Saturday, October 26, 2019

Rate Limiting Enzymes | NEET PG | FMGE


Important RATE LIMITING ENZYMES

FOR NEET PG / FMGE

Process
Enzyme
Glycolysis
PhosphoFructokinase-1
Gluconeogenesis
Fructose-1,6-Bisphosphate
Glycogenesis
Glycogen Synthase
Glycogenolysis
Glycogen Phosphorylase
HMP Shunt
Glucose 6 Phosphate Dehydrogenase
Urea Cycle
Carbomyl Phosphate Synthase-1 (CPS-1)
Ketogenesis
HMG CoA Synthase
Fatty acid Synthesis
Acetyl CoA Carboxylase or Malonyl CoA Synthase
Cholesterol Synthesis
HMG CoA Reductase
Bile Acid Synthesis
7 α Hydroxylase
Heme Synthesis
ALA Synthase
Denovo Purine Pathway
PRPP Glutamyl Amino Transferase
Denovo Pyrimidine Synthesis
Eukaryotic organism: CPS II
Prokaryotic organism: ATC



These are the important Rate Limiting Enzymes which are frequently asked in Competitive exams like NEET PG, AIIMS, FMGE, etc.

I hope you liked the content.


_________________________________
Follow our Youtube channel: LINK
Follow our Instagram channel: LINK
_________________________________

Tuesday, October 8, 2019

Rheumatoid Arthritis for NEET PG | HARRISON BASED NOTES


Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown etiology characterized by symmetric polyarthritis.

Clinical Features:
Presenting symptoms: Early morning joint stiffness lasting more than 1 hour that eases with physical activity.

Most frequently involved joints: the wrists, MCP, and PIP joints (DIP is usually spared). Axial involvement is rare, if occurs most common site is cervical vertebrae.

Flexor tendon tenosynovitis – leading to decreased range of motion and reduced grip strength: “Trigger” fingers.

Hyperextension of the PIP joint with flexion of the DIP joint: “swan-neck deformity”.

Flexion of the PIP joint with hyperextension of the DIP joint: “boutonnière deformity

Subluxation of the first MCP joint with hyperextension of the first interphalangeal (IP) joint: “Z-line deformity”.

Inflammation about the ulnar styloid and tenosynovitis of the extensor carpi ulnaris may cause subluxation of the distal ulna, resulting in a “piano-key movement” of the ulnar styloid.




Other important points:

Most common pulmonary manifestation of RA: Pleuritis.

Most frequent site of cardiac involvement in RA: Pericardium.

Most common valvular abnormality in RA: Mitral Regurgitation.

Most common hematologic abnormality in RA: Normochromic Normocytic anemia.

Most common histopathologic type of Lymphoma in RA: Diffuse Large B cell Lymphoma.

Most common cause of death: Cardiovascular disease.

Caplan’s syndrome: RA + Pneumoconiosis that manifests as Pulmonary Nodules

Felty’s syndrome: Neutropenia + Splenomegaly + nodular RA.




Diagnosis:
Classification criteria for RA:



RA is diagnosed if score is ≥ 6.




Serum IgM RF – Positive in 75-80 % of the patient.

Serum anti-CCP antibodies – More specificity (95%).

Plain Radiograph: Reveals Osteopenia, symmetric joint space loss and subchondral erosions.

MRI: Reveals presence of Bone Marrow oedema.



Treatment:

Treatment may be divided into:
1.      NSAIDs
2.      Glucocorticoids
3.      Conventional DMARDs
4.      Biologic DMARDs

1.      NSAIDS:
NSAIDs are now considered to be adjunctive agents for management of symptoms uncontrolled by other measures. NSAIDs exhibit both analgesic and anti-inflammatory properties.


2.     Glucocorticoids:
Can be given in several ways:
First, low to moderate doses to achieve rapid disease control before the onset of fully effective DMARD therapy.
Second, a 1 to 2 week burst of glucocorticoids for the management of acute disease flares, with dose and duration guided by the severity of the exacerbation.


3.     Conventional DMARDs:
Conventional DMARDs includes: Methotrexate, Hydroxychloroquine, sulfasalazine and leflunomide.

Methotrexate is DMARD of choice for treatment of RA. It stimulates adenosine release from cells, producing an anti-inflammatory effect.


4.     Biologic DMARDs:
IL-1 receptor antagonist: Anakinra

Anti TNF agents: Infliximab, Golimumab, Certolizumab, etanercept.

Anti CD-20: Rituximab.

Anti IL-6: Tocilizumab

Abatacept: Inhibits T cell stimulation

Tofacitinib: Inhibits JAK1 and JAK3. It is an oral agent.


_________________________________
Follow our Youtube channel: LINK
Follow our Instagram channel: LINK

________________________________

Saturday, August 31, 2019

Anti-Retroviral Drugs | Mechanism | Mnemonic and Tricks

Hello medicos, this blog is about Anti-Retroviral Drugs. After reading this you will be knowing basic mechanism of drugs; and mnemonics and tricks to remember the full classification.

I.                    Nucleoside Reverse Transcriptase inhibitors (i.e. NRTIs):

Mechanism: Active forms of Nucleosides gets incorporated into the growing viral DNA and cause premature chain termination.

Examples are:
-          Zidovudine
-          Didanozine
-          Stavudine
-          Lamivudine
-          Abacavir

(These are very commonly used names, so I don’t want to burden your brain by providing a mnemonic for this).

II.                  Non-Nucleoside reverse transcriptase inhibitors (i.e. NNRTIs):

Mechanism: These drugs directly binds to the Reverse Transcriptase enzyme causing inhibition of its function.

Mnemonic for the name of these drugs is NEERD. So, why NERD? Because they are NOT with NRTIs. They are NNRTIs.

The drugs are:
-          Nevirapine
-          Efavirenz
-          Etravirine
-          Rilpivirine
-          Delaviridine

III.                Next is Nucleotide reverse transcriptase inhibitors (i.e. nRTI):

Only one drug to remember, which is Tenofovir.
You can remember it is a nucleoTide RT inhibitor, so it starts from T.
And we are using small or tiny ’n’ as a short form (nRTI).
From Tiny, you can remember Teno. That’s simple.

IV.                Fusion inhibitor:
As the name suggests, these drugs block the initial fusion of HIV with cell surface receptors. Basically, they bind to gp41 transmembrane protein.
Only one drug you need to remember in this category is Enfuvirtide.
As you can see it contains “FU” in the spelling. So Fusion Inhibitor can be remembered as "FU" containing drug, Enfuviritide.

V.                  CCR5 receptor blocker:

Drugs in this category bind to the host cells through CCR5 receptors, preventing interaction with gp41.
The drug's name is Maraviroc.
(this drug contains ROC in its name, so you can remember it as ROCK on CCR5 receptor i.e. Maraviroc)

VI.                Protease inhibitors:

All the drugs in this category contain the word “navir”

Examples are:
-          Indinavir,
-          Ritonavir,
-          Darunavir, and so on…

You can remember these three examples if you are familiar with Hindi, all 3 contain the name of food items or drink like A(I)nde, Roti and Daru.

VII.              Integrase inhibitors:

These drugs inhibit the action of integrase which is required for the insertion of the viral genome into the DNA of the host cell.

Examples are:
-          Raltegravir
-          Elvitegravir
-          Dolutegravir

All these drugs have the word “gravir” in their name.
You can remember these drugs by Mnemonic: RED Gravis.

So, this is the summary of the whole classification we have studied.




I hope this tricks and mnemonics helped you to remember Anti-retroviral drugs, which is very difficult to remember.


Follow our instagram channel: crazy.medicine