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Wednesday, May 31, 2017
CMS psychiatry form 4 question on tardive dyskinesia
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
Basal LES pressure - Increases / decreases?
Peristalsis - Increases / decreases?
In scleroderma:
Basal LES pressure - Increases / decreases?
Peristalsis - Increases / decreases?
This is high yield for CK!
Tuesday, May 30, 2017
Non lactose fermenters mnemonic
Monday, May 29, 2017
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
Sunday, May 28, 2017
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.
Saturday, May 27, 2017
Authors diary: Have fun while studying
I crack really lame jokes. It keeps me sane :P
Low Weight in Cerebral Palsy : Possibilities
Hi everyone ! Here's a short post on Causes of Weight loss or Poor gain of weight in Cerebral palsy (CP) patients.
1. Feeding problems due to motor deficit -
- Patients with CP have poor feeding due to problems with sucking and swallowing. - They may have palato-pharyngeal incoordination due to the UMN lesions - especially if there's an accompanying Bulbar or Pseudobulbar palsy.
-So there's impaired oral motor control.
- Repeated aspirations may be present.
2. GERD -
- Gastro esophageal reflux is a common co-morbidity with CP.
- This can be very bothersome for the baby and reduces appetite and may even cause repeated vomiting.
3. Reliance on Care taker -
- The child cannot use his own hands to feed a lot of times.
- This causes excess reliance on the caretaker.
- The caretaker may underfeed the baby weary of the aspirations and Dysphagia of the baby.
4. Poor hygiene -
- Poor hygiene practices are more likely to cause infections (Feco-oral ).
- This is more likely to cause undernutrition due to the infective agents.
Hope this felt clinically relevant and helpful to you !
Stay awesome !
~A.P.Burkholderia
Syndromes associated with Ventricular Septal Defect : Mnemonic
Here's a short post.
So a fair bit of genetic mutations are associated with VSD's.
Remember :
ACED 2
(As in You ACED your exam ! )
A- Apert Syndrome
Features are mainly Cranio-digital. Causes Craniosynostosis, Syndactyly and mandibulo-facial deformities.
C- Cri du chat Syndrome
Notorious for the kitten like cry.
Other features are hyperagrresivenes, skin tags in front of eyes , microcephaly and wide eyes.
E - Edwards Syndrome
Trisomy 18. Other features - Omphalocele , esophageal atresia, low set ears, Microcephaly, Ptosis and Rocker bottom feet , Hypertelorism. Also associated with ASDs.
D - DiGeorge Syndrome
CATCH 22
C - CHD
A - Abnormal facies
T - thymic aplasia
C - Cleft palate
H - Hypocalcemia
22 - Chr 22 abnormality.
D - Down Syndrome
(You all know about that one !)
That's all!
Hope this helped.
Happy Studying and like always , Stay awesome !
~ A.P.Burkholderia
Friday, May 26, 2017
Medicowesome secret project : Lets talk about 'adjustments'
You will understand how I feel,
Because you might have felt it for a few moments like I feel most of the time.”
I was diagnosed with clinical depression a year back. Although the labeling never led to any improvement but it made me understand that I have a medical problem and I need help. Being from a smaller city, where everyone knew each other, where life moved at its own pace and where things were easier to understand, moving to Delhi away from my family proved stressful for me. The constant pressure to fit in, to dress, talk, sit in a particular manner and being ridiculed for being little different only made things worse. There would be days in row when I wouldn't feel like getting up, the day would stretch far too long and I wouldn't understand what exactly was I going through. I would stay awake till 4am crying with feeling of helplessness. From being the topper of my school I became one of the lowest scorers of my class. Nothing would seem to motivate me to keep going because I had already given up. Fortunately, two failed suicide attempts made me feel like seeking for help. My treatment is ongoing. People close to me understand that it's something which I wasn't in control of. Depression is something which can break you into innumerable pieces, loosen your ability to look at positivity and get up to fight back with zeal. I hope you understand. - maybe this is what someone with depression goes through (I guess). So will you help them stay strong? :)
Thanks Purnima Bhatia for sharing this story ( a part of it is hers, rest is fiction ) with us and spread awareness on the matter. :)
Ewing's Sarcoma- A review.
Common in males than females.
Types of barium-contrast imaging.
Hello everybody!
Let's quickly revise the types of Barium investigations.
So to enlist the investigations are: Barium swallow, barium meal, barium follow-through, and barium enema.
The barium swallow, barium meal, and barium follow-through are together also called an upper gastrointestinal series (study), whereas the barium enema is called a lower gastrointestinal series (study).
Procedure:
In upper gastrointestinal series examinations, the barium sulfate is mixed with water and swallowed orally, whereas in the lower gastrointestinal series (barium enema), the barium contrast agent is administered as an enema through a small tube inserted into the rectum.
Let's review individual examinations breifly:
Barium swallow X-ray examinations are used to study the pharynx and esophagus.
Barium meal examinations are used to study the lower esophagus, stomach and duodenum.
Barium follow through examinations are used to study the small intestine.
Enteroclysis also called small bowel enema is a Barium X-ray examination used to display individual loops of the small intestine by intubating the jejunum with a small tube and administering Barium sulfate followed by methylcellulose or air.
Barium enema examinations are used to study the large intestine and rectum.
Hope this was useful!
Let's learn Together!
-Medha.
Thursday, May 25, 2017
Authors' diary: How to study during Ramzaan
Wednesday, May 24, 2017
Autism and ADHD : The clinical intersection
Autism and Attention - Deficit Hyperactivity Disorder (ADHD) may co - occur in upto 80% of children and they share about 50 - 75% of their genetic factors and pathologic features, thus resulting in some clinical intersection.
NBME 7 question on muscle weakness
CMS neurology form 2 question on fibromuscular dysplasia with paresis, occulomotor palsy
CMS neurology form 2 question on headache, seizures, urinary incontinence, broad based gait
NBME 7 question on intoxication
Tuesday, May 23, 2017
Fact of the day : Pinenes for refreshing your Airways
Did you know? One of the reasons your lungs feel refreshed ( increased mental focus and energy ) when you walk through the shades of beautiful pine forest is because of an anti - inflammatory compound called alpha -Pinene, that is found in conifers. It is used as a bronchodilator in the treatment of asthma and is abundantly present in marijuana.
- Jaskunwar Singh
Pill induced esophagitis mnemonic
Pill induced esophagitis is caused by a pill! :D
Causes of pill induced esophagitis mnemonic: A PILL.
Aspirin
Alendronate
Antibiotics like tetracycline, clindamycin
Potassium chloride
Iron
Less water
Lying down immediately
Interesting anatomy correlation:
The most common sites of injury are the proximal esophagus near the compression from the aortic arch and the distal esophagus in patients with left atrial enlargement.
The typical endoscopic appearance of pill-induced esophageal injury is a discrete ulcer with relatively normal surrounding mucosa.
That's all!
-IkaN
Motor nuclei in the brainstem : An overview
2. Branchial motor efferent - 4
3. Visceral motor efferent - 4
- Sach somite gives rise to a particular set of muscles called its myotome.
So this is simple.
There are 3 pre otic somites giving rise to distinct groups of extraocular muscles supplied by their own cranial nerve.
Muscles -
All Extra ocular muscles except Lateral Rectus and Superior oblique.
Nerve -
Oculomotor nerve (III)
Nucleus -
Oculomotor nucleus in the Upper Midbrain.
Muscles -
Superior oblique.
Nerve -
Trochlear nerve (IV)
Nucleus -
Trochlear motor nucleus in the Lower Midbrain.
Muscles -
Lateral Rectus.
Nerve -
Abducent nerve (VI)
Nucleus -
Abducent motor nucleus in the Pons.
All muscles of the tongue except Palatoglossus
Nerve -
Hypoglossal I'm nerve (XII)
Nucleus -
Hypoglossal nucleus in the Medulla.
All muscles of mastication + TT (Tensor tympani + Tensor veli Palatini) + Digastric anterior belly. ( And Meckel cartilage)
Nerve -
Mandibular branch of Trigeminal
Nucleus -
All muscles of facial expressions + Stapedius + Digastric posterior belly. ( And Reichter cartilage)
Nerve -
Facial nerve (VII)
Nucleus -
Stylopharyngeus
Nerve -
Glossopharyngeal nerve (IX)
Nucleus -
- All muscles of Soft palate ( except Tensor veli which is up in the 1st arch) by the 4th. + cricothyroid muscle of Larynx.
Nerve -
4th arch - Superior laryngeal nerve of the Vagus.(X)
Nucleus -
Sphincter pupillae - Constricts pupil
Nerve -
Oculomotor nerve
Nucleus -
Lacrimal glands, nasal mucosal, sinuses mucosal glands and pharynx mucosal - Secretomotor.
Facial nerve (Greater Petrosal)
Nucleus -
Submandibular glands , sublingual glands - Secretomotor.
Facial nerve (Chorda tympani)
Nucleus -
Parotid gland
Glosspharyngeal nerve (Lesser Petrosal)
Nucleus -
Monday, May 22, 2017
Lacunar strokes : An Overview
Fact of the day: Marchiafava-Bignami disease
Marchiafava-Bignami disease is a rare disorder of demyelination or necrosis of the corpus callosum and adjacent subcortical white matter that occurs predominantly in malnourished alcoholics. Dementia, spasticity, dysarthria, and inability to walk may present as an acute, subacute or chronic condition.
Lesions appear as hypodense areas in portions of the corpus callosum on CT and as discrete or confluent areas of decreased T1 signal and increased T2 signal on MRI. Alcohol abusers without liver disease, amnesia, or cognitive dysfunction show thinning of the corpus callosum at autopsy and on MRI, suggesting that alcohol or malnutrition damages the corpus callosum commonly in the absence of the necrotic lesions of Marchiafava-Bignami disease.
Interesting, isn't it?
-IkaN
Sunday, May 21, 2017
Atrial fibrillation begets Atrial fibrillation: Explanation
Hi ! Short post on pathophysiology of Atrial Fibrillation!
- Atrial Fibrillation is a fairly common disorder of rhythm, where the atria begin to beat at random , irregular and very high rates. Like 300-600 beats / min !
- Some of these MANY contractions get transmitted to the ventricles causing an Irregular , yet High , Ventricular rate - around 100-160 per minute or even higher.
Now how this occurs is a very interesting yet much-ignored mechanism.
- Due to some pre existing factors like Rheumatic heart disease , Myocardial ischemia or Thyroid abnormalities among many others, the atria get electrically irritated and begin to fire on their own.
- These ectopic foci are common along the opening of the pulmonary veins = called the pulmonary sleeve.
This area of hyperactivity and automaticity begins to fire from the left Atrium creating a wavefront of abnormal impulses.
- Say one of these myocytes becomes ectopic one day and produces an abnormal wavefront. This wavefront progresses across the atrium and in turn stimulates the other Atrial myocytes to inturn fire ectopically -- causing formation of multiple Daughter ectopic foci.
- These daughter ectopic foci produce daughter wavelets that then propagate through the atria , in turn producing more duaghter wavefronts.
- Eventually there are A LOT of Atrial foci causing multiple wavelets to produce multiple electrical wavefronts.
- Thus A-Fib causes multiple wavefronts which in turn cause more wavefronts eventually propogating A fib as a positive feedback mechanism.
- In the long term, due to this constant irregular beating there is fibrosis and electrophysiological remodelling making the atrium more irritable and automatic.
Thus A-Fib begets A-Fib!
Hope you liked this !
Happy Studying !
Stay awesome.
~A.P.Burkholderia
Saturday, May 20, 2017
Mitral Regurgitation Begets Mitral Regurgitation : Explanation
Hi everyone ,just a short explanation of the famous phrase 'MR begets MR'.
Here goes.
And it'll pour in 130 ml into the LV.
Happy studying !
~ A.P. Burkholderia
Microbiology of Actinomyces vs Nocardia mnemonic
Hello! Let's go back to Microbiology today.
Nocardia typically appear as delicate filamentous gram-positive branching rods that appear similar to Actinomyces species.
Nocardia can usually be differentiated from Actinomyces by acid-fast staining, as Nocardia typically exhibit varying degrees of acid fastness due to the mycolic acid content of the cell wall.
Another useful clue is that Nocardia grow under aerobic conditions, whereas Actinomyces grow under anaerobic conditions.
How to remember this? Remember one mnemonic, the other one is the other one. Okay?
So let's start with nocardia.
nocarDIA. nocarDICA. ACID fast!
noCARDIA. Heart needs oxygen. Aerobic organism.
Therefore, the other one, Actinomyces is anaerobic, non acid fast.
Treatment mnemonic: PANT
Penicillin Actinomyces
Nocardia TMP-SMX
That's all!
-IkaN
Tay-Sachs disease notes and mnemonic
Plasma Proteins Mnemonic
Lets discuss plasma proteins.
1.How do we classify them?
- They are classified into Albumin, Globulin and Fibrinogen.
- Globulins are further classified into Alpha , Beta Globulins and Gamma Globulin.
- Alpha Globulin is further divided into Alpha 1 and Alpha 2 Globulins.
- Positive acute-phase proteins increase in inflammation e.g., C-reactive protein, mannose-binding protein, complement factors, ferritin, ceruloplasmin, serum amyloid A and haptoglobin.
- Negative acute-phase proteins decrease in inflammation. Examples include albumin, transferrin, transthyretin, retinol-binding protein, antithrombin, transcortin.
Friday, May 19, 2017
No cyanosis in cyanide poisoning. Why?
I was reading about cyanide poisoning today and saw "Cherry red skin" in the clinical manifestations. I know that carbon monoxide poisoning causes a cherry red color to blood. But why cyanide?
The curiosity lead to this post.
In normal cellular metabolism, most adenosine triphosphate (ATP) is generated from oxidative phosphorylation. .
Cyanide avidly binds to the ferric ion (Fe3+) of cytochrome oxidase a3, inhibiting this final enzyme in the mitochondrial cytochrome complex. When this enzyme's activity is blocked, oxidative phosphorylation ceases. The cell must then switch to anaerobic metabolism of glucose to generate ATP.
Anaerobic metabolism leads to the formation of lactic acid and the development of metabolic acidosis. Hydrogen ions produced by ATP hydrolysis are no longer consumed in aerobic ATP production, exacerbating this acidosis. Serum bicarbonate decreases as it buffers excess acid, leading to an increased anion gap.
Despite an ample oxygen supply, cells cannot utilize oxygen because of their poisoned electron transport chain. This functional (or "histotoxic”) hypoxia is particularly deleterious to the cardiovascular and central nervous systems (especially the basal ganglia).
Because of the decreased utilization of oxygen by tissues, the venous oxyhemoglobin concentration will be high, making venous blood appear bright red.
Therefore, despite hypotension, apnea, and/or bradycardia, the patient does not usually appear cyanotic in the setting of cyanide poisoning.
Clinical features:
Central nervous system toxicity is the most prominent in cyanide toxicity – Headache, anxiety, confusion, vertigo, coma, seizures.
Which should you suspect cyanide poisoning?
Victims of fires
Reported ingestions
Treatment with sodium nitroprusside
Antidote:
Hydroxocobalamin
Sodium thiosulfate
Nitrites (to induce methemoglobinemia)
That's all!
-IkaN
Thursday, May 18, 2017
CT scans and role of Contrast enhancement
Contrast enhancement and it's role in CT scan
The concept of Contrast enhancement in radiology is not new and it has been in practice even before the Advent of CT scans.
CT scan as a modality of imaging was invented by a British engineer Godfrey Hounsfield in the year 1972.
Purpose of Contrast enhancement
Contrast enhancement is a method of exaggerating the visible difference between adjacent structures on scan by administrating contrast agents.The term Contrast enhancement in CT scan includes usage of radio opaque substances for better visualization of the anatomic structures as well as better localization and characterization of the pathologies, better differentiation of the pathology from the normal surrounding structures.
Principle of Contrast enhancement
The diffusion of contrast agents from the blood stream to the body tissue is physiologically limited. In pathologies such as cancer, blood vessels grow (angioneogenesis) with increased leaking of contrast agents resulting in lesions much more visible on Contrast enhanced scans.
In CNS, contrast diffusion is limited by Blood brain barrier. Disruption of BBB lead to enhancement after administration of contrast agents.
Indications of Non Contrast CT (NCCT )
For detection of
1.Stones in kidney,ureter, cbd
2.Calcification
3. Fat in various tumors
4. Head injury
5. Acute hemorrhage
6. Stroke
7. SAH
CECT
The pathologic lesions show enhancement or attenuation depending upon the phase of contrast enhancement. So if you are looking for a particular pathology,it is important to know in which phase of CECT to look for.
For that purpose,I've enumerated the phase in which CT scan is done and can be recorded.
1. Non enhanced phase (NECT)
Uses are same as those of Ncct. Many a times this scan is done before administration of the dye to compare pre and post contrast enhancement study.
Calcification, fat in tumors, inflammation and infarction can be seen in this phase well.
2. Early arterial phase (15-20 secs post injection)
When contrast is still in the arteries, it has not enhanced the organs.
This phase is useful to look for vascular abnormalities such as aneurysms, vascular stenosis, etc
3. Late arterial phase (35-40 secs post injection)
Sometimes known as arterial phase.
All the structures that get their blood supply from arteries will show optimal enhancement in this phase.
4. Hepatic or late portal phase (70-80 secs post injection)
Liver parenchyma enhance trough blood supply by portal vein and some enhancement of hepatic veins.
5. Nephrogenic phase (100 secs post injection)
This is when all of the renal parenchyma including medulla enhances. Particularly helpful for small renal cell carcinoma which are otherwise missed.
6. Delayed phase (6-10 mins post injection) called as wash out phase or equilibrium phase
Washout of contrast in all abdominal structures except for fibrotic tissues which become relatively more dense in this phase.
Factors affecting CECT
The timings depend on
1. Organs to be scanned and focussed
2. Type of CT machine available, number of slice
3. Amount of contrast given depending upon the body weight of the patient
4. Injection rate of the contrast
5. Route by which contrast given. (Mainly IV but can be oral,rectal too)
Lesions / pathologies visualized on CECT
1. Liver tumors
Due to it's dual blood supply, 80% by portal vein and 20% by hepatic artery normal parenchymal enhancement maximally in hepatic phase . On the contrary, all all liver tumors are supplied 100% by hepatic artery. So hyper vascular tumors are best seen in late arterial phase. Hypovascular tumors on the other hand are better seen in hepatic phase.
2. Fibrotic lesions
Fibrotic lesions like cholangiocarcinoma and fibrotic mets hold contrast much longer than normal parenchyma hence best seen in delayed phase.
3. Pancreatic tumors most of them being hypovascular are seen best in late arterial phase. In cases of acute pancreatitis, late arterial phase best detects necrosis. Remember chronic pancreatitis can be very well appreciated on NCCT due to calcification.
4. Anastomosis leakage
CECT done in post op patients to check anastomosis leakage. Oral contrast play a role here for check scans done in post op bowel anastomosis.
5. Pulmonary embolism -
Good quality scans are required to delineate the emboli in the pulmonary vasculature.
6.CT angiography
For vascular studies.
Dr. Shil Pill
Diabetes insipidus and water deprivation test
Theophylline toxicity mnemonic
Chest x-ray - Left Lung.
Lingula : The tongue like extension and the alleged counterpart of the middle lobe has 2 parts to it : Superior and Inferior.
Basal lobe has 4 segments namely : Superior, Posterior, Medial, Lateral.
Basal Lobe:
Wednesday, May 17, 2017
“PILL” Esophagitis.
Hello!
Let's review a very common preventable condition of pill/drug induced esophagitis.
It is occurs due to prolonged contact of the esophageal mucosa with a medication, which acts like the damaging agent.
Medications implicated in
“pill”esophagitis are :
Tetracycline
Potassium chloride
Ferrous sulfate
Nonsteroidal antiinflammatory drugs
Alendronate.
Most often the offending tablet is ingested at bedtime with inadequate water, this leads to prolonged contact u of the drug with the esophageal mucosa leading to focal damage and esophagitis.
This causes acute discomfort followed by progressive retrosternal pain, odynophagia, and dysphagia.
Endoscopy reveals a focal lesion localized to one of the anatomic narrowed regions of the esophagus or an unsuspected pathologic narrowing.
Treatment is supportive.
Antacids, topical anesthetics, bland or liquid diets are often used.
Let's Learn Together!
-Medha.
Flow volume loop explanation video and mnemonic
I explain the flow volume loops seen in obstructive lung diseases, restrictive lung diseases, intrathoracic and extrathoracic - fixed variable obstruction in this video with mnemonics! :)
Chest X-ray - Right Lung!
Hello everybody!
So today let's go through the Right lung segments as seen on a Chest x-ray with the help of images.
This will help us identify the exact location of the pathology and the possible etiology for the same.
So the Right lung has 3 lobes.
Upper
Middle
Lower.
Let's start with the right UPPER LOBE.
It has 3 segments.
Now moving to the MIDDLE LOBE .
It has 2 segments Medial and Lateral.
Tuesday, May 16, 2017
Difference between cauda equina syndrome and conus medullaris (with mnemonics)
With mnemonics because they make life easier! (And because it is the IkaN style of doing things)
Aortic stenosis murmur explained
The systolic crescendo decrescendo murmur of AS
Early vs late systolic murmur - Which is more severe?
Why there is a soft S2 and paradoxical splitting of the second heart sound in AS?
And mnemonics! Yaay! :D
Cortisol and eosinophils
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?
Bankart's and Hill Sach's lesion mnemonic
These two lesions occuring in relation with shoulder dislocation can stump someone if asked in an MCQ as to which lesion is specifically related to which structure.
Remember the sentence-
" Sacks of money are deposited in a bank"
In a similar way, the head of humerus is 'deposited' (articulates within) the glenoid cavity.
Thus,
Hill Sach's lesion occurs on the humeral head.
Bankart's lesion occurs on the anterior glenoid labrum.
Now, how to remember whether is it the anterior or the posterior labrum?
Remember that anterior dislocation of the humeral head is the commonest occurence. That will leave no confusion.
That's all!
-Sushrut Dongargaonkar
How to interpret a Chest X-ray.
Hello everybody, so today's post will be a little long so kindly bear with me.
I hope that this post helps you and makes interpretation of an x-ray less daunting and more fun.
So let's get started.
Step 1:
Always place the x-ray in a such a way so that it seems you are facing the patient.
So naturally this is only possible with AP(Anteroposterior) and PA (Posteroanterior) views.
The technicians mark the X-ray indicating the side but chest x-rays are sort of independent of side markers due to the position of the left ventricle and the aortic knuckle.
Step 2:
To interpret a chest x-ray you need to think in layers as in from outside-in or from inside-out, with one type of structure at a time.
Do a targeted search rather than just staring at the radiograph, an abnormality is unlikely to strike unless you look for it in a planned manner.
Your eyes should scan each part of the film and one should always look twice in the regions where mistakes are more likely, like the Apices in a PA view and the region over the spine in a lateral view.
Step 3:
Scan the whole radiograph in a sequence:
Identify AP or PA view.
Check for side markers.
Radiographic exposure.
Check for integrity of bony cage.
Begin with lung Apices.
Upper middle and lower zones.
Check the Cardiophrenic angles.
Mediastinal structures.
Soft tissues.
Step 4:
Then Detect the lesion : Where is the lesion and what structures are affected by it. Starting with
Trachea and Bronchi:
Position,shift and deviation.
Mediastinal Lines:
Paratracheal stripes: visible or lost.
Aortopulmonary Window: Fullness or normal.
Paraspinal Lines: bulging or normal.
Hilum and Cardiac prominences, and see cardiogenic or mediastinal cause for the prominence.
Lungs :
Check for the Lung Volumes, Right or left lung densities,Diffuse lung abnormalities.
Whether the lesion is Pulmonary or Extrapulmonary. If pulmonary whether it is focal or diffuse.
Pleura and Fissures : Check for pleural effusion and pleural based masses.
Bones :
Focal injuries
Rib fractures, Notching.
Shoulder girdle and clavicles .
Step 5:
Directed search in an apparently normal chest x-ray.
Lungs :
See the Hidden lung areas like retrocardiac and retroclavicular areas.
Also check for Pulmonary Embolism.
Mediastinum : Check for the Posterior mediastinal masses and hilar masses.
Step 6:
Describe the Lesion :
Location and Extent of the lesion.
Characteristics in the form of :
Shape
Homogeneity
Calcification
Necrosis
Associated features of trachea, lungs fissures etc.
Step 7:
In the end.
Put up a provisional diagnosis.
Differentiate from the closer/similar diagnoses.
Put up a final diagnosis.
A breif description on the Management.
Viola! We are through our way describing a chest x-ray!
Reading any radiograph has its learning curve and the more we see the more we learn.
Try and describe all the radiographs you see hence forth in the manner mentioned above or anyway you like it but follow a definite protocol and don't miss any important points.
I hope this post was helpful.
Let's Learn Together!
-Medha.
Monday, May 15, 2017
A neonate with cyanotic heart disease (Case #2)
Similar to the case we discussed last time (A neonate with cyanotic heart disease #1), let's narrow our differential.
Step 2 CK: Immunization schedule in the US mnemonic
I did not create the mnemonic, I just created the table to put it all together for quick revision :)
Sunday, May 14, 2017
Why some people hate cheese!
Hello everybody!
So today let's learn a bit about how our brain circuits work.
Some people hate cheese. Like seriously?
How can you miss the warm fussy feeling you get while eating warm molten cheese in a Fondue!
Well some people might not feel any bit of it and rather feel disgusted when presented with cheese.( I feel bad for them )
Anyway let's see how these things work.
Why aversive to cheese per say?
Cheese is the food that most frequently triggers aversion.
Among those with an aversion to cheese, 20% say they are intolerant to lactose. In 50% of cases, at least one of their family members does not like cheese either. These stats suggested that there is a genetic origin to this aversion, which might be related to lactose intolerance.
To find out what happens in the brain, people who like cheese and who do not were selected and participated in a functional magnetic resonance imaging (fMRI) study.
They observed that the ventral pallidum which is activated in people who are hungry was totally inactive in people who had an aversion to cheese but was active for all other food types. Also the Globus Pallidus and Substantia Nigra part ( the reward circuit) was more active in people who had aversion to cheese than in those who do.
So in conclusion, the areas of reward centres of our brain the Globus Pallidus and Substantia Nigra have two types of neurons with complementary activity , one relating to the rewarding aspect of food and other to it's aversive nature.
So now we have a breif idea as to how the brains are wired differently and how we all our special in our own ways!
Let's learn Together!
-Medha.
Femoral Nerve Mnemonic
Lets discuss Femoral nerve today. Doesn't femoral nerve sound feminine? Also I am writing this post on Mothers Day, what a coincidence!
Root value: L2-L4
(Ladies work 24 hours.)
Motor innervation:
It innervates following muscles:
- Anterior division branches innervates
- Sartorius
- Illiacus
- Pectineus
- Posterior division branches (innervates Quadriceps femoris)
- Rectus femoris
- Vastus medialis
- Vastus lateralis
- Vastus intermedius
How to remember it? @_@
Queens hardly get time to SIP coffee ^_^
Sensory innervation:
Anterior division branches provides sensation to anteromedial asepct of the thigh, consists of 2 branches:
- Medial cutaneous nerve of thigh
- Intermediate cutaneous nerve
Posterior division:
- Saphenous nerve : provides sensation to anteromedial aspect of lower leg.
- Infrapatellar branches to knee :pierces the sartorius and fasica lata medial to the knee, and provides cutaneous innervation to the skin anteriorly over the patella.
Monteggia and Galeazzi fracture mnemonic
One can get confused on hours end as to what fracture is related to what bone. Hope this mnemonic comes in handy!
1. MUFC( Manchester united fan club)
- Monteggia upper ulnar fracture
With radial head dislocation
2. GFR low(Glomerular filtration rate)
- Galeazzi fracture radial, lower
With distal radio ulnar subluxation
That's all!
-Sushrut Dongargaonkar
Laughter Disorders - It might not be funny!
ranging from genuine and spontaneous to simulated (fake), stimulated (tickling), induced (by drugs) or even pathological.