03-07 Absorption Physio; Malabsorptive D/O Flashcards

Question 1

Q

Hartnup Dz 101

Answer

A

A.D. mutation in renal & GI neutral AA (tryptophan, histidine, phenylalanine) transport in both gut and kidneys

<ul>
<li>Usually Hartnup is asymptomatic
<ul>
<li>depends on genetics/penetrance</li>
</ul>
</li>
<li>Can lead to pellagra b/c tryptophan is a neutral AA that is broken down into niacin in the liver
<ul>
<li>niacin deficiency leads to pellagra</li>
<li>Rarely: niacin def → cerebellar ataxia & psychosis</li>
</ul>
</li>
<li>Niacin deficiency rare b/c
<ul>
<li>other dietary sources</li>
<li>can still absorp Trp as part of an oligopeptide that cgets absorbed paracellularly</li>
</ul>
</li>
</ul>

Question 2

Q

Cystinuria 101

Answer

A

Autosomal recessive defect in SC3A1 dibasic AA transporter in gut and kidney

<ul>
<li>Cystine least soluble of dibasic AAs (cystine, ornithine, arginine, lysine)</li>
<li>precipitates in acid milieu of kidney→cystine kidney stones
<ul>
<li>see crystal here</li>
</ul>
</li>
</ul>

Question 3

Q

Loss of enterohepatic circulation can cause deficiencies in?

Answer

A

Fat-soluble vitamins Vit A, D, E, K

Question 4

Q

coloretic diarrheais caused by

Answer

A

caused by bile salts irritating the colon

<ul>
<li>can happen s/p T.I. resection</li>
</ul>

Irritation of colon leads to increase extrusion of Cl- ions

<ul>
<li>Na+ follows</li>
<li>H2O follows</li>
<li>diarrhea follows</li>
</ul>

Question 5

Q

scalloped duodenal folds should make you think of

Answer

A

Celiac Dz

Question 6

Q

OBJECTIVE: describe normal digestion and absorption (including where it's absorbed) of carbs

Answer

A

LOCATION OF CARB ABSORPTION

<ul>
<li>Very little in the duodenum</li>
<li>Most in jejunum</li>
<li>Less in distal small bowel</li>
<li>None in colon*
<ul>
<li>*2-20% of starches don't get absorbed→colon→ bacteria breakdown to SFACs (e.g.propionate, acetate, butyrate) + gas→ SCFAs absorbed by colonic enterocytes</li>
</ul>
</li>
</ul>

STEPS OF CARB DIGESTION AND ABSORPTION

<ol>
<li>Physical denaturation
<ul>
<li>mastication and antral grinding</li>
</ul>
</li>
<li>intraluminal digestion
<ul>
<li>starch--amylase--> oligosaccharides</li>
<li>both salivary (‪↓‬ effective b/c inactivated ‪↓‬ stomach pH) and pancreatic</li>
</ul>
</li>
<li>brush border digestion
<ul>
<li>di- & oligo-saccharides--b.b. disaccharidases—>monos</li>
<li>see image here</li>
</ul>
</li>
<li>transport (see image on reverse)</li>
</ol>

<ul>
<li>Apical membrane: Two proteins

<ul>
<li>Fructose: Facilitated diffusion (GLUT5)</li>
<li>Gluc& Galactose: Active transport (Na/gluc transport - SGLT1)</li>
</ul>
</li>
<li>Basolateral membrane: Single protein
<ul>
<li>Facilitated diffusion (GLUT2)</li>
</ul>
</li>
</ul>

Question 7

Q

OBJECTIVE: describe normal digestion and absorption of protein

Answer

A

Similar to carbs

<ul>
<li>Major proteins hydrolyzed to oligopeptides and amino acids within the lumen</li>
</ul>

Unlikecarbohydrates

<ul>
<li>BOTH small polymers AND amino acids are absorbable</li>
<li>Proenzymes require conversion</li>
</ul>

STEPS OF DIGESTION AND ABSORPTION

<ol>
<li>Mechanical breakdown</li>
<li>Gastric hydrolysis
<ol>
<li>↓ gastric pH causes minimal protein hydrolysis</li>
<li>Gastric pepsinogen activated by acid to pepsin
<ul>
<li>Optimum pH ~2; inactivated by pancreatic juice</li>
<li>Partially digests 10-15% of dietary protein</li>
<li>NOT essential for protein digestion</li>
</ul>
</li>
</ol>
</li>
<li>Trypsin and luminal (premucosal) digestion
<ol>
<li>Pancreas releases trypsinogen
<ul>
<li>Activated by brush border enterokinase (and trypsin!)</li>
</ul>
</li>
<li>Trypsin
<ul>
<li>The key! activates 4 other peptidases</li>
<li>Quickly inactivates itself via autodigestion</li>
</ul>
</li>
<li>Brush border
<ul>
<li>Hydrolyzes larger peptides (3-8 AAs)</li>
</ul>
</li>
</ol>
</li>
<li>Absorption
<ol>
<li>Apical membrane AA transporters
<ul>
<li>Redundant: overlap for chemically similar AAs</li>
</ul>
</li>
<li>Di-, tri-, tetra- absorbed intact via carrier molecules
<ul>
<li>Cytosolic peptidases then hydrolyze to AA’s</li>
</ul>
</li>
<li>Paracellular route for intact peptides</li>
</ol>
</li>
</ol>

Question 8

Q

OBJECTIVE: describe normal digestion and absorption of fats

Answer

A

<ol>
<li>Emulsified by the motion of chewing and antral grinding

<ul>
<li>provides more surface area for the lipases</li>
<li>bile salt stabilize this emulsion</li>
</ul>
</li>
<li>Fat —gastric/lingual lipases→ TALs & DALs
<ul>
<li>special acid and pepsin resistant lipase</li>
<li>inactivated once in duodenum by
<ul>
<li>neutral pH</li>
<li>trypsin digests it</li>
</ul>
</li>
</ul>
</li>
<li>CCK & GIP → ↑ biliary and pancreatic lipase secretions (bile salts, panc lipase)
<ul>
<li>TALs/DALs—panc.lipase→ MAG + 2FAs</li>
<li>panc lipase needs co-factors
<ul>
<li>neutral pH</li>
<li>co-lipase</li>
<li>bile salts</li>
</ul>
</li>
</ul>
</li>
<li>Micells form w/ bile salts & phospholipids → absorbed</li>
<li>Chylomicrons formed in enterocytes</li>
<li>Post-processing of dietary fat</li>
</ol>

Question 9

Q

OBJECTIVE: describe normal digestion and absorption of vitamin B12

—Name one things that can go wrong at each step to cause B12 deficiency

Answer

A

see image here

<ol>
<li>Decreased Intrinsic Factor secretion
<ul>
<li>Pernicious anemia, Gastrectomy</li>
</ul>
</li>
<li>Increased R factor B12 binding
<ul>
<li>Pancreatic insufficiency</li>
</ul>
</li>
<li>Increased bacterial B12 uptake
<ul>
<li>Bacterial overgrowth</li>
</ul>
</li>
<li>Decreased ileal B12 absorption
<ul>
<li>Crohn’s disease, ileal resection</li>
</ul>
</li>
</ol>

Question 10

Q

OBJECTIVE: Describe/define the different pathophysiologic defects causing maldigestion and malabsorption involving the following steps incarbohydrate digestion and absorption: intraluminal digestion, intraluminal transfer to mucosa, mucosal digestion, mucosal processing, mucosal export

Answer

A

See image

Question 11

Q

OBJECTIVE: Describe/define the different pathophysiologic defects causing maldigestion and malabsorption involving the following steps inprotein digestion and absorption: intraluminal digestion, intraluminal transfer to mucosa, mucosal digestion, mucosal processing, mucosal export

Answer

A

See image

Question 12

Q

OBJECTIVE: Describe/define the different pathophysiologic defects causing maldigestion and malabsorption involving the following steps in fat digestion and absorption: intraluminal digestion, intraluminal transfer to mucosa, mucosal digestion, mucosal processing, mucosal export

Answer

A

See image

Question 13

Q

OBJECTIVE: Describe/define the different pathophysiologic defects causing maldigestion and malabsorption involving the following steps infat absorption(only).

Answer

A

see image

Question 14

Q

OBJECTIVE: Describe the clinical manifestations and pathophysiologic mechanisms of lactase deficiency.

Answer

A

<ul>
<li>bloating, pain, gas, diarrhea that improves w/ fasting</li>
</ul>

PATHOPHYSIOLOGY

<ul>
<li>lactase activity is lower:
<ul>
<li>with age</li>
<li>in non-Northern Europeans</li>
<li>sometimes after infections or inflammation</li>
</ul>
</li>
<li>lactose in the gut:
<ul>
<li>acts as osmotic laxative</li>
<li>is fermented into:
<ul>
<li>SCFAs → omsotic lax</li>
<li>H2, methane → farts</li>
</ul>
</li>
</ul>
</li>
</ul>

Question 15

Q

OBJECTIVE: Describe the clinical manifestations and pathophysiologic mechanisms of pancreatic insufficiency.

Answer

A

CLINICAL MANIFESTATIONS

<ul>
<li>steatorrhea</li>
<li>fat soluble vitamin malabsorption</li>
<li>frequently, insulin dependent diabetes</li>
<li>Other well known sequelae:
<ul>
<li>metabolic bone disease</li>
<li>B12 deficiency</li>
<li>oxalate kidney stones</li>
</ul>
</li>
</ul>

PATHOPHYSIOLOGY

Carb Malabsorption

<ul>
<li>Amylase production</li>
<li>Bicarbonate (optimal pH) and Cl- for amylase</li>
</ul>

Protein Malabsorption

<ul>
<li>Pancreatic proteases (zymogens and active)</li>
</ul>

Fat Malabsorption

<ul>
<li>↓ Bicarbonate (optimal pH)</li>
<li>↓ Lipase, colipase</li>
<li>steatorrhea → ↑ oxalate absorption by fat binding Ca/Mg (saponification) →  not enough Ca/Mg to bind and prevent oxalate absorption</li>
</ul>

Vitamin/Mineral Malabsorption

<ul>
<li>B12 (cobalamin) Deficiency

<ul>
<li>Insufficient pancreatic proteases to digest dietary R factors that bind cobalamin</li>
</ul>
</li>
<li>Metabolic bone disease
<ul>
<li>Vit D deficiency (along w/ A, D, & E)</li>
</ul>
</li>
</ul>

Refer to notes “Pancreatic Function/Disorders of the Exocrine Pancreas" for pathophysiology.

Question 16

Q

OBJECTIVE: Describe the clinical manifestations and pathophysiologic mechanisms of Bile salt deficiency.

Answer

A

CLINICAL MANIFESTATIONS

<ul>
<li>steatorrhea</li>
<li>Deficiency of Vitamins A, D, E and/or K</li>
</ul>

PATHOPHYSIOLOGY

<ul>
<li> Often caused by resection of the terminal ileum where 95% of bile salts are reabsorbed</li>
<li>leads to inability to form micelles</li>
</ul>

Question 17

Q

OBJECTIVE: Describe the clinical manifestations and pathophysiologic mechanisms of celiac disease.

Answer

A

CLINICAL MANIFESTATIONS

<ul>
<li>"panmalabsorption"</li>
<li>iron deficiency anemia (b/c of )</li>
<li>unintended weight loss</li>
<li>diarrhea</li>
</ul>

PATHOPHYSIOLOGY

<ul>
<li>allergic rxn to gliadin within epithelium and subepithelium of the proximal small bowel</li>
<li>•HLA-DQ2 OR HLA-DQ8 genotype required
<ul>
<li>but not sufficient</li>
</ul>
</li>
<li>Fe-def happens because theduodenum (the site where divalent ions are absorbed) is affected</li>
<li>weight loss because the villi of the small bowel are eroded decreasing the surface area for absorption
<ul>
<li>see histo image here</li>
</ul>
</li>
<li>diarrhea b/c:
<ul>
<li>destroys neuroendocrine cells→ impairs CCK/Secretin release → decreased pancreaticobiliary secretion and steatorrhea</li>
<li>↓ brush border hydrolases, peptidases, transport proteins → CHO and protein malabsorption</li>
<li>↓ villous structure → ↓ surface area</li>
<li>↑ inflam mediators → ↑intestinal secretion</li>
</ul>
</li>
</ul>

Question 18

Q

OBJECTIVE: Describe the clinical manifestations and pathophysiologic mechanisms of small bowel bacterial overgrowth.

Answer

A

CLINICAL MANIFESTATIONS

<ul>
<li>steatorrhea</li>
<li>sx of ADEK absorption</li>
<li>B12 (cobalamin) deficiency sx
<ul>
<li>megaloblastic anemia (could also be 2° to folate def)
<ul>
<li>hypersegmented neutrophils</li>
</ul>
</li>
<li>neuro ∆s (not caused by low folate)</li>
<li>atrophic glossitis, etc.</li>
</ul>
</li>
</ul>

PATHOPHYSIOLOGY

<ul>
<li>bacteria dis-conjugate bile salts → makes them absorbable so quickly they can't work → fat malabsorption → A, D, E, K and steatorrhea</li>
<li>Bacteria can also bind B12</li>
</ul>

Question 19

Q

OBJECTIVE: Describe the clinical manifestations and pathophysiologic mechanisms of abetalipoproteinemia.

Answer

A

CLINICAL MANIFESTATIONS

<ul>
<li>infancy fat malaborption</li>
<li>low VLDL</li>
<li>Vit ADEK deficiencies</li>
</ul>

PATHOPHYSIOLOGY

<ul>
<li>inherited mutation in microscopmal triglyceride transfer proteins</li>
<li>apo B-48 and B-100 deficiencies → No ApoB48 to form chylomircrons</li>
</ul>

Question 20

Q

OBJECTIVE: Describe the clinical manifestations and pathophysiologic mechanisms of Whipple's disease.

Answer

A

CLINICAL MANIFESTATIONS

<ul>
<li>Fat malabsorption
<ul>
<li>Fatty acid diarrhea</li>
</ul>
</li>
<li>Protein losing enteropathy
<ul>
<li>Edema, ascites, pleural effusion</li>
<li>Lymphopenia-susceptible to infection</li>
</ul>
</li>
</ul>

PATHOPHYSIOLOGY

T. whipplei infection

may be acquired from exposure to dust borne soil in individuals with impaired cellular immunity

Bacteria grow within “foamy” macrophages in lamina propria, mesentery and lymph nodes → enlarge → lymphangiectasia

Question 21

Q

OBJECTIVE: List the signs and symptoms of maldigestion and malabsorption of major nutrients and vitamins

Answer

A

.bleck

Question 22

Q

OBJECTIVE: define diarrhea

Answer

A

Fluid secretion and/or failure to absorb water and electrolytes

Question 23

Q

OBJECTIVE: define maldigestion

Answer

A

Failure to break down complex nutrients

Question 24

Q

OBJECTIVE: define malabsorption

Answer

A

Failure to absorb products of digestion

Question 25

Q

These are serum glucose and H2 breath test results from a lactose challenge test in a normal individual.

<ul>
<li>How would these results look in someone w/ lactase deficiency?</li>
</ul>

Question 26

Q

Bacterial overgrowth

<ul>
<li>predisposing factors</li>
<li>presentation</li>
<li>Diagnosis</li>
<li>pathophys</li>
</ul>

Answer

A

PREDIPOSING FACTORS

<ol>
<li>Anatomic derangements
<ul>
<li>Ileocecal resection, fistula</li>
</ul>
</li>
<li>Achlorhydria
<ul>
<li>H+ is an antibiotic that ↓ bacterial flora</li>
</ul>
</li>
<li>Stasis
<ul>
<li>Impaired motility and aging, impaired MMC’s (migrating motor complexes)</li>
</ul>
</li>
</ol>

PRESENTATION

<ul>
<li>most pts: nonspecific sx of bloating, flatulence, or abd discomfort, or asymptomatic</li>
<li>Many pts w/ severe have diarrhea or steatorrhea</li>
<li>Rarely wt loss due to severe diarrhea, malabsorption, or poor oral intake</li>
</ul>

DIAGNOSIS

<ul>
<li>Quantitative small bowel culture</li>
<li>(+) Breath test for H₂, methane production after eating carbs</li>
</ul>

PATHOPHYS

<ul>
<li>> 10⁶ aerobes/anaerobes per ml → deconjugation of bile salts → fat malabsorption

<ul>
<li>Deconjugated bile salts, unionized at duodenal pH, do not form micells</li>
</ul>
</li>
<li>Make SCFAs →H₂, CO₂, and methane</li>
<li>Bacterial toxins damage mucosa</li>
<li>•Bacterial bind B12 (cobalamin)
<ul>
<li>Megaloblastic anemia, and all the rest</li>
</ul>
</li>
</ul>

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03-07 Absorption Physio; Malabsorptive D/O Flashcards

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