Gastrointestinal Diseases Part2

SUBJECT:PEDIATRICS DATE:JUNE 30,2008 TOPIC: GIT 2 LECTURER: DR. RUBY ANN L. PUNONGBAYAN TRANSGROUP: TAMPON NI BINDOY

INTUSSUSCEPTION

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Hydrostatic reduction vs. “air” enema

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Occurs when a portion of the alimentary tract is telescoped into an adjacent segment

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Most common cause of intestinal obstruction bet.3 mos6yrs.old; M > F

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Unknown cause in most cases

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Correlation with adenovirus

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Most often ileocolic & ileoileocolic

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Upper portion of bowel (intussusceptum) invaginates into the lower part (intussuscipiens) dragging its mesentery along with it into the enveloping loopmesentery constricts & obstructs venous returnintussusceptum engorgesedema & bleeding from the mucosa leads to bloody stool

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Severe paroxysmal colicky pain that recurs at frequent intervals with straining efforts; legs & knees are flexed with loud crying

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Ulcers are deep lesions that breach the integrity of the epithelium & penetrate through the muscularis mucosa.

•

If not reduced-shocklike state

•

•

60% of infants pass currant jelly stool

Erosions are superficial & stop short of the muscularis propria.

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Palpation of abdomen: slightly tender sausage-shaped mass in the RUQ which may increase in size & firmness during a paroxysm of pain

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Both lesions occur in inflammation or gastritis

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Pathogenesis incompletely understood

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Ulceration occurs when aggressive factors (gastric acid, digestive enzymes, H.pylori) overwhelm the natural barriers that protect the gastroduodenal lining (bicarbonate-mucus barrier, gastric epithelial cells, mucosal blood flow, PGs)

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May be present in either parent of an affected child

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Gastroduodenal inflammation due to H.pylori found primarily in the mucus layer covering gastric epithelial cells

•

H.pylori produces urease that catalyzes conversion of urea in the gastric juice to NH3 & HCO3 which buffer the gastric acid

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Classic symptom of epigastric pain alleviated by ingestion of food is present only in a minority of children

Plain abdominal X-ray: (+)density

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Barium enema: filling defect or cupping in the head of barium; coiled-spring sign (thin rim of barium trapped around the invaginating part within the intussuscipiens)

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Ultrasound: tubular mass & a doughnut or target appearance

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Tx: reduction of an acute intussusception is an emergency procedure; if with signs of shock, peritoneal irritation or intestinal perforation, reduction is not done

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Success rate of X-ray reduction is 50% if symptoms are present >48 hrs & 70-90% if reduction is done within the 1st 48 hrs

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Resection with end-to-end anastomosis is done if manual operative reduction fails.

the

presence

of

gastric

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PEPTIC ULCER DISEASE

MA RY YVE TTE ALL AIN TIN A RAP LH SHE RYL BAR T HEI NRI CH PIP OY KC JAM CEC ILLE DEN ESS E VIN CE HO OPS CES XTI AN LAI NEY RIZ KIX EZR A GOL DIE BUF F MO NA AM MA AN ADI KC PEN G KAR LA A LPH E AAR ON KYT H ANN E EIS A KRI NG CAN DY ISA Y MA RCO JOS HUA FAR S RAI N JAS SIE MIK A SHA

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Majority with poorly localized pain

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After 6 yrs old, clinical features may be similar to those in adults; dull or aching pain, GI blood loss, have exacerbations & remissions

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Typical ulcer pain with prompt relief after antacids found in <33% of patients

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Dx: Endoscopy – method of choice

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Test H.pylori if there is documented duodenal/gastric ulcer or MALT lymphoma (antral micronodules representing lymphoid follicles)-biopsy (from antrum, body & transition zone of stomach); rapid urease test done in biopsy sample

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Ab detection of H.pylori in blood, urine, saliva & stool (low sensitivity & specificity in low prevalence areas); Ag detection in stool; urea breath test

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Tx: with H.pylori who have ulcers, MALT lymphoma, atrophic gastritis with intestinal metaplasia; cost-benefit ratio of eradicating H.pylori (at least 2 antibiotics & a potent antacid for 1-2 wks)

STRESS ULCER DISEASE •

Underlying causes of secondary PUD not fully understood

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Factors that interfere with host defense mechanisms are involved (mucosal blood flow, PG synthesis, acid/mucus production)

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Infants: related to infection or dehydration

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Older children: related to trauma

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Antacids (AlMg salts)neutralize acid;H2 receptor blockers suppress acid secretion; Hydrogen pump inhibitors

GASTROENTERITIS 2 types of acute infectious diarrhea:

1. Noninflammatory – enterotoxin production by bacteria, destruction of villus by viruses, adherence by parasites

2. Inflammatory – due to bacteria that invade the intestine directly or produce cytotoxins **Chronic or persistent diarrhea - >14 days duration may be due to infection or any enteropathogen infecting an immunocompromised host or residual symptoms due to damage to the intestine

Etiology •

Inflammatory: C.jejuni, Shigella, Yersinia

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Noninflammatory: EPEC, ETEC, V.cholera

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Antibiotics are given to select patients with bacterial enteritis to shorten the clinical course, to decrease excretion of the causative organism, or to prevent complications

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Viral: rotavirus, adenovirus, astrovirus, Norwalk, calicivirus

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Parasitic: G.lamblia, E.histolytica, B.coli, Strongyloides, spore-forming protozoa

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Other causes: anatomic defects, malabsorption, endocrinopathies, food poisoning, neoplasms, miscellaneous (milk allergy, immunodeficiency states, laxative abuse, ulcerative colitis, motility disorders)

C.difficile,

EIEC,

Salmonella,

General Approach •

Assess the degree of dehydration & provide fluid & electrolyte replacement.

Curling ulcers – associated w/ burns (>25%)

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Prevent spread of the enteropathogen.

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Cushing ulcer – head trauma/surgery

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Associated with hemorrhage or perforation

Determine etiologic agent in selected cases & provide specific therapy if indicated.

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Drug-related: due to NSAIDs

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Tx: remove inciting cause; control of gastric acidity for 6 wks is active

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Clinical Evaluation of Dehydration

> Mild (3-5%): normal or inc.pulse, dec.UO, thirsty, normal PE

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> Moderate (7-10%): inc.HR, little or no UO, irritable/lethargic, sunken eyes & fontanel, dec.tears, dry mucous membranes, mild tenting of the skin, delayed capillary refill, cool and pale

Average composition of diarrhea:

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For older children, mild, moderate, and severe dehydration represent 3%, 6%, and 9% respectively of BW lost.

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Sodium –

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Potassium – 25 mEq/L

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Bicarbonate –15 mEq/L

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Volume of stool should be measured and an equal volume of replacement solution should be given

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Replace stool ml/ml every 1-6 hrs

General Approach •

Ask about oral intake; frequency & volume of stool output; general appearance & activity of the child; frequency of urination; recent travel; use of antimicrobials; intake of seafood, contaminated water, uncooked meat or unwashed vegetables; duration of diarrhea; presence of blood; other symptoms (fever, tenesmus, vomiting)

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Stool culture: if HUS is suspected; bloody diarrhea; stool with fecal leukocytes; during outbreak; immunocompromised patients

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Management of dehydration is the cornerstone.

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Rapid rehydration with replacement of ongoing losses during the 1st 4-6 hrs

55 mEq/L

Composition of ORS

Solution

Glucose Na

K

Cl Base

WHO solution

111

90

20

80

30

Pedialyte

140

45

20

35

30

Glucolyte

165

50

20

42

28

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Reintroduce food once rehydration is complete!

Hydrite

55

45

10

40

15

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Antidiarrheals generally not recommended!

Glucost

55

45

10

40

5

Cholyte

111

45

20

42

28

Clinical Syndromes

Servidrat

140

56

20

46

30

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Gatorade

58

14.6 3.5

General rule: occurring in <1 hr – chemical poisoning, toxins from fish or shellfish

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Vomiting & diarrhea 1-6 hrs – S.aureus

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Watery diarrhea, abdominal cramps 8-72 hrs – Salmonella

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Bloody diarrhea >15 hrs – Shigella, Salmonella

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Neurologic symptoms 0-6 hrs- fish, shellfish, MSG; 0-24 hrs – mushroom; 18-24 hrs – C.botulinum

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Severity of disease depends on the amount inoculated into the food or water

Approximate Electrolyte Consumed Fluids

Composition

HCO3

of

Na

K

Cl

Apple juice

0.4

26

---

---

11.9

Coca-cola

4.3

0.1

---

13.4

10.9

Gatorade

21

2.5

17

---

5.9

Ginger ale

3.5

0.1

---

3.6

9

Milk

22

36

28

30

4.9

Commonly

CHO g/dl

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> Severe (10-15%): rapid and weak pulse, dec. BP, no UO, very sunken eyes and fontanel, no tears, parched mucous membranes, tenting of the skin, very delayed capillary refill, cold and mottled

Diagnosis of food borne or water borne illness is considered when >2 persons have ingested common food/water develop a similar acute illness.

Orange juice 0.2

49

---

50

10.4 PLAN C

* Not recommended for oral rehydration therapy

ASSESSMENT OF DIARRHEA PATIENTS FOR DEHYDRATION (WHO)

Age

First give 30 ml/kg in:

Then give 70 ml/kg in:

< 1 year old > 1 year old

1 hour 30 minutes

5 hours 2 ½ hours

PLAN A 3 rules for treating diarrhea at home: 1.

2.

3.

Give the child more fluids than usual to prevent dehydration (give these fluids until the diarrhea stops). Give the child plenty of food to prevent malnutrition (give an extra meal daily for 2 weeks). Take the child to the health worker if the child does not get better in 3 days or develops any of the following: Many watery stools

CHRONIC DIARRHEA •

Increased total daily stool output with increased stool water content

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Diarrhea that lasts more than 2 weeks

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Results from altered intestinal water and electrolyte transport

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GI tract of an infant handles 285 ml/kg/day of fluid (intake plus intestinal secretion) with a stool output of 5-10 g/kg/day

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Stool output in infants & children contains approximately per liter, 20-25 mEq of Na, 50-70 mEq of K, 20-25 mEq of Cl

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Mechanisms responsible for the absorptive capacity are caused by the function of several transport proteins located at the brush border membrane of the small and large intestine

Repeated vomiting Marked thirst Eating or drinking poorly Fever Blood in the stool

If the child will be given ORS solution at home:

< 24 months

Amount of ORS to give after each loose stool 50-100 ml

Amount of ORS to provide for use at home 500 ml/day

2-10 years old

100-200 ml

1000 ml/day

> 10 years old

As much as wanted

2000 ml/day

PLAN B •

Approximate amount of ORS required (in ml) can also be calculated by multiplying the patient’s weight (in kg) times 75

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Reassess after 4 hours.

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If the child vomits, wait 10 minutes and then continue giving ORS but more slowly (a spoonful every 2-3 mins).

Pathophysiologic mechanisms: •

Osmotic diarrhea

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Secretory diarrhea

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Mutations in apical membrane transport proteins

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Reduction in anatomic surface area

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Alteration in intestinal motility



Osmotic diarrhea – due to the presence of nonabsorbable solutes in the GIT; classic ex: lactose intolerance due to lactase enzyme deficiency causes:

malabsorption of water-soluble nutrients, excessive intake of carbonated fluids & nonabsorbable solutes

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Age

Stops with fasting, has a low pH, (+) reducing substances



Secretory diarrhea – activation of intracellular mediators like cAMP, cGMP that stimulate active Cl secretion from the crypt cells & inhibit the neutral coupled NaCl absorption; toxin-mediated injury to the tight junctions

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Phase IV: hormonal studies (VIP, gastrin, secretin)

Treatment Classic ex: cholera, E.coli enterotoxins, Clostridium

difficile, vasoactive peptides

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Maintain adequate nutritional intake to permit normal growth & development

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If diarrhea is due to CHO intolerance, have a trial period of decreased lactose or sucrose.

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Use predigested formula (Pregestimil or Alimentum) for postgastroenteritis malabsorption syndrome

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Secretory type: consider nutritional support (most likely due to congenital defect in transport proteins)

Continues with fasting, extremely watery stool, high

volume

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Mutational defects in ion transport protein – congenital defect in Na-H exchange, Cl-HCO3 exchange

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Reduction in anatomic surface area – short bowel syndrome, celiac disease

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Altered intestinal motility – due to malnutrition, intestinal pseudo-obstruction syndrome, DM

2 major etiologic factors:

ACUTE PANCREATITIS •

Most common pancreatic disorder in children

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Common causes: blunt abdominal injury, mumps & other viral illnesses, multisystem disease, congenital anomalies, biliary microlithiasis, drugs & toxins

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Pancreas

1. Intraluminal factors – involved in the digestion process; pancreatic, liver & brush border membrane disorders

2. Mucosal factors – involved in the digestion & transport of nutrients across the mucosa; bacterial, viral, parasitic, fungal agents

Pathogenesis

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Theory: following an insult, lysosomal hydrolase colocalizes with pancreatic proenzymes within the acinar cell- pancreastasis with continued synthesis of enzymes occur--proenzymes are activated by cathepsin leading to autodigestion, further activation & release of active proteases-- lecithin is activated by phospholipase A2 into the toxic lysolecithin

Evaluation of Chronic Diarrhea

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Phase I: history, PE, stool exam (pH, reducing substances), stool culture, stool for C. difficile toxin, CBC, ESR, electrolytes, serum creatinine

Phase II: sweat chloride, 72-hr stool collection for fat, stool electrolytes & osmolality, stool for phenolphthalein, Mg sulfate, PO4

Phase III: endoscopy, small bowel biopsy, sigmoisdoscopy or colonoscopy, barium

Clinical Manifestations •

Severe, steady abdominal pain (epigastric or in either upper quadrant, appears acutely ill), persistent vomiting, fever

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Pain increases in intensity for 24-48 hrs with vomiting

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Severe acute type: rare in children; severe nausea, vomiting, shock, jaundice, high fever, Cullen sign, Grey Turner sign, necrotic pancreas; mortality rate of 25% related to the systemic inflammatory response syndrome with multiple organ dysfunction

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Diagnosis

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Uncomplicated cases: recover over 4-5 days

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If associated with trauma or systemic disease: prognosis is related to the associated medical conditions

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ERCP or magnetic resonance cholangiopancreatography: recurrent pancreatitis

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Acute cases: serum amylase and lipase

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Amylase elevated for up to 4 days

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Serum lipase is more specific for acute inflammatory pancreatitis; rises by 4-8 hrs, peaks at 24-48 hrs & remains elevated 8-14 days longer than serum amylase

LIVER DISEASE

Ultrasound & CT scan of the abdomen show pancreatic enlargement, a hypoechoic, sonolucent edematous pancreas, mass, fluid collection, abscess

Metabolic Functions of the liver:

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•

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At least 20% of children with acute pancreatitis have normal imaging Cullen’s sign

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Carbohydrate metabolism

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Protein metabolism

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Lipid metabolism

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Biotransformation

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Hepatic excretory function

Manifestations of Liver Disease •

Alteration in liver structure & function

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Pathologic manifestations:

Treatment •

Medical mgt: to relieve pain and to restore metabolic homeostasis

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Analgesia

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Fluid electrolyte & mineral balance restored & maintained

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Prophylactic antibiotics useful in severe cases to prevent infected pancreatic necrosis

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Inflammation or necrosis – viruses, drus, toxins, hypoxia, IEM, immunologic disorders

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Cholestasis – response to injury due to extra- or intrahepatic obstruction to bile flow; accumulation in serum of substances normally excreted in bile

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Cirrhosis

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Tumors

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Treatment

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Refeed when vomiting has resolved, serum amylase is falling, and clinical symptoms are resolving

1. Hepatomegaly – increase in the number or size of the

Endoscopic therapy – if due to anatomic abnormalities (strictures or stones)

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Severe acute type: enteral alimentation is superior to TPN within 2-3 days of onset, antibiotics, gastric acid suppression, peritoneal lavage (to reduce risk of secondary infection)

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Prognosis

cells in the liver, inflammation, infiltration, increased size or vascular space, increased size of biliary space

2. Jaundice – unconjugated type may indicate increased production, hemolysis, reduced hepatic removal or altered metabolism; conjugated type reflects decreased excretion by damaged hepatic parenchymal cells or disease of biliary tract due to sepsis, endocrine or metabolic disease, inflammation of the liver or obstruction

3. Pruritus – multifactorial; retained bile components

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Clinical manifestations:

the presence of liver dysfunction

Sexual transmission

5. Palmar erythema – due to vasodilation & increased blood flow

6. Xanthoma – elevated cholesterol may cause deposition of lipid in the dermis & subcutaneous tissue

7. Portal hypertension – >10mmHg difference between the portal vein & systemic veins

8. Ascites – portal hypertension & hepatic insufficiency are also present

9. Variceal hemorrhage – results from increased pressure within the varix which leads to changes in the diameter of the varix & increased wall tension

10. Encephalopathy – prominent or subtle neurologic dysfunctions; may be due to altered ammonium metabolism, synergistic neurotoxins, or “false neurotransmitters” with plasma amino acid imbalance

11. Endocrine abnormalities – adults>children 12. Renal dysfunction – systemic disease or toxins may affect both organs simultaneously; altered water & sodium activity, impaired concentrating ability; hepatorenal syndrome – functional renal failure in patients with endstage liver disease

13. Pulmonary involvement – hepatopulmonary syndrome – triad of hypoxemia, intrapulmonary vascular dilations & liver disease

HBV

HCV

HDV

HEV

HGV

Nucleic acid Incubati on (mean)

RNA

DNA

RNA

RNA

RNA

RNA

30 days

100120 days

7-9 wks

2-4 mos

40 days

Percutaneous transmission Fecaloral transmission

rare

com mon

com mon

com mon

no

Un k now n com mon

com mon

no

no

no

com mon

rare

rare

rare

rare

HAV

HBV

HCV

HDV

HEV

HGV

no

prob ably no

rare

yes

no

yes

yes

rare

prob ably no

•

anti-HAV, IgM anti-HAV

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Anti-HBsAg, IgM anti-HBsAg, anti-HBcAg, anti-HBeAg

•

Anti-HCV

•

Anti-HDV

•

Anti-HEV, IgM anti-HEV

•

Anti-HGV

Hepatitis B Antigens & Antibodies •

First clinical evidence of HBV infection is elevation of ALT levels which occurs about 6-7 wks after exposure

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Anti-HBcAg – most valuable single serologic marker of acute HBV infection because it is present as early as HbsAg and continues to be present later in the course of the disease when HBsAg has disappeared

•

HBcAg – inner portion of the virion that encodes the viral DNA

•

HBeAg – serves as a marker of active viral replication; identification of infected people at increased risk of transmitting HBV

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HBsAg – first serologic marker to appear & its rise coincides with the onset of symptoms; detection of acutely or chronically infected people; antigen used in hepatitis B vaccine

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Anti-HBs – identification of people who have resolved infections with HBV; determination of immunity after immunization

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Anti-HBe – identification of infected people with lower risk of transmitting HBV

system due to gram (-) enteric organisms

HAV

com mon

Transno com rare placent mon al transmission Chronic no yes yes infectio n Fulmina rare yes rare nt disease IDENTIFIED ANTIBODIES:

14. Recurrent cholangitis – ascending infection of the biliary

VIRAL HEPATITIS

rare

no

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4. Spider angioma – due to altered estrogen metabolism in

Anti-HBc – identification of people with acute, resolved, or chronic HBV infection

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IgM anti-HBc – identification of people with acute or recent HBV infections (including HBsAg-negative people during the “window” phase of infection)

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