هتلاقي واحد كلاون دلوقت بيذاكر ف ال ٥٠٠ محاضره فسيو عشان عليهم ٩ درجات ويسيب محاضره البايو الي عليها ٣ درجات مضمونين والله.
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شباب عشان انا عكست بين الخطوتين بس في الريكورد
-تصنيع ال carbamoyl P بيحول
2ATP to 2 ADP.
-تصنيع ال Arginosuccinate بيحول
ATP to AMP.
-تصنيع ال carbamoyl P بيحول
2ATP to 2 ADP.
-تصنيع ال Arginosuccinate بيحول
ATP to AMP.
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بص علي دول كدا وبعون الله تضمن ال ٣ درجات:-
-major source of ammonia is transdeamination reactions but there is minor sources as purine and pyrimidine deamination and bacterial putrefaction.
-main site for deamination reactions is liver.
-anabolic pathways for ammonia
Used for synthesis of non-essential amino acids as glutamine.
-ammonia from most tissue especially brain go to liver in the form of glutamine.
-ammonia from muscles go to liver in the form of alanine.
-ammonia produced in kidney excreted directly in urine and not go to liver.
-urea cycle occur in liver only in mitochondria and cytosol.
-the rate limiting enzyme is carbamoyl phosphate synthetase-1 and this enzyme activated by Mg and Mn and n-acetylglutamate.
-reactions used ATP is formation of carbamoyl phosphate and arginosuccinate.
-amino acids used in urea cycle is Arginine - aspartate - ornithine.
-ornithine is regenerated every urea cycle.
-one of links between urea cycle and TCA cycle is fumarate.
-the first amino group enter urea cycle carried by carbamoyl phosphate.
-the 2nd amino group transferred for citrulline from aspartate.
-the carbon source in urea cycle is CO2.
-carbamoyl phosphate and citrulline only produced in mitochondria.
-nitrogen attoms in urea produced from NH3 and aspartate.
-Brain is very sensitive for ammonia toxicity.
-in renal failure urea level increased and ammonia level is normal.
-in liver failure ammonia level increase.
-type 1 hyperammonemia caused by deficiency in CPS-1.
-type2 caused by deficiency in ornithine transcarbamoylase( the most common type).
-citrullinimia type-1 due to deficiency in arginosuccinate synthetase.
-citrullinimia type-2 due to deficiency in citrin(transport of aspartate).
-arginosuccinic aciduria due to deficiency in arginosuucinate lyase.
-HHH due to deficiency in ornithine transport.
-homocitrulline produced when carbamoyl phosphate react with lysine. مهمه
-ammonia is toxic to Brain because its depelate alpha ketoglutarate which is essential for TCA cycle so ATP production will decrease.
-major source of ammonia is transdeamination reactions but there is minor sources as purine and pyrimidine deamination and bacterial putrefaction.
-main site for deamination reactions is liver.
-anabolic pathways for ammonia
Used for synthesis of non-essential amino acids as glutamine.
-ammonia from most tissue especially brain go to liver in the form of glutamine.
-ammonia from muscles go to liver in the form of alanine.
-ammonia produced in kidney excreted directly in urine and not go to liver.
-urea cycle occur in liver only in mitochondria and cytosol.
-the rate limiting enzyme is carbamoyl phosphate synthetase-1 and this enzyme activated by Mg and Mn and n-acetylglutamate.
-reactions used ATP is formation of carbamoyl phosphate and arginosuccinate.
-amino acids used in urea cycle is Arginine - aspartate - ornithine.
-ornithine is regenerated every urea cycle.
-one of links between urea cycle and TCA cycle is fumarate.
-the first amino group enter urea cycle carried by carbamoyl phosphate.
-the 2nd amino group transferred for citrulline from aspartate.
-the carbon source in urea cycle is CO2.
-carbamoyl phosphate and citrulline only produced in mitochondria.
-nitrogen attoms in urea produced from NH3 and aspartate.
-Brain is very sensitive for ammonia toxicity.
-in renal failure urea level increased and ammonia level is normal.
-in liver failure ammonia level increase.
-type 1 hyperammonemia caused by deficiency in CPS-1.
-type2 caused by deficiency in ornithine transcarbamoylase( the most common type).
-citrullinimia type-1 due to deficiency in arginosuccinate synthetase.
-citrullinimia type-2 due to deficiency in citrin(transport of aspartate).
-arginosuccinic aciduria due to deficiency in arginosuucinate lyase.
-HHH due to deficiency in ornithine transport.
-homocitrulline produced when carbamoyl phosphate react with lysine. مهمه
-ammonia is toxic to Brain because its depelate alpha ketoglutarate which is essential for TCA cycle so ATP production will decrease.
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وبردو لو جت مسأله ف الامتحان اعتقد معظمكم فاكر قانون حساب التركيز
A sample/C sample = A standard/C standard
بيبقي ف المسأله مدي ٣ قيم وعايزك تحسب ال C sample.
طيب في قانون ف الكتاب كاتب فيه حاجه اسمها ال Blank كل ما عليك هيبقي القانون زي ما هو بس هتطرح قيمه ال A بتاعه ال blank من قيمه ال A بتاعه ال sample.
A sample/C sample = A standard/C standard
بيبقي ف المسأله مدي ٣ قيم وعايزك تحسب ال C sample.
طيب في قانون ف الكتاب كاتب فيه حاجه اسمها ال Blank كل ما عليك هيبقي القانون زي ما هو بس هتطرح قيمه ال A بتاعه ال blank من قيمه ال A بتاعه ال sample.
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Forwarded from ساعد تسعد |Sa3ed Tas3ad 4th
📌حل أسئلة البايو عملي
*هييجي مسألة عن ال jaundice وسؤال من دول
1-Test that indicate synthetic function of the liver
- Serum total protein, albumin, globulin, A/G ratio
- prothrombin time
2-Test that indicate excretory function of the liver
- Serum bilirubin (total+conjugated+unconjugated)
- urine bilirubin,bile salts, urobilinogen
3-Which is more spesific indicator of liver disease AST or ALT and why
ALT, because ALT is present predominantly in the liver while AST is present in liver + RBCs + cardiac muscle + skeletal muscles ,so damage in these sites will lead to increase in serum AST level ,so ALT is more specific than AST.
4-Which enzyme is more spesific for obstructive jaundice
ALP or GGT and why
GGt is more specific
Because ggt is present predominantly in the liver while ALP is present in liver+Bone+placenta+kidney+intestine ,so damage in these sites will lead to increase in serum ALP level ,so GGT is more specific than ALP.
5-Normal bilirubin level: 0.2 to 1.2 mg/dl
Direct: 0.1 to 0.4
indirect: 0.2 to 0.7
6-Principle of malloy and evelyn test
-Bilirubin reacts with diazo reagent to form purple color azobilirubin
-water soluble bilirubin ( conjugated ) reacts fast with diazo (direct reaction)
-free Bilirubin (unconjugated) reacts very slowly and requires an accelerator or solubilizer as methanol (indirect reaction)
7-How to differentiate gilbert syndrome from hemolytic jaundice
By analysis of RBCs (full blood count+reticulocyte count+blood film) + LDH + hepatoglobin measurement to exclude hemolysis
8-Which is more sever gilbert or crejler najjar syndrome and why
crejler najjar syndrome
Because gilbert cause mild unconjugated hyperbilirubinaemia while crejler najjar cause severe unconjugated hyperbilirubinaemia in neonatal period leading to kernicterus+death
9-What is dubin jonson syndrome
-congenital benign hyperbilirubinaemia + hyperbilirubinuria
The Cause:-due to defect in the transfer of conjugated Bilirubin into billiary canaliculus
10-Causes of decreased albumin blood level
1-liver disease ( decrease the synthesis )
2-malnutrition
3-kidney disease (leading to albuminuria)
11-Causes of prolonged PT other
than liver disease
1-malnutrition
2-vit K deficiency
3-using of anticoagulants
🔻لا تنسوا إخواننا في فلسطين، ودثرونا أيضًا في دعواتكم.
*هييجي مسألة عن ال jaundice وسؤال من دول
1-Test that indicate synthetic function of the liver
- Serum total protein, albumin, globulin, A/G ratio
- prothrombin time
2-Test that indicate excretory function of the liver
- Serum bilirubin (total+conjugated+unconjugated)
- urine bilirubin,bile salts, urobilinogen
3-Which is more spesific indicator of liver disease AST or ALT and why
ALT, because ALT is present predominantly in the liver while AST is present in liver + RBCs + cardiac muscle + skeletal muscles ,so damage in these sites will lead to increase in serum AST level ,so ALT is more specific than AST.
4-Which enzyme is more spesific for obstructive jaundice
ALP or GGT and why
GGt is more specific
Because ggt is present predominantly in the liver while ALP is present in liver+Bone+placenta+kidney+intestine ,so damage in these sites will lead to increase in serum ALP level ,so GGT is more specific than ALP.
5-Normal bilirubin level: 0.2 to 1.2 mg/dl
Direct: 0.1 to 0.4
indirect: 0.2 to 0.7
6-Principle of malloy and evelyn test
-Bilirubin reacts with diazo reagent to form purple color azobilirubin
-water soluble bilirubin ( conjugated ) reacts fast with diazo (direct reaction)
-free Bilirubin (unconjugated) reacts very slowly and requires an accelerator or solubilizer as methanol (indirect reaction)
7-How to differentiate gilbert syndrome from hemolytic jaundice
By analysis of RBCs (full blood count+reticulocyte count+blood film) + LDH + hepatoglobin measurement to exclude hemolysis
8-Which is more sever gilbert or crejler najjar syndrome and why
crejler najjar syndrome
Because gilbert cause mild unconjugated hyperbilirubinaemia while crejler najjar cause severe unconjugated hyperbilirubinaemia in neonatal period leading to kernicterus+death
9-What is dubin jonson syndrome
-congenital benign hyperbilirubinaemia + hyperbilirubinuria
The Cause:-due to defect in the transfer of conjugated Bilirubin into billiary canaliculus
10-Causes of decreased albumin blood level
1-liver disease ( decrease the synthesis )
2-malnutrition
3-kidney disease (leading to albuminuria)
11-Causes of prolonged PT other
than liver disease
1-malnutrition
2-vit K deficiency
3-using of anticoagulants
🔻لا تنسوا إخواننا في فلسطين، ودثرونا أيضًا في دعواتكم.
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شباب حاجه بس وقع فيها ناس من زمايلي السنه الي فاتت :-
في جزء تقريبا عندكم ف الفسيو ليه علاقه ب ال jaundice ف لما جه ف الامتحان بتاعنا في ناس حليته علي انه سؤال بايو واجابته ك فسيو كانت غير اجابته ك بايو ف خدوا بالكم من الspot الي واقفين عليها هيا سؤال اي.
في جزء تقريبا عندكم ف الفسيو ليه علاقه ب ال jaundice ف لما جه ف الامتحان بتاعنا في ناس حليته علي انه سؤال بايو واجابته ك فسيو كانت غير اجابته ك بايو ف خدوا بالكم من الspot الي واقفين عليها هيا سؤال اي.
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بوستات الرجاله عندي ع الفيس كلها فرحه عن ان خلاص معدش فيه حفظ سلايدز باثولوجي ولا هيستو تاني مستنيكم السنه الجيه وانتوا بتمتحنوا عملي الكلينيكال كلو اوسكي وكل الناس الي عندها social phobia هتتكشف علي حقيقتها.😂
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السنه الي فاتت ف الريسيرش بتاعي عملتوا معايا الواجب ف جه وقت رد الدين😂
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اهم اسئله المقالي لبايو ال GIT يا شباب:-
-sources of ammonia in our body?
-what is the fate of ammonia?( Anabolic and catabolic)
-what is the relation between TCA and urea cycle?
-give short account on HHH syndrome?
-why ammonia is toxic?
-sources of ammonia in our body?
-what is the fate of ammonia?( Anabolic and catabolic)
-what is the relation between TCA and urea cycle?
-give short account on HHH syndrome?
-why ammonia is toxic?
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