Medicine and surgery

1. Absorption and Malabsorption

2. Learning Objectives
• At the end of this lecture, students should be able
to:
• 1. Identify the major pathophysiological
mechanisms responsible for generalized
malabsorption and malabsorption of specific
nutrients.
• 2. Construct a differential diagnosis for a patient
with suspected malabsorption with items listed in
the order of relative likelihood.
• 3. Identify the most appropriate tests to identify
malabsorption of specific nutrients.

3. Gastrointestinal Tract
• A series of organs connected in series to the
outside world whose function is:
• 1. Efficient uptake from a mixed intake of
sufficient amounts of fuel (hexoses, amino
acids, fatty acids) and essential chemicals (I.e.,
those that cannot be synthesized).

4. Gastrointestinal Tract
• 2. Exclusion of other, potentially harmful,
organic and inorganic compounds and
infectious agents.

5. Normal Digestion and Absorption

6. Efficiency of Small Bowel Absorption:
not perfect
• Nutrients
Fat 93-95% of triglyceride
Starch 80-95% depending on
type
Disaccharides 96-98%
Protein 95-99%
Minerals Iron 6-20% depending on
body iron status

8. MALDIGESTION AND
MALABSORPTION
• Maldigestion: defective hydrolysis of nutrients
Malabsorption: defective mucosal absorption.
• Although this distinction may be useful on
pathophysiologic grounds, the clinical
presentation and complications of
maldigestion and malabsorption are similar.
• When the distinction between these terms is
not of clinical relevance, only the terms
absorption and malabsorption are used.

9. What is malabsorption syndrome?
• The main role of your small intestine is to
absorb nutrients from the food you eat into
your bloodstream.
• Malabsorption syndrome refers to a number
of disorders in which the small intestine
cannot absorb enough of certain nutrients and
fluids.

10. What is malabsorption syndrome?
• The term malabsorption denotes disorders in
which there is a disruption of digestion and
nutrients absorption. This may lead to
malnutrition and a variety of anaemias.
• Impairment can be single or multiple
depending on the abnormality.

11. ETIOLOGY AND PATHOPHYSIOLOGY
• From a pathophysiologic point of view,
mechanisms causing malabsorption can be
divided into:
• Premucosal (luminal) factors,
• Mucosal factors, and
• Postmucosal factors (vascular and lymphatic

12. ETIOLOGY AND PATHOPHYSIOLOGY
• For clinical purposes, this approach is of
limited value, because the various clinical
pictures caused by malabsorption syndromes
are determined mainly by the nature of the
malabsorbed substrates.
• We therefore discuss the mechanisms causing
malabsorption on the basis of the
malabsorbed substrate.

13. PATHOPHYSIOLOGY
• Digestion is by enzymatic hydrolysis which is
initiated by intraluminal processes requiring
gastric,pancreatic, and biliary secretions.
• The final products of digestion are absorbed
through the intestinal epithelial cells.

14. PATHOPHYSIOLOGY
• Malabsorption constitutes the pathological
interference with the normal physiological
sequence of:
• Digestion (intraluminal process),
• Absorption (mucosal process) and
• Transport (postmucosal events) of nutrients.

15. Clinical Clues to Nutrient
Malabsorption
• Weight loss, fatigue, “out of gas”
• Intake of excess calories without weight gain
• Diarrhea: bulky, oily stools (fat)
liquid stools (carbohydrates)
• Excess flatus

16. Clinical Clues to Nutrient
Malabsorption
• Evidence of vitamin/mineral deficiencies:
glossitis, cheilosis (iron/B vitamins),
acrodermatitis (zinc), dry skin and hair
(essential fatty acids)
• Anemia: microcytic - iron deficiency,
macrocytic - folate/B-12 deficiency
• osteopenia/osteoporosis: Vit D/calcium
• night blindness; Vitamin A
• easy bruising: Vitamin K

17. Steatorrhea

18. Angular Cheilosis: Deficiencies
Vitamin B-12 Iron Folate B vitamins

19. Glossitis: Deficiencies of Vitamin B-12,
Iron Folate, Niacin

20. Red tongue with burning sensation
B-12 deficiency with hypersegmented PMNs

21. Zinc Deficiency
Acrodermatitis

22. Acrodermatitis: Loss of hair, skin rash
and diarrhea due to zinc deficiency

23. Examples of Malabsorption
• Luminal Maldigestion: Fat, Chronic
pancreatitis
• Mucosal Maldigestion: Disaccharide, Lactase
deficiency
• Mucosal Maldigestion/Malabsorption:
Generalized malabsorption, Celiac sprue,
Bacterial overgrowth

24. Luminal Digestion of Fat
• Requires pancreatic lipases
• Requires conjugated bile acids (salts) from the
liver
• No small intestinal back-up available

25. Chronic Pancreatitis
• Often due to long-standing alcohol use,
Marked destruction of ducts/acini
• Reduced secretion of digestive
enzymes, fluid, bicarbonate.Lipases most
affected
• Anatomic damage assessed by ERCP or
endoscopic ultrasound (EUS) or pancreatic
calcifications on x-rays

27. ERCP view
of Chronic Pancreatitis
Endoscopic Retrograde
CholangioPancreatography
Single arrow points to bile
duct compressed by
fibrotic
pancreas
Double arrow points to
dilated
pancreatic duct with short
stubby side branches

28. Chronic Pancreatitis: Manifestations
• Weight loss
• Malabsorption of fat due to loss/inactivation of
pancreatic enzymes
• Bulky, oily stool, Steatorrhea is predominant abnormality
• Loss of protein/carbohydrate in stool is much less as back-
up mechanisms exist for protein/ carbohydrate digestion
• Fat soluble vitamin deficiency may occur in long-standing
severe cases
• Edema/hypoproteinemia
• Due to malnutrition with decreased hepatic
synthesis of albumin/serum proteins

29. Mucosal Maldigestion
Disaccharide
• Lactase deficiency
• Any malabsorbed carbohydrate
• Lactase: enterocyte brush-border disaccharidase
found in nursing mammals.
• Lactase splits lactose in milk to the
monosaccharides glucose and galactose for
absorption.

30. Mucosal Maldigestion
• Normally little of the enzyme is made by villus
enterocytes after weaning
• exceptions are groups of humans who exhibit
unusual persistence of lactase throughout
adulthood
• northern Europeans and other "dairying" cultures
• Symptoms occur upon ingestion of lactose by
lactase-deficient individuals

31. Mucosal Maldigestion/Malabsorption
• Generalized malabsorption
• Celiac sprue
• Bacterial overgrowth
• Celiac sprue is an Immune-mediated destruction
of enterocytes in response to ingestion of the
protein gluten found in wheat and certain other
grains. A fraction termed gliadin contains the
immunogenic material

32. Celiac sprue I
• Small intestinal villi are damaged or destroyed
- "flat gut" appearance.
• Mature digesting and transporting enterocytes
are virtually absent.

33. Celiac sprue II
• Patchy disease - usually affects proximal intestine more
than distal intestine (? why).
• Mucosal digestion and absorption are both severely
impaired.
• Characteristic antibodies used in diagnosis: IgA
antibodies to tissue transglutaminase or gliadin.
• Nice review: New England Journal of Medicine
357:1731, 2007

34. Clinical Manifestations of Sprue
• Weight loss, often with increased appetite
• Bulky, oily stools – steatorrhea - fat malabsorption
• Flatus/frothy stools – carbohydrate malabsorption
• Anemia – deficiencies of iron, folate
• Osteopenic bone disease – Vitamin D and calcium
malabsorption
• Edema/hypoproteinemia – protein deficiency and
malnutrition
• Cheilosis and glossitis – B vitamin deficiencies

35. Celiac sprue
• The degree of malabsorption depends on the
severity and
• extent of the disease: how much of the small
bowel is affected
• and how severely?

36. Malabsorbed nutrient in Celiac sprue
• Iron (why is this so??)
• Fat
• Fat-soluble vitamins
• Carbohydrate
• Protein
• Water-soluble vitamins
• Other minerals
• (Bile acids - rarely)

37. Bacterial Overgrowth-I
• Definition: overgrowth of bacteria in small bowel
due to anatomic or motility factors.
• Clinical consequences:
• Deconjugation of bile acids by bacterial enzymes
• Loss of deconjugated bile acids in stool
• Decreased bile acid pool - not enough for lipid
digestion/absorption
• Damage to enterocytes by bacteria

38. Bacterial Overgrowth-II
• Clinical consequences:
• Intraluminal consumption of nutrients by
bacteria (competition)
• Carbohydrates, amino acids
• Vitamin B-12, iron
• Damage to small bowel enterocytes causing a
sprue-like histologic appearance
• Mild to severe generalized malabsorption

39. CLINICAL FEATURES AND EVALUATION
• Diagnosis of malabsorption requires
suspecting its presence, confirming its
existence, and demonstrating its cause.
• History and Physical Examination

40. CLINICAL FEATURES
• Diarrhea, often steatorrhea is the most common
feature. Watery, diurnal and nocturnal, bulky,
frequent stools are the clinical hallmark of overt
malabsorption.
• It is due to impaired water, electrolyte absorption
or irritation from unabsorbed fatty acid.
• Bloating, flatulence and abdominal discomfort
also seen.

41. CLINICAL FEATURES
• Cramping pain suggests obstructive intestinal
segment especially if it persist after
defecation. Eg; Crohn’s disease
• Weight loss can be significant despite
increased oral intake of nutrients.
• Growth retardation,failure to thrive, delayed
puberty are seen in children.

42. CLINICAL FEATURES
• Swelling or oedema are seen due to loss of
protein.
• Anaemias, commonly from vitamin B12, folic acid
and iron deficiency presenting as fatigue and
weakness.
• Muscle cramp from decreased vitamin D, calcium
absorption and they lead to osteomalacia and
osteoporosis.
• Bleeding tendencies are seen from vitamin K and
other coagulation factor deficiencies.

43. CLINICAL FEATURES
• Others: hyperphagia , Easy bruisability,
ecchymoses, petechiae , Glossitis, cheilosis,
stomatitis, Acrodermatitis, scaly dermatitis ,
Follicular hyperkeratosis , Hyperpigmented
dermatitis ,
• Thin nails with spoon-shaped deformity ,
Perifollicular hemorrhage , Spiral or curly hair . ,
Kidney stones , Amenorrhea, impotence,
infertility , Night blindness, xerophthalmia ,
Peripheral neuropathy , Neurologic symptoms,
ataxia .

44. DIAGNOSIS
• As a baseline,the estimation of full blood
count,ESR,haematinics in the form of
folate,B12and iron status and serum albumin
with serum calcium,phosphate and
magnesium have to be done.

45. INVESTIGATION OF MALABSORPTION
• 1. Consider possibility of malabsorption based on
clinical clues
• Identify nutrient deficiencies
• Document impaired digestion and/or absorption of
nutrients
• 4. Identify causative process and treat appropriately

46. Approach to Thinking about
Malabsorption
• . How many nutrients?
• Single nutrient (i.e., Vitamin B-12)
• Subset of nutrients (i.e., fats)
• Generalized malabsorption (i.e., several nutrients)
• 2. What type of nutrient?
• Fat, carbohydrate, protein, vitamins,
• minerals or combinations
• 3. Pathophysiologic process likely to be involved?
• Luminal maldigestion
• Mucosal maldigestion
• Mucosal malabsorption

47. Tests of Malabsorption:
what types are available?
• Screening tests
• Quantitate nutrient malabsorption
• Specific diagnostic tests

48. • Screening tests – simple, cheap, fast
• Stool smear with fat stain
• CBC for evidence of anemia
• Cholesterol/carotene blood levels
• Stool osmotic gap for carbohydrates
• Weight loss/clinical clues

49. • Blood Cell Count: Hematocrit,
hemoglobin(Decreased in iron, vitamin B12, and
folate malabsorption or with blood loss)
• Mean corpuscular hemoglobin or mean
corpuscular volume(Decreased in iron
malabsorption; increased in folate and vitamin
B12 malabsorption )
• White blood cells, differential(Decreased in
vitamin B12 and folate malabsorption; low
lymphocyte count in lymphangiectasia).

50. • Biochemical Tests (Serum ):
Triglycerides(Decreased in severe fat
malabsorption)
• Cholesterol(Decreased in bile acid
malabsorption or severe fat malabsorption)

51. • Albumin(Decreased in severe malnutrition,
lymphangiectasia, protein-losing enteropathy)
• Alkaline phosphatase(Increased in calcium and
vitamin D malabsorption (severe steatorrhea);
decreased in zinc deficiency)
• Calcium, phosphorus, magnesium(Decreased
in extensive small intestinal mucosal disease,
after extensive intestinal resection, or in
vitamin D deficiency)

52. • Zinc(Decreased in extensive small intestinal
mucosal disease or intestinal resection)
• Iron, ferritin(Decreased in celiac disease, in
other extensive small intestinal mucosal
diseases, and with chronic blood loss)

53. • Other Serum Tests : Prothrombin
time(Prolonged in vitamin K malabsorption) β-
Carotene(Decreased in fat malabsorption from
hepatobiliary or intestinal diseases)
Immunoglobulins(Decreased in
lymphangiectasia, diffuse lymphoma)

54. • Folic acid(Decreased in extensive small
intestinal mucosal diseases, with
anticonvulsant use, in pregnancy; may be
increased in small intestinal bacterial
overgrowth ) Vitamin B12(Decreased after
gastrectomy, in pernicious anemia, terminal
ileal disease, and small intestinal bacterial
overgrowth) Methylmalonic acid(Markedly
elevated in vitamin B12 deficiency)

55. • Homocysteine(Markedly elevated in vitamin
B12 or folate deficiency)Stool Tests :
Fat(Qualitative or quantitative increase in fat
malabsorption) Elastase,
chymotrypsin(Decreased concentration and
output in exocrine pancreatic insufficiency)
pH(Less than 5.5 in carbohydrate
malabsorption

56. • Biopsy :
• Examination of endoscopic biopsy specimens from the
duodenum may be diagnostic or highly suggestive of a
variety of small bowel disorders resulting in
malabsorption ; follow-up small intestinal biopsy can
be used to assess treatment effects. two or three
jumbo duodenal or jejunal biopsy specimens usually
are sufficient to allow histologic sectioning parallel to
the villi and crypts. Specimens also may be obtained
with smaller forceps, although the number of
specimens obtained must then be increased to four to
six. Charaterstic histological feature of malabsorption is
villous atrophy.

57. • Aspiration :
• Fluid aspirated from the descending part of the
duodenum may be examined microscopically for
Giardia lamblia or cultured to detect bacterial
overgrowth in patients with diffuse small intestinal
motility disorders .
• ABDOMINAL IMAGING
• Small Bowel Follow-through and Small Bowel
Enteroclysis
• Abdominal Computed Tomography
• Magnetic Resonance Imaging of the Small Intestine

58. • Quantitate nutrient malabsorption: messy,
take time, accurate and quantitative
• 72-hour fecal fat
• D-xylose excretion (monosaccharide)
• Schilling’s test for B-12 absorption (no longer
available)
• Breath hydrogen test (carbohydrate)

59. 72-hour Fecal Fat Test

60. Hydrogen Breath Test for Carbohydrate
Malabsorption
• Principle: malabsorbed sugar passes into colon
bacteria produce hydrogen gas. H2 diffuses into
blood and is excreted by lungs
• Practice: Administer 25-50 grams of glucose or
other sugar orally
• Measure hydrogen in exhaled breath at 2-4 hours
• Variants: Other sugars can be employed to test
for specific disaccharidase or transporter defects,
lactase deficiency, glucose-galactose
malabsorption

62. Tools for Evaluation of Malabsorption:
diagnosis of underlying disease
once you have identified a small
group of possible diseases.

63. • Radiographs of the small bowel to delineate
anatomy
• Endoscopic retrograde cholangiopancreatography
(ERCP) to define the anatomy of biliary and
pancreatic ducts
• Pancreatic secretory function tests
• Small bowel biopsy and/or antibody tests for
celiac sprue
• Quantitative small bowel bacterial culture, bile
acid or glucose breath tests for bacterial
overgrowth

64. DDX of villous atrophy
• 1- celiac diseas
• 2- tropical sprue
• 3- Infection (due to Giardia lamblia,
Cryptosporidium)
• 4-AIDS enteropathy
• 5- Whipple's disease
• 6-Drug-induced enteropathy (NSAIDs, colchicine,
neomycin)
• 7-Food protein hypersensitivity (rye, barley, egg,
fish, rice, poultry)

65. DDX of villous atrophy
• 8-Immunodeficiency (hypogammaglobulinemia)
• 9-Lymphoma
• 10-Prolonged folate or cobalamin deficiency
• 11- Crohn's disease
• 12-Protein-calorie malnutrition
• 13- zollinger Ellison syndrome
• 14- Chronic radiation damage
• 15-Traumatic injury

66. Treatment of malabsorptive diseases
• must be directed against the underlying
condition, if possible. In addition, nutritional
deficits must be corrected.
• In pancreatic insufficiency, in disorders of
intestinal fat absorption, and in short bowel
syndrome, medium-chain triglycerides can be
used as a source of dietary calories, these
patients, therefore, should consume a diet rich in
carbohydrates and medium-chain triglycerides

67. Treatment of malabsorptive diseases
• In bile acid malabsorption after extensive ileal
resections, intestinal fat absorption can be improved
markedly by oral administration of natural conjugated
bile acids or of synthetic cholylsarcosine. Replacement
of conjugated bile acids also reduces urinary oxalate
excretion and therefore should protect against
development of kidney stones.
• Patients with cystic fibrosis or short bowel syndrome
who are unable to absorb vitamin D from their diet
may benefit from treatment with an ultraviolet lamp,
which emits ultraviolet radiation similar to sunlight.

68. Treatment of malabsorptive diseases
• In patients with malabsorption and an intact
colon, fluid depletion must be avoided to prevent
kidney stones associated with hyperoxaluria.[326]
In patients with malabsorption syndrome, special
care should be given to the replacement of
vitamins, iron, calcium, and trace elements to
avoid deficiency syndromes.
• In patients with diarrhea, symptomatic treatment
with opiates or loperamide can increase the time
available for absorption of nutrients.