Chronic granulomatous disease - Catalase positive organisms mnemonic

CGD (chronic granulomatous disease)

Diagnosis: Negative Nitroblue tetrazolium reduction.

NADPH oxidase deficiency: Susceptible to Catalase+ organisms.

I had got this mnemonic on someone's (arghlblargh) tumblr but I can't seem to find it so I'll publish it here!

“The Recoiling Red Asp wasn’t Sorry towards the moaning Cat because it had Noheart.”

Recoiling  = E.coli
Red  = Serratia
Asp = Aspergillus
Sorry = S. Aureus
Moaning  = Pseudomonas
Cat = Catalase + organism
NoHeart = Nocardia

Study group discussion: Extra books for USMLE

Could someone suggest books to use for mle step 1? Everyday someone new tells me that the kaplan book is not good for a particular subject.

Haha

BRS + Kaplan for physiology
Road map to gross anatomy
Biochemistry Kaplan (Pretty good)
Goljan for pathology
Microbiology Kaplan (more than enough)
Pharmacology Kaplan
Behavioral Kaplan + BRS + a lot of resources online and it's never enough

What about the other subsections of anatomy?

Umm which subsections? Embryology and Histology isn't high yield.

Oh alright. Neuroanatomy?

That's a pain! There are these anki flashcards I found on neuro.. I'll send you guys the link when I'm home. Thanks!

Do all brain stem sections for step 1. Any image on neuro and you need to identify the tracts/structures!

Ah. Why don't you try clinical neuroanatomy made ridiculously simple? I have heard its a recommended book for USMLE Step 1.

Ridiculously simple series is good!

Neuroanatomy one is really short and nice.

I've read the neuroanatomy book too. It's good.

Related post:
Preparing for the USMLE Step 1 exam
I have no idea about USMLE Step 1
USMLE for Indian medical students

Study group discussion: Anti-viral drugs used in herpes

Name the DNA polymerase inhibitor antiviral drugs.
(Hint - Drugs used against herpes virus)

Acyclovir and related drugs too.

One more drug which is used in resistant cases of herpes.. It's foscarnet!

Which drug is used for herpes ophthalmicus?

The drug of choice for CMV retinitis - Ganciclovir.

Study group discussion: JVP in pulmonary hypertension and tricuspid regurgitation

One question...Giant "a" wave in JVP will be due to which of the two.. Pulmonary hypertension or tricuspid regurgitation?

I would go for pulmonary hypertension.. Because Tricuspid stenosis causes giant a waves whereas tricuspid regurgitation causes giant v waves. I'm not sure, correct me if I'm wrong. a wave is due to atrial contraction.

Ya that's what I think is right too... But I get to see different answer at different places. Ok... Pulmonary hypertension it is then!

What abnormal wave does the other cause then?

It's like all the blood is regurgitating into the atria when the ventricles are contracting.. So it'll cause a giant cv wave. The a wave should remain normal. I don't get why pulmonary hypertension should cause a giant A wave though.. I get that the back flow should hypertrophy the right atrium and right ventricle so maybe that's why!?

Study group discussion: Anti-tubercular drugs

Name the first line anti - tuberculosis drug which is a static drug?

Ethambutol.

Name the bactericidal drugs.

Bedaquiline.

Bedaquiline isn't approved in India yet! It's still undergoing trials, according to the TOI.

Woah.

HRZS.

Which of the HRZES drug has the best CNS penetration?

It's pyrazinamide.

Which of the drug doesn't penetrate the CNS?

It's the aminoglycoside.

Streptomycin!

Which of these drugs you don't prescribe in children? And why?

Ethambutol? Because kids can't tell you if they're going color blind

Correct.

Which of the drugs you don't give if the patient is receiving HIV drugs?

Rifampicin?

Right.

Instead of it which drug you give?

Rifabutin.

Why don't we give?

Rifampicin is a cytochrome enzyme inducer.

Hence, it will reduce the concentration of PI and NNRTI.

Which TB drug causes orange color tears? Can't recall!

Rifampicin.

Study group discussion: Sulfonamides, Trimethoprim Sulfamethoxazole and other sulfa drugs

One extra review question session for today!

Give one example of longest acting sulphonamides.

Sulfadoxine!

Which are the other drugs with a sulfa structure?

Diuretics - Loop, thiazide and also acetazolamide. Except ethacrynic acid.

So any more drugs?

Hint- one anti-leprosy, anti-hypertension, and another one anti-diabetic.

Dapsone.

Correct!

Umm Sulfonylureas.

The hint was in the name! Correct!

Which anti hypertensive though? :O

Diazoxide :)

Ahh!

Side effects of diazoxide?

Ahh..Steven Johnson syndrome?

I'm looking for the very unique side effect which helps in treating a tumor.

Diazoxide has an anti-insulin effect.. It's used in insulinomas.

Ooh.

And what's the unique side effect of Minoxidil?

Minoxidil was used as an antihypertensive, but it caused hair growth. So they used it topically for hair loss!

If the dose of sulfamethoxazole in cotrimoxazole is 100 mg. What is the dose of trimethoprim

It's always given in the ration of 1:5
One part trimethoprim to 5 parts sulfamethoxazole

Ohh so 20 mg trimethoprim

Yup.

What is fixed drug eruptions?

Every time you eat the drug..you get a specific skin reaction at the same place every single time.

Name the site of action of smx and tm. How do they produce the sequential blockade?

Folate synthase SMX and TMP DHFRase

Sulfo doesn't inhibit the enzyme..its not the main action

Prevents formation of dihydrofolate?  Folate synthase right?

No. It's an antimetabolite. Structure similar to PABA. It attaches itself in place of PABA ..hence the mechanism of action!

One last question. Name other drugs which inhibit dihydrofolate reductase ?

Methotrexate.

Hint-  anti- epileptic drugs and one anti malarial.

Oh yes. Anti malarial! Pyrimethamine!

Correct!

Is it phenytoin?

Yes!

That's why these drugs are not given in pregnancy!

I guessed because of the megaloblastic anemia side effect!

High chances of NTD due to folic acid deficiency.

Oh well IkaN..It's all inter related :)

Totally! Medicine <3

Nice session!

Study group discussion: Tetracyclines

Which are the broad spectrum antibiotics?

Chloramphenicol and tetracycline.

Which tetracycline causes cholestatic jaundice?

It's chlortetracycline.

Doxycycline is secreted in feces. So in which conditions it is preferred?

Renal comprise.

Exactly!

Which is the common side effect of all tetracyclines?

Photosensitivity :)

Which tetracycline is used in SIADH?

Demeclocycline is used in SIADH.

What happens when you give outdated tetracycline?

Fanconi's syndrome!

Study group discussion: Fluoroquinolones

Review questions please!

You are asking questions?

No, I was waiting from them! :)

Haha review questions then!

Which enzyme does fluoroquinolones inhibit in gram negative and gram positive bacteria?

DNA gyrase!

Umm specific types of it in both gram negative and gram positive bacteria.

Topoisomerase 2 in gram negative and topoisomerase 4 in gram positive.

What are the side effects of quinolones?

Tendon rupture, photo toxicity!

Can cause convulsion.. Because they are also GABA inhibitory.

Somnolence. You don't prescribe them to people who drive for the same reason.

QT prolongation.

Nausea, vomiting and taste disturbance.

Tendon rupture in elderly people taking steroids.

QT prolongation only in gemifloxacin, lomefloxacin, moxifloxacin and levofloxacin.

Why don't you give it in pregnant ladies and young children?

In children, it can cause some defects in bone/cartilage formation. So it'll cause bending of long bones and stuff.

Yup. It causes defect in collagen.. Articular rupture and tendonitis!

Okie moving on.. Name the respiratory fluoroquinolones.

There are four of them. They have been termed that because they can be given to patients suffering from COPD.

Gatifloxacin, gemifloxacin, levofloxacin, moxifloxacin.

Could you explain the concept of respiratory fluoroquinolones a lil bit more? It's a new concept to me.  sorry! Why can't you give the others to someone with COPD?

They are especially used for lower RTI and upper RTI.. Cause they inhibit anaerobic, gram positive, atypical as well as gram negative aerobes. The others do that too..but these are especially preferred for respiratory infections.

Study group experience #10

Tissues that are exclusively dependent on glucose for metabolism 

Vitamins (Antioxidants, Vitamin E and vitamins in egg) 

HNPCC (Lynch syndrome) and microsatellite instability 

Peutz Jegher's Syndrome 

Iron metabolism 

Management of Parkinson's disease (USMLE oriented case)

Gate control theory of pain 

QT prolongation 

Mechanism of pulsus paradoxus in severe acute bronchial asthma 

Sickle cell anemia

Heparin, warfarin and the anti-fibrinolytics

Aminoglycoside review questions and mnemonics 

Zidovudine 

Heparin induced thrombocytopenia and leech therapy 

Virchow's triad 

Mechanism of hypercoagulability in obesity and smoking 

Type 2 polyglandular syndrome 

Most common site of intraperitoneal abscess 

I love how when people are unable to answer questions, the person who asks gives hints, clues and mini questions to lead to the right answer. This creative thinking and understanding process is what I love most about the study group <3

How to join the study group

Study group discussion: Zidovudine

Review questions!

Full form of HAART?

Highly active anti retroviral therapy.

Which is more toxic.. Zidovudine or acyclovir? And why?

Zidovudine due to bone marrow suppression.

Yes! It causes BM suppression.

Actually, both of these drugs cause it..but zidovudine causes it at a much severe level.
Acyclovir and zidovudine have to be activated to their respective triphosphate. Zidovudine uses the host cell enzymes for this but acyclovir uses the viral enzyme FIRST and then the host cell enzyme. Hence in cases of zidovudine the toxicity is very high.

Wow what a concept!

The myelosuppression is so bad.. That you have to give blood transfusion and growth factors.

It effects the mitochondria of the cells too I guess.

AZT induces significant toxic effects in humans exposed to therapeutic doses...
Cytogenetic observations on H9-AZT cells showed an increase in chromosomal aberrations and nuclear fragmentation when compared with unexposed H9 cells...
The toxicities explored here suggest that the mechanisms of AZT induced cytotoxicity in bone marrow of the patients chronically exposed to the drug in vivo may involve both chromosomal and mitochondrial DNA damage.

Study group discussion: HNPCC (Lynch syndrome) and microsatellite instability

Just was mentioned in lecture: What is the cause of lynch syndrome (the specific cause)?

It's HNPCC. DNA mismatch repair affected.

Yes, a bit more specific! Which part of MMR?

I think it's micro satellite instability or MSH2.

Msh2 is one of them, correct!

MLH1 as well.

Mhmm. One more?

Donno any more T_T

Apparently MSH6 as well :)

Could you sum them all up? What is lynch syndrome..What are it's features?

Ovarian, Colon and Endometrial carcinoma are the features. You do the molecular talk!

Lynch syndrome (also known as HNPCC) increases the chance of colon cancer up to 80% along with increasing chances of other sorts of cancer.

It is caused by disruption of Mismatch Repair system due to mutations in 3 MMR factors : MSH2, MSH6, and MLH1

What about the microsatellite instability pathway? Which syndrome was that?

Oh I found out.. Microsatellite instability is found particularly in cells which are expressing mismatch repair defects. HNPCC is one of the of the most important syndromes where this happens. However its not an "exclusive feature" of MMR defects.

The microsatellite  instability is the evidence that the MMR isn't working properly and can't detect insertion-deletion loops that forms in the S phase. Googled and paraphrased.

Ah makes sense. Thanks!

Elaborate on the term microsatellite instability.

Umm it's kind of complex.. Usually you detect DNA by PCR, right?

Yup. You amplify the DNA!

So if while PCR, little microfragments of DNA split up which weren't there originally. They are called microsatellites. They were made during PCR. So if those are created, it means the fragment has microsatellite instability.

So these are abnormal?

They occur naturally.. But usually detected by MMR and dispatched if MMR doesn't work...
They will be present!

Yep!

Got it. Thanks!

Study group discussion: Peutz Jegher's Syndrome

What's Puetz jegher syndrome?

Hamartomatous polyp with pigmentation on lips.

Study link! http://medicowesome.blogspot.ae/2014/10/tumors-of-colon-and-of-polyposis.html

Another life problem solved! Haha thanks!

Lkb1 is involved in PJS. How?

Peutz Jegher's Syndrome mnemonic:
Remember the initial letters of the disease - PJS.
P: Pigmented oral mucosa
J: Jejunal polyps
S: STK 11 defect
Thank you  IkaN!

Oh nice. LKB1 kinase activity is lost due to somatic mutations. In Peutz Jegher's Syndrome, that is.

Study group discussion: Mechanism of pulsus paradoxus in severe acute bronchial asthma

Which one of the following does not cause pulsus paradoxus?

a. Severe aortic regurgitation
b. Cardiac tamponade
c. Constrictive pericarditis
d. Acute severe bronchial asthma