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