Baclofen for treatment of alcohol dependence

Hello!

Recent evidence suggest that the gamma-aminobutyric acid-B receptor agonist baclofen is a promising agent for the treatment of alcoholism.

Yep!

Baclofen produces an effortless decrease or suppression of alcohol craving. It decreases alcohol consumption including in those with poor motivation. The drug causes few side effects and does not add to the intoxication effect of alcohol.

It benefits patients with alcohol dependence (even those who are still in precontemplation stage of motivation!)

Research has shown that baclofen reduces withdrawal symptoms of alcohol and is safe in those with liver impairment.

Although further studies that compare long-term alcohol-related outcome of baclofen with established drugs such as naltrexone and disulfiram are needed.

Interesting, isn't it?

-IkaN

More than what you know about vitamins!

Hello! :)

These were the questions asked during my pharmacology vivas. And I found it fascinating after studying. I have never studied these points about vitamins before! 

Q. Which vitamin deficiency is related with lowering of seizure threshold?

Ans. Pyridoxine Vitamin B6. 

Why? As it is associated with synthesis of neurotransmitter GABA. Therefore, it is indicated during isoniazid induced convulsions. :)

Q. Why laropiprant (20mg) + Niacin (1g) is used in combination?

Ans. Nicotinic acid (a derivative) results in flushing of face.

Why? Vasodilation of cutaneous vessels.

Therefore, we combine it with specific anti-flushing drug called laropiprant.

Q. In hyperemesis gravidarum, what do you give for associated Wernicke's encephalopathy following hyperemesis? 

Ans. I thought of anti-emetics at first but the answer is vitamin B1. (Wernicke's encephalopathy doesn't always result from alcohol :P )

That's for today.
Take care. :)
-Upasana Y.

Lacunar infarction notes + mnemonic

Lacunar infarcts are small (0.2 to 15 mm in diameter) noncortical infarcts caused by occlusion of a single penetrating branch of a large cerebral artery.

Pathophysiology:
Lipohyalinosis of the penetrating arteries. (Mnemonic: L for Lipohyalinosis, L for Lacunar)
Microatheroma of the origin of the penetrating arteries.
Lacunar stroke is usually related to a chronic vasculopathy associated with systemic hypertension.

Clinical features:
Penetrating artery occlusions usually cause symptoms that develop over a short period of time, typically minutes to hours. However, a stuttering course may ensue, as with large artery thrombosis, and symptoms sometimes evolve over several days.

As a general rule, lacunar syndromes lack findings such as aphasia, agnosia, neglect, apraxia, or hemianopsia (so-called "cortical" signs). Monoplegia, stupor, coma, loss of consciousness, and seizures also are typically absent.

These syndromes are common :
● Pure motor hemiparesis
● Pure sensory stroke
● Ataxic hemiparesis
● Sensorimotor stroke
● Dysarthria-clumsy hand syndrome

Pure motor hemiparesis: Characterized by weakness involving the face, arm, and leg on one side of the body in the absence of "cortical" signs (aphasia, agnosia, neglect, apraxia, or hemianopsia) or sensory deficit.

Artery / structure involved: Posterior limb of the internal capsule.

Mnemonic: PM - Pure Motor, Posterior limb of internal capsule.

Pure sensory stroke: Numbness of the face, arm, and leg on one side of the body in the absence of motor deficit or "cortical" signs.

Artery / structure involved: Thalamogeniculate branches of the posterior cerebral artery (Ventral posterolateral and ventral posteromedial nuclei)

Mnemonic: MIST
Motor - Internal capsule
Sensory - Thalamus

Ataxic hemiparesis: Ipsilateral weakness and limb ataxia that is out of proportion to the motor deficit. Some patients may exhibit dysarthria, nystagmus, and gait deviation towards the affected side. As with other lacunar syndromes, the above-mentioned "cortical" signs are absent.

Artery / structure involved:  Fibres of the fronto-ponto-cerebellar system in the internal capsule / corona radiata.

Sensorimotor stroke: Characterized by weakness and numbness of the face, arm, and leg on one side of the body in the absence of the aforementioned "cortical" signs.

Artery / structure involved: Sensorimotor strokes arise from infarcts involving the posterolateral thalamus and posterior limb of the internal capsule. The exact vascular anatomy is debated. 

Dysarthria-clumsy hand syndrome: Facial weakness, dysarthria, dysphagia, and slight weakness and clumsiness of one hand are characteristic. There are no sensory deficits or "cortical" signs.

Artery / structure involved: Lacunar infarctions of the anterior limb of the internal capsule, genu of the internal capsule, or corona radiata.

Treatment:
Intravenous alteplase (recombinant tissue-type plasminogen activator or rt-PA) improves outcomes for patients with ischemic stroke in general if administered within 4.5 hours of symptom onset. The available evidence suggests that intravenous thrombolysis is beneficial for patients with lacunar stroke. Most patients with acute ischemic stroke who are not eligible for thrombolytic therapy should be treated with aspirin.

That's all!
-IkaN

Changes in glomerular dynamics mnemonic

Hello everyone!

If you forgot the afferent - efferent stuff from step 1, I have a mnemonic.

Remember ACE ID, PDA ANC.

Step 2 CK: Management of thromboembolic stroke

Here are my notes. The most simplified version you'll get. 

That's all!

-IkaN

So I've been questioned the most about the last point, regarding heparin. Here's the source and reading material:

There are additional situations of high thrombotic risk after ischemic stroke where anticoagulation may be beneficial but for which there are little or no data. These include mechanical heart valves, carotid artery dissection, and large artery atherosclerotic stenosis.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031793/

Drugs used to lower BP acutely in severe preeclampsia mnemonic

Drugs used to lower blood pressure acutely in severe preeclampsia (Maternal hypertensive crisis) mnemonic

"Lower Hypertension Now"

Labetalol iv preferred (Avoid in bradycardia)

Hydralazine iv

Nifedipine oral

That's all!
-IkaN

Micturition and Neurological diseases

Here, presenting you a detailed description of Pathologies of Bladder in Neurology. I believe this is the best resource on this topic available online for free. :)

Diaphragmatic hernia : Mnemonic and Review

Here's a short post on the key points about Congenital Diaphragmatic Hernia.

So there's deficiency in the diaphragm during development causing abdominal contents to budge into the Thorax.

There are 2 main types -->

1. Bochdalek.

2. Morgagni.

Now out of these 2, Bochdalek is commoner.
(It's hard to remember the word Bochdalek. I struggle with it every day. )

You can memorize it by realising that it rhymes with ' Scotch da Lake '
(Which means a lake of scotch in Punjabi)

Key points about Bochdalek -
BBBB

- Back  - Located posteriorly
- Big - Bigger than the Morgagni form
- Bad - Poor prognosis
- Bag and Mask Contra indicated. 

Also realise - Bochdalek
So it's got an L in it. L = Left. So it's more common on the left side. These hernia classically cause a scaphoid abdomen and Mediastinal shift to the opposite side.

Morgagni can be remembered by the opposite of the BBB
So it's
- Not on the back - Anteriorly
- Not Big - Small sized.
- Not as Bad - Prognosis is alright.

Also realise - Morgagni
It's got an R in it = Right. So it's more common on the right side. And it contains the Transverse colon generally.

So that's all !
Happy studying! 
Stay awesome !

~ A.P.Burkholderia 

Croup : Review of key points

Here's a short Mnemonic/Review of Important facts about Croup - Acute Tracheobronchitis !

Remember :
CROUPS

C - Common respiratory disease
R - Respiratory viruses like Parainfluenza
O - Oxygen Treatment (Humidified)
U - Ugly Cough - Barking / Seal like cough
P - Prodrome of illness followed by Inspiratory Stridor
S - Steeple sign on X Ray

It's helpful to remember Acute EPIGLOTTITIS as the complete opposite of CROUPS using similar ideas.

- Not as common.
- Caused by Bacteria generally (Strep , Hib)
- Oxygen Therapy + AntiBiotics
- Ugly - Sniffing dog like position + Drooling
- Prodrome not particularly, but Stormy acute onset.
- Shows Thumb print appearance on X Ray.

Hope this helped !
Happy Studying !
Stay awesome.

~ A.P.Burkholderia

CMS neurology form 2: Question on numbness, tingling and decreased grip strength

Disclaimer: This is an CMS neurology form 2 question for step 2 CK. If you are planning to take USMLE step 2 CK in the future, I would recommend that you DO NOT read this post because it will bias your assessments.

Differentiating C8 radiculopathy from ulnar neuropathy

Hello. This is a very short post (because I am super busy studying)

It's on differentiating C8 radiculopathy from Ulnar neuropathy based on a question I solved the other day. How would you differentiate the two in clinical practice?

C8 radiculopathy:
- Thumb abduction weakness: abductor pollicis brevis (C8, T1)

- Triceps affected (C6, C7, C8)

- Radiculopathies are often painful.

Ulnar neuropathy:
- Hand intrinsics (C8, T1) affected:
Palmar and dorsal interossei
Lumbricals III & IV
Abductor/opponens/flexor digiti minimi

- Basically, all hand intrinsics except for the median-supplied "LOAF" muscles (lumbricals I & II, opponens/ abductor/flexor pollicis brevis)

- Triceps not affected.

- Focal neuropathies aren't painful.

Conclusion: The ulnar nerve innervates all intrinsic hand muscles, except the abductor and flexor pollicis brevis, opponens pollicis, and lateral two lumbricals, which are innervated by C8 and T1 via the median nerve which helps differentiating the ulnar neuropathy from C8 radiculopathy.

That's all!
-IkaN

Pills of knowledge in Ophthalm- Anterior ciliary artery

The point where the anterior ciliary artery pierces the sclera is often marked by a pigment. This is of particular importance while cauterization as in a bid to make everything look neat and shiny, the pigmented part shouldn't be cauterized as it will cause necrosis of the structures supplied by the artery. 

Effects of Angiotensin-II on GFR

So this is a highly confusing topic. No matter how many times you read it, some amount of doubt is always there in your mind. So an advice to the readers, bookmark this post because you will be needing to read it more than once to get the drift.

First of all, let us review the effects of Angiotensin II on Glomerulus.

It constricts both the afferent and efferent arterioles but preferentially increases efferent resistance. Why? 3 reasons:

1. Efferent arterioles have a smaller diameter in their basal state.

2. Ang II stimulates the release of vasodilator NO from the afferent arteriole.

3. Ang II minimizes vasoconstriction at the afferent arteriole via the stimulation of Ang II type 2 (AT-2) receptors, which result in vasodilatation through a CYP450 dependent pathway.

The net effect of preferential rise in efferent arteriolar resistance is that the glomerular pressure is increased or stabilized(in hypoperfusion states), which helps to maintain or increase GFR. But in the long run, lots of fluid have been filtered out leaving behind the proteins which raise the colloid osmotic pressure, eventually enough to overrule the hydrostatic pressure and hence it leads to decrease in GFR.

Ang II also reduces GFR by causing constriction of the mesangial cells which reduces the effective surface area for filtration. 


-VM