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
At histology patient presents with foamy macrophages. What's organism Is infecting these macrophages
Tropheryma whippelii WHIPPLES DISEASE
25
Explain how T. Whippelii affects macrophages
Gram-positive infection – >macrophage eat T.WHIPPELLII – >not kill only partially destroy – >organism remains @ lysosomes
26
Which layer of the mucosa does the macrophages infiltrate to? How does the infiltration of macrophages into the lamina propria affect fat absorption ?
Lamina propria Macrophages compresses thin-walled lacteals – >chylomicrons not brought in – > fat malabsorption + steatorrhoea
27
In Whipple disease what other areas of the body are infected
CNS Heart valves Sinovium of joint = arthralgia arthritis Lymph nodes of SI STEATORRHEA
28
Patient presents with arthritis cardiac valve issues CMS issues with fat malabsorption and stay at a rear what does he have? Macrophages are foamy
Wipple disease
29
Explain what Abetalipoproteinaemia is
Autosomal recessive deficiency of apolipoprotein B 48+ B100 B48 = need to make chylomicron therefore fat malabsorption B100 = absence plasmin VLDL + LDL
30
what is the most common small bowel cancer?
Carcinoid tumour
31
How does the carcinoid tumour @ small-bowel grow? | What does this polyp like nodule secrete?
Grows as a submucosal polyp like nodule that secreta serotonin into the portal vein
32
Explain the biochem and how it is not a carcinoid syndrome
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
Explain why metastasis to the liver makes the carcinoid tumour a carcinoid syndrome
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
At what point do you get carcinoid syndrome and carcinoid heart disease in carcinoid tumour of the small-bowel?
When you get metastases to the liver so that serotonin is dumped into the hepatic vein
35
What can carcinoid syndrome symptoms be triggered by?
Alcohol + emotional stress
36
Explain why patients with carcinoid tumour have right-sided fibrosis and not left-sided fibrosis Explain What Valve issues you get
Serotonin goes to the right heart – >long Long has monoamine oxidase therefore converted to 5HiAA