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

Cataplesy and cataplexy mnemonic

Awesomite: Hi! Urgent mnemonic help. So can you tell me how I can remember this -

A case with dyspnea and blurring of vision

A 63-year-old male presented with increasing fatigability and dyspnoea for 2 months, and headache and blurring of vision for past 15 days. Physical examination was significant for pallor, mild hepatomegaly and a palpable spleen (2 cm).
Labs showed:
Hemoglobin concentration of 4.0 g/dL
Total white cell count of 25000/cmm
Platelet count of 60000/cmm
Monoclonal gammopathy (M spike) was seen in gamma globulin region, which turned out to be IgM on immunofixation.
Fundus examination revealed venous dilatation, tortuosity and superficial retinal hemorrhages.

Diagnosis? Treatment?

Tetanus are Anaerobic! Can Oxygen infusion into the wound, heal tetanus?

Think about it for a moment! Then look for the answer.

Non-Hodgkins lymphoma treatment (CHOP regimen) mnemonic

Hey!

If you can't remember the drugs used in the CHOP regimen of Non-hodgkin's lymhoma, I have a mnemonic for you.

Hodgkins lymphoma treatment (ABVD regimen) mnemonic

Hey!

If you can't remember the drugs used in the ABVD regimen of Hodgkin's lymhoma, I have a mnemonic for you.

Study group discussion: ADP fibrinogen test

What is ADP (Adenosine diphosphate) fibrinogen test?

ADP, formed by Ib receptor, acts on IIb IIIa receptor through fibrinogen and causes aggregation.

In vWD and Bernard Soulier disease (Ib defect), if you add ADP, aggregation would take place and test will be normal as it acts on IIb IIIa receptor.

In glanzmann thrombasthenia, the IIb IIIa receptor is deficient. ADP can not act on the receptor, if added. That's why, the test becomes abnormal.

Therefore, the test is normal in vWD, Bernard soulier disease and abnormal in glanzmann thrombasthenia.

Explained by Abhishek Shukla

Homocysteine metabolism notes for USMLE

Hey!

Let's do a quick and dirty Q&A post :D

Homocysteine metabolism

PATCHED: When the tonsils shows a membrane

Hello everyone.

I'm back with a simple mnemonic to deal with a questionably common but very important issue: The Patch On The Tonsil.

Difference between neuroleptic malignant syndrome and serotonin syndrome

Neuroleptic malignant syndrome:
Evolves over one to three days.
Sluggish neuromuscular responses (Rigidity, bradyreflexia)
Typical course: Mental status changes appear first, followed by rigidity, then hyperthermia, and autonomic dysfunction (Tachycardia, high BP, tachypnea)

Step 2 CK: AML (Acute myelogenous leukemia) notes

Hello! So these are my notes on AML :)

Treatment of AML mnemonic

Hi.

The mnemonic for treatment of AML is ABCD!

Fever : What questions to ask your patient and why

Fever
So we're familiar with the definition and measurement of fever. But while taking a case or interacting with a patient with this simple and most basic symptom , what all should we ask for to make sure we don't miss out on anything ?

Here's a list of things your Historytaking should elicit :

Ask for :

1. Onset and Duration.
When did the fever begin - and for how long has it lasted. (This would give a clue whether the person suffers from an Acute Febrile Illness - which can generally be attributed to Infectious Disease , or a rather Chronic form of fever which could be due to Granulomatous diseases or even Neoplastic and Autoimmune conditions )

2. Progression.
(Has it worsened or Become better since its onset. This gives a clue about the present status of the patient. )

3. Chills , Rigors , Sweat .
(It's essential to include the presence or absence  of chills+Rigors + Sweat immediately in the fever description. Presence of Chills and Rigors indicate any infectious process in the body and can be found in Malaria and UTI's among other conditions. Sweating after feeling hot and then cold  is characteristically associated with Malaria)
(Important : Presence of the B Symptoms - which are Night Sweats ; Fever ; Weight loss. Seen with Lymphomas and TB)

4. Periodicity .
(It's of extreme value to understand the pattern of the fever.
If the fever is present throughout the day with a variation of not more than 1°C it is of the Continuous Type : As seen in Enteric Fever and even UTI's .
If the fever is present throughout the day but the variation is more than 1°C it is of the 'Remittent' variety. It may not be possible to distinguish between these 2 on history alone.
Intermittent is when the fever stays only for some duration during the day and the patient is afebrile during the remaining part )

5. Diurnal variation ?
(Night rise of fever could be suggestive of Tuberculosis)

6. Associated with Rash or any Spots ?
(Viral exanthems like Dengue , Chikungunya , Zika or even Rickettsial diseases commonly present with some form of rashes)
(Another possibility could be a primary Skin condition induced fever )

7. Arthralgia , Myalgia ?   
(Arboviruses like Dengue and Chikungunya are infamous for these. Arthralgia is especially debilitating in Chikungunya fever. Body ache is also common in both. Retro-orbital pain and Bifrontal headache are common with Dengue.)

8.  Icterus , High colored urine.
(Presence of these  - especially during the post monsoon season should raise suspicion of Leptospirosis or Acute Viral hepatitis. Enteric fever may be considered)

9. Cough , weight loss?
(Presence of these should raise query of TB or Pneumonia )

10. Dysuria, urgency , frequency?
( UTI is a common cause of AFI especially in Diabetics )

11. Altered sensorium, photophobia , vomiting ?
( Characteristic of Meningitis /Encephalitis)

12. Eating outside , GI disturbances ? (Enteric fever or Gastroenteritis should be suspected )

I hope this gave a crisp summary of how a fever case can be approached . Goodbye ! Happy-Treating !
A.P.Burkholderia

Study group discussion: Why are agglutinates not seen in warm type autoimmune hemolytic anemia?

Why are agglutinates not seen in warm type autoimmune hemolytic anemia?

Because the antibody is IgG. IgG is called incomplete antibody.

RBCs have a strong negative charge on their surface called zeta potential. So the shortest distance attainable between two RBCs is 18nm. IgM molecule has a large pemtameric structure, so it has a distance of 30 nm between two binding sites. Hence, it is able to agglutinate RBCs.

But the small IgG molecule has only 12 nm gap between two binding sites. So it can't bind to multiple RBCs and hence fails to agglutinate them.

So it just coats the RBCs, which is taken to spleen to be killed.

That's all!

Thank you, Divya, for explaining this to us =)

-IkaN

Marijuana and cannabinoids intoxication mnemonic

Hey!

So in this post, imma gonna talk about what happens when you smoke weed yo.

The symptoms of marijuana intoxication are:

Munchies (Polyphagia)
Autonomic hyperactivity (Mild hypertension, dry mouth)
Racing heart (Tachycardia)
Injection (Scleral, conjunctival injection)
Judgement impaired
Uphoria (Euphoria)
Anxiety
Nystagmus
Ataxia

Treatment? Intoxication is self-limited to several hours. Interestingly, the treatment for marijuana intoxication and withdrawal are exactly the same: supportive care only.

That's all!

Don't do pot, you dope, you :P

-IkaN