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 Gastroenterology & Liver disease

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كاتب الموضوعرسالة
dr saad
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مُساهمةموضوع: Gastroenterology & Liver disease    الجمعة 01 أبريل 2011, 20:43

Diarrhea
Session with Dr. Maimoona
Diarrhea
Acute & Chronic
 
2 weeks more
Causes:
I. Infections:
 Protozoa:
Amoeba  , Giardia
 Bacteria:
E. Coli , Klibsiella , Shigella  , salmonella 
Vibrio cholera  watery diarrhea
Staph. Aureus (milk products)
Campylobacter  (pets at home)
Yersinia 
C. difficile   diarrhea, pseudomembranous colitis
 Viruses:
HIV (common cause)   3 months + lymphadenopathy + wt loss
Rota virus, adenovirus
 Fungal in immunocompromised
Cryptosporidium
 Lyme disease  Liptospirae
 Mycobacteria: intestinal TB
Note:
C. botulinium  botulism (preserved food)
C. Perfringins  food poisoning / gas gangrene
C. tetini  tetanus
The underlined words are important causative organisms
  Means Bloody
Note:
Algid Malaria: malaria superimposed by Salmonella
 Common cause of septic shock
II. Inflammatory Bowel Disease  Crohn's – Ulcerative colitis
III. Malignancy:
Intestinal lymphoma, Colon carcinoma, Pancreas carcinoma, Medullar
carcinoma of thyroid
IV. Malabsorption:
1- Celiac disease (not all patients present with diarrhea)
*malabsorption*
CBC: dimorphic picture
Microcytosis & macrocytosis
Hypochromic & hyperchromic
D.D. Celiac Disease
Combined deficiency (folate – Fe)
They have hypo Ca+2
2- Tropical sprue (hot humid countries)
Probably due to E. coli (traveler's diarrhea)
3- Whipple's disease (malabsorption due to trophyrhyma whipple
"bacteria")
Note
Hemolytic anemia  peripheral blood film  reticulocytosis
Usually patients also suffer Lymphadenopathy, hepatosplenomegaly, arthritis,
malabsorption and, skin pigmentation.
Tetracycline should be prescribed for 1 year
Periodic acid Sheff (PAS)  positive (+)
4- Blind loop syndrome (malabsorption) , short loop
5- Pancreatic (chronic) malabsorption
Chronic pancreatitis – cystic fibrosis - carcinoma
6- Post-gastrectomy , resection of colon
V. Endocrine:
 Thyrotoxicosis
 Addison's (hypotension & diarrhea)
 DM (autoimmune neuropathy)
 Glucagonoma
 VIP tumor
 Pheochromocytoma
 Hypoparathyroidism
 Carcinoind (flushing face)
VI. Drugs:
 Antibiotics  mainly clindamycin
 Laxatives
 Cytotoxic
VII. Idiopathic: Irritable bowel syndrome, diverticular disease
In History:
- The amount and frequency
- Consistency: watery
- Associates with bleeding: Amoeba, IBD, Shigella, Salmonella, E. Coli
- Fever: Infections, IBD
- Tenesmus or not: Giardiasis & Amoebiasis
- Abdominal Pain  IBD and malignancy
- Loss of weight: HIV, IBD, and malignancy
- Family History
- Laxatives, eat outside the house, house hold diarrhea (ACUTE)
Investigations of a patient with diarrhea:
1- Stool analysis: Blood – Mucus – Protozoa e.g. trophozoid
Cuture  bacteria
&
Sensitivity
2- CBC
- Anemia
- Leukocytosis
- Thrombocytosis: bone marrow  to confirm safe anemia
3- ESR
4- U and E
- Hypo K+
- Hyper Na+
- Renal failure (due to fluid loss)
5- Left: hypoalbuminemia
6- Serology:
HIV+ for ulcerative colitis pANCA, ASCA + CMV IgM
7- Endoscopy
8- Enema
9- Salmonella titer
10- Abdominal X-Ray:  toxic mega colon
Differential Diagnosis of Diarrhea:
1- Infection
2- IBD
3- Malignancy
4- Malabsorption
5- Endocrine
6- Drugs
7- Idiopathic
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عدد المساهمات : 176
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مُساهمةموضوع: رد: Gastroenterology & Liver disease    الجمعة 01 أبريل 2011, 20:44

Inflammatory Bowel Disease
Clinically we cannot differentiate between ulcerative colitis and Crohn's unless
fistula develops.
Presentation: mainly diarrhea.
I- Ulcerative Colitis
1- Intestine: diarrhea (bloody) - pain - malabsorption - tenesmus
2- Skin: erythema nodosum, pyoderma gangrnosum
3- Amylodosis,
4- Arthropathy
5- Thromboembolic disease
6- Both: ant. Uveitis, conjectivitis, episcleritis, iritis, ankylosing spondylitis,
sacroilitis, sclerosing cholangitis
7- Fatty liver, autoimmune hepatitis.
Complications:
1- Toxic megacolon (most severe complication)
Tachycardia, anemia, hypotension, dilated transverse colon more than 6cm
If not improved in 24 to 48 hours -> total Colonectomy should be preformed
immediately.
(Chest x-ray)
2- Malignancy:
More with Ulcerative Colitis
A patient with Ulcerative Colitis for more than 10 years must have an annual
endoscopy.
3- Amylodosis (in both)
4- Thrombosis.
II- Chron's
Terminal ilium  B12 deficiency
Intestinal obstruction - stricture
Fistula (entero - enteric or vesical).
Perianal (abscess - tags)
Grading
I- Mild
Diarrhea > 5/day
No anemia
No fever
Normal albumin
II- Moderate
(In between)
III- Severe
Diarrhea > 10/day
Fever
Tachycardia
Hypotension
Hypoabuminia (edema)
Treatment
I- Salphasalazine (Paraaminosalicylic acid)
II- Steroids (Pridnisolone)
If the patient suffers Chron’s:
Add metronidazole (antibiotic covers anaerobes)
Investigations
1- CBC
2- U&E
3- Left
4- Barium enema
5- Endoscopy (Chron's skiplesion) coplet stones
6- Biopsy
7- Stool (to exclude infections)
8- Abdominal x-ray
* Vitamin deficiency (B12)  numbness.
* Gallstone (both).
* Exudates stones Crohn's (Child)
Ulcerative Colitis
(Non-smokers)
Symptoms:
1- Bloody diarrhea.
2- Tenesmus.
3- Abdominal pain (lower).
If severe:
- More frequent diarrhea more than 10 times per day
4- Fever
5- Weight loss.
6- Signs of anemia, hypoalbuminemia.
If only rectum (proctitis).
1- Constipation.
2- Blood in stool.
Signs:
1- Clubbing, leukonychia.
2- If fulminant: diarrhea mixed with blood & mucus.
3- Abdominal tenderness , distention (toxic megacolon)
Extra-intestinal signs:
1- Skin: erythema nodosum, Pyoderma gangrinosum.
2- Eye: uvitis, conjunctivitis, iritis, episcleitis.
3- Mouth: aphtous ulcer.
4- Arthropathy.
5- Amyloidosis.
6- Thromboembolic disease.
Other unrelated to disease activity:
1- Sclerosing cholangitis.
2- Fatty liver, autoimmune hepatitis.
3- Ankylosing spondylitis, sacroilitus.
Complications:
1- Toxic megacolon.
2- Malignancy.
3- Thrombosis.
4- Bleeding  dehydration.
5- Perforation.
6- Amyloidosis.
Crohn’s Disease
Granulomatous – transmural – skip lesion.
Terminal ilium (any where)
Symptoms:
Diarrhea, malabsorption, abdominal pain, right iliac fossa pain, rectal
bleeding (less than U C), weight loss, fever.
Signs:
1- Clubbing.
2- Perianal skin tags, fistula, stricture, abscess.
3- Weight loss.
4- Fever.
5- Anemia
6- Hypoproteinemia.
Abdomen: tender, mass.
Extra-intestinal: as in Ulcerative Colitis
Complications:
1- Stricture (intestinal obstruction).
2- Fistula (enteroenteric , vescal or vaginal).
3- Renal disease due to ureteric compression.
4- Fe- folate- B12 deficiency.
5- Malignancy.
6- Amyloidosis.
Relapsing of Crohn's
Session with Dr. Faiza Qari (5th year tutor)
► A known case of Crohn's dis. presents to the ER with vomiting &
abdominal distention, what might be the causes of his complains?
1- Intestinal obstruction:
 abdominal pain
 abdominal distention
 vomiting (repeated attacks)
 constipation
2- Relapsing of Crohn's
3- Gastric or duodenal ulcer  heart burn
4- Peritonitis  severe abdominal pain
5- Colon cancer  weight loss
► Relapsing of Crohn's  other important history:
* Past history  since the time of 1st diagnosis
- Times admitted to hospital
- Procedures (what happened?)
- Any relapses
- Any ICU admissions
* Last colonoscopy
* Abdominal pain, bleeding diarrhea, bleeding/rectum, abdominal distension,
repeated mouth ulcer, loss of appetite, weight loss, repeated fissures & fistulae
* Intestinal manifestations of Crohn's:
- Anemia (iron deficiency)  chronic illness
- Appendicitis (Right Iliac mass)
* Extra-intestinal manifestations of Crohn's:
- Arthritis  sacroiliac joint  back pain
Or mono-arthritis
- Liver  hepatitis, gall stone …
- Phlebitis  DVT…
- Renal stones
- Skin rash  Erythema Nodosum
► Crohn's affect  small intestine > large intestine

Vomiting
Weight loss
► Most important investigations:
- CBC:
WBC normal
Hb ↓  microcytic hypochromic anemia
Platelet ↑↑↑  (1) postsplenectomy (↑)
(2) Relapse of Crohn's
- ESR  activity of disease
- LFT
CLD
Dr.Maimoona
When a patient presents with hepatic symptoms, 1st search for acute causes of
illness then ask about chronic.
ETIOLOGY:
(1) infection:
- hepatitis
• B  sexually
• C  blood transfusion / vertical from mother to child
- Schistosomiasis (Bilharziasis)
- Hydatid cyst  by compression, not hepatocellular.
- TB  most common in KSA.
- HIV  usually acute, but chronic if patient lives long enough.
(2) Alcohol  always take History of alcohol.
* Most likely jobs to be alcoholic & drug abusers:
- Cops & Army.
- People working at port of entry.
REMEMBER! These infections are causes of acute, not chronic liver
disease:
- CMV
- Toxoplasmosis
- EBV
- Malaria
(3) Autoimmune  all CTD: SLE, RA, Wegner's Granulomatosis.
(4) Metabolic:
• Wilson's disease  autosomal recessive.
Diagnosed by:
 Low ceruloplasmin (serum).
 High 24 hr urine cupper.
• hemochromatosis  autosomal recessive.
Diagnosed by:
 Serum iron, ferretin.
 Liver biopsy  diagnostic.
(5) Drugs  remember 1 or 2 only
• Anti-Tuberculosis.
• Methotrexate.
• Anti-epileptics  sodium valporate, phenytoin, tegretol.
(6) Primary biliary cirrhosis:
Classically pt present with:
 Young female .
 Itching 1 or 2 years before any liver involvement.
Diagnosed by:
 Anti-Mitochondrial Abs.
 IgM Abs.
 High ALP.
All these 3 are raised in these patients.
(7) Malignancy  metastasis.
(Cool budd chiare syndrome:
Hepatic vein thrombosis.
Causes:  all causes of DVT
90% of pt
Present:
 acute abdominal distention  main
 Others.
Do liver scan  find  uptake in caudate lobe.
(9) Cardiac cirrhosis.
(10) Idiopathic.
(11) fatty liver  NEVER say it, because it is TOO RARE, & if you mentioned it in the
exam ( في البداية ) you will lose marks
Dr Maimoona says "don't remember it".
Decompensation of CLD shows up by Complications:
(1) Portal Hypertension:
• variceal Hrg.
• Splenomegaly.
• Ascites.
(2) Hepatocellular Ca.  this is #1
(3) Hypersplenism.  pancytopenia.
(4) Bleeding tendency.
(5) Hepatic encephalopathy.
(6) SBP. (spontaneous bacterial peritonitis)
(7) Hepatorenal syndrome  if you mentioned this, Dr Maimoona will tell you
to talk about something that is more important.
Hepatic Encephalopathy:
50 years old lady admitted through ER, who is known case of CLD secondary to
HCV.
C/O: altered level of conciseness (complaint & HPI)

Hepatic encephalopathy
How do you manage?
(1) Take History of what ppt. of a patient to have an encephalopathy:
History of precipitating factor:
- Infection:
• SBP: spontaneous bacterial peritonitis 
• Sore throat, respiratory, UTI, leg ulcer…etc.
- Constipation.
- Hemorrhage (bleeding):
Upper/Lower GI bleeding  globulin  high urea.
- High protein diet  high urea.
- Drugs: analgesics, sedatives & tranquilizers.
- Causes of electrolytes imbalance:
• Overuse of diuretics.
• Gastroenteritis  vomiting & diarrhea.
- Dehydration: vomiting, diarrhea, burn.
- Excess alcohol.
- Heart failure.
- Hepatoma (hcc).
(2) Examination of pt who already has CLD & came with hepatic
encephalopathy:
1- Glasgow coma scale (1st)  consciousness.
2- Vital signs:
-Temp  infection.
-Blood Pressure  look for postural hypotension (Ascites).
-Pulse  tachycardia due to infection or loss of fluid.
3- Fluid status: (2nd)
• Fluid overload (from liver failure)  pleural effusion, Ascites, lower limb
edema.
• Dehydration  mucus membrane, auxiliary sweating, postural
hypotension.
4- PR = per rectum Ex (digital rectal Ex) (3rd)  bleeding: 'melena' in all hepatic
encephalopathy.
5- Evidence of infection: (4th)
• Chest.
• SBP (spontaneous bacterial peritonitis) abdominal tenderness.
6- Hepatic bruit 'hepatoma'.
+ CLD stigma.
(3) Everyday follows up:
1- Glasgow-coma scale.
2- Flapping tremor (asterixis).
3- Constructional apraxia: draw a 5 pointed star (better) or draw a square.
Investigations:
That should be done to all patients:
(1) CBC:
- Leukocytosis  infection.
- Cytopenia  hypersplenism & vasculitis (CTD).
• Anemia.
• Leucopenia.
• Thrombocytopenia.
(2) LFT:
In cirrhotic liver: cells are distorted  enzymes not secreted = normal LFT.
1- Hepatocellular Ca   enzymes.
2- Obstructive (primary biliary cirrhosis)  ALP.
3- Bilirubin.
4- PT, PTT (coagulation profile) clotting factors.
5- Albumin level  if <13  pt is prone to develop SBP.
(3) Urea & electrolytes:
1- Low K  diuretic.
2- Low Na  dilutional or diuretic.
3- prerenal failure  increase urea & creatinine.
(4) Blood glucose  hypoglycemic, because there is no gluconeogenesis in liver.
(5) Hepatitis B & C serology  most common in KSA.
(6) α-fetoprotein (AFP) & abdominal US  every 6 months  for hepatoma.
*NOTE:
If all these didn't help you, then you'll do the other tests if symptoms are suggestive (but
in a written exam, you have to write them all) 
(7) Abdominal US/CT (only 1, if US didn't help: do CT)
1- Liver:
 1st  size of liver?  If shrunken  order a biopsy.
 2nd  macronodular (alcohol) or micronodular.
 3rd  lesion (masses)  metastasis, tumor, hydatid cyst.
2- Dilatation of biliary tract  obstruction  stones … etc.
3- Ascites.
4- Spleen  enlarged  hypersplenism.
5- Any other masses  LN / metastasis.
(Cool CXR:
• Evidence of infection.
• Fluids overload  pulmonary edema.
• HF.
• Malignancy  metastasis, 1° tumor.
(9) UGI endoscopy: to know source of bleeding.
- Oesophageal varices.
- Peptic ulcer  because liver can't metabolize. endogenous gastrin
 ttt: PPI (proton pump inhibitor).
(10) Liver biopsy: (invasive procedure, keep it at last).
Only in patient with non-shrunken liver & he has Hepatitis B or C.
 To know activity of the virus, & treatment.
(11) ascitic tap: diagnostic/relief  for gram stain , culture & sensitivity,
cytology, protein, glucose "see below".
(12) If Pt. not known to have CLD, presented with hepatic encephalopathy, do:
-HBV, HCV.
-ANA profile.
-Young Pt: metabolic causes.
Others:
- Blood culture.
- Urine analysis.
- Urine culture & sensitivity.
- Ammonia.
- ECG in electrolytes disturbance.
SBP:
- Patient should have Ascites to develop it
- CLD
- Abdominal pain
Diagnosis:
P/C:
Abdominal pain, distention, fever, decrease bowel sounds, worsening hepatic
encephalopathy, tenderness.
Or in the absence of signs:
Ascetic tap:
1- WBC >500, neutrophil >250 neutrophils/ μl  diagnostic.
2- Gram staining.
3- Culture  E. coli  most common.
After tap, pt. will be on antibiotic empirically, then if +ve SBP (SBP is
documented)  life-long prophylactic antibiotic.
Management:
- Bed rest.
- Low salt/low protein diet.
- Intake/output chart.
- Daily weighting: the goal of diuretic therapy is daily weight loss of 0.5-1
mg/day.
- Daily examination of 2 signs: constructional apraxia, flapping tremor asterixis:
see if improver with ttt.
- Daily urea & electrolytes if disturbed.
1- laxative: lactulose.
Aim: 2-3 bowel motion daily, lactic acid lactose disaccharide change pH of colon
flora  no overgrowth of bacteria.
2- Antibiotic  3rd generation cephalosporin SBP.
3- Fluid status management:
o Dehydration  give fluid.
o Fluid overload  diuretic:
• loop diuretic, quick action till spironolactone takeover.
• spironolactone, aldactone, antialdosteron (aldosterone cause Na &
water retention)  take 3 days to work.
4- Proton pump inhibitor 'prophylaxis'.
5- β-blocker inderal decrease portal pressure.
If patient out of encephalopathy:
Discharge on:
1- Lasix.
2- Spironolactone.
3- Proton pumps inhibitor.
If it is not diuretic albumin.
& the following investigation:
1- Urea & electrolytes.
2- Alpha-fetoprotein Q 6 months.
3- Abdominal U/S Q 6 months.
4-CBC
Ascites Management:
- Salt restriction.
- Diuretic: loop diuretic & spironolactone.
- Diagnostic paracentesis.
- In refractory ascites: fluid overload that is none responsive to a sodiumrestricted
diet & high-dose diuretic: -TIPS -shunt - therapeutic paracentesis Q
2/52. If child C >>liver transplant.
- In large volume paracentesis: concomitant administration of IV colloid (5-8g
albumin/L ascites removed).
SBP management:
-ttt: empiric IV antibiotic therapy 3rd generation cephalosporin (ceftriaxone or
cefotaxime) depending on renal function, or quinolone( ciprofloxacin).
- Then long life/2ry prophylaxis: norfloxacin 400 mg PO qd.
- If total protein < 10g give antibiotic as prophylaxis even if no SBP.
- In GI bleeding start antibiotic prophylaxis 2nd generation cephalosporin or
quinolone.
Coagulopathy management:
- Vit. K IV 10mg/day for 3 consecutive days.
- In active bleeding or invasive procedure: fresh frozen plasma & platelets
transfusion.
GI bleeding management:
- ICU admission.
- ABC  resuscitation with IV fluid fast drip till blood available.
- Lab tests CBC, U & E, coagulation profile, cross matching.
- NGT.
- Octreotide infusion, bolus then infusion acutely reduces portal pressures &
controls variceal bleeding with very few side effects, improving the diagnostic &
therapeutic success of subsequent endoscopy.
- Vasopressin: cardiovascular risk in ICU w. cardiac monitoring, + nitroglycerin.
- Endoscopy for variceal ligation banding, sclerotherapy.
- TIPS, shunt surgery: if child B not responding to therapeutic endoscopy to
relief portal hypertension, then liver transplant.
- Balloon tamponade: dangerous esophageal rupture.
- Discharge on b-blocker Propranolol : reduce portal pressure & lower the risk of
recurrent bleeding.
- Endoscopy every year.
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dr saad
Admin


عدد المساهمات : 176
تاريخ التسجيل : 12/12/2010
العمر : 35
الموقع : http://medsurgery.ba7r.org

مُساهمةموضوع: رد: Gastroenterology & Liver disease    الجمعة 01 أبريل 2011, 20:45

Chronic liver disease
Dr. Hisham Akbar
• Definition
• Types
• Causes
• Manifestations
• Treatment
Types:
A. According to pathology:
1. Traditional:
• Chronic persistent
• Chronic lobular
• Chronic active
• Liver cirrhosis
2. Metavir
3. Knodells
B. According to etiology:
1. Necrotic
2. Post necrotic
Depends on taking liver specimen to show:
• Degree of inflammation
• Staging = of the degree of fibrosis
Role of liver biopsy in chronic hepatitis:
1. To establish the diagnosis
2. For the detection or exclusion of other diseases
3. For grading
4. For staging
5. Evaluation of therapeutic effect
Note:
• Initially the inflammatory cells limited in the portal tract  then in a
lobule  then spreads to the portal vein.
• The liver histological specimen is usually stained with H&E.
• Cirrhosis: is the complete distraction of hepatic nodules. Moreover, a
patient with hepatic cirrhosis is more liable to develop HCC.
Classification of CLD according to the cause:
1. Infection : viral hepatitis ( B, C, D )
2. Autoimmune hepatitis
3. Alcoholic
4. Drugs ( methotrexate, isonizaid, methyldopa, … )
5. Metabolic  fatty liver
6. Cholestatic  1ry & 2ry biliary cirrhosis
 sclerosing cholangitis
7. Infiltrative
8. Vascular problem ( cardiac cirrhosis )
9. Neoplastic  benign
 Malignant  1ry
 2ry
10. Idiopathic
Note:
• 4 months are needed to develop HBVs Abs
• 1-2 weeks are needed to develop HBVc Abs  IgM  then IgG
Therefore 1. HBVs Abs remains for 4 months or more
2. HBVs Abs  (Positive + )
3. Persistent vireamia  detected by  PCR
Natural History of hepatitis B in adult by:
Acute HBV
 95 % recovery & immunity
 5 % chronic hepatitis
Note:
• If the patient becomes jaundiced – feverish – ill , that signifies that his
immune system is intact and is trying to defend the body against the
disease
• Chronicity risk  by aging (  age   chronicity )
• Mode of transmission :
 Neonate : vertical infection from the mother to the fetus ( 90%
chronic )
 Adult: horizontal infection
• Even if the patient is Asymptomatic but has persistent viremia, he has
the same chance of infection with HCC as a patient who is
Symptomatic.
CLD
Classification of autoimmune hepatitis:
Types Serum auto Abs Auto Ag
I 1. Serum anti nuclear
2. Anti mitochondria
3. anti-smooth Abs
- Double stranded DNA
in some but target Ags.
- In liver disease not fully
defined action.
II 1. Anti liver & kidney LK
2. Microsomal ( Abs type I
LKM )
- Cytochrome P450 11D
- Cytochrome 8 + 18
III Antisoluble liver Ag -
The interpretation of aggregated score is:
• Type I in female at menopause and teenage years.
• Type II & III more in children
• If the score of the criteria is 15 before ttt and greater than 17 after ttt :
 It’s Definitive autoimmune hepatitis
• If the score of the criteria is 10 – 15 before ttt & 12 – 17 after ttt
 It’s Probably autoimmune hepatitis
Alcoholic Liver Disease
Depends on:
• Amount per day
• More than 10 years consumption
• Genetic predisposition
Results in:
• Acute alcoholic hepatitis
• Fatty liver change
• Cirrhosis
Manifestations of CLD:
• Asymptomatic
• Symptomatic   Extra abdominal manifestation
1. Fatigue
2. Spider nevi
3. Enlarged or Shrunken liver
4. Enlarged spleen
5. Finger clubbing
6. Collapsing pulse
7. Kayser-Fleischer ring
8. Xanthelasma
9. Parotid swelling  alcoholic
10. Palmer erythema  Thenar
 Hypothenar
 Pulp of fingers
11. Gynecomastia  the most common cause is
diuretics ( Spironolactone / Aldactone ) .
12. Dupetrine contraction (common cause is occupational –
manual working).
13. Advanced disease  Ascites
 Bruising
 Esophageal varices
 Extra hepatic manifestation of hepatitis: mixed cryoglobulinemia
1. Rash
2. Glumerulonephritis  membranoproliferative
3. porphyria cutanea tarda hepatocellular ca
4. Arthritis
5. Vasculitis
6. Angioneuretic edema
Acquisition of HDV infection:
 Co-infection: simultaneous introduction of HBV – HDV
 Super infection: introduction of HDV into HBVs Ag (positive) host
Chronic
hepatitis
Asymptomatic
carrier
Cirrhosis
HCC
Persistent infection
Death
Natural Hiostory of HCV :
Acute infection
Clinical Sequelae :
Acute hepatitis
Chronic HBV / HDV
hepatitis
Fulminant hepatitis
HDV / HBV
Co-infection
HDV super
infection
to HBV
< or = 15 %
Resolution ( Risk
for subsequent
infection is
unknown )
> or = 85 %
Persistent
infection
Treatment
• Treat the cause
• Treat the complications :
1. Hepatorenal syndrome
2. Encephalopathy ( lactose, flagel )
3. Bleeding  a. ABC first.
b. Endoscopy: sclerotherapy
c. TIPS for  bleeding
 ascites
4. Ascites ( diuretic )
5. SBP (most common E.coli )  neutrophile
6. Hepatoma
Persistent infection
Non-Progressive
liver injury
Normal ALT Elevated ALT
Progressive
liver injury
Fibrosis &
Cirrhosis Death
HBV pt. might develop HCC
HCC without cirrhosis
but HCV pt. must have
cirrhosis to develop HCC
Treatment of chronic hepatitis:
A. Interferon (INF ) :
But not in Saudi patients since they fulfill the criteria for ttt with INF.
1. It's effective in treatment if the infection is recent (not more than 2
years), but most Saudi patients have established the infection since
childhood (more than 30 years).
2. INF is effective only if the liver enzymes are elevated twice the normal,
which does not apply to Saudi patients. (They have high liver enzymes
but not as twice).
3. Most of the viruses here in Saudi Arabia are pre-coremutant viruses
which are resistant to INF  so, once you stop the ttt viremia it will
rise again.
4. It should not be given to a patient with an autoimmune disease such as
SLE, RA.
5. Also it should not be prescribed to patients with leukopenia and
thrombocytopenia (CBC).
New combination: - INF + Ribavirine
- Pegylated INF
B. Nucleoside
INF
Moderate to
severe
necroinflammation
Fibrosis
HCV RNA ( + ve)
Persist elevated
ALT
C. Liver transplantation :
- Not all HCC are sent for assessment of liver transplantation.
- Only in case of Liver failure
- Most of deaths occur  early = infection
Late = rejection
- Nowadays, transplantation of the left lobe enhances the liver to be a
complete one within 6 months. The donor’s liver will grow another left lobe to
replace the donated lobe.
How to diagnose HCV?
1. ELISA : detect HCV Abs  Generation 1
 Generation 2
 Generation 3
- If ELISA is (positive) that means the patient has the Abs  has the
infection for at least 6 months.
- If liver enzymes > 1000 it means the infection is acute.
- Incubation period for HCV ( 30 – 90 days )
- After 1 month the patient starts to have an increase  in liver enzymes
either  clinical
Or  subclinical
2. PCR (positive): only after 2 weeks of the infection.
3. RIBA: Recombinant Immuno Blotting Assay = detects Abs earlier than
ELISA.
Q: PCR (+) increase in liver enzymes, what is to be done?
We cannot start the treatment for any patient with HCV unless:
1. Decompensate CLD e.g. reaching the stage of Ascites – varices
2. Alpha IF or Rebavirine is contraindicated for a reason or the other.
So, when we discover HCV infections we should decide in which stage is the
patient by taking History & physical examination.
1. Jaundice
2. Hematemesis
3. Asterixis
4. Lower limb edema
5. Epistaxis
6. Bleeding gum
7. Abdominal pain & distention
α-IF ( S.C ) + Ribavirine ( tablets ) = ttt of HCV + CLD
Could be used with any patient with compensated CLD and has no
contraindication to medication.
Decompensation (Ascites - Encephalopathy- varices)
Investigations:
1. Baseline CBC  because  α -IF cause  leukopenia ( neutropenia )
 Thrombocytopenia
- So we need to know his baseline.
- If the patient is already leukopenic, he is not a good candidate for
α-IF.
2. Left  synthetic function ( PT – PTT – Albumin )
 Excretory function (bilirubin)
• α-IF should not be given to any autoimmune pt. e.g. SLE , RA.
Because it will worse the condition.
• α-IF can cause thyroid dysfunction  hypo ( common )
 & hyperthyroidism
& this S/E is the only S/E of a-IF which is not reversible. That's why we
need to do TFT ( T3 – TSH ).
• Rebavirine should not be given to a pregnant patient can't control
her because it is teratogenic.
• Rebavirine could cause hemolysis so it shouldn’t ever be given to
patient with hemolytic anemia.
• Rebavirine until now doesn’t have an exact defined dose. So, a
follow-up is need.
• Rebavirine could cause impaired renal function. So, a baseline
should be done on RFT.
End ttt Response ( ETR )
Sustained Viral Response ( SVR )
After finishing ttt (6 or 12 months),
& liver enzymes (negative)
& PCR (negative)
 It is ETR
But my aim is to have PCR (negative) after 6 months of stopping ttt.
 At this time it's (SVR).
1st time the HCV was discovered was in 1989
α-IF for 6 months  response  6 %
After 1994  extended monotherapy  for 1y  15 %
In 1998 α-IF + Rebavirin  response  41 %
HCV  6 genotypes  type I & IV (requires a year) disresponse to
α-IF – Rebavirine
 While genotype II & III (requires 6 months)
cause better response 60%.
 Some patients could have co-infection of I & II
It fails many times due to mutation in genotype, that is why we give
pegylated IF.
Polyethylene glycol + α-IF  pegylated IF  In type IV after 1y
(41 % response).
 In type II / III
(~ 80 % response).
Factors affecting response:
1. Younger than 40 years.
2. Female better than male.
3. Genotype II is & III better than I & IV.
4. Degree of cirrhosis.
5. Viral load.
EVR = Early Virologic Response
الرجوع الى أعلى الصفحة اذهب الى الأسفل
http://medsurgery.ba7r.org
 
Gastroenterology & Liver disease
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