Presentation on theme: "Gangguan Sistem Pencernaan"— Presentation transcript:
1Gangguan Sistem Pencernaan Patofisiologi GiziGangguan Sistem Pencernaanpenyakit gastrointestinalgangguan akibat diarepenyakit hati
2Intraluminal stage: Physical and Enzymatic digestion Intestinal stage:Further hydrolysis of carbohydratesMucosal cell uptake and transport of hydrolyzed productsFormation of chylomicrons from TAG and cholesterolTransport across the epithelial cells to lymphatics or blood vessels
3Deranged stageClinical syndromePathophysiologyIntraluminal stageDigestion of fats, proteinsPancreatic damage, pancreatitis, cystic fibrosis, carcinomaDecreased production of pancreatic enzymesZollinger-Ellison syndromeInactivation of pancreatic enzymes by excess gastric acidSolubilization of fatBiliary tract obstruction, cholestatic liver diseaseInadequate delivery of bile to the duodenum or disruption of the enterohepatic circulationPreabsorption, modification of particular nutrientsPernicious anemiaDeficiency of intrinsic factor required for vit B12 absorptionIron deficiency from impaired absorptionInadequate dietary ascorbic acid, citric acid: phytates, tannates, in the dietTapeworm infectionCompetitive uptake of vitamin B12 by bacteria or worms
4Deranged stageClinical syndromePathophysiologyIntestinal stageMucosal cell digestionLactase deficiencyInability to hydrolyze lactose into absorbable monosacharidesMucosal uptake and transportCrohn’s disease, celiac sprue, postinfectious sprueReduction of absorptive surface area, mucosal cell injuryTransport stageLymphatic transportLymphoma, TBC,Obstruction to intestinal lacteal or ducts
5Gastritis Acute erosive Gastritis -Focal inflammatory lesions of the mucosa.-Sometimes the erosions extend into the deeper layers of the wall (beyond the lamina propria) to form acute ulcers.-Produced by alcohol, drugs (corticosteroids and NSAIDs) or infections with Helicobacter pylori or virus.-After severe stress (severe burns, trauma, shock, and sepsis) the gastritis may develop into a life-threatening condition with stress ulcers and haemorrhage.
7Gastritis long-lasting inflammation of the gastric wall. The superficial layers are infiltrated with lymphocytes and plasma cells.Atrophia develops with loss of both parietal and chief cells.Helicobacter pylori are the chief cause of chronic gastritis in the antrum.The loss of parietal cells leads to achlorhydria (absent HCl production), and to deficiency of intrinsic factor.Vitamin B12 is not absorbed in the ileum in the absence of intrinsic factor, so the result is pernicious anaemia.
8Peptic ulcer diseasemucusal ulcer in an acid- producing zone in the distal stomach or the proximal duodenum.Helicobacter pylori infection of the stomach and the colonisation of the upper gastrointestinal tract with this bacteria, destroys the protective system, and at the same time provokes excess acid secretion.Pain complains typically occur a few hours following a meal or awaken the patient at night, points out Epigastric painsBleeding : hematemesis -melena
10Peptic Ulcer: risk factors drugs (ASA, NSAIDs and corticoids),hyperparathyroidism (the high Ca2+ level stimulates gastric acid secretion),gastrin-producing tumours of the pancreas .increased pepsinogen from the chief cells,increased parietal cell mass,Strong alcoholic beverages.Caffein (stimulates gastric acid secretion).Genetic
11Diarrhoeaincreased stool frequency and implies larger than normal stool weightZollinger-Ellisons syndrome with tremendous gastric secretionBacterial or Secretory diarrhoea is caused by increased Cl secretion and reduced Na+ reabsorption. Enterotoxins from bacteria on the microvillus surface affect the toxin receptors, which increases the cAMP level in the cell. This in turn activates the chloride- channel and inhibits the NaCl reabsorption process.Inflammatory diarrhoea is caused by mucosal destruction with outflow of fluid and blood such as in ulcerative colitis.
12DiarrhoeaOsmotic diarrhoea caused by active substances in the gut lumen. These substances are normal nutrients in case of malabsorption, or non-absorbable substances taken for some reason or other.Diarrhoea following ileal resection. Bile acids are normally reabsorbed in the terminal ileum. Following ileal resection the bile acids enter the colon. Bile acids are toxic to the colonic mucosa and stimulate colonic secretion of large volumes,
14slow colonic motility: Colon irritableabdominal pain (diffuse or localised to the left iliac fossa), which is relieved by defecation or flatulence.There are often frequent small-volume stools, but the patient feels that the emptying is incomplete. The abdomen is distended. This is a condition with painful spasms causing constipation alternating with mucous diarrhoea.The condition is related to stress and sedentary life style, and is relieved by daily exercise.
15DiverticulosisDiverticulosis or diverticular disease is a condition with herniation of the mucosa through the muscular layers of the colon, caused by increased intraluminal pressure.if they are inflamed the condition is called diverticulitis. Persons with disturbed stool-habits are likely to develop increased intraluminal pressure during defaecation, and they may develop hernias at weak spots in the gut wall.The incidence is high in inactive persons and low in vegetarians or in persons with a high dietary fibre content.Mild clinical cases can be treated with light daily exercise such as walking in a hilly environment. Emergency cases may need surgery.
16Constipationfrequently caused by a low fibre intake in sedentary persons. They often exhibit irregular defaecation habits, and irrational use of laxatives. Such habits suppress the natural reflexes.The condition is improved by a high-fibre diet or by daily walking. Suppositories may be necessary, but long-term use of laxatives is contraindicated.
18Jaundice (icterus)The normal [bilirubin] in blood plasma is up to 17 mg /l or 29 mmol/ lThe threshold for visible jaundice (icterus) is a [bilirubin] in blood plasma above 18 mg /l or 30 mM in most people.Three types of icterus can be distinguished:Prehepatic or haemolytic icterusIntrahepatic icterusisPosthepatic icterus
20Prehepatic or haemolytic icterus Haemolytic anaemia causes haemolytic jaundice.Increased destruction of red cells (haemolysis) increases the bilirubin production to the extent that the hepatocytes cannot conjugate the bilirubin as rapidly as it is formed (the key hole enzyme is glucuronyl transferase).The neurotoxic free bilirubin in blood plasma rises much above normal, and large quantities of urobilinogen is excreted in the urine.
21Intrahepatic icterusis Caused by poor hepatocyte function.Damages of the hepatocytes by infections, tumours, or toxic agents impair the uptake, transport and conjugation of bilirubin.Absence of glucuronyl transferase or inhibition of the enzyme by steroids block conjugation of bilirubin.
22Posthepatic icteruscaused by cholestasis due to gallstones or pancreatic tumours.Gallstones or tumour masses obstruct the bile ducts, which is causing extrahepatic cholestasis with impaired excretion of conjugated bilirubin to the intestine.conjugated bilirubin reflux to the blood. Most of the bilirubin in plasma is therefore conjugated and some of it strongly bound to plasma albumin.