Skeletal muscle relaxants are drugs that affect skeletal muscle function by decreasing muscle tone. There are two main types: neuromuscular blockers that interfere with transmission at the neuromuscular junction and have no central nervous system activity, often used during surgery; and centrally-acting muscle relaxants that are used to alleviate musculoskeletal pain and spasms by acting in the central nervous system. Anemia is a condition in which the number of red blood cells or their oxygen-carrying capacity is insufficient, defined as a hemoglobin level below 13 g/dL for men and 12 g/dL for non-pregnant women. Anemia can be caused by blood loss, decreased red blood cell production, or increased red

1. Skeletal Muscle Relaxants By: Aditya Arya

2. A Muscle relaxant is a drug which affects skeletal muscle function and decreases the muscle tone. It may be used to alleviate symptoms such as muscle spasms, pain, and hyperreflexia. The term "muscle relaxant" is used to refer to two major therapeutic groups: Neuromuscular blockers and Spasmolytics. Neuromuscular blockers act by interfering with transmission at the neuromuscular end plate and have no CNS activity. They are often used during surgical procedures and in intensive care and emergency medicine to cause paralysis .

3. Spasmolytics, also known as Centrally-acting muscle relaxants: Are used to alleviate musculoskeletal pain and spasms and to reduce spasticity in a variety of neurological conditions. While both neuromuscular blockers and spasmolytics are often grouped together as muscle relaxants.

6. Neuromuscular blocking drugs : Block neuromuscular transmission at the neuromuscular junction, causing paralysis of the affected skeletal muscles. This is accomplished either by acting presynaptically via the inhibition of acetylcholine (ACh) synthesis or release, or by acting postsynaptically at the acetylcholine receptors of the motor nerve end-plate. While there are drugs that act presynaptically (such as botulinu toxin and tetrodotoxin), the clinically-relevant drugs work postsynaptically.

7. Clinically , neuromuscular block is used adjunctively to anesthesia to produce paralysis, so that surgery, especially intra-abdominal and intra-thoracic surgeries, can be conducted with fewer complications. Because the appropriate dose of neuromuscular blocking drug may paralyze muscles required for breathing (i.e. the diaphragm), mechanical ventilation should be available to maintain adequate respiration.

8. These drugs fall into two groups: Non-depolarizing blocking agents : These agents constitute the majority of the clinically-relevant neuromuscular blockers. They act by competitively blocking the binding of ACh to its receptors, and in some cases, they also directly block the ionotropic activity of the ACh receptors. Depolarizing blocking agents : These agents act by depolarizing the plasma membrane of the skeletal muscle fiber. This persistent depolarization makes the muscle fiber resistant to further stimulation by ACh.

9. Steps in neuromuscular transmission

11. Connective Tissue Covering Skeletal Muscle 

12. Microstructure of Skeletal Muscle 

13. Within the Sarcoplasm 

14. Neuromuscular Junction 

15. Actin & Myosin Relationship 

17. Non-depolarizing blocking agents: A neuromuscular nondepolarizing agent is a form of neuromuscular blocker which do not depolarize the motor end plate. Tubocurarine: Found in curare of the South American plant Pareira, Chonodendron tomentosum , is the prototypical non-depolarizing neuromuscular blocker. It has a slow onset (>5 min) and a long duration of action (1–2 hours). Side effects include hypotension. It is excreted in the urine.

21. Atracurium besylate : Intermediate-acting safe in liver and kidney disease; bradycardia may result during surgical manipulations, esp ophthal-mologic, ENT, or laparoscopy (treat with atropine or glycopyrrolate); precipitates in alkaline pH; can cause HA release at higher doses. Probably most used in veterinary medicine.

26. Competitive blockade reversed by neostigmine (Ns)

33. Depolarizing blocking agents: A neuromuscular depolarizing agent is a form of neuromuscular blocker which depolarize the motor end plate. An example is succinylcholine. Depolarizing blocking agents work by depolarizing the plasma membrane of the muscle fiber, similar to acetylcholine. This differs from acetylcholine, which is rapidly degraded and only transiently depolarizes the muscle.

34. There are two phases to the depolarizing block. During phase I ( depolarizing phase ), they cause muscular fasciculations (muscle twitches) while they are depolarizing the muscle fibers. Eventually, after sufficient depolarization has occurred, phase II ( desensitizing phase ) sets in and the muscle is no longer responsive to acetylcholine released by the motoneurons. At this point, full neuromuscular block has been achieved

44. THANK YOU

45. Centrally acting: (spasmolytic drugs)

48. Carisoprodol : It has a favorable muscle relaxant : Sedative activity ratio with weak analgesic, antipyretic and anticholinergic actions in addition . Uses: Musculoskeletal disorders associated with muscle spasm Chlorzoxazone: It is pharmacologically similar to mephenesin Longer duration of action Better tolerated orally

49. Chlormezanone : It has antianxiety and hypnotic as well : Has been used for Tension associated with increased muscle tone Methocarbamol: It is less sedative and longer acting than mephenesin Uses: Reflex muscle spasms and Chronic neurological diseases Used i.v without producing thrombophlebitis and haemolysis: Used for orthopedic procedures and tetanus

50. Diazepam : It is a prototype of benzodiazapines which act in the brain on specific receptors enhancing GABAergic transmission : Uses: It is particularly valuable in spinal injuries and tetanus. Comined with analgesic, it is popular for rheumatic disorders associated with muscle spasm. Baclofen: This analogue of the inhibitory transmitter GABA acts as a selective GABA B RECEPTOR AGONIST . GABA Receptors have been divided into : GABA A receptor: Intrinsic ion channel receptor : increases cl conductance which is blocked by bicuculline facilitated by BZDs GABA B receptor G protein coupled receptor hyperpolarizes neurones by increasing k conductance and altering Ca 2+ flux

51. Site of Action: Act in the spinal cord where it depresses both polysynaptic and monosynaptic reflexes Absorbed orally and is primarily excreted unchanged in urine with a t1/2 of 3-4 hours. Side Effects: Drowsiness Mental confusion Weakness Ataxia

55. BLOOD

56. Anaemia: Anemia ( meaning lack of blood ) is a decrease in number of red blood cells (RBCs) or less than the normal quantity of hemoglobin in the blood. However, it can include decreased oxygen-binding ability of each hemoglobin molecule due to deformity or lack in numerical development as in some other types of hemoglobin deficiency.

61. WHO's Hemoglobin thresholds used to define anemia (1 g/dL = 0.6206 mmol/L) Age or gender group Hb threshold (g/dl) Hb threshold (mmol/l) Children (0.5–5.0 yrs) 11.0 6.8 Children (5–12 yrs) 11.5 7.1 Teens (12–15 yrs) 12.0 7.4 Women, non-pregnant (>15yrs) 12.0 7.4 Women, pregnant 11.0 6.8 Men (>15yrs) 13.0 8.1

62. Peripheral blood smear microscopy of a patient with iron-deficiency anemia.

66. Normocytic: Normocytic anemia: Normocytic anemia occurs when the overall hemoglobin levels are always decreased, but the red blood cell size (Mean corpuscular volume) remains normal. Causes include: Acute blood loss Anemia of chronic disease Aplastic anemia (bone marrow failure) Hemolytic anemia

67. Dimorphic: When two causes of anemia act simultaneously, e.g., macrocytic hypochromic, due to hookworm infestation leading to deficiency of both iron and vitamin B 12 or folic acid or following a blood transfusion more than one abnormality of red cell indices may be seen. Evidence for multiple causes appears with an elevated RBC distribution width (RDW), which suggests a wider-than-normal range of red cell sizes.

68. Heinz body anemia: Heinz bodies form in the cytoplasm of RBCs and appear like small dark dots under the microscope. There are many causes of Heinz body anemia, and some forms can be drug induced. It is triggered in cats by eating onionsor acetaminophen (paracetamol). It can be triggered in dogs by ingesting onions or zinc, and in horses by ingesting dry red maple leaves

69. Refractory anemia : Refractory anemia is an anemia which does not respond to treatment. It is often seen secondary to myelodysplastic syndromes. Iron deficiency anemia may also be refractory as a clinical manifestation of gastrointestinal problems which disrupt iron metabolism