Jaundice Flashcards

1
Q

سطح بیلیبیرون چقدر باشه میتونیم زردی رو در sclera تشخیص بدیم؟

A

the presence of scleral icterus indicates a serum bilirubin level of at least 51 μmol/L (3 mg/dL).

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2
Q

رسوب بیلی روبین در بافت ها در چه بیماری هایی رخ میده؟

A

is a sign of either liver disease or, less often, a hemolytic disorder or disorder of bilirubin metabolism.

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3
Q

اگر که شک کردیم به scleral icterus،

گزینه دوممون برای معاینه کجایه؟

A

underneath the tongue

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4
Q

مکانیسم سبز شدن پوست در icterus?

A

if the process is long-standing;

the green color is produced by oxidation of bilirubin to biliverdin.

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5
Q

Ddx of yellowish of skin?

A

1-jaundice

2-carotenoderma

3-the use of the drug quinacrine

4-and excessive exposure to phenols.

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6
Q

نحوه افتراق jaundice از carotenoderma?

A

In jaundice the yellow coloration of the skin is uniformly distributed over the body, whereas in carotenoderma the pigment is concentrated on the palms, soles, forehead, and nasolabial folds.

✅Carotenoderma can be distinguished from jaundice by the sparing of the sclerae.

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7
Q

بیلی روبین یوریا خودشو چجوری نشون میده؟

و چه اطلاعاتی ازش به دست میاریم؟

A

darkening of the urine, which is due to the renal excretion of conjugated bilirubin.

Patients often describe their urine as tea- or cola-colored. ☕️🥤

Bilirubinuria indicates an elevation of the direct serum bilirubin fraction and, therefore, the presence of liver or biliary disease.

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8
Q

بیلیروبین direct و indirect چیه؟

A

direct : conjugated

indirect bilirubin: unconjugated bilirubin

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9
Q

چرا مقدار ‏ calculated indirect bilirubin ، برای ارزیایی دقیق و ریلایبل نیس؟

A

Unconjugated bilirubin also reacts with diazo reagents, albeit slowly, even when the accelerator is absent. Thus the calculated indirect bilirubin may underestimate the true amount of unconjugated bilirubin in circulation.
چون مصرف میشه، کمتر نشونش میده

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10
Q

What is the normal serum bilirubin concentration?

A

1-1.5 mg/dl

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11
Q

چه زمانی میگیم فرد Unconjugated hyper bilirubinaemia داره؟

A

Unconjugated hyper- bilirubinemia is present when the direct fraction is <15% of the total serum bilirubin.

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12
Q

در کدام بیماری conjugated Bilirubinaemia داریم ولی Bilirubinuria نداریم؟

A

in jaundiced patients with liver disease+ prolonged cholestasis

because the delta bilirubin, although conjugated, is covalently bound to albumin and therefore not filtered by the renal glomeruli.

The delta bilirubin is formed in serum when hepatic excretion of bilirubin glucuronides is impaired and the glucuronides accumulate in serum.

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13
Q

با چه تستی در بیماری کهدMildly elevated direct fraction داره، چجوری میتونیم وجود Conjugated hyperbilirubinaemia را تایید کنیم؟

A

detection of bilirubin in urine via dipstick test is extremely helpful to confirm the presence of conjugated hyperbilirubinemia

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14
Q

در اپروچ به Hyperbilirubinaemia، برای پیدا کردن علت ۳ رویکردی که پیش میگیریم چیه؟

A

۱- ایا Overproduction بیلیروبین داریم؟

۲-ایا uptake, conjugation, excretionش دچار مشکله؟

۳-ایا به خاطر اسیب هپاتوسیت ها و Bile ducts ریختن تو خون؟

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15
Q

اولین و دومین اقدام تشخیصی ما در برخوزد با بیماری که زردی داره؟

A

1-the initial step is to perform appropriate blood tests in order to determine whether the patient has an isolated elevation of serum bilirubin.

2-If so, is the bilirubin elevation due to an increased unconjugated or conjugated fraction?

3-If the hyperbilirubinemia is accompanied by other liver test abnormalities, is the disorder hepatocellular or cholestatic?

4-If cholestatic, is it intra or extrahepatic?

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16
Q

مهم ترین بخش Hx کسی که با زردی ای اومده که هنوز علتش رو نمبدونیم؟

A

Medical history

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17
Q

چه سوالایی رو حتما باید در شرح حال زردی بپرسیم؟

A

the use of or exposure to any chemical or medication, whether physician-prescribed, over- the-counter, complementary, or alternative medicines (e.g., herbal and vitamin preparations) or other drugs such as anabolic steroids.

The patient should be carefully questioned about possible parenteral exposures, including transfusions, intravenous and intranasal drug use, tattooing, and sexual activity.

Other important points include recent travel history; exposure to people with jaundice; exposure to possibly contaminated foods; occupational exposure to hepatotoxins; alcohol consumption; the duration of jaundice; and the presence of any accompanying signs and symptoms, such as arthralgias, myalgias, rash, anorexia, weight loss, abdominal pain, fever, pruritus, and changes in the urine and stool.

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18
Q

اگر در معایته بیماری که با زردی اومده متوجه temporal & proximal muscle wasting شیم به چی شک میمنیم؟

A

Temporal and proximal muscle wasting suggests long-standing disease such as pancreatic cancer or cirrhosis.

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19
Q

علایم stigmata of chronic liver disease چی ان و همراهی شون با زردی به نفع کدام بیماری کبدی عه؟

A

Stigmata of chronic liver disease, including spider nevi, palmar erythema, gynecomastia, caput medusae, Dupuytren’s contractures, parotid gland enlargement, and testicular atrophy, are commonly seen in advanced alcoholic (Laennec’s) cirrhosis and occasionally in other types of cirrhosis.

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20
Q

بزرگ بودن virchow node یا peri umbilical nodes به نفع چیه؟

A

An enlarged left supraclavicular node (Virchow’s node) or a periumbilical nodule (Sister Mary Joseph’s nodule) suggests an abdominal malignancy.

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21
Q

در معاینه شکم بیماری که با زردی اومده چیا برامون مهمه؟

A

The abdominal examination should focus on the size and consistency of the liver,

on whether the spleen is palpable and hence enlarged,

and on whether ascites is present.

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22
Q

بزرگ بودن لوب چپ کبد و طحال در زردی چی رو به ذهنمون میاره؟

A

Patients with cirrhosis may have an enlarged left lobe of the liver, which is felt below the xiphoid, and an enlarged spleen.

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23
Q

ملیگننسی کبد در معاینه خودشو چطور نشون میده؟

A

A grossly enlarged nodular liver or an obvious abdominal mass suggests malignancy.

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24
Q

بزرگ بودن کبد و تندر بودنش در زردی چی رو به ذهنمون میاره؟ ۴

A

1-viral or
2-alcoholic hepatitis;
3-an infiltrative process such as amyloidosis;
4-or, less often, an acutely congested liver secondary to right-sided heart failure.

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25
Q

در بیماری که با زردی اومده، اگر تندرنس شدید داشته باشه در RUQ و در دم دچار resp arrest شه، به چی شک میکنیم؟

A

Severe right-upper-quadrant tenderness with respiratory arrest on inspiration (Murphy’s sign) suggests cholecystitis.

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26
Q

در بیماری که آسیت و زردی داره چی میاد ب ذهنمون ؟ ۲

A

1-cirrhosis

2-malignancy with peritoneal spread

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27
Q

در initial evaluation بیماری که با زردی اومده چه لب تست هایی رو درخواست میدیم؟ ۵

A

total and direct serum bilirubin measurement with fractionation

serum aminotransferase

alkaline phosphatase

albumin concentrations

prothrombin time tests

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28
Q

فرق الگوی hepatocellular و cholestatic?

A

Patients with a hepatocellular process generally have a rise in the aminotransferases that is disproportionate to that in ALP, whereas patients with a cholestatic process have a rise in ALP that is disproportionate to that of the aminotransferases.

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29
Q

با کدوم تست ها liver function را برررسی میکنیم؟

A

albumin level and a prothrombin time

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30
Q

اگر در بررسی هایی که برای بیمار زردی انجام دادیم ببینیم که البومین پایینه ، نشونه چیه؟ ۲

A

A low albumin level suggests a chronic process such as cirrhosis or cancer.

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31
Q

اگر در بررسی هایی که برای بیمار زردی انجام دادیم ببینیم که البومین نرماله، نشونه چیه؟

A

A normal albumin level is suggestive of a more acute process such as viral hepatitis or choledocholithiasis.

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32
Q

اگر در بررسی هایی که برای بیمار زردی انجام دادیم ببینیم که PT بالاعه ، نشونه چیه؟

A

An elevated prothrombin time indicates either
1-vitamin K deficiency due to prolonged jaundice and malabsorption of vitamin K
2-or significant hepatocellular dysfunction.

The failure of the prothrombin time to correct with parenteral administration of vitamin K indicates severe hepatocellular injury.

33
Q

علل isolated indirect hyperbilirubinemia?

A

🌸Hemolytic disorders

🌸Ineffective erythropoiesis
in cobalamin, folate, and iron deficiencies.

🌸Increased bilirubin production

  1. Massive blood transfusion
  2. Resorption of hematoma

🌸Drugs

  1. Rifampin
  2. Probenecid
  3. Ribavirin
  4. Protease inhibitors (Atazanavir, Indinavir)

E. Inherited conditions
1. Crigler-Najjar types I and II 2. Gilbert’s syndrome

34
Q

اگر کسی در زمینه بیماری های همولیتیک دچار زردی با بیلیروبین بالای 5mg/dl شده، نشونه چیه؟ 3

A

1-coexistent renal or
2-hepatocellular dysfunction
3-or in acute hemolysis, such as a sickle cell crisis.

35
Q

سه مکانیسم هایپر بیلی؟

A

Hyperbilirubinemia may result from
(1) overproduction of bilirubin;

(2) impaired uptake, conjugation, or excretion of bilirubin;
(3) regurgitation of unconjugated or conjugated bilirubin from damaged hepatocytes or bile ducts.

36
Q

بیماری های همولیتیک ارثی که میتونن زردی بدن چیان و سطح معمول بیلی روبین دراینا؟

A
Inherited disorders include 
spherocytosis, 
sickle cell anemia, 
thalassemia, 
and deficiency of red cell enzymes such as pyruvate kinase and glucose-6-phosphate dehydrogenase. 

In these conditions, the serum bilirubin level rarely exceeds 5 mg/dL.

37
Q

در بررسی زردی در بیمارانی همولیز مزمن دارن چی بزامون مهمه؟

A

In evaluating jaundice in patients with chronic hemolysis, it is important to remember the high incidence of pigmented (calcium bilirubinate) gallstones found in these patients, which increases the likelihood of choledocholithiasis as an alternative explanation for hyperbilirubinemia.

یعنی ممکنه اون سنگه علت زردی باشه

38
Q

What are Acquired hemolytic disorders in which lead to jaundice?

A

microangiopathic hemolytic anemia (e.g., hemolytic-uremic syndrome)

, paroxysmal nocturnal hemoglobinuria

, spur cell anemia

, immune hemolysis

, and parasitic infections (e.g., malaria and babesiosis).

39
Q

ریفامپین و پروبنسید با چه مکانیسمی هایپر بیلی میدن؟

A

by diminishing hepatic uptake

40
Q

Crigler-Najjar type I چیه؟

A

Crigler-Najjar type I is an exceptionally rare condition found in neonates and characterized by severe jaundice (bilirubin >20 mg/dL]) and neurologic impairment due to kernicterus, frequently leading to death in infancy or childhood.

These patients have a complete absence of bilirubin UDPGT activity; are totally unable to conjugate bilirubin; and hence cannot excrete it.

41
Q

ویژگی های Crigler-Najjar type II؟

A

Crigler-Najjar type II is somewhat more common than type I.

Patients live into adulthood with serum bilirubin levels of (6–25 mg/dL).

Mutation in UDPGT gene cause the reduction—typically ≤10%—of the enzyme’s activity.

Despite marked jaundice, these patients usually survive into adulthood,

42
Q

زردی به همراه لرز شدید ناگهانی به نفع چیه؟

A

Jaundice associated with the sudden onset of severe right-upper- quadrant pain and shaking chills suggests choledocholithiasis and ascending cholangitis.

43
Q

اگر مریض هیستوری ارترالژی میالژی قبل زردی رو بده به نفع چیه؟

A

A history of arthralgias and myalgias predating jaundice suggests hepatitis, either viral or drug-related.

44
Q

علل ارثی Conjugated Hyperbilirubinemia

A

Dubin-Johnson syndrome and Rotor syndrome

Patients with either condition present with asymptomatic jaundice.

The defect in Dubin- Johnson syndrome is the presence of mutations in the gene for MRP2. These patients have altered excretion of bilirubin into the bilirubin bile ducts.

45
Q

چه دارویی رو به کریگر نجار های ۲ مبدیم؟

A

Bilirubin UDPGT activity can be induced by the administration of phenobarbital, which can reduce serum bilirubin levels in these patients.

46
Q

چیا بیمار کریگر نجار رو مستعد کرنیکتروس میکند؟

A

they may be susceptible to kernicterus under the stress of concurrent illness or surgery.

47
Q

سندرم گیلبرت چیه؟

A

Gilbert’s syndrome is also marked by the impaired conjugation of bilirubin due to reduced bilirubin UDPGT activity (typically 10–35% of normal).

Patients with Gilbert’s syndrome have mild unconjugated hyperbilirubinemia, with serum levels almost always < (6 mg/dL).
The serum levels may fluctuate.

Unlike both Crigler-Najjar syndromes, Gilbert’s syndrome is very common.

The reported incidence is 3–7% of the population, with males predominating over females by a ratio of 1.5–7:1.

48
Q

بیمار گیلبرتی چه زمانی دچار ایکتر میشه؟

A

jaundice is often identified only during periods of stress, concurrent illness, alcohol use, or fasting.

49
Q

پاتوفیزیولوژی سندرم Rotor?

A

Rotor syndrome may represent a deficiency of the major hepatic drug reuptake transporters

50
Q

علل هپاتوسلولار زردی؟

A
Viral hepatitis:
Hepatitis A, B, C, D, and E
Epstein-Barr virus
Cytomegalovirus
Herpes simplex virus

Alcoholic hepatitis

Chronic liver disease and cirrhosis

Drug toxicity
Predictable, dose-dependent (e.g., acetaminophen)
Unpredictable, idiosyncratic (e.g., isoniazid)

Environmental toxins
Vinyl chloride
Jamaica bush tea—pyrrolizidine alkaloids
Kava Kava
Wild mushrooms—Amanita phalloides, A. verna

Wilson’s disease

Autoimmune hepatitis

51
Q

اپیدمیولوژی ویلسون؟

A

Wilson’s disease occurs primarily in young adults.

52
Q

اپیدمیولوژی هپاتیت اتوایمیون؟

A

Autoimmune hepatitis is typically seen in young to middle-aged women

but may affect men and women of any age.

53
Q

ایا ار رو ازمایش مینونیم بفهیمیم علت الگوی هپاتوسلولار توکسینه یا وایرال یا الکل؟

A

Alcoholic hepatitis can be differentiated from viral and toxin-related hepatitis by the pattern of the aminotransferases:

patients with alcoholic hepatitis typically have an AST-to-ALT ratio of at least 2:1, and the AST level rarely exceeds 300 U/L.

Patients with acute viral hepatitis and toxin-related injury severe enough to produce jaundice typically have aminotransferase levels >500 U/L, with the ALT greater than or equal to the AST.

54
Q

بیماری اومده با ALT AST بالا که ۲۵ برابر uln عه. چه ننیجه ای میگیری؟

A

While ALT and AST values <8 times normal may be seen in either hepatocellular or cholestatic liver disease, values 25 times normal or higher are seen primarily in acute hepatocellular diseases.

55
Q

ایا امینوترنسفراز نرمال رد کننده بیماری های کبدی عه؟

A

Patients with jaundice from cirrhosis can have normal or only slightly elevated aminotransferase levels.

56
Q

قدم بعدی بعد از اینکه معلوم شد بیمار الگوش هپاتوسلولاره؟

A
When the clinician determines that a patient has a hepatocellular disease, appropriate testing for acute viral hepatitis includes a :
1-hepatitis A IgM antibody 
2-hepatitis B surface antigen 
3-and core IgM antibody assay
4-a hepatitis C viral RNA test, 

5-and, depending on the circumstances, a hepatitis E IgM antibody.

57
Q

چرا از هپاتیت c انتی بادی شو چک نمیکنیم و RNA چک میکنیم؟

A

Because it can take many weeks for hepatitis C antibody to become detectable, its assay is an unreliable test if acute hepatitis C is suspected.

58
Q

اگه به هپاتیت اتوایمیون شک داشتیم چه تست هایی رو در مرحله اول درخولست میدیم؟

A

Testing for autoimmune hepatitis usually includes an antinuclear antibody assay and measurement of specific immunoglobulins.

59
Q

اگر در زردی الگومون کلستاتیک شد قدم بعدی چیه؟

A

When the pattern of the liver tests suggests a cholestatic disorder, the next step is to determine whether it is intra- or extrahepatic cholestasis

The next appropriate test is an ultrasound.

60
Q

مریض اومده با زردی و الگوی کلستاتیک. سونوش کردیم. از کجا بفهمیم مجاری داخل کبد درگیر سده یا extrahepatic?

A

The absence of biliary dilation suggests intrahepatic cholestasis,

while its presence indicates extrahepatic cholestasis.

61
Q

مریض اومده با زردی و الگوی کلستاتیک. سونوش کردیم. اگه نرمال باشه ولش میکنیم؟

A

False-negative results occur in patients with :

1-partial obstruction of the common bile duct

2- in patients with cirrhosis

3- primary sclerosing cholangitis (PSC), in which scarring prevents the intrahepatic ducts from dilating.

62
Q

برتری اصلی mrcp به سونو در visualize کردن کجاهاس؟

A

CT scanning and MRCP are better than ultrasonography for assess- ing the head of the pancreas and for identifying choledocholithiasis in the distal common bile duct, particularly when the ducts are not dilated.

63
Q

گولد استاندارد تشخیص choledocholithiasis?

A

ERCP is the “gold standard” for identifying choledocholithiasis.

Beyond its diagnostic capabilities, ERCP allows therapeutic interventions, including the removal of common bile duct stones and the placement of stents.

64
Q

اندیکاسیون ptc کیه؟

A

PTC can provide the same information as ERCP and it also allows for intervention in patients in whom ERCP is unsuccessful due to proximal biliary obstruction or altered gastrointestinal anatomy.

65
Q

کدوم بیماری هایی که به صورت تیپیک الگوی هپاتوسلولار دارن ممکنه الگوی کلستاتیک بدن؟

A

Both hepatitis B and C viruses can cause cholestatic hepatitis (fibrosing cholestatic hepatitis).

This disease variant has been reported in patients who have undergone solid organ transplantation.

Hepatitis A and E, alcoholic hepatitis, and EBV or CMV infections may also present as cholestatic liver disease.

66
Q

شایع ترین داروهایی که کلستاز کبدی میدن؟

A

Drugs most commonly associated with cholestasis are the anabolic and contraceptive steroids.

Cholestatic hepatitis has been reported with chlorpromazine, imipramine, tolbutamide, sulindac, cimetidine, and erythromycin estolate.

It also occurs in patients taking trimethoprim; sulfamethoxazole; and penicillin-based antibiotics such as ampicillin, dicloxacillin, and clavulanic acid.

Rarely, cholestasis may be chronic and associated with progressive fibrosis despite early discontinuation of the offending drug.

Chronic cholestasis has been associated with chlorpromazine and prochlorperazine.

67
Q

What is PBC?

روش تشخیص؟

A

Primary biliary cholangitis is an autoimmune disease predominantly affecting middle-aged women and characterized by progressive destruction of interlobular bile ducts.

The diagnosis is made by the detection of antimitochondrial antibody, which is found in 95% of patients.

68
Q

What is PSC?

پاتوگونومیکش چیع؟

A

Primary sclerosing cholangitis is characterized by the destruction and fibrosis of larger bile ducts.

The diagnosis of PSC is made with cholangiography (either MRCP or ERCP), which demonstrates the pathognomonic segmental strictures.

69
Q

کوموربیدیتی PSC چیع؟

A

Approximately 75% of patients with PSC have inflammatory bowel disease.

70
Q

کلستاز بارداری چیه؟

تریگرش چیه؟

A

Cholestasis of pregnancy occurs in the second and third trimesters and resolves after delivery.

Its cause is unknown, but the condition is probably inherited, and cholestasis can be triggered by estrogen administration.

71
Q

علل malignant extrahepatic cholestasis؟ 5

A

1-pancreatic

2, gallbladder

3, ampullary cancers

4-cholangiocarcinoma

5-Hilar lymphadenopathy due to metastases from other cancers may cause obstruction of the extrahepatic biliary tree.

72
Q

Ddx of cholangiocarcinoma?

A

This malignancy is most commonly associated with PSC and is exceptionally difficult to diagnose because its appearance is often identical to that of PSC.

73
Q

در بین تومورهایی که میتونن علت زردی باشن، کدومشون رو میشه با جراحی برداشت و نتیجه خوبی گرفت؟

A

Ampullary carcinoma has the highest surgical cure rate of all the tumors that present as painless jaundice.

Pancreatic and gallbladder tumors as well as cholangiocarcinoma are rarely resectable and have poor prognoses.

74
Q

What is the most common cause of extrahepatic cholestasis?

A

Choledocholithiasis

75
Q

علایم Choledocholithiasis?

A

The clinical presentation can range from mild right-upper-quadrant discomfort with only minimal elevations of enzyme test values

to ascending cholangitis with jaundice, sepsis, and circulatory collapse.

76
Q

تشخیص افتراقی مهم PSC به عنوان علت اکستراهپاتیک کلستاز چیه و چرا مهمه؟

A

IgG4-associated cholangitis is marked by stricturing of the biliary tree.

It is critical that the clinician differentiate this condition from PSC as it is responsive to glucocorticoid therapy.

77
Q

ایا پانکراتیت ممکنه Extrahepatic Cholestasis بده؟

A

In rare instances, chronic pancreatitis causes strictures of the distal common bile duct, where it passes through the head of the pancreas.

78
Q

What is AIDS cholangiopathy ؟

A

AIDS cholangiopathy is a condition that is usually due to infection of the bile duct epithelium with CMV or cryptosporidia and has a cholangiographic appearance similar to that of PSC.

The affected patients usually present with greatly elevated serum alkaline phosphatase levels (mean, 800 IU/L), but the bilirubin level is often near normal.

These patients do not typically present with jaundice.