Gi Week 2 Objective 5

Front 1

What are some of the manifestations of malabsorption? (Access Medicine: malabsorption)

Back 1

steatorrhea; diarrhea; weight loss; muscle wasting; microcytic anaemia; macrocytic anaemia; parasthesia; tetany; (positive Trousseau and Chvostek signs); bone pain; pathologic fractures; skeletal deformities; bleeding tendency ie. ecchymoses, epistaxis; edema

Front 2

Steatorrhea is manifested when which nutrients are malabsorbed?

Back 2

triglycerides, FA's, phospholipids, cholesterol

N.B. fat soluble vitamins: A,D,E,K

Front 3

Diarrhea is manifested when which nutrients are malabsorbed?

Back 3

fats; CHO's

Front 4

Weight loss/muscle wasting is manifested when which nutrients are malabsorbed?

Back 4

fat; protein; CHO's

Front 5

Microcytic anaemia is manifested when which nutrients are malabsorbed?

Back 5

iron

Front 6

Macrocytic anaemia is manifested when which nutrients are malabsorbed?

Back 6

Vitamin B12 and/or folic acid

Front 7

Parasthesia, tetany, positive Trousseau and Chvostek signs are manifested when which nutrients are malabsorbed?

Back 7

Ca, Vit D, Mg

Front 8

Bone pain, pathologic fractures, skeletal deformities are manifested when which nutrients are malabsorbed?

Back 8

Ca, Vit D

Front 9

Bleeding tendency is manifested when which nutrients are malabsorbed?

Back 9

Vit K

Front 10

Edema is manifested when which nutrients are malabsorbed?

Back 10

Protein

Front 11

The pathogenesis of malabsorption can result from defects in the three phases of normal digestion and absorption. What are these three phases? (Access Medicine: malabsorption)

Back 11

Intraluminal, mucosal, absorptive

Front 12

What may account for defects in intraluminal digestion?

Back 12

Bile salt insufficiency; pancreatic enzyme insufficiency

Front 13

Which conditions may be associated with pancreatic insufficiency?

Back 13

chronic pancreatitis, cystic fibrosis, pancreatic ca, (also, pancreatic enzymes may be sufficient but can be inactived by excess acid in the duodenum as in Zollinger-Ellison syndrome)

N.B. from pathology that ca of the head of the pancreas leads to painless jaundice

Front 14

What are the manifestations of pancreatic insufficiency?

Back 14

SIGNIFICANT steatorrhea resulting in weight loss, gaseous distention, and flatulence; digestion of pro's and CHO's affected to a much lesser degree (not usually clinically significant)

Front 15

Which conditions are associated with bile salt insufficiency?

Back 15

-biliary obstruction; cholestatic liver diseases; Crohn's disease (because bile salts are resorbed from terminal ileum); resection of terminal ileum
-destruction of bile salts from bacterial overgrowth, massive acid hypersecretion, meds that bind bile salts (cholestyramine)

Front 16

What are the manifestions of bile salt insufficiency?

Back 16

MILD steatorrhea, minimal weight loss, impaired absorption of fat-soluble vits resulting in bleeding tendency, osteoporosis, hypocalcemia

Front 17

What may account for defects in the mucosal phase of absorption?

Back 17

-loss of intestinal mucosal surface area: resection, sprues (including celiac disease), lymphoma
-loss of brush border enzymes: rare congenital disorders (manifest in children), lactase deficiency (can manifest in adults)

Front 18

What are the manifestations of defects in the mucosal phase of absorption?

Back 18

-malabsorption of ALL nutrients leads to weight loss, muscle wasting, diarrhea, steatorrhea, gaseous distention, flatulence, etc.

Front 19

What may account for defects in the absorptive phase of digestion?

Back 19

obstruction of lymphatic system resulting in impaired absorption of chylomicrons and lipoproteins

Front 20

What should be included in a Ddx for malabsorptive disorders? (MD Consult: Sleisingers & Fordtran's table 98-6)

Back 20

-Inflammatory Bowel disease: Crohn's disease & ulcerative colitis;
-Sprues: tropical, Celiac disease;
-Cystic fibrosis;
-Infectious causes: bacterial overgrowth; parasitic infection; tuberculosis (of sm. intestine?)
-Endocrine causes: adrenal insufficiency; hyper/hypothyrodisim; diabetes mellitus;
-Neoplasms: Zollinger-Ellison disease; carcinoid tumour, lymphoma
-HIV patient: MAC
-Intestinal pathology: fistulas, diverticulitis, ischaemia
-Pancreatitis
-Cholestasis

Front 21

Which part of the GI system does Ulcerative colitis affect?

Back 21

colon only

Front 22

Which part of the GI system does Crohn's disease affect?

Back 22

patchy involvement of any segment of GI tract from mouth to anus

Front 23

How do Crohn's and ulcerative colitis differ in pathology, symptoms, etc?

Back 23

Crohn's:
-any segment of GI tract
-transmural inflammation (including mesentaries and lymphatics) therefore pain may be localized and sharp
-fibrosis (may lead to palpable masses)
-distribution: 30% small bowel only; 50% small and large bowel; 20% colon only
-more common in Europeans and Jewish persons
-sx: colicky, post-prandial ab pain; diarrhea less common; fever frequent
-onset b/w 15-30 yrs
- not ammenable to surgery! (85% recurrence with resection)
-pathophys: believe that a normal bacterial Ag may start inflammatory process

Ulcerative Colitis:
-affects rectum to cecum only
-not transmural (mucosal layer only) therefore pain is more diffuse
-sx: RECTAL BLEEDING & diarrhea
-onset: 20-50 yrs
-unknown aetiology

Front 24

What is the pathophysiology of Celiac disease?

Back 24

- gluten-induced enteropathy
- gliadin portion of gluten molecule is toxic to enterocytes leading to mucosal damage and therefore malabsorption

Front 25

What are the classic features of Celiac Disease?

Back 25

diarrhea, weight loss, malnutrition, osteomalacia (bone pain)

N.B. that sub-clinical presentations are becoming more common

Front 26

Which area of the GI tract is afflicted by Celiac disease?

Back 26

duodenum to jejunoileum and is usually more severe proximally

Front 27

Which laboratory tests are used to aid in the diagnosis of Celiac disease?

Back 27

1. Endomysial antibody (IgA EMA) Sens: 85-98 Spec: 97-100
2. Tissue transglutamase antibody (IgA tTG) Sens: 90-98 Spec: 94-97