malabsorption Flashcards
Proximal SI absorptives?
Calcium
Iron
Folic acid
Distal SI absorptives?
Vitamin B12
Bile acids
Primary bile acids
Cholic acid
Chenodeoxycholic acid
Synthesized in the liver from cholesterol (~500mg/d)
Secondary bile acids
Deoxycholic acid
Lythocholic acid
Synthesized from primary bile acids in the intestine by bacterial enzymes.
Conjugation of BA (to what and where)
taurine
glycine
liver
terminal ileum active Na+ absorption
Deconjugation BA (how and where)
colonic bacteria
reabsorb in colon and jejunum
Fat Absorption- Intraluminal phase
Lipolysis accure from stomach to jejunum
20-30% by gastric lipase (pH 4.5-6)
70-80% in duodenum/jejunum by pancreatic lipase
Impaired lipolysis
lipase secretion reduction:
Chronic pancreatitis
cystic fibrosis
PH:
Gastrinoma
lipolysis can be maintained by 5% of max pancreatic lipase secretion
micelle structure
inner- fatty acids
intermidiate- glycerol
out- conjugated bile salts (lack of those will damage micelle formation)
Fat Absorption- Mucosal & Delivery phase
Lipids enter the enterocytes
re-esterification to triglycerides
creation of Chylomicrons: β-lipoprotein triglycerides Cholesterol phospholipids
leave by lymphatic system
Abetalipoproteinemia
Failure in chylomicron formation prevents exit of lipids
histological Lipid- laden enterocytes
Medium Chain triglycerides
coconut oil
Do not require pancreatic lipolysis as they can be absorbed intact
Absorbed more efficiently than LCTs
do not require chylomicron formation to exit
exit is via the portal vein and not via lymphatis
Short Chain Fatty Acids
primarily acetate, propionate, and butyrate
Butyrate is the primary nutrient for colonic epithel
stimulate colonic NaCl and fluid absorption
Diversion colitis
Carbohydrate Absorption
only in the small intestine
only as monosaccharides
Disaccharides & starch are digested by pancreatic amylase & brush-border disaccharidase
Na-dependent transporter (SGLT1) Absorption
Lactase deficiency
Protein Absorption
only di- and tripeptides absorption
pepsin and trypsin
disorders are rare
Trypsin
Secreted as trypsinogen by the pancreas
Activated by brush-border enzyme enterokinase
Pepsin
secreted as pepsinogen from gastric chief cells
Activates by pH < 5
Water soluble vitamins
dietary & microbiome
absorption occurs via specific carriers, mostly in the proximal SI
(except for B12)
vitamins B1-12 names
1- thiamine
2- riboflavin
3- niacin
5- pantothenic acid
6- pyridoxine
7- biotin
9- folate
12- cobalamin
C- ascorbic acid
cobalamin
bound to proteins
chewing and pepsin hydrolyz to free Cbl
stomach-
haptocorrin together are resistant to acid and pepsin digestion
upper small intestine-
trypsin and chymotrypsin release from HC
binds to intrinsic factor (synthesized by parietal cells)
resistant to digestive enzymes present in upper GI
terminal ileum-
specific receptor uptake
IF degraded in lysosome
circulation-
transcobalamin II carries Cbl to liver
Fat soluble vitamins
ADEK
incorporation into micelles => package into chylomicrons
Deficiencies can be due to fat malabsorption
iron
no excerition
10% absorbed mostly in proximal small intestine
ferrous (Fe2+) > ferric (Fe3+)
+3 to +2 by Ascorbic acid (facilitate absorption)
Water Absorption
92% small intestine, rest in colon Diffusion through membrane Water channels (aquaporins) Transporters highly dependent on Na and glucose absorption
Lactase Deficiency
Lactose is a disaccharide present in milk
lactase present at Brash- border
Primary: genetically determined
Secondary: associated with small intestine mucosal diseases (celiac, etc.)
Pernicious Anemia
Autoimmune
parietal cell destruction - prevents B12-IF complex formation
Anti-IF
Anti-parietal cells (reacts with H/K ATPase in parietal cells
Pernicious Anemia symptoms
lemon-yellow waxy pallor
symptomatic anemia
smooth tongue
neurologic deficits
Pernicious Anemia treatment
parentral B12
Hereditary Hemochromatosis
accumulation of Iron due to increased absorption
Hereditary Hemochromatosis etiology
HFE mutation => decreased Hepcidin levels => increase absorption
Hereditary Hemochromatosis treatment
phlebotomies
iron cheletors
celiac morphology
villi flattening and increased mucosal lymphocytic infiltration
celiac location
mainly the proximal small intestine
celiac trigger
Abnormal immunologic response to gliadin
Small Intestine Bacterial Overgrowth (SIBO) etiology
Anatomical stasis- diverticuli, fistulas and strictures, intestine bypass
Functional stasis- diabetic dysmotility, scleroderma
Small Intestine Bacterial Overgrowth (SIBO) cause
Colonic- type bacterial proliferation in the SI
Small Intestine Bacterial Overgrowth (SIBO) Symptoms
Diarrhea
bloating
Iron deficiency
Steatorrhea: colonic bacteria in small intestine -> deconjugation of bile acids
Macrocytic anemia: cobalamin consumption by the bacteria, Folate level is increased due to production by the bacteria
Small Intestine Bacterial Overgrowth (SIBO) Treatment
Antibiotics
Short bowel syndrome etiology
result of extensive SI resection (Crohn’s, mesenteric ischemia)
In rare cases- congenital
Short bowel syndrome symptoms depend on
length of, and identity of specific segment that was resected
Residual disease in the remaining segment
Short bowel syndrome symptoms
Multiple nutritional deficiencies
Multifactorial diarrhea
Renal calcium oxalate stones: Increased fatty acid bind calcium -> increase in free oxalate -> increased absorption
Increase in cholesterol gallstones: Decreased bile acid pool size -> cholesterol supersaturation
Gastric acid hypersecretion
Short bowel syndrome treatment
Oral rehydration solutions, MCTs, vitamin
TPN
GLP-2 analogue (Gattex, atrophy of remaining intestine)
Bariatric surgeries types
restrictive:
vertical sleeve
gastric band
malabsorptive:
roux-en-y bypass
deudenal switch
Roux-en-Y Gastric Bypass
demand daily vitamins postoperatively
Roux-en-Y Gastric Bypass deficiencies risk
Vitamin B12: low IF
fat-soluble vitamins A, D, E, and K.
Fe, B9, Ca: normally absorb mainly in duodenum & proximal jejunum.
Ca deficiency exacerbates by vitamin D deficiency
Prolonged vomiting may result in thiamine (vitamin B1) deficiency, which can lead to Wernicke’s encephalopathy
