Study group discussion: Drugs that cause urinary calculi

Which diuretic agent is asociated with development of kidney stones?

Loop diuretics.
Potassium sparing diuretics.

So... Almost all of them?
Nope. Osmotic diuretics don't!

And thiazides are used for treating kidney stones!

Loop diuretics, carbonic anhydrase inhibitors and triamterene (Not all potassium sparing diuretics) are the ones that cause calculi.
Mechanism: Loops and CAI cause metabolic abnormalities.

Why only Triamterene?
The exact mechanism by which Triamterene promotes urinary calculus formation is unclear, although it is hypothesized that precipitation of triamterene and its metabolites provides a scaffold for nucleation and subsequent calculus growth.

Which carbonic anhydrase inhibitor cause renal stones? And what's the mechanism?

Prolonged use of carbonic anhydrase inhibitors may lead to a hyperchloremic metabolic acidosis, in which urinary pH is increased and urinary citrate is decreased.
Acidification of urine prevents calcium and phosphate stones but causes uric acid and cysteine stones. Link: http://medicowesome.blogspot.in/2012/12/acidification-of-urine.html

Speaking of stones, which antiretroviral drug causes nephrolithiasis?

Acyclovir?

I didn't know this. Just Googled and found that they cause crystalluria and obstructive nephropathy as well.

Indinavir was the drug I was asked about in a test.

A summary of drugs that cause stones (Source: ncbi)

Urinary calculi can be induced by a number of medications used to treat a variety of conditions.
Loop diuretics, carbonic anhydrase inhibitors, and abused laxatives can cause metabolic abnormalities that facilitate the formation of stones. Correction of the metabolic abnormality can eliminate or greatly attenuate stone activity

Magnesium trisilicate; ciprofloxacin; sulfa medications; triamterene; ephedrine, alone or in combination with guaifenesin; and indinavir may induce calculi via urinary supersaturation. Eliminating such calculi usually involves discontinuation of the medication or initiation of alternate therapy.

Thanks!

Study group experience #4

Discussions so far -

Histrionic personality disorder, Munchausen syndrome and MSBP  

Dissociative identity disorder, Post-Traumatic Stress Disorder and Shutter Island  

Migraine, aura and floaters  

Schizophrenia and Schizotypal disorder 

Malignant hypertension discussion 

Renal tubular acidosis types mnemonic 

How to do percussion (A clinically oriented topic) 

Cause of decreased glucose levels in CSF in bacterial meningitis  

Respiratory physiology (Interesting read for first years) 

Physiology books  

Transpulmonary pressure 

Case control and cohort study mnemonic  

Legionella confusion   

Compliance of the lungs  

Urinalysis  

Lateral spinothalamic tract mnemonic  

Trial of scar  

Management of ARDS 

Diagnostic tests for pulmonary embolism  

Amyloid  

Bone tumors 

Myocardial infarction markers  

Right ventricular infarction 

ECG sign of left ventricular aneurysm 

When I first thought of the group, negative thoughts poured in and everyone thought it was a bad idea: What if I get too many spam messages? All you'll receive is advertisements! You'll lose your Whatsapp privacy! It's too risky man! Why would you do something so stupid? Give your number to the internet?

But one person encouraged me: Eh? So what? Business men take risks all the time. Keep a verification so the spammers can't get it. Block people, duh! Why is that feature available on Whatsapp? You can always throw away your number or change it.

For everyone who benefits from the group discussions, you guys should totally thank that positive soul for this!

What I learnt by making the study group:

Don't be so negative, don't fear the bad stuff so much.

Be courageous. Take calculated risks.

Encourage people, no matter how crazy they sound.

It's takes just one person to make a life changing decision, make sure it's you.

*OMG I STILL CAN'T BELIEVE IT WORKED OUT SO WELL AND I'M TALKING TO YOU GUYS EVERYDAY*

-IkaN

Equilibrium potential value of an ion and how to apply it to action potential ?

The equilibrium potential value of an ion or the Em value.

I will try making some sense out of this confusing term.

1. Ions across a cell membrane have two forces acting on them, the concentration gradient and the electrical gradient. Since, Na,K and Cl are the most abundant of ions, it is only needed to know the Em of these three ions.

2. The Em is the value of the membrane potential at which both the concentration gradient force and the electrical gradient force are equal and opposite. This means that these two forces will cancel each other and there will be no net flow of ions across the membrane.

3. Also, remember whenever given the chance ( permeability ) the ion will try to reach a stability, that is it will try to achieve a membrane potential equal to its Equilibrium potential.

There is an equation called the Nernst equation to measure the Em value. When you solve this equation the values of Em are

Na- (+61Mv)
K   ( -94.1Mv)
Cl  (-70Mv)

Lets apply these terms, to the action potential

Study group discussion: ECG sign of left ventricular aneurysm

On ECG after an MI infarction..What is the sign for left ventricular aneurysm?

It's persistent ST segment elevation. After MI, the ST segment does rise, but it falls gradually too, reaching a normal. But if its elevated then its aneurysm.

In any specific leads?

The same leads where infarction shows up.

2, 3 and AVF leads.

So basically the ST segment doesnot fall back to normal right?

Yup.

Great didn't know that concept.

Study group discussion: Right ventricular infarction

Since it's MI..Review question.. Name a disease associated with right ventricular infarction?

Atherosclerosis?

I meant name a cause for right ventricular infarction, other than atherosclerosis.

It's pulmonary embolism.

The pulmonary embolus puts the right side of heart in strain and it dilates. This dilation obstructs the right coronary artery. This was my viva question on an ECG of right ventricular infarct.

So does not it lead to hypertrophy of the right ventricle?
In an acute setting, no.
If the pulmonary thromboembolism  is chronic it will cause pulmonary hypertension. Then it causes right ventricular failure.

So the acute pulmonary embolus should be the answer.

Ohh that makes some sense! Good one!

Study group discussion: Myocardial infarction markers

Which is the reinfarction cardiac marker?

It's CK MB. The levels fall in 3-4 days. So if you get a reinfarction and see your troponin you can't be sure if it's from last time.

CK MB falls in 36-48 hrs.

Why isn't it myoglobin? Myoglobin rises and falls the fastest.

Because myoglobin is not a specific cardiac marker.

No but in these cases, it is the most preferred. Cause it returns to normal within 24 hours.

Dunno.

I think the time after which re-infarction occurs also matters.

Do let us know.

These things are confusing. Good thing is we are trying to sort them out.

Yes, it is.

We had a confusion between myoglobin and CK MB in the diagnosis of re-infarction.

The answer is CK MB simply because it is cardiac specific and falls within 2 days.

The only use for myoglobin is ruling out a Myocardial Infarction, early. (Cause it's the first to rise and is very sensitive!)

If the levels are not up, it's not a MI.
If myoglobin levels are up - it could be a skeletal muscle injury or a MI, you don't know until you look at the other markers.

Even though myoglobin levels fall early, it is not used for the diagnosis of reinfarction because it's not specific and if the levels are up after an infarction, it could mean something else as well.

Harrison says both CK MB and myoglobin can be used for reinfarction. I would hate the question maker for asking us to choose between the two & go with CK MB because it's specific.

Woah... Awesome discussion... Thank you everyone for the cocepts... I so love this group.

Study group discussion: Amyloid

Does anyone have awesome things for amylodosis pathology?

Another concept you must understand is that the protein deposits in tissues depending upon where it was derived from.

For example, amyloid from immunoglobulins deposit in tissues of mesodermal origin like kidneys, heart, muscle, tongue.

When it's due to chronic inflammatory disease, it involves parenchymal organs like liver adrenals and pancreas.

Good concept.

Review question! Which amyloid protein is associated with Alzheimers disease?

Beta amyloid

Yes!

And why are patients with downs syndrome more susceptible to early Alzheimers?

Extra chromosome 21 which means extra copy of the presilline gene, I think.

Absolutely right!

Great.

Never knew that!

Oh oh one more!

Which condition is associated with amyloid deposition in the thyroid gland?

Are we talking about the medullary thyroid carcinoma?

Yep. The amyloid deposits are derived from calcitonin in that condition!

Which is the one in patients on dialysis?

Beta micro globulin?
B2 - microglobulin is seen in dialysis associated amyloid.
Derived from the MHC class 1 protein.

Yes. It's because the beta micro globulin is not filtered from the dialysis membrane.

Excellent stuff.

Study group discussion: Bone tumors

Osteoclastoma is a giant cell tumor, right?

And these giant cells can be differentiated from other giant cells on the basis of the number of nucleoli present?

 Yo

These giant cells will have about a 100 nucleoli

Osteogenic sarcoma is osteosarcoma. it is a malignant tumor

 names are confusing
 Osteosarcoma, osteoblastoma, osteoclastoma
 The other two are benign?

GCT(osteoclastoma) is a special variant bone tumor
Does not come under either benign or malignant
 Based on number of giant celss an osteoclastoma is loosely classified from typical to aggressive to malignant
 More giant cells and less stroma its benign, less giant cells more stroma its aggressive.

Osteoblastoma is a rare primary neoplasm of bone, categorized as a benign bone tumor that is closely related to osteoid osteoma. It differs from osteoid osteoma in its ability to grow larger than 2.0 cm in diameter and its aggressive behavior in bone.

Turner's syndrome mnemonic

Turner's syndrome mnemonic

Cystic hygroma, webbed neck: You can't turn your neck because of it.

Aortic coarction: Aorta takes a sharp turn.

Some toxicology mnemonics

Acetaminophen toxicity is treated with N acetyl cyteine.
Mnemonic: ACETaminophen ACETyl cysteine!

Ethylene glycol is metabolized to oxalic acid. Ethylene glycol is found in anti freeze.
Mnemonic: Freeze your EGO.
Anti freeze
Ethylene Glycol
Oxalic acid

Methanol is metabolized to formic acid by alcohol dehydrogenase which causes visual disturbances. It is treated with fomepizole.
Mnemonic: There's more to me (FoMEpizol) than what meets (Methanol) the eye (Blindness).

Study group discussion: Diagnostic tests for pulmonary embolism

What is the commonest sign on ecg for PE?

Nonspecific ST changes?
Nope.

SQ3 T3 something like that?
Nope.

Most common sign is sinus tachycardia. Most specific is S1q3t3 pattern..Positive only in 20-30% cases.

Ohhh!! Nice question.

Ooh.. We tend to forget common ones when looking out for rare signs!

What is the screening test for PE?

Screening test is d-dimer. If d-dimer is negative you virtually exclude the diagnosis of PE.

Which is the most specific diagnostic test for pulmonary embolism?

Pulmonary angiography.

Depends if the person is low risk or high risk! CT angiography is done though.

Which is the most preferred test for PE?

Spiral CT is preferred next to know location, size and blah blah.

What about VQ scan?

That's done if the patient is allergic to contrast.
Or has kidney failure.
Or CT isn't available.
Or the patient is pregnant.

In our hospital setting angiography would key since most patients can't afford CT.

Oh. But its invasive..and can be very harmful. It's only preferred when you are planning for thrombectomy..Or as a last resort to diagnose PE if all the other test are negative but d-dimer is positive.

Well money for a CT can feed a peasants family for a year.

True.

Venous doppler is preferred when CT or V/Q are inconclusive.

Whats d-dimer?
The clot thingy. It interlocks fibrin strands.

It is released from the thrombus.

Fibrin is non specific for clots
Because it is elevated in some other conditions as well. So d dimer to the rescue!
*Fibrin degradation products are.

Study group discussion: Management of ARDS

Anyone over here who knows the management of ARDS?

PEEP

Positive end expiratory pressure and 100% oxygen.

It's like during expiration your alveoli collapse, especially in ARDS since their surfactant is gone, so to prevent that collapse you give a bout of positive pressure at the end of expiration.
I don't know how they generate it but this is the mechanism!

Aah.

PEEP is continuous flow generated at certain fixed pressure that stops the alveoli from collapsing during the expiration. Pressure usually kept around 5

So the pressure is kept continuous during the whole time?

Yeah it's continuous during the both inspiration and expiration!

Umm then why is it called "End expiratory"?

That's a very good question actually. Don't know exactly why it's named that way!

Ever heard of low tidal volume ventilation? Aka lung protective ventilation? Aka baby lung concept?
It's used in managing ARDS. Since many alveoli are fluid filled and the patient effectively will have lesser tidal volume than normal. If we give the normal tidal volume the patent alveoli will burst due to barotrauma!
Inspite of normal tidal volume - 8-12ml/kg, we give 4-6ml/kg body weight for ARDS.

Also, you treat the underlying cause of ARDS.

You even have to restrict fluid overload. That's the other most important point!

Yeah read that too, diuretics are beneficial to some extent. Steroids are of no use.

Yup.

Also NO (Nitrogen oxide) is of no use.

Yeah for ARDS. During the various trails for the treatment of ARDS they observed that increasing the tidal volume lead to worsening most probably due to inflammation due to repeated opening and closing of alveoli with each inspiration and expiration ultimately affecting the structure of alveoli and their ability to perform their job. Low tidal volume along with PEEP significantly reduced the mortality in the patients with ARDS. So that the standard treatment at present.

I read there is other device called high RR..it provides respiratory rate of 15 to 20 cycles per SECOND.

It has a very low tidal volume but..Almost 1-2 ml / kg

Study group discussion: Trial of scar

Can anyone tell me about the "Trial of scar" after C section procedures?
I have heard of trial of labour, not sure if its the same thing!

My searches lead me to trial of labour as well ..I guess they are.

It's especially indicated in cases of borderline cephalopelvic disproportion.

The obstetrician let's the lady go in to labour in a controlled environment. If the labour becomes to stressful and is prolonged unduly, the doctor immediately performs a C section

It's more like given the patient an opportunity to experience normal vaginal delivery.

Same thing i suppose can be applied to scar from previous C section.

You see the chances of rupture of the lower segment scar is highest during labour, so the patient is monitored especially for signs of impending scar rupture

Most common is pain and tenderness over the scar area.

A off topic thing due to c/s delivery a tv series named "the knick", a medicine based serie in the beginning of the 20th century in usa, i recommend it, the changes in surgery, hospitalization, treatments are baby steps, surgeons invent the tools they use, amazing!

Study group discussion: Lateral spinothalamic tract mnemonic

PAin and TEmperature sensation carried by LAteral spinothalamic tract. Mnemonic is "PaTeLa" (which is present knee).

Study group discussion: Urinalysis

Significance of difference findings in urine analysis-
1) WBC in urine - Pyelonephritis
2) RBC - Glomerulonephritis
3) Hyaline cast - No significance
4) Broad waxy cast - CRF
5) Dirty brown/granular cast - Acute tubular necrosis

RBC's may also be present in case of calculi or tumors!

Correct!

"Approach to hematuria"
1) Dipstick - blood positive
Microscopy- RBC negative
It is myoglobinuria.

2) Dipstick - blood positive
Microscopy- RBC positive
It may be kidney pathology or bladder.

In that case if RBC is isomorphic (not distorted) - urinary bladder pathology like stones, cystitis.

If RBC is Dysmorphic - Kidney pathology (When RBC is passing thru tubules shape get distorted)

The dysmorphic RBC are a characteristic of glomerular pathology not tubular.

Study group discussion: Compliance of the lungs

Can anyone simply compliance for me?

Compliance = Change in volume/change in pressure.

So it follows as lungs starting at zero before inspiration. At the end there will be 500mL of air. So 0.5L
The pressure of he lungs starting at -5cm H20 increases to -10cm after expiration.

It would be (Specific compliance)
0.5 L/ (-5cm H20 - (-10cm H20))
= 0.5L/5cm H20 = 0.1 per cm H20

Theres a few types of compliance. Static compliance and dynamic.
Static calculates the periods where here isnt any gas flow. So during the time where there isn't fas flow.
Dynamic calculates the periods of active(!) Inspiration.

But I know nothing about those two calculations.

What is dead space of lungs?

There are two types of dead space-

1.       Anatomical

2.       Physiological

Anatomical dead space is the area included in the first 16 generation of the bronchial tree. Its by virtue of the normal anatomical structure that this area is unable to take part of in the exchange of gases

The physiological dead space is when there is decreased blood supply to a particular part of the lung, but the air entering the same part is normal. Hence there is no exchange of gases. In other words there is an increase in V/Q ratio.

Extra-

Why secondary tuberculosis affects the upper lobe?

There is an entity called ventilation perfusion ratio (V/Q)

meaning the degree of air entering the alveoli of lung and the corresponding pulmonary blood supply to the same. The normal value of the V/Q ratio is 0.8

Pulmonary blood capillaries are a low pressure system, with an average pressure of 25/8 mm of Hg. Out here comes the effect of gravity, pulmonary blood is unable to perfuse the upper lobes that well .

On the other hand, Air when it enters the lungs it enters the upper lobes better than the middle and lower lobes

This fact can be applied to

Study group discussion: Legionella confusion

A few days back, we had a discussion on legionella.

Legionella affects three systems - Lungs, GIT (diarrhoea) and CNS (Altered sensorium, confusion, etc).

Why does it cause CNS symptoms?

Study group discussion: Case control and cohort study mnemonic

Any mnemonic for case control study vs cohort study and how to identify which study to conduct or not?

Study group discussion: Transpulmonary pressure

What is transpulmonary pressure and its significance?

I remember it's something like... General lung pressure without alveolar pressure. I don't know.

It's the difference between the intrapleural pressure and the alveolar pressure. The athmosphere pressure is constant, but air still needs to flow in and out of our lungs, so we adjust the pressure inside our body.

The basic principle is that air flows from higher pressures to lower, so we constantly change the pressure in our lungs to higher or lower than the atmosphere.

Transpulmonary pressure (when everything is fine) is always positive.

I'm getting what he is saying, go on!

Transpulmonary pressure is always positive, intrapleural is always negative and alveolar fluctuates.

That's how I remember from my physiology classes, anyway.

Yeah, alveolar fluctuates so that air can flow in and out easily.

Transpulmonary pressure is basically the elasticity of the lungs. The recoil.

Since atmospheric pressure is relatively constant, pressure in the lungs must be higher or lower than atmospheric pressure for air to flow between the atmosphere and the alveoli. It is nothing but the elastic recoiling of the lungs. If 'transpulmonary pressure' = 0 (alveolar pressure = intrapleural pressure), such as when the lungs are removed from the chest cavity or air enters the intrapleural space (a pneumothorax), the lungs collapse as a result of their inherent elastic recoil. Under physiological conditions the transpulmonary pressure is always positive; intrapleural pressure is always negative and relatively large, while alveolar pressure moves from slightly positive to slightly negative as a person breathes. For a given lung volume the transpulmonary pressure is equal and opposite to the elastic recoil pressure of the lung.