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
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.
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.
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!
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.
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!
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.
Name some hyperdynamic states
Fever, anemia
Beriberi
Infections
Paget disease
Hyperthyroidism
Infections are hyperdynamic cause they cause fever.
Hahaha true
What about any valvular heart disease?
Aortic regurgitation
Pregnancy
AV malformation
Correct!
Why beri beri is a high CO state which leads to heart failure?
I don't know but is it due to Beri beri due to B1 deficiency?
For carbohydrate metabolism, B1 is required so for fulfilling body energy demands body has to burn other fuels fats and protein. They are limited and generate less energy so body need more cycles/min with more CO to wash out the products of metabolism to maintain metabolism. If condition not treated the heart gets hypertrophied and will eventually fail.
Yes. Beri beri leads to increased metabolic demand and increased need for blood flow causing high output cardiac failure.
*Review question session on SLE*
Which is the most sensitive antibody?
ANA
Most specific?
Ds DNA
Drug induced lupus?
Anti histone
I have mnemonics on these!
Please share!
http://immense-immunology-insight.blogspot.ae/2013/12/its-never-lupus-mnemonics.html
Most common type of lung involvement in SLE?
Pleurisy
Skin changes in SLE?
Malar rash
Discoid rash
Butterfly rash, discoid lesions
And?
Photosenstivity
Good.
How do you differentiate between discoid lupus and SLE?
Discoid lupus is a milder form of SLE.
I will approach the question in a different way.. Do we do skin biopsy in SLE?
Yes.
And what test we do?
Band test.
Correct!
Where?? Which level of the skin?
Between dermis and epidermis.
Dermo-epidermal junction. Correct!
So what do you think will be the difference in DLE and SLE?
Skin biopsy shows a green band under fluorescence.
In DLE..you will have a positive band test only in regional areas.
Whereas in SLE..the test is common all over the body, and not only the affected areas.
Ok so this differentiates DLE vs SLE.
Never heard about this thing. Thanks all!
This crazy skin test.
I didn't know this either. Amazing.
Also, nephritis is much more common in SLE.
Wire loop deposit.
Great!!
Which drugs cause drug induced SLE?
There is a very big list for sure.
The most common causes to remember are
1) Procainamide
2) Hydralazine
3) Isoniazid
Easy question would be..Which drugs don't cause SLE.
Yes. Because they are related to acetylators. The slow and fast acetylators.
Can you explain I mean how does it effect? The slow and fast acetylators?
I'm not sure.. But the slow acetylators are more prone to DILE. I'll cross check and let you know
Slow acetylators metabolize the drug slowly.. Hence a higher chance of toxicity.
Presumably, this is because acetylation of the aromatic amine or hydrazine functional group leads to a non-toxic product. Several other drugs which have been implicated in drug-induced lupus also contain an aromatic amine or hydrazine group. The clinical and laboratory characteristics of drug-induced and idiopathic lupus are similar but the degree to which the pathophysiological mechanisms are related, if at all, is unknown.
Source: http://www.ncbi.nlm.nih.gov/pubmed/7011656
Complex.
Ok so which symptoms you won't see in drug induced lupus?
Donno.. I know they'll disappear on discontinuation of the medication.
You won't see
CNS involvement and renal involvement in drug induced.
One last.
What happens to complement levels in lupus flare up?
Decreases.
Brilliant.
And what happens to dsDNA in flare up?
And what about levels of complement and anti ds Dna in drug induced lupus?
Anti dsDNA levels decrease in the lupus flare up.
Lol hope I am not bugging you guys!! Haha so I will answer the last one!!
Oh you're not. Medicine is addicting.
If we knew the answers we'd be jumping and answering :P
Haha yeah medicine is addicting once you get to know some of it.
You just can't back off! If when you have learnt there is much more that you don't know!
Complement levels and anti dsDNA levels are normal in drug induced lupus.
They do have positive ANA.
Ah. Makes sense.
Alright guys! It was wonderful! Keep learning medicine.
And keep rocking!
What is secondary anti-phospholipid syndrome?
Anti-phospholipid antibody syndrome?
In antiphospholipid syndrome, your body mistakenly produces antibodies against proteins that bind phospholipids.
Antibodies bind with phospholipid of every cell membrane?
It can be idiopathic or secondary when associated with another autoimmune dissorder as lupus. Oh, secondary can also be caused by infections (syphilis, HIV) or medication
It causes thrombosis, abortions, strokes...
Treatment?
Steroids.
Any specific steroid that is preferably used?
Don't know.
Mainly blood thinners and steroidal
Sapporo criteria used for APLA.
Interesting.
APLA is also a cause of recurrent abortions.
In fact I have seen a case female reproductiveage group having habitual abortions and anticardiolipin antibodies positive.
What is the significance of anticardolipin antibody?
(Microbiology related)
Syphillis test?
Yes, it gives false positive results.
APLA is differential diagnosis for false positive for syphilis.
Cool!
Here's an interesting thing I read.. Let me put it in a form of a hypothetical question.
A person suffers from chronic hemolysis due to sickle cell anemia. Has a high MCV. Which vitamin is he most likely to be deficient in?
Folic acid.
Correct!
Why not B12?
Cause it is stored in the body in high doses.
Yes :D
Folic acid on the other hand gets extinguished very fast.
Exactly!
And in every case of excessive RBC production..you always give folic acid supplements. Like even in thalassemia.. And other various chronic hemolytic conditions.
Ooh.
Why are alcoholics more prone to B9 deficiency?
Cause they eat less maybe. The commonest cause of deficiency is reduced intake in case of folic acid.
Correct!
Alcohol affects the body's ability to absorb folate and also increases folate in the urine. Many alcohol abusers have poor quality diets that do not provide the suggested intake of folate.
Systolic BP decreases in inspiration.....then what about JVP? It also decreases...But I'm not getting how?
During inspiration, there is increased negative pressure in the thorax..therefore the venous blood is forced to enter the heart. Hence the JVP reduces because the suction effect is more. But the venous blood supply to the heart reduces..that is via the pulmonary veins. Resulting in a reduced cardiac output. And reduced systolic. The left side of the heart I mean.
During inspiration a negative pressure is created which sucks the blood into the heart. That's why blood from the veins goes into the heart, the pressure or the JVP decreases (less volume).
Conditions where you dont see fall in blood pressure or JVP during inspiration?
Cardiac tamponade
Constrictive pericarditis
Restrictive cardiomyopathy
Yes, when the heart can't fill up blood!
*someone had a confusion on rise or fall in JVP in tamponade, this was explained by Sakkan*
Most kussmaul sign is positive in cardiac tamponade. That is paradoxical rise in JVP in inspiration.
In cardiac tamponade.. Due to increased external pressure on the right side of heart..the blood can't enter during inspiration. This leads to rise in JVP.
This also leads to bulging of the interventricular septum Upon the left ventricle. This decreases the preasure more than the normal fall of 10 mm of Hg.
Related to this.. Cardiac tamponade has a classical triad..called becks traid. That is silent chest, increased JVP and reduced BP.
Muffled heartsound.
Yeah cause the pericardial fluid accumulation dampens the sounds.
Yeah JVP will be elevated in cardiac tamponade! Thanks for a nice explanation.
What's holiday heart syndrome?
Atrial fibrillation.. Due to alcohol.
Heart takes a holiday with you :P
Yup when people do binge drinking for the first time. Or after a long time!
Meaning of fibrillation?
I'm not clear about it.
It's paroxysmal..The patient can die. It's like when your atria dont contract in one motion.
There are several simultaneous impulses generated that stimulate the atria. Hence rather then contracting in a syncitium the atria simply fibrillate. Meaning many many sad attempts at contraction, none of them strong enough to push blood in the ventricles.
Thank you!
Flutter is like a less severe form of fibrillation.
