Mnemonic for Caustic Esophageal injury

Hi everyone! 

Here is a short mnemonic! 

ACidic Substance = Coagulation Necrosis ( Protein denaturation) - 

results in Eschar - prevents further acid penetration & thereby severe injury.

ALakaline Substance = Liquefactive Necrosis (Cell membrane dissolution) - deeper penetration results in more severe injuries. 

1st step = Serial CXR & abdominal x-ray to identify perforation

If no perforation or respiratory distress then Upper GI endoscopy within 24 hours to assess severity for esophageal damage. 

Thank you! 

Pediatrics | Pulmonary & Critical Care | CK Uworld

PDA dependent Congenital Heart Diseases mnemonic for step 2 CK

 

 

Pediatrics Allergy & Immunology UWorld Step 2 CK

 

Conus medullaris syndrome vs. Cauda equina syndrome

Both of these are orthopedic/neurosurgical emergencies! But in general, CM syndrome is more severe than CE syndrome.

Here's a comparison between the two...

Rett syndrome notes

Hello friends!

Today we are going to learn about Rett syndrome. 

*Frequency : 1 in 15,000.

*90% of the cases are SPORADIC

*5-10% are X-Linked Dominant, so more common in females. 

(Remember males get only one X chromosome from mother whereas females get X chromosome each from mother and father).

*Mutation in gene : MeCP2.

*Virtually always seen in girls because males usually die in utero or shortly after birth.

*Important finding : Decreased pontine NE and Nigro-striatal Dopamine levels.

Clinical features : 

*At birth : Normal growth and normal head circumference.

*Normal attainment of milestones till 5-6 months of age, later there will be progressive regression of language (both receptive and expressive) and motor milestones.

*It causes Acquired Microcephaly.

*Hallmark : Repetitive hand writing movements with loss of purposeful movements.

*It can cause 5 As:

Apnea (intermittent)

Ataxia

Autistic behaviour

Arrhythmias

Acquired Microcephaly

*In addition to all of these, cyanosis, GTCS can also be seen.

*Staging :

Stage 1 : Onset stage (6-18 months)

Stage 2 : Rapid destructive (1-4 years) - 

Stage 3 : Plateau phase (2-10 years)

Stage 4 : Late motor phase (decreased motor movts) - Scoliosis can occur.

*Imaging : No pathognomonic finding. However, significant reduction on brain weight upto 60-80% is often seen.

*HPE : Decreased synapses, dendritic length and branching.

*Treatment : Supportive.

Hope it will help :)

Madhuri.

Coronary artery anatomy mnemonic and video for visualization

Let's learn about the coronary artery anatomy today (and never forget it!)

Watch the video. Text and images below.

Funnel Plot

-also called as Begg’s plot
-type of scatter plot
-used to examine biases in meta-analyses

An ideal funnel plot is symmetric.
If no biases, 95% of studies lie within the triangle.

Acute Liver Failure in a nutshell.

Acute Liver Failure is defined as the acute onset of severe liver injury with encephalopathy and ↓ synthetic function (INR ≥ 1.5 ) in a patient without  cirrhosis or underlying known liver disease.

Acute Liver Failure.

Acquired coagulopathy

Apart from congenital disorders, various clinical scenarios can give rise to altered hemostatic patterns leading to the state of so-called "acquired coagulopathy".

1.) Due to Factor inhibitors:
Classically it is seen in pregnant patients and those with lymphoproliferative disorders like CLL. However, it could be idiopathic.
Usually, it leads to the acquired factor Vlll and V deficiency.

Mixing studies are employed to differentiate between acquired and congenital factor deficiency. Failure of correction of clotting assays after mixing studies suggests the presence of inhibitors.

2.) Amyloidosis
Sequestration of Factor X by amyloid fibrils leads to an acquired deficiency-like state. Amyloid vasculopathy along with factor X deficiency often leads to purpura and ecchymosis in these patients.

3.) Myeloproliferative neoplasms
Apart from acquired vWD due to loss of HMW vWF multimers, acquired factor V deficiency can also be seen. This has been attributed to adherence of Factor V to megakaryoblasts similar to the relation between factor X and amyloid fibrils. However, severe clinical manifestations might not necessarily reflect upon clotting assays or factor levels with the latter suggesting functional factor V deficiency.

3.) Thrombotic microangiopathies and DIC
Usually leads to both thrombotic and bleeding manifestations. The spectrum of TMA includes HUS, aHUS, TTP, HELLP syndrome, DIC, cAPLA, scleroderma renal crisis, malignant hypertension, and radiation or HSCT-induced vasculopathy.

4.) Coagulopathy of liver failure
Classically seen in the setting of fulminant liver injury which may be due to the infections, drugs, autoimmune hepatitis, ischemic hepatitis/shock liver, or rarely in Wilson's disease due to massive hepatocyte destruction.
One of the hallmark lab findings includes normal factor VIII levels. This is due to the fact that factor VIII, unlike other factors, is chiefly produced by endothelial cells rather than by hepatocytes. In fact, due to its reduced metabolism by hepatocytes in the state of liver failure, factor VIIl levels are often elevated.

Other miscellaneous causes include Acute fatty liver of pregnancy, fat embolism syndrome, amniotic fluid embolism, and other pregnancy-associated complications.

- Kirtan Patolia

Mnemonic for Dawn & Somogyi phenomenon

Hello everyone....

A diabetic patient who is taking NPH insulin regularly at early evening time presents with early morning headache. He also feels very stressed & tiredness. 

I have checked that he is hyperglycemic.

Suddenly I think about Dawn & Somogyi phenomenon. But I have a confusion between that 2 terms.

So I make a mnemonic…

Here it is ..

Dawn & Somogyi phenomenon

In both Early Morning High Glucose 

= Due to ⬆️ GH & Cortisol Surge 

What is the difference ??

Treatment resistant depression notes

Hi! Quick notes for a friend :)

Treatment resistant depression: Major depressive episodes that do not respond satisfactorily to at least two trials of antidepressant monotherapy.



Things to consider:
Assess adherence
Identify comorbidities
Reassess diagnosis

Treatment strategies:
Augmentation (adding a treatment)
Switching treatment

ACCF/AHA versus ESC guidelines: Pharmacologic therapies for management of HFrEF

Hello everyone!

This video is based on the ACC/AHA guidelines from 2013 in addition to ACC/AHA 2017 update vs ESC guidelines from 2016. I recommend watching at 2x speed because I talk too slow :P

 

Work up of thyroid nodule

Hello,

Here is the shorter version of this post: Investigating thyroid nodule for Step 2 CK (link: https://www.medicowesome.com/2016/06/step-2-ck-investigating-thyroid-nodule.html)

So - if you find a thyroid nodule on physical examination - what do you do next?

WhiteBoard Summary: Lichen Planus

Hi guys, let’s talk dermatology.

Lichen Planus is a papulosquamous disease that affects skin, nails and mucous membrane, caused by cell-mediated immunity of unknown aetiology. Here’s a (not-so-white) whiteboard summary.

[Please click on the image to enhance it]

- Morphological variants can be hypertrophic, atrophic, erosive, follicular, annular, vesicular, bullous, actinic or pemphigoid.

- Lichenoid reaction can be caused by drugs (thiazides, antimalarials, penicillamine, gold) and even in Graft vs. Host disease.

- Those with steroid resistance/ intolerance are treated by hydroxyquine, methotrexate or sulfasalazine.

- Psoralens can also be used along with UV-A radiation.

- Patient education regarding self-limiting and recurrent nature of the disease is important.

- Ashish Singh

A-a Gradient

A-a gradient =[PAO2 - PaO2]
where:

A-a gradient = difference between alveolar PO2 and arterial PO2

PAO2 = alveolar PO2 (calculated from the alveolar gas equation)

PaO2 = arterial PO2 (measured in arterial blood)

PAO2 =150 - PaCo2/0.8

Normal range for A-a gradient is

10-15 mm Hg

ALL causes of hypoxemia lead to ↑ A-a gradient, EXCEPT:

Hypoventilation, high altitude, upper airway obstruction (e.g. epiglottitis from Haemophilus influenzae, or croup from parainfluenza virus)

Everything else will cause ↑ A-a gradient (e.g. shunt, V/Q mismatch, etc.).  

It's much better to remember the exceptions, then everything else becomes the rule!

Also to adjust for age, the thumb rule to calculate A-a gradient is :

Age /4   plus 4

A-a gradient >30 is considered elevated regardless of age.

Bhopalwala. H

Catheter Removal Timing

Removal — Following diagnosis of catheter-related infection, catheter removal is warranted in the following circumstances :

●Severe sepsis

●Hemodynamic instability

●Endocarditis or evidence of metastatic infection

●Erythema or exudate due to suppurative thrombophlebitis

●Persistent bacteremia after 72 hours of antimicrobial therapy to which the organism is susceptible

Source :Uptodate

Bhopalwala. H

Lung Biopsy in VAP

Lung biopsy in Ventilator-associated Pneumonia may be reserved for patients in whom infiltrates are progressive despite antibiotic therapy or patients in whom a non-infectious etiology is suspected.

The purpose of acquiring tissue under these circumstances is to identify a pathogen that may have been missed with previous sampling or a pathogen that is difficult to culture (eg, fungus, herpes viruses) or to identify a noninfectious process masquerading as infection (eg, cancer, cryptogenic organizing pneumonitis, lymphangitis, interstitial pneumonitis, vasculitis).

Source: Uptodate

Bhopalwala. H

Right to left shunt causing Hypoxemia

A right-to-left shunt exists when blood passes from the right to the left side of the heart without being oxygenated. There are two types of right-to-left shunts:

●Anatomic shunts exist when the alveoli are bypassed. Examples include intracardiac shunts, pulmonary arteriovenous malformations (AVMs), and hepatopulmonary syndrome.

●Physiologic shunts exist when non-ventilated alveoli are perfused. Examples include atelectasis and diseases with alveolar filling (eg, pneumonia, acute respiratory distress syndrome).

Right-to-left shunts cause extreme V/Q mismatch, with a V/Q ratio of zero in some lung regions. The net effect is hypoxemia, which is difficult to correct with supplemental oxygen.

The degree of shunt can be quantified from the shunt equation:

Qs/Qt  =  (CcO2  -  CaO2)  ÷  (CcO2  -  CvO2)

where Qs/Qt is the shunt fraction, CcO2 is the end-capillary oxygen content, CaO2 is the arterial oxygen content, and CvO2 is the mixed venous oxygen content. CaO2 and CvO2 are calculated from arterial and mixed venous blood gas measurements, respectively. CcO2 is estimated from the PAO2.

Source: UpToDate

Bhopalwala. H

Causes of Hypoventilation

Hypoventilation — 

The lung alveolus is a space in which gas makes up 100 percent of the contents. This means that once the partial pressure of one gas rises, the other must decrease. Both arterial (PaCO₂) and alveolar (PACO₂) carbon dioxide tension increase during hypoventilation, which causes the alveolar oxygen tension (PAO₂) to decrease. As a result, diffusion of oxygen from the alveolus to the pulmonary capillary declines with a net effect of hypoxemia and hypercapnia. Because the respiratory quotient (Defined as CO_{2 eliminated}/O_{2 consumed}) is assumed to be 0.8, hypoventilation affects PaCO₂more than O₂.

Hypoxemia due to pure hypoventilation (ie, in the absence of an elevated A-a gradient) can be identified by two characteristics. First, it readily corrects with a small increase in the fraction of inspired oxygen (FiO₂). Second, the paCO₂ is elevated. An exception exists when the hypoventilation is prolonged because atelectasis can occur, which will increase the A-a gradient . Abnormalities that cause pure hypoventilation include:

●CNS depression, such as drug overdose, structural CNS lesions, or ischemic CNS lesions that impact the respiratory center

●Obesity hypoventilation (Pickwickian) syndrome

●Impaired neural conduction, such as amyotrophic lateral sclerosis, Guillain-Barré syndrome, high cervical spine injury, phrenic nerve paralysis, or aminoglycoside blockade

●Muscular weakness, such as myasthenia gravis, idiopathic diaphragmatic paralysis, polymyositis, muscular dystrophy, or severe hypothyroidism

●Poor chest wall elasticity, such as a flail chest or kyphoscoliosis

Bhopalwala. H