Slide 5 GI

What are Inflammatory Bowel Diseases (IBDs)? A. Infectious diseases caused by bacteria only B. A group of diseases including ulcerative colitis and Crohn’s disease C. Liver disorders affecting bile production D. Gastric acid disorders only

B. A group of diseases including ulcerative colitis and Crohn’s disease

What is the primary difference in location between ulcerative colitis and Crohn’s disease? A. Both only affect the stomach B. Ulcerative colitis affects the large intestine, Crohn’s can affect any part of the GI tract (especially small intestine) C. Crohn’s only affects the rectum D. Both affect only the esophagus

B. Ulcerative colitis affects the large intestine, Crohn’s can affect any part of the GI tract (especially small intestine)

What is the key difference in tissue depth involvement between ulcerative colitis and Crohn’s disease? A. Ulcerative colitis is full thickness, Crohn’s is not B. Crohn’s is full thickness while ulcerative colitis is not C. Both are full thickness D. Neither involves the mucosa

B. Crohn’s is full thickness while ulcerative colitis is not

Why is full-thickness intestinal disease dangerous? A. It reduces acid production B. It increases vitamin absorption C. It can lead to leakage causing peritonitis and fistulas D. It improves motility

C. It can lead to leakage causing peritonitis and fistulas

What is a fistula? A. A type of immune cell B. A surgical procedure C. An abnormal connection between two organs D. A digestive enzyme

C. An abnormal connection between two organs

What causes fistulas in Crohn’s disease? A. Surface inflammation only B. Viral infection C. Full-thickness inflammation D. Excess mucus secretion

C. Full-thickness inflammation

What is the function of T cells in immunity? A. Produce bile B. Perform phagocytosis and destroy pathogens C. Produce insulin D. Store glucose

B. Perform phagocytosis and destroy pathogens

How are T cells classified? A. IgA and IgG B. Plasma and memory cells C. CD4 (helper) and CD8 (cytotoxic) D. Alpha and beta cells

C. CD4 (helper) and CD8 (cytotoxic)

What is the role of B cells? A. Kill infected cells directly B. Produce antibodies and present pathogens to T cells C. Perform digestion D. Produce hormones

B. Produce antibodies and present pathogens to T cells

Which T helper cells are increased in Crohn’s disease? A. Th2 only B. Th1 and Th17 C. Th3 only D. Regulatory T cells only

B. Th1 and Th17

Which T helper cells are increased in ulcerative colitis? A. Th1 B. Th17 C. Th2 D. Th0

C. Th2

Why is TNF-α important in IBD management? A. It decreases inflammation B. Controlling TNF-α helps control symptoms and disease progression C. It regulates blood sugar D. It only affects digestion of fats

B. Controlling TNF-α helps control symptoms and disease progression

How is TNF targeted therapeutically? A. With antibiotics B. With monoclonal antibodies (-mab drugs) C. With antivirals D. With antihistamines

B. With monoclonal antibodies (-mab drugs)

What are common symptoms of ulcerative colitis? A. Constipation and weight gain B. Diarrhea, bloody stools, and abdominal cramps C. Chest pain and dizziness D. Joint pain only

B. Diarrhea, bloody stools, and abdominal cramps

What serious complication can ulcerative colitis cause? A. Kidney failure B. Toxic megacolon with risk of perforation C. Liver cancer D. Stroke

B. Toxic megacolon with risk of perforation

What is the treatment approach for ulcerative colitis? A. Surgery only B. Antibiotics and corticosteroids initially, then aminosalicylates and immunosuppressants C. Antivirals only D. No treatment required

B. Antibiotics and corticosteroids initially, then aminosalicylates and immunosuppressants

What type of damage can Crohn’s disease cause? A. Only mucosal irritation B. Transmural (full-thickness) infections and perforations C. Only superficial redness D. No tissue damage

B. Transmural (full-thickness) infections and perforations

What complications are associated with Crohn’s disease in the small intestine? A. Only acid reflux B. Adhesions, perforation, and fistulas C. Only constipation D. Lung fibrosis

B. Adhesions, perforation, and fistulas

What are adhesions? A. Hormones regulating digestion B. Fibrous bands that connect organs and restrict movement C. Blood cells D. Enzymes

B. Fibrous bands that connect organs and restrict movement

What are skip lesions in Crohn’s disease? A. Continuous inflammation throughout the intestine B. Patchy areas of inflammation separated by normal tissue C. Only rectal involvement D. Uniform stomach inflammation

B. Patchy areas of inflammation separated by normal tissue

What systemic problems can Crohn’s disease cause? A. Only GI symptoms B. Anemia and malabsorption C. Only skin issues D. No systemic effects

B. Anemia and malabsorption

Why is Crohn’s disease considered systemic? A. It affects only one organ B. It affects multiple organs beyond the GI tract C. It only affects the skin D. It only affects blood vessels

B. It affects multiple organs beyond the GI tract

How is Crohn’s disease treated? A. No treatment B. Antibiotics PRN, corticosteroids, then aminosalicylates and immunosuppressants C. Only antivirals D. Only surgery

B. Antibiotics PRN, corticosteroids, then aminosalicylates and immunosuppressants

Compared to ulcerative colitis, Crohn’s disease has: A. Fewer complications B. Less inflammation C. More complications, adhesions, and peritonitis risk D. No symptoms

C. More complications, adhesions, and peritonitis risk

What are supportive therapies for IBD? A. High-fat diet only B. Fluid diet, vitamin supplementation, and low-fat diet C. No dietary changes D. High protein diet only

B. Fluid diet, vitamin supplementation, and low-fat diet

What is maintenance therapy for IBD? A. Antibiotics only B. Aminosalicylates like aspirin C. Insulin D. Opioids

B. Aminosalicylates like aspirin

When are corticosteroids used in IBD? A. Long-term maintenance B. Acute exacerbations only C. Never used D. Only for infections

B. Acute exacerbations only

What is the purpose of immunosuppressants in IBD? A. Immediate symptom relief B. Long-term disease control C. Cure the disease D. Replace all other drugs

B. Long-term disease control

How is 6-MP metabolized? A. Only renally B. Via xanthine oxidase and TPMT C. Only in the stomach D. Only via bile

B. Via xanthine oxidase and TPMT

What is the major interaction with 6-MP? A. Ibuprofen increases metabolism B. Allopurinol inhibits xanthine oxidase → increases toxicity C. Aspirin decreases toxicity D. Metformin enhances clearance

B. Allopurinol inhibits xanthine oxidase → increases toxicity

What are common immunosuppressant side effects? A. Weight loss only B. Bone marrow suppression, hepatotoxicity, cancer risk C. Hair growth D. Vision improvement

B. Bone marrow suppression, hepatotoxicity, cancer risk

What are cyclosporine toxicities? A. Cardiotoxicity only B. Nephrotoxicity, neurotoxicity, hepatotoxicity C. Lung cancer D. Hearing loss

B. Nephrotoxicity, neurotoxicity, hepatotoxicity

What is the primary use of anti-TNF drugs? A. Diabetes B. Crohn’s disease C. Hypertension D. Asthma

B. Crohn’s disease

What is the mechanism of anti-integrin drugs? A. Increase inflammation B. Block leukocyte migration by inhibiting integrin–selectin interaction C. Kill bacteria D. Increase TNF production

B. Block leukocyte migration by inhibiting integrin–selectin interaction

What is the role of anti–IL-23 drugs? A. Increase immune response B. Reduce chronic inflammation by blocking IL-23 C. Stimulate digestion D. Increase cytokines

B. Reduce chronic inflammation by blocking IL-23

Which drugs are anti-TNF antibodies? A. Methotrexate, azathioprine B. Infliximab, Adalimumab, Certolizumab, Golimumab C. Budesonide, prednisone D. Aspirin, ibuprofen

B. Infliximab, Adalimumab, Certolizumab, Golimumab

Which drugs are anti-integrin antibodies? A. Natalizumab and Vedolizumab B. Infliximab and Adalimumab C. Ustekinumab only D. Methotrexate only

A. Natalizumab and Vedolizumab

Which drugs are anti–IL-23 antibodies? A. Azathioprine, methotrexate B. Ustekinumab, Risankizumab, Mirikizumab C. Cyclosporine, tacrolimus D. Aspirin, mesalamine

B. Ustekinumab, Risankizumab, Mirikizumab

What is azathioprine’s mechanism? A. COX inhibition B. Purine analog prodrug inhibiting DNA synthesis C. TNF inhibition D. Calcium channel blockade

B. Purine analog prodrug inhibiting DNA synthesis

What is methotrexate’s mechanism? A. TNF blockade B. DHFR inhibition → inhibits DNA synthesis C. Histamine blockade D. Sodium channel inhibition

B. DHFR inhibition → inhibits DNA synthesis

What is cyclosporine’s mechanism? A. COX inhibition B. Calcineurin inhibition → prevents T cell activation C. TNF inhibition D. DNA replication enhancement

B. Calcineurin inhibition → prevents T cell activation

Which are Janus kinase inhibitors? A. Budesonide, prednisone B. Tofacitinib, Upadacitinib C. Infliximab, adalimumab D. Mesalamine, sulfasalazine

B. Tofacitinib, Upadacitinib

What are side effects of Janus kinase inhibitors? A. Weight loss B. Diarrhea, increased cholesterol, infections C. Hair growth D. Hypertension only

B. Diarrhea, increased cholesterol, infections

Which drugs are S1PR modulators? A. Ozanimod, Etrasimod B. Methotrexate C. Infliximab D. Aspirin

A. Ozanimod, Etrasimod

Where are S1P receptors located? A. Only liver cells B. Immune cells and lymphatic endothelial cells C. Only neurons D. Only muscle cells

B. Immune cells and lymphatic endothelial cells