Thursday, February 12, 2015
Study group discussion: Colored side effects
Study group discussion: Acute myelogenous leukemia
A 67-year-old man presents to his physician with a 10-day history of fatigue, bleeding gums, cellulitis, and a recent weight loss of 9 kg (20 lb). On physical examination, the patient is pale but has no evidence of lymphadenopathy or hepatosplenomegaly. Results of a complete blood count are as follows: WBC count: 18,300/mm3 (75% blastocytes, 20% lymphocytes) Hemoglobin: 9.1 g/dL Hematocrit: 29% Platelet count: 98,000/mm3 diagnosis?
He has acute myelogenous leukemia. It's acute because of the blasts.
Yes, acute myelogenous leukemia.
What could be find in marrow biopsy?
Lots of cells! Sometimes there could be fibrosis though which would lead to a dry tap.
Can anyone tell why the platelet count is affected? (Conceptual review question)
Isn't it in normal limits? 100k-150k?
Then why did he have bleeding gums?
Megakaryocyte lineage affected.
Yup the excessive growth of myeloid series doesn't not allow growth of megakaryocyte.
It is AML M5.
Isn't the bleeding gums due to thrombocytopenia?
I have seen a patient with type 5 AML in my hospital. They don't have bleeding gums. Rather a swelling of gums due to infiltration of leukemic cells. Gingival infiltration it's called I think.
Chloroma.
What's chloroma?
Infiltration of leukaemic cells in soft tissues.
That happens in ALL too, right? The infiltration of leukaemic cells into tissues?
Yes, I think.
I had seen a picture with a child having a chloroma of the orbit.
I thought the WBC count goes in lakhs in AML.
The count doesn't really help because sometimes the counts are comparable to a normal infection.
Oh.
What do we use for differentiating leukemia from infection?
The LAP.
What are the other causes of leukemoid reaction?
The major causes of leukemoid reactions are severe infections, intoxications, malignancies, severe hemorrhage, or acute hemolysis.
Source: http://www.ncbi.nlm.nih.gov/pubmed/16962944
Study group discussion: Pharmacological treatment of UTI in pregnancy
Sharing some of the knowledge I learnt!
So what is the treatment of Urinary tract infection?
Antibiotic according to urine culture report.
Yeah what's the most common cause?
E.coli
So what the treatment prescribed?
Norfloxacin. It's excreted unchanged in the urine.
The most commonly is trimethoprim sulfamethoxazole. But that's in case of chronic uti, right?
So the question I wanted to ask is what would you prescribe in a pregnant lady? Which drug.. Sulphamethoxazole and trimethoprim?
No. Its a PABA agonist.. Will inhibit folate synthesis. Risk factor for NTD.
NTD means?
Ntd-neural tube defects.
Amoxicillin and ampicillin. Those are the ones preferred for any infection.
Nitrofurantoin too.
That's prophylactically. Atleast that's what we were taught.
Even nalidixic acid.
Yeah! Not to give TMP-SMX that's what was the main point I wanted to convey.
Study group discussion: Thyroid, weight and ophthalmoplegia
We were told by our Pediatrics teacher that thyroid status and weight changes are not related. Weight gain in hypothyroidism, in fact due to myxoedema and not due to slow metabolism.
But almost every other book I read say weight changes are a part of symptomatology of thyroid disorders.
Would someone enlighten me about this?
In myxedema there is reduced breakdown of glycosoamimoglycans. Plus there is free fluid retention. A lot of factors come into play. I'll look it up and send a good resource on it.
And haan..also iy read in a book..that in thyrotoxicosis..30% of patients will have weight gain. So therefore, maybe the weight status are not characteristic to changes in thyroid profile.
Maybe.
The cause of the weight gain in hypothyroid individuals is also complex, and not always related to excess fat accumulation. Most of the extra weight gained in hypothyroid individuals is due to excess accumulation of salt and water.
Source: http://www.thyroid.org/weight-loss-and-thyroid
So, 'obesity' should not ideally be mentioned in symptoms of hypothyroidism?
Weight gain should be mentioned
Along with the various other signs and symptoms. The complete clinical picture is specific to thyroid diseases.
The mechanism maybe varied but weight gain is a symptom and should always be a differential for hypothyroidism.
Yup.
Also, in Grave's ophthalmopathy, GSGs are deposited in the retro orbital space. Shouldn't this be seen instead in hypothyroidism where there is reduced breakdown of GSGs?
It's because of autoimmunity
The antibodies stimulate deposition of GAGs. Has nothing to do with the effect of thyroid hormones. That's why, ophthalmoplegia can not be treated by anti thyroid medications.
Oh!
What is the treatment of ophthalmoplegia in Grave's?
It is symptomatic. Lubricants, steroids is all what we can prescribe.
Yes, steroids. To suppress the immune system.
Steroids are especially given in retinal pathologies.
What about a permanent cure?
I don't know about any permanent cure.
It's radioactive iodine 131 or thyroidectomy.
Permanent cure for opthalmopathy?
Hemithyroidectomy. Or if the graves is not too bad, we can give thyroid peroxidase inhibitors? And sometimes it will resolve by itself?
I was told the retro-orbital lipofibroblasts requires surgical removal of the mass behind the eye, but the lid lag will resolve once the thyrotoxicosis resolves?
Yes.
There are different surgeries for the opthalmoplegia..Don't remember the names.
Study group discussion: Cardiac biomarkers
Which all troponins are used as cardiac biomarkers?
I and T.
Troponin- T type 2.
Correct!
Which biomarker is used to differentiate breathlessness of cardiac origin from that of COPD?
BNP.
Correct!
BNP?
Brain natriuretic peptide.
Woah. I didn't know this.
Yeah. BNP is a marker for heart failure.
It's also used to monitor COPD patients.. That is the levels will increase if there is cor pulmonale
Also pro BNP.
BNP is present in ventricles. The ANP (Atrial natriuretic peptide) version in atria.
Amazing!
Study group discussion: Alcohol and liver enzymes
Kawasaki disease mnemonic and notes
Study group discussion: Vasculitis
Study group discussion: Classification of enzymes
Wednesday, February 11, 2015
Study group discussion: Competitive and non competitive inhibition
Define Km value of an enzyme.
In types of enzyme inhibition..Where does the value km and where does the value Vmax decrease?
It is the substrate concentration at which reaction rate is half the maximum rate.
Study links!
http://medicowesome.blogspot.ae/2013/12/competitive-and-non-competitive.html
http://medicowesome.blogspot.ae/2013/11/competitive-vs-non-competitive.html
In types of enzyme inhibition..Where does the value km and where does the value Vmax decrease?
Vmax decreases in non competitive inhibiton.
Kmax in competitive.
There is one more thing.. Uncompetitive inhibition.
Anybody knows about that?
Some placental enzyme inhibited by phenylalanine. Donno for sure.
Biochemistry.. It's fun when you have recently read it.
Study group discussion: Malaria
Review questions! Which are the types of parasites for malaria?
Plasmodium species!
Vivax, falciparum, ovale, malariae.
One more.
Plasmodium knowelsi.
How do you differentiate cause of malaria based on the fever
It's quartan in malarie.. After every third day.
It's tertian in the rest of them.. Every alternate day.
What's algid malaria?
Circulatory collapse
Fever and shock. That's algid malaria.
Which are the rapid diagnostic test for malaria?
Dip stick test
Pfhrp
Pfldh
Of HRP and LDH , which is specific for falciparum malaria?
HRP?
True.
LDH just shows infection with plasmodium. Not which sub type.
But what was the significance of LDH? I read somewhere it's super important.
It detects all other forms. Hrp is just to check whether it is falci or not.
Which forms have a latent phase in liver?
P. vivax & P. ovale
What is the clinical significance of liver forms?
They remain dormant in ovale & vivax, also known as hypnozoites & they cause relapse.
Yes.
Drug of choice for relapse?
Primaquine!
Why do we give primaquine in P. Falciparum malaria?
To destroy gametes!
Yes. Gametocides. It helps in control of spread. 45 mg is gametocidal.
Which test is more preferred if you are suspecting relapse?
Peripheral blood smear is preferred.
Correct!
Why don't you perform rapid diagnostic test when you are suspecting a relapse for malaria?
You don't do rapid diagnostic test cause.. These remain positive several weeks after an initial infection.
So it will show positive even if it's fever for some other cause.
I was asked this in viva, why we combine chloroquine and primaquine in combination?
In Vivax, primaquine is used for hypnozoites.
Which is the gold standard for detecting malaria?
Gold standard is that centrifuge thing.
QBC? Quantitative Buffy Coat? We add acridine orange?
Hmm. Peripheral blood smear is gold standard. Never heard of buffy test. Could be because in the buffy coat what you get is WBC's in maximal amount. Plasmodium are within RBC.
How will you diagnose cerebral malaria?
You can't diagnose malaria by CSF.
It's on clinical symptoms. Based on altered sensorium and coma you diagnose it.
Interesting.
But first you infuse glucose to rule out hypoglycaemia..If the patient fails to improve then its cerebral malaria.
Yes, I remember that.
Which anti malarial drug can cause hypoglycaemia?
Quinine and chloroquine too.
Correct!
Introduction to the new author
Study group discussion: Typhoid
When do complications of typhoid happen? Which week?
3rd week, intestinal perforation.
Correct. 3rd week is the week for complications.
Describe fever in typhoid?
Step ladder..the fever increases in the first week step by step. Later it becomes continuous.
When do rose spots appear?
End of first week.
Shape of ulcers?
Typhoid are longitudinal or parallel to the axis of the gut.
Most sensitive test?
WIDAL?
Widal is neither sensitive or specific.
Bone marrow for typhoid?
Yes, typhoid infects the RE cells..Hence, if the culture is inconclusive, there is higher chance of positivity from a bone marrow culture.
Urine and gall bladder cultures can also be performed.