Gastro Flashcards by Rachel Longwell

Physiology

What’s the difference in the myenteric and meissners plexus

Myenteric- peristalsis

Meissners- controls mucous glands

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Where is the majority of iron absorbed?

Duodenum

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

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

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Outline the major steps in CHO digestion

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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What do the following enzymes break down
Maltase
Sucrase
Lactase

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

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What happens in glucose galactose malabsorption

Where is the defect

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

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What causes fructose malabsorption

What causes hereditary fructose intolerance

Glut 2 and 5 transporter defects

AR defect of adalase B

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

Chains of amino acids

Carboxy end and nh3 end

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Proteins
Outline metabolism
What stomach enzymes induce and inhibit this

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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How can amino acids be absorbed

As single amino acids

Broker down within luminal cells via peptidases

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What are examples of monosaccharides

What are examples of polysaccharides

Glucose, galactose and fructose

Sucrose and lactulose

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

Turners and noonans
Protein and fat malabsorption
Immunoglobulins and lymphocytes

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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

Severe fat deficiency- can’t make chylomicrons 
Vitamin E deficiency
Retinitis pigmentiosa
Peripheral neuropathy 
Acanthocytes

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When we eat fats what form are they normally in?

Triglycerides

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Outline fat digestion

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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Outline fat absorption

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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What is the difference between saturated and unsaturated fats

Saturated=single bonds only

Unsaturated= double bonds

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What is different in neonates regarding fat digestion

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

Can be absorbed directly into the portal venous system

Useful for malabsorption or chylothoracies

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

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

Kasai
Before 12 weeks
Liver transplant

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

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

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What is is seen on biopsy of alagille syndrome

Bile duct paucity

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Bile duct disease

What is an example of a bile acid transporter disease

Persistent familial intrahepatic cholestasis

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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?

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

What are carbohydrates stored as in the liver

Glycogen

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

AR | Serpin1a

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

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

Jaundice | Other than haemolysis, what else can cause unconjugated hyperbili

Enzyme defects- Gilbert’s and crigler Najjar | UDP Glucuronyl transferase

What are genetic causes of conjugated hyperbili | What test will help differentiate the two?

Dublin Johnson Rotor Urinary coproporphyrin- increased in DJ, reduced in rotor

``` Wilson disease Which chromosome and gene Signs Characteristic blood test What happens to serum copper Diagnostic test ```

``` 13 ATP7B Neuropsychiatric- early Parkinson’s, liver failure, KF rings AST:ALT ratio 4:1 Raised or decreased Caeruloplasmin- low ```

Wilson’s First line chelation therapy Other useful treatments

Penicillamine | Zinc EDTA

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

Smooth muscle and ANA Liver kidney 2

Does hepatitis A normally cause liver failure? | How should you be treated if post exposure

No | Vaccine plus IG

``` Hepatitis B What antibodies/antigens are seen: - vaccinated - active infection - active replication - past infection ```

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

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

Granotti crosti | Salmon pink papules to face and buttocks

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

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

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

Cirrhosis and HCC | YES

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

IL10 | Immunodeficiencies

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

Patchy anywhere from mouth to anus, glanulomas, transmural, strictures and fistulae. Spares rectum Can have perianal disease Growth faltering More! NOD 2

What is the general pattern of inflammation in UC | Which ANCA is likely to be positive

Pancolitis Patchy, mucosal, no granulomas P ANCA

What 2 rashes are commonly seen in Crohn’s disease

Erythema nodosum | Pyoderma gangrenosum

What is faecal calprotectin a marker of? | What does it correlate severity of

Neutrophil derived inflammation | UC not CD

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

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

What is the main cause of intestinal damage in coeliac disease

Unchecked activation of T lymphocytes

How do infilximab and adalimumab compare and differ

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

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

HLA d2 and 8 All need a biopsy No No

Coeliac disease | What might you seen in the stool

Fatty acid crystals and raised reducing substances (general malabsorption)

What 3 syndrome last does coeliac disease associate with

Downs turners and Williams

What rash is associated with coeliac disease ? | If found alone is it diagnostic?

Dermatitis herpeteformis | Yes

Other than coeliac disease what can cause villlous atrophy

``` Giardia and rotavirus Whipples Soy milk and protein intolerance Eosinophilic gastritis Lymphoma GVHD ```

What is the most common type of oesophageal atresia

OA with distal TOF

Where are iron magnesium and calcium mainly absorbed

Duodenum and jejunum

What is the main physiological cause of reflux?

Transient lower eosophageal sphincter relaxation

What is the most likely causative agent in EOE | How many eosinophils are needed to be seed on microscopy

Milk | >20 per high powered field

How do PPIs work?

Bind to the HKATPase pump

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

Side on=tracheal | End on=oesophageal

What do the fore mid and hindgut make up? | When does the primatove gut start to develop

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

Where is intrinsic factor secreted from?

Parietal cells of the body of the stomach

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

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

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

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

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

Gram neg bacillus | Gastritis, peptic ulcers (mostly duodenal) and cancer- mostly lymphoma or adenocarcinoma

``` 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? ```

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

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

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

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

Coca Cola

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

Positive reducing substances, fat and fat crystals | Low stool PH

Are antibiotics recommended with shigella infection

Yes

How might yersinia present

Pseudo appendicitis

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

RET Rectal suction biopsy Downs. Ondine’s curse

``` Peutz jeghers syndrome Inheritance Gene Findings When does cancer surveillance start ```

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

FAPC Inheritance When do polyps start Screening

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

Secretory and osmotic diarrhoea How do they differ Examples of each

Secretory- low osmotic gap, high volume, persists with fasting. CF. Channel pump disorders Osmotic- high osmotic gap, improves with fasting. Coeliac, lactose intolerance

What can pyloric atresia be associated with

Epidermolysis bullosa

What rash is associated with zinc deficiency

Acrodermatitis enteropathica

What is the usual defect in malrotation

Counterclockwise rotation 270deg around sup mesenteric artery

What are the 3 most common genes associated with pancreatitis in children What is the difference between swachmann diamond syn and Pearson syn

PRSS 1 SPINK 1 CFTR SD- BM failure Pearson- sideroblastic

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

Around 80%

How much calories per gram of: Fat Carb Protein

Fat-9 | Protein and carb- 4

``` 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 ```

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

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

Intestinal protein loss Poor digestion- GB or pancreas issue malabsorption

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

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

``` 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 ```

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

Where is b12 absorbed | What does the colon secrete

Terminal ileum | Potassium and bicarb

What structures form from the foregut midgut and hindgut | What is the blood supply

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

Which vascular lesions can cause oesophageal obstruction

Double aortic arches and aberrant right subclavian

How beneficial is EEN at inducing remission in IBD

80%

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?

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

What is the triad of swachmann diamond syndrome

Short stature, pancreatic insufficiency and bone marrow failure

What persists to cause a meckels | What is the rule of 2s

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

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

1 low GGT and less severe than 2 3 high GGT Obstetric cholestasis AR

IPEX syndrome What gene is abnormal What is commonly seen

FOXP3 gene | Early diabetes, severe diarrhoea and dermatitis

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

Lipid content Omega 3 is kinder Ursodeoxycolic acid

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

Short bowel syndrome | Reduce TPN requirements. Increase villus height

How does citrulline associate with small bowel mass

Low in short bowel syndrome. Correlates to severity

What is goats milk low in?

Folate

Gastro Flashcards

(95 cards)