DISORDERS OF THE ACCESSORY ORGANS OF DIGESTION

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DISORDERS OF THE ACCESSORY ORGANS OF DIGESTION

• DISORDERS OF THE LIVER,GALLBLADDER PANCREAS,GI
  TRACT AND CANCERS OF THE ACCESSORY ORGANS

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PORTAL HYPERTENSION

• HIGH BLOOD PRESSURE IN PORTAL VENOUS SYSTEM
• (normal pressure 3 mmHg /
  hypertension start at 10 mmHg)
• INCREASED PRESSURE CAUSES VARICES( collateral
  vessels) ACROSS ESOPHAGUS, ANTERIOR ABDOMINAL
  WALL AND RECTUM
• CAUSED BY OBSTRUCTION OR IMPEDE BLOOD FLOW
  BUILDING OF ARTERIOVENUS SHUNTS

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PORTAL HYPERTENSIONPATHOPYSIOLOGY

• INTRAHEPATIC CAUSES VASCULAR REMODELING WITH
  INTRAHEPATIC SHUNTS,THROMBOSIS,INFLAMATION OR
  FIBROSIS CIRRHOSIS( most common cause), VIRAL
  HEPATITIS OR SCHISTOSOMIASIS
• POSTHEPATIC CAUSES FROM VEIN THROMBOSIS,
  CARDIAC RIGHT SIDE FALIURE OR CONSTRICTIVE
  PERICARDITIS BLOOD BACK UP INCREASED PRESSURE
  IN PORTAL SYSTEM
• PREHAPATIC CAUSE THROMBOSIS OR NARROWING OF
  PORTAL VEINS
• HEPATOPULMONARY SYSTEM AND PORTOPULMONARY
  HYPERTENSION CAUSED BY RELASE OF NITRIC OXIDE
  AND CO2 MICROVASCULAR INTRAPULMONARY
  VASODILATION . CLINICAL MANIFESTATION
  NONSPECIFIC, DYSPNEA AND DIGITAL CLUBBING.
  

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PORTAL HYPERTENSION CLINICAL MANIFESTATION

• BLOOD VOMITING BLEEDING OF ESOPHAGEAL VARICES
• ANEMIA AND MELENA (slow chronic bleeding)
• RUPTURE OF E.VARICES PAINLESS, VOMITING DARK
  BLOOD( mortality in one year 30-60)
• HEMORRHODILA VARICES RECTAL BLEEDING,
  HEMATOCHEZIA (maroon colored stools)

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PORTAL HYPERTENSIONEVALUATION AND TREATMENT

• NO EFFECTIVE DEFINITIVE TREATMENT
• BETA BLOCKERS FOR VARICES BLEEDING PREVENTION
• EMERGENCY TREATMENT FOR BLEEDING VARICES
• FLUID RESUCITATION
• ANTIBIOTICS
• VASOACTIVE DRUGS
• ENDOSCOPING BAND LIGATION / COMPRESSION VIA TUBE
  OR BALOON
• SURGICAL SHUNTS PLACEMENT( TIPS)
• LIVER TRANSPLANT

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SPLENOMEGALY

• ENLARGMENT OF THE SPLEEN
• CAUSED BY INCREASED PRESSURE IN THE SPLENIC VEIN
• THROMBOCYTOPENIA (decreased platelet count)
• INCREASED BLEEDING

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ASCITES

• CAUSES
• MOST COMMON COMPLICATION OF CIRRHOSIS
• HEART FALIURE
• CONSTRICTIVE PERICARDITIS
• ABDOMINAL MALIGNANCIES
• NEPHROTIC SYNDROM
• MALNUTRITION

• ACCUMULATION OF FLUID IN PERITONEAL CAVITY
• (THRID SPACE)

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ASCITES PATHOPHYSIOLOGY

• CONTRIBIUTING FACTORS PORTAL HYPERTENSION,
  SPLANCHNIC VASODILATION, HEPATOCYTE FALIURE AND
  SODIUM RETENTION
• OVERFLOW THEORY RENAL SODIUM RETENTION IS
  STIMULATED BY PORTAL HYPERTENSION INTRAVASCULAR
  HYPERVOLEMIA AND OVERFLOW IN PERITONEAL CAVITY
• UNDERFILL THEORY INCREASED HYDROSTATIC HEPATIC
  SINUSODIAL PRESSURE / DECREASED ONCOTIC PLASMA
  PRESSURE WEEPING LYMPH FLUID FROM LIVER
• ARTERIAL VASODILATION THEORY CIRCULATING NITIC
  OXIDE ARTERIAL VASODILATION STIMULATION OF
  RENAL SODIUM RETENSION THROUGH RENIN -
  ANGIOTENSIN ALDOSTERONE INTRARENAL BLOOD FLOW
  CHANGE

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ASCITESCLINCAL MANIFESTATION

• ACCUMULATON OF ASCITIC FLIUD WEIGHT INCREASE
  AND ABDOMINAL DISTENTION
• DIAPHRAM DISPLACEMENT DYSPNEA / DECREASED LUNG
  CAPACITY
• RESPIRATOTY RATE INCREASE
• PERIPHERAL EDEMA
• DILUTIONAL HYPONATREMIA
• BACTERIAL PERITONITIS IN 10 PATIENTS FEVER,
  CHILLS, PAIN

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ASCITESEVALUATION AND TREATMENT

• BLOOD TEST SERUM-ASCITES ALBUMIN GRADIENT- SAAG
• PARACENTESIS ASCITIC FLUID ASPIRATION FOR
  BATERIAL CUTURE / MICROSOPIC EVALUTAION
• TREATMENT DISCOMFORT RELIVE
• DIETARY SALT RESTRICTION
• VASSOPRESIN RECEPTOR 2 ANTAGONISTS
• ALBUMIN INJECTIONS
• ELECTROLYTE MONITORING
• PALLATIVE MESSURE DYSPNEA RELIVE - PARACENTESIS
• PERITIONITIS PREVENTION ANTIBIOTICS
• POTASSIUM-SPARING DIURETICS (Amiloride Midamor
  or Triamterene -Dyrenium)

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HEPATIC ENCEPHALOPATHY

• Brain cells called astrocytes from a 51-year-old
  alcoholic patient with cirrhosis who died in a
  coma (hepatic encephalopathy

• IMPARED COGNITIVE FUNCTION
• ASTERIXIS FLAPPING TREMOR
• EEG CHANGES
• RAPID BY ACUTE HEPATITIS
• SLOW WITH CHRONIC LIVER DISEASE
• RISKS GI BLEED, ELECTROLYTE IMBALANCE, INCREASED
  DIETERY PROTEIN, HYPOXIA,

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HEPATIC ENCEPHALOPHATYPATHOPHYSIOLOGY

• NEUROTOXIN AND ENDPRODUCTS (AMMONIA) ABSORBTION
  FROM GI TRACT CIRCULATION TO THE BRAIN
• INCREASED BRAIN BARRIER PREMEABILITY
• ASTROCRYTE MOST VUNERABLE AMMONIA
  DETOXIFICATION CAUSES EDEMA AND OXIDATION
• GLUTAMINE (METABOLIZED AMMONIA) ALTERS CEREBRAL
  BLOOD FLOW BRAIN HERNIATION AND DEATH
• GAMMA-AMINOBUTYRIC ACID (GABA) CONTIBUTES TO
  REDUCED LEVELS OF CONSCIOUSNESS

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HEPATIC ENCEPHALOPATHY CLINICAL MANIFESTATION

• PERSONALITY CHANGE
• MEMORY LOSS
• LETHARGY
• SLEEP DISTURBANCES
• CONFUSION
• FLAPPING TREMOR
• STUPOR
• CONVULSION
• COMA
• DEATH

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HEPATIC ENCEPHALOPHATYEVALUATION AND TREATMENT

• EEG
• BLOOD AMMONIA LEVELS
• TREATMENT
• FLUID AND ELECRTOLYTE IMBALANCE CORRECTION
• AMMONIA REDUTION
• LIVER METABOLISED DRUGS WITHDRAW
• DIETARY PROTEIN INTAKE RESTRICTION
• LACTULOSE ADMINISTRATION
• ANTIBIOTICS
• SODIUM BENZONATE FOR AMMONIA DETOX

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JAUNDICE

• ICTERUS YELLOW / GREEINISH SKIN PIGMENTATION
• CAUSED BY HYPERBILIRUBINEMIA( TOTAL BIL. gt 2.5
  -3MG/DL)
• EXRTAHEPATIC - OBSTRUTION OF BILE FLOW(GALLSTONE)
• INRTAHEPATIC OBSTRUCTION CAUSED BY CIRRHOSIS OR
  HEPATITIS
• EXCESSIVE PRODUTION - EXCESSIVE HEMOLYSIS OF RED
  BLOOD CELLS
• NEWBORNS IMPARIED BILIRUBIN UPTAKE AND
  CONJUGATION

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JAUNDICE PATHOPHYSIOLOGY

• OBSTRUCTIVE JAUNDICE
• EXTRA HEPATIC - GALLSTONE, TUMOR, COPRESSION FROM
  EDEMA OF PANCREATITIS
• INTRAHEPATIC OBSTRUTION OF BILE CANALICULI
  BILE ELEVATION IN PLASMA
• HEMOLYTIC JAUNDICE
• EXCESSIVE HEMOLYSIS UNCONJUGATED
  HYPERBILIRUBINEMIA NOT H2O SOLUBLE NOT
  EXCRETED BY URIN ( SICKLE CELL DISEASE)
• METABOLIC DISEASES ( GILBERT DISEASE - ELEVATION
  OF UNCONJUGATED BILIRUBIN W/O LIVER DISEASE
  SYMPTOMS)
• HEPATOCELLULAR JAUNDICE
• LIVER CELL FALIURE TO CONJUGATE BILIRUBIN (
  GENETIC DEFECT, HEPATITIS, BILARY CIRRHOSIS)

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JAUNDICE CLINICAL MANIFESTATIONAND TREATMENT

• URIN DARKENING JAUNDICE PRECOURSOR
• FEVER,CHILLS,PAIN
• ANOREXIA, MALAISE, FATIGUE
• XANTHOMAS(SKIN CHOLESTEROL DEPOSITS)
• PRURITUS

• TREATMENT CONSITS OF CORRECTING THE CAUSE

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HEPATORENAL SYNDROME (HRS)

• COMPLICATION OF ADVANCED LIVER DISEASE
  FUNCTIONAL RENAL FALIURE

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HRS - PATHOPHYSIOLOGY

• CAUSED BY CIRRHOSIS OR HEPATITIS ARTERIAL
  VASODILATION RENAL VASOCONSTRICTION DECREASED
  BLOOD FLOW REVERSIBLE RENAL FALIURE
• TYPE 1- RAPID AND PROGRESSIVE RENAL FALIURE
• TYPE 2- CHRONIC AND STABLE/ REFRACTORY ASCITES
• OLIGURIA SUDDEN DECREASE OF BLOOD VOLUME AND
  GLOMERULAR FILTRATION ( BLEEDING, HYPOTENSION
  LIVER FALIURE)

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HRS MANIFESTAION, EVALUATION AND TREATMENT

• OLIGURIA, JAUNDICE, ASCITES, GI BLEEDSYSTOLIC
  HYPOTENSION, ANOREXIA, WEAKNESS, FATIGUE
• SERUM UREA AND CREATININ ELEVATION
• gt1.015 URIN SPECIFIC GRAVITY
• LOW URIN SODIUM CONCENTRATION
• TREATMENT
• SYTEMIC VASOCONSTRICTORS
• PENTOXIFYLLINE
• TIPS
• LIVER TRANSPLANT

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VIRAL HEPATITIS

• HEPATITIS G IS BLOOD- BORNE AND USUALLY NOT
  SIGNIFICANT CAUSE OF LIVER DISEASE

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HEPATITIS A

• INCUBATION 30 DAYS ( 4-6 WEEKS)
• ROUTE FECAL-ORAL, PARENERATAL, SEXUAL
• ONSET ACCUTE WITH FEVER/ FECAL SHEDDING 10-14
  DAYS BEFORE ONSET OF SYMPTOMS MOST CONTAGIOUS
• SEVERITY MILD
• NOT CHRONIC
• PROPHYLAXIS HYGIENE, IMMUNE SERUM GLOBULINE(
  FIRST IGM THEN IGG LEVEL INCREASE), VACCINE

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HEPATITIS B

• INCUBATION 60 -180 DAYS
• ROUTE PARENTERAL, SEXUAL
• ONSET - INSIDIOUS
• SEVERITY SEVERE( PROLONGED OR CHRONIC)
• CHRONIC INFECTION IN 15-30
• PROPHYLAXIS HYGIENE, VACCINE

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HEPATITIS C

• INCUBATION 35-72 DAYS
• ROUTE PARENTERAL
• ONSET INSIDIOUS
• SEVERITY MILD TO SEVERE
• CHRONIC MOST COMMON CAUSE OF CIRRHOSIS
• PROPHYLAXIS HYGIENE, SCREENING,INTERFERON ALPHA
  OR RIBAVIRIN, NO VACCINE(DIFFICULT BECAUSE HAS 6
  DIFFERENT GENOTYPES)

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HEPATITIS D

• INCUBATION 30-180 DAYS
• ROUTE PARENTERAL, SEXUAL, FECAL-ORAL
• ONSET INSIDIOUS
• SEVERITY- SEVERE
• CHRONIC
• PROPHYLAXIS HYGIENE, HBV VACCINE (OCCURS IN
  INDIVIDUALS WITH HEPATITIS B)

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HEPATITIS E

• INCUBATION 15-60 DAYS
• ROUTE FECAL-ORAL
• ONSET - ACUTE
• SEVERITY - SEVERE IN PREGNANT WOMAN
• NOT CHRONIC
• PROPHYLAXIS HYGIENE, SAFE WATER( COMMON IN
  DEVELOPING COUNTRIES)

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HEPATITIS G

• INCUBATION UNKNOWN
• ROUTE PARENTERAL, SEXUAL
• ONSET UNKNOWN
• SEVERITY UNKNOWN
• CHRONIC- UNKNOWN
• NO PROPHYLAXIS( DISOVERED IN 1990 NO
  ASSOCIATION WITH HEPATOCELL CARCINOMA)

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HEPATITIS PATHOPHYSIOLOGY

• HEPATIC CELL NECROSIS
• SCARING
• KUPFFER CELL HYPERPLASIA
• INFILTRATION BY MONONUCLEAR PHAGOCYTES
• CYTOXIC T-CELLS
• INFLAMMATION
• BILE CANALICULI OBSTRUCTION
• CHOLESTASIS
• MOST SEVERE DAMAGE BY HEP B AND C
• LIVER FALIURE
• INTESTINAL BLEEDING
• CARDIORESPIRATOTY INSUFFICIENCY AND RENAL FALIURE

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HEPATITIS CLINICAL MANIFESTATION

• SIMULAR IN ALL TYPES
• ABSENCE OF SYMPTOMS OR ACUTE ONSET
• ABNORMAL LIVER FUNCTION
• PRODOMAL PREICTERIC PHASE 2 WEEKS AFTER
  EXPOSURE, FATIGUE, ANOREXIA, MALAISE,
  NAUSEA,VOMITING, HEADACHE, HYPERALGIA
  (sensitivity to pain) RASH, PURPURA, ARTHRALGIAS
  ENDED WITH JAUNDICE
• ICTERIC PHASE - HEPATOCELLULAR DISTRUCTION AND
  BILE STASIS, MILD ITCH, PROLONGED PROTHROMBIN
  TIME
• RECOVERY PHASE RESOLUTION OF JAUNDICE, 6-8
  WEEKS AFTER EXPOSURE, NORMALISATION OF LIVER
  FUNCTIONS SOMETIMES TURNS IN CHRONIC ACTIVE
  HEP.

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FLUMINANT HEPATITIS

• RESULTS IN SEVERE IMPARMENT OR LIVER CELL
  NECROSIS
• SECONDARY TO HEP C OR HEP B
• TOXIC DRUG REACTION
• CONGENIAL METABOLIC DISORDERS
• EDEMA OF HEPATOCYTES
• NECROSIS AND INFLAMMATION
• TREATMENT SUPPORTIVE
• IRREVERSIBLE NECROSIS
• LIVER TRANSPLANT

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CIRRHOSIS

• IRREVERSIBLE INFLAMMATORY DISEASE
• FIBROSIS WITH LEUCOCYTE RELASE
• LIVER CELL REGENARTION REPLACED BY HYPOXIA,
  NECROSIS AND ATROPHY
• LIVER FALIURE
• SEVERITY DEPENDS ON THE CAUSE AND CELL DEATH RATE

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CHOLELITHIASIS (GALLSTONES)

• RISK FACTORS
• OBESITY
• RAPID WEIGHT LOSS
• MIDDLE AGE,
• FEMALE GENDER
• ORAL CONTRACEPTIVES USE
• HIGH DIETARY CHOLESTEROL
• GENE-ENVIRONMENTAL INTERACTIONS

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CHOLELITHIASIS PATHOPHYSIOLOGY

• CHOLESTEROL STONES MOST COMMON, CHOLESTEROL
  SUPERSATURATION OF BILE, FORMS CRYSTALS GROWTH
  IN MACROSTONES, DECREASED GALLBLADDER MOTILITY
• PIGMENTED STONESBILIARY TRACT OBSTRUCTION OR
  BACTERIAL DEGRADATION OF BILIARY LIPIDS
• CAUSES ENZYMATIC DEFECT, LOW BILE ACID
  SECRETION, DECREASED BILE SALT REABSORPTION,
  GALLBLADDER STASIS, GENETIC PREDISPOSITION

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CLINICAL MANIFESTATION OF GALLSTONES

• GASTRIC PAIN / RIGHT HYPOCHONDRIUM PAIN / COLIC
• FATTY FOOD INTOLERANCE
• HEARTBURN
• FLATULENCE
• EPIGASTRIC DISCOMFORT
• JAUNDICE
• FEVER
• COMPLICATION - PANCREATITIS

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GALLSTONES EVALUATION AND TREATMENT

• ORAL CHOLECYSTOGRAM
• INTRAVENOUS CHOLANGIOGRAPHY
• ABDOMINAL UTRASOUND
• LAPRASCOPIC CHOLECYSTECTOMY
• LITHOTRIPSY
• STONES DISSOLVING DRUGS BY SMALL STONES

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CHOLECYSTITIS

• CHRONIC OR ACUTE
• CAUSED BY LODING OF GALLSTONE IN BILE DUCT
• GALLBLADDER DISTENTION AND INFLAMMATION
• PAIN
• FEVER
• LEUCOCYTOSIS
• TREATMENT- PAIN CONTROL, FASTING, FLUIDS,
  ANTIBIOTICS

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ACUTE PANCREATITIS

• DEVELOPS AS RESULT OF AN INJURY OR DISRUPTION OF
  PANCREATIC ACINAR CELLS
• LEAKAGE OF PANCREATIC ENZYMES( TRYPIN,
  CHYMOTRYPSIN AND ELASTASE) INTO PANCREATIC TISSUE
• INFLAMMATION, EDEMA, VASCULAR DEMAGE, NECROSIS
  AND FIBROSIS

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ACUTE PANCREATITIS CLINICAL MANIFESTATION

• EPIGASTRIC OR MIDABDOMINAL PAIN
• BILATY TRACT OBSTRACTION
• PERITONEUM INFLAMMATION
• NASUEA , VOMITING
• ABDOMINAL DISTENTION
• BOWEL HYPERMOTILITY
• CAUSES ABDOMINAL COMPARTMENT SYNDROM

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ACTE PANCREATITIS EVALUATION AND TREATMENT

• ELEVATED SERUM AMYLASE AND LIPASE ( NORMAL
  LEVELS Plasma amylase 70-200 U/L. , Plasma
  lipase 7-58 U/L. )
• AMYLASE CREATIN CLEARENCE INCREASE
• ABDOMINAL ULTRASOUND IN FURTHER DEVELOPED CASES
• TREATMENT
• NARCOTICS (DEMEROL)
• NG TO SUCTION
• ENTERAL NUTRITION
• PARNTERAL FLUIDS
• CIMETIDINE
• ANTIBIOTICS

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CHRONIC PANCREATITIS

• ALCOHOL ABUSE MOST COMMON CAUSE
• OTHERS GALLSTONE OBSTRUCTION, OBESITY,
  AUTOIMMUNE DISORDERS, SMOKING OR IDIOPATHIC(25)
• COMMON LESIONS DESTRUCTION OF ACINAR CELLS,
  FIBROSIS, STRICTURES, CALCIFICATION, CYSTS
• ABDOMINAL PAIN, WEIGHT LOSS, SOMETIMES DIABETES
• INCRESES THE RISK OF PANCREATIC CANCER

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REFERENCES

• McCance, K.L., Huether, S.E., Brashers, V.L.,
  Rote, N.S. (2010). Pathophysiology The Biologic
  Basis for Disease in Adults and Children, 6th Ed.
  Maryland Heights Mosby Elsevier.