Hey!
HOCM is hypertrophic obstructive cardiomyopathy.
HOCM is the most common cause of sudden cardiac death in ADolescents.
HOCM is Autosomal Dominant.
Fun fact: Most common cause of sudden cardiac death in children in Aortic Stenosis.
-IkaN
Hey!
HOCM is hypertrophic obstructive cardiomyopathy.
HOCM is the most common cause of sudden cardiac death in ADolescents.
HOCM is Autosomal Dominant.
Fun fact: Most common cause of sudden cardiac death in children in Aortic Stenosis.
-IkaN
This is a discussion I had with a lot of people. My questions are put in inverted commas.
"I don't understand the next best step in the management in acute coronary syndromes. If there's ST elevation MI, you do angioplasty. But when there was a ST depression, they preferred heparin after aspirin even when angioplasty was in the options. Why is that? Why does the management change depending on elevation or depression?"
ST elevation means transmural ischemia so maybe angioplasty is the only way to restore flow. ST depression means subendocardial ischemia so occlusion isn't complete. Heparin and blood thinners might work.
"But then if you can do angioplasty (Catherization lab available), why give heparin?"
They do send for angioplasty later. Heparin can be given immediately to prevent the situation from getting worse.
"But then again, why wouldn't you do that with ST elevation too?"
ST elevation means the occlusion is complete. Heparin wouldnt be effective. In NSTEMI and unstable angina, there's still some lumen viable.
"Patients with MI with ST-segment depression should not be treated with fibrinolysis. Why isn't fibrinolysis done in ST depression angina?
We say that the occlusion isn't complete because there is subendocardial ischemia in ST depression and we give heparin to prevent further occlusion. But why not give streptokinase? Why not eradicate what is already formed instead of trying to prevent progression of clot?"
Because fibrinolysis treatment has it's own side effects and it's not effective in all the cases. It's contraindicated because studies have shown it does more harm than good in only ST depression.
Like, for example, there is reperfusion injury which would might make the only subendocardial infarct into a transmural one. 3 in ten patients end up with cerebral haemorrhage. There are so many other clauses.
Hence it's only indication is a transmural infarction.. The damage is already great. Irrespective of using t-PA the patient condition is critical.
That's all!
Thank you everyone who helped me out on this one.
-IkaN
By which mechanism, does medullary thyroid cancer cause secretory diarrhea?
Medullary thyroid carcinoma is usually associated with men syndrome in which we get VIPoma, which is associated with diarrhoea.
Upto date: "Systemic symptoms may occur due to hormonal secretion by the tumor. Tumor secretion of calcitonin, calcitonin-gene related peptide, or other substances can cause diarrhea or facial flushing in patients with advanced disease. In addition, occasional tumors secrete corticotropin (ACTH), causing ectopic Cushing's syndrome."
Colonic function was markedly impaired in three ways: (a) water absorption was decreased by half; (b) as the main excreted solutes were organic acids, a large electrolyte gap was recorded in faecal water, and (c) colonic transit time of the meal marker was very short, and was in agreement with the rapid transit of ingested radioopaque markers. These data strongly suggest that decreased absorption in the colon secondary to a motor disturbance is the main mechanism of diarrhoea in this case of medullary thyroid carcinoma, while calcitonin induced small intestinal fluid secretion suggested earlier is either non-existent, or only of minor importance.
Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1433550/
My dd for tumors and secretory diarrhea (someone wants to add):
- carcinoid tumor
- VIPoma
- Gastinoma
- Medullary thyroid cancer
Mnemonic for Macrocytosis (Non B12 causes):
ALPHA NERD
Alcohol
Liver disease
Pregnancy
Hemolysis (especially chronic)
Agglutination
Neoplasia (Including myelodysplasia)
Endocrine (Hypothyroidism)
Reticulocytosis
Drugs (Especially myelosuppressives like chemotherapy, anti-HIV meds)
This awesome mnemonic was written by Adnan Arif.
-IkaN
While Auscultating the Chest of patient and analysing Type of breathing, whether it's Bronchial or Vesicular.
Remember GRIP
1. Bronchial breathing:
Gap is present between Inspiration & expiration.
Respiration shows Inspiration & expiration equal length
Intensity is loud.
Pitch is high.
2. Vesicular Breathing:
Gap is absent.
Respiration shows Expiration is short.
Intensity is low.
Pitch is low.
This post was written by Adnan Arif. Thanks Adnan! (:
-IkaN
Related post: Abnormal breath sounds mnemonic
1. Durgs that inhibit hormone synthesis (Antithyroid drugs):
Propylthiouracil, methimazole, carbimazole.
Mnemonic: Professor Met Carby
2. Drugs that inhibit thyroid trapping (Ionic inhibitors):
Nitrates (NO3), thiocyanates (SCN), perchlorate (ClO4) .
Mnemonic: NTP
3. Inhibit hormone release:
Iodine, iodides of Na & K, organic iodides.
Mnemonic: I prevents release (Iodine, it's salts and organic form.)
4. Destroy thyroid tissue: Radioactive Iodine (I 131, I 123, I 125)
Mnemonic: Iodine normal is 128 (+3 &-3 are radioactive so is I 123)
That's all!
The mnemonics were submitted by Sareer. Thank you, Sareer, you're awesome.
-IkaN
When you are listening to a murmur, look for "SECRET Pi"
Site
Effect of posture
Character (Tapping, heaving, thrill)
Radiation ( Axilla, neck, shoulder)
Effect of Respiration
Timing
Pitch
This mnemonic was submitted by Adnan Arif =)
Thanks Adnan!
-IkaN