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Charcot’s joint of both elbow Charcot’s joint of both knee Charcot’s joint of both feet Q:What is Charcot’s joint? A: It is the complete destruction and disorganization of the joint buy cleocin gel 20 gm overnight delivery acne soap, usually secondary to loss of proprio- ception of the joint sense proven 20 gm cleocin gel acne 5 pocket jeans. However in some long case such as diabetes mellitus or any neurological case purchase cleocin gel 20gm without a prescription skin care with vitamin c, fundoscopy is usually necessary. Proceed as follows: Before examining the eyes, the patient should sit at the edge of the bed facing the examiner. Look at the face to see any facial asymmetry (in hemiplegia, Bell’s palsy), myasthenic, myotonic, tabetic face and thyrotoxic or hypothyroid face. Ptosis (complete or partial), squint, exophthalmos, eyebrows (fall of lateral one-third or all), xanthelasma, lid retraction, puffy face with baggy eyelids and heliotrope rash. Proceed as follows: • The patient should be examined either in sitting or lying down in a dark room. Opacity in media of the eye (cornea, anterior chamber, lens and vitreous) will appear as black specks or lines against red refex. Normal optic disc is rich in yellow colour, rest of fundus is rich in red colour). It appears darker than the surrounding retina and in young individuals has a central yellow point called ‘fovea centralis’. A: 3 types: • Primary (due to optic neuritis, compression in the optic nerve, glaucoma). Secondary to optic neuritis, which may be due to: • Demyelinating disease (multiple sclerosis). Optic atrophy is the degeneration of the optic nerve head, sometimes a sequel to optic neuritis. A: In this condition, there is infarction of anterior part of optic nerve resulting in acute severe loss of vision. Presentation of a Case: (Mention in Which Eye, Right or Left or Both) • There is bilateral papilloedema, more marked in right or left eye. Papilloedema (Left eye) Papilloedema (Right eye) Papilloedema with haemorrhage and exudates in fundus (malignant hypertension) Q:Could it be malignant hypertension? A: Transient obscurations of vision due to temporary impairment of retinal blood fow. B: Remember the following points: • Visual Acuity is usually preserved but may be affected in late stage. Stages are: • Early sign: Absence of spontaneous pulsation of retinal veins and increased pink or red colouration of the disc. A: It is the infammation of optic nerve head is called papillitis or intraocular optic neuritis. A: Infammation of the orbital or posterior portion of optic nerve is called retrobulbar optic neuritis or orbital optic neuritis. Central scotoma Present Absent, there is peripheral constriction of visual feld 5. A: It is characterized by a frontal lobe tumour compressing optic nerve causing ipsilateral optic atrophy but contralateral papilloedema due to raised intracranial pressure. Predisposing factors are: • Drugs: Tetracycline, nalidixic acid, oral contraceptive pill, Hypervitaminosis A, nitrofurantoin, sulphur drugs, phenytoin, steroid (both therapy and withdrawal). If no response, Surgical treatment: • Lumbo-peritoneal shunt or venticulo-peritoneal shunt, especially if progressive visual loss. A: As follows: • In mild case without macular involvement: there is no visual disturbance. My diagnosis is Hypertensive retinopathy (or grade 4, may be malignant hypertension). A: Unknown, probable mechanisms are: • Fibrinoid necrosis of the wall of small artery and arteriole, which results in end organ damage. A: 4 grades (Keith–Wagener–Barker classifcation): • Grade I: Thickening of arterial wall, increase tortuosity, narrowing of arteriole and increased light refex (silver wiring). Presentation of the Case: • There are few haemorrhages (mention the location), some are fame shaped and some are irregular in outline. Dot haemorrhage and Dot and blot haemorrhage Dot and blot haemorrhage microaneurysm (soft exudate) (hard exudate) Q:What is microaneurysm?

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Answer E buy cleocin gel line skin care gift baskets, neu- medications ropeptides are degraded by acetylcholinesterase in the 5 generic 20 gm cleocin gel mastercard anti-acne. Which one of the following drugs acts by inhibiting synapse order 20gm cleocin gel fast delivery skin care 99, is incorrect because other enzymes called pepti- neurotransmitter re-uptake? A heteroreceptor is a notably the barbiturates, self-induce metabolic enzymes, type of presynaptic receptor that is also located on the but this mechanism is not known to occur with opioid neuronal terminal but binds a different neurotransmitter analgesics. Answer B, pain intensity has greatly increased, than the one being released from the terminal. The sig- could also be true, but there is no information given in naling through this type of receptor usually causes the question to assume that this might be the case. Answer A, Answer C, the effciency of G protein coupling is presynaptic receptor, is a general term for any type of decreased, is a mechanism more noted for acute changes receptor located on the neuronal terminal. Answer C, after agonist administration, whereas down-regulation is Chapter 18 y Introduction to Central Nervous System Pharmacology 185 more likely with long-term or chronic administration of bipolar disorder acts at the level of signal transduction. Answer E, the patient is a “drug seeker” and Answer B, morphine, is incorrect as this opioid agonist addicted to opioid medications, is very unlikely because acts by receptor activation. Answer D, levodopa, is an metastatic lung cancer can be a very painful condition antiparkinsonian agent that acts by a strategy known and less than 4% of patients treated with opioid analge- as precursor loading, which feeds the biosynthetic sics develop substance abuse disorders. Anxiety is character- • Diazepam (Valium) ized by changes in mood (apprehension and fear), sympa- • Lorazepam (Ativan) thetic nervous system arousal, and hypervigilance. When • Midazolam (Versed) a anxiety becomes chronic, it can impair a person’s ability to • Triazolam (Halcion) b perform the activities of daily living. Moreover, chronic • Flumazenil (Romazicon) anxiety often leads to visceral organ dysfunction and unpleas- Barbiturates ant symptoms. For example, patients with chronic anxiety • Amobarbital (Amytal) may develop gastrointestinal, cardiovascular, and neurologic • Pentobarbital (Nembutal) problems, including diarrhea, tachycardia, sweating, tremors, • Phenobarbital (Luminal) and dizziness. Ultimately, anxiety can contribute to heart • Thiopental (Pentothal) disease and other disorders, including self-medication, which may lead to substance abuse. Antihistamines • Diphenhydramine (Benadryl) Neurologic Basis of Anxiety • Doxepin (Silenor) The neuronal pathways involved in anxiety disorders include • Hydroxyzine (Atarax) the sensory, cognitive, behavioral, motor, and autonomic pathways. Sensory systems, cortical processing, and memory Other Sedative-Hypnotic Drugs are involved in interpreting a stimulus to be dangerous • Zolpidem (Ambien) and creating a state of heightened arousal. Motor systems • Zaleplon (Sonata) and autonomic processing participate in the exaggerated • Eszopiclone (Lunesta) responses to an anxiety state. In experimental Also estazolam (ProSom), furazepam (Dalmane), oxazepam (Serax), temazepam (Restoril), and clorazepate (Tranxene). Electrical stimulation of the amygdala induces pharmaceutical agents in the world. The sedative part of signs of anxiety, whereas lesioning the amygdala or the their name refers to the ability of these agents to calm or administration of anxiolytic drugs prevents the behavioral reduce anxiety, known as an anxiolytic effect. The hypnotic and physiologic manifestations of anxiety during the antici- part of their name describes the ability of these agents to patory period. It is believed that long-term potentiation in induce drowsiness and promote sleep. This latter action is amygdala neurons establishes the memory of adverse events caused by a greater depression of central nervous system underlying anticipatory anxiety. A few agents, however, exert anxiolytic effects of Anxiety Disorders without causing sedation or hypnosis. The appropriate management of anxiety disorders requires This chapter describes the pharmacologic properties of an accurate diagnosis, and treatment may involve the use of benzodiazepines, barbiturates, and other sedative-hypnotic pharmacologic agents, psychotherapy, or both. Because of their greater safety, fewer Acute Anxiety adverse effects, and the availability of an antagonist, the Acute anxiety may develop in response to various factors, benzodiazepines have largely replaced the older barbiturates such as illness, separation from loved ones, or the anticipa- for these indications. Acute anxiety is often self-limiting 186 Chapter 19 y Sedative-Hypnotic and Anxiolytic Drugs 187 and may resolve in a few weeks to a few months without venlafaxine and duloxetine (see Chapter 22), are also used drug treatment. During a panic attack, an individual may feel an Other medications, such as benzodiazepines, may also be impending sense of doom that is often accompanied by used to treat associated symptoms, such as an exaggerated sweating, tachycardia, tremor, and other visceral symptoms. Five panic attacks during the early phase of therapy, and alpra- distinct patterns of brainwave activity occur during sleep, zolam and clonazepam are benzodiazepines that have grouped into the four stages of non-rapid eye movement been particularly useful in this regard. As an individual falls asleep, the high-frequency and low- Phobic Disorders amplitude activity of the alert state gradually diminishes Phobic disorders can be grouped into specifc phobia, social during stages 1 and 2 and is replaced by the low-frequency anxiety disorder (social phobia), or agoraphobia. Phobias are and high-amplitude activity of slow-wave sleep (stages 3 conditions in which an individual is overly fearful about a and 4). A normal adult cycles through the sleep which it might be diffcult or embarrassing to cope with a stages about every 90 minutes (Box 19-1).

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The most common causes of rectal bleeding in the infant period are a milk protein allergy and an anal fissure purchase cleocin gel 20gm without a prescription acne 24. The patient in the case presenta- tion has no physical examination finding purchase cheap cleocin gel on line acne treatment, so milk protein allergy is more likely purchase generic cleocin gel on-line acne tips. However, with a normal physical examination and no emesis, this diagnosis is unlikely. The abdominal pain is periumbilical, started 12 hours prior, is 9 out of 10 on the pain scale, and is constant, dull, and achy in nature. The acetaminophen her mother gave her did not reduce the pain, but is diminished only by lying supine. She is not hungry and has had one episode of nonbilious emesis 2 hours after the onset of the pain and one small, loose bowel movement. She denies dysuria, urinary frequency, and her last menses a week ago was normal; she denies having any sexual contact. On examination, she appears uncomfortable, has a heart rate of 110 beats/min, and a temperature of 100°F (37°C). Her abdominal examination reveals hypoactive bowel sounds, right rectus abdominis muscle rigidity, and tenderness to palpation, particularly in the periumbilical region. Her pelvic examination shows neither vaginal discharge nor cervical motion tenderness, but she has some abdomi- nal tenderness with gentle bimanual palpation. She has pain at the right lower quadrant when she flexes the right thigh and extends the hip to place her leg into the stirrup for the bimanual examination. She has no dysuria or sexual activity, and the pain appears unrelated to her menses. Her physical examination shows a quiet, rigid, tender abdomen, and positive psoas sign. Despite this adolescent’s denial of sexual activity, a urine pregnancy test should always be obtained in postmenarchal females. Considerations The definitive diagnosis of appendicitis is made once the pathologist finds inflam- mation histologically on the appendix specimen obtained by surgical removal. For this patient, the initial periumbilical abdominal pain followed by anorexia and vomit- ing suggests appendicitis. The pain of appendicitis classically begins periumbilically and then migrates to the right lower quadrant with maximal discomfort at McBurney point. However, the pain can occur laterally if the appendix is retrocecal or it can become diffuse if perforation occurs. If a patient presents early in the disease process, is lacking the characteristic physical examination findings, has inconclusive imaging findings, and thus has a questionable diagnosis, the child may be observed and undergo serial abdominal examinations for a few hours. However, once appendicitis seems likely, surgical management should occur in a timely fashion; perforation rates exceed 65% if diag- nosis is delayed beyond 36 to 48 hours from symptom onset. The most common complications of appendicitis are wound infection and intra-abdominal abscess or phlegmon formation, all of which occur more frequently with appendiceal perfora- tion. Other serious complications are sepsis, shock, ileus, peritonitis, and adhesions causing small bowel obstruction. A person’s life- time risk of appendicitis has been estimated at 6% to 20%, with the peak incidence in adolescence and a slight predilection for males. Appendicitis can develop via several mechanisms but a frequent cause is when the appendiceal lumen becomes obstructed, leading to vascular congestion followed by ischemia, gangrene, and ultimately perforation with spillage of contaminated material into the peritoneum. Obstruction can be caused intrinsically by inspissated fecal material (a fecalith) or by external compression from enlarged lymph nodes associated with bacterial or viral infections. A thorough history of the illness with close attention to symp- toms in other organ systems can help identify these causes; for example, subacute weight loss, sore throat, dysphagia, cough, jaundice, rash, vaginal discharge, and arthralgias do not typically occur with appendicitis. However, diarrhea can be present with appendicitis due to bowel inflammation or because enteric infection may have led to the initial appendiceal inflammation. Appendicitis usually begins with nonspecific symptoms of malaise and anorexia and then abdominal pain following in a few hours. Localization to the right lower quadrant may take 12 to 24 hours to appear, and pain will then be made worse with movement.

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The drug is similar to sumatriptan with regard to mechanism purchase cleocin gel 20gm otc acne 6 months postpartum, efficacy purchase cleocin gel on line amex skin care lotion, and time course—and is better tolerated purchase discount cleocin gel line skin care usa. Like other triptans, almotriptan can cause harmless, transient chest discomfort—but the incidence is very low (only 0. To avoid excessive vasospasm, almotriptan should not be administered within 24 hours of an ergot alkaloid or another triptan. The drug is similar to other triptans with regard to mechanism and side effects— but is less effective and has very different kinetics. Although the number of patients responding at 2 hours is low (37% to 46%), rates of headache recurrence are low too (7% to 23%)—lower than with any other triptan. To avoid excessive vasospasm, frovatriptan should not be administered within 24 hours of an ergot alkaloid or another triptan. The drug is at least as effective as oral sumatriptan and may have a faster onset. To avoid excessive vasospasm, eletriptan should not be administered within 24 hours of an ergot alkaloid or another triptan. P ro t o t y p e D r u g s Drugs for Migraine Headache Nonsteroidal Antiinflammatory Drugs Aspirin Selective Serotonin Receptor Agonists Sumatriptan Ergot Alkaloids Ergotamine Ergot Alkaloids Ergotamine Mechanism of Antimigraine Action. Ergotamine has complex actions, and the precise mechanism by which it aborts migraine is unknown. Ergotamine can alter transmission at serotonergic, dopaminergic, and alpha-adrenergic junctions. In cranial arteries, ergotamine acts directly to promote constriction and reduce the amplitude of pulsations. Ergotamine is used as a second-line drug used for stopping an ongoing migraine attack in patients who have not responded to a triptan. Owing to the risk for dependence (see later), ergotamine should not be taken daily on a long-term basis. Although the half-life of ergotamine is only 2 hours, pharmacologic effects can still be observed 24 hours after dosing. The drug can stimulate the chemoreceptor trigger zone, causing nausea and vomiting in about 10% of patients, thereby augmenting nausea and vomiting caused by the migraine itself. Other common side effects include weakness in the legs, myalgia, numbness and tingling in the fingers and toes, angina-like pain, and tachycardia or bradycardia. In addition to the adverse effects seen at therapeutic doses, overdose can cause ischemia secondary to constriction of peripheral arteries and arterioles: the extremities become cold, pale, and numb; muscle pain develops; and gangrene may eventually result. Patients should be informed about these responses and instructed to seek immediate medical attention if they develop. The risk for ergotism is highest in patients with sepsis, peripheral vascular disease, and renal or hepatic impairment. To avoid this problem, dosing with ergotamine and serotonin agonists should be separated by at least 24 hours. Regular daily use of ergotamine, even in moderate doses, can cause physical dependence. The withdrawal syndrome is characterized by headache, nausea, vomiting, and restlessness. Patients who experience these symptoms are likely to resume taking the drug, thereby perpetuating the cycle of dependence. To avoid dependence, dosage and duration of treatment must be restricted (see dosing guidelines later). In addition, the drug should not be taken during pregnancy because it can promote uterine contractions and hence might cause fetal harm or abortion. Intranasal dihydroergotamine is less effective than intranasal sumatriptan but is associated with a lower rate of migraine recurrence. Pharmacologic Effects The actions of dihydroergotamine are similar to those of ergotamine. Like ergotamine, dihydroergotamine alters transmission at serotonergic, dopaminergic, and alpha-adrenergic junctions. In contrast to ergotamine, dihydroergotamine causes little nausea and vomiting, no physical dependence, and minimal peripheral vasoconstriction (when used alone). Pharmacokinetics Dihydroergotamine may be administered parenterally or by nasal spray—but not by mouth (owing to extensive first-pass metabolism).

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Hence cheap cleocin gel 20gm visa skin care expiration date, drugs that selectively interfere with these unique microbial processes can cause serious injury to microorganisms while leaving mammalian cells intact order cleocin gel 20 gm fast delivery acne jeans men. Disruption of the Bacterial Cell Wall Unlike mammalian cells generic 20gm cleocin gel free shipping skin care routine for oily skin, bacteria are encased in a rigid cell wall. The protoplasm within this wall has a high concentration of solutes, making osmotic pressure within the bacterium high. If it were not for the cell wall, bacteria would absorb water, swell, and then burst. Because mammalian cells have no cell wall, drugs directed at this structure do not affect us. Inhibition of an Enzyme Unique to Bacteria The sulfonamides represent antibiotics that are selectively toxic because they inhibit an enzyme critical to bacterial survival but not to our survival. Specifically, sulfonamides inhibit an enzyme needed to make folic acid, a compound required by all cells, both mammalian and bacterial. Because we can use folic acid from dietary sources, sulfonamides are safe for human consumption. Because mammalian cells do not make their own folic acid, sulfonamide toxicity is limited to microbes. Disruption of Bacterial Protein Synthesis In bacteria, as in mammalian cells, protein synthesis is done by ribosomes. However, bacterial and mammalian ribosomes are not identical, and hence we can make drugs that disrupt function of one but not the other. As a result, we can impair protein synthesis in bacteria while leaving mammalian protein synthesis untouched. Classification of Antimicrobial Drugs Various schemes are employed to classify antimicrobial drugs. Classification by Susceptible Organism Antibiotics differ widely in their antimicrobial activity. Some agents, called narrow-spectrum antibiotics, are active against only a few species of microorganisms. In contrast, broad-spectrum antibiotics are active against a wide variety of microbes. As discussed later, narrow-spectrum drugs are generally preferred to broad-spectrum drugs. The table shows three major groups: antibacterial drugs, antifungal drugs, and antiviral drugs. In addition, the table subdivides the antibacterial drugs into narrow-spectrum and broad-spectrum agents and indicates the principal classes of bacteria against which they are active. We do not know why inhibition of protein synthesis by these agents results in cell death. However, in contrast to the aminoglycosides, these agents only slow microbial growth—they do not kill bacteria at clinically achievable concentrations. Members of this group include rifampin, metronidazole, and the fluoroquinolones (e. The result is either a decrease in the synthesis of essential cell constituents or synthesis of nonfunctional analogs of normal metabolites. When considering the antibacterial drugs, it is useful to distinguish between agents that are bactericidal and agents that are bacteriostatic. Bactericidal drugs are directly lethal to bacteria at clinically achievable concentrations. In contrast, bacteriostatic drugs can slow bacterial growth but do not cause cell death. When a bacteriostatic drug is used, elimination of bacteria must ultimately be accomplished by host defenses (i. Acquired Resistance to Antimicrobial Drugs In this section, we discuss bacterial resistance to antibiotics, which may be innate (natural, inborn) or acquired over time.

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