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DISORDERS OF THE ACCESSORY ORGANS OF DIGESTION

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Title: DISORDERS OF THE ACCESSORY ORGANS OF DIGESTION


1
DISORDERS OF THE ACCESSORY ORGANS OF DIGESTION
  • DISORDERS OF THE LIVER,GALLBLADDER PANCREAS,GI
    TRACT AND CANCERS OF THE ACCESSORY ORGANS

2
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

3
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.

4
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)

5
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

6
SPLENOMEGALY
  • ENLARGMENT OF THE SPLEEN
  • CAUSED BY INCREASED PRESSURE IN THE SPLENIC VEIN
  • THROMBOCYTOPENIA (decreased platelet count)
  • INCREASED BLEEDING

7
ASCITES
  • CAUSES
  • MOST COMMON COMPLICATION OF CIRRHOSIS
  • HEART FALIURE
  • CONSTRICTIVE PERICARDITIS
  • ABDOMINAL MALIGNANCIES
  • NEPHROTIC SYNDROM
  • MALNUTRITION
  • ACCUMULATION OF FLUID IN PERITONEAL CAVITY
  • (THRID SPACE)

8
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

9
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

10
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)

11
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,

12
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

13
HEPATIC ENCEPHALOPATHY CLINICAL MANIFESTATION
  • PERSONALITY CHANGE
  • MEMORY LOSS
  • LETHARGY
  • SLEEP DISTURBANCES
  • CONFUSION
  • FLAPPING TREMOR
  • STUPOR
  • CONVULSION
  • COMA
  • DEATH

14
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

15
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

16
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)

17
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

18
HEPATORENAL SYNDROME (HRS)
  • COMPLICATION OF ADVANCED LIVER DISEASE
    FUNCTIONAL RENAL FALIURE

19
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)

20
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

21
VIRAL HEPATITIS
  • HEPATITIS G IS BLOOD- BORNE AND USUALLY NOT
    SIGNIFICANT CAUSE OF LIVER DISEASE

22
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

23
HEPATITIS B
  • INCUBATION 60 -180 DAYS
  • ROUTE PARENTERAL, SEXUAL
  • ONSET - INSIDIOUS
  • SEVERITY SEVERE( PROLONGED OR CHRONIC)
  • CHRONIC INFECTION IN 15-30
  • PROPHYLAXIS HYGIENE, VACCINE

24
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)

25
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)

26
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)

27
HEPATITIS G
  • INCUBATION UNKNOWN
  • ROUTE PARENTERAL, SEXUAL
  • ONSET UNKNOWN
  • SEVERITY UNKNOWN
  • CHRONIC- UNKNOWN
  • NO PROPHYLAXIS( DISOVERED IN 1990 NO
    ASSOCIATION WITH HEPATOCELL CARCINOMA)

28
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

29
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.

30
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

31
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

32
CHOLELITHIASIS (GALLSTONES)
  • RISK FACTORS
  • OBESITY
  • RAPID WEIGHT LOSS
  • MIDDLE AGE,
  • FEMALE GENDER
  • ORAL CONTRACEPTIVES USE
  • HIGH DIETARY CHOLESTEROL
  • GENE-ENVIRONMENTAL INTERACTIONS

33
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

34
CLINICAL MANIFESTATION OF GALLSTONES
  • GASTRIC PAIN / RIGHT HYPOCHONDRIUM PAIN / COLIC
  • FATTY FOOD INTOLERANCE
  • HEARTBURN
  • FLATULENCE
  • EPIGASTRIC DISCOMFORT
  • JAUNDICE
  • FEVER
  • COMPLICATION - PANCREATITIS

35
GALLSTONES EVALUATION AND TREATMENT
  • ORAL CHOLECYSTOGRAM
  • INTRAVENOUS CHOLANGIOGRAPHY
  • ABDOMINAL UTRASOUND
  • LAPRASCOPIC CHOLECYSTECTOMY
  • LITHOTRIPSY
  • STONES DISSOLVING DRUGS BY SMALL STONES

36
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

37
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

38
ACUTE PANCREATITIS CLINICAL MANIFESTATION
  • EPIGASTRIC OR MIDABDOMINAL PAIN
  • BILATY TRACT OBSTRACTION
  • PERITONEUM INFLAMMATION
  • NASUEA , VOMITING
  • ABDOMINAL DISTENTION
  • BOWEL HYPERMOTILITY
  • CAUSES ABDOMINAL COMPARTMENT SYNDROM

39
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

40
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

41
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. 
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