Mitral Regurgitation Begets Mitral Regurgitation : Explanation

Hi everyone  ,just a short explanation of the famous phrase 'MR begets MR'.
Here goes.

- Mitral Regurgitation is a disease where the mitral valve is incompetent or insufficient and leaks or pukes when it should be shut. (Rather like a blithering idiot who keeps talking at the wrong time. =}. )

- So it allows the blood to puke back into the Left Atrium from the Ventricle during systole.

- So assume - 100 ml of blood would flow into LV from the LA normally which the LV would pump into the Aorta.

- Now because of the weird and incompetent valve , the LV can pump only like 70 ml into the Aorta and the rest of the 30 ml goes back into the LA.

- So now the LA volume is 30 ml + 100 ml
And it'll pour in 130 ml into the LV.

- So effectively, the LV has an overload of volume in it and over a period of time it would undergo Dilatational changes and increase in size.

- As the Ventricle increases in size , the mitral valve apparatus is stretched all the more.

-This is because the mitral valve is attached to the Ventricular myocardial tissue directly at the annulus as well as via the papillary muscles. Both of these are stretched. 

- The stretching causes further increase in MR. This causes further volume overload. Which causes further MR.

- Thus it is like a positive feedback response and a vicious cycle is formed.

This phenomenon is referred to as ' MR begets MR' which means MR basically causes Ventricular changes which stretch the heart and cause more MR which continues the cycle further.

Hope this helped !
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

Hello!

Tay-Sachs disease is an autosomal recessive, neurodegenerative disease.

Plasma Proteins Mnemonic

Hello Everyone,
 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.

Memorising the examples of them is simple. 

Examples of Beta Globulins can be remembered as follows:

         B PTH

B-Beta Lipoproteins(LDL)

P-Plasminogen

T-Transferrin

H-Hemopexin

Interesting Fact:

Acute-phase proteins are a class of proteins whose plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation. This response is called the acute-phase reaction.

• 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. 

Thats all,

Thank you,

Chaitanya Inge

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

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

Coccidioidomycosis mnemonic

Coccidioidomycosis is caused by Coccidioides immitis!

Diabetes insipidus and water deprivation test

In this video I talk about pyschogenic polydipsia, central diabetes insipidus, nephrogenic diabetes inspidius, water deprivation test :)

Theophylline toxicity mnemonic

Theophylline's effects arise from antagonism of adenosine receptors and indirect adrenergic activity.

It is used as a bronchodilator for patients with asthma or chronic obstructive pulmonary disease.

Chest x-ray - Left Lung.

Hello everybody!

Let's see the image correlations of the left lung today.

The left lung has an apical lobe ,lingula and a basal lobe.

Apical lobe has 2 segments: Anterior and posterior.
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.

Carefully observe how the identification of these segments differs while seeing an X-ray.

Apical lobe:

Basal Lobe:

So that's it with the interpretation of lung fields on X-rays!

Hope this is helpful!

-Medha.

“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 notes and mnemonics

Here are my notes on the flow volume loops!

Flow volume loop explanation video and mnemonic

Hello!

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! :)