Important for multiple choice questions (=
Pre-eclampsia
Post partum hemorrhage
Placental abruption
Gestational diabetes
Preterm delivery
Oligohydramnios
Growth restriction (Asymmetric IUGR, Head spared, Head abdominal ratio increased)
Still birth
-IkaN
Hey guys!!
In this post I will try to explain why Calcium gluconate is the first line drug in managing hyperkalemia.
First of all, please form a mental image of normal cardiac action potential with the-
1- Very steep phase 0 caused by Na+ influx,
[Note: Vmax is the rate of build-up of membrane potential in phase 0]
2- A short, sharp phase 1 caused by K+ efflux via Transient outward K+ channel
( and some books say Cl- influx)
3- Phase 2 plateau phase caused by Ca2+ influx and K+ efflux via slow delayed rectifier channels.
4- And finally, the downsloping, not so steep repolarization phase caused by K+ efflux via Ikr (Rapid delayed rectifier channels) and also a few other channels which you can afford to forget.
Now what changes Hyperkalemia bring in this sequence of normal action potential?
1. Initially it increases myocardial excitability by raising the RMP from -90mv to approx -75mv; hence bringing it closer to the threshold potential. This is coz of the K+ concentration gradient alteration.
2. But as Hyperkalemia progresses, it causes myocardial depression by decreasing Vmax, essentially slowing down phase 0, hence causing increase in QRS complex duration. This is because the no of Na+ channels activated decreases if RMP becomes less negative.
3. Conversely, it increases the rate of Repolarization, hence causing shortening of QT interval. This is because of a strange reason. The Ikr which I have mentioned above becomes more active if the extracellular K+ levels are high.
Now that we know what happens in Hyperkalemia, let us learn how calcium gluconate amends these changes.
1. It makes the threshold potential become less negative, thereby restoring the normal difference between it and RMP. Myocardial excitability amended!
2. It increases Vmax. Myocardial depression amended!
3. It acts on the SA node and AV node and increases their automaticity further rectifying myocardial depression.
A word of caution! In patients having Hyperkalemia due to digitalis toxicity, hypercalcemia can potentially kill the patient. So in such conditions we use calcium gluconate cautiously only if-
1. There is loss of P waves
2. Widened QRS complex.
Other treatment modalities:
1. Insulin with Dextrose
2. Beta-2 Agonists like Albuterol
Both 1 and 2 work by increasing the activity of Na+-K+ ATPase.
3. Bicarbonate. It will cause increased pH which will increase the activity of H+-K+ exchangers.
4. Haemodialysis if it's readily available
5. Ion exchange resins like Sodium Polystyrene Sulfonate along with a laxative like Sorbitol.
A question for you guys, Why is it recommended to give a laxative with an ion exchange resin? ;)
-VM
Patients with histoplasmosis who have hilar lymphadenopathy, arthralgias, and erythema nodosum can be mistakenly given the diagnosis of sarcoidosis (“pseudosarcoidosis.”)
Steroids mistakenly given for sarcoidosis can cause acute exacerbation of histoplasmosis.
Hellooo people!
After travelling from the Midbrain I we have reached the Pons.. which literally means a Bridge... So .... Let's study the important eponymous Pontine syndromes today...
1) Millard-Gubler Syndrome:
Lesion location:Pons
Structures affected: CN VII ,Corticospinal tracts!!
Clinical features: Ipsilateral peripheral facial palsy; contralateral hemiparesis ,CN VI not involved
Foville's Syndrome(Raymond-Foville) :
Lesion location:Pons
Structures affected:CN VII; lateral gaze center; Corticospinal tracts.
Clinical features • Ipsilateral facial palsy and horizontal gaze palsy; contralateral hemiparesis
Raymond's (Yelloly, Landry) Syndrome: Lesion Location: Pons
Structures affected: CN VI; Corticospinal tracts
Clinical Features: Ipsilateral abducens palsy; contralateral hemiparesis ,it is often lumped with Foville's syndrome.
There are other Pontine syndromes ...And an Anatomical classification of them makes them easy to understand !
I shall in the next post put up the respective syndromes along with associated diagrams..
Till then... Study Well Guys!
Also I would like to say... Medicine is not just science and theory but also an art to be understood.... So we all need to have the artists eyes and spot out the subtle presentations of the diseases in our patients and treat them with all our hearts!
-Medha!
Helloooo....
Well we all know about the Lhermitte’s sign... The famous Barber's Chair sign!
For the people who are reading for the first time... Lhermitte's sign is a sensation of tingling or electric shocks running down the back and legs on flexion of the neck.
Some other actions giving rise to similar sensations are: Neck rotation, arm abduction, coughing ,Yawning
It is common in multiple sclerosis, and other demyelinating diseases but can occur with other conditions involving the cervical spinal cord.
But...Some variants to Lhermitte’s sign have also been described.
1) Delayed typical Lhermitte phenomenon can follow contusion of the spinal cord from neck trauma.
2) Reverse Lhermitte phenomenon
Paresthesias induced by neck extension have been described in extrinsic compression of the cervical spinal cord.
3) Inverse Lhermitte's sign:
Upward moving paresthesias with neck flexion have been described in myelopathy from nitrous oxide inhalation.
I hope this was informative!
-Medha!😊
Following are some important signs and buzzwords that are testable ...And high yeild for entrances.
Olympian Brow: Bony prominence of the forehead caused by persistent or recurrent periostitis
Clavicular or Higoumenakia sign:Unilateral or bilateral thickening of the sternoclavicular third of the clavicle
Saber shins :Anterior bowing of the midportion of the tibia
Scaphoid scapula :Convexity along the medial border of the scapula
Hutchinson teeth:Peg-shaped upper central incisors; they erupt during 6th yr of life with abnormal enamel, resulting in a notch along the biting surface
Mulberry molars :Abnormal 1st lower (6 yr) molars characterized by small biting surface and excessive number of cusps
Saddle nose :Depression of the nasal root, a result of syphilitic rhinitis destroying adjacent bone and cartilage
Rhagades:Linear scars that extend in a spoke-like pattern from previous mucocutaneous fissures of the mouth, anus, and genitalia
Juvenile paresis :Latent meningovascular infection; it is rare and typically occurs during adolescence with behavioral changes, focal seizures, or loss of intellectual function
Juvenile tabes : Rare spinal cord involvement and cardiovascular involvement with aortitis
Hutchinson triad :Hutchinson teeth, interstitial keratitis, and 8th nerve deafness
Clutton joint :Unilateral or bilateral painless joint swelling (usually involving knees) from synovitis with sterile synovial fluid; spontaneous remission usually occurs after several weeks
Interstitial keratitis: Manifests with intense photophobia and lacrimation, followed within weeks or months by corneal opacification and complete blindness
8th nerve deafness: May be unilateral or bilateral, appears at any age, manifests initially as vertigo and high-tone hearing loss, and progresses to permanent deafness.
Well all these are late manifestations of congenital syphilis occuring after 2 years of life.
It is important to recognise these signs clinically and also on the exams...
-Medha.
Hey Awesomites
Yes, you read it right. The symptoms of psychosomatic disorders flit from one body part to another, and just too easily and quickly ( they love to travel a lot ;p ) . Just as one symptom is discovered, it disappears and another one emerges in some other part of the body.
The psychosomatic symptoms have been linked to a chameleon. Every time a medicine tries to pin them down, they become something different.
That's all
- Jaskunwar Singh
The colours of a chameleon are not more numerous and inconstant than the varieties of the hypochondriac and hysteric disease.
- Robert Whytt
Hey guys, this post will help you to remember the definitions of the four NYHA classes.
So first just remember two phrases-
"Patient with a heart disease" and "in ordinary or accustomed activities". For convenience I will use letters A and B to refer to these phrases respectively. Now I will just fill in the gap between them.
1. NYHA Class I:
A--- will not get dyspnea ---B.
2. NYHA Class II:
A--- will get dyspnea ---B.
3. NYHA Class III:
A--- will get dyspnea in less than ---B.
4. NYHA Class IV:
A--- will get dyspnea at rest.
This system of classification has its flaws since the definition of "ordinary and accustomed activities" is entirely subjective. Like for example if a rich businessman gets breathless after walking 1 km, you may label him as NYHA Class II, but the same case in a hard working labourer will have to be labelled as NYHA Class III.
And another thing that NYHA has recently clarified NYHA Class III a bit further, it has included self-care activities in it's spectrum. As a supposition, if a 56 year old male person gets breathless while shaving or bathing then it is NYHA Class III.
-VM
