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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

A

100 vs 55

25
Q

What vitamin is B1 and what sx do you get in deficiency

A

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
Q

What is vitamin B2 and what sx do you get in deficiency

A

Riboflavin

Photophobia, blurred vision
Magenta glottis
Stomatitis

27
Q

What is vitamin B3 deficiency and what does it cause when deficiency

A

Niacin

Pellegra- diarrhoea, dementia, dermatitis

28
Q

What is Vitamin B6 and what do you get in deficiency

A

Pyridoxine

Enzyme for decarboxylation and transamination so get diffuse breakdown
e.g. peripheral neuritis, stomatitis, glossitis

29
Q

What is vitamin B12 and what do you get in deficiency

A

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
Q

What is the name of Vitamin C deficiency and what are the symptoms

A

Scurvy
-Glossitis, gum hypertrophy, poor wound healing, gingivitis, weakness, jaundice, neuropathy

31
Q

What are symptoms of vitamin A deficiency

A

Retinal - blindness from keratomalacia (cornea softens and goes cloudy)

Teeth- faulty enamel
Bones- faulty epiphyseal plate
Poor growth

32
Q

What are is the syndrome of vitamin D deficiency and the signs

A

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
Q

What are the symptoms of Vitamin E deficiency

A

Cerebellar ataxia
Posterior column dysfunction
Peripheral neuropathy

34
Q

What co-factors if Vitamin K involved in

A

Factor 2, 7, 9, 10
Protein C + S

35
Q

what would you see in iron deficiency on iron studies

A

low serum iron
low ferritin
high transferrin

36
Q

What is congenital zinc deficiency called and what are the features

A

Acrodermatitis enteropathica
-perioral and perianal dermatitis
-alopecia
-anaemia
-recurrent infections especially candida
-anaemia
-poor wound healing

37
Q

What are the signs of hypercalcaemia
What is the relationship of calcium and magnesium

A

-Bony pain, renal stones, abdomen pain/constipation, confusion

Low Mg drives low calcium- can result in Vitamin D resistant rickets

38
Q

What is the condition of congenital copper deficiency called and its features

A

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
Q

What is the condition of copper excess, what genetic defect and what are the symptoms

A

Wilsons disease
Gene: ATP7B
Features
-Eyes; KF rings
-Brain: psychosis
-heart: cardiomyopathy
-liver: hepatitis, portal HTN
-renal: acute tubular acidosis

40
Q

What is the difference between Kwashiok and Marasmus

A

Marasmus- muscle wasting and depletion of fat stores

Kwashiok- generalised oedema and flaky peeling skin

41
Q

What does IFALD stand for and what are the causes/risk factors/symptoms/management

A

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
Q

What is intestinal failure

A

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
Q

In short gut syndrome, what length is associated with likely need for long term nutritional support

A

<40cm

44
Q

What motility disorders cause short gut syndrome

A

Gastroschisis
High level hirschsprungs
Chronic intestinal pseudo-obstruction

45
Q

What hormone is elevated in Prada-willi syndrome that stimulates appetite

A

Gherlin

46
Q

What is the difference in diarrhoea illness of these E. Coli
-Enterotoxic
-Enterohaemorrhagic
-Enteroinvasive
-Enteropathogenic

A

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
Q

What channel is affected in congenital Chloride diarrhoea and what does it do to the blood gas

A

Cl/HCO3 exchanger
Results in inability to reabsorb Cl and cannot excrete bicarbonate

Result= metabolic alkalosis with hypochloraemia

48
Q

What channel defect occurs in congenital sodium diarrhoea

What is the affect on the blood gas
What kind of stool do you get

A

Na/H channel defect- cannot absorb sodium or excrete hydrogen

Metabolic acidosis
Alkaline stool

49
Q

What pathology occurs in congenital Microvillus atrophy and tufting enteropathy

A

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
Q

What malfunctions in fructose malabsorption vs intolerance

A

Fructose malabsorption- GLUT5 transporter defect

Fructose intolerance- metabolism defect = due to fructose-1-phosphate-aldolase
Gene=ALDOB

51
Q

what is Zollinger-Ellison syndrome

A

Gastrin producing tumour. Results in increased parietal stimulation –> increased acid secretion –> gastric ulcers and chronic diarrhoea

52
Q

Name 4 causes of exocrine pancreatic insufficiency (genetic) and their features

A

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
Q

What genes are associated with hereditary pancreatisi

A

SPINK-1, PRSS

54
Q

What are the risk of developing coeliac in these people
-HLA matched sibling of a coeliac person
-Monozygotic twin
-1st degree relative

A

-30-40%
-70-100%
-5-10%

55
Q

What are drugs in the Calcinerin inhibitor group and what are their MOA and side effect profile

A

Tacrolimus and Cyclophosphamide
MOA: inhibit IL2 transcription so T-cells cannot proliferate

Side effects:
-Cyclosporin: nephrotoxicity, hairiness, gum hypertrophy, dyslipidaemia
-Tacrolimus: nephrotoxicity, HTN

56
Q

Describe the metabolism of Azathiopurine and what affects the dosing in various populations

A

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
Q

What is the MOA of methotrexate and what is the side effect profile

A

Anti-folate/anti-metabolite

Side effect- liver injury, lung fibrosis, Bone marrow suppression

RACP EXAM (9 decks)

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