BRACHIAL PLEXUS

Q.)  10 Yr old boy is diagnosed with an upper brachial plexus injury . He presents with his right upper arm at his side due to loss of abduction. Which of the following muscles are primarily responsible for abduction of the arm at the shoulder?

A. Deltoid and biceps brachii

B. Deltoid and supraspinatus

C. Deltoid and infraspinatus

D. Supraspinatus and infraspinatus

E. Coracobrachialis and supraspinatus

Ans:  B. The deltoid and supraspinatus muscles, which are innervated by the axillary and suprascapular nerves, respectively, are the primary abductors of the arm at the shoulder

Q.)  Injury to the  musculocutaneous nerve results in which of the following findings?

A. Weakness of abduction of the arm at the shoulder

B. Weakness of adduction of the arm at the shoulder

C. Weakness of extension of the forearm at the elbow

D. Weakness of flexion of the forearm at the elbow

E. Weakness of supination of the forearm and hand

Ans:  D. Injury to the musculocutaneous nerve will result in loss or weakness of flexion at the elbow due to paralysis of the biceps brachii and brachialis muscles.

Q.) A 22-year-old man is brought into the emergency department with a knife injury to the axilla. The physician suspects injury to the lower brachial plexus. Which of the following nerves is most likely to be affected?

A. Axillary

B. Musculocutaneous

C. Vagus

D. Radial

E. Ulnar

.

Ans:  E. The C8 and T1 portions of the lower brachial plexus make up the majority of the ulnar nerve.

Beta BLOCKER

Q) All are true except about Beta Blockers-
a. They are all water soluble
b. They should never be used in patients with diabetes
c. They are used in the treatment of heart failure, migraine and hypothyroidism
d. They should never be used in combination with digoxin

Ans: A,B,C,D.

Some beta blockers are water soluble and some are lipid soluble. Those that are water soluble are less likely to enter the brain and therefore cause less sleep disturbance and nightmares. They can be used with caution in patients with diabetes, but may blunt their awareness of hypoglycaemia and cause deterioration in their glucose tolerance. They are useful in the treatment of many conditions including angina, heart failure, myocardial infarction, arrhythmias, thyrotoxicosis, anxiety, migraine and glaucoma. They should not be used with verapamil because this may cause severe hypotension, heart failure and asystole, but may be useful when combined with digoxin to control the ventricular rate in atrial fibrillation, especially when associated with thyrotoxicosis.

MANNITOL

Q.) Mannitol true statements are-
a. This should be given to all patients with head injury and a reduced GCS
b. It is a loop diuretic similar in action to furosemide
c. It decreases cerebral blood flow by reducing blood viscosity and microcirculatory resistance
d. It may produce renal failure or hypotension if given in large doses

Ans: D

Mannitol is an osmotic diuretic that may be useful in patients with deepening coma, pupil inequality or deterioration in neurological function. It is an osmotic diuretic that reduces cerebral oedema by preventing movement of water from the vascular space into the cells via the creation of an osmotic gradient. This reduces brain volume and may prevent herniation by allowing more space for swelling or an expanding haematoma. It also has other neuroprotective effects, promoting cerebral blood flow and scavenging free

radicals.

ADENOSINE

Q.) Adenosine false are-
a. This has a half-life of approximately 10 min
b. It is a naturally occurring purine nucleoside
c. It is useful in the management of supraventricular and ventricular arrhythmias
d. It is the drug of choice to cardiovert patients with tachycardias related to Wolff–Parkinson–White syndrome

Ans: A, C, D.

Adenosine is a naturally occurring purine nucleoside that has a half-life of approximately 10 seconds, so its side effects, such as dyspnoea and bronchospasm, are short-lived. It is useful in supraventricular tachycardia via its action at the AV (atrioventricular) node. In Wolff–Parkinson–White (WPW) syndrome, adenosine (and other AV node-blocking drugs such as calcium channel blockers, b blockers and digoxin) may cause a faster ventricular rate from unopposed and potentially enhanced conduction through an accessory pathway. This may degenerate in ventricular fibrillation.


ADENOSINE  is a nucleoside that is administered as a rapid intravenous bolus for the acute termination of reentrant supraventricular arrhythmias. Rare cases of ventricular tachycardia ( These may be harmful in reentrant VT and so should be used for acute therapy only if the diagnosis is secure) in patients with otherwise normal hearts are thought to be DAD-mediated and can be terminated by adenosine. Adenosine also has been used to produce controlled hypotension during some surgical procedures and in the diagnosis of coronary artery disease. 
The effects of adenosine are mediated via specific GPCRs. Adenosine activates acetylcholine-sensitive K+ current in the atrium and sinus and AV nodes, resulting in shortening of action potential duration, hyperpolarization, and slowing of normal automaticity. Adenosine also inhibits the electrophysiological effects of increased cellular cyclic AMP that occur with sympathetic stimulation. Because adenosine thereby reduces Ca2+ currents, it can be antiarrhythmic by increasing AV nodal refractoriness and by inhibiting DADs elicited by sympathetic stimulation. Administration of an intravenous bolus of adenosine transiently slows sinus rate and AV nodal conduction velocity and increases AV nodal refractoriness. A bolus of adenosine can produce transient sympathetic activation by interacting with carotid baroreceptors; a continuous infusion can cause hypotension. 
 Adverse Effects : A major advantage of adenosine therapy is that adverse effects are short-lived because the drug is transported into cells and deaminated so rapidly. Transient asystole is common but usually lasts less than 5 seconds and is in fact the therapeutic goal. Most patients feel a sense of chest fullness and dyspnea when therapeutic doses (6–12 mg) of adenosine are administered. Rarely, an adenosine bolus can precipitate bronchospasm or atrial fibrillation.
Clinical Pharmacokinetics:  Adenosine is eliminated with a t1/2 of 10 seconds by carrier-mediated uptake in most cell types and subsequent metabolism by adenosine deaminase. Adenosine probably is the only antiarrhythmic drug whose efficacy requires a rapid bolus dose, preferably through a large central intravenous line; slow administration permits elimination of the drug prior to its arrival at the heart. The effects of adenosine are potentiated in patients receiving dipyridamole, an adenosine-uptake inhibitor, and in patients with cardiac transplants owing to denervation hypersensitivity. Methylxanthines (e.g., theophylline and caffeine) block adenosine receptors; therefore, larger than usual doses are required to produce an antiarrhythmic effect in patients who have consumed these agents in beverages or as therapy. 


source: Goodman Gilman textbook of pharmacology

NSAID-GASTRITIS

Q.) In NSAID-associated ulceration true are-

a. Adverse effects from NSAIDs are rare
b. Prostaglandins (PGE2 and PGI2) increase gastric acid secretion
c. Eradication of Helicobacter pylori will reduce the risk of NSAID-induced bleeding
d. Ibuprofen is less likely to cause serious gastrointestinal side effects than diclofenac.

Ans: D.

Adverse effects from NSAIDs (non-steroidal anti-inflammatory drugs) are common, especially as they are often given for long periods of time to elderly patients. NSAIDs inhibit cyclooxygenase and decrease the production of prostaglandins, which are protective, via a decrease in gastric acid secretion. Although eradicating H. pylori may help reduce the overall risk of ulceration in those starting long-term NSAID treatment that have dyspepsia or a history of ulceration, it is unlikely to reduce the risk of NSAID-induced bleeding or ulceration in those already on NSAIDs. Ibuprofen is the NSAID associated with the lowest risk of bleeding.


Important : 

Inhibition of Gastric Secretion:

Although intestinal chyme slightly stimulates gastric secretion during the early intestinal phase of stomach secretion, it paradoxically inhibits gastric secretion at other times. This inhibition results from at least two influences. The presence of food in the small intestine initiates a reverse enterogastric reflex, transmitted through the myenteric nervous system and extrinsic sympathetic and vagus nerves, that inhibits stomach secretion. This reflex can be initiated by distending the small bowel, by the presence of acid in the upper intestine, by the presence of protein breakdown products, or by irritation of the mucosa. This is part of the complex mechanism discussed in Chapter 63 for slowing stomach emptying when the intestines are already filled. The presence of acid, fat, protein breakdown products, hyperosmotic or hypo-osmotic fluids, or any irritating factor in the upper small intestine causes release of several intestinal hormones. One of these is secretin, which is especially important for control of pancreatic secretion. However, secretin opposes stomach secretion. Three other hormones-gastric inhibitory peptide (glucose-dependent insulinotropic peptide), vasoactive intestinal polypeptide, and somatostatin-also have slight to moderate effects in inhibiting gastric secretion PGE2,PGI2 both inhibit acid secretion.  source: Guyton textbook of physiology