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.
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!?
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.
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!
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!
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.
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.
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!
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.
In which form is iron absorbed?
Fe2+
Ferrous!
In which form is it stored?
Ferritin!
Fe3+
Study link! http://medicowesome.blogspot.ae/2013/11/ferrous-vs-ferric-mnemonic.html
In which form does heme contain iron?
Ferrous
Remember..Heme is always in the ferrous form when free..And in the ferric form when bound. In heme..it is an exception.
Others ferritin, transferrin..it is always in ferric form
Ohh. Interesting!
Antidote for choice for acute iron overdose?
Desferoxamine?
Yup. Desferrioxamine is given IV.. It is for acute iron overload.
Which antidote is preferred for chronic iron overdose then?
Oral drug.. Deferiprone.
Desferoxamin SC.
Name the three crisis of sickle cell anaemia.
Aplastic crisis
Vaso-occlusive crisis
Sequestration crisis
What causes aplastic crisis?
Parvovirus B19
*doubt discussion*
In sickle cell anemia what analgesic do we use? I've heard that morphine can cause vasoconstriction and that would make it worse, but I'm not sure that's true.
Yup, opiates are used.
One cause of death in sickle cell anemia is acute chest syndrome, if I give the patient morphine (that has a secondary coronary vasoconstrictor effect) that will kill the patient.
Correct.
Acute chest syndrome is due to occlusion of the pulmonary vessels.
The major issue hear is to given oxygen to the patient..Cause hypoxia aggravates the whole situation.
So I'm not supposed to worry about Myocardial Infarction?
Not that I've heard of.
Doesn't it cause CHF?
"The acute chest syndrome may mimic CHF however it is uncommon." Says the internet.
New drug for SCA. Read in Harrison. Azacytidine.
Mechanism of action of azacytidine?
Azacytidine increases HbF production and reduces anemia in sickle cell disease.
There's a drug which blocks gardos channel in RBC membrane. It's under trials too. It's the one I was talking about.
The mechanism is interesting because it prevents dehydration of the RBC.. That's the cause of sickling.
I like the sound of it - Gardos channel.
It's a potassium channel!
A greek god!
Me too.. It guards the RBC!
Gargoyle ..thats what my mind said.
Haha. They were guardians too!
Another interesting thing.. An anti fungal we use also blocks this channel in vitro!
Just had my first class of pain physiology. I loved it!
What was the most interesting thing that you learnt in class?
Melzack and Wall's theory. About the gate control of pain. I had to google the english term lol.
Aw that's so nice of you. It's an interesting concept. Why soldiers don't feel pain when they are injured in battle.. But feel it in the hospital.
What is it called in Brazilian? (I donno what language you'll speak)
Portuguese. In portuguese, it's 'teoria das comportas'
I feel better now for not recognising "Melzack and wall's theory" but I do remember learning teoria das comportas! hahahaha I have to Google the translation all the time too.
Must be because of increase in Endorphins and adrenaline?
Not exactly. You should read more about it!
The brain determines which stimuli are profitable to ignore over time. Thus, the brain controls the perception of pain quite directly, and can be "trained" to turn off forms of pain that are not "useful". This understanding led Melzack to assert that pain is in the brain.
Awesome stuff!
Came across a new question today. Let me ask you guys -
So what is Type II polyglandular autoimmune syndrome?
Schmidt syndrome?
Yes, also known as Schmidt syndrome.
What are the components?
Adrenal insufficiency (Addisons)
Hypothyroidism (hashimoto)
Also gonadal insufficiency
And ?
Abs pancreatic insufficiency!
Yeah, Type 1 DM.
Good job!
Which things in our body are exclusively dependent in glucose for energy?
The lens.
Correct
Liver too?
Nope.
Brain?
No. It uses ketone bodies too!
Muscle?
No.
Cornea?
Cornea correct!
Heart.
Heart, no.
Interesting: Heart can use lactate.
Sperm
No. Sperm uses fructose!
It's RBC!
Oh ya. They are exclusively dependent on glucose! RBC can't metabolize anything else!
How does smoking and obesity promote hypercoagulability?
Smoking increases reactive oxygen species. ROS reacts with LDLs causing increasing oxidized LDL, when deposited in intima becomes atherosclerotic plaques. Also ROS causes endothelial damage itself, increasing its permability to LDL.
Atherosclerotic plaques can rupture, exposing tissue factor. Or the plaque itself causes turbulent blood flow, increasing chance of thrombosis.
Nicotine causes vasculitis and thus causes turbulence of bood flow!
And obesity?
The various mechanisms by which obesity may cause thrombosis include: the actions of so-called adipocytokines from adipose tissue, e.g. leptin and adiponectin; increased activity of the coagulation cascade and decreased activity of the fibrinolytic cascade; increased inflammation; increased oxidative stress and endothelial dysfunction; and disturbances of lipids and glucose tolerance in association with the metabolic syndrome.
Source: Obesity and Thrombosis — ScienceDirect - http://www.sciencedirect.com/science/article/pii/S107858840600579X
What is Virchow's triad for thrombosis? Explain please.
Virchow's triad... If there is stasis (Blood ain't flowing to wash out the collected coagulation factors), hypercoagulability (More coagulation factors) or endothelial injury (Stuff that activates coagulation factors) there'll be a predisposition to thrombosis.
In Virchow's triad 2 things are missing:
1. Role of platelets
2. Coagulation system
