نتائج الامتحانات للصف الثالث متوسط لطلاب المدارس والخارجي

الدور الثاني 2021

في هذا الموضوع سيتم نشر نتائج الثالث متوسط للعام الدراسي 2021 للدور الثاني لطلاب المدارس وطلاب الخارجي اول باول
سيتم النشر حال الحصول عليها من التربية يرجى تحديث الصفحة بين فترة واخرى

المحافظات التي بجانبها علامة اضغط هنا باللون الازرق تعني تم تحميل النتائج بالاضافة وجود عبارة تم الرفع 

إعلان نتائج امتحانات الثالث المتوسط اليوم ان شاء الله 

#رابط النتائج أضغط أدناه : 👇 

https://t.me/joinchat/sb4SOgLVbJ5kMTUy

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PH.Jafar Jassim 11/03/2021 04:04:00 ص

تابع القراءه

               

سالازوبيرين Salazopyri

الاسم العلمي : 

• سلفاسالازين

سلفاسالازين هو علاج من مشتقات الامينوسليسيلات, يعمل على تثبيط عملية الإلتهاب في القولون.

تصنيف الدواء: مضادات الروماتزم المعدلة للمرض

الفئة: أمراض الجهاز الهضمي

العائلة الدوائية: مشتق حمض 5-الأمينوساليسليك.

الاعراض الجانبية للعلاج :

• فقدان الشهية          ~33%
• صداع                 ~33%
• غثيان                  ~33%
• قيء                   ~33%
• اضطراب المعدة   ~33%
• على ما يبدو قابل للانهيار oigospermia~33%
• الطفح الجلدي , حكة ,
• شرى
• حمة
• فقر الدم هاينز
• فقر الدم الانحلالي
• زراق
• عسر ضربات الدم: Pseudomononucleosis
• اضطرابات القلب: التهاب عضلة القلب
• اضطرابات الكبد: تقارير من السمية الكبدية ، بما في ذلك اختبارات وظائف الكبد مرتفعة
• اضطرابات الجهاز المناعي: الحساسية المفرطة
• اضطرابات الأيض والتغذية النظام: نقص حمض الفوليك
• الاضطرابات الكلوية والبولية: تحصي الكلية
• الاضطرابات التنفسية والصدرية والضيائية: آلام الفم البلعومية
• اضطرابات الجلد والأنسجة تحت الجلد: وذمة وعائية ، فرفرية
• اضطرابات الأوعية الدموية.

• ما هي استخدامات سالازوبيرين ؟

  يستخدم في علاج إلتهاب القولون المتقرح و في إلتهاب المفاصل الروماتويدي في البالغين و الْتِهاب المفاصل الروماتويدي اليفعِيّ

• ما هي موانع استخدام سالازوبيرين ؟

  يمنع استخدامه في المرضى الذين أظهروا فرط الحساسية للسلفاسالازين، أو للسالسيلات او للعلاجات الأخرى المحتوية على السولفوناميد أو لأي مكون آخر من مكونات العلاج، كما يمنع استخدامه في المرضى المصابين البُرْفيرِيَّة (خلل جيني في انتاج انزيمات معينة، يؤثر عادة على الكبد أو الجلد)، و المرضى المصابين بانسداد معوي أو انسداد في الجهاز التناسلي أو البولي.

  ما هي الاعراض الجانبية لسالازوبيرين ؟

  من أعراض العلاج الجانبية الشائعة: غثيان أو تقيؤ، فقدان الشهية، ألم في المعدة، عُقم في الذكور (قابل للعكس: يزول مع توقف العلاج) غثيان، طفح جلدي، صداع، إسهال، تغير لون البول إلى اللون الأصفر البرتقالي (نادراً).

  ما هي احتياطات استخدام سالازوبيرين ؟

  فئة السلامة أثناء الحمل: "بي"؛ لم تظهر الدراسات الحالية أضراراً على الجنين، و لكن يمنع استعماله في المرحلة الأخيرة من الحمل. يجب استشارة الطبيب قبل أخذ العلاج في حال كانت المريضة حامل أو تخطط للحمل. الرضاعة: قد يفرز العلاج في حليب الأم؛ يجب الحذر عند اعطائه للمرأة المرضع. قد يزيد العلاج من خطر حصول اضطرابات في الدم، مثل فقر الدم أو نقص شديد في الكريات البيض، لذاغ يجب استعماله بحذر و عمل فحزصات دورية لمكونات الدم. قد يرفع العلاج من خطر حصول فقر دم تحللي في مرضى التفول، لذا يجب استعماله بحذر. يجب استعمال العلاج بحذر في المرضى المصابين باعتلالات في وظائف الكلى أو الكبد. يجب استعمال العلاج بحذر في مرضى الربو بسبب خطر حصول حساسية حادّة. الأطفال: يفضل عدم إستعماله في الأطفالِ دون 2 سنة من العمر.

  ما هي التداخلات الدوائية لسالازوبيرين ؟

  إذا كنت تتناول أي من الأدوية التالية أخبر الطبيب أو الصيدلاني ، فقد تحتاج إلى تعديل الجرعة أو إجراء فحوصات معينة : مميعات الدم مثل الوارفرين، الميثوتريكسات، محصرات النستقبلات بيتا (مثل البروبرانولول)، الديجوكسين، حمض الفوليك، الميثامين.

  ما هي الأشكال الدوائية لسالازوبيرين ؟

  أقراص مغلفة 500 مغ

  ما هي ظروف تخزين سالازوبيرين ؟

  يحفظ العلاج في درجة حرارة الغرفة (25 درجة مئوية).

  كيفية استخدام سالازوبيرين ؟

  يجب اخذ الدواء كما قال لك الطبيب او الصيدلاني. يؤخذ مع الطعام مع كوب ماء كبير . عليك اخبار الطبيب اذا كنت تعاني من حساسية الكبريت كن حذرا إذا كان لديك نقص G6PD. نقص في انزيم نازعة هيدروجين الجلوكوز - 6 - الفوسفات فقد يحدث فقر الدم. هذا الدواء قد يغيير افرازات الجسم مثل لون البولالى اللون الأصفر أو البرتقالي. او الدموع والعرق، وقد يصبغ والأقمشة .

• اسم الشركة المصنعة ل سالازوبيرين ؟

  اسم الشركة المصنعة بالعربية فارمشيا
  اسم الشركة المصنعة بالإنجليزية Pharmacia
  

  أدوية بديلة لسالازوبيرين 

  • سلفاسالازين اقراص
  • سالازوبايرين اقراص
  • كولوبايرن
  • كولوسالازين
  • سالازوبايرن

  • _المراجع و المصادر

  • • Brunton, L. L., Knollmann, B. C., & Hilal-Dandan, R. G. (2018). Gilman’s the pharmacological basis of therapeutics. New York City.
    • DiPiro, J. T., Talbert, R. L., Yee, G. C., Matzke, G. R., Wells, B. G., & Posey, L. M. (2017). Pharmacotherapy: A Pathophysiologic Approach, 10 izdanje.
    • Medscape, Drugs, OTCs & Herbals. From: https://reference.medscape.com/drugs
    • Drugs.com, Drug Index A to Z. From: https://www.drugs.com/drug_information.html

    
    

0 تعليق

PH.Jafar Jassim 6/06/2021 12:07:00 ص

تابع القراءه

 

Hepatitis, Viral: C

D E FI N I T ION 

Hepatitis caused by infection with hepatitis C virus (HCV), often following a

chronic course ( 80% cases).

AETIOLOGYHCV 

is a small, enveloped, single-stranded RNA virus of the flavivirus family.

As it is an RNA virus, fidelity of replication is poor and mutation rates are high, resulting in

different HCV genotypes, and even in a single patient, many viral quasi-species may be

present.

Transmission

: Occurs via the parenteral route, and at-risk groups include recipients of blood

and blood products prior to blood screening, IV drug users, non-sterile acupuncture and

tattooing, those on haemodialysis and health care workers. Sexual and vertical transmission

is uncommon (1–5%, " risk in those co-infected with HIV).

Pathology/Pathogenesis

: Although HCV is hepatotropic, it is not thought that the virus is

directly hepatotoxic, rather that the humoral and cell-mediated response leads to hepatic

inflammation and necrosis. On liver biopsy, chronic hepatitis is seen and a characteristic

feature is lymphoid follicles in the portal tracts. Fatty change is also common and features

of cirrhosis may be present.

EPIDEMIOLOGY 

Common. Prevalence is 0.5–2% in developed countries, with higher

rates in certain areas (e.g. Middle East) because of poor sterilisation practices. Different HCV

genotypes have different geographical prevalence.

HISTORY

Ninety per cent of acute infections are asymptomatic with<10% becoming jaundiced with a

mild flu-like illness.

May be diagnosed after incidental abnormal LFT or in older individuals with complications of

cirrhosis.

EXAMINATION

There may be no signs or may be signs of chronic liver disease in long-standing infection.

Less common extra-hepatic manifestations include:

. skin rash, caused by mixed cryoglobulinaemia causing a small-vessel vasculitis; and

. renal dysfunction, caused by glomerulonephritis.

INVESTIGATIONS

Blood:

HCV serology

: Anti-HCV antibodies, either IgM (acute) or IgG (past exposure or chronic).

Reverse-transcriptase PCR

: Detection and genotyping of HCV RNA. Used to confirm antibody

testing; also recommended in patients with clinically suspected HCV infection but

negative serology.

LFT

: Acute infection causes " AST and ALT, mild " bilirubin. Chronic infection causes 2–8 times

elevation of AST and ALT, often fluctuating over time. Sometimes normal.

Liver biopsy

: To assess degree of inflammation and liver damage as transaminase levels bear

little correlation to histological changes. Also useful in diagnosing cirrhosis as patients

with cirrhosis will require monitoring for hepatocellular carcinoma.

MANAGEMENT

Prevention

 Screening of blood, blood products and organ donors, needle exchange schemes

for IV drug abusers, instrument sterilization. No vaccine available at present.

Medical:

Acute

 No specific management and mainly supportive (e.g. antipyretics, antiemetics,

cholestyramine). Specific antiviral treatment can be delayed for 3–6 months.

Hepatitis, Viral: C (continued)

Chronic

 Combined treatmentwith pegylated interferon-a (cytokine which augments natural

antiviral mechanisms) and ribavirin (guanosine nucleotide analogue) is the treatment

strategy of choice

. HCV genotype 1 or 4: 24–48 weeks

. HCV genotype 2 or 3: 12–24 weeks

Monitoring of HCV viral load is recommended after 12 weeks of treatment to determine

efficacy of treatment. Regular ultrasound of liver may be necessary if the patient has

cirrhosis.

COMPLICATIONS 

Fulminant hepatic failure in acute phase (0.5%), chronic HCV carriage,

cirrhosis and hepatocellular carcinoma. Less common are porphyria cutanea tarda, cryoglobulinaemia

and glomerulonephritis.

PROGNOSIS 

Approximately eighty per cent of exposed progress to chronic HCV infection,

and of these, 20–30% develop cirrhosis over 10–20 years.

0 تعليق

PH.Jafar Jassim 3/09/2021 01:30:00 ص

تابع القراءه

 

Cardiomyopathy

D E FI N I T ION

 Primary disease of the myocardium. Cardiomyopathy may be dilated, hypertrophic

or restrictive.

AETIOLOGY 

The majority are idiopathic.

Dilated:

 Post-viral myocarditis, alcohol, drugs (e.g. doxorubicin, cocaine), familial (25% of

idiopathic cases, usually autosomal dominant), thyrotoxicosis, haemochromatosis,

peripartum.

Hypertrophic:

 Up to 50% of cases are genetic (autosomal dominant) with mutations in

b-myosin, troponin T or a-tropomyosin (components of the contractile apparatus).

Restrictive:

 Amyloidosis, sarcoidosis, haemochromatosis.

EPIDEMIOLOGY 

Prevalence of dilated cardiomyopathy and hypertrophic cardiomyopathy

is 0.05–0.20%. Restrictive cardiomyopathy is rare.

HISTORY

Dilated:

 Symptoms of heart failure, arrhythmias, thromboembolism, family history of sudden

death.

Hypertrophic:

 Usually none. Syncope, angina, arrhythmias, family history of sudden death.

Restrictive:

 Dyspnoea, fatigue, arrhythmias, ankle or abdominal swelling.

Enquire about family history of sudden death.

EXAMINATION

Dilated:

 " JVP, displaced apex beat, functional mitral and tricuspid regurgitations, third heart

sound.

Hypertrophic:

 Jerky carotid pulse, double apex beat, ejection systolic murmur.

Restrictive:

 " JVP (Kussmaul’s sign: further " on inspiration), palpable apex beat, third heart

sound, ascites, ankle oedema, hepatomegaly.

INVESTIGATIONS

CXR: 

May show cardiomegaly, and signs of heart failure.

ECG:

All types: 

Non-specific ST changes, conduction defects, arrhythmias

Hypertrophic: 

Left-axis deviation, signs of left ventricular hypertrophy (see Aortic stenosis), Q

waves in inferior and lateral leads.

Restrictive: 

Low voltage complexes.

Echocardiography:

Dilated:

 Dilated ventricles with ‘global’ hypokinesia.

Hypertrophic: 

Ventricular hypertrophy (disproportionate septal involvement)

Restrictive: 

Non-dilated non-hypertrophied ventricles. Atrial enlargement, preserved systolic

function, diastolic dysfunction, granular or ‘sparkling’ appearance of myocardium in

amyloidosis.

Cardiac catheterization: 

May be necessary for measurement of pressures.

Endomyocardial biopsy: 

May be helpful in restrictive cardiomyopathy.

Pedigree or genetic analysis: Rarely necessary.

MANAGEMENT

Dilated:

 Treat heart failure and arrhythmias. Consider implantable cardiac defibrillators (ICD)

for recurrent VTs.

Hypertrophic: 

Treat arrhythmias with drugs, ICD for survivors of sudden death, reduce

outflow tract gradients, pacemaker, surgery (e.g. septal myomectomy, septal ablation

with ethanol). Screen family members with ECG or echocardiography.

Restrictive: 

No specific treatment. Manage the underlying cause.

Cardiac transplantation:

 May be considered in end-stage heart failure in all cardiomyopathy

types.

Cardiomyopathy (continued)

COMPLICATIONS

 Heart failure, arrhythmias (atrial and ventricular).

Dilated and hypertrophic cardiomyopathy:

 Sudden death and embolism.

Hypertrophic: 

Infective endocarditis.

PROGNOSIS

Dilated: 

Depends on the aetiology, New York Heart Association functional class and ejection

fraction.

Hypertrophic:

 Ventricular tachyarrhythmias are the major cause of sudden death.

Restrictive:

 Poor prognosis, many die within the first year after diagnosis.

0 تعليق

PH.Jafar Jassim 3/08/2021 01:15:00 ص

تابع القراءه

 Hepatitis, viral: B and D

D E FI N I T ION 

Hepatitis caused by infection with hepatitis B virus (HBV), which may follow

an acute or chronic (defined as viraemia and hepatic inflammation continuing>6 months)

course.

Hepatitis D virus (HDV), a defective virus, may only co-infect with HBV or superinfect persons

who are already carriers of HBV.

AETIOLOGYHBV 

is an enveloped, partially double-stranded DNA virus. Transmission is by

sexual contact, blood and vertical transmission. Various viral proteins are produced,

including core antigen (HBcAg), surface antigen (HBsAg) and e antigen (HBeAg). HBeAg is

a marker of " infectivity.

HDV is a single-stranded RNA virus coated with HBsAg.

Antibody- and cell-mediated immune responses to viral replication lead to liver inflammation

and hepatocyte necrosis. Histology can be variable, from mild to severe inflammation and

changes of cirrhosis.

ASSOCIATIONS/RISKFACTORS 

Hepatitis B infection is associated with IV drug abuse,

unscreened blood and blood products, infants of HbeAg-positive mothers and sexual contact

with HBV carriers. Risk of persistant HBV infection varies with age, with younger individuals,

especially babies, more likely to develop chronic carriage. Genetic factors are associated with

" rates of viral clearance.

EPIDEMIOLOGY 

Common. 350 million worldwide infected with HBV; 1–2 million deaths

annually. Common in Southeast Asia, Africa and Mediterranean countries. HDV also found

worldwide. HBV is relatively uncommon in the UK.

H ISTORY

Incubation period 3–6 months; 1- to 2-week prodrome of malaise, headache, anorexia,

nausea, vomiting, diarrhoea and RUQ pain.

May experience serum-sickness-type illness (e.g. fever, arthralgia, polyarthritis, urticaria,

maculopapular rash).

Jaundice then develops with dark urine and pale stools.

Recovery is usual within 4–8 weeks. One per cent may develop fulminant liver failure.

Chronic carriage may be diagnosed after routine LFT testing or if cirrhosis or decompensation

develops.

EXAMINATION

Acute: 

Jaundice, pyrexia, tender hepatomegaly, splenomegaly and cervical lymphadenopathy

in 10–20%. Occasionally, urticaria/maculopapular rash.

Chronic: 

May have no findings; signs of chronic liver disease or decompensation.

INVESTIGATIONS

Viral serology:

Acute HBV: HbsAg positive, IgM anti-HbcAg.

Chronic HBV: 

HbsAg positive, IgG anti-HBcAg, HbeAg positive or negative (latter in precore

mutant variant).

HBV cleared or immunity:

 Anti-HBsAg positive, IgG anti-HBcAg.

HDV infection:

 Detected by IgM or IgG against HDV.

PCR: 

For detection of HBV DNA is the most sensitive measure of ongoing viral

replication.

LFT:

 "" AST and ALT. " Bilirubin. " AlkPhos.

Clotting: " PT in severe disease.

Liver biopsy:

 Percutaneous, or transjugular if clotting is deranged or ascites is present.

MANAGEMENT

Prevention: 

Blood screening, instrument sterilization, safe sex practices.

Hepatitis, viral: B and D (continued)

Passive immunization: 

Hepatitis B immunoglobulin (HBIG) following acute exposure and to

neonates born to HbeAg-positive mothers (in addition to active immunization).

Active immunization:

 Recombinant HbsAg vaccine for individuals at risk and neonates born

to HBV-positive mothers. Immunization against HBV protects against HDV.

Acute HBV hepatitis:

 Symptomatic treatment with bed rest, antiemetics, antipyretics and

cholestyramine for pruritus. Notification to the consultant in communicable disease

control.

Chronic HBV:

Indications for treatment with antivirals: HbeAg-positive or HbeAg-negative chronic

hepatitis (depending on ALT and HBV DNA levels), compensated cirrhosis and HBV DNA

>2,000 IU/mL, decompensated cirrhosis and detectable HBV DNA by PCR.

Patients may be treated with interferon alpha (standard or pegylated, which has " half-life), or

nucleos/tide analogues (adefovir, entecavir, telbivudine, tenofovir, lamivudine). The role

of lamivudine as primary therapy has diminished due to high rates of drug resistance.

Interferon alpha is a cytokine which augments natural antiviral mechanisms. Side-effects

include flu-like symptoms, fever, chills, myalgia, headaches, bone marrow suppression

and depression, necessitating discontinuation in 5–10% of patients.

COMPLICATIONS

 Fulminant hepatic failure (1%), chronic HBV infection (
10% adults,

much higher in neonates), cirrhosis and hepatocellular carcinoma, extrahepatic immune

complex disorders including glomerulonephritis, polyarteritis nodosa. Superinfection with

HDV may lead to acute liver failure or more rapidly progressive disease.

PROGNOSIS 

In adults, 10% infections become chronic, and of these, 20–30% will

develop cirrhosis. Factors predictive of a good response to interferon include high serum

transaminases, low HBV DNA, active histological changes and the absence of complicating

diseases.

0 تعليق

PH.Jafar Jassim 3/07/2021 12:04:00 ص

تابع القراءه

 Hepatitis, viral: A and E

D E FI N I T ION 

Hepatitis caused by infection with the RNA viruses, hepatitis A (HAV) or

hepatitis E virus (HEV), that follow an acute course without progression to chronic carriage.

AE T IOLOGY HAV

 is a picornavirus and HEV is a calicivirus. Both are small non-enveloped

single-stranded linear RNA viruses of
7500 nucleotides, with transmission by the

faecal–oral route.

Both viruses replicate in hepatocytes and are secreted into bile. Liver inflammation and

hepatocyte necrosis is caused by the immune response, with targeting of infected cells by

CD8þ T cells and natural killer cells. Histology shows inflammatory cell infiltration

(neutrophils, macrophages, eosinophils and lymphocytes) of the portal tracts, zone 3

necrosis and bile duct proliferation.

E P IDEMIOLOGY HAV

 is endemic in the developing world, infection often occurs subclinically.

In the developed world, better sanitation means that seroprevalence is lower,

age of exposure " and hence is more likely to be symptomatic. Annual UK incidence is

5000 cases (seroprevalence
5%).

HEV is endemic in Asia, Africa and Central America.

H ISTORY 

Incubation period for HAV or HEV is 3–6 weeks.

Prodromal period:

 Malaise, anorexia (distaste for cigarettes in smokers), fever, nausea and

vomiting.

Hepatitis: 

Prodrome followed by dark urine, pale stools and jaundice lasting
3 weeks.

Occasionally, itching and jaundice last several weeks in HAV infection (owing to

cholestatic hepatitis).

EXAMINA T I ON

 Pyrexia, jaundice, tender hepatomegaly, spleen may be palpable (20%).

Absence of stigmata of chronic liver disease, although a few spider naevi may appear,

transiently.

INVE S T I G A T IONS

Blood: 

LFT ("" AST and ALT, " bilirubin, " AlkPhos), " ESR. In severe cases, # albumin and

" platelets.

Viral serology:

Hepatitis A: Anti-HAV IgM (during acute illness, disappearing after 3–5 months), anti-HAV

IgG (recovery phase and lifelong persistence).

Hepatitis E: 

Anti-HEV IgM (" 1–4 weeks after onset of illness), anti-HEV IgG. Hepatitis B and C

viral serology is also necessary to rule out these infections.

Urinalysis:

 Positive for bilirubin, " urobilinogen.

MANAGEMENT 

No specific management. Bed rest and symptomatic treatment (e.g.

antipyretics, antiemetics). Colestyramine for severe pruritus.

Prevention and control:

Public health: Safe water, sanitation, food hygiene standards. Both are notifiable diseases.

Personal hygiene and sensible dietary precautions when travelling.

Immunization (HAV only): Passive immunization with IM human immunoglobulin is only

effective for a short period. Active immunization with attenuated HAV vaccine offers safe

and effective immunity for those travelling to endemic areas, high-risk individuals (e.g.

residents of institutions).

COM P L IC A T I ONS 

Fulminant hepatic failure develops in 0.1% cases of HAV, 1–2%of HEV

but up to 20% in pregnant women. Cholestatic hepatitis with prolonged jaundice and

pruritus may develop after HAV infection.

Hepatitis, viral: A and E (continued)

Post-hepatitis syndrome: Continued malaise for weeks to months.

PROGNOSIS 

Recovery is usual within 3–6 weeks. Occasionally, a relapse during recovery.

There are no chronic sequelae. Fulminant hepatic failure carries an 80% mortality.

0 تعليق

PH.Jafar Jassim 3/06/2021 12:04:00 ص

تابع القراءه

 

Hepatitis, autoimmune

D E FI N I T ION

 Chronic hepatitis of unknown aetiology, characterized by autoimmune

features, hyperglobulinaemia and the presence of circulating autoantibodies.

AE T IOLOGY 

In a genetically predisposed individual, an environmental agent (e.g. viruses

or drugs) may lead to hepatocyte expression of HLA antigens which then become the

focus of a principally T-cell-mediated autoimmune attack. The raised titres of ANA, ASM

and anti-liver/kidney microsomes (anti-LKM) are not thought to directly injure the liver.

The chronic inflammatory changes are similar to those seen in chronic viral hepatitis with

lymphoid infiltration of the portal tracts and hepatocyte necrosis, leading to fibrosis and,

eventually, cirrhosis. Two major forms:

Type I (classic)

: ANA, anti-smooth muscle antibodies (ASMA), anti-actin antibodies (AAA),

anti-soluble liver antigen (anti-SLA).

Type 2

: Antibodies to liver/kidney microsomes (ALKM-1, directed at an epitope of CYP2D6),

antibodies to a liver cytosol antigen (ALC-1).

Patients with variant forms of autoimmune hepatitis have clinical and serologic findings of

autoimmune hepatitis plus features of PBC or PSC.

E P IDEMIOLOGY 

Type 1

 autoimmune hepatitis occurs in all age groups (although mainly

in young women). 

Type 2 

is generally a disease of girls and young women.

H ISTORY 

May be asymptomatic and discovered incidentally by abnormal LFT.

Insidious onset

: Malaise, fatigue, anorexia, weight loss, nausea, jaundice, amenorrhoea,

epistaxis.

Acute hepatitis (25%)

: Fever, anorexia, jaundice, nausea, vomiting, diarrhoea, RUQ pain.

Some may also present with serum sickness (e.g. arthralgia, polyarthritis, maculopapular

rash).

May be associated with keratoconjuctivitis sicca.

Personal or family history of autoimmune disease, e.g. type 1 diabetes mellitus and vitiligo.

It is important to take a full history to rule out other potential causes of liver disease

(e.g. alcohol, drugs).

EXAMINA T I ON

 Stigmata of chronic liver disease, e.g. spider naevi (see Cirrhosis).

Ascites, oedema and encephalopathy are late features.

Cushingoid features (e.g. rounded face, cutaneous striae, acne, hirsuitism) may be present

even before the administration of steroids.

INVE S T I G A T IONS

Blood

: LFT: "" AST and ALT, "" GGT, " AlkPhos, " bilirubin, # albumin in severe disease.

Clotting

: " PT in severe disease. FBC: Mild # Hb, also # platelets and WCC from

hypersplenism if portal hypertension present.

Hypergammaglobulinaemia is typical (polyclonal gammopathy) with the presence of ANA,

ASMA or anti-LKM autoantibodies.

Liver biopsy: Needed to establish the diagnosis. Shows interface hepatitis or cirrhosis.

Other investigations: To rule out other causes of liver disease, e.g. viral serology (hepatitis B

and C) caeruloplasmin and urinary copper (Wilson’s disease), ferritin and transferrin

saturation (haemochromatosis), a1-antitrypsin (a1-antitrypsin deficiency) and antimitochondrial

antibodies (PBC).

Ultrasound, CT or MRI of liver and abdomen: To visualize structural lesions.

ERCP: To rule out PSC.

MANAGEMENT

Indications: Aminotransferases >10 the upper limit of normal, symptomatic, histology:

significant interface hepatitis, bridging necrosis or multiacinar necrosis.

Hepatitis, autoimmune (continued)

Immunosuppression

 with steroids (e.g. prednisolone), followed by maintenance treatment

with gradual reduction in dose (treatment is often long term). Azathioprine or

6-mercaptopurine (6-MP) may be used in the maintenance phase as a steroid-sparing

agent with frequent monitoring of LFT and FBC. (Test for TPMT1 activity before starting

azathioprine or 6-MP.)

Monitor

: Ultrasound and a-fetoprotein level every 6–12 months in patients with cirrhosis (to

detect hepatocellular carcinoma). Repeat liver biopsies for evidence of disease progression

(<2 years).

Hepatitis A and B vaccinations.

Liver transplant

: For patients who are refractory to or intolerant of immunosuppressive

therapy and those with end-stage disease.

COMPLICATIONS 

Fulminant hepatic failure. Cirrhosis and complications of portal hypertension

(e.g. varices, ascites). Hepatocellular carcinoma. Side-effects of corticosteroid

treatment.

PROGNOSIS 

Older patients with type 1 autoimmune hepatitis are more likely to have

cirrhosis at presentation but may be more likely to respond to treatment. Approximately 80%

achieve remission by 3 years. Thirty five to 50% remain in remission when immunosuppression

is withdrawn. Fifty percent require lifelong maintenance. Five-year survival rate is 85% if

treated and 50% if untreated. Five-year survival after liver transplantation is >80%.

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PH.Jafar Jassim 3/05/2021 07:47:00 ص

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Acute respiratory distress syndrome (ARDS)

D E FI N I T ION 

Syndrome of acute and persistent lung inflammation with increased vascular

permeability. Characterized by:

. acute onset;

. bilateral infiltrates consistent with pulmonary oedema;

. hypoxaemia: PaO2/FiO2
200mmHg regardless of the level of positive end-expiratory

pressure (PEEP);

. no clinical evidence for " left atrial pressure (pulmonary capillary wedge pressure

(PCWP)
18 mmHg).

. ARDS is the severe end of the spectrum of ‘acute lung injury’ (ALI).

AETIOLOGY

Severe insult to the lungs or other organs induces the release of inflammatory

mediators, increased capillary permeability, pulmonary oedema, impaired gas exchange

and # lung compliance. Common causes include: sepsis, aspiration, pneumonia, pancreatitis,

trauma/burns, transfusion (massive, transfusion-related lung injury), transplantation

(bone marrow, lung) and drug overdose/reaction.

Patients progress through three pathologic stages: exudative, proliferative and fibrotic stage.

EPIDEMIOLOGY 

Annual UK incidence1 in 6000.

HISTORY

Rapid deterioration of respiratory function, dyspnoea, respiratory distress,

cough, symptoms of aetiology.

EXAMINATION

Cyanosis, tachypnoea, tachycardia, widespread inspiratory crepitations.

Hypoxia refractory to oxygen treatment.

Signs are usually bilateral but may be asymmetrical in early stages.

INVESTIGATIONS

CXR: 

Bilateral alveolar and interstitial shadowing.

Blood: 

FBC, U&E, LFT, ESR/CRP, amylase, clotting, ABG, blood culture, sputum culture.

Plasma BNP < 100 pg/mL may distinguish ARDS/ALI from heart failure, but higher levels can

neither confirm heart failure nor exclude ARDS/ALI in critically ill patients.

Echocardiography: 

Severe aortic or mitral valve dysfunction or # LVEF favours haemodynamic

oedema over ARDS.

Pulmonary artery catheterization: 

PCWP
18mmHg(however " PCWP does not exclude

ARDS as patients with ARDS may have concomitant left ventricular dysfunction).

Bronchoscopy:

 If the cause cannot be determined from the history, and to exclude

differentials, e.g. diffuse alveolar haemorrhage (frothy blood in all airways, haemosiderin-

laden macrophage from lavage fluid), lavage fluid for microbiology (mycobacteria,

Legionella pneumophila, Pneumocystis, respiratory viruses) and cytology (eosinophils,

viral inclusion bodies and cancer cells).

MANAGEMENT

Respiratory support:

Supplemental oxygen (FiO2: 50–60%). Almost all patients require

intubation and mechanical ventilation.

Fully supported volume limited and pressure limited modes are both acceptable. The tidal

volume, respiratory rate, PEEP and FiO2 are managed according to the strategy of low tidal

volume ventilation (LTVV). The rationale for LTVV is that smaller tidal volumes are less

likely to generate alveolar overdistension and ventilator-associated lung injury. LTVV

frequently requires ‘permissive hypercapnic ventilation’, a ventilatory strategy that

accepts alveolar hypoventilation in order to maintain a low alveolar pressure and minimize

the complications of alveolar overdistension. The lowest plateau airway pressure possible

should be targeted.

Sedation and analgesia:

 To improve tolerance of mechanical ventilation and to # oxygen

consumption. Neuromuscular blockade should be used only when sedation alone is

inadequate.

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PH.Jafar Jassim 2/16/2021 11:55:00 م

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Aortic dissection

DEFINITION

 A condition where a tear in the aortic intima allows blood to surge into the aortic wall, causing a split between the inner and outer tunica media, and creating a false lumen.

AETIOLOGY 

Degenerative changes in the smooth muscle of the aortic media are the predisposing event. Common causes and predisposing factors are:

• hypertension;
• aortic atherosclerosis;
• connective tissue disease (e.g. SLE, Marfan’s, Ehlers–Danlos);
• congenital cardiac abnormalities (e.g. aortic coarctation);
• aortitis (e.g. Takayasu’s aortitis, tertiary syphilis);
• iatrogenic (e.g. during angiography or angioplasty);
• trauma;
• crack cocaine.

Stanford classification divides dissection into

•  type A with ascending aorta tear (most common);
•  type B with descending aorta tear distal to the left subclavian artery.

Expansion of the false aneurysm may obstruct the subclavian, carotid, coeliac and renal

arteries.

EPIDEMIOLOGY

 Most common in < between 40 and 60 years.

HISTORY

 Sudden central ‘tearing’ pain, may radiate to the back (may mimic an MI).Aortic dissection can lead to occlusion of the aorta and its branches:

Carotid obstruction: Hemiparesis, dysphasia, blackout.

Coronary artery obstruction: Chest pain (angina or MI).

Subclavian obstruction: Ataxia, loss of consciousness.

Anterior spinal artery: Paraplegia.

Coeliac obstruction: Severe abdominal pain (ischaemic bowel).

Renal artery obstruction: Anuria, renal failure.

EXAMINATION 

Murmur on the back below left scapula, descending to abdomen.

Blood pressure (BP):

 Hypertension (BP discrepancy between arms of >20 mmHg), wide pulse pressure. If hypotensive may signify tamponade, check for pulsus paradoxus.

Aortic insufficiency: 

Collapsing pulse, early diastolic murmur over aortic area.Unequal arm pulses.

There may be a palpable abdominal mass.

INVESTIGATIONS

Bloods: FBC, cross-match 10 units of blood, U&E (renal function), clotting.

CXR: Widened mediastinum, localized bulge in the aortic arch.

ECG: Often normal. Signs of left ventricular hypertrophy or inferior MI if dissection compromises the ostia of the right coronary artery.

CT-thorax: False lumen of dissection can be visualized.

Echocardiography: Transoesophageal is highly specific.

Cardiac catheterization and aortography.

MANAGEMENT

Acute: If suspected, CT-thorax should be performed urgently concurrent to resuscitation.

Resuscitate and restore blood volume with blood products. Monitor pulse and BP in both arms, central venous pressure monitoring, urinary catheter. Best managed in ITU setting.

 

Type A dissection: 

Treated surgically. Emergency surgery because of the risk of cardiac tamponade. Affected aorta is replaced by a tube graft. Aortic valve may also be replaced. 

Type B dissection:

 Can be treated medically, surgically or by endovascular stenting. Control BP and prevent further dissection with IV nitroprusside and/or IV labetalol (use calcium channel blocker if b-blocker contraindicated). Surgical repair may be appropriate for patients with intractable or recurrent pain, aortic expansion, end-organ ischemia or progression of dissection, and has similar outcome rates. Endovascular repair is a newer technique using endovascular stents and is available in some centres, although evidence of benefit is still lacking (ADSORB trial results pending). 

COMPLICATIONS

 Aortic rupture, cardiac tamponade, pulmonary oedema, MI, syncope, cerebrovascular, renal, mesenteric or spinal ischaemia. 

PROGNOSIS 

Untreated mortality: 30% at 24 h, 75% at 2 weeks. 

Operative mortality of 5–10%. A further 10% have neurological sequelae. 

Prognosis for type B better than type A.

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PH.Jafar Jassim 1/31/2021 12:04:00 ص

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