Appendix – Joke

A nonsurgical noninflammatory chat with the appendix
Interview done
by Srt.😜

Name    :  appendix

Surname   :vermiform
called   :      vestigeal

Address: mcburneys point, right iliac fossa gated community.

Cell numb:ask the pathologist 😝 for cell numb and type.

Email id
(  password:  I think is fecolith😝  )        

facebook status:married to miss o.appendix (mesoappendix)

Watsapp group:adorable abdomen

Fav music:bowel sounds

Fav dance:persistalsa (intestinal salsa dance😜)

Fav tv show:grays  anatomy (very romantic😝😷)

favourite indoor game:hide n seek . Sometimes I hide beneath the liver n in the pelvis to confuse the radiologist .but they hav discovered a cat which can find me there too….CAT scan😪.

Fav subj :maths.
I keep counting the follicles in the ovary, fimbria of the fallopian tube n villi of the intestine.

Fav outdoor game: free style swimming in  formalin solution.

Nature:silent but wen I fight I become red with anger (appendicitis)
And can even create tsunami in the abdomen (peritonitis) and send the owner of the abdomen to motuary n then to obituary .😜

One last message to the viewers:save us from the serial killers ( ie from the  genlsurgeons.)

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Midazolam Nasal Spray for Seizures

A nasal spray formulation of midazolam may diminish repeated seizures and lower the risk of generalized tonic-clonic seizures in hospitalized epilepsy patients, researchers found.

In a retrospective analysis of data from a German university epilepsy center, those given intranasal midazolam during or right after a seizure remained free of seizures longer than those not given the drug (5.83 hours versus 2.37 hours), according to Lara Kay, a doctoral candidate at Philipps University in Marburg in Germany, and colleagues.

Those who didn’t get the drug also had a higher risk of generalized tonic-clonic seizures over the next 24 hours (odds ratio 4.67, 95% CI 1.06 to 2.12), they reported online in Epilepsia.

The researchers noted that it’s important to give anticonvulsants quickly, easily, and safely when managing repetitive and prolonged seizures, both in the hospital and in the community setting.

The gold standard treatment in such cases is intravenous lorazepam, but getting venous access may be a challenge during a seizure, and it may not be possible for a caregiver to do so outside of a hospital in an emergency situation.

Other formulations for home use have included rectal diazepam, which hasn’t had good uptake for a number of reasons, including stigma and shame, the researchers said. There’s also buccal midazolam, which has been approved in Europe.

Intranasal midazolam is an emerging technique for periprocedural sedation and for acute seizure control. The idea is to have a formulation that allows for rapid and easy administration. It’s been studied in home use, with no differences in efficacy or complications when compared with intravenous diazepam.

Now the researchers are looking at its in-hospital effects. Since 2008, the hospital’s epilepsy center has used intranasal midazolam to treat seizures and prevent seizure clusters and tonic-clonic seizures.

Kay and colleagues reviewed the records of 75 patients, mean age 35, who were treated with intranasal midazolam at their center, during or right after an epileptic seizure from 2008 to 2014.

The nasal spray was manufactured by the hospital’s pharmacy, and it delivered a dose of 2.5 mg midazolam per puff. The average dose per patient was 5 mg, or two sprays. It took a median time of 2.17 minutes to give intranasal midazolam.

They found that over the next 12 hours, the number of seizures was significantly lower for those who took intranasal midazolam. The median seizure-free interval was significantly longer for those who had the nasal spray than for those who didn’t (P=0.015).

They noted that the likelihood of a patient developing a subsequent seizure was four higher in first hour and fell gradually after 12 hours (OR 4.33, 95% CI 1.30-14.47 and OR 1.5, 95% CI 1.06-2.12, respectively).

Patients who didn’t receive intranasal midazolam had a much higher likelihood of experiencing a generalized tonic-clonic seizure during a 24-hour observation period than those who didn’t get the drug (P=0.009).

Only four patients (5.3%) had an adverse event. Three patients had nasal irritation, while in the fourth, administration was delayed by the patient’s ictal automatisms and head turning.

There were no serious adverse events and the treatment was generally well-tolerated, the researchers said.

“This study provides evidence that ictal and immediate postictal administration of intranasal midazolam is a well-tolerated procedure and prevents subsequent seizures for a 12-hour period and especially generalized tonic-clonic seizures for a 24-hour period,” they concluded.

They added that intranasal midazolam is “easy to employ, and it can be delivered from any position. Even during a seizure, it takes little time to administer the dose, and patients do not need to be restrained.”

The study was limited by its retrospective, observational nature and lack of randomization, and the results need to be confirmed in larger randomized trials, the researchers said.

Another challenge is that there’s no commercial preparation available, but it still may be an inexpensive way to reduce the costs of morbidity and mortality associated with seizure activity, they concluded.

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Bezold-Jarisch Reflex

Bezold-Jarisch Reflex

Eponym for a triad of responses (apnea, bradycardia, and hypotension)

A cardiovascular decompressor reflex involving a marked increase in vagal (parasympathetic) efferent discharge to the heart, elicited by stimulation of chemoreceptors, primarily in the left ventricle & hypopnea. This causes a slowing of the heart beat (bradycardia) and dilatation of the peripheral blood vessels with resulting lowering of the blood pressure.

Reflex cardiovascular depression with vasodilation and bradycardia has been variously termed vasovagal syncope, the Bezold–Jarisch reflex and neurocardiogenic syncope

The concept was originated by a German physiologist Albert von Bezold in 1867, later revised by an Austrian dermatologist Adolf Jarisch in 1937.

Miller’s Anesthesia 7 th Ed.p. 409

The Bezold-Jarisch Reflex responds to noxious ventricular stimuli sensed by chemoreceptors and mechanoreceptors within the LV wall by inducing the triad of hypotension, bradycardia, and coronary artery dilatation.  The activated receptors communicate along unmyelinated vagal afferent type C fibers.  These fibers reflexively increase parasympathetic tone.  Because it invokes bradycardia, the Bezold-Jarisch reflex is thought of as a cardioprotective reflex.  This reflex has been implicated in the physiologic response to a range of cardiovascular conditions such as myocardial ischemia or infarction, thrombolysis, or revascularization and syncope.  Natriuretic peptide receptors stimulated by endogenous ANP or BNP may modulate the Bezold-Jarisch reflex.  Thus, the Bezold-Jarisch reflex may be less pronounced in patients with cardiac hypertrophy or atrial fibrillation.

Stoelting’s Anesthesia and Co-Existing Disease 5 th Ed.p.74-5

The underlying mechanism responsible for bradycardia and asystole during spinal and epidural anesthesia is not known. Proposed theories include reflex-induced bradycardia resulting from decreased venous return and activation of vagal reflex arcs mediated by baroreceptors and stretch receptors in the sinus node resulting in a paradoxical Bezold-Jarisch response. Another possible mechanism is the unopposed parasympathetic nervous system activity that results from the anesthetic-induced sympathectomy. Blockade of cardiac accelerator fibers originating from thoracic sympathetic ganglia (T1-4) may alter the balance of autonomic nervous system input to the heart resulting in the emergence of relatively unopposed parasympathetic influences on the SA node and AV node. Secondary factors such as hypovolemia, opioid administration, sedation, hypercarbia, concurrent medical illnesses, and long-term use of medications that slow the heart rate could also contribute to development of bradycardia.The following source would not be used for board references, but is here to further illustrate the concept of the Bezold-Jarisch reflex.

British Journal of Anaesthesia 2001; volume 86; p. 859–68

Reflex cardiovascular depression with vasodilation and bradycardia has been variously termed vasovagal syncope, the Bezold–Jarisch reflex and neurocardiogenic syncope. The circulatory response changes from the normal maintenance of arterial pressure, to parasympathetic activation and sympathetic inhibition, causing hypotension. This change is triggered by reduced cardiac venous return as well as through affective mechanisms such as pain or fear. It is probably mediated in part via afferent nerves from the heart, but also by various non-cardiac baroreceptors which may become paradoxically active. This response may occur during regional anesthesia, hemorrhage or supine inferior vena cava compression in pregnancy; these factors are additive when combined. In these circumstances hypotension may be more severe than that caused by bradycardia alone, because of unappreciated vasodilation. Treatment includes the restoration of venous return and correction of absolute Blood volume deficits. Ephedrine is the most logical choice of single drug to correct the changes because of its combined action on the heart and peripheral blood vessels. Epinephrine must be used early in established cardiac arrest, especially after high regional anesthesia.

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