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RACP EXAM > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Where is most water reabsorbed

A

90% in jejunum and ileum
10% in the colon

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2
Q

Where is bicarbonate secreted and resorbed

A

Secreted by Pancreatic fluid to neutralise gastric acid

Reabsorbed in the jejunum

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3
Q

what is the function of the following cells
-parietal cells
-endochromaffin cells
-chief cells
-G-cells
-D-cells
-Mucus cells

A

-parietal cells: secrete HCl
-Endochromaffin cells: secrete histamine which promotes HCl production by parietal cells
-Chief cells; secrete pepsinogen- needed for protein digestion
-G-cells: secrete gastrin which promotes the parietal cells to secrete HCl
-D-Cells: secretes somatostatin- inhibits G-cells, endocromaffin cells and parietal cells to reduce gastric acid secretion

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4
Q

What 3 things stimulate HCl secretion

A

-Vagal nerve- releases EACh to activate ECE and parietal cells
-Endochromaffin cells- secrete histamine which binds to H2 receptors on parietal cells to increase HCl secretion
-Gastrin- released into blood stream and binds to ECE cells to stimulate histamine release

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5
Q

How does ibuprofen causes ulcers

A

COX inhibitor
COX 1 + 2 enzymes result in the synthesis of prostaglandins E2 and I2. These bind to parietal cells to reduce HCl secretion.
Prostaglandins also activate the mucus cells to secrete more protective mucus and bicarbonate

Blockage = increased stomach acid, reduced mucus, reduced bicarbonate which can result in ulceration

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6
Q

How does the sympathetic NS reduce stomach acid production

A

Inhibits G-cells (reduced gastrin = reduced parietal and ECE cell stimulation) and stimulates D-cells to make more somatostatin

Net effect = inhibition of HCl production

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7
Q

What affect do CCK and secretin have on gastric acid

A

Reduce it

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8
Q

What is absorbed at
-the duodenum and jejunum
-ileum

A

-most proteins/fat/water/salts
-ileum= bile salts and B12

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9
Q

Describe the process of fat absorption

A

-Fat enters mouth
-broken down by lingular lipase secreted by Ebner’s gland
-enters stomach; acid breaks down further
-In duodenum, fat entering triggers the release of CCK from the pancreas. CCK stimulates gallbladder contraction
-Pancreas releases lipase which breaks down the fat to Free fatty acids and monoglycerides.
-Bile salts then coat the fat and make a MICELLE which is absorbed directly into the enterocyte
-In the enterocyte, micelle breaks down
-Short and medium chain fatty acids are taken up directly into portal blood
-Long chain fatty acids travel to the endoplasmic reticulum; made into triglycerides which conjugate to make lipoproteins. Many lipoproteins= chylomicron
-Chylomicron is absorbed into the lymphatic system and empties into the thoracic duct

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10
Q

What is the role of CCK in fat absorption

A

stimulates the gallbladder to release bilesalts into the duodenum.

Stimulated on arrival of fat into the duodenum. Secreted by the pancreas

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11
Q

Describe the digestion of carbohydrates

A

Salivary parotid amylase breaks down
In the duodenum, amylase is secreted by pancreas, which helps further break down polysaccharides to disaccharides

Enterocytes have a brush boarder with enzymes
-sucrase: breaks down sucrose -> fructose and glucose
-lactase: breaks down lactose –> glucose and galactose
-maltase: breaks down maltose to 2x glucose

Na/K ATPase pump on enterocyte basomembrane pumps sodium out of cell to make sodium gradient
-Glucose or Galactose/Na co-transporter absorbed into the enterocyte
-Exits into blood stream via GLUT-2 transporter

Fructose absorbed by GLUT-5 transporter on apical membrane. Can exit via GLUT-5 transporter OR be phosphorylated in the cell to glucose and exit via GLUT-2 transporter

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12
Q

What are features of a glucose/galactose malabsorption and why do they occur

What is the management

A

Severe diarrhoea, hypoglycaemia, glucosuria

AR defect in sodium/glucose transporter (SGLT1). Result = inability to absorb glucose and galactose.

Manage- fructose as this uses GLUT 5 transporter

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13
Q

How is Fructose absorbed

A

GLUT-5 transporter on apical membrane

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14
Q

If you have a sucrase/isomalatase deficiency what won’t you absorb and how will you present

A

Sucrose ==> glucose + fructose
Maltose= 2x glucose

Main symptom is severe toddlers diarrhoea when fruit is introduced as increased fructose is present and not absorbed

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15
Q

What percentage of fat is not absorbed for there to be ‘malabsorption’

A

> 6%

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16
Q

Describe protein digestion

A

Amino acids broken down in stomach acid.

Enter duodenum. Enzymes from pancreas release- chymotripsinogen, trypsinogen and elastase.

Brush boarder enzyme enterokinase activates typsinogen –> trypsin which in turn activates chymotripsinogen to chymotrypsin. Enzymes break the protein down to dipeptides and tripeptides

Enzymes on the brush boarder break down the protein further

Absorbed into the cell using hydrogen/peptide transporter.

Absorbed across the basomembrane using sodium-peptide cotransporter

Travel to liver in portal blood

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17
Q

What is the role of gastrin

A

“GO” hormone of digestion
-stimulates parietal cells to secrete gastric acid
-stimulates pancreas
-stimulates Intrinsic factor release
-Stimulates Chief cells to release pepsinogen

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18
Q

What is the role of secretin

A

“STOP” hormone of digestion- stimulated by intra-luminal acid secretion
-stimulate pancreatic bicarb secretion
-reduces stomach acid
-prevents gastric emptying

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19
Q

What is the role of CCK

A

Cholecystokinin pancreozymin
-stimulated by intraluminal food
-stimulates gallbladder contraction
-stimulates pancreatic release of enzymes and bicarbonate
-reduces gastric emptying

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20
Q

What affect does increased GIP have on insulin

A

Stimulates insulin production

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21
Q

What is the role of GIP

A

Gastric inhibitory protein
-inhibits gastric emptying
-induces insulin secretion

Stimulated by glucose/protein/fats

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22
Q

What is the role of VIP

A

Vasoactive Inhibitory Protein
“FIGHT OR FLIGHT” protein
-sympathetic neural stimulation = reduced HCl and Pepsin secretion by parietal and chief cells
-reduced gastric motility
-increased secretion of insulin

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23
Q

What affect do both VIP and GIP have on insulin

A

increase the secretion insulin

24
Q

How many calories / kg/ day does an infant need vs a child

25
What vitamin is B1 and what sx do you get in deficiency
B1= Thiamine- get Beri Beri Wet beriberi = CHF causing shortness of breath and oedema Dry Beri Beri= demyelination and axonal degeneration peripheral to proximal. Get tingling, loss of reflexes, weakness, cramping of muscles. Eventually can get aphonia (laryngeal nerve), ptosis (optic nerve) Late stage- wernickes encephalopathy, coma, death
26
What is vitamin B2 and what sx do you get in deficiency
Riboflavin Photophobia, blurred vision Magenta glottis Stomatitis
27
What is vitamin B3 deficiency and what does it cause when deficiency
Niacin Pellegra- diarrhoea, dementia, dermatitis
28
What is Vitamin B6 and what do you get in deficiency
Pyridoxine Enzyme for decarboxylation and transamination so get diffuse breakdown e.g. peripheral neuritis, stomatitis, glossitis
29
What is vitamin B12 and what do you get in deficiency
Cobalamin Important in DNA /RNA repair and synthesis, RBC synthesis and lipid synthesis -Lipid: degeneration of myelin sheath = spinal cord degerneration -DNA/RNA:Beefy red tongue / glossitis -RBC: macroblastic anaemia Causes: -diet -stomach fundoscopy (where Intrinsic factor secreted from parietal cells) -ileum resection (absorbed via enterocytes) -pernicious anaemia
30
What is the name of Vitamin C deficiency and what are the symptoms
Scurvy -Glossitis, gum hypertrophy, poor wound healing, gingivitis, weakness, jaundice, neuropathy
31
What are symptoms of vitamin A deficiency
Retinal - blindness from keratomalacia (cornea softens and goes cloudy) Teeth- faulty enamel Bones- faulty epiphyseal plate Poor growth
32
What are is the syndrome of vitamin D deficiency and the signs
Rickets Bony signs: frontal bossing, wide open fontanelle, bowed legs, swelling of ankles and wrist, rachitic rosary, minimal trauma fracture Non-bony: delayed gross motor development, poor linear growth
33
What are the symptoms of Vitamin E deficiency
Cerebellar ataxia Posterior column dysfunction Peripheral neuropathy
34
What co-factors if Vitamin K involved in
Factor 2, 7, 9, 10 Protein C + S
35
what would you see in iron deficiency on iron studies
low serum iron low ferritin high transferrin
36
What is congenital zinc deficiency called and what are the features
Acrodermatitis enteropathica -perioral and perianal dermatitis -alopecia -anaemia -recurrent infections especially candida -anaemia -poor wound healing
37
What are the signs of hypercalcaemia What is the relationship of calcium and magnesium
-Bony pain, renal stones, abdomen pain/constipation, confusion Low Mg drives low calcium- can result in Vitamin D resistant rickets
38
What is the condition of congenital copper deficiency called and its features
Menkes Kinky hair Disorder of copper transport Result = kinky hair, demyelination of nervous tissue and facility of large blood vessels. results in death before age 3
39
What is the condition of copper excess, what genetic defect and what are the symptoms
Wilsons disease Gene: ATP7B Features -Eyes; KF rings -Brain: psychosis -heart: cardiomyopathy -liver: hepatitis, portal HTN -renal: acute tubular acidosis
40
What is the difference between Kwashiok and Marasmus
Marasmus- muscle wasting and depletion of fat stores Kwashiok- generalised oedema and flaky peeling skin
41
What does IFALD stand for and what are the causes/risk factors/symptoms/management
Intestinal failure associated liver disease -TPN associated liver disease -Liver disease associated with chronic use of TPN Risk factors: prolonged TPN use, prematurity, lack of enteral nutrition, bacterial gut overgrowth, CVC infections Symptoms: cholestasis, hepatic fibrosis, and can develop portal hypertension and liver failure Management -prevent: early enteral nutrition, prevent CVC infection -manage: introduce fish oil fatty acids (SMOF), ursodeoxycholic acid- improves bile acid flow and reduces gallbladder stasis
42
What is intestinal failure
Inadequate small bowel available to support nutrition and growth -unable to absorb enough nutrients, water and electrolytes -require IV nutrition to sustain growth and health
43
In short gut syndrome, what length is associated with likely need for long term nutritional support
<40cm
44
What motility disorders cause short gut syndrome
Gastroschisis High level hirschsprungs Chronic intestinal pseudo-obstruction
45
What hormone is elevated in Prada-willi syndrome that stimulates appetite
Gherlin
46
What is the difference in diarrhoea illness of these E. Coli -Enterotoxic -Enterohaemorrhagic -Enteroinvasive -Enteropathogenic
Enterotoxic: produces a toxin that results in pores forming in the apical surface. Leak Cl/Na/water into the lumen to cause secretory diarrhoea Enterhaemorrhagic: produces Shigella toxin- E.Coli 0157:H7 is associated with HUS. Toxin causes inflammation of endothelial cells resulting in microangiopathy, platelet aggregation and AKI Enteroinvasive E.Coli: uses adhesive proteins to invade enterocytes and uses the cell machinery to multiple. Causes severe mucosal damage and inflammation --> profuse watery diarrhoea and fever Enteropathogenic" common toddlers diarrhoea
47
What channel is affected in congenital Chloride diarrhoea and what does it do to the blood gas
Cl/HCO3 exchanger Results in inability to reabsorb Cl and cannot excrete bicarbonate Result= metabolic alkalosis with hypochloraemia
48
What channel defect occurs in congenital sodium diarrhoea What is the affect on the blood gas What kind of stool do you get
Na/H channel defect- cannot absorb sodium or excrete hydrogen Metabolic acidosis Alkaline stool
49
What pathology occurs in congenital Microvillus atrophy and tufting enteropathy
have epithelial cell aplasia in the microvillus surface with microvilli atrophy and in tufting enteropathy get tufts of epithelia cells extruding from the epithelia cells on biopsy Results in severe secretory diarrhoea from birth Require PN Require Gut transplant
50
What malfunctions in fructose malabsorption vs intolerance
Fructose malabsorption- GLUT5 transporter defect Fructose intolerance- metabolism defect = due to fructose-1-phosphate-aldolase Gene=ALDOB
51
what is Zollinger-Ellison syndrome
Gastrin producing tumour. Results in increased parietal stimulation --> increased acid secretion --> gastric ulcers and chronic diarrhoea
52
Name 4 causes of exocrine pancreatic insufficiency (genetic) and their features
Cystic fibrosis- CFTR mutation Schwann-Diamond syndrome: SBDS mutation - neutropenia, bone abnormalities, acinar duct aplasia leading to exocrine pancreatic insufficiency Pearson Syndrome- fibrosis of exocrine gland, sideroblastic anaemia Johnson-Blizzard syndrome- fibrosis of pancreatic gland, severe nasal hypoplasia
53
What genes are associated with hereditary pancreatisi
SPINK-1, PRSS
54
What are the risk of developing coeliac in these people -HLA matched sibling of a coeliac person -Monozygotic twin -1st degree relative
-30-40% -70-100% -5-10%
55
What are drugs in the Calcinerin inhibitor group and what are their MOA and side effect profile
Tacrolimus and Cyclophosphamide MOA: inhibit IL2 transcription so T-cells cannot proliferate Side effects: -Cyclosporin: nephrotoxicity, hairiness, gum hypertrophy, dyslipidaemia -Tacrolimus: nephrotoxicity, HTN
56
Describe the metabolism of Azathiopurine and what affects the dosing in various populations
Azathiopurine works to inhibit DNA purine synthesis Broken to 6-Metacaptopurine. From there can be metabolised to 6-thioguanine OR to 6-MMP by the enzyme TPMT. 6-MMP= liver toxicity 6-TG= bone marrow suppression If too little TPMT, get increased 6-TG levels and can cause profuse bone marrow suppression Avoid in homozygous
57
What is the MOA of methotrexate and what is the side effect profile
Anti-folate/anti-metabolite Side effect- liver injury, lung fibrosis, Bone marrow suppression

RACP EXAM (9 decks)

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