About me

Hey Awesomites!

Well, I am not a new author here. I am honored to write so many posts for the blog . Let me introduce myself so that all of you can know about me...

Treatment of cholesterol-induced Alzheimer's

Hey awesomites!

Pathology done! Now lets know about its pharmacology here :)

Cranial Nerve Exits Mnemonic (2 2 4 4 )

Hey guys, Jay here!

This is a very simple self explanatory image which I made.

Brain abscess notes

Brain abscess notes

Here's what I studied =)

Causes
- Direct spread (Paranasal sinusitis, otitis media, mastoiditis, dental infection)
- Head trauma or surgical procedure
- Hematogenous spread (Pneumonia, endocarditis)

Organisms:
- Streptococci
- Bacteroides
- Pseudomonas
- Hemophilus
- Enterobacteriaceae
- MRSA (Head trauma, neurosurgical procedure)

Symptoms:
- Headache > 75% patients
- Fever only in 50% patients (Important: Absence of fever should not exclude the diagnosis)
- Focal neurologic deficits > 60% patients
- Other symptoms - Papilledema, nausea, vomiting, drowsiness, confusion
Hemiparesis - Frontal lobe abscess
Dysphasia - Temporal lobe abscess
Nystagmus, ataxia - Cerebellar abscess

Neuroimaging:
- MRI is better than CT.
- Ring enhancing lesion with surrounding edema on neuro imaging studies is seen.
- Most accurate: Brain biopsy
High yield: Biopsy is essential to distinguish brain abscess from cancer and also to determine the precise organism.

Don'ts: Do NOT do a LP. CSF analysis doesn't contribute to diagnosis or therapy. Increases the risk of herniation.

Extra: Abscesses due to Listeria have blood culture positive > 85% of the time.

Differentials:
- Meningitis
- Meningoencephalitis
- Brain tumors (Cancer can give fever)

Treatment:
- Empirical antibiotics should be modified after results of gram stain and culture.
- Surgical drainage.
- Prophylactic anticonvulsant therapy (High risk [>35%] of seizures)
- Glucocorticoids are reserved for substantial periabscess edema and mass effect due to increased ICP.
- Serial MRI or CT scan monthly to document resolution of abscess.

That's all!
-IkaN

Hypercholesterolemia and the Alzheimer's disease

Hey awesomites!

All of you know that cholesterol is synthesized locally in brain as well as peripherally in liver, both separated by a line of blood-brain barrier. But what about the case of hypercholesterolemia and how it eventually leads to increased amyloid depositions. what is the ultimate link between high serum levels of cholesterol and the Alzheimer's disease?

Enteric nervous system (ENS)

Recently, while studying pharmacology, I came to know about the third system of ANS - Enteric nervous system, apart from sympathetic and parasympathetic systems .

Here is some information of ENS:

It consists of highly organized neurons situated in the wall of GI tract.

It mainly includes Auerbach's plexus and Meissner's plexus.

The most interesting point about ENS is this network receives preganglionic fibers from the parasympathetic system and from postganglionic sympathetic neurons.

ENS controls GI motility, secretions, mucosal blood flow.

ENS causes relaxation or stimulation of smooth muscles.

Non-cholinergic excitatory transmitters such as substance - P plays a modulatory role in controlling ENS!

~Ojas

What is the difference? : Meconium vs. Meconium Ileus

Hey Folks, Jay here!

Meconium is the very first stool ("poop") of a Neonate. This is mainly composed of the material that it ingested during its intrauterine life. This can include, amniotic fluid, mucus, bile, intestinal epithelium cells, lanugo and water.

Classical Findings of RDS Infant!

Hi awesomites, Jay here! This is a short description on Classical clinical findings of a Neonatal Respiratory Distress Syndrome(RDS or NRDS) infant.

Scarlet fever notes and mnemonic

Hello. How are you awesomites?

Let's talk about scarlet fever today!

Scarlet fever, also known as scarlatina, is characterize by exudative pharyngitis, fever and scarlatiniform rash.

It's caused by erythrogenic toxin producing GABHS (Group A Beta Hemolytic Streptococci)

Characterized by:
- Fever, headache
- Sore throat, circumoral pallor
- Sandpaper rash (Pinpoint, erythematous blanchable papules), erythema trunk, pastia lines
- Lymphadenopathy

Diagnosis:
- Rapid antigen detection test is specific, but not sensitive.
- If it is negative, do throat culture.
- Elevated ASO, DNAse maybe seen.

Treatment:
- Treatment as long as 9 days after the onset of symptoms prevents rheumatic fever.
- Oral penicillin, amoxicillin for 10 days.
- Cephalosporins, macrolides are alternatives. (Penicillin resistant group A staphylococcus doesn't exist.)
- If adherence problem, intramuscular benzathine penicillin G.

That's all!
The only fever I have is for Scarlett Johansson =P
-IkaN

Erythroblastosis fetalis (HDNF)

It is a condition that develops when Rh-negative women is pregnant with Rh-positive baby .
It causes phagocytosis of the fetus's RBC's (Baby inherits Rh positive antigen from father ).
As mother is Rh-negative , exposure to fetus's antigen causes development of anti-Rh agglutinins .
These agglutinins(mostly IgG antibody ) diffuse through the placenta and enters fetus blood cells and leads to phagocytosis of the RBCs ,which leads to release of hemoglobin into blood !Then fetus's macrophages converts the hemoglobin into bilirubin ,which causes baby skin to become yellow(jaundiced).Although the severe form of anemia is responsible for many deaths of infants ,many children who barely survive the anemia exhibit permanent mental impairment , because of precipitation of bilirubin in the neuronal cells  ,causing destruction of many cells , condition known as Kernicterus

It usually doesn't affect the first child ,since sensitization occurs during parturition.However ,if Rh-negative mother was sensitized earlier with Rh antigen then first child can get affected .

Treatment:
1)One treatment of HDNF is to replace the neonate's blood with Rh-negative blood .About 400ml of Rh negative blood is infused over a period of 1.5 or more  hours ,while neonate's own blood is removed,the process may be repeated several times during the first week of life ,to prevent Kernicterus .

Prevention:
Anti-D antibody is administered to the expectant mother ,starting at 28-30 weeks of gestation.The anti -D antibody is also administered to Rh-negative women who deliver Rh -positive babies to prevent sensitization of the mothers to the D antigen .This greatly reduces the risk of developing large amounts of D antibodies during second pregnancy !

~ojas

DON'T use Perfumes to test Olfactory nerve!!! But why?

Hi folks,

Our Neurology professor said not to use Perfumes to test Olfactory nerve in Cranial nerve testing. But why?

The updated Glasgow Coma Scale

Hi Awesomites,

The Glasgow coma scale or GCS as we know it has changed since its inception in 1974.

So lets go!

Main differences are 

• We no longer use the term "Pain", but "Pressure"
• We no longer recommend "Sternal Rub", but "Trapezius Pinch" or "Supraorbital notch pressure" or careful "Fingertip pressure"(Peripheral stimulation)
• "To speech" is changed to "To Sound"
• "To pain" is changed to "To pressure"
• "Inappropriate speech" is changed to "Words"
• "Incomprehensible speech" is changed to "Sounds"
• Flexion is defined two way now as "Normal flexion" and "Abnormal flexion"

The differences between 1974 and 2014 updates are as follows.

You can read more details on the update, in this link. Download the pdf in the page which is the original paper.

Thanks,

With love,

Jay :) 

Anatomy of the larynx: Cartilages

Here's an awesome video on the anatomy of the larynx by A. P. Burkholderia!

Isn't he just awesome? :D

Beta HCG notes

Where is beta HCG produced? 

Syncytiotrophoblast.

Step 2 CK: Goodpastures syndrome notes

Hello!
Here's a short post on Goodpastures syndrome!

Cocaine in the brain - "The Addiction"

Hey Awesomites!

Here I will be talking about a social problem amongst the youngsters - “Addiction to cocaine”. 

Menstrual cycle and related problems

Here are some common menstural complaints that I studied today during my posting that I would like to share with you. There are many more though. Comment if you think I have missed out on something!

Contrast induced nephropathy notes

Features of contrast induced nephropathy

- Due to iodinated contrast agents (Other agents that cause AKI: Gadolinium for MRI, sodium phosphate solutions as purgatives)
- Prevented by use of non ionic contrast agents, IV hydration, acetyl cysteine.
- Serum Creatinine rises 24-48 hours after exposure. Resolves in a week.
- FeNa low, benign urinary sediment.
- Risk increases in CKD, Diabetic nephropathy, multiple myeloma.

Brachial plexus mnemonic

This was probably the most important answer you must have encountered during your 1st year.

Here are tricks to remember Brachial Plexus!

Analgesic nephropathy notes

Analgesic nephropathy

Characterized by:
Renal insufficiency
Papillary necrosis

Due to:
Toxic drug levels in inner medulla
Causes chronic tubulointerstitial damage
Results from papillary ischemia due to vasoconstriction of medullary blood vessels (vasa recta)

Caused by:
Phenacetin containing preparations
Aspirin
Caffeine

Symptoms:
Polyuria (Due to impaired concentrating ability)
NAGMA (Due to tubular damage)
Hematuria (Due to sloughed necrotic papilla)
Sterile pyuria and WBC casts may also be seen
Ureteric colic, obstruction (Due to sloughed necrotic papilla)

At increased risk of:
Premature aging
Atherosclerotic vascular disease
Urinary tract cancer

That's all!
-IkaN

Radial nerve mnemonic

I am gonna put radial nerve in the simplest form mostly including mnemonics how to learn it's huge muscles supply!

Remember when you were in 1st year and how these nerves used to test your patience?! Let's make it easy.

-Nerve root: C5-T1

-Sensory nerve supply:
Skin of dorsal surface of forearm
Lateral side of the dorsal part of palm
Lateral 3 & 1/2 digits

-Motor nerve supply:
(It supplies extensor compartment)
Here is mnemonic
S: Supinator.
I: Extensor indices.
D: Extensor Digitorum.
B: Brachioradialis.
A: Anconeus.
T: Triceps.
C: Extensor carpi radialis longus.
C: Extensor carpi radialis brevis .
A: Anconeus.
P: Extensor pollicis brevis.
P: Extensor pollicis Longus.
CU: Extensor carpi ulnaries.
ED: Extensor digiti minimi.

So mnemonic is
SID (C)CAP(P) (Read it as cap!) BAT Cu-ed.

Remember:
Cu = Extensor carpi ulnaris (Supplied by radial nerve not ulnar nerve as it is extensor muscle)

~ Ojas

Treatment of TTP mnemonic

Safia made a mnemonic of TTP and sent it to Medicowesome, hoping it would help someone. So sweet!

Treatment of TTP: CART
C: corticosteroids
A: asprin
R: rituximab
T: transfusion

In emergency situations, transfuse blood first!

Thanks Safia.

-IkaN

Cranial nerves type mnemonics

Here is one of the mnemonics which I made to remember types of cranial nerves
1)Olfactory  -Sensory
2)Optic.  -Sensory
3)Occulomotor-Motor
4)Pathetic(Trochlear)-Motor
5) Trigeminal-Mixed
6)Abducens-Motor
7)Facial-Mixed
8) Auditory-Sensory
9) Glossopharyngeal-Mixed
10)Vagus-Mixed
11)Spinal accessory-Motor
12) Hypoglossal-motor

"Some say marry money but my brother says beautiful bride matters more!"

S-Sensory ;M-Motor ;B-Both (Mixed)

~Ojas

Contraindications of thrombolytic therapy

BISHOPS

B = Bleeding disorder .
I = Intracranial Hemorrhage.
S = Stroke past 3 months .
H = Head injury past 3 months .
O =Oesophageal varices.
P = Pregnancy.
S =Surgery.

Made by: Khushboo shaikh
Written by: Ojas gite

Step 2 CK: Mortality benefit in Congestive Heart Failure (CHF)

Another USMLE Step 2 CK important topic :D

Things that have a mortality benefit in CHF mnemonic: "ABCDES"
A: ACEI and ARBS
B: Beta blockers
CD: implantable Cardiac Defibirillator
E: Epelerenone
S: Spironolactone

Reading material from UpToDate! =)

T wave Inversion Mnemonic

In this post, I'll be sharing a mnemonic to remember the causes of T wave inversion.

Cleft lip and palate

Hi friends,

Here's a quick way to remember the cause of Cleft lip and Cleft palate.

LMN
Cleft Lip - failure of fusion of Maxillary and median Nasal prominences!

PPP
Cleft Palate - failure of fusion of two Palatine Processes!

That's all!

-Rippie

Alport syndrome notes

Alport syndrome notes

If we were parts of the ECG, you'd be the QT segment, cutie!

I know it isn't Valentine's day, but hey, do we need a day to be all lovey dovey and flirty? xD

Hypercalcemia and hypocalcemia - ECG

Hey!

Hypocalcaemia causes QTc prolongation primarily by prolonging the ST segment.

In hypercalcemia, the ST segment is short.

And since I am a mnemonic queen:

Prinzmetal's angina notes

Hello!

Here are my notes on Prinzmetal's angina:

1. Ischemic pain at rest.
2. Diagnosed by transient ST elevation.
3. Nitrates and calcium channel blockers are used for treatment.

About me

Hello guys!!! =D
I am Vinayak, the newest author here.

I would start this mini-autobiography by expressing my gratitude to the coordination of all those zillion coincidences which ended up as me writing for this blog. :)

I have written a few articles for this awesome blog till now but this one took me the most time and brains. It is always challenging to write or say about oneself, it's like being honest without being truthful.

I belong to a very small town in Odisha situated alongside its border with Jharkhand; and like all towns situated at the border, it's pretty backward. I currently live in Mumbai, I first visited this city when I was seven years old to visit my grandfather who was admitted in JJ Hospital, at that time I never would have thought that it would be the same hospital I would become a doctor in many years later. From that moment, it was my dream to live in this city one day, and now everyday I wake up I am happy because I am living my dream! :)

"I believe that imagination is stronger than knowledge, that dreams are more powerful than facts, that hope always tiumphs over experience, that laughter is the only cure for grief and that love is stronger than death." This is my favorite quote. I also believe that "mistakes" should not be frowned upon and berated, that your evolution as a person, as a student, as a family member, as a professional is the result of a "trillion mistakes". One should be so confident about his failures that he is able to fail at the time and place of his own choosing.

As you can gather from the above article, I aspire to be a philosophical writer one day. :D

That'll be all for now! I hope one day I can come back to this article and add another paragraph about living the dream I have right now. :) Thanks IkaN for giving me this oppurtunity!

-VM

Cephalosporins : A mnemonic to get you out of the Cepho-pocalypse

Hello Everyone !
I have with me today a somewhat easy way to remember the Cephalosporins. To rescue you of the Cepha-pocalypse, if you will. Rid you of your Cepha-problems with some Cepha-lutions. (Had to say that. Sorry for the Cephalameness ;;) .)

So the 1st Generation are 3 drugs .
Remember : ZoLeDrox:
So add cef everywhere now
CefaZoline
CephaLexine
CephaDroxil

Now the 2nd Generation.
Remember : ChloroFuro carbons
So CefaChlor And Cefuroxime
(2nd is the least imp generation. So to hell with it. )

The 3rd Generation  is the most important.
So first the Parenteral  ones.
Remember:
Cef (Pronounce Saif like Saif Ali Khan)  Opera (like Oprah Winfrey)
Taxi me
Cefti(Like Safety) ke liye
Axe and
Cefta ke liye not even a
Dime (like the money dime)

So add Cef to Opera and Taxi-me to get Cefoperazone And Cefotaxime.
And further add Cefti / Cefta to the next two respectively to get :
Ceftriaxone
And Ceftazidime
So that gives you 4 Parenteral drugs.  Cefoperazone Cefotaxime Ceftriaxone Ceftazidime.

Now Oral ones.
(Whenever I think of 'Oral' - Denaerys Targaryean comes to my mind. God knows the reason for this Ceph-oral Problems ;;) )

Remember : Denaerys Xi (pronounce Chi) Beauty
Add Cef related prefixes to each of the 3 words to get your drugs.
Cefdinir  Cefixime And Ceftibuten.

And That, friends, is the story of the Cephalosporins. Now there's 4th and 5th generations too. But doing them all together can lead to a Cepha-tastrophe. ;;) That's all this time. Hope you found this helpful. Let me know what other topics you'll would like to learn in an easier way.
Bye :)

~A.P.Burkholderia

Membranous glomerulonephritis notes

Hey!
This post is on membranous glomerulonephritis :D

Carbohydrate Loading

I learnt this concept today while going through Harper's. This is especially for the fitness enthusiasts, since learning it can help you to build up your stamina better.

Energy for Muscle Contraction

Let us start by subdividing muscle fibers into two types: Type I (Slow twitch, Oxidative) and Type II (Fast twitch, Glycolytic).

Step 2 CK: Abdominal aortic aneurysm notes

Hey, here are my notes :)

Role of Glucocorticoids in Developmental events

Glucocorticoids in the fetus are either of maternal origin or syntheiszed from placental progesterone in the fetal adrenal cortex(which lacks zona reticularis). Glucocorticoids are essential for a lot of developmental events, but three of them are most important which goes as follows.

Erythropoietin therapy

Here are some important things you should know about erythropoietin therapy.

It is used in patients on dialysis.

Resistance to erythropoietin is most commonly due to iron deficiency.

Adverse effects are associated with rapid rise in hematocrit and hemoglobin - Hypertension, Thrombosis.

Other side effects are: Headache, flu like symptoms, red cell aplasia.

Did you know?

Erythropoietin was the first human hematopoietic growth factor to be isolated.

Erythropoietin was originally purified from urine of patients with severe anemia.

It is banned by the International Olympics Committee.

That's all!
-IkaN

Gap Junctions and Connexin Mutations

Let's start with a brief description of Gap Junctions. Take two empty cardboard boxes, assume they are cells. Bore a hole in each one of them and then enter a small straw in it. Then arrange the two boxes(cells) in such a way that the two straws are aligned perfectly with each other and that their cavities form a continuous column, so that if you pour water in one box it should completely go into the other one without even a single drop falling in between them.

Causes of priapism

Hello lovely medical students!

Priapism is persistent, painful erection that develops without sexual simulation.

Here are a few causes of priapism:

Prazosin
(Mnemonic: PRazosin causes PRiapism)

Trazodone
(Mnemonic: Trazodone causes a boner - TrazoBone)

Perineal or genital trauma

Neurogenic lesions

Sickle cell disease and leukemia

Always check medications first, since it is often drug induced.

That's all!
-IkaN

Medicowesome on Telegram

It's like the broadcast list on Whatsapp

https://t.me/medicowesome

Nephrotoxic antimicrobials

Hello! In this post, I'll be talking about nephrotoxic antimicrobials.

Let's start with Aminoglycosides!

Aminoglycoside toxicity manifests in the form of tubular necrosis.

Did you know AKI due to Aminoglycosides manifest 5-7 days after therapy even after the drug has been discontinued? :O

Aminoglycosides accumulate in the renal cortex and cause non oliguric AKI. Hypomagnesemia is a common finding.

Amphotericin B also causes tubular necrosis. It binds to tubular membrane cholesterol and introduces pores. Clinical findings include polyuria, hypomagnesemia, hypocalcemia and NAGMA.

Mnemonic for nephrotoxic drugs: Drugs with A!

Aminoglycosides
Amphotericin B 
Antivirals like acyclovir, tenofovir, cidofovir, foscarnet, pentamidine.
(Cause tubular toxicity)

Antibiotics like penicillin, cephalosporins, quinolones, sulfonamides, rifampin.
(Cause acute interstitial nephritis)

Remember, in acute interstitial nephritis, WBCs, WBC casts and urine eosinophils will be seen. However, in AKI, the urine sediment will show granular casts.

That's all!
The predominant feeling I have is that if gratitude (=
-IkaN

Pathophysiology of Absence Seizures

Currently, the best understood of the primary generalized seizures is the Absence Seizure(also called Petit Mal seizure).

So we will focus on it. In contrast to secondary generalized seizures, where synchronicity begins in a specific foci in the brain within an aggregate of neurons and then spreads to the entire brain; the primary generalized seizures arises from central brain regions like Thalamus and then spreads rapidly to both hemishpheres.

To understand the pathophysiology of absence seizures, we first have to be acquainted with the physiology of slow-wave(Stage 3) sleep; since they both have similar EEG reading patterns; i.e., the 3-per-second spike-and-wave activity.

In the awake state, the thalamocortical circuits are in "transmission" mode, whereby incoming sensory informations are faithfully transmitted to the cerebral cortex. Whereas in slow-wave sleep, these circuits are in"burst" mode, because of the bursting activity of a unqiue, dendritic T-type Calcium channel in the thalamus which alters the incoming sensory signals in such a way that the output signals to the cortex have an oscillatory firing rate; but no sensory information is transmitted to the cortex. Something similar happens in Absence Seizure.

In absence seizure, there is abnormal, abrupt activation of this T-type calcium channel in the awake state. This has been postulated to be due to hyperpolarizaion of relay cells in thalamus which in turn is due to increased GABAergic input from the reticular nuclei. 

Hence, drugs that block T-type calcium channels (Ethosuximide, Valproate, Lamotrigine, Clonazepam) are used in the treatment of these seizures while Barbiturates which augment the GABAergic activity in the reticulothalamic relay circuits exacerbate the condition. 

-VM

Pathophysiology of Secondary Generalized Seizures

To understand the pathophysiology of seizures in brief, lets take the following case.

“Two brothers, Ram and Shyam were playing chess. When all of  a sudden Ram noticed that his 40-year old brother seemed to be daydreaming  and seemed to be confused and having a petrified stare for about 20 seconds. Then suddenly his right hand began to bend into an awkward position and then to shake. The shaking grew worse, progressing gradually from the hand to the arm and then to the entire right side of the body. Then his body stiffened for about 15 seconds, followed by shaking movements of all four limbs that lasted another 30 seconds or so. Then he became limp and unconscious.”

1. Now here Rob first showed the symptoms of daydreaming, confusion and petrified stare, this is known as Aura. Since its a behavioural disturbance, we can guess that the foci of this seizure activity is in the temporal lobe(hippocampus, amygdala etc).

2. So there is abnormal synchronous electrical activity(ASET) somewhere in the temporal lobe which could have been due to any pathology like tumour, tuberculoma, stroke, viral encephalitis, neurocysticercosis etc.

3. It took the seizure activity 20 seconds to override the Surround inhibition  of the temporal lobe and then spread to the neighbouring areas.

4. Next there is contraction of muscles followed by shaking first in his right hand, then arm, then the complete right side. This means now the abnormal synchronous electrical activity(ASET) has spread to the left motor cortex and progressively involved the entire homunculus.

5. Next this tonic-clonic activity involves the entire body. This means that ASET has spread to the contralateral hemishphere via corpus callosum and other commissures and that it has involved Thalamus, which is the gateway to the entire cerebral cortex. Now since it is bilateral, we can call it a Generalized seizure.

6. Lets learn the mechanism of Tonic-Clonic seizure(Grand Mal seizure) activity.

A: First there is sudden inhibition of all GABAergic activity leading to overriding       of the Surround Inhibition, causing contraction of both agonist and antagonist group of muscles, referred to as the Tonic phase.

B: Then the GABA-mediated inhibition is gradually restored and while increasing it starts      oscillating with the excitatory activity mediated by Glutamate via its NMDA and AMPA receptors. If this oscillation involves the motor cortex, there is shaking movements, referred to as Clonic phase.

C: Ultimately the GABA-mediated inhibition prevails, resulting in all the muscles               becoming flaccid and the patient becomes unconscious until normal brain function is restored.   

-VM

Radiolucent stones mnemonic and uric acid calculi

Good morning! =)

I was studying about radiolucent kidney stones and thought of sharing what I learnt with you all.

Mnemonic for radiolucent renal calculi: CATIX URL
Cysteine
Adenine (2,8-Dihydroxyadenine)
Triamterene
Indinavir
Uric acid
RadioLucent

Another mnemonic for medication stones: GUEST MIC
Guaifenesin stones (Radiolucent)
Ephedrine stones (Radiolucent)
Sulphonamides stones (Radiolucent)
Triamterene stones (Poorly radiopaque)
Magnesium trisilicate stones (Poorly radiopaque)
Indinavir stones (Radiolucent)
Cephalosporins stones (Radiolucent)

If you are asked to choose the radiolucent one between Orotic acid stones and cysteine stones, choose orotic acid. It is radiolucent, cystine is poorly radioopaque.

Magnesium ammonia phosphate (struvite) and Cystine calculi are less radiodense and are more difficult to visualize. Uric acid, orotic acid, xanthine, triamterene, dihydroxy­adenine, and indinavir calculi are radiolucent and might not be seen on a plain radiograph.
(Source.)

Predisposing factors for uric acid stones:
1. Low urinary pH
2. High uric acid excretion

Treatment for uric acid stones:
1. Alkalinization of urine
(Sodium bicarbonate, potassium citrate)
2. Increase fruits, veggies. Decrease animal flesh.
3. XOI - Allopurinol, Febuxostat

Alkalinization of urine mnemonic: ABC.
Alkalinization. Bicarbonate. Citrate.
(Sodium bicarbonate and potassium citrate are used for alkalinization of urine)

That's all!
-IkaN

Study group discussion: Cold agglutinin disease and extravascular hemolysis in liver

We were discussing a MCQ from pathologystudent.

Here's the question:

On a routine physical examination of an elderly male patient with no other medical problems, you note that his earlobes and fingertips are pale and slightly bluish. A CBC shows a hemoglobin of 10.6 g/dL (12 – 16) and an MCV of 88 (80 -100). Numerous red blood cell agglutinates are seen on the blood smear, made by smart technologists in your laboratory. Which of the following statements is true?

1. The antibody bound to the patient’s red blood cells in this disorder is probably IgG
2. Complement is probably bound to the patient’s red cells
3. The spleen is the main site of red cell destruction in this patient
4. 1 and 3
5. 1, 2, and 3

1 is not true. It's cold agglutinin disease. The main antibody is IgM here.

2 is correct since complement is involved.

The main site of destruction is liver macrophages (Kupffer cells). Therefore, 3 is incorrect.

Is there a specific reason for it?

Liver RECs have loads of C3 specific receptors. So most extravascular hemolysis that occurs in cold agglutinin disease is in the liver.

Another common mechanism of hemolysis in cold agglutinin disease is direct complement mediated intravascular hemolysis.

There's C3b on RBC and macrophage has CR3 (Complement receptor 3).

Liver macrophages lack the capacity of spleen to sequester cells. Hence, here the RBC destruction in liver occurs by phagocytosis predominantly.

Thanks, Divya, for explaining this.

Tourette syndrome mnemonic

Hello!

For those who don't know -

Tourette syndrome is a disorder involving multiple motor and vocal tics, for at least a year, before 18 years of age.
Mnemonic: T for Tourette, T for Tics!

Tourette syndrome is associated with ADHD and OCD.

Mnemonic: TAO!
Tourette - ADHD, OCD.

Treatment - Antipsychotics like tetrabenazine, risperidone, fluphenazine are preferred.
Clonidine and Clonazepam maybe useful.

That's all!

-IkaN

Step 2 CK: CLL notes and staging mnemonic

Hey!

Chronic lymphocytic leukemia is proliferation of normal B lymphocytes that function abnormally.

The WBC count in CLL is > 20,000/flL with 80-98% lymphocytes.

Smudge cells are seen in CLL.

Staging of CLL mnemonic

High  LSAT score :D

Stage 0: High WBC
Stage 1: Lymphadenopathy
Stage 2: Splenomegaly + Hepatomegaly
Stage 3: Anemia
Stage 4: Thrombocytopenia

For stage 0 and stage 1, no treatment is required.

Therapy is indicated for patients with advanced stage disease, high tumor burden, severe disease-related "B" symptoms, or repeated infections.

Hepatosplenomegaly, anemia and thrombocytopenia are preferably treated with fludarabine and rituximab (FR).

For refractory cases, cyclophosphamide can be used (FCR regimen)

Older individuals (> 65 years of age) can be treated with ibrutinib, a bruton’s tyrosine kinase (BTK) inhibitor (preferred) or chlorambucil plus anti-CD20 monoclonal antibodies.

Autoimmune hemolysis or thrombocytopenia is treated with prednisone (Autoimmune warm IgG antibodies)

CLL has a good prognosis compared to other leukemias. Most common cause of death is due to infection.

That's all!
-IkaN

Bulbar and pseudobulbar palsy mnemonic

Hello! This is a mini post on bulbar and pseudobulbar palsy.

Bulbar palsy is the paralysis of the muscles supplied by the cranial nerves coming out from the bulb also known as the medulla (Cranial nerves 9, 10, 12) and it is lower motor neuron palsy.

Pseudobulbar palsy is paralysis of the same cranial nerves but the upper motor neuron type. Mostly due to lesions in the brain.

Mnemonic: pseUdo has a U for UMN lesion.

That's all!
-IkaN