By T. Aila. Dartmouth College.
If you lose track of what number you are on 100mg aurogra for sale erectile dysfunction caused by prostate surgery, no problem—just start over at One cheap aurogra 100mg line impotence nerve. Another breath-counting meditation is similar to this one, but we will be count- ing backwards. This is somewhat akin to the methods used in hypnosis, where the client counts backwards from 100, and by the time he or she reaches the lower numbers, they are fully hypnotized. Start the breathing method used in the first meditation, making sure you are physically comfortable in your chair. No, simply forget about the counting, and simply enjoy the process of breath- ing. At this point, you can actually move into the Breath-Watching meditation, which is the first visualization meditation we will try. TLFeBOOK M editation E xercises / 145 Visualization Meditations Much has been written and claimed for visualizations. They are a way of direct- ing our intent, or our will, in whichever direction we desire. It is said that to make something happen, you must see it happening in your mind. For our purposes, we might be more interested in the ability of visualization to hone our concentration and allow us to forget our troubles for a while. In our first visualization meditation, Breath Watching, we will be doing just that: watching our breath. Breathe deeply and slowly, feeling the breath fill you up with lightness and health. Once you are settled in your breathing rhythm, you can start your visualization. Perhaps you can imagine that the air looks like a golden liquid, or a white vapor. My students have come up with all manner of ideas for what air looks like. As you continue your breathing, see the air around you in your chosen color and consistency. It travels down to your lungs, and actually goes all the way down to your lower abdomen, to a point just below your navel. By the end of the inhale, you should have a full breath of air, and your attention is directed at your lower abdomen. As you begin to exhale, follow the breath as it leaves your abdomen, goes through your body to the base of your spine, follows the spine all the way up to your head, and then travels over the top of your head and back out your nose into the world. That was one cycle of breathing, a simple enough thing really, but your mind followed an imaginary path- way throughout your upper body. Continue the exercise, watching the next inhale travel down the front of your body, and then up your spine, over your head, and out your nose on the exhale. Sometimes you just are not in the mood, and you can develop resentment for meditation if you attempt to do it during those times. What this meditation does first is to improve your thought and imagination processes, a benefit of special interest to us as we get older. Secondly, this exercise is great for those times when you wish you could get away on a vacation, but for economic or practical reasons, cannot. Once you are comfortably settled in, start concentrating on your breath- ing. Spend a little while enjoying the breathing process and getting into that relaxed state. At whichever point you wish, continuing the breathing uninterrupted, switch your attention to a little scene that you play in your mind. That scene is your favor- ite vacation spot, whether it is the beach, the mountains, the woods, or Las Vegas! See the colors, smell the smells, hear the bustle of nature (or people) flowing around and through you. Take as much time as you need in establishing the initial scene, and add as much detail as you are able. Walk around, see things from different angles and heights, hear new sounds and smell new odors. Often after a meditation, it can be difficult to return to the everyday world. When you are ready to leave your vacation spot, visualize yourself returning to the place where you began the trip. Slowly bring your concentration back to your breathing, perhaps watch- ing the breath come down the front of the body and exit up the spine and out the nose. TLFeBOOK M editation E xercises / 147 Relaxation Meditations Although all of the previously discussed meditations are relaxing, these next two are specifically designed to relax your body as well as your mind.
A venous tial activation of clotting factors in the blood (Table 57–1) purchase 100mg aurogra with amex erectile dysfunction diabetes reversible, thrombus is less cohesive than an arterial thrombus 100 mg aurogra amex erectile dysfunction treatment chandigarh, and an and growth of ﬁbrous tissue (ﬁbrin) into the blood clot to embolus can easily become detached and travel to other parts make it more stable and to repair the tear (opening) in the of the body. Overall, normal hemostasis is a com- Venous thrombi cause disease by two mechanisms. First, plex process involving numerous interacting activators and thrombosis causes local congestion, edema, and perhaps in- inhibitors, including endothelial factors, platelets, and blood ﬂammation by impairing normal outﬂow of venous blood coagulation factors (Box 57–1). Sec- TABLE 57–1 Blood Coagulation Factors Number Name Functions I Fibrinogen Forms ﬁbrin, the insoluble protein strands that compose the supporting frame- work of a blood clot. II Prothrombin Forms thrombin, which catalyzes the conversion of ﬁbrinogen to ﬁbrin III Thromboplastin Converts prothrombin to thrombin IV Calcium Catalyzes the conversion of prothrombin to thrombin V Labile factor Required for formation of active thromboplastin VII Proconvertin or stable factor Accelerates action of tissue thromboplastin VIII Antihemophilic factor Promotes breakdown of platelets and formation of active platelet thromboplastin IX Christmas factor Similar to factor VIII X Stuart factor Promotes action of thromboplastin XI Plasma thromboplastin antecedent Promotes platelet aggregation and breakdown, with subsequent release of platelet thromboplastin XII Hageman factor Similar to factor XI XIII Fibrin-stabilizing factor Converts ﬁbrin meshwork to the dense, tight mass of the completely formed clot 834 SECTION 9 DRUGS AFFECTING THE CARDIOVASCULAR SYSTEM BOX 57–1 HEMOSTASIS AND THROMBOSIS The blood vessels and blood normally maintain a balance between The cell membrane of a platelet contains a coat of glycopro- procoagulant and anticoagulant factors that favors anticoagulation teins that prevents the platelet from adhering to normal endothe- and keeps the blood ﬂuid. Injury to blood vessels and tissues lium but allows it to adhere to damaged areas of endothelium and causes complex reactions and interactions among vascular en- subendothelial collagen in the blood vessel wall. It also contains dothelial cells, platelets, and blood coagulation factors that shift receptors for ADP, collagen, blood coagulation factors such as the balance toward procoagulation and thrombosis. Breakdown of the cell mem- Endothelial Cells brane releases arachidonic acid (which can be metabolized to produce thromboxane A2) and allows leakage of platelet contents Endothelial cells play a role in all aspects of hemostasis and throm- (eg, thromboplastin and other clotting factors), which function to bosis. Normal endothelium helps to prevent thrombosis by produc- stop bleeding. However, endothelium pro- ADP, ﬁbrinogen, histamine, platelet-derived growth factor, sero- motes thrombosis when its continuity is lost (eg, the blood vessel tonin, von Willebrand factor, enzymes that produce thromboxane wall is torn by rupture of atherosclerotic plaque, hypertension, A2, and other substances. The cytoplasm also contains contractile trauma), its function is altered, or when blood flow is altered or proteins that contract storage granules so they empty their con- becomes static. After a blood clot is formed, the endothelium also tents and help a platelet plug to retract and plug a hole in a torn induces its dissolution and restoration of blood ﬂow. Antithrombotic Functions The only known function of platelets is hemostasis. When • Synthesizes and releases prostacyclin (prostaglandin I2), which platelets come in contact with a damaged vascular surface, they inhibits platelet aggregation become activated and undergo changes in structure and function. The thrombus blocks the tear in the blood vessel and phate (ADP), a platelet product that promotes platelet aggregation prevents further leakage of blood. Platelets usually disappear • Produces plasminogen activators (eg, tissue-type or tPA) in re- from a blood clot within 24 hours and are replaced by fibrin. These activators convert inactive plasminogen to plasmin, of activation, adhesion, aggregation, and procoagulation. Platelet activation occurs when agonists such as thrombin, colla- • Produces thrombomodulin, a protein that helps prevent forma- gen, ADP, or epinephrine bind to their speciﬁc receptors on tion of intravascular thrombi by inhibiting thrombin-mediated the platelet cell membrane surface. Thrombomodulin also reacts with throm- Willebrand factor, which aids platelet adhesion to blood vessel bin to activate proteins C and S, which inhibit the plasma cas- walls. Normally, the balance be- Platelet adhesion involves changes in platelets that allow them to tween proﬁbrinolysis and antiﬁbrinolysis favors ﬁbrinolysis adhere to endothelial cells and subendothelial collagen exposed by (clot dissolution). Adhesion is mediated by interactions be- sclerosis, ﬁbrinolysis may be limited and thrombosis enhanced. In capillaries, factor serves as a site for subendothelial platelet adhesion and where blood shear rates are high, platelets also can bind indirectly as a carrier for blood coagulation factor VIII in plasma. Von Willebrand factor disease states are associated with increased or altered produc- is synthesized by endothelial cells and megakaryocytes. It requires the Platelets (also called thrombocytes) are fragments of large cells binding of extracellular fibrinogen to platelet fibrinogen recep- called megakaryocytes. The fibrinogen receptor is located on a complex of two and released into the bloodstream, where they circulate for ap- glycoproteins (GPIIb and IIIa) in the platelet cell membrane. Each activated GP IIb/IIIa CHAPTER 57 DRUGS THAT AFFECT BLOOD COAGULATION 835 BOX 57–1 HEMOSTASIS AND THROMBOSIS (Continued) complex is capable of binding a single fibrinogen molecule. Blood Coagulation However, a fibrinogen molecule may bind to receptors on adja- The blood coagulation process causes hemostasis within 1 to cent activated platelets, thus acting as a bridge to connect the 2 minutes. Activated GP IIb/IIIa complexes can also bind von are normally present in blood and tissues as inactive precursors Willebrand factor and promote platelet aggregation when fi- and formation of a meshwork of ﬁbrin strands that cements blood brinogen is lacking. Major phases in- Aggregated platelets produce and release thromboxane A2, clude release of thromboplastin by disintegrating platelets and which acts with ADP from platelet storage granules to promote damaged tissue; conversion of prothrombin to thrombin, which re- additional GP IIb/IIIa activation, platelet secretion, and aggre- quires thromboplastin and calcium ions; and conversion of ﬁ- gate formation. The exposure of functional GP IIb/IIIa com- brinogen to ﬁbrin by thrombin. Collagen stimulates additional aggrega- when blood passes out of a blood vessel, are needed for normal he- tion by increasing the production of thromboxane A2 and storage mostasis. The intrinsic pathway occurs in the vascular system; the granule secretion. Although the pathways are Overall, aggregated platelets release substances that recruit initially separate, the terminal steps (ie, activation of factor X and new platelets and stimulate additional aggregation. If the opening is small, the platelet tact with collagen in the injured vessel wall and coagulation fac- plug can stop blood loss.
Regimens vary from a single dose before chemotherapy to doses every Drugs used to prevent or treat nausea and vomiting belong 4 to 6 hours for 24 to 48 hours cheap 100mg aurogra with mastercard impotence stress. With this short-term use 100 mg aurogra erectile dysfunction use it or lose it, to several different therapeutic classifications, and most adverse effects are mild (eg, euphoria, insomnia, mild fluid have anticholinergic, antidopaminergic, antihistaminic, or retention). Most antiemetics prevent or relieve nausea and vomiting by acting on the Benzodiazepine Antianxiety Drugs vomiting center, CTZ, cerebral cortex, vestibular apparatus, or a combination of these. They pro- duce relaxation and inhibit cerebral cortex input to the vom- iting center. They are often prescribed for clients who Phenothiazines experience anticipatory nausea and vomiting before admin- istration of anticancer drugs. Lorazepam (Ativan) is com- Phenothiazines, of which chlorpromazine (Thorazine) is the monly used. These drugs have widespread effects on 5-Hydroxytryptamine3 (5-HT3 or the body. Their therapeutic effects in nausea and vomiting (as Serotonin) Receptor Antagonists in psychosis) are attributed to their ability to block dopamine from receptor sites in the brain and CTZ (antidopaminergic Ondansetron (Zofran), granisetron (Kytril), and dolasetron effects). When used as antiemetics, phenothiazines act on the (Anzemet) are used to prevent or treat moderate to severe CTZ and the vomiting center. Not all phenothiazines are nausea and vomiting associated with cancer chemotherapy, effective antiemetics. Some anticancer Phenothiazines are usually effective in preventing or treat- drugs apparently cause nausea and vomiting by combining ing nausea and vomiting induced by drugs, radiation therapy, with a subset of 5-HT3 receptors located in the CTZ and GI surgery, and most other stimuli, but are usually ineffective in tract. These drugs cause sedation; prochlorper- activation by emetogenic anticancer drugs. Adverse effects are usually mild to moderate, and common ones include diarrhea, headache, dizziness, constipation, muscle aches, and transient elevation Antihistamines of liver enzymes. Its half-life Antihistamines are used primarily to prevent histamine from is 3 to 5. With oral drug, ac- Antihistamines used as antiemetic agents are the classic tion begins in 30 to 60 minutes and peaks in about 2 hours. The drugs are thought to relieve nausea Granisetron has a half-life of 6 hours with oral drug and and vomiting by blocking the action of acetylcholine in the 5 to 9 hours with IV drug; its half-life in patients with liver brain (anticholinergic effects). Action begins rapidly with IV 904 SECTION 10 DRUGS AFFECTING THE DIGESTIVE SYSTEM Drugs at a Glance: Antiemetic Drugs Routes and Dosage Ranges Generic/Trade Name Adults Children Phenothiazines Prochlorperazine (Compazine) PO 5–10 mg 3 or 4 times daily (sustained-release >10 kg: PO 0. Maximum dose, 100 mg single dose, 15 min before cessation of anesthe- Prevention or treatment of PONV, IV 0. Phosphorated carbohydrate PO 15–30 mL repeated at 15-min intervals until PO 5–10 mL repeated at 15-min intervals until solution (Emetrol) vomiting ceases vomiting ceases Scopolamine (Transderm Scop) Motion sickness, PO, SC, 0. With intramuscular (IM) Dolasetron has a half-life of about 7 hours with both IV use, action onset occurs in 10 to 15 minutes and peaks in and oral drug, which is extended to 11 hours in patients with 60 to 90 minutes. Action onset and peak occur rapidly 3 minutes and peaks in 60 to 90 minutes. Adverse effects in- with IV administration; onset is rapid and peak occurs in 1 to clude sedation, restlessness, and extrapyramidal reactions 2 hours with oral drug. Metoclopramide may increase the effects of alcohol and cyclosporine (by increasing their absorption) and decrease Miscellaneous Antiemetics the effects of cimetidine and digoxin (by accelerating passage through the GI tract and decreasing time for absorption). Dronabinol is a cannabinoid (derivative of marijuana) used Phosphorated carbohydrate solution (Emetrol) is a in the management of nausea and vomiting associated with hyperosmolar solution with phosphoric acid. Dronabi- reduce smooth muscle contraction in the GI tract and is avail- nol causes the same adverse effects as marijuana, includ- able over the counter. Withdrawal symptoms (eg, insomnia, irritability, restless- ness, others) may occur if dronabinol is abruptly stopped. Onset occurs within 12 hours, with peak intensity within Indications for Use 24 hours and dissipation within 96 hours. These symptoms are most likely to occur with high doses or prolonged use. Antiemetic drugs are indicated to prevent and treat nausea Sleep disturbances may persist for several weeks. As a result, it can de- antiemetic drugs are ineffective or only a few doses are crease nausea and vomiting associated with gastroparesis and needed. Metoclopramide also has central antiemetic effects; it antagonizes the action of dopamine, a Contraindications to Use catecholamine neurotransmitter. Metoclopramide is given orally in diabetic gastroparesis and esophageal reflux. Large Antiemetic drugs are usually contraindicated when their use doses of the drug are given intravenously during chemother- may prevent or delay diagnosis, when signs and symptoms of apy with cisplatin (Platinol) and other emetogenic antineo- drug toxicity may be masked, and for routine use to prevent plastic drugs. A Interventions few studies have investigated its antiemetic activity in hu- Use measures to prevent or minimize nausea and vomiting: mans. Results indicated that ginger was comparable sights and odors; excessive ingestion of food, alcohol, or to metoclopramide and that both treatments were more effec- nonsteroidal anti-inﬂammatory drugs). Similar results were obtained in another study with tration of analgesics before painful diagnostic tests and 120 patients having gynecologic surgery; in this study, meto- dressing changes or other therapeutic measures may be clopramide was given orally. The general consensus • Administer antiemetic drugs 30 to 60 minutes before a seems to be that it is premature to recommend ginger for any nausea-producing event (eg, radiation therapy, cancer therapeutic use until long-term, controlled studies are done.
Background from animal experiments 115 Extra- Bag fusal 2 fibre muscle fibre α β Ia II γ γ Bag s d 1 fibre Chain fibres Primary endings Secondary endings Capsule Fig generic 100 mg aurogra overnight delivery impotence only with wife. The capsule of the spindle (dotted line) contains intra-fusal muscle ﬁbres – the so-called nuclear bag (bag1 and bag2) and chain ﬁbres discount 100 mg aurogra mastercard erectile dysfunction studies. The primary ending spirals around the central region of the bag and chain ﬁbres and gives rise to a single large group Ia afferent. Secondary endings are more distal (asterisks), on either side of the central region (although shown on only one side, for simplicity), mainly on chain ﬁbres but also on the static bag2 ﬁbre, and give rise to several group II afferent axons. Chain ﬁbres and static bag2 ﬁbres receive efferent innervation from static fusimotor ( s) neurones, while dynamic bag1 ﬁbres receive efferent innervation from dynamic fusimotor ( d) neurones. Onlythe innervationofbag1 ﬁbresisrepresented, but some bag2 ﬁbres also receive innervation. The main innervation of extra-fusal muscle ﬁbres comes from large ( ) efferents. Differences in spindles within a single species seem to be greater than the morphological differences between species. In the cat, there are differences in spindle morphology in different muscles Morphological differences between feline and Complex spindles involving more than one spindle human spindles or a spindle/tendon organ combination, and spin- dles in tandem with two or more spindles end to The differences are summarised by Prochazka & end, are common in neck muscle. Some differences in conduction velocity of the afferent may be of some functional relevance. These morphological differences ever, overall, the human spindle is slightly longer 116 Muscle spindles and fusimotor drive Fig. Ambiguous responses of a spindle afferent during graded twitch-induced contractions of tibialis anterior. Upper traces, neural activity from the afferent; lower traces,rectiﬁed EMG, with the ampliﬁcation for (b ) twice that for (c ) and (d ). Upper trace, afferent potentials; lower trace, twitch force, calibration: 1 Nm. The potentials (upper trace)are displayed without ﬁltering, after passage through a digital delay line. The oscilloscope sweep was triggered by the potential, ﬁltered as in (b )–(e )(lower trace). The spindle is always shorter (iii) The human spindle contains more intrafusal than the muscle ﬁbres with which it is associated, ﬁbres (1–4 bag ﬁbres and up to 14 chain ﬁbres) than but muscle ﬁbres are longer in human muscles. This would produce a greater tendency for ending of the human spindle is distributed more human spindles to be stimulated when nearby mus- around bag ﬁbres than chain ﬁbres. However, weaker twitch contractions in (vii) The afferent and efferent axons appear to be Fig. Methodology 117 Spindle density therefore to increase the dynamic sensitivity of the primaryending. However,therearealsostatic effer- The facial muscles and the digastric lack identiﬁ- ents(notrepresentedinFig. The larger size than the dynamic efferent and, when number of spindles in other muscles varies from present, they innervate the long chain ﬁbre, so alter- <50 for intrinsic muscles of the hand to >1000 for ing the static behaviour of the primary ending. However, spindle density seems to be greatest for the muscles of the neck (where Methodology theymayhaveacomplexmorphology,particularlyin deep paraspinal muscles, see above) and the intrin- sic muscles of the hand. Discredited techniques Comparisons of tendon jerk and H reﬂex as (skeleto-fusimotor) neurones measures of fusimotor drive Underlying principle Theseneuronesinnervatebothintra-andextra-fusal muscle ﬁbres (Bessou, Emonet-Denand & Laporte,´ Based on the fact that the H reﬂex bypasses the mus- 1965) and, in the cat hindlimb, perhaps 30% spin- cle spindle while the tendon jerk does not, many dles receive such innervation. Their activity would authors have, following Paillard (1955), implicitly obligatorily result in a coupling of spindle excitation accepted that comparisons of the H reﬂex and ten- and muscle contraction. However, this is unlikely don jerk can be used to provide a reliable measure of to account for the consistent ﬁnding that voluntary fusimotor activity. As a result of such comparisons, effort results in parallel activation of muscle and and of the uncritical use of local anaesthetic nerve muscle spindle endings because (i) during pressure blocks, it became accepted that (i) there is a sig- block experiments to the point of paralysis (presum- niﬁcant level of background fusimotor drive in the ably blocking large axons before small axons), relaxedstate,particularlyindynamic motoraxons; voluntary effort can still activate spindle endings (ii) this background fusimotor drive sensitises spin- (Burke, Hagbarth & Skuse, 1979); (ii) speciﬁc search dleendingstopercussionintherelaxedstate;and(iii) for a coupling of spindle discharge to EMG activity withoutthisbackgroundfusimotordrivetherewould using spike-triggered averaging has been unreward- be no tendon jerk. These views have been the sub- ing in one study (Gandevia, Burke & McKeon, 1986a) ject of critical reappraisal, as have many of the con- though not in a subsequent study (Kakuda, Miwa & clusions about motor control mechanisms in health Nagaoka, 1998); and (iii) there have been anecdotal and disease that were based on them (Burke, 1983; reports of changes in spindle discharge that could e. Each of the above statements is be produced in relaxed muscles without the appear- probably erroneous: there is now substantial experi- anceofdetectableEMG(Gandeviaetal. There clusions about fusimotor function cannot be drawn is anatomical evidence of innervation of human fromsuchcomparisons(e. Burke,McKeon&Skuse, spindles and suggestive evidence that this may be 1981a,b;Burke, Gandevia & McKeon, 1983, 1984; physiologically signiﬁcant: corticospinal volleys and Morita et al. In general, efferents innervate the Because of the properties of the tendon, tendon dynamic bag1 ﬁbre (cf. The afferent volley for the EPSP, the rising phase of which may be some 5– soleus tendon jerk reaches the popliteal fossa some 10 ms, much longer than the 1–2 ms rising phase 4–5 ms after percussion on the Achilles tendon, of the EPSP produced by a single electrical stimu- reaches a peak some 5–10 ms later and lasts some lus to the tibial nerve (Burke, Gandevia & McKeon, 30–40 ms (Burke, Gandevia & McKeon, 1983). There is thus greater opportunity for oligo- to the extreme sensitivity of primary spindle end- synaptic inputs to affect the motoneurone discharge ings, it is not necessary to percuss the appropri- withthetendonjerkthantheHreﬂex. Notwithstand- ate tendon directly: percussion on a bony protu- ing, the rising phase of the electrically evoked EPSP berance will result in a vibration wave that trav- is briefer than might be expected given the opportu- els along the bone exciting muscle spindles in nity for dispersion of the volley created by the long nearby muscles and, in subjects with brisk ten- conduction pathway (much longer than in the cat), don jerks, may produce tendon jerks in multiple theslowerconductionvelocitiesofgroupIaafferents muscles throughout the limb – the phenomenon of −1 (maximally∼60–70ms inthelowerlimb,i. The muscle spin- −1 of Ia conduction velocities (∼60–70 m s down to dle is not the only receptor responsive to ten- −1 ∼48 m s ; see Chapter 7,pp.
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