released?

A
157
Q

What are the main components of bile?

A
158
Q

Describe the movement of the large intestine

A
  • Slow (5-10 cm/h) to allow a lot of water to be reabsorbed
  • Proximal colon also elicits ‘antipropulsive’ contractions to impede propulsion and keep food in that region for longer. In the transverse and descending portions there are localised segmental contractions of circular muscle called haustral contractions, which helps to shuffle contents forwards and backwards. Also, there are short propulsive movements every 30 mins.
159
Q

How are the “valleys” called in the small intestine (basically opposite of villi)?

A

Crypts of Lieberkühn

160
Q

Explain the concept of enteral feeding

A

Enteral feeding is the delivery of a fluid past into the upper GI tract (Magensonde)

For patients with upper GI trauma (oesophagus) –> can’t swallow and chew food normally)

161
Q

What are the healthy eating guidelines?

A
  • at at least 5 portions of a variety of fruit and vegetables every day
  • Base meals on potatoes, bread, rice, pasta or other starchy carbohydrates; choosing wholegrain versions where possible
  • Have some dairy or dairy alternatives (such as soya drinks); choosing lower fat and lower sugar options
  • Eat some beans, pulses, fish, eggs, meat and other proteins (including 2 portions of fish every week, one of which should be oily)
  • Choose unsaturated oils and spreads and eat in small amounts
  • Drink 6-8 cups/glasses of fluid a day
162
Q

How does the circular muscle in the large intestine differ from the rest GI tract?

A

It is discontinous and bundles of muscles from the the taeniae coli (longitudinal muscle )

163
Q

What kind of Neurons are present in the enteric nervous system?

A

Sensory: respond to mechanical, thermal, osmotic and chemical stimuli.

Motor: axons terminate on smooth muscle cells of the circular or longitudinal layers, secretory cells of the gastrointestinal tract, or gastrointestinal blood vessels.

Interneurons: neurons between neurons integrate the sensory input and effector output.

164
Q

What are the functions of the large intestine?

A
  • To reabsorb water and nutrients
  • to eliminate waste
  • To provide habitat for gut bacteria
165
Q

Why does the number of goblet cells in the small intestine increase as it goes further along?

A

Because chyme is constantly dehydrated–> more mucus and goblet cells are needed to lubricate small intestine

166
Q

Explain the mechanism of celiac disease?

A
  1. A protein of gluten (Gliadin) is not broken down by Stomach acid –> binds to IgA in the small intestine
  2. The complex binds to TfR (overexpressed) and is transcytosed into lamina propia
  3. Enzyme tissue transglutaminase (tTG) cuts off the amide group from the protein.
  4. Deamidated gliadin is phagocytosed by the macrophages and presented by MHC II molecules.
  5. This leads to the activation of the immune system causing the destruction of epithelial cells.
167
Q

Parenteral feeding

A

Bypass of GI tract and delivery of nutrients into the blood

–> can be necessary for some (if not able to digest food/ or excrete food)

168
Q

What is the main cell type for absorption in the small intestine?

What are their distinctive features?

A

Enterocytes

  • Simple Columnar shaped, on villi
  • have microvilli at the apical surface (2000/cell, 1µm (1/1000 of villi)
  • abundant rough ER + mitochondria
  • have a lifespan of 1-6 days
169
Q

Summarise stomach movment

A

20% Peristalsis –> directed, organised moving down of food (controlled by Vagus)

80% Segmentation –> weaker, mixing of chime –> moves liquid parts of food towards pyloric sphincter, solid parts towards the body

170
Q

Which parts of the oesophagus are controlled by which kind of muscle?

A

Upper oesophageal sphincter: skeletal muscle (constrictor pharyngeal medius + constrictor pharynges inferior)

Middle part: a mixture of both: skeletal and SM

Lower oesophageal sphincter/ lower oesophagus: Smooth muscle

–> though Skeletal muscle: not under voluntary control

171
Q

Which anatomical region of the stomach secretes Gastrin?

A

The Pyloric Antrum

172
Q

What are the effects of gastrin?

A

Increases gastric acid production (via histamine release)

Also increases secretion of pancreatic juice and bile

173
Q

What do very high levels of Cholecystokinin lead to?

A

It can lead to shutting down of gut function –> to protect duodenum from acid and more food that it can handle

174
Q

What is Ghrelin secreted by?

Where does it bind to?

What is its effect?

A
  • It is secreted by the stomach
  • It binds to the hypothalamic receptor
  • It has a short-term effect and increases hunger/urge to eat
175
Q

Which role does the liver play in protein metabolism?

A
  • generation of secreted proteins from amino acids
  • transamination to create essential AA
  • Transamination to create substrates for ATP production
  • GNG
176
Q

What is the mechanism by which Agpr regulates appetite?

A
  1. Agpr binds to MC4R receptor in paraventricular nuclei
  2. It inhibits it. –> inhibition of “full” signal
177
Q

Next to Bacteriodetes what is the other main group of bacteria in the gut?

A

Bifidobacteria

  • gram +
  • non-sporeforming
  • lactic acid producing bacteria
  • –> “friendly bacteria” —> thought to prevent comonisation
178
Q

Summarise the mechanisms of how Vitamin D3 effects calcium absorption

A
  • Enhances the transport of Ca2+through the cytosol
  • Increases the levels of calbindin
  • Increases rate of extrusion across basolateral membrane by increasing the level of Ca2+ATPase in the membrane.
179
Q

Which type of epithelium can be found in the stomach?

A

Simple columnar epithelium

180
Q

How is Calcium transported inside the cell?

Why?

A

Calcium in a signaling molecule inside the cells –> needs to be inactivated for passing:

Binds to Binding molecule: Calbindin

181
Q

What is jaundice?

A

“Turning yellow “

–> Yellow discolouration of eyes and skin due to high leves of bilirubin

182
Q

Is appetite controlled voluntarily or centrally?

A

Though it can be influenced voluntarily, it is controlled centrally by the hyporthalamus

183
Q

Why does the oesophagus require tonical activity anyway?

A

It is the swallowing centre –> can actively swallow food

184
Q

What are the characteristics of Follicle-Associated-Endothelium?

A

FAE has

  • Fewer goblet cells
  • M cells are present
  • lies above sub-endothelial dome (payers patch)
185
Q

Which effect does Peptide YY 3-36 has on the hypothalamic nuclei?

A

It inhibits NPY and stimulates POMC production

186
Q

Where are payers patches found?

A

In the small intestine with highest concentration in the distal ileum

187
Q

What is the name of the vessels in the liver which hold mixed blood from the hepatic portal vein and the hepatic artery?

What are their characteristics?

A

They are called sinusoid, specialised capillary

Wider than normal –> slower flow

Fenestration –> leaky

188
Q

What are the main anatomical regions of the stomach and their respective functions?

A
189
Q

In which two categories can GALT be subdevided?

Name examples for each

A

GALT = Gut Associated Lymphatic tissue

1. Organsied sites

  • Payers patches
  • Lymphocytes in mesnterial lymph nodules (drain lymph from villi)

2. Disorganised sites

  • Lymphocytes in lamina propria and interstitial space
190
Q

Explain the role of the small intestine in carbohydrate metabolism

A

Pancreatic amylase breaks down sugar into disachharids and some medium sized sachharides

–> Sucrose, Lactose, Maltose, Trehalose (disaccharides)

–> Maltotriose, ⍺-Dextrin

Disaccharides than broken down by membrane-bound enzymes

191
Q

What is the main pathway by which triglycerides are formed in the enterocyte?

A

Monoglyceride acylation

Other pathway:

Phosphatidic Acid Pathway

192
Q

What are the characteristics/Mechanism of Ulcerative colitis?

A

Autoimmune disorder - T cells destroy the cells lining the walls of large intestine

Can be made worse by stress and diet

–> Normally starts at anus and goes up the large intestine

193
Q

What are the three main functions of the liver?

A
  • Metabolic and catabolic functions: synthesis and utilization of carbohydrates, lipids and proteins.
  • Secretory and excretory functions: synthesis and secretion of bile and waste products
  • Detoxification and immunological functions: breakdown of ingested pathogens and processing of drugs
194
Q

What is the pathophysiological role of mycobacteria in the large intestine?

A
  • Gut bacteria populations help to maintain and prime the immunological system
  • Inappropriate population or loss of commensal bacteria can predispose to infection and illness throughout the body
  • —> Potential value in ‘faecal transplant’ to re-instate bacteria (remember the potential role of the appendix!)
195
Q

Where are enteroendocrine cells in the small intestine found?

Which shape do they have?

A

At the bottom of the crypts

Roughly columnar shape

196
Q
A
197
Q

What is an acute pancreatitis?

A

An acute inflammatory process that leads to necrosis of the pancreatic parenchyma.

198
Q

Explain the structure and secretory products of a paneth cell

A

Paneth cells secret:

  • lysozyme: an antibacterial enzyme
  • glycoproteins: to protect local cells from enzymes
  • zinc: a common cofactor for lysozymes
199
Q

Summarise the function of the enteric nervous system

A

SPAM –> It controls

  • Sensation
  • Perfusion
  • Absorption (alteration by expression of luminal transport proteins
  • Motility
200
Q

What are possible later signs of liver disease?

A
  • Peripheral swelling
  • Abdominal bloating
  • Bruising
  • Vomiting of blood
  • Confusion and somnolence
201
Q

Which factors influence the associated risk of disease?

A
  • geographic location
  • age (highest risk 55-64)
  • ethnicity
  • social class (lower= higher risk)
  • Smoking
202
Q

Which anatomical regions of the stomach secrete mucus only?

A

Cardia and Pyloric canal

203
Q

What are the main characteristics of the lining of the oesophagus?

A

Non-keratinizing stratified squamous epithelium

–> resists extreme temperatures and textures

Lubrication: mucus secreting glands (+saliva) –> to cunduct food

204
Q

Which cells secrete Glucose-dependent insulinotropic peptide (Gastric inhibitory peptide)?

Where are they located?

A

It is secreted by K cells in the duodenum and jejeum

205
Q

What is an oesophageal sphincter?

Where are they located?

Explain how they change during swallowing.

A

It is a narrowing of the oesophagus due to muscular tension around

Upper: right after pharynx (narrowest)

Lower: at T10: Diaphragm and muscle

(Middle through the trachea and aortic arch)

When no food conducted: they are closed. they open when swallowing food

206
Q

How would you investigate somone who you’d suspect to have chronic pancreatitis?

A
  • PlainXray
  • CT scan
  • Faecal elastase
207
Q

Explain the role and process of the small intestine in fat metabolism

A

When arriving in the duodenum: lipids are mainly undigested

Bile emulsifies fats and forms lipid droplets (increased surface area)

Now: Luminal digestion: pancreatic lipase (also needs colipase) cleave triglycerides to give monoglycerides and free fatty acids

They form Micelles

Micelles are taken up by the cell, and triglycerides are resynthesized via monoglyceride acylation pathway and phosphatidic pathway

Form chylomicrons which travel to the lymph

208
Q

What happens during the cephalic phase of gastric secretion?

A

Tase, smell thought etc. of food induce small response to prepare for food

–> Vagus releases ACh –> histamine release –> stimulates parietal cells to produce HCl and pepsinogen

209
Q

Define chronic liver failure

A

Chronic hepatic failure occurs where there is a deterioration in liver function superimposed on chronic liver disease.

210
Q

Oesophageal cancer: Where does which type of oesophageal cancer occur?

A

In upper 2/3 of esophagus:

  • Squamous cell carcinoma

In lower 1/3 of oesophagus:

  • Adenocarcinoma
211
Q

What are the two characterisations of liver cirrhosis?

A
  • Necrosis of liver tissue followed by
  • fibrosis and liver nodule formation

–> leads to portal hypertension

212
Q

What is the effect of the commuication of the two plexi in the GI tract?

A

The myenteric plexus communicates directly with the submucosal plexus to make ‘local’ decisions based on ‘local’ signals

213
Q

What structures can be affected with problems with the oesophagus?

A

Passes through thorax –>basically all thoracic structures (heart, lungs etc) can be affeted

214
Q

What is an Anastamosis and which role does it play in short bowel syndrome?

A

It is the connection of the small intestine to the colon which can reduce reliance on parenteral nutrition

215
Q

What is the role of hepatic Kupffer cells?

Where are they located?

A

Immunological cells (hepatic macrophages, stellate shpaed)

–> located in the sinusoid, attached to the endothelial wall

Can phagocytose pathogens and toxic substance and release cytokines and activate hepatic stellate cells

216
Q

How much is the estimated biomass of he microbiom in a newborn and in an adult human?

A

Newborn: Thoght to have 0 = sterile

Adult = 1500g

217
Q

By which nerve is the external anal sphincter controlled?

A

By the pudendal nerve

218
Q

What do the acinar cells in the pancreas secrete?

A

A very enzyme rich (mostly inactivated), viscous secrete

219
Q

Which factors influence the neurones in the Arcuate nucleus?

A

It is Influenced by free floating hormones, Neural input etc.

–> complex control mechanism

220
Q

Name some more signs of chronic liver malfunciton

A
  • Xanthelasma - sharply demarcated yellowish deposit of cholesterol underneath the skin, usually on or around the eyelids.
  • Finger Clubbing
  • Pruritus - itchy skin causes scratch marks.
  • Ascites and dilated veins of the abdomen
  • Hepatomegaly - enlarged liver
  • oedema
  • weight loss
  • bruising
  • Caput medusa: distended and engorged paraumbilical veins, which are seen radiating from the umbilicus
221
Q

How does IgA prevent pathogens to enter the organism?

A

IgA bound to pathogens prevent the adherence to mucus and therefore entry to the organism

222
Q

How can you subdivide Acute liver failure?

A
  • Hyperacute liver failure is when encephalopathy occurs within seven days of the onset of jaundice.
  • Acute liver failure is when encephalopathy occurs after 8-28 days of jaundice.
  • Subacute liver failure is when encephalopathy occurs 5-12 weeks after the onset of jaundice.
223
Q

What are the symptoms of celiac disease and how can it be managed?

A

Symptoms:

  • Abdominal distension (bloating)
  • Diarrhoea
  • Sometimes dermititis herpetiformis

Management:

  • Gluten free diet
224
Q

What is a schema to investigate abdominal pain? (Greek)

A

S ite

O Onset

C character

R adiation

A ssociations

T ime

E Relief of symptoms

S everity

225
Q

What is Koilonychia?

A

Deformation of nails (often due to Fe- lack anaemia)

226
Q

What influences energy intake?

A

Biology

activity in enveirnoment+ individual

food consumption

individual psychology

food production

social influence

227
Q

With which four defense mechanism is the Mucosa-associated?

A
  • Physical barrier –> Glycocalyx, Epithelial wall, Brush border and also peristalsis to keep things moving
  • Chemical barrier —> Gastric Actid+ bactericidal enzymes from paneth cells
  • Bacterial protection –> Bacteria prime immunity + prevent the colonisation of pathogenic bacteria
  • Immunological –> Gut-Associated Lymphatic Tissue)
228
Q

Which problems can short bowel syndrome lead to?

A

–> Reduction of absorptive surface area leading to:

It can lead to dehydration, malnutrition because of malabsorption of macro and micronutrients

–> Always presents dysfunction if removed tissue

229
Q

What are the characteristics of cholestatic jaundice?

A
  • High Conjugated bilirubin.
  • Pale stool.
  • Dark Urine.
  • Abnormal liver biochemistry
230
Q

What is Ranitidine and what is its target?

A

Drug to reduce stomach activity/ gastric acid production

Histamine receptor inhibitor

231
Q

Where in the colon is water predominantly reabsorbed?

A

In the proximal colon, where the chyme is more fluid like

232
Q

To which stimulus do the pancreatic acinar cells secrete enzymes?

Explain the physiological function

A
  1. Hormonal:
  • Mixed meal components are detected by I cells in the small intestine
  • Secret Cholecystokinin
  • Binds to CCK1 receptor
  1. Central control:
    * ACh from the vagus

Both Mechanisms:

  • activated Phospholipase C –> increases cytosolic Calcium

–> triggers exocytosis of enzymatic granules

233
Q

What are the three main functions of the gall bladder (gall) ?

A
  • Emulsification and absorption of fat: to increase surface area for lipase activity
  • Cholesterol homeostasis: excreting excess as needed
  • Toxin excretion: endogenous (e.g. bilirubin) and exogenous (e.g. drugs)
234
Q
A
235
Q

Into how many lobes can the liver be split and how are they called?

What are they separated by?

A

Can be split into two lobes: right and left separated by the falciform ligament

236
Q

What effect has isolates Cholecystokinin on bicarbonate?

Which effect has isolated Secretin on bicarbonate secretion?

Which effect have CCK and secretin together on bicarbonate secretion?

A
237
Q

How do you call difficulties swallowing?

A

Dysphagia

238
Q

Which cell in the small intestine secretes gastrin?

A

G-cell

239
Q

What is the distinctive feature of the jejunum?

A

Large submucosal folds called plicae circularis. These are similar to the folds in the rest of the small intestine, but they are considerably larger and closer together. They look much more like frills than folds.

240
Q

Explain the movement of the migrating motor complex

A

Occurs when fasting

241
Q

What are the two (three) major cell classes in the pancreas?

A
  1. Exocrine acini cells –> secrete digestive enzymes
  2. Islets of endocrine cells –> not connected to ducts system, highly vascularized
  3. Connective tissue
242
Q

What is the function of the secretory component bound to IgA?

A
  1. Helps IgA to get to apical membrane thorugh the cell
  2. Protects it from enzymatic break down and gastric acid degradation
243
Q

Which arteries supply which part of the colon?

A

Midgut (ascending + proximal 2/3 of the transverse colon)

  • Middle colic artery (branch of the superior mesenteric artery)

Hindgut:

  • Inferior mesenteric artery
244
Q

Explain the role of the small intestine in protein metabolism

A

Trypsinogen is activated by enterokinase (on enterocytes)

–> Trypsin

Trypsin breaks down proteins + activates further enzymes

Brush border enzymes convert protein into Aminoacids, Di-/Tripeptides which are either directly absorbed or

Di/Tripeptides broken down by brush border enzymes (Di/Tripeptidases)

245
Q

What are the physiological role of the microbiome in the colon?

A
  • Synthesise and excrete Vitamin K (important for coagulation; it is almost exclusively produced by gut bacteria)
  • Prevent pathogen colonisation by competing for attachment sites and nutrition.
  • Antagonise other bacteria which can inhibit or kill non-indigenous species.
  • Stimulate the production of cross-recative antibodies.
  • Stimulate development of some tissues.
  • Fibre can be broken down.
  • Links with drug metabolism, insulin reistance, bile acid metabolism, lipid metabolism and obesity.
246
Q

What are the symptoms of an Colorectal cancer?

A

Asymptomatic (incidental anaemia)

Change in Bowel Habit

  • Diarrhoea
  • Constipation

Blood in Stool

Acute intestinal obstruction

247
Q

How is Heme Iron taken up and processed in the gut?

A
  • Uptake via heme carrier protein 1 (HCP-1) + via receptor-mediated endocytosis.
  • Fe2+liberated by Hemeoxygenase.
248
Q

What leptin abnormalities are there?

What can they lead to?

A

In many obese people: leptin resistance

But there is also a rare congenital leptin deficiency leading to obesity

249
Q

Which hormone is being produced by S cells in the small intestine?

A

Secretin

250
Q
A
251
Q

What is the small structural unit of the liver?

A

Liver lobule

Hexagon shaped, portal triads at each corner of the hexagon.

Sinusoids drain into a central vein

Hepatocytes are arranged, that each hepatocyte has a bile and a sinusoid facing side

252
Q

Which stomach cells produce gastrin?

A

G-cells

253
Q

What is omenprazole and when is it discibed? What does it target?

A

Perscribed wen too much reflux:

Proton pump inhibitor –> inhibits HCL produciton

254
Q

What is the cause of cholestatic jaundice?

A

Cholestatic jaundice is caused by the failure of bile secretion by the liver or bile duct obstruction. This is divided into intrahepatic and extrahepatic cholestasis.

255
Q

Explain the processing and absorption of Lactose

A

Converted by lactase into glucose + galactose

Both: Absorbed: SGLT-1 + Excreted: GLUT-2

SGLT=Sodium GLucose linked transporter

256
Q

How do you manage chronic pancreatitis?

A
  • Stop alcohol and smoking
  • Small meals with low fat
  • PPI (block gastric acid production) and pancreatic supplements (take over tasks of pancreatic enzymes)
  • Analgesia
257
Q

What are the characteristics of irritable bowel syndrome?

A
  1. reucuurent abdominal pain
  2. Abnormal bowl movent: diarreah/ constipation

–> No damage to bowel (functional disorder)

258
Q

Which part of the hypothalamus sends out signals for appetite regulation?

What are its characteristics?

A
  • It is the Arcuate Nuclei located at the base of the brain
  • Uncomplete blood-brain barrier
259
Q

Summarise the livers blood supply

A

20% Hepatic artery for tissue oxygenation

80% from hepatic portal vein for nutrient supply and delivery of blood to be filtered

260
Q

Explain the absorbance of Vitamin B12 into the liver

A
    1. Binds to R-protein (in saliva) to not be broken down by HCL
  2. R Protein is being digested in duodenum
  3. Binds to Intrinsic Factor (IF) –> no digestion of vitamin
  4. Binds to cubulin receptor in distal ileum and taken up
  5. In cell:
  6. Complex dissociates and B12 binds to TCII (Trans-cobalamin 2)
  7. TCII complex pass-through basolateral membrane + taken up into liver cell via TCII receptors
  8. TCII boroken down into liver cell
261
Q

What is Hepatic encephalopathy?

A

Hepatic encephalopathy is the inevitable consequence of acute hepatic failure.

Accumulation of toxins, primarily derived from the gut, is thought to induce cerebral oedema and changes in the level of consciousness and eventually coma.

262
Q

What are the risk factors for cholorectal cancer?

A
  • Family History
  • Specific inherited conditions

–FAP, HNPCC, Lynch Syndrome

  • Uncontrolled Ulcerative Colitis
  • Age
  • Previous Polyps
263
Q
A
264
Q

How can the uptake of pathogens via M-cells cause damage to the organism?

A

It is also an ideal site of entry for pathogens

–> No enzymes, get phagocytosed over membrane

265
Q

Name the nine Regions of the abdomen where pain can be felt?

A
266
Q

What are the signs and symptoms of an acute pancreatitis?

A

Signs and symptoms include

  • severe abdominal pain
  • nausea
  • vomiting
  • diarrhoea
  • fever
  • shock.
267
Q

Explain the role of the pancreas in protein metabolism

A

Trypsin and Proteases convert longer protein chains into shorter peptides (di/tripeptides)

268
Q

What is the most common cause for Congential hyperbilirubinaemia?

A

Gilberts syndrome

  • mutation in the gene that codes for glucuronyl transferase (1st step to make bilirubin water soluble)
    *
269
Q

Which hormone is being produced by the I cells in the small intestine?

A

Cholecystokinin

270
Q

Summarise the treatment for Crohn’s disease

A

Anti-inflammatory medicaton

Antibiotics –> reduce Bacteria in

Maybe:

  • Immunosuppressants with severe symptoms
  • Removal of tissue –> does not cure the disease
271
Q

Explain the movement of potassium in the gastrointestinal tract

A

Potassium can diffuse freely paracellularly and normally exits lumen in the proximal gut and enters it in colon –> Faeces is K+ rich

(Also important in pumping Na+ into extracellular fluid via Na+/K+ ATPase for generating concentration gradient)

272
Q

Name the three major categories of jaundice

A
  1. haemolytic jaundice
  2. jaundice caused by congenital hyperbilirubinamias
  3. and cholestatic jaundice .
273
Q

What is different about the glycocalyx in the large intestine compared to the small intestine?

A

It is still present but does not contain brush border enzymes that break down carbohydrates

274
Q

How much water does the large intestine normally absorb per day?

A

Normally it absorbs around 1500ml

275
Q

List the 5 ways you could test for cholorectal cancer?

A
  • A: Abdominal X-Ray
  • B: CT Scan
  • C: Barium enema
  • D: Colonoscopy
  • E: CT Virtual colonoscopy
276
Q

What are the two types of liver cirrhosis?

What are they caused by?

A
  1. Micronodular
  • uniform, small nodules (<3mm)
  • Caused by Alkohol and biliary tract disease
  1. Macronodular
  • nodules of variable size
  • caused by chronic viral hepatitis
277
Q

Summarise the bilirubin metabolism

A
  1. Derives from break down of hemoglobin in the spleen
  2. In transported as unconjugated bilirubin bound to albumin to the liver
  3. In the liver: conjugated by glucuronyl transferase to bilirubin glucuronide
  4. Secreted into Bile
  5. Degradated by Bacteria into Urobilinogen
  • reabsorbed by the kidney and excreted in urine
  • Transformed into stercobilinogen (10% reabsorbed/ 90% transformed into stercobilin in feces)
278
Q

Which cells in the small intestine secrete somatostatin?

A

D cells

279
Q
A
280
Q

Explain the different proportions in the islet endocrine cells of the panceas

A

70% ß-cells : insulin

20% ⍺-cells : glucagon

10% 𝛅-cells: somatostatin

281
Q

What is the characteristic feature of hepatic endothelial cells?

A

Line sinusoids

–> fenestrated and therefore very leaky, allowing plasma and also larger molecules to pass through them

282
Q

How do you call the process of vomiting blood?

A

Haematemesis

(Kaffesatz –> krümelig)

283
Q

Which hepatic cells store vitamin A and produce Collagen when they get activated?

A

Hepatic stellate cells

(located para sinusoid)

284
Q
A
285
Q

Explain the processing of Ion. (Fe2+) once being taken up into the blood?

A
  • Fe2+moves across baslolateralmembrane via ferroportin.
  • Hephaestinis a transmembrane copper-dependent ferroxidase that converts Fe2+to Fe3+.
  • Fe3+binds to apo-transferrin, travels in blood as transferrin.
286
Q

aWhich pharmacological interventions can you make to inhibit gastric acid production and what are their targets?

A

Omenprazole: protone pump inhibitor

Ranitidine: Histamin receptor inhibitor

287
Q

Which hormone is being produced by D-cells in the small intestine?

A

Somatostatin

288
Q

What are the risk factors of pancreatic cancer?

A
  • Smoking
  • Drinkinng
  • Obesity
  • Family

–Especially rare conditions such as MEN

289
Q

Which shape does hepatocytes have?

How are they organised?

A

Cuboidal

Organised in sheaths so every cell faces sinusoid and bile canal

290
Q

Explain the processing and storage of Ion (Fe2+) in the cytosol

A
  • binds to apoferritin in cytosol to form ferritin micelle.
  • Ferritin is globular protein complex. Fe2+is oxidised to Fe3+which crystallises within protein shell

–> One ferritin Can bind many Fe3+ (up to 4.000) and is formed whith excess dietary Fe3+ uptake

291
Q

What is the hepatorenal syndrome?

Explain its likely mechanism

A
  • reduced renal blood flow due to cortical vasoconstriction as a result to liver failure. may result from the accumulation of a vasoactive substance, thought to be endotoxin, which is usually cleared in the liver.

It is often irreversible and rapidly fatal - patients who develop hepatorenal syndrome have a 95% chance of dying from it, and a mean survival of under 2 weeks. Resolution only occurs if there is dramatic improvement of liver function e.g. via liver transplantation.

292
Q

What are the main functions of the oesophagus?

A

Conduit for food, drink and swallowed secretions from pharynx to stomach

293
Q

By what is Peptide YY-3-36 secreted?

What does it bind to?

What are its effects?

A

It is secreted by the ileum and colon

It binds to the hypothalamic receptors

It decreased hunger and short-term eating behaviors

294
Q

How do you call black, tarry stool from digested blood?

A

Melaena

295
Q

What kind of muscle contraction does the oesophagus use to conduct food?

A

Peristalsis: Contraction above bolus, relaxation below bolus

296
Q

Which component of the lymphocyte binds to which receptor to allow migration into the endothelium?

A

L-selection on lymphocytes binds to Mucosal addressin cell adhesion Molecule 1 (MAdCAM-1) to allow slowing down and rolling into tissue

297
Q

What are the systemic and local complications of an acute pancreatitis?

A

Systemic:

  • •Hypovolaemia
  • •Hypoxia
  • •Hypocalcaemia
  • •Hyperglycaemia
  • •DIC (all coagulation facots used –> causes bleeding)
  • •Multiple organ failure

Local:

  • •Pancreatic necrosis
  • •Fluid collections – mature into pseduocysts
  • •Splenic vein thrombosis/pseudoaneurysm
  • •Chronic Pancreatitis
298
Q

Which role does the liver play in carbohydrate metabolism?

A
  • Glycogen (storage (for 24h fasting) and synthesis)
  • an important role in Cori cycle –> anaerobic respiration

(liver recycles muscle lactate to glucose)

(Lactate —> pyruvate—> GNS –> Glucose)

299
Q

is the main function of the myenteric plexus?

A

In intrinsically controls

  • Motility
300
Q

What are the major functions of the stomach?

A
  1. Digestion: Breaking down food into smaller pieces (acid+ movement)
  2. The reservoir of food until intestine is ready to digest food
  3. Immunological: Killing of parasites and bacteria (acidic environment)
301
Q

What is the function of payers patches?

What do they require to develp?

A

They are “immune sensors” –> monitor local bacteria and protect against pathogenic bacteria

Therefore: They require exposure to bacteria (–> Less found in people who grew up in sterile environment

302
Q

How are the gastric fold called and what is their function?

A

Rugae –> to allow expansion of stomach

303
Q

What is odynophagia?

A

Pain when swallowing

304
Q

What is the main function of the parietal cells in the stomach?

A

To secrete HCL

Also secrete intrinsic factor (important in B12 absorption)

Year 1 LSS (12 decks)

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