Patofisiologi Gizi

Gangguan Sistem Pencernaan

• penyakit gastrointestinal • gangguan akibat diare• penyakit hati

Intraluminal stage:Intraluminal stage: Physical and Physical and

Enzymatic digestionEnzymatic digestion

Intestinal stage: Further hydrolysis of carbohydratesMucosal cell uptake and transport of hydrolyzed productsFormation of chylomicrons from TAG and cholesterol

Transport across the Transport across the epithelial cells to epithelial cells to lymphatics or blood lymphatics or blood vesselsvessels

Deranged stage Clinical syndrome Pathophysiology

Intraluminal stage

Digestion of fats, proteins

Pancreatic damage, pancreatitis, cystic fibrosis, carcinoma

Decreased production of pancreatic enzymes

Zollinger-Ellison syndrome

Inactivation of pancreatic enzymes by excess gastric acid

Solubilization of fat Biliary tract obstruction, cholestatic liver disease

Inadequate delivery of bile to the duodenum or disruption of the enterohepatic circulation

Preabsorption, modification of particular nutrients

Pernicious anemia Deficiency of intrinsic factor required for vit B12 absorption

Iron deficiency from impaired absorption

Inadequate dietary ascorbic acid, citric acid: phytates, tannates, in the diet

Tapeworm infection Competitive uptake of vitamin B12 by bacteria or worms

Deranged stage

Clinical syndrome

Pathophysiology

Intestinal stage

Mucosal cell digestion

Lactase deficiency

Inability to hydrolyze lactose into absorbable monosacharides

Mucosal uptake and transport

Crohn’s disease, celiac sprue, postinfectious sprue

Reduction of absorptive surface area, mucosal cell injury

Transport stage

Lymphatic transport

Lymphoma, TBC,

Obstruction to intestinal lacteal or ducts

GastritisGastritis

Acute erosive GastritisAcute erosive Gastritis-Focal inflammatory lesions -Focal inflammatory lesions of the mucosa. of the mucosa.

-Sometimes the erosions extend into the deeper layers -Sometimes the erosions extend into the deeper layers of the wall (beyond the lamina propria) to form of the wall (beyond the lamina propria) to form acute acute ulcersulcers. .

-Produced by alcohol, drugs (corticosteroids and -Produced by alcohol, drugs (corticosteroids and NSAIDs) or infections with Helicobacter pylori or virus. NSAIDs) or infections with Helicobacter pylori or virus.

-After severe stress (severe burns, trauma, shock, and -After severe stress (severe burns, trauma, shock, and sepsis) the gastritis may develop into a life-threatening sepsis) the gastritis may develop into a life-threatening condition with stress ulcers and haemorrhage. condition with stress ulcers and haemorrhage.

Gastric UlcerGastric Ulcer

Gastritis Gastritis

long-lasting inflammation of the gastric wall. long-lasting inflammation of the gastric wall. The superficial layers are infiltrated with lymphocytes The superficial layers are infiltrated with lymphocytes

and plasma cells. and plasma cells. Atrophia develops with loss of both parietal and chief Atrophia develops with loss of both parietal and chief

cells. cells. Helicobacter pyloriHelicobacter pylori are the chief cause of chronic are the chief cause of chronic

gastritis in the antrum. gastritis in the antrum. The loss of parietal cells leads to The loss of parietal cells leads to achlorhydria achlorhydria (absent (absent

HCl production), and to deficiency of HCl production), and to deficiency of intrinsic intrinsic factor.factor. Vitamin B12 is not absorbed in the ileum in the Vitamin B12 is not absorbed in the ileum in the

absence of intrinsic factor, so the result is absence of intrinsic factor, so the result is pernicious pernicious anaemiaanaemia..

Peptic ulcer diseasePeptic ulcer disease

mucusal ulcer in an acid- producing zone in mucusal ulcer in an acid- producing zone in the distal stomach or the proximal the distal stomach or the proximal duodenum. duodenum.

Helicobacter pylori Helicobacter pylori infection of the stomach infection of the stomach and the colonisation of the upper and the colonisation of the upper gastrointestinal tract with this bacteria, gastrointestinal tract with this bacteria, destroys the protective system, and at the destroys the protective system, and at the same time provokes excess acid secretion.same time provokes excess acid secretion.

Pain complains typically occur a few hours Pain complains typically occur a few hours following a meal or awaken the patient at following a meal or awaken the patient at night, points out Epigastric painsnight, points out Epigastric pains

Bleeding : hematemesis -melenaBleeding : hematemesis -melena

Peptic Ulcer DiseasePeptic Ulcer Disease

Peptic Ulcer: risk Peptic Ulcer: risk factorsfactors drugsdrugs (ASA, NSAIDs and corticoids), (ASA, NSAIDs and corticoids), hyperparathyroidismhyperparathyroidism (the high Ca2+ level (the high Ca2+ level

stimulates gastric acid secretion), stimulates gastric acid secretion), gastrin-producing tumours gastrin-producing tumours of the pancreas .of the pancreas . increasedincreased pepsinogen pepsinogen from the chief cells, from the chief cells, increased parietal cell mass, increased parietal cell mass, Strong alcoholic beverages. Strong alcoholic beverages. Caffein (stimulates gastric acid secretion).Caffein (stimulates gastric acid secretion). GeneticGenetic

DiarrhoeaDiarrhoea

increased stool frequency increased stool frequency and implies larger than and implies larger than normal stool weightnormal stool weight

Zollinger-Ellisons syndromeZollinger-Ellisons syndrome with tremendous with tremendous gastric secretiongastric secretion

Bacterial or Secretory diarrhoeaBacterial or Secretory diarrhoea is caused by is caused by increased Cl secretion and reduced Na+ increased Cl secretion and reduced Na+ reabsorption. Enterotoxins from bacteria on the reabsorption. Enterotoxins from bacteria on the microvillus surface affect the toxin receptors, microvillus surface affect the toxin receptors, which increases the cAMP level in the cell. This in which increases the cAMP level in the cell. This in turn activates the chloride- channel and inhibits turn activates the chloride- channel and inhibits the NaCl reabsorption process.the NaCl reabsorption process.

Inflammatory diarrhoeaInflammatory diarrhoea is caused by mucosal is caused by mucosal destruction with outflow of fluid and blood such destruction with outflow of fluid and blood such as in ulcerative colitis.as in ulcerative colitis.

Diarrhoea Diarrhoea

Osmotic diarrhoeaOsmotic diarrhoea caused by active caused by active substances in the gut lumen. These substances in the gut lumen. These substances are normal nutrients in case of substances are normal nutrients in case of malabsorption, or non-absorbable malabsorption, or non-absorbable substances taken for some reason or substances taken for some reason or other.other.

Diarrhoea following ileal resectionDiarrhoea following ileal resection. Bile . Bile acids are normally reabsorbed in the acids are normally reabsorbed in the terminal ileum. Following ileal resection terminal ileum. Following ileal resection the bile acids enter the colon. Bile acids the bile acids enter the colon. Bile acids are toxic to the colonic mucosa and are toxic to the colonic mucosa and stimulate colonic secretion of large stimulate colonic secretion of large volumes,volumes,

slow colonic motility:slow colonic motility:Colon irritableColon irritable abdominal pain (diffuse or localised to the left iliac abdominal pain (diffuse or localised to the left iliac

fossa), which is relieved by defecation or flatulence. fossa), which is relieved by defecation or flatulence.

There are often frequent small-volume stools, but There are often frequent small-volume stools, but the patient feels that the emptying is incomplete. the patient feels that the emptying is incomplete. The abdomen is distended. This is a condition with The abdomen is distended. This is a condition with painful spasms causing constipation alternating with painful spasms causing constipation alternating with mucous diarrhoea. mucous diarrhoea.

The condition is related to stress and sedentary life The condition is related to stress and sedentary life style, and is relieved by daily exercise. style, and is relieved by daily exercise.

DiverticulosisDiverticulosis

DiverticulosisDiverticulosis or or diverticular disease diverticular disease is a condition with is a condition with herniation of the mucosa through the muscular layers of herniation of the mucosa through the muscular layers of the colon, caused by increased intraluminal pressure. the colon, caused by increased intraluminal pressure.

if they are inflamed the condition is called if they are inflamed the condition is called diverticulitisdiverticulitis. . Persons with disturbed stool-habits are likely to develop Persons with disturbed stool-habits are likely to develop increased intraluminal pressure during defaecation, and increased intraluminal pressure during defaecation, and they may develop hernias at weak spots in the gut wall. they may develop hernias at weak spots in the gut wall.

The incidence is high in inactive persons and low in The incidence is high in inactive persons and low in vegetarians or in persons with a high dietary fibre vegetarians or in persons with a high dietary fibre content. content.

Mild clinical cases can be treated with light daily exercise Mild clinical cases can be treated with light daily exercise such as walking in a hilly environment. Emergency cases such as walking in a hilly environment. Emergency cases may need surgery.may need surgery.

ConstipationConstipation

frequently caused by a low fibre intake frequently caused by a low fibre intake in sedentary persons. They often exhibit in sedentary persons. They often exhibit irregular irregular defaecation habits, and defaecation habits, and irrational use of laxatives. Such habits irrational use of laxatives. Such habits suppress the natural reflexes.suppress the natural reflexes.

The condition is improved by a high-fibre The condition is improved by a high-fibre diet or by daily walking. Suppositories diet or by daily walking. Suppositories may be necessary, but long-term use of may be necessary, but long-term use of laxatives is contraindicated.laxatives is contraindicated.

Jaundice (icterus)Jaundice (icterus)

The normal [bilirubin] in blood plasma is up to The normal [bilirubin] in blood plasma is up to 17 mg /l or 29 mmol/ l 17 mg /l or 29 mmol/ l The threshold for visible jaundice (icterus) is a The threshold for visible jaundice (icterus) is a [bilirubin] in blood plasma [bilirubin] in blood plasma above 18 mg /l or above 18 mg /l or 30 mM 30 mM in most people.in most people.

Three types of icterus can be distinguished:Three types of icterus can be distinguished:

a.a. Prehepatic or haemolytic icterusPrehepatic or haemolytic icterus b.b. Intrahepatic icterusisIntrahepatic icterusis c.c. Posthepatic icterusPosthepatic icterus

Regulation of Bile ReleaseRegulation of Bile Release

Prehepatic or Prehepatic or haemolytic icterushaemolytic icterus• Haemolytic anaemia causes haemolytic Haemolytic anaemia causes haemolytic

jaundice. jaundice.

• Increased destruction of red cells (haemolysis) Increased destruction of red cells (haemolysis) increases the bilirubin production to the extent increases the bilirubin production to the extent that the hepatocytes cannot conjugate the that the hepatocytes cannot conjugate the bilirubin as rapidly as it is formed (the key hole bilirubin as rapidly as it is formed (the key hole enzyme is enzyme is glucuronyl transferaseglucuronyl transferase). ).

• The neurotoxic free bilirubin in blood plasma The neurotoxic free bilirubin in blood plasma rises much above normal, and large quantities rises much above normal, and large quantities of urobilinogen is excreted in the urine.of urobilinogen is excreted in the urine.

Intrahepatic Intrahepatic icterusisicterusis Caused by poor hepatocyte function.Caused by poor hepatocyte function.

Damages of the hepatocytes by infections, Damages of the hepatocytes by infections, tumours, or toxic agents impair the uptake, tumours, or toxic agents impair the uptake, transport and conjugation of bilirubin. transport and conjugation of bilirubin.

AbsenceAbsence of glucuronyl transferase or of glucuronyl transferase or inhibition of the enzyme by steroids inhibition of the enzyme by steroids block block conjugation of bilirubin.conjugation of bilirubin.

Posthepatic Posthepatic icterusicterus

caused 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.

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