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FRACP > Gastro > Flashcards

Gastro Flashcards

1
Q

Physiology

What’s the difference in the myenteric and meissners plexus

A

Myenteric- peristalsis

Meissners- controls mucous glands

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2
Q

Where is the majority of iron absorbed?

A

Duodenum

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3
Q

Carb physiology
What are the 2 major forms of starch and how do they differ
What else can make up starch

A

Amylose- has 1,4 bonds only
Amylopectin has 1,4 and 1,6 bonds
Glycogen

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4
Q

Outline the major steps in CHO digestion

A

Chewed in the mouth. Some amylase action- partial hydrolysis
Nothing but churning in the stomach
Most happens in the small intestine-pancreatic amylase causes hydrolysis
Brush border enzymes break into glucose

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5
Q

What do the following enzymes break down
Maltase
Sucrase
Lactase

A 
Maltase= Maltose- 2xglucose 
Sucrase= Sucrose- glucose and fructose
Lactase= Lactose- glucose and galactose
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6
Q

What happens in glucose galactose malabsorption

Where is the defect

A

Glucosuria and reducing substances in the urine on breast milk introduction
Na glucose channel

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7
Q

What causes fructose malabsorption

What causes hereditary fructose intolerance

A

Glut 2 and 5 transporter defects

AR defect of adalase B

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8
Q

Protein absorption
What are proteins made up of
What are the 2 ends

A

Chains of amino acids

Carboxy end and nh3 end

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9
Q

Proteins
Outline metabolism
What stomach enzymes induce and inhibit this

A

Chewed in the mouth
Pepsinogen goes to pepsin in the stomach and breaks peptide bonds
Pancreatic enzymes induced by enterokinase
Trypsinogen to trypsin which allows all other enzymes to work within the duodenum

Gastrin and secretin. Somatostatin inhibits

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10
Q

How can amino acids be absorbed

A

As single amino acids

Broker down within luminal cells via peptidases

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11
Q

What are examples of monosaccharides

What are examples of polysaccharides

A

Glucose, galactose and fructose

Sucrose and lactulose

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12
Q

Lymphangiectasia
What two syndromes is it associated with
What is it
What two other things will be low

A

Turners and noonans
Protein and fat malabsorption
Immunoglobulins and lymphocytes

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13
Q 
Abetalipoproteinaemia 
What is it? 
What is a common complication
What eye disorder is seen
What nero signs are there 
What is seen on blood film
A 
Severe fat deficiency- can’t make chylomicrons 
Vitamin E deficiency
Retinitis pigmentiosa
Peripheral neuropathy 
Acanthocytes
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14
Q

When we eat fats what form are they normally in?

A

Triglycerides

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15
Q

Outline fat digestion

A

Emulsified in the stomach
Broken down by pancreatic lipases in small intestine to free fatty acids
Combine with bile salts to form mixed micelles

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16
Q

Outline fat absorption

A

Free fatty acids enter cells
Back to triglycerides
Form a chylomicron
Go to the lymphatic system then to the blood via thoracic duct

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17
Q

What is the difference between saturated and unsaturated fats

A

Saturated=single bonds only

Unsaturated= double bonds

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18
Q

What is different in neonates regarding fat digestion

A

Have stomach and linguine lipase that can work in the stomach and break down short and medium fas which is more common in milk

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19
Q

What is different about medium fatty acid metabolism and why is this useful?

A

Can be absorbed directly into the portal venous system

Useful for malabsorption or chylothoracies

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20
Q 
Biliary atresia 
What will syndromic BA have? 
Does it normally associate with IUGR?
What is seen on ultrasound? 
What is seen on biopsy?
A

Congenital heart disease and poly/asplenia
No!
Contracted bile duct. Dilated ports hepatis
Black pigment and reversal of hepatic artery to vein ratio

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21
Q

Biliary atresia
What surgical procedure is performed
When is it best preformed
What is the ultimate treatment

A

Kasai
Before 12 weeks
Liver transplant

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22
Q

Alagille syndrome
What are the 2 common genetic forms
What phenotypically is seen

A

JAG 1, NOTCH2
Normal if Notch 2, otherwise triangle face, broad forehead, posterior embryotoxin, butterfly vertebrae, peripheral pulmonary stenosis

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23
Q

What is is seen on biopsy of alagille syndrome

A

Bile duct paucity

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24
Q

Bile duct disease

What is an example of a bile acid transporter disease

A

Persistent familial intrahepatic cholestasis

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25
Q

Paracetamol overdose
What are 3 examples of potentially toxic ingestions
When after ingestion should the level be taken
When should NAC be started?
What is the toxic metabolite that builds up?
What does NAC do?

A 
>10g, >200mg/kg, staggered subtheraputic overdoses 
4 hrs 
Before 8 hrs 
NAPQI 
Restores glutathione
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26
Q

What are carbohydrates stored as in the liver

A

Glycogen

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27
Q

Alpha 1 AT DEF
What is the inheritance
What is the gene

A

AR

Serpin1a

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28
Q

Alpha 1 AT def
What is the normal function of the protein
What is the severe form called- what happens
When does lung disease typically present
How should family members be screened

A

To prevent lung damage against neutrophil elastase
ZZ disease- hepatocytes cant secrete the protein
Adolescence or adulthood
Screen alpha 1 AT Levels

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29
Q

Jaundice

Other than haemolysis, what else can cause unconjugated hyperbili

A

Enzyme defects- Gilbert’s and crigler Najjar

UDP Glucuronyl transferase

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30
Q

What are genetic causes of conjugated hyperbili

What test will help differentiate the two?

A

Dublin Johnson
Rotor

Urinary coproporphyrin- increased in DJ, reduced in rotor

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31
Q 
Wilson disease 
Which chromosome and gene 
Signs 
Characteristic blood test 
What happens to serum copper 
Diagnostic test
A 
13 ATP7B
Neuropsychiatric- early Parkinson’s, liver failure, KF rings 
AST:ALT ratio 4:1
Raised or decreased 
Caeruloplasmin- low
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32
Q

Wilson’s
First line chelation therapy
Other useful treatments

A

Penicillamine

Zinc EDTA

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33
Q

Types of autoantibodies-
Autoimmune hepatitis 1
Autoimmune hepatitis 2
Which type is more common in kids?

A

Smooth muscle and ANA
Liver kidney
2

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34
Q

Does hepatitis A normally cause liver failure?

How should you be treated if post exposure

A

No

Vaccine plus IG

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35
Q 
Hepatitis B 
What antibodies/antigens are seen:
- vaccinated 
- active infection
- active replication 
- past infection
A

Anti HepB s
Hep b S
Hep b E
Anti s and c

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36
Q

What rash is found in kids with active hep b. What does it look like?

A

Granotti crosti

Salmon pink papules to face and buttocks

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37
Q

Hepatitis B
What phase is treatment normally targeted
What meds are given
How do you manage an infant with a mum with active infection
What other infection can occur simultaneously

A

Clearance phase- chronic active hepatitis
Interferon alpha and nucleoside analogues- combination therapy
Give vaccine and IG
Hep D

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38
Q

Hepatitis C
What are the main complications
Is breast feeding safe?

A

Cirrhosis and HCC

YES

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39
Q

Early onset IBD
Which IL is commonly associated?
What else is commonly seen

A

IL10

Immunodeficiencies

40
Q

What is the general pattern of inflammation in Crohn’s disease

What might the first signs of disease be?

Are systemic features and extra intestinal disease more or less likely than UC

What gene defect is seen most commonly

A

Patchy anywhere from mouth to anus, glanulomas, transmural, strictures and fistulae.
Spares rectum
Can have perianal disease

Growth faltering

More!

NOD 2

41
Q

What is the general pattern of inflammation in UC

Which ANCA is likely to be positive

A

Pancolitis
Patchy, mucosal, no granulomas
P ANCA

42
Q

What 2 rashes are commonly seen in Crohn’s disease

A

Erythema nodosum

Pyoderma gangrenosum

43
Q

What is faecal calprotectin a marker of?

What does it correlate severity of

A

Neutrophil derived inflammation

UC not CD

44
Q

Azathioprine
How does it work
Why do metabolites need to be monitored
How is it monitored and what does the results indicate
What can be given to help
What should be checked prior to starting and what indicates not to start it
What is the risk of lymphoma

A

Direct action of T cells
Changed in the liver to 6MCP. Can cause BM Suppression
6TG levels- low= possible poor compliance. High= toxicity possible
Allopurinol
TMPT status- if heterozygous or homozygous don’t give
4x general ppn

45
Q

What is the main cause of intestinal damage in coeliac disease

A

Unchecked activation of T lymphocytes

46
Q

How do infilximab and adalimumab compare and differ

A

Both anti TNF alpha
Inflix is IV, Ada is SC
Ada is humanised

47
Q

What test has the best negative predictive value in coeliac disease- HLA or anti TTG
How is diagnosis in diabetes different?
Do you need symptoms to make a diagnosis
Do you need a biopsy of positive HLA and antibodies x2

A

HLA d2 and 8
All need a biopsy
No
No

48
Q

Coeliac disease

What might you seen in the stool

A

Fatty acid crystals and raised reducing substances (general malabsorption)

49
Q

What 3 syndrome last does coeliac disease associate with

A

Downs turners and Williams

50
Q

What rash is associated with coeliac disease ?

If found alone is it diagnostic?

A

Dermatitis herpeteformis

Yes

51
Q

Other than coeliac disease what can cause villlous atrophy

A 
Giardia and rotavirus 
Whipples 
Soy milk and protein intolerance 
Eosinophilic gastritis 
Lymphoma 
GVHD
52
Q

What is the most common type of oesophageal atresia

A

OA with distal TOF

53
Q

Where are iron magnesium and calcium mainly absorbed

A

Duodenum and jejunum

54
Q

What is the main physiological cause of reflux?

A

Transient lower eosophageal sphincter relaxation

55
Q

What is the most likely causative agent in EOE

How many eosinophils are needed to be seed on microscopy

A

Milk

>20 per high powered field

56
Q

How do PPIs work?

A

Bind to the HKATPase pump

57
Q

Swallowed coins, how do you tell if they’re in the trachea or oesophagus?

A

Side on=tracheal

End on=oesophageal

58
Q

What do the fore mid and hindgut make up?

When does the primatove gut start to develop

A

From 4 weeks
Fore- until the cbd insertion at the duodenum
Mid- until mid transverse colon
Hind- until anal canal

59
Q

Where is intrinsic factor secreted from?

A

Parietal cells of the body of the stomach

60
Q

What are the three hormones the stomach secretes? What do they do

A

Gastric- increased acid secretion and motility.
Somatostatin- inhibits gastrin and insulin
Pepsinogen- cleaved to pepsin and useful
Digestive hormone

61
Q

Pyloric stenosis
What factors make it more likely
What medication can cause it

A

B and O blood groups
Son of a mum who had it
Erythromycin

62
Q

H pylori
What type of bacteria is it?
What three things does it cause?

A

Gram neg bacillus

Gastritis, peptic ulcers (mostly duodenal) and cancer- mostly lymphoma or adenocarcinoma

63
Q 
H pylori 
How does it usually present in kids
What is the best diagnostic test? 
What is used to monitor treatment effect? 
What is the treatment?
A

Non specific abdominal pain
Gastroscopy plus biopsy
Urease breath test
Amox, Clari and ppi for 2 weeks

64
Q

What usually causes zollinger Ellison syndrome
What is it associated with
How is it diagnosed

A

Gastrinoma
TS and NF1
Non healing ulcer with high fasting gastrin levels

65
Q

What might be useful for a plant (phyto) bezoar?

A

Coca Cola

66
Q

What is likely to be found in the stools of lactose intolerance

A

Positive reducing substances, fat and fat crystals

Low stool PH

67
Q

Are antibiotics recommended with shigella infection

A

Yes

68
Q

How might yersinia present

A

Pseudo appendicitis

69
Q

What is the genetic association with hirschsprung disease
What is the gold standard investigation.
What syndromes make it more likely

A

RET
Rectal suction biopsy
Downs. Ondine’s curse

70
Q 
Peutz jeghers syndrome
Inheritance 
Gene 
Findings 
When does cancer surveillance start
A

AD
STK11
Mucocutaneous pigmentation, small intestinal polyps and increased malignancies- breast and reproductive
8 yrs

71
Q

FAPC
Inheritance
When do polyps start
Screening

A

AD
Adolescence. Multiple polyps with 100% malignant change
Annual colonoscopy

72
Q

Secretory and osmotic diarrhoea
How do they differ
Examples of each

A

Secretory- low osmotic gap, high volume, persists with fasting. CF. Channel pump disorders

Osmotic- high osmotic gap, improves with fasting. Coeliac, lactose intolerance

73
Q

What can pyloric atresia be associated with

A

Epidermolysis bullosa

74
Q

What rash is associated with zinc deficiency

A

Acrodermatitis enteropathica

75
Q

What is the usual defect in malrotation

A

Counterclockwise rotation 270deg around sup mesenteric artery

76
Q

What are the 3 most common genes associated with pancreatitis in children

What is the difference between swachmann diamond syn and Pearson syn

A

PRSS 1
SPINK 1
CFTR

SD- BM failure
Pearson- sideroblastic

77
Q

How successful is EEN at inducing remission in Crohn’s disease

A

Around 80%

78
Q

How much calories per gram of:
Fat
Carb
Protein

A

Fat-9

Protein and carb- 4

79
Q 
Smith lemil opitz syndrome 
What causes the disease 
How phenotypically do they present 
What GI and neuro issues do they have
What is the diagnostic test 
What may be useful to treat
A

Reduced 7 dehydroxycholesterol resuctase enzyme
Microcephaly with fused fingers and toes
Bowel obstruction and pyloric stenosis
Cataracts seizures and hypotonia
Increased serum DOC
Cholesterol supps and simvastatin

80
Q

Stool interp
What does alpha 1AT show
What do fatty globules show? Crystals

A

Intestinal protein loss
Poor digestion- GB or pancreas issue
malabsorption

81
Q

Stool interp

What is a low stool ph? What does it show? What test should be done next. What level are you looking for

A

<5.3
Fermentation- CHO malabsorption so monosacchiarides and disaccharides are in the stool
Looking for reducing sugars- >0.5% or 2+

82
Q 
Stool interp 
How do you calculate stool osmolality 
What is normal
What does high indicate 
What does low indicate 
What does high na indicate- what is high 
What does high cl indicate- what is high
A

290 -2(na + k)
50-100
Osmotic- can’t absorb
Secretory- secreting too many electrolytes

High na- secretory diarrhoea- above 70
High cl- congenital chloride losing diarrhoea- above 20

83
Q

Where is b12 absorbed

What does the colon secrete

A

Terminal ileum

Potassium and bicarb

84
Q

What structures form from the foregut midgut and hindgut

What is the blood supply

A

Fore- until duodenum (where bile duct enters) - coeliac artery
Mid- until transverse colon- sup mesenteric artery
Hind- until anus- inf mesenteric artery

85
Q

Which vascular lesions can cause oesophageal obstruction

A

Double aortic arches and aberrant right subclavian

86
Q

How beneficial is EEN at inducing remission in IBD

A

80%

87
Q

How is azathioprine metabolised
Why should TMPT test be done before. When should it not be given? When should 50% dose be given instead?
What is the active form called. What do low levels show? High levels?

A

To 6MP in liver then 6TG
To ensure can break down 6MP. Homozygote- don’t give. Hetero 50% dose
6TG. Low is poor compliance. High- potentially toxic- give allopurinol

88
Q

What is the triad of swachmann diamond syndrome

A

Short stature, pancreatic insufficiency and bone marrow failure

89
Q

What persists to cause a meckels

What is the rule of 2s

A

Vitelline duct

2% ppn. Men to women 2:1. 2 fr from IC valve and 2 inches long

90
Q

How do you differentiate between the 3 types of PFICC
What might be seen in the obstetric history
What is the inheritance

A

1 low GGT and less severe than 2
3 high GGT

Obstetric cholestasis
AR

91
Q

IPEX syndrome
What gene is abnormal
What is commonly seen

A

FOXP3 gene

Early diabetes, severe diarrhoea and dermatitis

92
Q

What is the main cause of liver disease in TPN usage?
What is better soy or fish oil
What medication might be useful in treatment

A

Lipid content
Omega 3 is kinder
Ursodeoxycolic acid

93
Q

GLP2 analogues
What are they used for
What do they help? How?

A

Short bowel syndrome

Reduce TPN requirements. Increase villus height

94
Q

How does citrulline associate with small bowel mass

A

Low in short bowel syndrome. Correlates to severity

95
Q

What is goats milk low in?

A

Folate

FRACP (23 decks)

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