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The decrease in effective circulating arterial volume due to this patient`s liver disease is responsible for ADH secretion in this patient. Hyponatremia is defined as plasma sodium concentration less than 135 mEq/L. Most patients with hyponatremia are asymptomatic. Symptoms do not usually appear until the plasma sodium level drops below 120 mEq per L. Hyponatremia can be developed in cases of excess water intake that exceed the excretory capacity of the kidneys. Other causes include impared renal functions and ability to excrete excess water, or inappropriate secretion of ADH. Acute severe hyponatremia (i.e., less than 125 mmol per L) usually is associated with neurologic symptoms and should be treated urgently because of the high risk of cerebral edema and hyponatremic encephalopathy. Treat with 3% NaCl to begin with (100 ml infused over 10 minutes and repeated once if needed). Transition to 0.9% NaCl/vaptans at sodium levels > 125 mEq/L.<br/>
'''Educational Objective:''' Acute severe hyponatremia (i.e., less than 125 mmol per L) usually is associated with neurologic symptoms and should be treated with 3% NaCl to begin with (100 ml infused over 10 minutes and repeated once if needed). Transition to 0.9% NaCl/vaptans at sodium levels > 125 mEq/L.<br/>
'''References:''' http://www.wikidoc.org/index.php/Hyponatremia_resident_survival_guide +
The decrease in effective circulating arterial volume due to this patient`s liver disease is responsible for ADH secretion in this patient. Hyponatremia is defined as plasma sodium concentration less than 135 mEq/L. Most patients with hyponatremia are asymptomatic. Symptoms do not usually appear until the plasma sodium level drops below 120 mEq per L. Hyponatremia can be developed in cases of excess water intake that exceed the excretory capacity of the kidneys. Other causes include impaired renal functions and ability to excrete excess water, or inappropriate secretion of ADH. In asymptomatic euvolemic hyponatremia, fluid restriction (less than 1 to 1.5 L per day) is the mainstay of the treatment.<br/>
'''Educational Objective:''' In asymptomatic euvolemic hyponatremia, fluid restriction (less than 1 to 1.5 L per day) is the mainstay of the treatment.<br/>
'''References:''' http://www.wikidoc.org/index.php/Hyponatremia +
Cluster headaches are recurring bouts of excruciating unilateral headache attacks of extreme intensity. The duration of a typical CH attack ranges from about 15 to 180 minutes. Most untreated attacks (about 75%) last less than 60 minutes.
The onset of an attack is rapid and most often without preliminary signs that are characteristic in migraine. Preliminary sensations of pain in the general area of attack, referred to as "shadows", may signal an imminent CH, or these symptoms may linger after an attack has passed, or even between attacks. Though a CH is strictly unilateral, there are some documented cases of "side-shift" between cluster periods, extremely rare, simultaneously (within the same cluster period) bilateral headache.
The pain occurs on one side only (unilateral), around the eye (orbital), particularly above the eye (supraorbital), in the temple (temporal), in any combination. The pain of CH is remarkably greater than in other headache conditions, including severe migraine. The term "headache" does not adequately convey the severity of the condition; the disease may be the most painful condition known to medical science. The pain is described as stabbing, burning or squeezing and may be located near or behind the eye and at the back of the head or neck.
Prevention:
Preventive treatments are used to reduce or elimination cluster headache attacks; they are generally used in combination with abortive and transitional techniques.
1.Verapamil
The recommended first-line preventative therapy is verapamil, a calcium channel blocker. Verapamil was previously underused in people with cluster headache.
Steroids
There is little evidence to support a long-term benefit from steroids, but they may be used until other medications take effect as they appear to be effective at three days. They are generally discontinued after 8–10 days of treatment.
2.Surgery
Nerve simulators may be an option in the small number of people who do not improve with medications. Two procedures, deep brain stimulation or occipital nerve stimulation, may be useful; early experience shows a benefit in about 60% of cases. It typically takes weeks or months for this benefit to appear. A non-invasive method using transcutaneous electrical nerve stimulation (TENS) is being studied.
A number of surgical procedures, such as a rhizotomy or microvascular decompression, may also be considered, but evidence to support them is limited and there are cases of people ending up worse off.
3.Other
Lithium, methysergide, and topiramate are recommended alternative treatments, although there is little evidence supporting the use of topiramate or methysergide. This is also true for melatonin and ergotamine. Valproate, sumatriptan and oxygen are not recommended as preventative measures. Botox injection have shown mixed success.
Management:
Treatment for cluster headache is divided into three primary categories: abortive, transitional, and preventative. There are two primary treatments for acute CH: oxygen and triptans, but they are underused due to misdiagnosis of the syndrome. During bouts of headaches, triggers such as alcohol, nitroglycerine and naps during the day should be avoided.
1.Oxygen
Oxygen therapy may help people with CH, but it does not help prevent future episodes. Typically it is given via a non-rebreather mask at 12-15 liters per minute for 15–20 minutes. Around 70% improve within 15 minutes. It is unclear if hyperbaric oxygen therapy is better than high flow oxygen.
2.Triptans
The other primarily recommended treatment of acute attacks is subcutaneous or intranasal sumatriptan. Sumatriptan and zolmitriptan have both been shown to improve symptoms during an attack with sumatriptan being superior. Because of the vasoconstrictive action of triptans, they are contraindicated in people with ischemic heart disease.
3.Opioids
The use of opioid medication in management of CH is not recommended; they may make headache syndromes worse and their long-term use is associated with dependency, addiction and withdrawal syndromes. Prescription of opioid medication may additionally lead to a delay in diagnosis, undertreatment, and mismanagement.
Other
The vasoconstricting ergot compounds may be useful, but have not been well studied in acute attacks.<br/>
'''Educational Objective:''' Since the patient has unilateral headache with tearing, redness and rhinorrhoea the diagnosis is 100% cluster headache. The treatment for an acute attack is Sumatriptan and oxygen via nasal cannula . However, cluster headache is prevented by using calcium channel blockers like verapamil, cyproheptadine, topiramate, valproate, lithium carbonate and amitriptyline .<br/>
'''References:'''
This is a classical history of Benign paroxysomal positional vertigo (BPPV). BPPV is a disorder of the vestibular system usually affecting balance. Patients often describe their first experience occurring while turning their head in bed or while driving a car .
The vertigo is brief in duration — 5 seconds to 30 seconds.It is often associated with nausea. No other neurological deficits are noted. However care must be taken and a posterior circulation stroke should be kept in mine while treating these patients.
'''Educational Objective'''
A vertigo lasting for a few seconds and associated or brought about by change in position is Benign positional vertigo unless proved otherwise.<br/>
'''Educational Objective:''' <br/>
'''References:''' +
The treatment of choice for this condition is the Epley canalith repositional maneuver which is effective in approximately 80% of patients. The treatment employs gravity to move the calcium build-up that causes the condition). The particle repositioning maneuver (Epley Maneuver) can be performed during a clinic visit by specially trained otolaryngologists, neurologists, chiropractors, physical therapists, or audiologists. The maneuver is relatively simple but few general health practitioners know how to perform it.
Treatment may also be achieved with the use of a device such as "The DizzyFIX", a device that enables patients and health practitioners to guide themselves through the particle repositioning maneuver. The maneuver can be conducted at home and repeated as often as needed. Other devices, such as a head over heels "rotational chair", are also available at some tertiary care centers .The Epley maneuver (particle repositioning) does not address the actual presence of the particles (otoconia), rather it changes their location. The maneuver moves these particles from areas in the inner ear which cause symptoms, such as vertigo, and repositions them into areas where they do not cause these problems.<br/>
'''Educational Objective:''' <br/>
'''References:''' +
The patients presents with classical symptoms of stroke. The patient has all the risk factors for stroke like diabetes, hypertension and hypercholesteremia. The patient presents with facial asymmetry , one-sided facial droop, asymmetrical smile, difficulty completely closing one eye, and impaired tearing and salivation on left side . the multiple red papule suggesting Zoster is a distraction . Irrespective of the conditions stroke has to be ruled out first and hence CT Scan is the next best step to rule out stroke. Acyclovir may be started later after stroke is ruled out.
'''Educational Objective''' If the patient has symptoms of stroke or stroke mimicking symptoms a CT scan should be performed immediately and stroke should be ruled out first before initiating any kind of therapy.<br/>
'''Educational Objective:''' <br/>
'''References:''' +
Chronic metformin use for more than 10- 15 years cause Vit B12 deficiency by exhaustion of the stores. It presents as a peripheral neuropathy often misdiagnosed as diabetic neuropathy. The Other side efect of metformin is lactic acidosis. This B12 deficiency should be treated by stopping the offending agent and replenishing b12 stores.<br/>
'''Educational Objective:''' <br/>
'''References:''' +
The Glasgow Coma Scale or GCS is a neurological scale that aims to give a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment. A patient is assessed against the criteria of the scale, and the resulting points give a patient score between 3 (indicating deep unconsciousness) and either 14 (original scale) or 15 (the more widely used modified or revised scale).
The scale is composed of three tests: eye, verbal and motor responses. The three values separately as well as their sum are considered. The lowest possible GCS (the sum) is 3 (deep coma or death), while the highest is 15 (fully awake person).
Eye response (E)
There are four grades starting with the most severe:
#No eye opening
#Eye opening in response to pain stimulus. (a peripheral pain stimulus, such as squeezing the lunula area of the patient's fingernail is more effective than a central stimulus such as a trapezius squeeze, due to a grimacing effect).
#Eye opening to speech. (Not to be confused with the awakening of a sleeping person; such patients receive a score of 4, not 3.)
#Eyes opening spontaneously
Verbal response (V)
There are five grades starting with the most severe:
#No verbal response
#Incomprehensible sounds. (Moaning but no words.)
#Inappropriate words. (Random or exclamatory articulated speech, but no conversational exchange)
#Confused. (The patient responds to questions coherently but there is some disorientation and confusion.)
#Oriented. (Patient responds coherently and appropriately to questions such as the patient’s name and age, where they are and why, the year, month, etc.)
Motor response (M)
There are six grades:
#No motor response
#Extension to pain (extensor posturing: abduction of arm, external rotation of shoulder, supination of forearm, extension of wrist, decerebrate response)
#Abnormal flexion to pain (flexor posturing: adduction of arm, internal rotation of shoulder, pronation of forearm, flexion of wrist, decorticate response)
#Flexion/Withdrawal to pain (flexion of elbow, supination of forearm, flexion of wrist when supra-orbital pressure applied ; pulls part of body away when nailbed pinched)
#Localizes to pain. (Purposeful movements towards painful stimuli; e.g., hand crosses mid-line and gets above clavicle when supra-orbital pressure applied.)
#Obeys commands. (The patient does simple things as asked.)
Interpretation
Individual elements as well as the sum of the score are important. Hence, the score is expressed in the form "GCS 9 = E2 V4 M3 at 07:35".
Generally, brain injury is classified as:
*Severe, with GCS < 9
*Moderate, GCS 9–12 (controversial)
*Minor, GCS ≥ 13.
Tracheal intubation and severe facial/eye swelling or damage make it impossible to test the verbal and eye responses. In these circumstances, the score is given as 1 with a modifier attached e.g. "E1c" where "c" = closed, or "V1t" where t = tube. A composite might be "GCS 5tc". This would mean, for example, eyes closed because of swelling = 1, intubated = 1, leaving a motor score of 3 for "abnormal flexion". Often the 1 is left out, so the scale reads Ec or Vt.
'''Education Objective'''
A score of <9 is a sign of impending respiratory failure and all patients must be intubated first before starting any treatment<br/>
'''Educational Objective:''' <br/>
'''References:'''
This is a clear case of 'Rhinitis medicamentosa'. The patient classically presents with a running nose which first improves after using topical decongestants but worsens aftera few days due to rebound congestion. This is a very common side-effect of topical decongestants.
Rhinitis medicamentosa (or RM) is a condition of rebound nasal congestion brought on by extended use of topical decongestants (e.g. oxymetazoline, phenylephrine, and xylometazoline nasal sprays) that work by constricting blood vessels in the lining of the nose. This condition typically occurs after 5 to 7 days of use of such medications. Patients often try increasing both the dose and the frequency of nasal sprays upon the onset of RM, worsening the condition. The swelling of the nasal passages caused by rebound congestion may eventually result in polyps that block nasal breathing until surgically removed.
Topical nasal sprays act as an agonist to sympathetic α1 receptors in the blood vessels of the nose, signaling those vessels to contract. By decreasing blood flow to the lining of the nose, the tissue becomes less congested and mucous production is slowed. However, after several days use of these products these receptors become downregulated requiring more frequent and higher doses to prevent the rebound congestion that results when the medicine wears off.
The treatment of RM involves withdrawal of the offending nasal spray. Both a "cold turkey" and a "weaning" approach can be used. Symptoms of congestion and runny nose can often be temporized by using prescription nasal steroid sprays 1 to 2 times daily for a few weeks. For very severe cases oral steroids may be necessary. Oral decongestant medications like pseudoephedrine can also help with the transition.
Other commercially available products such as Rhinostat may help ease withdrawal from physiological tolerance to the nasal decongestant by providing an easy means to dilute the spray gradually.
A study has shown that the anti-infective agent benzalkonium chloride, which is frequently added to topical nasal sprays, aggravates the condition by further increasing the rebound swelling.
Common issues that lead to overuse of topical decongestants:
1.Deviated septum
2.Upper respiratory tract infection
3.Vasomotor rhinitis
4.Cocaine abuse
5.Pregnancy (these products are not considered safe for pregnancy, however)
6.Chronic rhinosinusitis
7.Hypertrophy of the Inferior Turbinates
'''Eductional Objective'''
Rhinitis medicamentosa (or RM) is a condition of rebound nasal congestion brought on by extended use of topical decongestants (e.g. oxymetazoline, phenylephrine, and xylometazoline nasal sprays) that work by constricting blood vessels in the lining of the nose. This condition typically occurs after 5 to 7 days of use of such medications. Prevention is by stopping the drug after 3 days.<br/>
'''Educational Objective:''' <br/>
'''References:'''
The vast majority of cases of sinusitis are caused by viruses and will therefore resolve without antibiotics. However, if symptoms do not resolve within 10 days, amoxicillin is a reasonable antibiotic to use first for treatment with amoxicillin/clavulanate being indicated when the person's symptoms do not improve after 7 days on amoxicillin alone. Antibiotics are specifically not recommended in those with mild / moderate disease during the first week of infection due to risk of adverse effects, antibiotic resistance, and cost. Due to increasing resistance to amoxicillin the Infectious Diseases Society of America recommends amoxicillin-clavulanate as the treatment of choice for acute sinusitis. They also recommend against other commonly used antibiotics, including azithromycin, clarithromycin and trimethoprim/sulfamethoxazole, because of growing drug resistance.
Fluoroquinolones, and a newer macrolide antibiotic such as clarithromycin or a tetracycline like doxycycline, are used in those who have severe allergies to penicillins. Because of increasing resistance to amoxicillin the 2012 guideline of the Infectious Diseases Society of America recommends amoxicillin-clavulanate as the initial treatment of choice for bacterial sinusitis. The guidelines also recommend against other commonly used antibiotics, including azithromycin, clarithromycin and trimethoprim/sulfamethoxazole, because of growing drug resistance.
A short-course (3–7 days) of antibiotics seems to be just as effective as the typical longer-course (10–14 days) of antibiotics for those with clinically diagnosed acute-bacterial sinusitis without any other severe disease or complicating factors. The IDSA guideline suggest five to seven days of antibiotics is long enough to treat a bacterial infection without encouraging resistance. The guidelines still recommend children receive antibiotic treatment for ten days to two weeks.<br/>
'''Educational Objective:''' If failure of treatment even after 7 days of diagnosis the the patient should be started on 1. Amoxicillin-clavulanate 4g per day of amoxicillin equivalent,2. Levofloxacin 500 mg orally once daily, 3. Moxifloxacin400 mg orally once daily.<br/>
'''References:'''
A history of fever and seizures in a 11 month old child is highly suggestive of an infection . Since the patient is from Haiti where malaria and other parasitic infection are endemic an empirical therapy of anti malarial should be started right away . Since the thick and thin smears are negative malaria is ruled out and other infectons should be thought about. The next step in the management is do a lumbar puncture and rule out other infection like meningitis from encephalitis.
'''Educational objective''':
Rule out encephalitis and meningitis before starting empirical therapy in a case of unknown sezirues with fever. Lumbar puncture is always the next best step in the management.<br/>
'''Educational Objective:''' <br/>
'''References:''' +
Herpesviral Encephalitis can be treated with high-dose intravenous aciclovir. Without treatment, HSE results in rapid death in approximately 70% of cases; survivors suffer severe neurological damage. When treated, HSE is still fatal in one-third of cases, and causes serious long-term neurological damage in over half of survivors. Twenty percent of treated patients recover with minor damage. Only a small population of survivors (2.5%) regain completely normal brain function. Earlier treatment (within 48 hours of symptom onset) improves the chances of a good recovery. Rarely, treated individuals can have relapse of infection weeks to months later. While the herpes virus can be spread, encephalitis itself is not infectious. Other viruses can cause similar symptoms of encephalitis, though usually milder (human herpes virus-6, varicella zoster virus, Epstein-Barr, cytomegalovirus, coxsackievirus, etc.).<br/>
'''Educational Objective:''' Acyclovir is used to treat for HSV-encephalitis. The patient is treated for 3-4 weeks for a minimum.<br/>
'''References:''' +
Dengue fever, also known as breakbone fever, is an infectious tropical disease caused by the dengue virus. Symptoms include fever, headache, muscle and joint pains, and a characteristic skin rash that is similar to measles. In a small proportion of cases the disease develops into the life-threatening dengue hemorrhagic fever, resulting in bleeding, low levels of blood platelets and blood plasma leakage, or into dengue shock syndrome, where dangerously low blood pressure occurs.
There are no specific antiviral drugs for dengue, however maintaining proper fluid balance is important. Treatment depends on the symptoms. Those who are able to drink, are passing urine, have no "warning signs" and are otherwise healthy can be managed at home with daily follow up and oral rehydration therapy. Those who have other health problems, have "warning signs" or who cannot manage regular follow up should be cared for in hospital. In those with severe dengue cared should be provided in an area where there is access to an intensive care unit.
Intravenous hydration, if required, is typically only needed for one or two days. The rate of fluid administration is titrated to a urinary output of 0.5–1 mL/kg/h, stable vital signs and normalization of hematocrit. The smallest amount of fluid required to achieve this is recommended. Invasive medical procedures such as nasogastric intubation, intramuscular injections and arterial punctures are avoided, in view of the bleeding risk. Paracetamol (acetaminophen) is used for fever and discomfort while NSAIDs such as ibuprofen and aspirin are avoided as they might aggravate the risk of bleeding. Blood transfusion is initiated early in people presenting with unstable vital signs in the face of a decreasing hematocrit, rather than waiting for the hemoglobin concentration to decrease to some predetermined "transfusion trigger" level. Packed red blood cells or whole blood are recommended, while platelets and fresh frozen plasma are usually not. Corticosteroids do not appear to affect outcomes and may cause harm, thus are not recommended.
During the recovery phase intravenous fluids are discontinued to prevent a state of fluid overload. If fluid overload occurs and vital signs are stable, stopping further fluid may be all that is needed. If a person is outside of the critical phase, a loop diuretic such as furosemide may be used to eliminate excess fluid from the circulation.<br/>
'''Educational Objective:''' Serial platelet counts should be ordered once the patient is admitted. One should wait till platelets drop below 10,000 to start transfusion.<br/>
'''References:'''
The patient in this vignette most likely has idiopathic pulmonary fibrosis (IPF). IPF is a chronic and ultimately fatal disease characterized by a progressive decline in lung function. IPF belongs to a large group of more than 200 lung diseases known as interstitial lung diseases (ILD), characterized by the involvement of lung interstitium. The interstitium, the tissue between the air sacs in the lung, is the primary site of injury in interstitial lung diseases. However, these disorders frequently affect not only the interstitium, but also the airspaces, peripheral airways, and vessels.
Lung tissue from individuals with IPF shows a characteristic histopathologic pattern known as usual interstitial pneumonia (UIP). UIP is classically characterized by a “honeycombing” pattern on chest CT. Honeycombing is a lung condition defined by the presence of small cystic spaces with irregularly thickened walls composed of fibrous tissue. Interstitial lung disease and IPF in particular is characterized by honeycombing of the lower lobes of the lung.
The patient in this vignette displays a progressive course of decreasing lung function consistent with pulmonary dysfunction. Normally, FEV1/FVC is approximately 80%; higher values can indicate restrictive lung disease. Because this patient has an FEV1/FVC of 90%, he likely has restrictive lung disease. The patient’s chest CT shows classic honeycombing pattern of fibrosis in the lower lobes, which is classic for interstitial lung disease. There are many causes of interstitial lung disease, but the other options are ruled out by the negative laboratory findings.
Recent phase 3 trials have indicated that antifibrotic drugs and tyrosine kinase inhibitors reduce disease severity in patients with idiopathic pulmonary fibrosis (See review of 3 phase 3 trials by Hunninghake et al.)<br/>
'''Educational Objective:''' Idiopathic pulmonary fibrosis is a form of interstitial lung disease that is characterized by progressive pulmonary dysfunction and "honeycombing" appearance of the lung on CT.<br/>
'''References:''' Hunninghake GM. A new hope for idiopathic pulmonary fibrosis. N Engl J Med. 2014;370(22):2142-2143.<br>
Gross TJ, Hunninghake GW. Idiopathic pulmonary fibrosis. N Engl J Med. 2001;345(7):517-525.<br>
King Jr, Talmadge E, et al. A phase 3 trial of pirfenidone in patients with idiopathic pulmonary fibrosis. N Engl J Med. 2014; 370(22):2083-2092.<br>
First Aid 2015 page 611.
Silicosis is a form of occupational lung disease caused by inhalation of crystalline silica dust, and is marked by inflammation and scarring in the form of nodular lesions in the upper lobes of the lungs. When fine particles of silica dust are deposited in the lungs, macrophages that ingest the dust particles will set off an inflammation response by releasing tumor necrosis factors, interleukin-1, leukotriene B4 and other cytokines. In turn, these stimulate fibroblasts to proliferate and produce collagen around the silica particle, thus resulting in fibrosis and the formation of the nodular lesions.
Radiographically, chronic simple silicosis reveals a profusion of small (<10 mm in diameter) opacities, typically rounded, and predominating in the upper lung zones. These opacities are often referred to as “eggshell calcifications”.<br/>
'''Educational Objective:''' Silicosis is a pneumoconiosis associated with exposure to silica particles. It causes predominantly upper lobe disease and will classically demonstrate “eggshell calcification”.<br/>
'''References:''' Leung, Chi Chiu, Ignatius Tak Sun Yu, and Weihong Chen. "Silicosis." The Lancet 379.9830 (2012): 2008-2018.<br>
First Aid 2015 page 612<br>
First Aid 2014 page 606 +
Thioridazine is a typical antipsychotic that prolongs the QTc interval in a dose-dependent manner. It was previously widely used in the treatment of schizophrenia but was largely discontinued due to cardiotoxicity and retinopathy. The electrocardiogram from this patient demonstrates a widened QT interval. The QT interval represents electrical depolarization and repolarization of the ventricles. A lengthened QT interval is a marker for the potential of ventricular tachyarrhythmias like torsades de pointes and a risk factor for sudden death.<br>
'''Note:''' While First Aid 2014 claims that risperidone lengthens the QT interval and may cause torsades de pointes, there is no evidence that risperidone increases the risk of torsades de pointes (see review by Glassman et al.).<br/>
'''Educational Objective:''' Thioridazine potently prolongs the QT interval and has been documented to cause torsades de pointes.<br/>
'''References:''' Glassman AH, Bigger JT. Antipsychotic drugs: prolonged QTc interval, torsade de pointes, and sudden death. Am J Psychiatry. 2001;158(11):1774-82.<br>
First Aid 2015 page 283 (Long QT and Torsades de pointes)<br>
First Aid 2015 page 521 (Antipsychotics)<br>
First Aid 2014 page 277 (Long QT and Torsades de pointes)<br>
First Aid 2014 page 517 (Antipsychotics)<br> +
The patient in this vignette is self-administering diphenhydramine (Benadryl) to help her fall asleep. Diphenyhdramine is a Histamine H<sub>1</sub> blocker. The H<sub>1</sub> receptor is linked to an intracellular G-protein (G<sub>q</sub>) that activates phospholipase C and the phosphatidylinositol (PIP2) signaling pathway. Antihistamines, which act on this receptor, are used as anti-allergy drugs. By blocking histamine binding of the H1 receptor, diphenhydramine blocks G<sub>q</sub> activation.<br/>
'''Educational Objective:''' Antihistamines act on the H<sub>1</sub> receptors and are used as anti-allergy drugs. By blocking histamine binding of the H1 receptor, diphenhydramine blocks G<sub>q</sub> activation.<br/>
'''References:''' Leurs R, Smit MJ, Timmerman H. Molecular pharmacological aspects of histamine receptors. Pharmacol Ther. 1995;66(3):413-463.<br>
First Aid 2015 page 248. +
The patient in this vignette has fallen unconscious due to severe hypotension from nitrate overdose. Isosorbide dinitrate is a commonly prescribed drug used to treat angina pectoris. It is most commonly administered sublingually. Patients experiencing angina when doing certain physical activities can often prevent symptoms by taking nitroglycerin 5 to 10 minutes before the activity. Isosorbine dinitrate is converted to nitric oxide by mitochondrial aldehyde dehydrogenase. Nitric oxide is a potent vasodilator that decreases vascular tone by increasing intracellular cGMP. Nitric oxide preferentially dilates veins compared to arterioles, thereby decreasing venous system pressure and cardiovascular preload. Because both end diastolic volume and blood pressure are decreased, myocardial oxygen consumption is decreased and angina is attenuated.
Nitric oxide, known as the 'endothelium-derived relaxing factor', or 'EDRF', is biosynthesized endogenously from L-arginine, oxygen, and NADPH by various nitric oxide synthase (NOS) enzymes.<br/>
'''Educational Objective:''' Endothelial nitric oxide synthase (ENOS) produces the vasodilator nitric oxide from L-Arginine.<br/>
'''References:''' First Aid 2015 page 106<br>
First Aid 2014 page 299 +
The patient in this vignette has contracted a subtype of hypersensitivity pneumonitis called “Bird Fancier’s Lung”. This disease is caused by the exposure to avian proteins present in the dry dust of the droppings and sometimes in the feathers of a variety of birds. People who work with birds or own many birds are at risk. Bird hobbyists and pet store workers may also be at risk. This question requires that test takers calculate the Aveolar-arterial (A-a) oxygen gradient. Recall that the equation for A-a gradient is PAO<sub>2</sub> - PaO<sub>2</sub>. PaO<sub>2</sub> can be measured in the patient’s blood. PAO<sub>2</sub> is given by the following equation:
'''150 - (PaCO<sub>2</sub>/0.8) = 150 - (40/0.8) = 100'''
The A-a gradient is the PAO<sub>2</sub> - PaO<sub>2</sub>:
'''100 - 70 = 30 mmHg'''<br/>
'''Educational Objective:''' The Aveolar-arterial (A-a) gradient is defined as the difference between PAO2 and PaO2. “Bird Fancier’s Lung” is a type IV hypersensitivity reaction.<br/>
'''References:''' First Aid 2014 page 605 (Hypersensitivity pneumonitis)<br>
Funke M, Fellrath JM. Hypersensitivity pneumonitis secondary to lovebirds: a new cause of bird fancier's disease. Eur Respir J. 2008;32(2):517-21. +
Antipsychotics can cause SIADH resulting in the dilutional hyponatremia.<br/>
'''Educational Objective:''' Antipsychotics can cause SIADH, which is commonly observed in schizophrenic patients. SIADH results in dilutional hyponatremia.<br/>
'''References:''' http://www.ncbi.nlm.nih.gov/pubmed/20082537
http://www.wikidoc.org/index.php/Clinical_depression_history_and_symptoms
http://www.wikidoc.org/index.php/Serotonin_syndrome
http://www.wikidoc.org/index.php/Hyponatremia_history_and_symptoms
http://www.wikidoc.org/index.php/Malignant_hyperthermia +