Gastro Flashcards
(42 cards)
Which vitamin deficiency?
Macrocytic anaemia, elevated homocysteine, peripheral neuropathy, memory loss, cognitive defects
Causes?
B12 cobalamin
Animal source - strict vegans (Inc breastfed)
Ileal resection
Crohn’s
Pernicious anaemia
Deficiency in Vit B9
Folate
Macrocytic anaemia, elevated homocysteine, deficiency in pregnancy women causes birth defects
Which vitamin deficiency?
Pellagra.
Aggression, dermatitis, insomnia, weakness, mental confusion, diarrhoea
Sources?
Causes?
Niacin B3
Three Ds” - dermatitis, diarrhoea, dementia
In advanced cases pellagra causes dementia and death
Milk and eggs
Malabsorptive diseases, anorexia nervosa
Alcoholism, prolonged Isoniazid therapy
Which vitamin deficiency?
Ariboflavinosis
Cheilosis, high sensitivity to sunlight, angular cheilitis, glossitis, dermatitis or pseudo syphilis or pharyngitis
Source?
Causes/prevelance
Riboflavin B2
Meat, Fish, eggs, milk, yeast, vegetables
Prolonged phototherapy in Prems
High prevalence in adolescent females
Low socioeconomic status
Which vitamin deficiency?
Beriberi (what is it?)
Wright loss, emotional disturbances, Wernicke’s encephalopathy (impaired sensory perception), weakness and pain in limbs, arrythmias, oedema
Source?
Thiamin B1
Infantile Beriberi - congestive heart failure, neuritis, hoarseness or aphonia, absence of deep tendon reflexes anorexia
Yeast, legumes, meat, milk, Vegetables
Treatment of Wilson’s disease
Common first line - D penicillamine
Penicillamine can chelate heavy metals such as lead, copper, and mercury and form a soluble complex that is renally excreted in the urine.
It is an α-amino acid metabolite of penicillin, although it has no antibiotic properties.
Trientene is an alternative option.
Zinc salts may also be used to bind intestinal copper
First line induction therapy of Crohn’s with pancolitis and terminal ileitis without perianal disease
Exclusive enteral nutrition
Shown to have high mucosal healing rates than steroids with comparable rates of clinical remission
EEN required dedicated patient and family
Steroids used if EEN not feasible
First line therapy for mild Crohn’s disease after successful induction therapy
Methotrexate or azathioprine
Mtx is generally avoided in post pubertal girls as it is a folate antagonist
Mechanism of absorption of Fructose
Absorbed directly via the brush border of the small intestine, after absorption it enters the hepatic portal vein and is directed toward the liver
Transport across into cell by GLUT5 in apical membrane and out of cell by GLUT2 via basement membrane into blood vessel (Na independent facilitated diffusion)
Note: as sucrose comes into contact with small intestine the enzyme sucrase catalyses the cleavge of sucrose into 1 X glucose and 1x fructose
Mechanised of absorption of glucose/galactose in small intestine
SGLT 1 Na/K ATPase transporters in intestine and exits cell via GLUT2
SGLT = sodium glucose linked transporter
Complications of Hep A infection
Uncommon - pancreatitis, acute liver failure (older patients), prolonged cholestatic syndrome with fat malabsorption for months
Type 1 autoimmune hepatitis
Symptoms
Bloods
10-20yo, 78% F
Hepatic encephalopathy, coagulopathy, jaundice
Anti SMA, ANA, pANCA
Pronounced IgG increase, IgA normal
Associations HLA B8, DR3, DR4
Good prognosis
Type 2 autoimmune hepatitis
Age
SX
Bloods
Associations
2-14yo, 89% F
antiLKM1 antibodies
Moderate IgG increase, occasional IgA decrease
HLA B14, DR3
IgA deficiency
More aggressive and higher relapse rates that classical type 1
Ix for Meckel’s diverticulum
99mTachnetium pertechnetate scan
Mucous secreting cells of the ectopic gastric mucosa take up pertechnetate, permitting visualisation of Meckel diverticulum
Sensitivity 85% specificity 95%
RET gene
Hirshsrpungs disease
Also associated with EDNRB, andEDN3genes
DG551D
Cystic fibrosis
Less common than F508
JAG1
Alagille syndrome
Also associated with NOTCH2
ATP7B gene
Wilson’s disease
Congenital sucrase-isomaltase deficiency
- gene, inheritance
- pathophysiology
- presentation
- Ix
SI gene, autosomal recessive
Unable to break down disaccharides: sucrose (fruit/table sugar) and maltose (grains)
Sx appear after infant begins consuming fruit/juice/grains
After consumption -> stomach cramps, bloating, excessive gas production, diarrhoea.
Can have explosive watery diarrhoea leading to dehydration
Can have malnutrition and FTT
Tissue Bx: disaccharidase assay
Sucrose hydrogen breath test
Stool - increase total sugars. Low reducing sugars (monosaccharides)
Helicobacter pyloriincreases risk of which malignancies
Epidemiology studies have shown that individuals infected withH. pylorihave an increased risk of gastric adenocarcinoma. Studies have also shown that individuals infected withH. pylorihave an increased risk of gastric mucosa-associated lymphoid tissue (MALT) lymphoma, a rare cancer of the stomach. Gastric MALT lymphoma is frequently associated (72-98%) with chronic inflammationas a result of the presence ofH.pylori.
Conversely, risk of oesophageal adenocarcinoma may be reduced inH. pylori-infected individuals.
acute hepatic GVHD
LFTs/Bili?
Timeline
aminotransferase levels may rise markedly in the absence of elevated bilirubin, ALP, and GGT levels, mimicking viral hepatitis.
Acute hepatic GVHD can present both early (days 14–21) and late (>day 70) after allogeneic SCT.
Chronic hepatic GVHD blood picture
In chronic hepatic GVHD, serum aminotransferase levels are not as markedly elevated and cholestasis is more prominent with marked rises in serum conjugated bilirubin, GGT, and ALP levels.
Veno-occlusive disease clinical picture
VOD or SOSsecondary to sinusoidal endothelial damage and subsequent thrombotic/fibrotic occlusion of hepatic sinusoids and venules. There is a clinical syndrome of:
Jaundice and hyperbilirubinaemia
Right upper quadrant pain, generally with tender hepatomegaly.
Weight gain and ascites
What is absorbed in the Duodenum and proximal jejunum
Ca, Mg, PO4, iron, folic acid.