Medicollabowesome: Topic of the month - Diabetes Mellitus

NPH and hypoglycemia mnemonic

Mnemonic is NPH.

Immunotherapy for Prostate cancer

Hey Awesomites

Immunotherapy is now an emerging and much promising intervention in the treatment of prostate cancer, apart from the traditional cancer treatments - chemotherapy, radiation and surgery.

Neuroblastoma mnemonic

Hello!

The term neuroblastoma is commonly used to refer to a spectrum of neuroblastic tumors (including neuroblastomas, ganglioneuroblastomas, and ganglioneuromas) that arise from primitive sympathetic ganglion cells and, like paragangliomas and pheochromocytomas, have the capacity to synthesize and secrete catecholamines.

Remember the N myc mnemonic for neuroblastoma :

N - Neuroblastoma, N myc gene
M - Crosses midline (differentiates from Wilms)
MY - MYoclonus (Opoclonus myoclonus)
C - Calcifications in tumor present
C - Catecholamine secretion

You can also remember "High BP" for additional findings seen in neuroblastoma:

Horner syndrome
Heterochromia iridis (different colors of the iris or portions of the iris)
Hypertension
Homovanillic acid and vanillylmandelic acid elevated in urine
Bombesin positive
Back pain
Bone pain
Beckwith-wiedemann syndrome association
Posterior mediastinum or retroPeritoneal mass
Pseudorosette
Purple skin lesions
Proptosis
Periorbital ecchymoses

That's all!
-IkaN

GLP-1 analogues mnemonics

Hello!

Mechanism of action of GLP 1 analogues
- Increase glucose dependent insulin release
- Decrease glucagon release

Glargine insulin mnemonic

Mini post!

Diabetes insipidus and water deprivation test

In this video I talk about pyschogenic polydipsia, central diabetes insipidus, nephrogenic diabetes inspidius, water deprivation test :)

Cortisol and eosinophils

Today, I forgot the relationship between cortisol and esosinophils. Completely screwed up a practice question because I couldn't remember it.

Now I made a mnemonic to remember this :D

Mnemonic: In hypERcortisolism, Eosinophils Reduce.

Why do corticosteroids cause eosionopenia? Why does hypocortisolism cause an increase in eosinophil count?

Dwarfism vs Cretinism

Hello Everyone,
   How do we differentiate between dwarfism and cretinism?
Just remember GIRL

G- Growth- Reduced in both
I- IQ- Normal in pituitary dwarfism and decreased in cretenism
R-Reproduction-Absent or delayed puberty in both
L-Limbs- Proportionate in Dwarfs and Disproportionate in cretins.
                (C follows D)(cretins have disproportionate limbs)

What are features seen in a cretin?
Remember 5P's

1. Pot-bellied
2. Pale
3. Puffy-faced child
4. Protruding umbilicus
5. Protuberant tongue

That's all,
Thank you,
Chaitanya Inge

Fact of the day : Testosterone administration impairs 'cognitive reflection' in men

Hey Awesomites

You must have tried solving brain teasers at some point of time.. right? Ok so how many of you tried to solve it right at that instant ( sensing your gut reaction ), but guessed it wrong? If so, you might be having loads of testosterone in your veins!

Congenital adrenal hyperplasia mnemonic

Hey, do you know a way to remember the Congenital Adrenal Hyperplasia and it's enzyme deficiencies?

It's the same mnemonic that everyone uses:

The 1 looks like an up arrow for increase

First digit for blood pressure
Second digit for sex hormones

11 hydroxylase deficiency:

1 - BP - High (Hypertension) 

1 - Sex steroids - High (Virilization in females) 

21 hydroxylase deficiency:

2 - BP - Low (Hypotension)

1 - Sex steroids - High (Virilization in females)

17 hydroxylase deficiency:

1 - BP - High (Hypertension) 

7 - Sex steroids - No increase

There was a point in my life where I forgot which digit stood for what. I have a mnemonic for that as well... It's a vulgar mnemonic.

I think of erection, first the blood goes into the corpora cavernosa and then the penis is erect. I remember the sequence of digits by - "First comes the blood, then comes the boner."
First digit - BP
Second digit - sex steroids

An easier alternative submitted by Dev:
Just remember AT
A - Aldosterone

T - Testosterone

I modified it to cat.

Meow. 

-IkaN 

Addisons disease mnemonic

Hey!
Do you have a mnemonic for adrenal insufficiency?

Cranial nerve III damage (Oculomotor nerve damage mnemonic)

Hello!

The CN III has both motor (central) and parasympathetic (peripheral) components.

Which fibers get affected in diabetes?
Which would lead to loss of pupillary light reflex?
Which fibers are compressed first?
Which would cause the down and out pupil?

Don't know? Check the video out!

C Peptide levels : An Overview

Hello everyone!So I ended up uttering 'C peptide' recently in my Medicine Viva and my professor screwed me over it.
(Clearly I didn't C it through :'D )
So I thought of doing a brief summary on it.
Here goes.

1. What is C peptide ?
- When pro- insulin is cleaved , it gives insulin and C peptide.
- C peptide in general has a longer half life than insulin and is easier to detect.
- The pathway is something like this :

Pre proinsulin produced in Rough Endoplasmic Reticulum of Pancreas --> Transported to the Golgi apparatus and cleaved to form Proinsulin -->  Packed into secretory granules --> In these granules proinsulin is converted to : Insulin and C peptide. 

- Traditionally it is said to have no intrinsic activity but recent studies say it might have anti oxidant and anti inflammatory properties.   

2. What does it indicate ?
- So , its presence indicates presence of Insulin in the body in a proportionate amount.
- Hence in a case of Hypoglycemia if C peptide levels are high, it's likely to be due to increased endogenous Insulin levels.

3. C peptide levels increased in -
- Insulinoma
- Sulfonylurea induced Hypoglycemia ( As they are Insulin Secretagogues)
- Type 2 Diabetes Mellitus ( Hyperinsulinism due to resistance)
- Insulin Resistance states like Obesity , PCOS , Cushing's.

4. C peptide levels reduced in -
- Type 1 Diabetes as Insulin secretion is reduced
- Latent Autoimmune Diabetes of Adult (LADA )
- Factitious hypoglycemia - Due to excess exogenous Insulin administration.
- Hypoglycemia due IGF secreting tumors.

So if you get a patient with Hypoglycemia with elevated insulin levels , C peptide levels help you decide if due to exogenous Insulin , or Endogenous Insulin  ( Sulfonylurea induced or Insulinoma).

Hope this helped !
Stay awesome.
Happy studying!
~ A.P Burkholderia.

Infants of Diabetic Mothers (IDM) : A clinical overview

Hello

With the prevalence of insulin - dependent diabetes mellitus and maternal hyperglycemia, serious consequences to the ingrowing foetus may occur during its organogenesis. Lets have a quick review of the clinical problems in the infants of diabetic mothers ( IDM ) with some lame mnemonics :p -

GENERAL BUILT :
- Macrosomia ( birth weight >4,000 gm ) resulting in difficult labor and complications such as traumatic asphyxia, shoulder dystocia, BP injury, etc.
- Large for gestational age

CONGENITAL ANOMALIES :-

1. CARDIOVASCULAR - mnemonic : CASTeD
- Cyanotic heart disease
- Asymmetric septal hypertrophy ( resulating in small LV )
- Septal defects ( VSD, ASD )
- Transposition of blood vessels
- Decreased cardiac output ( due to perinatal asphyxia and metabolic acidosis )

2. SKELETAL AND CNS -
- Caudal regression syndrome
- Mental retardation

3. NEURAL TUBE DEFECTS - mnemonic : HAM

- Holoprosencephaly

- Anencephaly

- Meningomyelocoele

4. RENAL and GENITOURINARY - mnemonic : HURT

- Hydronephrosis

- Urethral dysplasia

- Renal agenesis

- Thrombosis of renal vein

( patient presents with flank mass, intermittent hematuria, and thrombocytopenia )

5. GASTROINTESTINAL - mnemonic : GAS

- Gastrointestinal obstruction ( due to duodenal atresia )

- Anorectal malformations

- Small left colon syndrome

6. RESPIRATORY -
- Hyaline membrane disease ( Infantile RDS )
- Persistent Pulmonary Hypertension

7. METABOLIC changes -

- Hyperbilirubinemia ( due to polycythemia )

- Hypoglycemia occurs 30 - 90 mins post delivery which may take several days to resolve. Rebound hypoglycemia may occur in response to rapid, large boluses of glucose ( 10-15 mg/kg/min ).

- Hypocalcemia ( levels <7 mg/dL ) occurs within hours to days after birth due to a delay in PTH synthesis after birth, often accompanied with Hypomagnesemia.


Thats all
Hope this helps :)

- Jaskunwar Singh

Bromocriptine : Utility Review

Hi everyone ! Here's a brief review on the drug Bromocriptine which happens to be one of my favorite drugs. So here goes.

- Bromocriptine is a Dopaminergic agonist , specifically acting on the D2 Receptors.

- It is a very widely used drug , with various and multi systemic uses.

Uses :

1. Parkinson's disease.
- Bromocriptine and other D2 agonists like Rotigotine , Ropinirole and Pramipexole can be used to treat Parkinsonism.
- They act by providing a sort of  replacement for the depleted dopamine in the circuits of the basal ganglia.
- They are quite effective , especially in case of L Dopa resistance , or deterioration of symptoms when on L dopa.

2. Neuroleptic Malignant Syndrome.
- NMS is perhaps caused by D2 blockade due to drugs like Haloperidol and Fluphenazine.
- Thus it makes sense if you give this D2 agonist to treat this disorder.

3. Hyperprolactinemia.
- Dopamine acts as a Prolactin Inhibitory Factor (PIF) at the Hypthalamo-Pituitary level.
- In cases of Hyperprolactinemia where there is gynecomastia and galactorrhea,  giving D2 agonists counteracts the elevated prolactin levels.
- Thus it's useful in Anti psychotic/ Metoclopramide induced Hyperprolactinemia.
- Can be used in Ovulation induction due to elevated prolactin by a Pituitary adenoma.

4. Diabetes Mellitus.
- Bromocriptine modulates the Dopaminergic discharge at the Hypothalamus level.
- This modulates the circadian rhythm and resets the abnormal metabolic drive of the Hypothalamus and reduces the insulin resistance.
- The specific Quick Release formulation is used for this indication.
- It may be used in conjunction with Insulin and does not cause hypoglycemia.
- It cannot however be used for DKA

5. Acromegaly.
- Inhibits the excess Growth Hormone secretion by acting at the Hypothalamus level.

Hope this helped !
Happy studying and stay awesome!
~ A.P.Burkholderia

Pancreatic beta cell: Effect of sympathetic stimulation mnemonic

Fact of the day: High maternal cortisol good for foetal brain

Hey Awesomites

Neurodevelopment attained in the foetal period is greater than in any other period of an individual's life. Foetal exposure to "optimal levels" of maternal cortisol in third trimester has been linked to better cognitive and functional performance in the child.

Maternal cortisol acts on its receptors present in amygdala, hippocampus and the pre - frontal cortex ( PFC ) in high amounts. This hormone influences various stages of neurodevelopment including neurogenesis, axonal development, and myelination of nerve fibres and thus it leads to increased cortical thickness in frontal part of the brain and increased brain maturity.
( Source )

Thats all
- Jaskunwar Singh

Studying made simple: Ocular signs of thyrotoxicosis

Hey Awesomites

I read about ocular signs seen in patients with thyrotoxicosis. On googling and partly my work, studying these signs has become so simple to remember. -

Pathophysiology of myopathy caused during hypothyroidism and hyperthyroidism

Hello awesomites! Today's topic of discussion is - Myopathy in thyroid disease.

Interestingly, it is caused by both, hypothyroidism as well as hyperthyroidism.

What is myopathy?

It is a disease of muscle tissue where, ultimately, muscles get weak and are unable to perform work due to deficiency of ATP.

Why is there myopathy in hyperthyroidism?

The thyroid hormone is a catabolic hormone. Hyperthyroidism increases energy expenditure, glucose turnover, lipolysis, and protein breakdown (proteolysis). But here is the catch - Hyperthyroidism increases whole-body protein turnover and breakdown before any measurable changes in energy expenditure or glucose and fat metabolism, suggesting that amino acid and protein metabolism is an early and primary target for thyroid hormone action in humans. It was therefore concluded that the thyroid-hormone concentration may be an important factor in regulating muscle proteolysis. The altered protein metabolism causes myopathy.

Then, one may ask, why myopathy in hypothyroidism? Less thyroid hormone should lead to less protein breakdown, shouldn't it?

Well, this is a good question! Slightly complex and tricky to answer though. 

In hypothyroidism, there is abnormal glycogenolysis, defective mitochondrial oxidative metabolism and triglyceride storage.

Abnormal glycogenolysis and triglyceride storage: Less glucose is released and utilised because of this. The body starts using more proteins usually derived from muscles leading to myopathy.

Mitochondrial oxidative metabolism defect: Thyroid hormone is responsible for activation of bc1 complex also known as complex 3 & succinate dehydrogenase. Less activation of bc1 leads to less formation of ATP from glucose.... So again, the body switches to proteins from muscles as a source of energy!

That's all!
Stay cool :)

~Ojas