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GI Liver > Small-Bowel > Flashcards

Small-Bowel Flashcards

0
Q

Why does patient have polyhydramnios in duodenal atresia

A

Amnion fluid = swallowed + digestive by baby to decrease volume up a lot of fluid

If it can’t be digestive to atresia and get polyhydramnios a baby can’t pass it through rest of gut

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1
Q

What is duodenal atresia

What genetic condition is it associated with?

A

Congenital failure Of small bowel to canalise

Assoc with DOWNS

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2
Q

Give three clinical features of duodenal atresia

A

Double BiPolo

1.polyhydramnios

2.buildup of food @tract – > end@ blind loop – >
bile come in from duodenum – >
regurgitate out = bilious vomiting

  1. Double bubble sign = stomach + duodenum distension
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3
Q

What is Meckel’s true diverticulum

A

Failure vitelline duct to involute completely

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4
Q

What is a true Diverticulum

A

Outpouching of all three layers of bowel wall

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5
Q

At a clinical examination under the umbilicus you feel something firm but soft what is this?
What are the rule of 2’s?

A

Stool

FITY%!!!
2 Feet from ileocecal valve
2 Inches
2 Types = gastric + pancreatic
first 2 Years of life
2% of pop – most common anomaly of GI tract
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6
Q

Presentation of Meckels Diverticulum

A

BIVO

Bleeding, intussusception, volvulus, obstruction near terminal Ilium

RLQ pain, Melena

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7
Q

What is a volvulus?
What can it lead to?
Where are the common locations of volvulus in adults + infants/children

A

Twisting of bowl along mesentery

Obstructed bowel, decreased blood supply
– > infarction

@Adults = SIGMOD colon
@Infants/children = midgut – Caecum
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8
Q

Define intussusception

Explain how intussusception occurs

A

Telescoping proximal segment of bowel into distal segment

there’s something peristalsis hooks on to + grabs bowel + drags it forward–>
Bowel dragged along direction of peristalsis – >drag blood supply = infarction – > currant jelly stools

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9
Q

What is the leading edge i.e. underlying cause that allowed bowel to get dragged forward?

A

Idiopathic/Kid gets a viral infection – >

lymphoid hyperplasia –> wall thickens – >

terminal ileum = dragged to cecum

In adults = tumour pulled into the lumen

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10
Q

What are the two types of small-bowel infarction and how can they occur?

SYMPTOMS?!?!?!???

A

Transmural infarction:

Vasculitis (polyarteritis nodosa) + AF – >
thrombosis/embolism of artery = SMA

Lupus anticoagulant/polycythaemia vera – > thrombosis of vein

Mucosal infarction:

Hypotension – >decrease BF slightly – >mucosa furthest away from blood supply = ischaemic

Abdominal pain, Decreased bowel sounds,
bloody diarrhoea = redcurrant jelly stools

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11
Q

What are the three types of lactose intolerance is?

A

Primary = absence of lactase persistence allele
@Asian African Native American

Secondary = gastroenteritis(rotavirus) + AI disease
– > Lose brush border (lactase @ tips of villi)

AR Congenital lactase deficiency = rare due to defective gene

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12
Q

What does the stool, the breath, And lactose intolerance test show?

A

Stool = decreased PH

Breath = Increased hydrogen content with LI test

LI test = lactone administration – >
abdominal distension + serum glucose increases by less than 20

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13
Q

What is coeliac disease?

A

Auto immune-mediated damage of small-bowel villi

due to intolerance to Gliadin @gluten @wheat + grain

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14
Q

What are the genes involved in coeliac?

A

7 + 3 = 10
Coeliac HSR

HLA– DQ(2 +8)

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15
Q

How is the Gliadin transformed in the gut?

Explain how deamidated Gliadin results in tissue damage?

A

Gilead then the amidated by
tissue trans gut aminase

Deamidated Gliadin = presented by APCs via MHC2– >

T-helper cell mediates tissue damage -
⬆️p(T-cell lymphoma)

16
Q

How do children and adults present with coeliac disease ?

A

@Kids = abdominal distension + diarrhoea

@Adults = bloating + chronic diarrhoea

17
Q

How does a patient at celiac disease get herpetiformis dermatitis

A

Get IgA deposition at dermal papillae tips – > destroy connection between dermis and epidermis = blister/Vesicle

18
Q

Lab findings of coeliac disease?

A

BAAA(get)LD

BBBBBlunt/flat villi + crypt hyperplasia

– auto IgA against Gliadin

– auto IgA against Endomysium

– auto IgA against Tissue transglutaminase

LLLLymphocytes @ lamina propria
⬇️bone DDDDDDensity

19
Q

What do you know about IgA concentration in coeliac disease patients?
What else do we check for instead?

A

IgA deficiency

Check for IgG

20
Q

What does the duodenal biopsy show?

Where does damage occur in the bowel in coeliac disease

A

Flattening of the villi +
hyperplasia of crypts +
intraepithelial lymphocytes @ lamina propria

Damage: duodenum >jejunum + ileum

21
Q

Patient presents with refractory coeliac disease despite claiming food dietary control in terms of gluten. What’s the differential diagnosis?

A

– Small bowel carcinoma

T-cell lymphoma/EATL = Enteropathy associated T-cell lymphoma

22
Q

What is tropical sprue due to ?

A

Unknown organism – >damage to small-bowel villi

– >malabsorption

23
Q

What is the difference between tropical sprue and coeliac disease ?

A

TIJA

TS @tropical regions

Infectious diarrhoea – >TS

Jejunum (folic acid) deficiency) + Ilium(vitB12 deficiency >duodenum

respond to Antibiotics

24
Q

At histology patient presents with foamy macrophages. What’s organism Is infecting these macrophages

A

Tropheryma whippelii WHIPPLES DISEASE

25
Q

Explain how T. Whippelii affects macrophages

A

Gram-positive infection – >macrophage eat T.WHIPPELLII – >not kill only partially destroy
– >organism remains @ lysosomes

26
Q

Which layer of the mucosa does the macrophages infiltrate to?

How does the infiltration of macrophages into the lamina propria affect fat absorption ?

A

Lamina propria

Macrophages compresses thin-walled lacteals – >chylomicrons not brought in – >
fat malabsorption + steatorrhoea

27
Q

In Whipple disease what other areas of the body are infected

A

CNS

Heart valves

Sinovium of joint = arthralgia arthritis

Lymph nodes of SI

STEATORRHEA

28
Q

Patient presents with arthritis cardiac valve issues CMS issues with fat malabsorption and stay at a rear what does he have? Macrophages are foamy

A

Wipple disease

29
Q

Explain what Abetalipoproteinaemia is

A

Autosomal recessive deficiency of apolipoprotein B 48+ B100

B48 = need to make chylomicron therefore fat malabsorption

B100 = absence plasmin VLDL + LDL

30
Q

what is the most common small bowel cancer?

A

Carcinoid tumour

31
Q

How does the carcinoid tumour @ small-bowel grow?

What does this polyp like nodule secrete?

A

Grows as a submucosal polyp like nodule that secreta serotonin into the portal vein

32
Q

Explain the biochem and how it is not a carcinoid syndrome

A

Secretes serotonin into PV – >going to liver – >
MAO converts serotonin 5HIAA – >Excrete at urine

Not carcinoid syndrome as serotonin Does not going to the systemic circuit ie all serotonin is destroyed by the liver

33
Q

Explain why metastasis to the liver makes the carcinoid tumour a carcinoid syndrome

A

Serotonin dumped into the hepatic vein via portosystemic shunt’s which can get into the systemic circuit

Bronchospasm, diarrhoea, flushing of skin = carcinoid Syndrome

34
Q

At what point do you get carcinoid syndrome and carcinoid heart disease in carcinoid tumour of the small-bowel?

A

When you get metastases to the liver so that serotonin is dumped into the hepatic vein

35
Q

What can carcinoid syndrome symptoms be triggered by?

A

Alcohol + emotional stress

36
Q

Explain why patients with carcinoid tumour have right-sided fibrosis and not left-sided fibrosis

Explain What Valve issues you get

A

Serotonin goes to the right heart – >long

Long has monoamine oxidase therefore converted to 5HiAA

GI Liver (11 decks)

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