Digestive system Flashcards

Question

What are the most common diseases of GI tract?

Answer 1

- Peptic ulcers - Lactose intolerance - Appendicitis - Infections by bacterial pathogens

Answer 2

1) Helicobacter pylori colonises epithelial cells of the stomach or duodenum. 2) More HCl is secreted than normal to kill bacteria 3) Increased acidity damages stomach lining (mucous membranes) 4) chronic inflammation leads to atrophy of stomach wall and gastric malignant tumors Can be treated with simple antibiotics.

Answer 3

Lactase (enzyme on intestinal brush border) is normally present in all children under 4. In some adults, their lactase may be deficient, so they cannot digest and absorb lactose. Accumulation of undigested lactose prevents normal water absorption which leads to diarrhea. This lactose is than digested by bacteria (Lactobacillus, bifidobacterium) in colon to produce gases. Gases lead to bloating, crumps and flatulence.

Answer 4

- lymphatic nodules in appendix swell, leading to inflammation - peritonitis (appendix ruptures and infection enters peritoneum) is life threatening

Answer 5

1) Caused by E. Coli, Salmonella, Vibrio cholerae, Campylobacter 2) colonisation and/or toxin release 3) upregulation of cAMP 4) more CFTR activated 5) lots of Cl- is released in GI 6) water follows by osmos 7) diarrhea 140 000 deaths per year.

Answer 6

- 1.2-1.5 kg (one of the largest organs in the body), comparable to the brain - 2000 L of blood passes through liver every day Functions: 1) Blood detoxification: - chemical modification of drugs - converting more toxic substances into less toxic ones (alcohol, urea) using various enzymes - excretion of resulting molecules into bile 2) Carbohydrate metabolism: - synthesis and storage of glycogen (glycogenesis) - depolymerisation of glycogen into free glucose on demand (glycogenolysis) - gluconeogenesis (synthesis of glucose from non-hexose precursors) - converting fructose and galactose into glucose 3) Lipid metabolism: - synthesis of triglycerides - synthesis of cholesterol and excreting it into bile 4) Protein synthesis: - albumin - plasma transport proteins (many of alpha and beta globulins) - clotting factors (fibrinogen, prothrombin) - complement proteins 5) secretion of bile to aid in emulsifying lipids: - synthesis of bile salts - conjugation and excretion of bilirubin 6) Secondary endocrine function: - insulin-like growth factor (triggered by growth hormone) - angiotensinogen - hepcidin - vitamin D

Answer 7

- the product of haem (haemoglobin multiring cofactor) degradation after erythrocyte and myoglobin destruction - powerful antioxidant - pigment Metabolism in spleen: 1) heme oxidized to biliverdin (in macrophages) 2) biliverdin reduced to unconjucated bilirubin (in macrophages) Metabolism in liver: 3) unconjucated bilirubin to conjugated bilirubin 4) excreted into duodenum (small intestine) through bile Metabolism in colon: 5) conjugated bilirubin into urobilinogen (by gut bacteria) 6) urobilinogen to stercobilin, making faeces brown (by air exposure) Metabolism in kidney: 6.1) urobilinogen to urobilin, making urine yellow (by air exposure)

Answer 8

- Made of hexagonal lobules - Each of them has a central vein in the middle - there are 6 hepatic portal veins, hepatic arteries and bile ductules on each lobule corner - central vein, portal veins and arteries are connected to each other with sinusoids which deliver blood to hepatocytes - 70% of surface area of hepatocytes faces sinusoids, increasing the efficiency of blood-cell exchange - bile canaliculi connect hepatocytes with bile ductules

Answer 9

- Green - Contain no enzymes - Contains bile salts (cholic acid/chenodeoxycholic acid + glycine/taurine). Bile acids are cholesterol-based with a carboxyl group added. - Also contains bilirubin and cholesterol - Drugs and xenobiotics are cleared from blood, detoxified and excreted in bile - Made by hepatocytes --> bile canaliculi --> bile ductules --> common hepatic duct --> gallbladder (storage and concentration) --> common bile duct --> sphincter of Oddi (also connects pancreas) --> duodenum.

Answer 10

- bile salts on 2 opposite sides (2 particles per side, 4 in total) - phospholipids - monoglycerides - diglycerides

Answer 11

- The main source of glucose during the fasting state - Liver glycogen is enough for 4-5 hours of fasting in the resting state (1.5 hours for increased physical activity) - Glucagon triggers glycogen depolymerisation - Insulin triggers glycogenesis in the fed state - Both insulin and glucagon are produced by pancreas

Answer 12

- Paracetamol poisoning - Alcohol poisoning - Mushroom poisoning - Hepatitis A, B and C - Bacterial infections (Salmonella, Campy), originating from bacterial toxins from GI tract or from blood - Gall stones - Non-alcoholic fatty liver disease (metabolic dysfunction associated steatotic liver disease)

Answer 13

A) Increases lipid synthesis (activation of enzymes SREBP-1) and decreases lipid degradation (beta-oxidation; inhibition of enzymes PPARα and AMPK). Leads to lipid accumulation and hence fatty liver disease. - Decreased function of individual hepatocytes due to large fat droplets in their cytoplam. B) Increased production of reactive oxygen species (activation of the enzyme cytochrome P450s). Kupffer cells release proinflammatory cytokines, which increase immune response from macrophages, neutrophils, T cells. - Hepatocytes die (apoptosis), scarring tissue accumulates, hence cirrhosis. Ethanol also makes the tight junctions in the colon weaker, destroying intestinal barriers.

Answer 14

Specialised macrophages residing in the liver. The largest population of phagocytes in the body.

Answer 15

Normally, most of paracetamol is converted into non-toxic APAP (glucuronide and sulphate metabolites). But with higher doses, the amount of highly reactive NAPQI increases and not enough of it is detoxified into mercapturic acid and cysteine conjugates. NAPQI reacts with mitochondrial proteins, induces oxidative stress. This leads to mitochondria damage, decreased ATP production. Cells die by necrosis. This leads to acute liver failure.

Answer 16

A) Alpha-amanitin (cyclic peptide from 8 amino acids) binds to RNA polymerase II and inhibits it. No protein expression, cells stop functioning (apoptosis). B) Alpha-amanitin leads to an increased amount of reactive oxygen species by an unknown mechanism. Results in acute liver failure.

Answer 17

Hepatitis A: - acute but mild symptoms - hepatitis A virus spreads by the fecal-oral route (contaminated food) - no long-term effects Hepatitis B: - serious infection, lasts for 4-6 weeks - hepatitis B virus spreads by biological fluids (blood and sexual route) - 10 times more contagious than hepatitis C - often have long-term effects like cirrhosis due to chronic inflammation - often triggers the development of hepatocellular carcinoma before cirrhosis - DNA virus Hepatitis C: - hepatitis C virus spreads only through blood-to-blood contact - the rest is analogical to hepatitis B, but C develops more quickly and more deadlier - hepatocellular carcinoma often develops after cirrhosis - RNA virus

Answer 18

1) avoiding immune detection by immune system dysregulation 2) DNA integration to non-stop virus production in hepatocytes 3) activated tumour formation by: - inflammation - invasion and metastasis - angiogenesis - mutations - resisting apoptosis - evading growth suppressors - increased signalling for proliferation 4) deregulation of cell bioenergetics (hypoxia and lactic acid accumulation)

Answer 19

- caused by precipitated cholesterol due to fatty diet or lack of bile salts - 16% of adults - bile builds up in the liver - in worst cases, mucosa of gall bladder becomes atrophied and scarred

Answer 20

1) Citrate transporters (NaCT) are blocked or less inserted in the membranes 2) Less citrate means downregulation of lipid synthesis (less activated Acetyl-CoA carboxylase to produce malonyl-CoA) 3) Lipid accumulation decreases 4) Insulin sensitivity increases

Answer 21

Yellowing of skin and eyes. Caused by the accumulation of bilirubin in the body, which cannot be processed by the liver. The sign of liver failure.

Answer 22

- significantly varies in size, but 90 g is average Functions: - secretion of hormones at islet of Langerhans (2% of the organ): glucagon at alpha-cells; insulin and amylin (function similar to glucagon) at beta-cells; somatostatin (inhibits release of gastrin, glucagon and insulin) at D/delta-cells. - secretion of digestive enzymes (20 in total) at acini (98% of the organ) - secretion of bicarbonate at duct cells to make alkaline environment at small intestine

Answer 23

- Insulin dominates (glucagon is still present, though). - Insulin release is triggered by elevated glucose in the blood - Insulin triggers glucose uptake into liver, muscles and adipose tissue. This decreases blood glucose to premeal level. - Leads to increased glucose oxidation - increased synthesis of glycogen, fat and proteins

Answer 24

- Glucagon dominates (some insulin is still present) - Glucagon acts to elevate blood glucose levels by releasing glucose from the storages - increases glycogenolysis, gluconeogenesis and ketogenesis

Answer 25

- diabetes mellitus - pancreatitis

Answer 26

Type I: - autoimmune (autoantibodies recognise specific peptides at the beta-cells such as insulin itself or glutamic acid decarboxylase). Beta-cells are destroyed, resulting at insulin deficiency - more common in children - acute symptoms, requires life-long insulin injections - 8-10% of cases Type II: - beta cells are present but defective insulin secretion and tissues have decreased sensitivity to insulin, often as a result of obesity - in beta cells, too much lipids and glucose cause oxidative stress and formation of reactive oxygen species, not allowing Ca2+ to trigger insulin release through exocytosis. - in muscles and liver, reactive oxygen species lead to chronic inflammation, which interferes with insulin binding - in adipose tissue, hypoxia of hypertrophied cells also leads to chronic inflammation, preventing binding to insulin - more common at 40+ adults - symptoms develop slowly - 90% of cases

Answer 27

Affects the part of pancreas responsible for digestive enzyme production. Alcohol and some medications irritate ducts, directly leading to chronic inflammation. Blocked by gall stones (or tumour) ducts leads to build up of enzymes, resulting in autodigestion and chronic inflammation. Chronic inflammation leads to scarring and loss of functional parts of the organ.

Digestive system Flashcards

(51 cards)