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In Capsule Series

Liver

Liver
Introduction:
- Liver is the largest & heaviest internal organ in the body (1500gm). - Liver is the master of metabolism, it's involved with almost all i biochemical pathways that allow growth, fight disease, supply nutrients, provide energy & aid reproduction. - Liver cells (hepatocytes) go thousands of complex

biochemical reactions every second in order to perform these function. In brief, you can't live without liver

Anatomy:
- The liver is located behind the lower ribs, right below diaphragm on i right side of abdomen separated superiorly by falciform ligament & inferiorly by ligamentum teres. N.B. - Rhight lobe is much larger & has 2 additional lobes caudate & quadrate lobe).

Histology:
- Hepatic lobule: is the basic unit for liver function:
Portal vein
Hepatic artery

Bile duct hepatocytes

Space of disse.
Blood sinusoid

Bile canaliculi Central vein

N.B: The walls of i sinusoids consist of endothelial & macrophage cells known as "Kupffer cells" - These kupffer cells phagocytose damaged & aging RBCs, bacteia, viruses & immune complexes. 1
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Blood Supply of i liver:
- Liver has double bl. Supply hepatic artery 1/3 Portal vein 2/3 iiihepatic artery carries oxygenated blood.

Liver

Portal vein brining blood from the intestine & spleen.

Venous drainage:
Drainage is via the hepatic veins into the inferior vena cava.

Portal circulation:
Portal vein (Blood from gut) Hepatic artery So, there is mixed bl. In blood sinusoid Hepatic vein I.V.C

Liver function:

The liver is the main industrial centre of i body. - Liver is very important in proper protein, carbohydrate & fat metabolism. - Making bile. - Detoxification: filtering of i blood.

You can spend a lifetime studying the liver and still not understand all of its physiology!!
N.B: The liver has great reserve power, it using only a small amount of its full potential, it can loss 3 4 of its cells before it stops functioning. So, this great reserve power means that diseases that affect i liver show no symptoms in early stages, & this makes the prognosis worse.

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Liver

N.B: Liver cells can regenerate themselves, this regenerative ability allows diseased liver to return to normal function in some cases. Very few organs in i body have this ability. So, the first lines in any symptoms of any liver dis. Are: - Many patients with (any liver diseases) are a symptomatic, for years, others may show generalized weakness, anorexia, malaise & weight loss.

Rule of 6 in Hepatology:
Pathogenesis (AE) of Ascites in hepatic patient . 6 items. ttt of Ascites in hepatic patient. ......... 6 items ppt factors of hepatic encephalopathy.... 6 Items. c/p of hepatic encephalopathy (precoma)... 6 Items. ttt of hepatic encephalopathy............. 6 items. c/p of portal hypertension ............. 6 Items complications of portal hypertension.. 6 Items. Investigations of portal hypertension.. 6 Items. ttt of portal hypertension (O.varices)...6 Items. Prevention of O.varices6 Items. Complications of hepatitis ...6 Items. Causes of hepatomegally 6 Items.

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In Capsule Series

Liver

Liver Cirrhosis
Def.: Cirrhosis is defined as irreversible hepatic injury,
characterized by fibrosis & regeneration nodules ending in loss of normal liver architecture. N.B: fibrosis without regeneration module is not cirrhosis.

Pathogenesis:
iThe main damage in cirrhosis is triggered by scaring (fibrosis) that occurs from injuries due to alcohol, viruses,.. iiIn response to the scaring, liver cells regenerate in abnormal pattern & form nodules around i scar. iiiThe scar tissue & regenerated nodules block the flow of blood and bile through the liver, preventing it from working as it should.

Aetiology:
1- Alcoholic cirrhosis (laennic's cirrhosis). 2- Post hepatitis cirrhosis, Bilharziasis. 3- Cardiac cirrhosis 4- Biliary cirrhosis bile 5- Metabolic Haemochromatosis Hepatolenticular dengeration 6- Iatrogenic: Methotrexate, INH, Methyldopa 7- Idiopathic (cryptogenic) cirrhosis. 8- Others : Severe malnutrition. Syphilis. 1 antitrypsin deficiency.

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Liver

Classification of cirrhosis:
- Aetiological classification acc. To aetiology. - Morphological classification: Micro-nodular < 3mm, same size. Macronodular > 3 mm, variable size. Mixed.

Clinical picture:
Symptoms:
a- Asymptomatic (latent cirrhosis): Compensated liver cirrhosis (No LCF or pH Many patients with liver cirrhosis are asymptomatic for years, others may show generalized

weakness, anorexia, malaise & weight loss. b- Symptomatic (Manifest cirrhosis):

Symptoms of i cause

Liver cell failure (LCF)

Portal hypertension (pH)

i- Symptoms of I cause : e.g.: Post hepatitis: symptoms of hepatitis (history) Haemochromatosis: Bronzed DM. Hepatolenticular degeneration: extrapyramidal manifestations. ii- Symptoms of liver cell failure: easy fatigueencephalopathy.. see later. iii- Symptoms of portal hypertension: distension, splenmegally, varices see later.

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Signs:
1 signs of i cause.

Liver

2 signs of liver cell failure: palmer erythema, flapping tremor, 3 signs of portal hypertension: splenomegally. 4 Liver: firm, sharp border shrunken liver. Complication hepatoma: N.B1 : The liver is shrunken in all types of cirrhosis except in - Cardiac cirrhosis. - biliary cirrhosis - early cases of liver cirrhosis N.B2 : Causes of shrunken liver: Cirrhosis, fibrosis, necrosis.

Investigation:
iiiiiiivInvestigation for i cause. Investigation for liver cell failure (liver function test). Investigation for portal hypertension. Investigation for cirrhosis biopsy is the surest D ultrasound - CT vInvestigation for complication (hepatoma) Tumur marker (-feoto ptn.) (carboxy prothrombin)

Treatment:
- Liver damage from cirrhosis can't be reversed, but treatment can stop or delay further progression and reduce

complications. iiiTreatment of i cause. Treatment of liver cell failure. 6


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iiiivTreatment of portal hypertension.

Liver

Drugs to decrease liver fibrosis (Antifibrotic) it's still under trial Colchecine collagen destruction. penicilamine collagen synthesis.

v-

Hepatic transplantation is the best hope but many patient are not suitable.

1- Alcoholic Cirrhosis
Aetiology:
Alcoholic cirrhosis usually develops after more than 10 years of heavy drinking. How ? 1- Alcohal appetite & malopserption nutritional cirrhosis. 2- Alcohol Alcohol H + + Acetaldhyde dehydrogenase
Direct Hepatotoxic

Pathology:

- Path. Of cirrhosis itself (def.) - Micronodular cirrhosis. - Mallory bodies: Oesinophilic deposits.

Clinical picture:
1- C/P of cirrhosis itself. (LCF > pH) 2- C/P of i cause (Alchoholism) 3- History of prolonged alcohol intake > 10 y` 4- Acute alcoholic hepatitis vomiting enlarged tender liver.

5- Other features of ch. alchohlism: GIT: Gastritis, hepatitis, pancreatitis, malabsorptions. CNS: Korsakow's syndromes: tremore, Amenesia. blood: haemolytic anaemia. Immune: recurrent infection.

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Metabolic: Hypoglycaemia, hyperlipidaemia. Bilateral parotid enlargement. Investigation: general inv. For cirrhosis.

Liver

Treatment:
Stop alcohol intake. General measures for cirrhosis. Essential aa - cholchiaia cortisone

N.B: Alcoholic liver diseases: 1- Fatty liver (reversible) : Alcohol fat entery to hepatocyte. fat secretion from hepatocyte. 2- Alcoholic hepatic: mimic viral hepatitis + IgA N.B: if i ratio of SGOT: SGPT > 2:1 suggest alcohol hepatitis. 3- Cirrhosis (LCF > PH)

2- Post hepatitis Cirrhosis


Aetiology: Pathology:
Pathology of cirrhosis itself. Ground glass appearance +ve orcien stain virus features of chronic active hepatitis. following virus B,C & D.

Clinical picture:
Clinical picture of cirrhosis. Past history of virus hepatitis. (see later) 8
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Liver

Investigation:
Investigation for cirrhosis. Detection of hepatitis markers.

Treatment:
General measures for cirrhosis. ttt of chronic active hepatitis. Hepatitis B vaccine for prevention.

3- Bilharziasis
(pH > LCF) In past, it was thought that B leads to fibrosis only no.. B can lead to cirrhosis with marked fibrosis by 2 mechanisms. 1- Combined AE virus C. 2- Ag Ab complex.

4- Cardiac Cirrhosis
Aetiology: Due to chronic liver congestion
1- RSHF 2- Tricuspid valve disease. 3- Constrictive percarditis & pericardial effusion 4- Inferior vena cava obstruction. 5- Budd-chiari syndrome (hepatic V. obst.) 6- Veno-occlusive disease. (small interhepatic veins). (v.rare & v.late)

Pathology: The same as any cirrhosis.

Clinical picture:
General features of cirrhosis.

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Liver is enlarged, tender, soft then firm & sharp border. N.B: Portal hypertension occurs before liver cell failure.

Liver

Investigation: - The same as cirrhosis.


- Investigation for i cause.

Treatment:
General measures for cirrhosis. ttt of the causes e.g.: heart failure. N.B: again: cardiac cirrhosis is very early & very late. N.B: Budd. Chiari syndrome: - It's obstruction of large hepatic veins. by: thrombosis, obstruction (tumour). C / P: acute stage: - enlarged, tender liver - Abd. Pain Ascites chronic stage: feature of cardiac cirrhosis.

5- Biliary Cirrhosis
- It's cirrhosis caused by prolonged biliary obstruction. - Bile is very irritant to the hepatocyte if retained.

(A) Primary biliary cirrhosis:


Pathogenesis Autoimmune disease leading to destruction of intrahepatic bile duct.

Clinical picture:

30-50 4`
Asymptomatic ( 13 ) Fatigue (most common). Pruritis occurs months before jaundice because retention of bile salts can occur before significant retention of bilirubin. 10
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Jaundice Clubbing. Hepatomegaly Vit A, D, E, K Vit D Osteomalacia Vit K Hge

Liver

associated immune disorders: SLE, 30% of patients have thyroid disorders. Xanthelasma 2ry to hypercholesterolemia + manifestiations of cirrhosis.

DD: Medical causes of itching:


1- 1ry biliary cirrhosis. 2- Obst. Jaundice. 3- DM 4- CRF 5- Heamolytic aneamia 6- Polycythemia 7- Leukemia 8- Lymphoma

Investigation:
It's autoimmune so, there is: antimitochondrial antibody: +ve in 95% IgM Liver biopsy is diagnostic.

Treatment:
Immunosuppressive: Pencillamine, Azathioprine. N.B Cortisone is contraindicated as it increases osteomalacia and osteoprosis.

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Liver

B) Secondary biliary Cirrhosis: Extrahepatic: stone, stricture. N.B. Cancer head of pancreases usually of short duration so cirrhosis usually doesn't occur. Intrahepatic: See obstructive Jaundice. How to differentiate ( ) extrahepatic & intrahepati biliary obstruction? 1- US: to Inrahepatic lead constriction of Intrahepatic bile radicles. Extrahepatic biliary obst. diltation of intrahepatic bile radicles. 2- Cortisone test.

6 Heamochromatosis "bronzed diabtetes"


Def.: It's a disease characterized by of total body iron iron
deposition in several organs including liver.

Aetiology: hereditary disorder


: Excessive iron absorption due to absence of mucosal block (autosomal R) here, body iron reaches up to 60gm (N=4gm)

Clinical Picture:
- More common in (no menstruation) - Liver liver cirrhosis. 95%. - Heart Cardiomyopathy. - Skin Bronzed colour. 90% ( of melanocyte) - Pancreas Diabetes mellitus. 60% - Mental disturbance. - Testicular atrophy.

Complication: 20% of cases hepatoma.

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Liver

Investigation: serum iron, S.ferritin


Iron binding capacity : Liver biopsy MRI - ttt of cirrhosis (LCF PH) - ttt of i cause: repeated venesection: once/week, 500ml = 250 mg iron - Chelator: Desferal - Symptomatic ttt: DM, Cardiomyopathy,..

Treatment:

7- Hepatolenticular Degeneration "Wilson dis" Aetiology:


Decrease in "Ceruloplasmin" which is responsible for carring copper (autosomal R). So, copper now is free with poor excretion through i bile. Abnormal deposition

Clinical picture:
Liver acute hepatitis self limited, may progress to cirrhosis. Lentiform nucleus (Basal ganglia) extrapyramidal manifestation (Parkinsonism, chorea). Kidney renal tubule damage which lead to albuminuria & aminoaciduria. Eye Kayser Fleisher ring (green brown ring in i cornea)

Investigation:
blood copper level. ceruloplasmin level. Liver biopsy. Treatment: ttt of cirrhosis (LCF PH) ttt of i cause : Penicillamine (Chalator) K sulphide cu symptomatic ttt 13
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In Capsule Series Liver Cell Failure


Aetiology: 1- Infections: viral hepatitis. B, C, D 2- Chemicals: Alcohol

Liver

D DT, Halothan, Paracetamel, INH 3- Physical: Severe burns & hyperthermia. 4- Terminal stage of - Liver cirrhosis. - obstructive jaundice - chronic hepatitis. - malignancy

Clinical Picture of liver cell failure:


: - Fatigue, anorexia, loss of weight - Fever. - Foetor hepaticus. - Jaundice - Ascites - Encephalopathy - Skin manifestations. - Endocrinal manifestations. (Hormonal) - Cardiovascular manifestations. - Haematological manifestations. - Hepatorenal syndrome. 1- Fatigue, anorexia, loss of weight. 2- Fever: (low grade & prolonged)

d. to: i- necrosis of liver cell release of pyrogens heat regulating centre

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Liver

ii- Bacteramia due to failure of the liver to clear bacteria from the circulation.

3- Foeter hepaticus:
It's musty, slightly fecal smell increased by constipation & by defecation. It's d. to methylmercaptan (which is normally absorbed from intestine & detoxicated in liver) but in liver cell failure it bypass hepatic detoxication excreted in mouth with breath.

4- Jaundice: Failure of liver to deal bilirubin (see later)

5- Ascites: Pathogenesis:
important factor. N.B.: Patient liver cirrhosis & ascites with normal albumin suspect other causes of ascites e.g.: T.B peritonitis. ii. Portal hypertension: This factor alone can't produce ascites, it only leads to localization of the transudate to peritoneal cavity. N.B: Experimentally, even ligation of portal vein doesn't cause ascites. iii- aldosterone: d.to In liver failure destruction of aldosterone. Hypoalbuminaemia hypovolamia RBF renin angiotensin II aldosterone. iv. ADH d. to liver failure.

1- Hypoalbuminaemia ( < 3gm%) which is the most

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v. Lymphorrhea:

Liver

post sinusoidal obstruction lymph production into peritoneum. (liver weepin) vi. Associated factors: SBP, malignancy, T.B. peritonitis.

Spontenous bacterial peritonitis: (SBP)


Infection of the peritoneal cavity in absence of known aetiology. occurs in 10% of cirrhotic patients. d. to loss of detoxification function of the liver. The prognosis is very bad. c/p: i deterioration of liver function, e.g.: increasing

encephalopathy, ascites or jaundice. ii- resistance to diuretics may be a sign of SBP. iii- High fever, sever abdominal pain, tenderness. Diagnosis: The key to the diagnosis of SBP is examination of the ascetic fluid: Polymorephonuclear leukocytes count (PMN) > 250 cells / mm3. Culture: monomicrobial e.g: E.cali.

Treatment:
Cefotaxime: 2 gm t.d.sIV

Investigations of a case of ascites:


1- diagnostic aspiration with: a. albumin determination. b. Cell count c. Culture & sensitivity test: ZN for T.B. d. Amylase to exclude pancreatic ascites.

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N.B: significance of cell count: An ascetic fluid with RBCs suggests malignancy.

Liver

An ascetic fluid with WBCs > 250/mm3 suggests SBP.

2- Investigation for the cause: Liver function tests e.g.: serum albumin. Laparoscope for peritoneal tumors or T.B.

Treatment:
1- Salt restriction.

2- Spirnolactone in full dose 100-400mg/ d drug of choice. 3- Lasix (40-80mg/d) N.B: The maximum amount of fluid transported from peritoneum to the blood is 500-700 cc/d, so any more lasix general dehyderations of the body without improvement of ascites. 4- Tapping (paracentesis) is not indicated except in: 3 cases. Sampling. To releife respiratory distress. To releife compression on the hidney. 5- Albumin (infusion) 6- Peritoneo-venous shunt: le veen shunt. N.B: Ascites must not be treated if there are marked

manifestations of liver cell failure. **Refractory ascites: Ascites not responding to salt, fluid restriction & lasix (up to 120mg) + spirnolactone (up to 400mg) for > 2 weeks.

6- Skin manifestations: (VDM)


i- Palmar erythema: erythema in head of metacarpal bones, thinner & hypothinner eminence with central pallor.

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ii- Spider navi: Each navi is a dilated arteriole with radiating capillaries.

Liver

Compression of the central arteriole causes blanching of the radiating capillaries. It occurs in the distribution of SVC: (Above the nipple line) N.B: Pulmar erythema & spider navi are attributed to VDM e.g: hyperoestrogenism. iii- Paper money skin: Numerous small vessels scattered in skin over bony areas, dorsum of foot & hand, forhead, chest. iv- White nail: white zone at the tip of the nail. v- Xanthelasma: (cholesterol deposits)

7- Endocrinal manifestations: d.to oestrogen


[

Gynaecomastia. Female distribution of suprapubic hair. Impotence, libido & testicular atrophy.

Amenorrhea & sterility. Atrophy of breast & libido.

- Aldoeterone - ADH N.B. : - Gynaecomastia is occasionally unilateral. - The cause of gynaecomastia is still questionable, but it is probably related to oestrogen or to treatment with spironolactone. 8- Cardiovascular manifestations: (VDM) i- Hyperdynamic circulation: due to: Anaemia. 18
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Toxic product are vasodilators (VDM) ii- Cyanosis & clubbing : d.to Opening of intrapulmonary A.V. shunt. d. to (VDM) Portopulmnary shunt. Basal lung collapse d. to ascites.

Liver

9- Haematological manifestations:
i- Anaemia: Normocytic normochromic: BM depression by toxins. hyprsplenism. Microcytic hypochromic: Iron deficiency d. to ch. Blood loss. Macrocytic: Vit B12 & folic acid deficiency. ii- Bleeding tendency: d. to Hypoprothrombinaema. Hypofibrinoginaemia. vit. K factors II, VII, IX, X 1972 hypersplenism thrombocytopenia.

10- Hepato-renal Syndrome:


It's acute renal failure with no renal pathology in patients with chronic liver disease. Exactly cause is unknown. May be due to: i-acc. Of VDM e.g: Nitric oxide (No) ii- Hypoalbuminaemia hypovolaemia RBF GFR. The prognosis is very bad. Liver transplantation is the best choice. 19
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Liver

11- Hepatic Encephalopathy:


Def.: It's a neuropsychiatric manifestations in patients with liver cell failure.

Precipitating factors:
1- GIT Bleeding. 2- ptn intake. 3- Old Blood transfusion. 4- Aspiration of ascites. 5- Diuretics (lasix) 6- aldoesterone N.B1.: Ammonia interferes with creb's cycle
3 glutamine CNS). (glutamic acid NH

ammonia

K+

N.B2.: Hypokalemia glucose entery to cell e.g: cerebral cells coma.

Clinical picture:
Pre coma: 2 A + 2 S + 2 D Coma i- Pre Coma: 2A + 2 S + 2D Disorientation: for time, place, persons. Disorders behaviour: childishness, phasic excitation & depression Sleep: reversed sleep rhythm, any metabolic error can do that. Speech: slow, slurred or monotonous. Apathy: slow response to questions. Asterixis: (Flapping tremors).

ii- Coma: Irritable coma.

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N.B: DD of irritable coma: - Hypoglycemic coma. - Hepatic coma.

Liver

Treatment of hepatic encephalopathy:


the site of bleeding. 2- Diet: .ptn: restricted.

1- Hospitalization in ICU, endoscope must be done to localize

. CHo: CHO ptn breakdown as a source of energy. . Fats: Fats in small amount mild diarrhea which is useful to wash intestine. 3- Enema / 4h wash the colon. 4- Neomycin 1gm/6h orally. 5- Lactulose (15ml 3 times/day) osmotic diarrhea wash the colon. fermented into organic acid. NH3 + H+ NH4 (non absorbable) 6- Liver transplantation.

Investigations of LCF:
Liver function tests. US, CT Investigations for the cause. Investigations of ascites. N.B.: Biopsy is very difficult d. to bleeding & Ascites.

Treatment of LCF:
Treatment of the cause.

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Liver

Treatment of ascites: provide that the features of LCF are not sever. Treatment of encephalopathy. Liver transplantation.

Acute (Fulminant) Hepatic Failure (FHF) Def.: It's an acute liver failure with rapid development of hepatic
encephalopathy & coagulopathy within 8 weeks in patients without pre-existing liver disease. N.B: Hyperacute liver failure within 2 weeks. Acute liver failure within 2-8 weeks. Sub acute liver failure 8 weeks -6 months.

Aetiology:
Viral hepatiis B, C. Paracetomal toxicity ( > 15gm = 30 tab) Alcohol toxicity. Acute fatty liver of pregnancy.

Clinical picture: (Encephalopathy & coagulopathy)


Encephalopathy (pre coma & coma) Coagulopathy (bleeding) Jaundice : rare The condition usually ends by death due to bleeding, respiratory & circulatory failure (shock), cerebral odema & other organ failure.

Investigations:
S. Bilirubin : Exceeding 23mg Poor prognosis S. albumin : Normal, prothrombine time prolonged.

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Treatment:
- The treatment of encephalopathy + ttt of complication - Hepatic transplantation.

Liver

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In Capsule Series Portal Hypertension


Def.: Elevation of portal venous pressure above 12mm Hg Aetiology: The most common cause at all is L.cirrhosis other causes extremely rare. i- Supra hepatic cardiac cirrhosis - RSHF, TS, pericarditis, IVC obstruction & Budd.ch.s. ii- Hepatic (most common): sinusoidal & post sinusoidal: Liver cirrhosis "the most common cause". Veno-occlusive disease. pre sinusoidal Schistosomiasis: peri-portal fibrosis. Congenital fibrosis of portal tract. Hodgkin's lymphoma, leukemia.

Liver

iii- Infrahepatic: Portal vein thrombosis (Tumour).


N.B.: Cirrhosis is the main cause of portal htn. By: 1- The trauma that caused cirrhosis creates an arterio-venous fistula ( ) hepatic a & portal v. 2- Liver fibrosis & regenerative nodules increase i portal pressure by compression.

Pathophysiology:
Portal vien is formed by i union of i superior mesenteric & splenic vien. So, portal hypertension lead to: Spleen congestion. Intestinal congestion.
Sup. Mes. V.

Liver

spleen

S.intestine

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Liver

Porto-systemic shunt. In attempt to decompress the portal hypertension.

Clinical Picture:
(1) Splenomegaly:

- Dragging pain in i left hypochondrium. - May be the only clinical evidence of portal hypertension. - May be associated with hypersplenism, which by turn lead to pancytopenia & bleeding tendency. N.B.: No relation ( ) size of spleen & severity of portal hypertension.

(2) Intestinal congestion:


- Distension - Dyspepsia.

(3) Liver: firm & sharp border (cirrhotic liver) (4) Ascites: Portal hypertension is a localizing factor rather than a
cause. (5) Encephalopathy: - Precoma:2A, 2S, 2D. - Irritable come.

- AE of encephalopathy:
i- The blood bypasses i the liver via i collaterals so, the toxic metabolites pass directly to the brain to produce i

encephalopathy. ii- Porto systemic shunt operations

(6) Porto-systemic shunt:


In attempt to decompress the portal hypertension.

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Main sites of i collaterals:Site Portal C. Systemic C. Azygos vein of

Liver

Clinical presentation Oesophageal with bleeding or varices without

1- Lower end of Coronary oesophagus veins stomach 2Around

i Umbilical vein Veins of ant. Caput medusa in flaciform Abdominal wall & Inferior rectal May be mistaken for rectal vein hemorrhoids

umbilicus

ligament 3- Anal canal Superior middle veins

N.B.: Actually piles never occurs, this is because: - Too far from i portal vein to transmit pressure. - Perianal sphincters are always in tonic contraction that compress i veins.

Complications of portal hypertension:


1- Oesophageal varices. 2- Ascites 3- Portosystemic encephalopathy. 4- Hypersplenism. 5- Congestive gastropathy (bleeding) 6- Renal failure.

Oesophageal varices:
Def: dilated, elongated, tortuous veins located at lower end of i oesophagus. AE: I can say that portal hypertension is the only cause of oesophageal varices & no one can blame me !!.

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In Capsule Series C/P:


- Approximately 90% of cirrhotic patients
1 3

Liver

will

develop

oesophageal varices, over 10 years, but only bleed.

of these will

- Bleeding is likely to occur with large varices, red signs on varices (diagnosed by endoscope) and in severe liver disease. i- before rupture: Asymptomatic (silent) dysphagia (v. rare) ii- At rupture: Painless massive hematemesis. melena. N.B: Because other etiologies of upper gastrointestinal bleeding are also common in cirrhotics (gastritis, peptic ulcer) variceal bleeding should be confirmed with endoscope (even in patient with known varices).

Investigation of portal hypertension:


(oesophageal varices)

1- Endoscopy:
Detect early varices. Detect signs of impending rupture (red signs). Detect active bleeding & its site. Can be used for sclerotherapy of varices. 2- Doppler or duplex ultrasound detect pressure, Bl. Velocity, patency.

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Liver

3- Free & wedged hepatic venous pressure: Catheter is introduced into SVC IVC hepatic vein (free hepatic venous pressure) then pushed till it is wedged in hepatic sinusoids (wedged hepatic v. pressure)

Portal Pressure = Wedged Free 4- Splenoportography:


needle introduced into i spleen inject dye for patency of portal vein.

5- Evaluation of i liver: liver function test, liver biopsy. 6- Barium swallow: can be used to detect oesophageal varices
& Barium enema to detect bilharzial polypi.

Treatment of portal hypertension:


1- ttt of oesophageal varices. 2- ttt of porto-systemic encephalopathy. 3- ttt of Ascites.

Treatment of oesophageal varices:


During attack:

1- Volume resuscitation & correction of coagulopthy: Bl. Transfusion, vit K. 2- Endoscopy to detect i site of bleeding. 3- Pharmacological ttt: vasopressin, somatostatin, octreotide. * Vasopressin: (pitressin) -V.C of mesenteric & hepatic arteriole Portal inflow portal v. pressure Hge - Dose: 20 unit in 200ml glucose 5% over 20 min.

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Liver

- SE: generalized V.C may result in peripheral vascular ischemia, Ischemic heart disease & hypertension so, we may use nitrate with vasopressine. * Somatostatin or octreotide are more safer.

N.B: Whatever drug is used, it's inadvisable to continue drug


therapy for more than 1 to 2 days. N.B: Pharmacological therapy can be initiated as soon as variceal hge is suspected, even before diagnostic endoscope. 4- Injection sclerotherapy and / or band ligation: (through an upper endoscopy). - The efficacy of rubber band ligation is similar to sclerotherapy with fewer esophageal complications: esophageal ulceration, stricture. 5- Sengstaken- Blakemore tube: mechanical compress of oesophageal varices. Diagnostic value: used in haematemesis, if i bleeding doesn't stop source is not i oesophagus. Therapeutic value: - If bleeding doesn't stop by conservative treatment. - If endoscope is not immediately available. S/E: esophageal perforation & ischemia Especially in inexperienced hand. 6- When all the above measures fail, Transjugular intrahepatic portosystemic shunt (TIPS) or portosystemic shunt are considered.

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3 1ry 3 2ry

Liver

Prevention:

1ry prevention
2- Large varices: B. blocker: cop.

(silent varices)

1- Small varices: no treatment is required.

Nitrates: venodilator 3- Impending rupture: injection sclerotherapy or band ligation.

Secondary prevention: d
(Prevention of recurrent variceal bleeding) 1- B blocker (propranolo): the risk of rebleeding up to 40%. 2- Repeated injection sclerotherapy or band ligation till varices disappear. 3- TIPS or portosystemic shunt are considered in patient who rebleed during above measures.

- TIPS (transjugular Intrahepatic porto-systemic shunt): inserting short metal tube through neck vein (Jugular) liver (hepatic) & connect portal vein with hepatic vein (portosystemic). - It requires only light sedation & local anesthesia. - Porto-systemic shunt: * Portocaval * mesenterico caval * lienorenal minimal encephalopathy. 2 types : Distal (warren op). : proximal. - HASSAB op (minor surgery): splenectomy & o.devascularzation

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In Capsule Series

Liver

Gastro-Intestinal Bleeding
* Upper GIT bleeding: - Site of bleeding: is proximal to ligament of Treitz. (distal duodenum) - Presentation: - Haematemesis - Melaena - Occult blood in stool * Lower GIT bleeding: - Site of bleeding: is distal to ligament of Treitz. - Presentation: - Heamatochezia (Bleeding per rectum) - Melaena - Occult blood in stool Haematemesis: - Vomiting of blood - Blood may be: red in color: if immediately after bleeding coffee ground (Melenemesis): when blood is in contact with gastric acid for at least 1 hour. * AE: Esophageal: - Esophageal varices - cancer Esophagitis - Mallory weiss tear * Gastro-duodenal: Duodenal ulcer

- Gastric ulcer - Gastritis - Cancer stomach

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Liver

* Systemic (general) causes: - Haemorrhagic blood diseases. - Haemorrhagic fever. - Severe hypertension. - Heparine therapy. Mallory weiss tear: mucosal tear due to repeated vomiting. ttt : self limited, vasopressin may be used

*** D of haematemesis: 1- Clinical history: Cause 1- O. varices 2- Peptic ulcer Question to detect I cause History of cirrhosis, confusion? Epigastric pain, dyspepsia, heart burn?

3- Gastritis

History of drug intake e.g: Aspirin, Alcohol, NSAID? Epigastric pain?

4- Cancer stomach 5- Mallory-weiss 6- Coagulation defect

Weight loss, Meat dyspepsia Preceded by severe vomiting? Oral anticoagulant? History of cautaneous or orifice bleeding?

2- Nasogastric tube: usually +ve for blood 3- Endoscopy to localize i site of bleeding. 4- Angiograpy: done if endoscope fails to show i site of bleeding. 5- Lab: Aneamia urea: (breakdown of blood)

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In Capsule Series
* of heamatemesis: 1- Resuscitation: IV fluid & blood transfusion if necessary. 2- Endoscopy 3- of i cause: e.g: O. varices: see page 27 peptic ulcer: IV omeprazole. 4- Iron therapy: given in chronic cases presenting with iron deficiency anaemia. D D of haematemesis: - differentiation of i cause - Heamoptysis

Liver

- False haematemesis: Ingestion of blood after bleeding from i nose, mouth or pharynx then vomiting of this blood.

Melaena:
- Passage of black tarry stool due to presence of digested blood. - It indicates that heamorrhage has remained for 8 hours in the GIT

* AE: Site of bleeding: is not merely above ligament of Treitz but may extended up to right colon. So, AE of melaena = iiiAE if upper GIT bleeding (heamatemyesis) Jejunum & ileum: 2T + 2C Typhoid ulcer T.B enteritis Cancer head of pancrease Crohn's disease

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iiiColon: Rhight sided tumor Ulcerative colitis. D D of dark stool: - melaena - Iron ingestion - haemolytic Jaundice. * Diagnosis & of melaena; The same as

Liver

haematemesis Haematochezia:
- Passage of bright red blood per rectum. - Usually indicate that lesion distal to Rh. Colon

* AE: - Hemorrhoids - Diverticulosis. - Colitis - Colonic Cancer: usually present with chronic occult bleeding.

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Liver

D of Haematochezia:
1- Clinical history 2- PR examination 3- Colonoscop 4- Barium enema 5- Nasogastric tube: -ve 6- Lab: Aneamia

Occult GIT blood loss:


- normal appearing stool - hemoccult +ve

N.B: C/P of GIT hge: 1- C/P of i type of hge. 2- Hypovolemic shock 3- Recurrent GIT hge lead to iron deficiency anaemia. 4- C/P of i aetiology

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In Capsule Series
Hepatitis
Def: is an infilammation of i liver AE of hepatitis

Liver

Infectious

Non infectious * Alcohol * DDT Halothan * Paracetamol - INH

Viral
* 5 major hepatitis viruses: A, B, C, D, E * Recently F & G * Other viruses: CMV EPV, herps simplex A RNA

Non viral
* Malaria * Leptospirosis * Brucellosis

Viral genome

B DNA

C RNA

Transmission

Fecooral

Parenteral sexual transplacental 2-6 m 0.5-1%

IP Mortality rate (fulmination)

2-6 w < 0.2%

Parenteral sexual (V.rare, anal only) 2-6 m 0.5%

D RNA (incomplete virus with HBs Ag coat) Parenteral sexual

E RNA

Feco-oral

2-6 m Up to 10%

Chronicity Malignancy Prophylaxis Immunoglobulin vaccine

No No Non specific Yes (havrix)

5% Yes Specific Yes (HB vaccine (0,1,6m)

50-70% Yes -

50-70% Yes -

2-6 w 0.2% (in pregnant women 20%) No No No

No No Supervision (vaccination of blood against HBV) donation

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Causes of Hepatomegally:
Fascioliasis. T.B.

Liver

1- Infections: Hepatitis, Bilhariziasis, Amoebiasis,

2- Inflammation: Connective tissue disease & rheumatic disease. 3- Infiltration: Fatty liver, glycogen storage disease & amyloidosis. 4- Maligmency: 1ry & 2ry, Leukemia, Lymphoma. 5- Congestive liver. 6- Cholestasis: obst. Jaundice particularly extrahepatic. N.B: Most common causes of hepatomegally: Viral hepatitis fatty liver. N.B: Mild enlargement: < 5cm from costal margine e.g. : liver cirrhosis moderate enlargement 5-8 cm from C.margine Severe enlargement > 8cm below c.margine e.g. Leuk. Lymphoma, Amyloidosis.

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In Capsule Series

Liver

Approach to Asymptomatic patient with elevated transmaineses:


Careful history e.g.: alcoholdrug. & physical examinations suggest chronic liver disease

Yes

No

Presisten of SGOT & SGPT

Persistent of SGOT only

- Viral hepatitis merker: A, B, C - In young : autiommune markers ; ANA, AMA - Genetic disorders markers: Iron, Copper, 1 antitrypsin

Possible none-hepatic source, e.g.: muscle source Alcohol

-ve results Alcohol, obesity, DM, hyperlipidemia as risk factors

+ve results Consider liver biopsy to assess stage of disease

No

yes Fatty liver Diagnosis unclear Consider liver biopsy for diagnosis Treat as appropriate

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In Capsule Series

G.I.T.

Malabsorption Syndrome
** Def:
- Failure of absorption of one or more of the nutrient (fat, ptn, CHO, minerals, vit.), - Steatorrhea (fatty stool) remains the main mark of malabsorption. (>6gm/d).

** Causes:
IGastric Causes: 1- Gastrectomy. 2- Atrophic gastritis. 3- Cancer stomach achlorhydria (HCl) Bact. Contamination of intestine. 4- Zollinger-Ellison's syndrome hyperchlorhydria HCl inhibits pancreatic lipase. IIHepato-biliary Causes: 1- Liver cirrhosis 2- Chronic hepatitis. 3- Biliary obstruction. 4- Biliary fistula. IIIPancreatic Causes: 1- Chronic pancreatitis 2- Cystic fibrosis dis. Of pancreas. 3- Cancer head of pancreas. 4- Pancreatectomy.

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IVIntestinal Causes: A) Primary steatorrhea:

G.I.T.

1- Tropical sprue: unknown aetiology but may be: Bacterial infection. folic acid deficiency. 2- Non-tropical sprue (Gluten sensitive enteropathy) inborn sensitivity to gluten (a ptn commonly found in wheat) Ag. Ab reaction impairs absorption of all food elements d. to damage of intestinal mucosa. B) Secondary to intestinal diseases: 1- Short gut syndrome: extensive intestinal resection absorptive surface. 2- Stagnant (blind) loop syndrome: part of S.I. is narrowed so, there is stagnation of intestinal content bacterial growth which compete the host for vit B12 & other contents. e.g.: strictures of S.I, Diverticulosis. Hypothyroidism, intestinal myoputhy. 3- Systemic diseases: Diabetic neuropathy, amyloidosis, collagenosis. 4- Infection: Bacterial over growth. T.B enteritis, Giardia, Strongeloides. 5- Inflammation: Crohn's disease. Irradiation. 6- Iatrogenic: * Dendivan (anticoagulant). * Neomycin.
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7- Lymphatic obstruction: Lymphoma

G.I.T.

Whipple's dis. (mainly affects MAN) Malabs. Syndrome, Anemia, Neuropathy, lymphadenopathy.

** Clinical picture:
IGeneral manifestations: 1- loss of weight. 3- fever 2- fatigue. 4- clubbing of fingers.

II- Intestinal manifestations: 1- Steatorrhea: Stool is Pale, bulky, offensive, floats on water, greasy, glistening. 2- Diarrhea: diarrhea. 3- Audible intestinal sounds (borborygmi). 4- Distension, colics. III- Nutritional deficiency: ptn muscle wasting, oedema. Fats loss of weight. CHO hypoglycaemia. Minerals: Iron anaemia. Na Muscle cramps, hypotension. K arrhythmia. Ca, Mg tetany. Iodine Goitre. Vitamins: A night blindness, follicular hyperkeratosis. malabsorption usually results in

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In Capsule Series
D Rickets, osteomalacia. E infertility. K Bleeding tendensy. C Scurvy B1 Beri Beri B2 glossitis gastritis

G.I.T.

B3 Diarrhea, Dermatitis, Dementia. B6 peripheral neuritis. B12 Megaloblastic anaemia. IV- C/P of the cause: - History of surgical operation. - T.B: toxaemia, chest infection.

** Investigation:
I- Biochemical investigation: 1- Estimation of foecal fat: n= 6 gm/d in steatorrhea >6 gm/d. if split fat intestinal dis. Non split fat pancreatic dis. 2- Pancreatic function tests. 3- Sugar curve flat curve 4- D-xylose test: normally, 25 gm D-xylose orally 5h urine should contrain at least 5 gm (20%) - if < 5 gm in 5h urine malabsorption. IIHaematological Investigations:
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G.I.T.

1- Blood picture: Anaemia. (Microcytic anemia due to iron deficiency or macrocytic anemia due to vit B12 or Folate malabsorption. 2- Plasma ptn: hypoproteinaemia. 3- Serum electrolytes. 4- Prothrombin IIItime: may prolonged bec. of

malabsorption of vit. K. Radiological investigations: - CT - MRI - U.S. - Barium meals: - S.I. Dilated >25mm - loss of feathery app. IVAspiration of Jejunal content then culture.

** Treatment: 1

of the cause:

- T.B entritis anti tuberculous drugs. - Stricture surgical - Tropical sprue antibiotic & folic acid. - Gluten sensitive ent. cortisone. elimination of gluten from diet. 2- Diet: Low fat, low fibers, non irritant diet. 3- Parentral vitamins, minerals, fluid. 4- Synptomatic

: - Antidiarrheal drugs Difenoxylate (Lomotial). Loperamide (Loperazin).

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G.I.T.

Diarrhea
Def:
It means liquidity of stool and / or quantity (N=150-200g/d) or frequency (N: 4 motions/d).

AE:
I- AE of acute diarrhea: 1- Infection: * Bacterial: Salmonella E.coli * Viral: Rota virus Norwalk virus * Protozoa: E.histolytica Malaria Giaradia * Helminthes: Ascaris, strongyloids stercoralis. 2- Iatrogenic: * Laxatives * Chemotherapy * Para $ 3- Toxins: * Antibiotic * Allopurinol * Mg cont. antacid. Shigella Cholera

* Bacterial: staph, E.coli * Lead 4- Diet: * Unripe fruit * Mashroom.


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* arscenic * Alcohol

In Capsule Series
5- Nervous: psychological stress e.g: before examination.

G.I.T.

II. AE of chronic diarrhea: - The same as malabsorption syndrome.

Mechanisms of Diarrhea:
i. Osmotic diarrhea: Substance in intestineal lumen maintain fluid & prevent absorption (e.g: lactulose,

sorbitol, mg laxative). iiSecretory diarrhea: secretion of water &

electrolytes into the lumen (watery D) e.g: cholera. iiiAbnormality of intestineal motility: e.g:

Thyrotoxicosis, IBS, D neuropathy. ivAbnormality of intestineal mucosa. e.g:

inflammation.

N.B: - Osmotic diarrhea: Stops with fasting. - Secretory diarrhea: Continues with fasting. - Complication:
H2O dehyderation. K hypokalemia. HCO3 Acidosis.

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G.I.T.

- Diagnosis:
1- History analaysis: - Frequency: >4/d diarrhea - Consistency: - watery: infilammation - greasy: malabsorption. - Associated symptoms: * Abd pain: all causes except drug induced & Thyrotoxicosis. * Nausea & vomiting: Acute infections. * Fever: infection, inflammation. * Constipation: IBS. 2- Examination: * abdominal tenderness * bowel sounds * degree of general hydration * examination per rectum: to exclude rectal mass or blood. 3- Investigations: 4S not every patient who presents with diarrhea needs to be evaluated with these expensive tests, watchfull waiting & symptomatic therapy with oral fluid are very enough. * Stool examination: - for ova, cysts & parasite - stool osmolarity - fat assay. * Sigmoidoscopy: if large bowel cause suspected.
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G.I.T.

* Small bowel radiology: if small bowel cause suspected. * Serological tests: + other invest. Of malabsorption syndrome in case of chronic diarrhea (see before).

Treatment: 3 S
- Specific Symptomatic Supportive - Specific: of the cause. - Symptomatic: * Anti D: Difenoxylate (lomotil) Loperamide (loperazine) * Anti emetic: motilium - Supportive: - Diet: fat, irritant, light diet - of complication: Fuid. K HCO3

Dysentery
Def:
Diarrhea + Tenesmus + Blood + mucous in stool. Tenesmus: painful defecation with sense of

incomplete bowel evacuation.

AE: A: Amoebic dysentery


B: Bacillary dysentery, B dysentery. C: Cancer colon, rectum. D: Diverticolosis. M: Malaria R: Renal failure G: Giardia (v.v. rare).

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In Capsule Series Dysentery Scheme:


- Causative organism - Mode of infection - C/P: * Asymptomatic * Symptomatic * Complication - Investigation: - : 4S 3S

G.I.T.

Amoebic dysentery
Causative organism: E. histolytica (cyst) Mode of infection: feaco-oral. C/P: Asymptomatic symptomatic complication 1- Asymptomatic: cysts in lumen. 2- Symptomatic: Acute chronic Acute: Symptoms: dysentery: - Diarrhea - Tenesmus - blood in stool - mucous in stool. N.B: Diarrhea: mild (8/d) Signs: - Local: Tenderness in colon esp. ceacum & sigmoid. - General: - No fever: (superficial lesion) - No dehyderation (mild diarrhea)
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Chronic: - recurrent attacks of acute dysentery.

G.I.T.

- sometimes the patient may present by pain (caecum, appendix, T. colon). 3- Complication: Local: Amoeboma Systemic: Amoebic hepatitis (see liver).

Investigations: 4S
- Stool examination: cyst, mucous, blood. - Sigmoidoscopy: flask shaped ulcer with intervening healthy mucosa. - Small bowel radiology - Serological tests.

ttt : 3 S
- Specific (antiamoebic) - Symptomatic - Supportive
Like diarrhea

* Antiamoebic drugs: I- Luminal: used for of cysts (chronic amoeba) 1- Halogenated quinoline e.g: di-Iodo-hydroxy quinoline SE: Neuropathy, goiter Dose: 500 mg t.d.s for 2 w

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In Capsule Series
2- Phenanthroline quinines (Entobex) 500 mg t.d.s for 2 w 3- Diloxanide: 4- Furamide 500 mg t.d.s for 1 w

G.I.T.

5- Antibiotic: paromomycin & erythromycin are directly amoebicidal. II- Systemic drugs: (Acute & extra intest. Manifestation): Have no effect on cyst in intestinal lumen 1- Emetine: SE: Cardiotoxicity 2- Dehydroemetine: less toxic 3- Chloroquine: used in hepatic amoebiasis. III- Lumin & systemic (Mixed): - Metronidazole (Flagyl) - Dose: 500 mg t.d.s for 10 days. - SE: nausea, metallic taste.

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G.I.T.

Bacillary dysentery
Causative organism: G-ve bacilli (shigella) Mode of infection: feaco-oral. C/P: Asymptomatic Symptomatic: 1st phase: 1-2 days (mild) fever colic diarrhea 2nd phase: 1-2 dysentery: (diarrhea tenesmus mucous blood in stool). Diarrhea: severe 15-20 /d Tenesmus: (colic) General signs: fever & dehydration. symptomatic complication

Complication:
Bacteramia: (urethritis arthritis iridocyclitis)

Investigation: 4S
- Stool examination: Culture: shigella pus (WBCs) - Sigmoidoscopy: diffuse inflammation with dirty yellowish pseudomembrane. - Small bowel radiology. - Serological test.

ttt : - Specific
- Symptomatic - Supportive Specific ttt: - Ampicillin: 500 mg / 6h - Tetracycline: 2.5 gm in single oral dose. - Septrin (Co. Trimexazole) 2 tab twice daily for 5 days.
Like diarrhea

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G.I.T.

Bilharzial dysentery
- Causative organisms: S.mansoni - Mode of infection: infection occurs when i parasite penetrates i skin duing swimming in infected water. C/P: Asymptomatic symptomatic Symptomatic: (1) Dysentery (severe) Diarrhea Tenesmus Mucous Blood in stool (2) Bleeding per rectum (3) Pericolic mass in left iliac fossa. (4) HSM, clubbing. complication

Complications:
- Liver B - B cor pulmonale

- Investigations:
- Stool analysis: ova

3S + 2 B

- Sigmoidoscopy: ulcers or polyps mainly in rectosigmoid area. - Serological test: by ELISA - Barium enema: polyps. - Blood picture: Anemia esinophilia.

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Treatment: - Specific - Symptomatic - Supportive 1- Praziquntel 2- Niridazole 3- Antimonial drugs. 4- Metrifonate 5- Mirazid. Praziquentel: is i most effective drug.
Like diarrhea

G.I.T.

Specific ttt : (antibilharzial drugs):

mech. of action: cell membrane permeability to ca marked contraction. & spastic paralysis of worm. Dose: 40mg/ kg single dose or 20mg/ kg 3 times / w`. S/E: headache, nausea, vomiting, pruritis, fever, elevation of liver enzymes.

Vomiting
Def.: forceful expulsion of gastric content into mouth. Mech.: (vomiting reflex) : stimulus centre response (vomiting) stimulus: - peripheral e.g.: GIT - Centeral e.g.: ICT - Metabolic e.g.: ureamia
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In Capsule Series
centre : vomiting centre in medulla. Response: vomiting. Pylorus is closed. cardia is opened contraction of diaphragm. AE: I- Peripheral causes: (GIT causes) - Gastritis - Hepatitis - peptic ulcer cancer stomach - pancreatitis - Appendicitis

G.I.T.

- Cholecystitis - peritonitis - pyloric opstruction intestinal opstruction. II- Central causes: - Psychic : bad smell, sight. - Hysterical. - ICT: Tumour , Hge. - Pain: migraine, MI, renal colic. III- Metabolic causes: - Renal failure. - Liver cell failure. - Acidosis (DKA). - Alkalosis. - Electrolyte: Ca, Na, or K IV- Iatrogenic: M : morphine. A : Alcohol. D : Digitials. MAD

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V- Pregnancy: * Diagnosis of a case of vomiting: Clinical History analysis. examination. Investigation.

G.I.T.

I- History analysis:
1- Time of vomiting: * Early morning : - Pregnancy - ICT - Alcohol * During meal : * After meal by:
1 2

oesoph. Obstruction oesoph. Regurge.

h : Gu

2-4 h : Du > 8h : Intestinal obstruction. (2) Associated nausea: upper GIT causes. - No nausea: ICT (3) Associated Abd. Pain: (GIT causes) * peritonitis * pancreatitis N.B.: Vomiting relief pain: Gu. * intestinal obst. * cholecystitis

- painless vomiting: Neurological causes:

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(4) Associated headache: ICT. (5) History of drug intake : MAD (6) Biliary symptoms:

G.I.T.

- Jaundice - Pruritise - Abd. Pain - Color of urine & stool. (7) Frequency: Persistent in peritonitis. II- Examination of vomiting: i. Content : undigested food: pyloric obst. bile: below ampulla of vater blood: ulcer, cancer, Mallory weiss $ F.B.: gall stone. ii- Odour: offensive: Malignancy, int. obstruction. III- Investigations: inv. For the causes.

ttt:

* Specific: for i cause * Symptomatic: Antiemetic * motilum * primpran IV nutrition Antidiarrheal * Supportive: correct dehyderation & electrolyte imbalance

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In Capsule Series Acute Pancreatitis


AE: - gall stone - Alcohol - Viral infection e.g.: mumps - Hyper lipidemia. N.B.: gall stone is the most common causes

G.I.T.

back regurge of trypsin enzyme (autodigestion)

C/P:
- Abd. Pain: epigastric pain radiating to back. - Nausea & vomiting. - Tenderness & rigidity. - Cullen sign: umbilical ecchymosis. - Grey turner's sign: ecchymosis in flanks.

Complications:
- Abscess. - Hypocalcemia. - DIC - HF, Renal failure, Respiratory failure. Investigation: - Serum amylase: (5 times) - X ray, US, CT: gall stones. - swollen pancreas - calcification.

ttt:
- Nasogastric suction. - IV nutrition. - Somatostatin infusion
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G.I.T.

Chronic Pancreatitis
AE: chronic alcoholism C/P: Triad i- Abd. Pain: radiate to i back. ii- DM iii- steatorhea (malabsorption $)

Investigation:
- Like acute pancreatitis. - Calcification ttt: stop alcohol + symptomatic pain: Analgesics ttt of DM ttt of steatorhea Cancer Head of Pancreas painless obstructive jaundice loss of weight Anoroxia Cancer Body of Pancreas Pain: radiate to back Jaundice: rare.

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G.I.T.

Inflammatory Bowel Disease


- Crohn's disease & ulcerative colitis are both chronic inflammatory diseases of the GIT. - Aetiology: is still questionable. Most probably autoimmuno. (The local Tcells are angry with something in common food !!). Genetic factor: play a great role. Infections (T.B, measles): not confirmed. Psychological factor may play a role.
Pathology: Site: Crohn's disease Affects any part of GIT from mouth to anus, esp. terminal ileum (70%). Ulcerative colitis - Limited to colon & rectum. - Terminal ileum can be affected in 5% only

Layers Granuloma

All three (transmural) - Mucosa only No Yes in (30%) N.B: finding of granuloma = crohn's disease Crypt abscesses No Yes (30%) N.B: finding of crypt abscesses = ulcerative colitis Fibrosis Server No Pattern of colonic Skip lesions Continuous involvement involvement

C/P:
Sex Age Smoking Abd. Pain: Diarrhea Equal No specific age incidence smokers Prominent Yes Slightly more in 30-40 4` in incidence in smokers (80% non smokers) Less prominent Yes (severe & sometimes dysentery)

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Crohn's disease per Uncommon

G.I.T.
Ulcerative colitis Common

Bleeding rectum Anal & oral lesions Yes No Bowel obstruction May be No Malabsorption May be No syndrome Intestinal fistula May by No B12 deficiency May be No Carcinoma risk Minor High Systemic (extra The same intestinal) manifestations skeletal : Arthritis, skin: erythema nodosa pyoderma gangrenosa. Liver: fatty liver sclerosing cholangitis Eye: uveitis, iritis Crohn's disease Ulcerative colitis Investigation Radiological colon, - deep ulcers (cobble - shortened absence of hustra stone), area of narrowing in i (lead pipe sign) ileum. - pseudo polyposis - Skip lesion 15%. - Fistula & strictures. Colonoscopy & - Show involvement - Limited to i mucosa biopsy of i entire bowel & may have crypt wall granuloma abscesses. formation.

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In Capsule Series
Medical

G.I.T.

Treatment:
Medical ttt:

Surgical

1- Sulfasalazine: reduce inflammation esp in ulcerative colitis. 2- Cortisone: (prednisolone): This active disease 40-60mg/d. 3- Immuno suppressants: Azathioprine (Imuran). 4- Antibiotics: Metronidazole & ciprofloxacin. is i main ttt for

Surgical ttt:
Indications: * Failure of medical ttt. * Complications

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