Monday, October 31, 2016

Fever : What questions to ask your patient and why

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 !

Sunday, October 30, 2016

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 =)


Saturday, October 29, 2016

Marijuana and cannabinoids intoxication mnemonic

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)

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

Step 2 CK: Treatment of narcolepsy and cataplexy

Treatment of Narcolepsy:
Patients with sleepiness severe enough to require medication can be treated with stimulant medications.

IPC and CrPC mnemonics

This post is for Indian medical students only.

IPC 319, 320, 323, 324, 325, 326, 334, 335 mnemonic


Narcolepsy mnemonic


This post is on narcolepsy.

For those who don't know, narcolepsy is characterized by:

Crown rump length and gestational sac diameter

The crown rump length in mm is calculated by subtracting 42 from the gestational age in number of days.

The gestational sac diameter in mm is calculated by subtracting 30 from the gestational age in number of days.

Friday, October 28, 2016

Step 2 CK: Treatment of bipolar disorder

For acute maniac episode:
Give antipsychotic (preferably IM) like Olanzapine, Haloperidol first because they act fast.

Long term treatment for Bipolar disorder: Mood stabilizer like lithium.

If patient is on mood stabilizer and presents with maniac episode: Give antipsychotic.

For patients who have a history of multiple recurrences or have a partial but inadequate response to a maintenance drug that is tolerated, add a second drug:

Common combinations include lithium or valproate:
- Plus  a second-generation antipsychotic, such as quetiapine, long-acting injectable risperidone, ziprasidone, or olanzapine
- Lamotrigine
- Carbamazepine

Step 2 CK: Treatment of anxiety disorders

Patient is in a panic attack:
Use benzodiazepines because they act fast.

Long term treatment for panic disorder:

Long term treatment for GAD:

Tuesday, October 25, 2016

IPC 300, 302, 307, 308 and 309 mnemonic


Here are some Indian Penal Code mnemonics :)

Study group discussion: Bradycardia

Name the causes of bradycardia!

Physiological bradycardia is seen during sleep and in athletes.

In typhoid fever, yellow fever and brucellosis, we see relative bradycardia.

Pathological bradycardia is seen in hypothermia, hypothyroidism, raised intracranial tension & inferior wall myocardial infarction, hypertension, bradyarrhythmia, etc.

What is relative bradycardia?

Indices of obesity mnemonic

Let's mnemonic-fy everything!

Saturday, October 22, 2016

Authors diary: IkaN's real name (Meaning and pronunciation of Nakeya)


IkaN from Medicowesome here!
This video and post is from the authors diary! :D

People have been asking me what my real name is and how I pronounce it so I thought of making a video on it.

There you go! :)

Wolff–Chaikoff effect mnemonic


Here's an awesome mnemonic on Wolff–Chaikoff effect sent to us by Hari!

For those of you who don't know what Wolff–Chaikoff effect is, it is a reduction in thyroid hormone levels caused by ingestion of a large amount of iodine.

Thursday, October 20, 2016

Schizophrenia subtypes mnemonic

Schizophrenia types mnemonic: CURDP

Diagnosis vs. Prognosis! Which is which?

When I was in 1st year I used to mistake these two parts of patient care very much. Let’s try to understand these concepts.

Diagnosis (Dx) – The identified disease/condition that the person has. We get to a diagnosis, after considering all the symptoms, and signs.

Prognosis – What’s going to happen in future for the patient regarding this disease.

Wednesday, October 19, 2016

Step 2 CK: ADHD treatment

Hello! This post is on the treatment of Attention Deficit Hyperactive Disorder (ADHD)!

Cognitive behavioural therapy is the first line of treatment for ADHD.

As for pharmacotherapy, FDA has approved two types of medications — stimulants and non-stimulants.

Monday, October 17, 2016

Study group discussion: Dopamine, prolactin, Parkinson's disease and Schizophrenia

A schizophrenic presents with galactorrhea. The patient’s medication regimen includes haloperidol. Blockade of which  neurotransmitters is responsible for this patient's clinical presentation?

Dopamine. Since it is a Prolactin Inhibitor - Inhibition of Dopamine causes hyperprolatctinemia.

Doubt: Level of dopamine also decreases in Parkinson's disease. So can hyperprolactinemia also be seen in Parkinson's disease?

In Parkinson's, there is loss of dopamine only in the substantia niagra.

There are 4 main dopaminergic pathways in the CNS:
1. Nigrostrial pathway which is involved in Parkinson's disease.
2. Mesolimbic pathway involved in Schizophrenia.
3. Paraventricular pathway involved in satiety.
4. Tuberoinfundibular pathway involved in prolactin secretion.

Drugs can affect all pathways, that's why, the side effects. But Parkinson's only hits the nigrostrial pathway.

Sunday, October 16, 2016

Study group discussion: Dead space

What is dead space?

Physiologic or total dead space is the sum of anatomic dead space and alveolar dead space. Anatomic dead space is the volume of gas within the conducting zone (as opposed to the transitional and respiratory zones) and includes the trachea, bronchus, bronchioles, and terminal bronchioles; it is approximately 2 mL/kg in the upright position. Alveolar dead space is the volume of gas within unperfused alveoli (and thus not participating in gas exchange either); it is usually negligible in the healthy, awake patient.

Flexion of the head decreases dead space. Why?

Flexion of head decreases anatomical dead space. Therefore, physiological dead space will also be decreased.

Neck extension and jaw protrusion can increase the dead space twofold.

Supine position decreases dead space and the dead space increases in upright position. Why?

In upright position, there is decreased perfusion to the uppermost alveoli.

Intubation decreases dead space by 70 ml approx. Why?

The size of the ET tube is smaller than the trachea. Therefore, reduction in the dead space.

Administration of bronchodilator increases dead space. Why?

The conduction zone, from the nose to the respiratory bronchioles, is dead space. Bronchodilators dilate the brochus and bronchioles and not the alveoli, increasing dead space.

Certain anaesthetics, like halothane and sevoflurane, cause bronchodilation. Hence, an important concept and MCQ.

The cause of increased dead space in general anesthesia is multifactorial, including loss of skeletal muscle tone and loss of bronchoconstrictor tone.

That's all!

Pray that my goals are completed on a timely basis. I need your prayers.


Apoptosis - Quick review

Apoptosis is ' Programmed Cell death'

It is a physiologic and a Pathologic phenomenon.

There are 2 pathways of apoptosis-
A. Extrinsic pathway- a/ w activation of caspase 8
B. Intrinsic pathway- a/w activation of caspase 9

Most striking feature- Absence of inflammation.
Earliest feature- Cell shrinkage
Most characteristic feature- Nuclear pyknosis

Friday, October 14, 2016

Diabetes Mellitus - Oral Treatment

Diabetes Mellitus (DM) is a heterogeneous group of disorders, characterised by hyperglycaemia and it's complications.

Hyperglycaemia according to American Diabetes Association is when
1. Fasting Blood Sugar level is more than or equal to 126mg/dL
2. Post prandial Blood sugar is more than or equal to 200mg/dL

The interesting part is here
DM Type 2 is either because of
i) increased glucose production by the liver ( when a person is sleeping) or
ii) impaired insulin secretion ( usually noticed after meals as insulin reserves are not sufficient or there is insulin resistance)

Let's talk of 2 scenarios,
In case i) Fasting blood glucose is high and
In case ii) Post Prandial blood glucose is high.

For case i), Metformin which is said to decrease the glucose production from liver is a better treatment option.
(Remember, Metformin also works against Insulin Resistance, so it also works in case ii !)

For case ii), since the problem is with insulin secretion or its resistance, Insulin Secretagogs work the best! Sulfonylurea increase the insulin secretion from ß cells in the pancreas, thereby tackling the problem.
Remember, Sulfonylureas are commonly used after Metformin!

If you want a super drug :P to tackle both these scenarios then Metformin and Thiazolidinediones are your best options. However, the side effect profile of the latter one is worrisome so used less often.

Here's one of my favourite quotes, Hardwork beats talent when talent doesn't work hard !
That's all!

- Rippie

Wednesday, October 12, 2016

Lights, Pokemon, Seizures!

Did you know light can induce seizures?

Photic-induced seizures — Photosensitivity has received considerable attention as a seizure trigger. The light stimulation may come from a natural or artificial source, in particular television shows and video games.

Deviation of the tongue, jaw, uvula and lips in cranial nerve palsy mnemonic

Hello! Long time no see (From my side :D )

So in this post, I'll be taking about what deviates where with a mnemonic! Yaay!
What? Jaw, tongue, lips and uvula.

Let's start with LMN lesions of the respective cranial nerves.

Tuesday, October 11, 2016

Two interesting facts.

Hey awesomites! Happened to read two interesting things today-

1. The Y sperm is relatively lighter due to the acrocentric chromosome, amounting to the relatively skewed sex ratio towards males across the globe.

2. Homeobox gene 8 controls the expression of forelimbs, messing with it causes alters the position of the forelimbs.

That's all!

Monday, October 3, 2016

Concepts vs mnemonics

"There are two ways to learn something - One is through pure logic  ie, from first principles (building up a concept). The other is mnemonics (To help retrieve info quickly... To avoid all the time and thinking taken to derive it).

The best thing is to learn both ways. If you forget the mnemonic, you can derive it from the concept. If you forget the concept, you'd at least have the mnemonic." - SG

Many people question whether mnemonics really help. This is what I have to say in explanation. Learn both like SG said. They'll help if you manage to remember, if you forget, you can use your knowledge and understanding to come to the same conclusion.

That's all!

SG is a good friend and is very philosophical on learning. These are some random thoughts that she sent and I thought of sharing them because I strongly agree!


Sunday, October 2, 2016

Transmission of toxoplasmosis

Toxoplasmosis is transmitted through:
Cat bite
Orofecal route
Cat scratch

This is a tricky question if you haven't revised parasitology. You'll vaguely remember the association with cats, so you'll be tempted to pick one which mentions the word cat.

Remember, toxoplasmosis is transmitted through cat feces, so orofecal route is the correct answer.

That's all!

Saturday, October 1, 2016