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Pathophysiology of the digestive system and the liver

Ministry of Health of Ukraine

BOHOMOLETS NATIONAL MEDICAL UNIVERSITY

Pathophysiology department

Lecturer:

PhD Antsupova V.V.

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  • Ingestion of food
  • Digestion
  • mechanical digestion of food particles
  • breaks up food particles
  • Motility
  • movements of organs and food
  • mechanical digestion of food particles
  • Secretion
  • secretion of digestive juices
  • chemical digestion of food particles
  • Absorption
  • absorption of digestion products to

blood or lymphatic vessels

  • Storage and Elimination

- non-digested food particles

  • Protective function – mechanical, chemical, immunological
  • not only GIT organs but also the body as a whole, against the potential harmful food

components

THE GASTROINTESTINAL TRACT - function

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THE GASTROINTESTINAL TRACT - function

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CARBOHYDRATE DIGESTION AND ABSORPTION

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PROTEIN DIGESTION AND ABSORPTION

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FAT DIGESTION AND ABSORPTION

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THE GASTROINTESTINAL TRACT - absorption

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THE GASTROINTESTINAL TRACT - structure

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DISORDERS OF THE DIGESTIVE SYSTEM

  • Disorders of the digestive system have serious consequences for the activity of the organism as a whole
  • congenital malformations
  • traumatic processes
  • inflammatory processes
  • neoplastic processes
  • infectious processes

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  • Digestive system communicates with the external environment through the intake of fluids and food
  • Toxic substances in food and fluids

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  • GIT itself contains toxic substances

- secretion components - enzymes, HCl

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- waste products of digestion of food, bacterial flora

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THE MOST COMMON DISORDERS of the digestive system

  • Motor dysfunction of smooth muscle of the individual parts of the digestive system

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  • Indigestion of food and absorption of nutrients - malabsorption syndrome

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  • Bleeding into the individual parts of the digestive tract

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  • Perforation of the wall of the digestive system with subsequent leakage of the contents to the peritoneal cavity

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  • Obstruction in moving of the contents of one part of the digestive system to the next section

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  • Circulation disorders in the wall of the individual parts of the digestive system

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CLINICAL MANIFESTATIONS

of GI dysfunction

  • Vomiting
  • Dyspepsia
  • Constipation
  • Diarrhea
  • Abdominal Pain
  • Gastrointestinal Bleeding

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Clinical manifestations of GI dysfunction - VOMITING

  • is the forceful emptying of stomach and intestinal contents through the mouth
  • the vomiting center lies in the medulla oblongata and includes the reticular formation and tractus solitarius nucleus
  • stimulation of the vomiting center occurs directly by irritants or indirectly.
  • the sudden expansion of the stomach and duodenum in the sudden accumulation of contents
  • Indirect - reflex response to intense pain - trauma of ovary, testis, uterus, bladder and kidneys

- stimulating the vomiting center, for example. metabolic acidosis or brain lesions

  • Direct - irritation of the stomach mucosa by toxic substances

Cause of:

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Symptoms

Malfunction

Disease

  • abdominal pain
  • esophagus
  • peptic ulcer
  • feeling of imperfect digestion
  • stomach
  • long-lasting reflux of stomach contents into the esophagus
  • bloating
  • duodenum
  • gastritis
  • nausea

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  • frequently it is functional (non-ulcer) dyspepsia

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  • dyspepsia similar to ulcer symptomatology: pain predominates

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  • dyspepsia similar to dysmotility symptomatology: nausea, vomiting, bloating

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  • For individual diseases of the upper GI, these symptoms can be combined in various ways

Clinical manifestations of GI dysfunction - DYSPEPSIA (malfunction of digestion)

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  • an increase in the frequency of defecation and the fluid content, volume, and weight of feces.

Clinical manifestation

- can be acute or chronic

  • systemic effects of prolonged diarrhea – dehydration, electrolyte imbalance (hyponatremia, hypokalemia), metabolic acidosis, and weight loss
  • manifestations of acute bacterial or viral infection - fever, with or without cramping pain, bloody stools
  • Steatorrhea (fat in the stools) and diarrhea are common signs of malabsorption syndrome

Clinical manifestations of GI dysfunction - DIARRHEA

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Factors determining the stool volume and consistency

  • water volume
  • the presence of undigested and resorbable food components
  • increased production of intestinal secretions

Pathomechanisms involved in the origination of diarrhea

  • osmotic activity of intestinal contents
  • increased fluid secretion into the lumen of the intestine
  • accelerated intestinal peristalsis

Clinical manifestations of GI dysfunction - DIARRHEA

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Clinical manifestations of GI dysfunction - DIARRHEA

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  • Osmotic diarrhea (large-volume diarrhea)
  • non-absorbable substance in the intestine draws water into the lumen by osmosis => excess of water and the non-absorbable substance => large-volume diarrhea
  • large oral doses of poorly absorbed ions, such as magnesium, sulfate, and phosphate, can increase intraluminal osmotic pressure
  • osmotic diarrhea disappears when ingestion of the osmotic substance stops
  • malabsorption related to lactase deficiency, pancreatic enzyme or bile salt deficiency, small intestine bacterial overgrowth, and celiac disease also cause diarrhea

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lactase deficiency

lactose, milk sugar, is not digested by the intestine => high osmotic activity => binds water => increase in the intestine volume content

Clinical manifestations of GI dysfunction - DIARRHEA

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  • Secretory diarrhea (large-volume diarrhea)
  • caused by excessive mucosal secretion of chloride- or bicarbonate-rich fluid or inhibition of net sodium absorption
  • infectious causes include viruses (e.g., rotavirus), bacterial enterotoxins (e.g., E. coli, Vibrio cholerae ), or exotoxins from overgrowth of Clostridium difficile following antibiotic therapy

Clinical manifestations of GI dysfunction - DIARRHEA

  • Small-volume diarrhea
  • caused by an inflammatory disorder of the intestine, such as ulcerative colitis, Crohn disease, or microscopic colitis
  • inflammation of the colon causes smooth muscle contraction, cramping pain, urgency, and frequency

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  • Motility diarrhea
  • caused by resection of the small intestine (short bowel syndrome), surgical bypass of an area of the intestine – diarrhea predominant, diabetic neuropathy, hyperthyroidism, and laxative abuse
  • excessive motility decreases transit time, mucosal surface contact, and opportunities for fluid absorption, resulting in diarrhea

Clinical manifestations of GI dysfunction - DIARRHEA

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  • difficult or infrequent defecation
  • it is associated with difficulty emptying of solid stool, which is usually painful

Clinical manifestation (min. two of the following for at least 3 months)

  1. straining with defecation at least 25% of the time
  2. lumpy or hard stools at least 25% of the time
  3. sensation of incomplete emptying at least 25% of the time
  4. manual maneuvers to facilitate stool evacuation for at least 25% of defecations
  5. fewer than three bowel movements per week

Clinical manifestations of GI dysfunction - CONSTIPATION

  • less frequent defecation
  • smaller stool volume
  • hard stools
  • blood in the stools
  • difficulty passing stools (straining)
  • feeling of bowel fullness and discomfort

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Clinical manifestations of GI dysfunction - CONSTIPATION

It is resulting from failure of:

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  • transporting the contents (mucus secretion -> colon - motion content)

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  • damage of nerve cells in the intestinal wall - regulation of peristalsis (congenital absence of the cells - a significant dilatation of the colon)

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  • neurogenic disorders (stroke, PD, spinal cord injury, MS) - neurotransmitters are altered or neural pathways are degenerated, resulting in delayed colon transit time

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  • endocrine and metabolic disorders associated with constipation (Diabetes mellitus, hypokalemia, hypercalcemia)

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  • weakened muscles of the abdominal wall - pain after operation

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  • inflamed hemorrhoids in the anal part - during defecation are quite painful

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  • physical activity stimulates peristalsis => sedentary lifestyle and lack of regular exercise are common causes of constipation

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  • often the result of a large number of diseases

Bleeding in the upper GIT

(esophagus, stomach, duodenum)

Bleeding in the lower GIT

(jejunum, ileum, colon, rectum)

  • esophageal varices
  • inflammation
  • hemorrhagic gastritis
  • tumors
  • gastric and duodenal ulcers
  • hemorrhoids

Clinical manifestations of GI dysfunction - GASTROINTESTINAL BLEEDING

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  • sudden and intense bleeding in the GIT is life threatening and manifests the presence of blood in the stool or vomit

Signs of bleeding in GIT

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  • Hematemesis

presence of blood in vomit, in the form of fresh blood or blood precipitates

  • blood in vomit in the form of "coffee grounds"

blood flows more slowly in the stomach - it's time for him to digest it - hemoglobin converts to acidic hematin (black)

  • Melena

dark stool caused by digested blood

  • Occult bleeding

chronically recurrent losses of small amounts of blood that usually results in anemia due to iron losses

Clinical manifestations of GI dysfunction - GASTROINTESTINAL BLEEDING

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  • malabsorption syndromes interfere with nutrient absorption
  • historically malabsorption disorders have been classified as maldigestion or malabsorption

maldigestion

malabsorption

  • failure of the chemical processes of digestion (intestinal lumen)
  • caused by deficiencies of enzymes (pancreatic lipase, intestinal lactase)
  • inadequate secretion of bile salts and inadequate reabsorption of bile in the ileum
  • failure of the intestinal mucosa to absorb (transport) the digested nutrients
  • result of mucosal disruption (gastric or intestinal resection, vascular disorders, or intestinal disease)
  • Small intestine excretes certain digestive enzymes and is also the most important area for the absorption of nutrients
  • Resorption area depends on the construction of normal mucosa, which is shaped into the villi.

Clinical manifestations of GI dysfunction - MALABSORPTION SYNDROMES

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  • Incomplete digestion of food can occur at several levels GIT due to malfunction of secretion of digestive juices

Disease

Manifestation

  • after gastrectomy

- malabsorption of proteins (poor digestion)

  • pancreas

(chronic inflamation)

- malabsorption of proteins, sugar and fat

(pancreas produces enzymes to digest all food components => undigested proteins, polysaccharides and lipids - present in the faeces)

  • liver or biliary tract

- malabsorption of fat - reduced secretion of bile into the duodenum - important for the digestion of fats

  • secretion of bile into the duodenum

- malabsorption of vitamins - failure of fat digestion => vitamins A, D, E and K (soluble only in fat) are not sufficiently resorbed

Clinical manifestations of GI dysfunction - MALABSORPTION SYNDROMES

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  • celiac and lactose intolerance are considered to be primary diseases of malabsorption in our geographical area.

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  • Celiac – malabsortion of proteins

- caused by the the allergic response in the small intestine to gluten - a protein present in different cereals

- resulting inflammation of the mucosa results in villus atrophy => significantly reduced resorption area/capacity of the small intestine

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  • Lactase Deficiency – malabsorption of sugar

- Lactase - lack of activity - enzyme which degrades lactose (milk sugar) => after the ingestion of milk, lactose present in the small intestine as an osmotically active agent (binds H2O => greatly increases the volume of the intestinal contents. In addition, lactose is decomposed by intestinal bacteria to gas and substances that irritate the mucous membranes.

This results in abdominal cramps, bloating and diarrhea often.

Clinical manifestations of GI dysfunction - MALABSORPTION SYNDROMES

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Disorders of the GastroIntestinal Tract

Esophagus

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  • Dysphagia
  • Achalasia
  • Gastroesophageal reflux

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Stomach

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  • Gastritis
  • Peptic Ulcer
  • Gastric Cancer

Intestinal system

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  • inflammatory bowel disease
  • Crohn disease
  • Ulcerative colitis
  • Colon Cancer
  • Ileus

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  • Dysphagia is characterized as swallowing disorders, which may be due to mechanical obstruction of the esophagus, or functional disorder that impairs esophageal motility

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  • Mechanical obstruction

- intrinsic - tumor, strictures

- extrinsic - originate outside the esophageal lumen and narrow the esophagus by pressing inward on the esophageal wall. The most common cause of extrinsic mechanical obstruction is tumor

Disorders of the GIT - DYSPHAGIA

  • Functional dysphagia

- caused by neural or muscular disorders that interfere with swallowing or peristalsis.

- typical causes of functional dysphagia in the upper esophagus - dermatomyositis (a muscle disease) and neurologic impairments caused by stroke, MS, PD, ALS

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  • Achalasia is a primary esophageal motility disorder characterized by an inability of the lower esophageal sphincter to relax and is constantly contracted

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  • Food accumulates in the upper part of the esophagus, which gradually dilates,
  • Food is degraded bacteria and occasionally there is a regurgitation

Disorders of the GIT - ACHALASIA

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  • Gastroesophageal reflux disease (GERD)

is the reflux of acid and pepsin from the stomach to the esophagus that causes esophagitis.

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  • HCl, pepsin and bile - induce mucosal inflammation, erosion and ulceration
  • It is a consequence of weaken function of the lower esophageal sphincter, delayed gastric emptying with an increase in the pressure of its content and weaken clearing function of the esophagus (lack of saliva, poor esophageal peristalsis, and decreased production of the esophageal mucosal glands).

Disorders of the GIT - GASTROESOPHAGEAL REFLUX DISEASE (GERD)

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Clinical manifestation:

  • heartburn, chronic cough, asthma attacks
  • abdominal pain (within 1 hour after meals, repeating)
  • symptoms may worsen if the individual lies down, or in the case of increasing intra-abdominal pressure (as a result of coughing, vomiting, or of hard stool)
  • symptoms may be present even if the acid is not present in the esophagus
  • heartburn can be seen as chest pain, which requires the exclusion of cardiac ischemia
  • alcohol or foods that contain acid (citrus fruits) can cause discomfort and worsen the syptoms

GASTROESOPHAGEAL REFLUX DISEASE (GERD)

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  • is a result of imbalance between the mucosal defense mechanisms in the esophagus, stomach and duodenum, and gastric mucosa-damaging mechanisms

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  • relates to digestion of mucous membrane and lower parts of the stomach, duodenum, and lower esophagus by HCl and pepsin

Disorders of the GIT – PEPTIC ULCER

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PEPTIC ULCER

Risk factors for peptic ulcer disease:

  • genetic predisposition
  • H.pylori infection of the gastric mucosa
  • age greater than 65 years
  • psychologic stress (mechanism unknown)
  • excessive use of alcohol
  • smoking
  • acute pancreatitis
  • chronic obstructive pulmonary disease
  • obesity
  • cirrhosis

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PEPTIC ULCER

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  • Types of Peptic Ulcers:

acute - quickly heal by the mucosa regeneration

chronic - penetrate deeper into the tissue, healing takes several weeks or months

  • Special types of ulcers:

Cushing - traumatic origin, or after surgery CNS (irritation of n. Vagus -> hypersecretion HCl)�Curling - traumatic origin, after burns (↑ levels of histamin -> hypersecretion HCl)�Zollinger - Ellison Syndrome - ↑ production of gastrin -> stimulates the secretion of HCl)�Stress ulcers - mucosal perfusion defect

PEPTIC ULCER

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PEPTIC ULCER

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  • Mucus-bicarbonate barrier
    • smooth adhesive mucus layer
    • pH gradient (lumen – epithelial surfice)
    • bicarbonate secretion by epithelial cells

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  • H+ disposal in gastric wall
    • mucoid barrier damage
    • back diffusion of H+ into the wall
    • mucosal blood flow

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  • Proliferation and epithelial repair
    • mitosis and cell migration along the basal membrane
    • mucoid cap after epithelial damage

EPITHELIAL GASTRODUODENAL BARRIER

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  • Mucus - bicarbonate layer

- protects the mucosa from autodigestion�- on the surface of the mucosa -> layer of mucus – non-permeable layer for acid and pepsin -> and prevent the intake of the hydrogen ion (H+) to the mucosal tissue which causes damage to the cells and subsequent digestion with pepsin�- in mucosa itself, a large amount of bicarbonate ions (HCO3-) is produced - buffering H+ ions that penetrate mucosa�- good blood flow

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  • Hlien – bikarbonátova vrstva -

EPITHELIAL GASTRODUODENAL BARRIER

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  • Mucoid cap
  • mechanisms associated with rapid repairing of the damage area
  • mucus with fibrin - form "fibrin cap" - strongly adhere to erosion - gives the condition of regeneration of the epithelium under it (preventing further penetration of aggressive agents)

EPITHELIAL GASTRODUODENAL BARRIER

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    • Mitosis and the cell migration along the basal layer

EPITHELIAL GASTRODUODENAL BARRIER

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Disorders of the GIT – PEPTIC ULCER

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Appendicitis is an inflammation of the vermiform appendix, which is a projection from the apex of the cecum

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Clinical manifestation:

  • pain is initially diffuse and poorly localizable (visceral pain), later when the inflammation transit to the parietal peritoneum, patients localize the pain in the right hypogastrium (somatization visceral pain)
  • the pain may be vague at first, increasing in intensity over 3 to 4 hours
  • right lower quadrant pain is associated with extension of the inflammation to the surrounding tissues
  • nausea, vomiting, and anorexia follow the onset of pain, and fever is common
  • diarrhea occurs in some individuals, particularly children; others have a sensation

of constipation

  • perforation, peritonitis, and abscess formation are the most serious complications of appendicitis

Disorders of the GIT – APPENDICITIS

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The exact cause of appendicitis is controversial.

  • obstruction of the lumen with stool, tumors, or foreign bodies with consequent increased intraluminal pressure, ischemia, bacterial infection, and inflammation is a common theory
  • regardless of the cause - intraluminal pressure increases (secretion of mucus and fluids continues), propagation of bacteria and leukocytes continues
  • the increased pressure decreases mucosal blood flow, and the appendix becomes hypoxic
  • the mucosa ulcerates, promoting bacterial or other microbial invasion with further inflammation and edema.
  • inflammation may involve the distal or entire appendix

Disorders of the GIT – APPENDICITIS

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Disorders of the GIT –

INFLAMMATORY BOWEL DISEASE

  • Ulcerative colitis and Crohn disease are chronic, relapsing inflammatory bowel diseases (IBDs) of unknown origin
  • both diseases are associated with genetic factors, alterations in epithelial cell barrier functions, immunopathology related to abnormal T-cell reactions to microflora and other luminal antigens, and varying phenotypes

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Disorders of the GIT –

INFLAMMATORY BOWEL DISEASE

Crohn disease - any part of the digestive tract - the most common - terminal part of the ileum

- inflammatory process affects all layers of the wall of the digestive tract -> ulcerations in the wall, the formation of fistulas and abscesses

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Ulcerative colitis - affects colon a rectum

- the process of fibrosis is not intensified

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  • is an idiopathic inflammatory disorder that affects any part of the gastrointestinal tract from the mouth to the anus
  • the distal small intestine and proximal large colon are most commonly affected by the disease
  • inflammation healing scars can lead to narrowing of the lumen and obstruction of the intestinal tract -> fibrosis

INFLAMMATORY BOWEL DISEASE

- Crohn disease

  • characteristic symptoms are abdominal pain and diarrhea
  • malabsorptions are the result of loss of functional mucosal absorptive surface
  • most often it is deficit of several food components and dehydration

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  • is a chronic inflammatory disease that causes ulceration of the colonic mucosa and extends proximally from the rectum into the colon
  • although the cause is unknown, dietary, infectious, genetic, and immunologic factors are all suggested causes (less common in smokers)
  • in oppposite to Crohn disease, the fibrosis process is not intensified
  • the primary lesions are continuous with no skip lesions, are limited to the mucosa, and are not transmural
  • the mucous layer is thinner than normal - impairment of the epithelial barrier

INFLAMMATORY BOWEL DISEASE

- Ulcerative Colitis

  • the inflammation damages the epithelial mucosal barrier with leak of fluids into the gut
  • the clinical symptoms are diarrhea, weight loss, abdominal pain and loss of blood in the faeces

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ABDOMINAL EMERGENCY

Accident origin

  • traumatic Haemoperitoneum - accumulation of large quantities of blood in the abdominal cavity due to e.g. traumatic rupture of the spleen, liver
  • Post-traumatic peritonitis - an accident puncture of an internal organ and a consequent release of its contents into the peritoneal cavity

Nontraumatic origin

  • Abdominal emergency of an inflammatory origin - 1) inflammation limited to a single organ with minimal spread to the surrounding peritoneal structures (appendicitis, chole-cystitis) - results in intraperitoneal abscess formation. 2) inflammation spreads to the peritoneal cavity - peritonitis
  • Abdominal emergency associated with intestinal obstruction
  • Abdominal emergency associated with bleeding in the digestive system - peptic ulcer and bowel disease, tumor process, bleeding disorder ...

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- is a serious condition that can have many causes

  • mechanical obstruction - obstruction in the lumen of the intestine and leads to compression of the wall
  • vascular obstruction - strangulation of blood vessel due to thrombosis or embolism
  • functional obstruction - due to the "paralysis" of the intestinal muscles

Pathogenesis – stagnation od the content, absorption and secretion, bacterial overgrowth, and hypoxia intestinal wall

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Clinical manifestation

  • vary according to the type of obstruction and its location in the intestinal system
  • may be colic pain (obstruction of the lumen) or permanent
  • vomiting and abdominal distension

Disorders of the GIT – ILEUS

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  • Caused by the obstruction of the intestinal lumen�- Intraluminal obturation - gallstones, swallowed foreign body lying in the lumen of the intestine�- Intramural obturation - malignant-benign tumors of the intestinal wall - obstacle is located in the walls of the intestines - cause intestinal obstruction and narrowing� - Extramural obturation - tumors in the peritoneal area, peritoneal adhesions - obstacle is outside of the intestine and acts of ambient pressure

ILEUS – Mechanical Ileus

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  • interruption of intestinal passage through the lumen

- strangulation of the of blood vessels with an interruption of the blood circulation, impaired nutrition of the intestinal wall (ischemia, ischemic necrosis of the intestinal wall)

- arising from the adhesions in abdominal surgery, herniation, intussusception (intestinal segment is inserted into an adjacent segment)

ILEUS – Mechanical Ileus

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  • Paralytic ileus - in paralysis, intestinal immobility, intestine vasculature failure, CNS disorders
  • Spastic ileus - there is a long spasm of various segments of the intestine

       - metabolic disorders, parathyroid diseases, spinal cord injury

    - this happens very rarely

ILEUS – Dynamic ileus

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Small intestine obstruction

  • most often caused by postoperative adhesions, Crohn's disease and hernias
  • proximal to the obstruction of the intestine, leads to dilatation, due to the accumulation of fluid and gas swallowed
  • dilate in turn stimulates secretion - increases peristalsis and intraluminal pressure�leading to loss of fluid and electrolytes in the 'third space’�

- vomiting occurs in the proximal localization of obstruction.

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Obstruction of the colon

  • tumors or anatomical abnormalities such as volvulus (part of the intestine completely turns around the mesenteric hinge)
  • constipation, abdominal pain, anorexia and vomiting later

INTESTINAL OBSTRUCTION

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Hepatic insufficiency

  • The pathological condition, in which the functional activity of the liver doesn’t maintain the homeostasis, leading to disruption of the functioning of the body.

On the basis of pathogenesis there are the following types of hepatic insufficiency:

  • Hepatocellular(in the dystrophic and necrotic lesions of the hepatocytes);
  • Exretory or cholestatic(as a result of the disturbance of the cholepoiesis and cholekinesis);
  • Hepato-vascular(in the blood circulation disturbances in the liver due to local (e.g., thrombosis, embolism) or general vascular disorders(e.g., right-heart failure, shock);
  • Combined

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HEPATIC INSUFFICIENCY

The degree of dysfunction

Clinical course

  • Total;
  • Partial
  • Immediate;
  • Acute;
  • Chronic

Pathogenesis

  • Hepatocellular;
  • Exretory;
  • Hepato-vascular;
  • Combined

Classified by:

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Hepatic coma

  • The pathological state caused by toxic damage of the CNS with severe disorders of its functions(loss of consciousness, absence of reflexes,and convulsions), blood circulation and respiration that occurs due to the severe hepatic insufficiency.

Depending on the causes and mechanisms of development there are three types of the hepatic coma:

  • Hepatocellular, or parenchymatous(as a result of the massive necrosis of the hepatocytes, e.g., in the viral hepatitis, toxic liver dystrophy, cirrhosis, acute disorders of the hepatic blood flow);
  • Portocaval, or shuntic that occurs in the portal hypertension syndrome( when toxic substances from the intestine entering via the portocaval anastomoses into the general circulation not being neutralized in the liver what is required);
  • Combined

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PATHOGENESIS OF HEPATIC COMA

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JAUNDICE

  • The syndrome that occurs in the high concentration of bilirubin in the blood which is characterized by the yellowing of the skin, mucous membranes, especially eyes, due to deposition of the bile pigments in them.

Depending on the primary localization of the pathological process and mechanism of occurrence there are the following types of the jaundice:

  • Prehepatic(suprahepatic), caused by the increased production of bilirubin primarily due to the increased breakdown of the red blood cells (the hemolytic jaundice);
  • Parenchymatous, caused by disorders of uptake, conjugation and exretion of bilirubin by the hepatocytes due to damages in various pathlogical processes at this level( the hepatocellular jaundice);
  • Posthepatic (subhepatic,mechanical, obstructive, cholestatic), occurs in obstruction of the bile outflow

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BILIRUBIN METABOLISM

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JAUNDICE: REVIEW

Prehepatic

Any etiological factor leading to hemolytic anemia.

Excessive hemolysis of RBC with formation of an excess of unconjugated bilirubin

In the blood: increased indirect(unconjugated) bilirubin;

In the stool: there is more stercobilin so it’s darker;

In the urine: it has more urobilin so it has more intense coloration.

Hepatic

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Hepatitis of any nature;

Toxic damage to the liver;

Liver carcinoma

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Disorders of uptake, conjugation and exretion of bilirubin by the hepatocytes due to their damage

In the blood: mixed hyperbilirubinemia( both direct and indirect one rise), cholalemia.

In the stool : there is less stercobilin so it’s lighter – hypocholia

In the urine: direct bilirubinuria + urobilinuria with an intense yellow color

Posthepatic

Tumors;

Biliary sclerosis;

Cholangitis;

Bile stones;

Pancreatitis with edema of the gland

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Compression or obstruction of bile ducts impeding bile outflow

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In the blood: direct bilirubinemia( increased content of conjugated bilirubin), cholalemia

In the stool: there is significantly less or no stercobilin – hypo-or acholia(colorless stool)

In the urine: direct bilirubinuria – the urine gets a dark yellow color (beer like)

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Causes:

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Leading mechanisms:

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Key features:

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