Step 2 CK: Psychiatry tip for possible depression questions

Hello! 

Whenever I come across a possible major depression question, I write SIGECAPS (full form at the end of the post) down and strike out the alphabets as and when I come across the symptoms.

For example, weight loss - strike out A for appetite change, fatigue because staying up at night - strike out S for sleep change, E for loss of energy.

Then re-read the stem and see for symptoms I missed out due to twisted wording (she stopped singing a month ago - strike out I for loss of interest)

It REALLY helps in figuring out 5/9 SIGECAPS for diagnosis of MDD because if you are not actively looking for the symptoms in the question stem, you'll miss them out. Also, if you are not counting, you might wrongly over diagnose MDD.

Writing it down also saves time because you don't have to keep re-reading the stem over and over.

It also helps getting the count right because if you have already striked out an alphabet, you can't strike it out again. So you won't get the count wrong for possible rephrasing of the same symptom in the question stem. (patient says she has lost appetite, there is weight loss - it is one alphabet in SIGECAPS, so you can't strike A out again - you will get the symptom count right!)

That's all!

I've read so many comments by students in forums where people get MDD wrong just because they didn't see the obvious 5/9 SIGECAPS. Don't miss it out guys, it's very easy to diagnose with this trick! :)
Hope that helps!

-IkaN

For those who don't know what SIGECAPS stands for :

S: Sleep changes: Increase during day or decreased sleep at night

I: Interest (loss): of interest in activities that used to interest them

G: Guilt (worthless): Devalue themselves, feel guilty

E: Energy (lack): common presenting symptom (fatigue) 

C: Cognition / Concentration: Reduced cognition &/or difficulty concentrating

A: Appetite (weight loss): Usually declined, occasionally increased

P: Psychomotor: Agitation (anxiety) or retardations (lethargic)

S: Suicide / preoccupation with death

Originally when a physician would write a prescription, the abbreviation “SIG” would be written which was to mean directions. The "E" CAPS was to remind the prescriber to write “Energy” capsules for depression (antidepressants).

Hence:  SIG:  E. CAPS

Therapist near me, BetterHelp

GLP-1 analogues mnemonics

Hello!

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

Motor Neurone Disease : Why and How to rule it out.

Hi everyone ! Here's a short post on How and why to rule out Motor Neuron diseases.

Motor Neurone Disease includes a group of conditions where the Motor Neurons of your body begin to degenerate.
If these neurons are located above the level of the Alpha motor neuron of spinal cord , the result is UMN lesions , like Primary Lateral Sclerosis.
If the degeneration occurs in the Alpha motor neurons themselves , the result is LMN type paralysis, like Spinal Muscular Atrophy..
A combination of the two - UMN + LMN features as seen in - Amyotrophic Lateral Sclerosis.

Now a few set of conditions are used as a way to exclude to MND.
MND itself isn't very common , and carries an extremely poor prognosis. Treatment options are extremely limited. So it's important to rule it out whenever you come across a Paraplegia , Quadriplegia, Bulbar or Pseudobulbar palsy patient .

An MND has No COBS.
C - No Cognitive changes
O - No Ocular motility involvement till late.
B - No Bladder bowel involvement till late.
S - No Sensory involvement.

There are a few exceptions to this -
Cognitive changes can be present if it's associated with Fronto temporal dementia. A lot of the familial cases are associated with this.

Behavorial changes can also be seen in a Pseudobulbar palsy patient. (More on that some other day !)

Sensory involvement may be seen in Hereditary spastic paraplegia - a variant of MND.

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

~ A.P.Burkholderia.

Clonus - A review.

Hello everybody!
Let's review Clonus breifly today.

So what is it?
It is a series of rhythmic involuntary muscular contractions induced by the sudden passive stretching of a muscle or tendon.

Clonus occurs most frequently at the ankle, knee, and wrist, occasionally elsewhere.

The important Clonus that we all frequently examine is the Ankle Clonus so let's see that in detail here.

Ankle clonus is a series of rhythmic alternating flexions and extensions of the ankle.

How to do it?
The leg and foot should be well relaxed, the knee and ankle in moderate flexion, and the foot slightly everted.
The examiner supports the leg, with one hand under the knee or the calf, grasps the foot from below with the other hand, and quickly dorsiflexes the foot while maintaining slight pressure on the sole at the end of the movement.
A single tap on the tendon to elicit the ankle jerk may occasionally provoke clonus.

Unsustained clonus fades away after a few beats; sustained clonus persists as long as the examiner continues to hold slight dorsiflexion pressure on the foot.

Unsustained (transient) symmetric ankle clonus may occur in normal individuals with physiologically fast Deep Tendon Reflexes. Nonorganic clonus occurs rarely. False clonus (pseudoclonus) in psychogenic disorders is poorly sustained and irregular in rate, rhythm, and excursion.

Sustained clonus is never normal. In severe spasticity, clonus may occur spontaneously or with the slightest stimulus. At the ankle, true clonus can usually be stopped by sharp passive plantar flexion  of the foot or the great toe; false clonus is not altered by such a maneuver

Mechanism:
Part one - For ankle clonus, the sudden stretch of the gastrosoleus muscle elicits a contraction essentially analogous to a stretch reflex that causes a contraction with resultant plantar flexion of the foot. The foot goes down. 
Part two - This contraction increases tension in the Golgi tendon organs in the gastrosoleus tendon, sending a volley of impulses via the Ib fibers that then inhibit the contraction of the gastrosoleus and facilitate contraction of its antagonist, the tibialis anterior muscle.  The foot goes up. 
This in turn passively stretches the gastrosoleus, and the cycle is repeated.

A simpler explanation is alternating stretch reflexes.

A few other Clonus' seen are :

1) Patellar clonus :
It consists of a series of rhythmic up-and-down movements of the patella. It may be elicited if the examiner grasps the patella between index finger and thumb and executes a sudden, sharp, downward thrust, holding downward pressure at the end of the movement. 

The leg should be extended and relaxed. Patellar clonus may appear when eliciting the patellar or suprapatellar reflex.

2) Wrist Clonus :
It is produced by a sudden passive extension of the wrist or fingers.

3) Jaw Clonus occurs occasionally.

So that's all about clonus.
Hope it was helpful!

Let's learn Together!
-Medha!

Alternate methods of Eliciting Toe Dorsiflexion in Corticospinal tract lesions.

Hello!

Let's review few minor signs of eliciting toe dorsiflexion when we are suspecting  a Corticospinal tract lesion.

Gordon’s sign :
Squeezing of calf muscles.

Schaefer’s sign :
Deep pressure on Achilles tendon.

Bing’s sign :
Pricking dorsum of foot with a pin.

Moniz’ sign :
Forceful passive plantar flexion at ankle.

Throckmorton’s sign :
Percussing over dorsal aspect of metatarsophalangeal joint of great toe just medial to Extensor Hallucis Longus tendon.

Marie Foix sign :
Squeezing the toes or strongly plantar   flexing toes or foot.

Gonda (Allen) :
Forceful downward stretching or snapping of second, third, or fourth toe; if response is difficult to obtain, flex toe slowly, press on nail, twist the toe, and hold it for a few seconds.

Stransky :
Small toe forcibly abducted, then released.

Allen and Cleckley :
Sharp upward flick of second toe or pressure applied to ball of toe.

Strümpell’s  phenomenon :
Forceful pressure over anterior tibial region.

Cornell response :
Scratching dorsum of foot along inner side of Extensor Hallucis Longus tendon.

All the above signs may not be always seen and sometimes these may be the Only signs present and hence it is necessary for us as students to screen as many patients as we can and increase our understanding and clinical acumen, cause the eyes can't see what the brain doesn't know.

Let's learn Together!
-Medha.

Tetralogy of fallot mnemonic

Hello!

Here is a short note on tetralogy of fallot. Tetralogy of fallot is a congenital disorder of heart. It shows four signs, as indicated in it's name (tetra).

Mnemonic for it is - PRVO virus ( parvo virus )

1. Pulmonary stenosis
2. Right ventricular hypertrophy
3. Ventricular septal defect
4. Overriding of aorta.

That's all :)

H@Mid.

Ano-Rectal anatomy: Above and below pectinate line

Here's an illustration I made :)

It shows the embryology, pathology, innervation, blood supply, venous drainage and lymphatic drainage on the rectum above and below pectinate line.

Examination of Subtle Hemiparesis - Barré's Sign.

Hello everybody!

So today let's learn about examination of subtle hemiparesis, a very important inspectory finding.

Sometimes patients with mild CST (Corticospinal Tract) lesions may have normal strength to routine testing, but the deficit may be brought out using ancillary maneuvers like the examination for pronator drift (Barré’s sign).

With the patient’s upper extremities outstretched to front, palms up and with the eyes closed, we have to observe the position of hands.
Normally patient should hold this position for at least 20 to 30 seconds and the palms will remain straight with the elbows straight, and the limbs horizontal.

Any deviation from this position should be similar on the two sides.

(One exception to the usual symmetry is that the dominant hand occasionally may pronate slightly more than the nondominant, perhaps because the nondominant extremities tend to be more flexible than the dominant extremities, making it more difficult to stretch the dominant hand to a horizontal position.)

However, greater pronation of the nondominant arm is sometimes an indication of subtle hemiparesis.

Three types of drifts may occur when the patient attempts to hold the arms outstretched with eyes closed: pyramidal drift, parietal drift, and cerebellar drift. In pronator drift (Barré’s sign) due to a pyramidal lesion, the arm sinks downward and there is accompanying pronation of the forearm.

In parietal drift, the arm usually rises and strays outward (updrift).  

With cerebellar drift, the arm drifts mainly outward, either at the same level, rising, or less often sinking.

The patient with a mild CST deficit may demonstrate “pronator drift” to varying degrees.

Mild drift : there is slight pronation of the hand and slight flexion of the elbow on the abnormal side. 

Severe drift : there is more prominent pronation and obvious flexion of the elbow, and there may be downward drift of the entire arm.

Mechanism: Because of the innervation pattern of the CST, the minimally weak CST innervated muscles are overcome by the non-CST muscles.

With a mild CST lesion, the minimally weak muscles in the upper extremity are the extensors, supinators, and abductors.  These are overcome by the uninvolved and therefore stronger muscles: the pronators, biceps, and internal rotators of the shoulder. As these overcome the slightly weakened CST innervated muscles, the hand pronates, the elbow  flexes, and the arm drifts downward.

The tendency to pronation and flexion in mild hemiparesis has also been attributed to subtle hypertonicity in the pronator and flexor muscle groups.

Imagine what would occur if this motion continued to the extreme: the hand would become hyperpronated, the elbow fully exed, and the shoulder internally rotated, that is, the position of spastic hemiparesis.

The abnormal upper limb positions in minimal pronator drift and in severe spastic hemiparesis are due to the same underlying phenomenon: strong non-CST muscles overcome variably weak CST muscles involved by the disease process.

The examination for pronator drift is a very important part of the neurologic examination. If only one motor test could be done on a patient, the best single test to use would probably be examining for drift.

Hope this was informative!
Let's learn Together!
-Medha.

Glargine insulin mnemonic

Mini post!

Pathophysiology of anorexia in chronic kidney disease

Normal appetite regulation: Appetite regulation involves the gastrointestinal tract (ghrelin as an appetite stimulant, and cholecystokinin, glucagon-like peptide-1, and neuropeptide YY as appetite inhibitors); the adipose tissue with leptin, a potent appetite inhibitor; the vagal system; and the brain, which integrates the stimuli in the hypothalamus area. Satiety relies on the melanocortin receptors with serotonin as the main neurotransmitter and is challenged with hunger peptides, namely, neuropeptide Y and agouti-related peptide.

What happens in CKD?

Pharmacotherapy for PTSD in pregnancy mnemonic

The two FDA approved drugs for PTSD are: Paroxetine and Sertaline.

Fact of the day: Valbenazine for treatment of tardive dyskinesia

Here's a cool fact: Valbenazine is a highly selective vesicular monoamine transporter 2 (VMAT2) inhibitor. It modulates dopamine release during nerve communication.

CMS psychiatry form 4 question on tardive dyskinesia

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.

Tetrology of Fallot Causes : Mnemonic and discussion

Hello everyone !

Tetrology of Fallot refers to the tetrad of features occuring in the heart -

1. Ventricular septal defect
2. Pulmonary stenosis
3. Right Ventricular Hypertrophy
4. Overriding aorta.

Now. The factors associated with this disease include a decent bit of things.  And while I was revising I remembered I didn't remember them at all. :) :) :) :) :)

-_-

So here's a mnemonic.
CATCH NATE

CATCH = CATCH 22 Syndrome
(DiGeorge Syndrome is represented by CATCH 22 popularly).

N - NOTCH 1 Gene mutations.
A - Alagille syndrome - Associated with a very peculiar set of features - Bile duct hypoplasia. So random .
T - Trisomies 13,18,21
E - Et cetera = Maternal Diabetes , Maternal progesterone , Drugs like Retinoic acid.

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

Step 2 CK: Manometric findings of achalasia and scleroderma

In achalasia:
Basal LES pressure - Increases / decreases?
Peristalsis - Increases / decreases?

In scleroderma:
Basal LES pressure - Increases / decreases?
Peristalsis - Increases / decreases?

This is high yield for CK!

Cauda equina syndrome

Hello!

What is cauda equina syndrome (CES)?
The cauda equina syndrome is caused by an intraspinal lesion caudal to the conus that injures two or more of the 18 nerve roots constituting the cauda equina within the lumbar spinal canal.

Cauda equina syndrome causes

Non lactose fermenters mnemonic

Shigella, Salmonella, Proteus, Yersinia - Motile or non motile? produces H2S or not?

Step 2 CK: Oral contraceptive pills and cancer

Hello!
Back with a mini post!

Wifi-allergy !

Now,being teenager we all know how much we are addicted to word "Wi-fi" or let's say  "Free Wi-fi".But today I came to know about a weird disorder "Wifi-allergy" .

Electromagnetic hypersensitivity is popularly known as "Wifi-allergy".
Adverse reaction to electromagnetic field is seen even if a victim is exposed to EM field below threshold level .
There are no scientific basis for Wi-fi allergy .

No scientific signs and symptoms are specified,but non-specific symptoms such as headache,fatigue,stress,sleep distractions,skin prickling,burning sensation,rashes pain,and acne in muscles,ringing in the ear,tinnitus,unexpected earache,memory loss,inability to concentrate,nausea,insomnia,fluctuation in heart rate,deteriorating vision,weakness and spasm of muscles,
bladder problems can develop.

Many of these symptoms overlaps with other syndromes such as Idiopathic Environmental Intolerance(IEI)

Cause:

No relation is found between exposure of electromagnetic field and symptoms.Studies shows it is a psychological disorder rather than a physiological .Many scientists claims that it is actually a nacebo effect.

Diagnosis:

Electromagnetic hypersensitivity is not an accepted diagnosis.No case definition /clinical practice guidelines are performed.No specific tests are performed.A French scientist Dr Belpomme has developed a technique using a computer and a Pulsed Eco-doppler which envelops diagnosis of electrical sensitivity.

Treatment:

There are no specific protocols for treatment of this psychological disorder.The basic treatment involes less use of devices which emits electromagnetic fields.

Stay awesome and cool:)
 
~Ojas

Lesions of the Central Nervous System.

Hello everybody!

So today we'll review a series of lesions and their presentation starting from the cortex till the spinal cord.

Will try and include as many lesions as I can without making it redundant or boring.

To start with.

1)Disorders of the Meninges and Ventricular System.

Many conditions can affect the meninges, like infections, neoplasia, sarcoidosis.The most common being infections.

Some meningeal infections may be extremely indolent and lack the classical signs associated with infection.
Chronic meningitis can also present as dementia or AMS.
Abnormalities of the ventricular system can occur due to congenital anomalies, such as aqueductal stenosis leading to dilatation of the ventricular system and may cause increased head circumference in children.
In adults, acquired conditions, such as normal pressure hydrocephalus usually present with evidence of increased intracranial pressure or with dementia, AMS, gait problems,difficulty with bladder control. The classic triad of Normal pressure hydrocephalus is - WET WHACKY WOBBLY.

2)Cerebral Hemisphere Disorders. Characteristic of unilateral hemispheric pathology is a “hemi” deficit.
Hemisensory loss,
Hemiparesis,
Hemianopsia,
Hemiseizures.

Other manifestations are hyperreflexia and pathologic reflexes.

Disease affecting the cerebral cortex behave differently from disease of subcortical structures.

Cortical involvement:
Aphasia,
Apraxia,
Astereognosis,
Impaired two-point discrimination, Memory loss,
Cognitive defects,
Focal seizures, or other abnormalities that reflect integrative role of the cortex.

Dominant hemisphere involvement:
Language dysfunction in the form of aphasia, alexia, or agraphia. 

Non dominant hemisphere involvement:
Higher cortical function disturbances involving functions other than language, such as apraxia.

Subcortical structures :
The clinical picture includes the hemidistribution of dysfunction but lacks those elements that are typically cortical (e.g., language disturbance, apraxia, seizures, dementia).

Certain processes involve wide areas of the cerebrum, causing diffuse dysfunction.

3) Basal Ganglia Disorders:
Diseases of the basal ganglia cause movement disorders such as Parkinson’s disease (PD) or Huntington's Disease. Movement disorders may be hypokinetic or hyperkinetic, referring to whether movement is in general decreased or increased.
PD causes bradykinesia and rigidity. Huntington’s disease, in contrast, causes increased movements, which are involuntary and beyond the patient’s control (chorea).  Tremor is a frequent accompaniment of basal ganglia disease.

4)Brainstem Disease: (So I have a  separate blog on these do check them out,where I have enlisted individual syndromes.)

The classic distinguishing feature of brainstem pathology is that deficits are “crossed,” with cranial nerve dysfunction on one side and a motor or sensory deficit on the opposite side.

There are often symptoms reflecting  dysfunction of other posterior fossa structures, such as vertigo, ataxia, dysphagia, nausea - vomiting, and abnormal eye movements.

Unless the process has impaired the reticular activating system, patients are normal, mentally awake, alert, able to converse (though perhaps dysarthric), not confused, and not aphasic. 

DeepTendon Reflexes are usually hyperactive with accompanying pathologic reflexes in the involved extremities; pain is rare untill Thalamus is involved and sphincter dysfunction occurs only if there is bilateral involvement.

5) Cranial Neuropathy Disease :
Selectively involve one, or more than one, cranial nerve.
The long tract abnormalities, vertigo, ataxia, and similar symptoms and findings that are otherwise characteristic of intrinsic brainstem disease are lacking.

Common cranial neuropathies include Optic neuropathy due to MS,
Third nerve palsy due to aneurysm
Bell’s palsy.
Involvement of more than one nerve occurs in conditions such as Lyme disease, sarcoidosis, and lesions involving the cavernous sinus

6)Cerebellar Disease:
Leads to combinations of tremor, incoordination, difficulty walking, dysarthria, and nystagmus, depending on the parts of the cerebellum involved. 

There is no weakness, sensory loss, pain, hyperreflexia, pathologic reflexes, sphincter dyscontrol, or abnormalities of higher cortical function.

Cerebellar abnormalities resulting​ from dysfunction of the cerebellar connections in the brainstem, usually are accompanied by other brainstem signs.

7)Spinal cord disorders:
Produce characteristic patterns of clinical abnormalities, with motor and sensory deficits in a certain distribution.

In addition to weakness below the level of the lesion, patients with spinal cord lesions also have paresthesias, numbness, tingling, and sensory loss with a discrete sensory level, usually on the trunk.

The pattern of weakness is typically more localizing than sensory abnormalities in lesions of the cervical spinal cord, while demonstration of a sensory level on the trunk is more helpful in localizing lesions of the thoracic cord.

Some important findings depicting the syndromes are :

Dorsal cord syndrome : Loss of position and vibratory sensation in the feet with preserved ankle jerks.

Central cord Syndrome (syringomyelia) :
Bilateral segmental sensory loss (i.e., sensory loss in the hands and forearms), not in a peripheral nerve distribution, with normal sensation in the legs and trunk and in the upper arms and neck.

Thoracic Cord Syndrome : Bilateral loss of position and vibratory sensation in the feet with a definite level of pinprick loss on the abdomen or chest.

Brown-Séquard syndrome : Loss of pinprick sensation on one side of the body with loss of position and vibration sensation on the other.

Intramedullary lesion or anterior extramedullary compression :
Loss of pinprick sensation over the legs and trunk with normal sensation in the perianal area.

Conus medullaris or L5–S1 cauda  equina lesion:
Loss of pinprick sensation in the perianal area and in the upper part of both posterior thighs.

Anterior Cord Syndrome :
Loss of pinprick sensation on the legs and trunk with normal position and vibration sense in the toes and fingers.

Phew😅 that was alot.
I hope this was helpful.
If you have any doubts or you need a detailed explanation of some part, do let me know.

Let's learn Together!
-Medha.

Authors diary: Have fun while studying

If you are not having fun while studying, you are doing it wrong.

I crack really lame jokes. It keeps me sane :P