27b. Maldigestion, Malabsorption Flashcards
How does mannitol work to prep the bowel?
It’s one of the sweeteners that doesn’t increase blood glucose as much as sucrose (has low glycemic index). Used as a sweetener for diabetic foods.
It is poorly digested in the small bowel, so it travels to the colon
At the colon, bacteria would transform it into short chain fatty acids (SCFAs) if they could, but they cannot so it ferments and produces CO2, H2, CH4.
Also causes osmotic diarrhea.
Rather than mannitol prep (which can cause explosion in bowel if cautery used), what would be safer to use?
Polyethylene glycol prep
CO2 insufflation rather than room air
Why might 2 people, after eating exactly the same things and getting the same E Coli, have different abilities to digest lactose a few weeks later?
Lactase is an enzyme in the brush border: a defect can be acquired or primary.
May be reversible.
Lactase deficiency is more common in african, asian, south american people so an injury like E Coli would affect them more than a N European whitey.
Why would people become lactose intolerant but not intolerant of sucrose or maltose?
- Lactase activity normally decreases after postnatal weaning
- Two enzymes hydrolyze maltose (have a backup plan for maltose)
- Sucrase (digests sucrose) is regulated by ingestion of food
- People are highly susceptable to acquired lactase deficiency after GI infections or inflammation.
What happens when lactase-deficient people consume lactose?
- water moves into the lumen of the small intestine due to osmolar effect of non-absorbed lactose
- significant increase in osmoles in small bowel: 1 mol Lactose is fermented to 4 mol lactate + 4 mol protons by bacteria
- also water, Co2, methane, H2 are produced by fermentation
In a normal person, what happens with serum glucose and breath H2 after consuming lactose?
Plasma glucose rises after glucose or lactose ingestion
H2 excreted by lungs is low
In a lactase-deficient person, what happens with serum glucose and breath H2 after consuming lactose?
Lactase-deficient individuals hydrolyze less lactose to glucose
Colonic bacteria metabolise the lactose that reaches the colon, resulting in higher H2 excretion by the lungs
What is Hartnup Disease?
What are the clinical manifestations?
congenital defect in Na-linked transporters in kidney, small intestine) for neutral AAs (tryptophan, histidine, phenylalanine)
May be no clinical manifestations, depending on diet. May be niacin deficiency -> pellagra.
What is cystinuria? What are the clinical manifestations?
Congenital defect in dibasic AA transporter in gut and kidney.
Cystine is the least soluble of the AAs that are affected – it precipitates in the kidney tubule and you pee it out.
Clinical manifestation = cystine kidney stones
With Hartnup Disease and Cysteinuria (inability to absorb certain types of AAs) why are there not usually clinical manifestations?
Because there is more than 1 way to absorb proteins: if your AA transport is defective for certain classes of AAs, you could absorb them as small peptides through the di- and tri-peptide transporter. There is also a paracellular route for protein absorption.
A Crohn’s patient has 80 cm of distal ileum resected – what vitamin levels should we keep an eye on?
Vit B12 - absorbed in distal ileum
Bile salts are also absorbed in distal ileum. If you get low in bile salts, you cannot absorb as much fat, and you cannot absorb as much fat-soluble vitamins (ADEK)
so keep an eye on B12, A, D, E, K levels!
What % of bile salts are reabsorbed in the terminal ileum? (what % is lost in feces)?
Via enterohepatic circulation, 95% of bile salts are reabsorbed in terminal ileum and returned to liver via hepatic portal vein.
5% is lost in feces
What are the 3 key roles of bile salts in fat digestion/absorption?
-Emulsification
-Increase pH for optimal function of pancreatic lipase
-Key to micelle formation
(also allow the absorption of ADEK vitamins)
Patient loses 10 cm of terminal ileum: how could this put her at risk for deficiency of ADEK and Vit B12?
Same question, but now the patient undergoes resection of the ileo-cecal valve as a kid due to Meckel’s diverticulum.
Terminal ileum = lack of bile salts reabsorption -> fat malabsorption, including ADEK and B12
ileo-cecal valve resection -> Bacterial Overgrowth Syndrome.
- Lack of valve allows colonic flora to enter the small intestines retrogradely, and they
- deconjugate the bile salts, leading to fat malabsorption.
- bind B12 causing deficiency –> megaloblastic anemia
- metabolize undigested proteins and carbs to produce SCFAs , H2, Co2, methane
- produce toxins that damage mucosa
What is Celiac Disease?
(Also known as Gluten Sensitive Enteropathy, celiac sprue)
Allergic reaction to gluten protein (gliadin) within the epithelium and subepithelium of the proximal small bowel. Causes crampy abd pain and iron-deficiency anemia
The gluten protein (gliadin) that causes Celiac is 19 AA long: how can it end up in the subepituelium (where it causes an allergic reaction)?
There is a paracellular route for intact peptides in addition to the AA transporters and transporters for small peptides
Celiac Disease: where does the inflammation occur?
What type of inflammation is it? what is the result?
Celiac (allergic/immune response to gliadin protein)
Inflammatory reaction mediated by both innate and adaptive immune systems
Location: upper small intestine
Lymphocytic infiltration of lamina propria
Causes atrophy of epithelium & villi
Celiac: what is the adaptive immune response to gliadin?
- Once gliadin gets into the lamina propria, enterocyte Tissue transGlutaminase (Ttg) deaminates gliadin
- Deamidated gliadin has high affinity for HLA-DQ2/8 on APCs (macrophages and dendritic cells)
- Gliadin/HLA DQ2/8 complex binds CD4+ TH1 cells
- Inflammatory cascade ensues with resultant villous injury and reactive crypt hyperplasia
- Activation and expansion of B-cells that produce antibodies (Ttg, gliadin)
What are some nutritional complications of chronic pancreatitis?
- Vit B12 deficiency (no pancreatic trypsin to separate R factor from B12)
- Metabolic bone disease (due to Vit D deficiency)
What disease?
Celiac: causes scalloped folds in the duodenum.
He didn’t say which of these pics is what. Bastard.
what is Whipple’s disease?
Infectious disease from bacillus.
Acquired from dust-borne soil in people with impaired immunity.
bacteria grow in macrophages –> cause lymphangiectasia = obstruction of the lymphatics.
Causes fat malabsorption.
(Pic is from lymphangiectasia, not necessarily from Whipple’s disease. lymphangiectasia causes edema, allows infection.)
