ILO WEEK 3 Flashcards

1
Q

The products of digestion and where they are released for absorption

A

Carbohydrates -> mono di and poly saccharides -> brush border to monosaccharides -> absorbed in small intestine Co-transport with sodium ions (pr facilitated diffusion for fructose)

Proteins -> digested in stomach and small intestines by multiple protease -> to peptides ->products of digestion are amino acids -> absorbed in small intestine -> active transport

Ribonuclease and deoxyribonuclease -> nucleotides -> active transport

Lipids -> triglycerides -> Fatty acids and monoacylglycerides -> Diffusion into intestinal cells, where they are combined with proteins to create chylomicrons or Simple diffusion for short

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2
Q

Describe the regulation of pancreatic secretion

A

Regulated by activity of the vagus nerve and hormones. Endocrine control is more important.
The cephalic phase:
Acinar cells and smooth muscle of the pancreas innervated by parasympathetic vagal nerves. Stimulation causes release of zymogen granules from acinar cells and increase in local blood flow. Sympathetic vasocnstriction reduces the blood flow
Under nervous control
(Sight, smell,Taste) Acetylcholine
The gastric phase:
Gastrin; secreted as a response to distension of the stomach and response of amino acids and peptides in the antrum
The intestinal phase:
>70% of total secretion; hormones secreted by the duodenal mucosa; Secretin released in response to low pH and stimulates secretion of bicarbonate rich fluid from ductal cells
CCK secreted when mucosal surface is bathed in monoglycerides, fatty acids, peptides, amino acids -> stimulates production of an enzyme-rich fluid from the acinar cells; also increases secretin effect
Alpha amylase is the only pancreatic enzyme that is released active

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3
Q

Discuss the dietary advice you would give to a patient with pancreatic insufficiency

A
  • low-fat
  • high-protein
  • high-calorie diet
  • with fat-soluble vitamin supplements
    
    PBL WEEK 3
  • lean meats, beans and lentils, clear soups, and dairy alternatives (such as flax milk and almond
  • milk)
  • Spinach, blueberries, cherries, and whole grains
    fruit instead of added sugars
    •Eat between six and eight small meals throughout the day to help recover from pancreatitis. This is easier on your digestive system than eating two or three large meals.
    •Use MCTs as your primary fat since this type of fat does not require pancreatic enzymes to be digested. MCTs can be found in coconut oil and palm kernel oil and is available at most health food stores.
    •Avoid eating too much fiber at once, as this can slow digestion and result in less-than-ideal absorption of nutrients from food. Fiber may also make your limited amount of enzymes less effective.
    •Take a multivitamin supplement to ensure that you’re getting the nutrition you need. You can find a great selection of multivitamins here.
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4
Q

Discuss possible strategies for improving patient compliance

A
  • Involve patients in making decisions
  • Forget; Doesn’t understand why has to take them; Doesn’t like shape taste etc. - Too many medications to take; lack of routine
  • Try to explain them the mechanism of drug; try to work through their issues
  • Imparting knowledge;
  • Modifying patient beliefs;
  • Patient communication;
  • Leaving the bias; and
  • Evaluating adherence.
  • Simplifying regimen characteristics;

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5
Q

The role of the Pancreas in the digestion of food in the human gut

A

Pancreatic juice with pancreatic enzymes:
Lipase -> works with bile salts and acids -> digests fats and fat soluble vitamins

NaHCO3-> secreted to neutralise the acidic stomach juice; enzymes only active in higher pH

Proteases -> trypsin, chymotrypsin, carboxypeptidase, elastase; wide range of peptide bonds; secreted as zymogens and activated in the gut lumen; trypsinogen activated by enterokinase (rest activated by trypsin)

Amylase -> alphaamylase; digests alpha1-4 bonds in starch and glycogen to disaccharides and oligosaccharides which are further digested by enzymes on the brush border of the mucosa

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6
Q

Different specificities of the pancreatic endopeptidases trypsin and chymotrypsin and the
structural basis for these specificities.

A

Trypsin:
• Trypsin acts on peptides with lysine and arginine on C- terminal side
• but not if there is a proline on the carboxyl side

Chymotrypsin:
• activated by trypsin
• acts on peptide bonds in which carboxyl group is provided by tyrosine and phenylalanine (uncharged forms, aromatic amino acids)

STRUCTURAL BASIS?!?

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7
Q

The actions of amylase on different dietary carbohydrates and the products released

A

Endoamylase, similar to salivary amylase
• Digests a 1-4 glucose-glucose bonds ONLY!

• Digests starch and glycogen to maltose, maltotriose and dextrins 
• Secreted in active form
The kinks in the amylose chain causes a helical structure characteristic of starch. The structure of cellulose is a zig zag or pleated pattern which is an ideal back bone for the plant cell wall.
Our enzymes can digest amylose but not cellulose.

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8
Q

Clinical tests available for pancreatic functions

A

Test of pancreatic damage:

  • Serum amylase
  • Urine amylase
  • Serum lipase

Test for pancreatic function:

  • Direct and indirect (tests based upon the principal that a pancreatic cleaves an absorbable substance from a non-absorbable molecule; not available in UK; DONT REALLY UNDERSTAND THIS!)function test
  • Faecal chymotrypsin
  • Faecal elastase

Faecal tests:
Measure pancreatic enzymes in faeces (chymotrypsin-> proteolytic enzymes -> low levels indicate insufficiency and elastase->if too high exocrine insufficiency-> uses ELISA kit )

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9
Q

Discuss absorption and transport of Iron from GIT

A

Non harm iron-> Ferric iron (3+) needs to be transformed into ferrous iron (2+) to be absorbed
transformed using: VITAMIN C FERROREDUCTASE
(DMI1 transporter absorbes it after) cotransport with H+
This happens mostly in duodenal enterocytes

Ham iron easily absorbed -> duodenal enterocytes as well by harm oxygenase

  • ferropotin transports it out of the tissues (in 2+ form and the enzymes change it back to 3+ later)

Transferrin -> transports IRON around the body (2X Fe3+)
Most goes into erythropoiesis
Rest goes:
- 10-20% to the liver stored in ferric form
ferropotin back to circulation
unless otherwise regulated by hepcidin

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10
Q

Describe utilisation of Iron in the human body

A
No mechanism to excrete iron!!!
Utilisation:
- total body content -> 4 g
- Bone marrow and RBCs -> 3g
- Reticuloendothelial system -> 200-500mg
- Myoglobin -> 200-300mg
- Enzymes -> 100mg
Most used for erythropoiesis
Rest is in the liver; stored or released when needed
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11
Q

Discuss regulation of iron metabolism in human body

A

Iron homeostasis:
Daily need 1-2mg/day
Western diet 15-20mg/day
Big iron loss in menstruation; need more
Role of Hepcidin (low iron hormone ->inhibits iron transport by binding to the iron export channel ferroportin)
40 g of iron circulates, only small amount of iron from the diet

HEPCIDIN:
- Inhibit function of ferropotin (iron release to circulation)
- Prevents release; decrease plasma iron concentrations
- Spleen macrophages!!!;
(Engulfing old RBC and digestion) BLOCKS it ; iron stays in spleen instead of going into circulation
- Inhibits absorption of iron in the small intestine

Hepsidin production and release:

  • inflammatory cytokines (IL-6)
  • Increase in plasma iron concentration -> close control
  • lipopolisaccharides

MAIN REGULATOR: HFE protein
HFE gene Hemohromatosis
interacts with other proteins to regulate iron absorption

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12
Q

Discuss about the causes and consequences of ‘Hereditary Haemochromatosis’

A

Mutation in HFE gene -> protein Hereditary Haemochromatosis
Autosomal recessive disorder Reduce Hepcidin production

Iron overload! Iron absorbed from intestine; plasma iron concentration increases; Hepsidin does not work

Body will absorb lots! -> severe consequences

More severe in males; females protected by menstuation and child birth
Raised serum ferritin
More then full saturation; some iron in plasma not bound; v. active metabolically; can cause tissue damage (cirrhosis; diabetes; bronzing of skin; arthritis); Restrictive cardiomyopathy

Treatment -> venesection!

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13
Q

Retrograded starch

A

some cooking pocesses and some storage processes cause recrystallisation of some starch -> becomes indigestible (mostly by pressure cooker or high pressure food processing or fridge)

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14
Q

Interpretation of the result of pancreatic tests

A

ADD THE TABLE (still don’t know how :P)

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15
Q

Acute pancreatitis

A

Gallstones; Alcohol; Infections itd itp

Acute inflammatory condition; From self limiting to fatal
Pancreatic insult-> activation of inactive enzyme precursors -> inflammatory cytokines
Sudden onset abdominal pain; nausea and vomiting; fever, hypotension, shock and multiorgan failure

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16
Q

Glycemic index

A

Foods compared for their likely effect on blood glucose levels; better to have slow rise than rapid rise and fall

17
Q

Serum Ferritin

A

directly related to the amount of iron that we have in macrophages and body stores;
Tiny amount in serum to RES iron stores

↓ in IDA
↑ in iron overload
NB. Acute phase protein; in presence of inflammation or tissue damage can rise inappropriately (↑ in tissue inflammation)

18
Q

storage and recycling of Iron in the human body

A

Storage:
- Ferritin (soluble, iron safe and readily available from RES; Haemosiderin (insoluble conglomerates of fern iron only slowly available)

Storred in liver and in bone marrow; sometimes in the spleen

Recycling:
RBC (Haemoglobin) when broken down to heme and globin; Heme absorbed into the cell lumen (to bilirubin and iron Fe3+) stored as ferritin
Iron from liver released when necessary (plasma levels fall or when more RBC need to be made)

19
Q

DMI1 Transporter

A

Absorption if iron and other metals: Mn, Zn,Cn,Cu

20
Q

Iron deficiency

A

If not enough in the diet -> Anemia (menstruation contributes to the problem)
Women require 50% more iron than men

GOLDEN RULE
• IDA in males & post menopausal females is due to GI blood loss until proven otherwise
• Young women; menstrual blood loss +/- pregnancy (500mg of IRON lost fro pregnancy)
GI investigations only for GI symptoms or blood in stool

21
Q

E.coli and cholera action on absorption:secretion ratio

A

E.coli antiabsorptive

Cholera -> prosecretory

22
Q

Using an image of the Small Intestine, define the locations of the Duodenum, Ileum and Jejunum.

A

Image not loading

23
Q

Using an image of the Large Intestine, identify the:

  • Ileocaecal Junction
  • Caecum
  • Appendix
  • Taenia Coli
  • Haustrations
  • Rectosigmoid Junction
A

Image not loading

24
Q

List the parts of the Large Intestine in order.

A
Ileocaecal Junction 
Caecum
Ascending Colon
Transverse Colon
Descending Colon
Sigmoid Colon
Rectum
25
Q

Name the constituent parts of the Midgut of the adult.

A
Duodenum (in part)
Jejunum
Ileum
Caecum
Appendix
Ascending Colon
Hepatic Flexure of the Colon
Transverse Colon (Prox. 2/3s.)
  • served by the superior mesenteric artery
26
Q

Name the constituent parts of the Hindgut of the adult.

A

Transverse Colon (Dist. 1/3, Splenic Flexure)
Descending Colon
Sigmoid Colon
Rectum
- served by the inferior mesenteric artery

27
Q

Discuss the histological differences between the Small and Large Intestines.

A

The Small Intestine is concerned with late stage digestion (mainly of fats and carbohydrates) and absorption of digested food.

To facilitate this, it’s mucosa is highly folded forming projecting villi and secretory crypts of Lieberkuhn. The folds themselves are lined with a fine brush-border made up of microvilli.

The Lamina Propria provides vasculature and lymphatics (l;acteals). Muscularis Mucusae layer.

Muscularis Externa has an circular and longitudinal layer of muscle to allow for peristalsis. Also provides immuno-surveillance with GALTs.

The large intestine comparatively simple. It completes absorption and re-absorbs water + sodium.

The mucosa is rich in crypts which secrete mucous, columnar absorptive cells make up the bulk of the epithelium. This epithelium is sloughed every six days.

The lamina propria and submucosa are the same as above.

The mucularis externa organises it’s circular layer of muscle as sphincters (at the anus) while the longitudinal layer is organised into taenia coli giving rise to haustrations.

28
Q

Provide an overview of the development of the intestines and the causation of embryological anomalies (in terms of the G.I Tract?)

A

General timeline:

  1. Formation of the primitive gut tube
  2. Basic sub-divisions of the gut tube take shape
  3. Definitive sub-divisions are made
  4. Cranio-Caudal patterning of the gut tube (junctions are formed)
  5. Radial patterning of the gut tube (temporary occlusion by proliferating endoderm is normal, but errors in it’s control can lead to stenosis in the final tract)
  6. Mesenteries of the gut tube form
    https: //web.duke.edu/anatomy/embryology/gi/gi.html
29
Q

Explain the general pattern of lymphatic drainage of the bowel and its clinical importance.

A

Duodenumal drainage -
Pancreatoduodenal and superior mesenteric nodes

Jejunum and Ileum - Superior mesenteric nodes

Ascending and transverse colon - superior mesenteric nodes

Descending and sigmoid colon - inferior mesenteric nodes

passes to the intestinal lymph trunks, cisterna chyli and finally the thoracic duct.

30
Q

Define Diarrhoea

A

Defined as three or more loose stools in a day and/or any increase in pattern for the individual for longer than 2 weeks and/or more than 200g of stool a day.

Acute less that two weeks, persistant more than two week and chronic more than 4 weeks.

31
Q

Describe the causes and pathogenic mechanisms of diarrhoea

A

Caused by anything that upsets normal absorption of fluids and salts (in the large intestine) or normal secretion of enzymes/ absorption in the small intestine.

The former causes a large volume of watery stools, the latter causes frequent, small volume stools which can contain blood and cause fever.

Typical causes are:

Baceria such as E.coli 0157 or Campylobacter sp.

0157 attaches to enterocytes and release shiga toxin, causing cell death. Can enter systemic circulation with an infectious dose as low as 10 CFU.

Campylobacter has a much higher dose, 9000 CFU which will usually cause disease when stomach pH is lowered. Can colonise the small and large intestine. It typically causes diarrhoea by killing enterocytes.

Viruses such as Norovirus

Faeco-oral infection. 10-100 virions sufficient for infection.

Parasites such as Giardia or Cryptosporidium

Giardia typically attaches the the epithelium of the duodenum causing inflammation of the villus surface, upsetting fat and carbohydrate absorption to produce a watery diarrhoea.

Cryptosporidium causes an inflammatory response resulting in increased permeability of the epithelium, loss of chloride and poor absorption. Produces a watery diarrhoea.

32
Q

Discuss the clinical features of gastroenteritis.

A

Think “D&V”

A self limiting D&V (sometimes or) will present around 12 hours after infection. Self limiting, and will usually resolve within 2 weeks.

Symptoms will deteriorate with dehydration/ poor re-hydration. S&S of as deteriorating patient will include confusion, palor, poor capillary refill time, poor skin turgor.

Specifics

  • 0157
    Incubates in 3-4 days and produces a bloody stool with abdominal tenderness. Fever is rare. Antibiotics is contraindicated as it will cause a triad of: microangiopathic haemolytic anaemia, acute renal failure and thrombocytopenia. Renal dialysis in 50% of patients, with mortality rate of 3-5%.
  • Campylobacter
    Sever abdominal pain, bloody stools. Nausea and fever but vomiting is usually absent.
  • Norovirus

Acute and severe D&V. “If anyone told you that it’s impossible to shit lots and vomit at the same time they’re liars”

33
Q

Discuss the investigation and management of infectious diarrhoea.

A

As per lecture guidance -

REHYDRATION. Illness is typically self limiting, so management with fluids is often the treatment.

Diagnosis is usually based on patient history, particularly travel or food. Culturing can allow for specifics but is generally obsolete.

In C Diff, antigen and toxin testing is sought. - Stop causative antiobiotics and recolonise with normal flora.

Viral - rapid onset.

Wash hands, maintain high standards of sanitation.

34
Q

Provide an overview of the anatomy and histology of the pancreas. Ideally with a drawn diagram.

A

Image isn’t loading but cover:

  • Head, neck, uncinate process body, tail.
  • Pancreatic, accessory, common bile ducts.
  • Spincter of Oddi, Ampulla of Vater
  • Gall Bladder
  • where it sits in relation to the duodenum

Understand that it is retroperitoneal with both endocrine (glucose regulation) and exocrine (digestion) functions.

It’s blood supply originates from the splenic artery for the body and tail, branches of the gastroduodenal + superior mesenteric arteries.

Nerves: vagus and splanchnic nerves

35
Q

Describe the process of Chronic Pancreatitis.

A

Principle causes are: alcohol, genetic factors, autoimmune disease. Generally, recurrent episodes of acute pancreatitis - which is handily remembered with I GET SMASHED.

Idiopathic
Gall stones (obstructive)
Ethanol (alcohol abuse)
Trauma
Steroids
Mumps (or viral infection, really.)
Autoimmune (increased levels of IgG and basal inflammation)
Scorpion Stings
Hypertriglyceridemia, hypercalcaemia, hyperparathyroidism.
ERCP (endoscopic retrograde cholangiopancreatography)
Drugs (vague AF, but an examples are sulphonamides).

Pathophysiology follows:

“The sentinel event” (above) causing acute pancreatitis, each event will cause additional fibrosis, leading to chronic pancreatitis which is heavily influenced by the loss of normal pancreatic architecture.

36
Q

Discuss the processes of digestion and absorption of carbohydrates

A

Digestion of carbohydrates starts in the mouth and finishes in the duodenum.

Salivary amylase converts food starch into disaccharides (Maltose) - it’s why bread changes flavour as you chew it.

The bolus is conducted through the oesophagus and stomach to the duodenum where it arrives as chyme.

Here, (pancreatic) amylase, maltases, sucrases and lactases continue the process in the brush border. Each act on maltose (think starch), sucrose (sugar in tea) and lactose (milk) respectively.

Maltose (disaccharide) produces glucose (monosaccharide). Sucrose (disaccharide) produces glucose and fructose. Lactose produces glucose and galactose.

These are then transported into the blood stream as monosaccharides.

37
Q

Discuss the processes of digestion and absorption of Proteins

A

This can be considered to start in the mouth with mechanical digestion (mastication or just “chewing”) but it mainly takes place in the stomach.

Here, pepsin digests proteins into short chains of amino acids.

The chyme moves to the duodenum, where pancreatic Trypsin, Elastase, Chymotrypsin, Carboxypeptidase, Depeptidase and Aminopeptidase further cleave the chains.

They are absorbed into the blood steam as amino acids.

38
Q

Discuss the processes of digestion and absorption of Lipids

A

This begins in small amounts in the mouth with Lingual Lipase and the stomach with Gastric Lipase.

It all really kicks off in the duodenum. Distention of the organ stimulates the release of bile, rich in bile salts which emulsifies fat (think washing up liquid and fat in a baking tray). Large lipid globules form small lipid globules.

This provides pancreatic lipases more surface area to work on: breaking fatty acids down into Glycerides.

Bile salts and these small lipid droplets form Micelles.

Micelles move to the brush border where long-chain fatty acids and monoglycerides diffuse out, and micelles remain in the chyme.

Triglycerides are formed from the fatty acids and monoglycerides, which diffuse into abnsorptive cells of the duodenum. Here, they aggregate with a protein coat to form Chylomicrons.

Chyomicrons are exocytosed into the lymphatic vessels and enter the blood at the subclavian vein.

39
Q

Describe the Migrating Motility Complex

A

An intraprandial, 4 stage cyclical contraction of the stomach and duodenum every 90 minutes to prepare the space for the next intake of food.

It is regulated by the hormone Motilin, produced by M Cells (These endocrine M Cells are not the same as M Cells in Peyers Patches) of the small intestine.

It is made up of four stages:

  1. A prolonged period of quiescence.
  2. An increased in contractions
  3. A peak of electrical and mechanical activity
  4. A lower frequency of contraction leading to stage 1.