#Clinical biochemistry

[theelementaryparticles]

Pipettes

[foreignmedgirl]

4.12 - 8.12.20

Only one more exam left! I’ve been trying to catch up on biochemistry and pediatrics. I barely got through pediatrics and didn’t manage to go through all the material so the exam wasn’t that great today.

Clinical biochem is tomorrow and then I’m free! Well only technically ... will be continuing with physiology and pathology introduction topics for USMLE. Then start systems/everything else. Super scary 😅 but I’ll get through that also!

Happy studying everyone, you can do it ☀️💪🏼

[zekarichan]

A summary for a part of the horrible "Inborn Errors of Metabolism" chapter.

[biochem2020]

Did some prep for my interview today. Really glad I've been able to use my pastel highlighters again after not having any physical work to do.

I'm finding learning about the different blood tests really interesting so hopefully I'm able to convey my interest and passion in my interview!

[akanshastyle]

Biosafety Measures for Prevention Against COVID- 19 Virus in Clinical bi...

[biomedgirl]

Just finished writing some notes on liver function tests. Clinical biochemistry is definitely my favourite module at the moment ☺️👩🏼‍🔬

[studyaidessaysuk]

Looking for clinical research writing service in the UK for Clinical biochemistry? Get a FREE quote. Best Price Guaranteed! Top Reviews.

[theelementaryparticles]

Kidney stone analysis

[poonamcmi]

How Do You Read Western Blotting Blot Data?

The Western Blotting (also known as the protein immunoblot) is a popular analytical technique in molecular biology and immunogenetics for detecting specific proteins in a sample of tissue homogenate or extract.

To separate a specific protein from a complex, the Western Blotting technique employs three steps: separation by size, transfer of protein to a solid support, and visualisation of target protein using a primary and secondary antibody. The primary antibody is a synthetic or animal-derived antibody that recognises and binds to a specific target protein. Before washing off excess antibody, the electrophoresis membrane is washed in a solution containing the primary antibody. A secondary antibody that recognises and binds to the primary antibody is added. The secondary antibody is visualised using a variety of techniques, including staining, immunofluorescence, and radioactivity, allowing for indirect detection of the specific target protein.

 Read More @ https://medium.com/@poonamdcmi/why-western-blotting-is-done-d9da101f41a7

Source Link @ https://www.coherentmarketinsights.com/market-insight/western-blotting-market-2711

[izzyl-ightstudyblr]

Be productive!

[chimken-snoup]

I’m sitting here in my clinical microbiology class wearing my lab coat realizing that in less than three years I’ll actually be able to call myself a real scientist and child me who used to look at dirt under her shitty toy microscope is jumping for joy :)

[biochem2020]

08/06/20

Just finished my interview!

I answered all the questions and the follow ups but I'm not sure I communicated the answers well enough.

Now I just have to wait and see.

Good luck to all of you who are having interviews or working on exams or assignments during this pandemic. It's not easy and we should all be so proud of ourselves! X

[biomedicool]

Liver function tests

AST/ALT ratio

If AST is higher than ALT, a muscle source of these enzymes should be considered. For example, muscle inflammation due to dermatomyositis may cause AST>ALT. Or complete liver necrosis 

Alcoholic fatty liver disease: AST > 8 times the ULN; ALT > 5 times the ULN

Nonalcoholic fatty liver disease: AST and ALT > 4 times the ULN

Acute viral hepatitis or toxin-related hepatitis with jaundice: AST and ALT > 25 times the ULN

Ischemic hepatopathy (ischemic hepatitis, shock liver): AST and ALT > 50 times the ULN (in addition the lactate dehydrogenase is often markedly elevated)

Chronic hepatitis C virus infection: Wide variability, typically normal to less than twice the ULN, rarely more than 10 times the ULN

Chronic hepatitis B virus infection: Levels fluctuate; the AST and ALT may be normal, though most patients have mild to moderate elevations (approximately twice the ULN); with exacerbations, levels are more than 10 times the ULN

[anamol-10]

This video describes how to do Calibration of Clinical Chemistry Analyzer Semi or Fully Automated in English.

www.anamollabs.com

[howdoesithappen]

Phenylketonuria (PKU)

1. In a nutshell Phenylketonuria or PKU is an inborn disorder of metabolism. The name of the condition denotes the presence of elevated levels of phenylpyruvate and phenylacetate in the urine. These two compounds are ketone bodies and accumulate when blood levels of phenylalanine rise above the normal reference range (0.06mmol/L - 0.1mmol/L). Hyperphenylalaninemia in PKU is a consequence of deleterious mutations in a gene that codes for the enzyme phenylalanine hydroxylase; this enzyme converts phenylalanine to the amino acid tyrosine. PKU detrimentally affects the developing brain and can cause irreversible mental retardation if it goes untreated. Screening of neonates is commonplace and necessary to avoid the potentially catastrophic clinical consequences of this condition.

Fig 1. The heel-prick test is routinely used to identify PKU in the neonate. 2. What causes it? PKU is a genetic disease, most commonly inherited in an autosomal recessive manner. Deleterious mutations in a single gene, the PAH gene, result in a deficiency of the enzyme phenylalanine hydroxylase. 

3. What are the symptoms? Untreated PKU can result in growth retardation, seizures, moderate-to-severe mental retardation, hypopigmentation and eczema. Cases where the treatment of PKU is only partial or ceased prematurely can cause a significant decline in IQ and increased incidences of behavioural and learning disabilities. 

4. What’s going on? Under normal circumstances the catabolism of phenylalanine is dependent on the enzyme phenylalanine hydroxylase. Through the action of this enzyme, phenylalanine is then converted to tyrosine. Tyrosine is an important non-essential amino acid that is a biosynthetic precursor for melanin and neurotransmitter development. In PKU, harmful mutations in the PAH gene (>600 have been described) result in the decreased production of phenylalanine hydroxylase which causes the substrate, phenylalanine, to accumulate. Tyrosine becomes an essential amino acid in PKU individuals as they can no longer synthesise it through dietary phenylalanine catabolism. Hyperphenylalaninemia affects the developing brain by disrupting energy production, protein synthesis and neurotransmitter homeostasis. Hypopigmentation in PKU is likely due to the inhibition of dopaquinone synthesis in melanocytes. Approximately 1% of PKU patients will also have defects in tetrahydrobiopterin (BH4) metabolism. This situation adds insult to injury as proper tetrahydrobiopterin metabolism is crucial for the formation of both phenylalanine hydroxylase and tryptophan and tyrosine hydroxylase. Thus, individuals with deranged tetrahydrobiopterin metabolism suffer from PKU and a lack of important serotenergic and catecholaminergic neurotransmitters. This further compounds and complicates the clinical picture and results in severe neurologic dysfunction.

Fig 2. Schematic diagram showing the metabolic fates of phenylalanine. (McPhee and Hammer, 2019).  5. How is it treated? Dietary restriction of phenylalanine is initiated once the condition is detected. It is necessary to continue dietary restriction of phenylalanine indefinitely, as even mild hyperphenylalaninemia can have detrimental effects on cognition and overall CNS health. Additionally, hyperphenylalaninemia, in the context of PKU, can also deprive the brain of adequate levels of other, important amino acids and supplementation is therefore recommended. 

6. That’s interesting... As women with PKU reach child-bearing age, fetal hyperphenylalaninemia due to in uterine exposure becomes a possibility. This can occur irrespective of the fetal genotype; neonates affected by this situation display microcephaly, congenital heart defects and profound developmental delay. Rigorous control of maternal phenylalanine prior to conception and up to birthing is essential in minimising the risk of significant fetal abnormalities in maternal PKU.