GASTROINTESTINAL Flashcards by megan king

infant
dark green emesis
fussiness
abdominal distention

midgut volvulous
(midgut malrotation)

can cause ischaemia to SMA - proximal bowel
IMA - lower gut

duojejunal flexure, jejunal loops lie on RIGHT side
ladd bands

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in Hurschsprung disease which area of colon lacks innervation

distal colon (rectum)

NCC migrate caudally

NCC develop in foregut mesenchyme
reach proximal colon 8 weeks
reach rectum 12th week
rectum always affected

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fibrous connection between umbilicus and ileum

incomplete obliteration of vitilline duct

umbilicus and ileum (not bladder)

conditions resulting from this:
persistent vittiline duct
meckels diverticulum
vitelline sinus
vitelline duct cyst

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patent urachus

failure of allantois to obliterate

fibrous band between umbilicus and bladder (not ileum) - urine

anomaly - urachal cyst

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gene affected in Lynch Syndrome (HNPCC)

MSH2, HLH1

hereditary non polyposis colorectal cancer

**AD
mismatch repair
microsatellite instability
always involves proximal colon
321 rule : 3 family members, 2 generations, 1 relative <50yo

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nausea
bloating
occassional vomiting post meals
T2DM
delayed gastric emptying

diabetic gastroparesis

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cause of diabetic gastroparesis

nerve damage from chronic hyperglycaemia

glycosylation of axon proteins
sortibol osmotic damage to neuron

barium swallow to rule out mechaniclal bowel obstruction
adult

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atherosclerosis
abdominal pain after eating
weight loss
PAD
CAD
diminished pedal pulses

celiac or mesentierc ischaemia

reduced blood flow to small intestine
acute or chronic

acute = embolic or thrombotic arterial obstruction
chronic = atherosclerotic stenosis (SMA common)
common asssoc findings:
atherosclerotic sequalae - PAD, CAD, pedal pulses

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diverticulosis is caused by

increased luminal pressure

herniatino of mucosa and submucosa through muscularis propria

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abnormal colonic motility
high dietary intake red meat
low fiber
obesity / low physical acivity

are risk factors of

diverticulosis

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glucagon acts on hepatocytes via

cAMP
activates protein kinase
(Gs)

activation of gycogen phosphoryalse

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what rash is associated with glucagonoma

necrolytic migratory erythema

often mouth and distal exremities

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what process is occuring in the liver with a glucagonoma

partial oxidation of fatty acids

glucoagon acts on hepatocytes
glycogen stores exhauseted
relies on fat breakdown - beta oxidation

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progressive dysphagia solid -> liquid
enlarged paratracheal lymphadenopathy
chest pain
wheezing, hoarseness
weight loss, cachectic

oesophageal cancer
SCC or adenocarcinoma

adenocarcinoma (lower 2/3) - assoc with GERD, obesity, barret oeseophagus
SCC (upper 2/3) - assoc with smoking, drinking, hot liquids, strictures

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risk factors of SCC of oesophagus

smoking
drinking
hot liquids
strictures

affects upper 2/3

risk factors of andeocarcioma oesophagus

GERD
Barrett oesophagus
obesity

affects lower 1/3

what is X

increased mucosal surface area
feathered appearance
larger caliber
thicker muscular walls
longer vasa rectae
fewer arcades

jejunum

Y = ileum

cause

perforation
retroperitoneal duodenum

2-4th segment retroperitoneal
m/c duodenal ulcer perforation

acute abdo pain
peritonitis
fever
free air on RADS

perforation
(duodenal ulcer)

injury caused by anterior vs posterior wall duodenal ulcers

anterior = perforation
posterior = haemorrhage (gastroduodenal artery)

m/c cause of petic ulcer disease - duodenal

H pylori

also zollinger-ellison disease

m/c cause of petic ulcer disease - gastric

NSAIDS

LN for gastric spread:
Primary: Celiac lymph nodes
Distant spread:
Virchow’s node
Sister Mary Joseph nodule
Irish node

location of node

Primary drainage: (gastric, hepatic, splenic)
Distant spread:
(left supraclavicular)
(periumbilical)
(left axillary)

abdo pain 1hr after eating weight loss HTN ectatic aorta pairs of arteries affected?

SMA IMA | mesenteric circulation: SMA, IMA, celiac increased BF after eating ## Footnote occluson -> collaterals kick in >2 arteries affected = symptoms splenic flexure common site (watershed area) ischaemia

name the cells at B | gastric biopsy - Zollinger Ellsion Syndrome

**parietal cells** large size central nucleus intensely acidophilic cytoplasm (pink) middle region of gastric gland ## Footnote A - gastric mucous cell D - vascular endothelial cell - lining capillary E - perivascular fibroblast - dark oblong mucleus

name the cells at C

**cheif cell ** basophilic cytoplasm numerous cytoplasmic vesicles granular appearance produce pepsin ## Footnote A - gastric mucous cell D - vascular endothelial cell - lining capillary E - perivascular fibroblast - dark oblong mucleus

veins part of the **portal** **vein** system

portal vein L gastric vein splenic vein superior mesenteric vein risk oesophageal varices | L gastric drains into inferior oesophageal vein ## Footnote haematamesis occurs with rupture of varices system at risk with: **cirrhosis schistosomiasis portal venous thrombosis**

veins part of the '**hepatic** **venous** sytem' | not part of portal system

hepatic vein IVC | drain blood from liver to IVC ## Footnote can be affected in **right heart failure** can cause cardiac cirrhosis TIPS procedure (portal-hepatic stent) can reliveve portal pressure --> but cause hepatic encephalopathy - ammonia accumulation (liver not working)

cecum recieves blood supply from

**ileocolic** artery (**SMA** branch)

abdo pain, vomiting large white worms stool immegration from India high pitched hyperacrive bowel sounds cough, eosinophilic pneumonitis

ascaris lumbroides (worm) | 35cm intestinal ingestion of eggs in food/water ## Footnote hatch in intestine released larvae infiltrate intestinal wall - haematogenous spread to lung mature in lung ascend bronchi travel back down oesophagus live 2 years no autoinfection

name 2 worms with autoinfection

**enterobius vermicularis** (round worm) - perianal pruritis i.e. pin worm **strongyloides stercoralis** (round worm) - penetrate intestinal wall