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2 months then RH for 4 months - Pregnant and lactating woman: PZA and Streptmycin CI. ERH (increased doses) for 48weeks, then RH twice Qweek x 7months. If resistance is a concern: ERH x 9months. Add Vit B6 with INH use. Breast-feeding is not contraindicated despite presence of small amounts of meds in milk. - HIV Positive: Same treatment with additional considerations: longer duration, Rifampin interaction with anti-HIV meds, directly-observed TB therapy should be used for all HIV pts, VitB6 mandatory with INH to reduce side effects. - Drug-resistant patient: Resistance only to INH = RZ with E or S x 6months or ER x 12 months. Others require expert intervention. - Extrapulmonary TB: 9months with same drugs if miliary, bone, meningeal, or joint TB. If bone: early surgical drainage and debridement of necrotic bone. Steriod therapy prevents cardiac constriction and neurologic complications from meningitis. - Latent TB: targeted testing to identify candidates, test for HIV, screen for prior TB Rx and current contraindications. Three regimens are considered: 1) Ideally: INH for 9months. Give Vit B6 if at risk to develop neuropathy (Pregnant, DM, HIV, alcoholic, uremia, Seizure disorder). 2) RZ x 2 months. 3) Rifampin x 4 months. Care must be taken if HIV patients on Nonnucleoside RT Inhibitors or Protease inhibitors. If Pregnant or lactating: INH QD or BID + Vit B6. - BCG Vaccine: recommended only on individual basis: e.g.: Healthcare worker with high % of multiresistant TB patients. CI if immune deficiency/impairement. - Steriod use in TB Rx: only in TB meningitis and TB pericarditis. PPD + is when: - >5mm: HIV+, Recent TB patient contact, CXR TB-like changes, Organ Transplant patients. - >10mm: Recent immigrant, IV drug user HIV-, TB lab personel, High risk medical personel, High risk medical conditions (Gastrectomy, GI bypass, DM, Silicosis, CRF, Leukemia, lymphoma, CA of HEENT or lung), kids<4yo or teens and adults exposed to TB patients. - >15mm: if no risk factors to TB. If PPD – then converts to <10mm => Repeat in 2 weeks (you cannot make a PPD- person become positive by repeated testing). If PPD is + => CXR: if abnormal => 3 AFB. TB prophylaxis now called latent TB: PPD + indicates 10% lifetime risk for active TB. - Exposed adult with PPD - => None - Exposed child<5yo with PPD - => INH x3months - PPD conversion but CXR - =>INH x6-12months
- Pregnant woman + HIV+ with PPD+/Conversion/Exposure to TB but no active disease: INHx 6-12months + Vit B6 Side Effects of TB drugs: All are hepatotoxic except Streptomycin. - INH: Hepatitis – Peripheral neuropathy - Rifampin: colors body secretions, contact lenses. Hepatitis, Renal Failure – drug interaction with OCP/Coumadin/Digoxin/Oral hypoglycemics/HIV meds - PZA: hyperuricemia, hepatotoxic, - ETB: Optic neuritis (reversible) - Streptomycin: VIII damage, nephrotoxic. Is there any correlation between lesion location and the develoment of post-stroke neuropsychiatric sequelae? A 69-year-old patient is admitted to the neurology service following a stroke. During the next few days, the staff observes that the patient has developed the clinical picture of mania. Which area of the brain has most likely been affected by the stroke? A. Left hemispheric lesions including Broca's area B. Left prefrontal cortex C. Midbrain lesion D. Right frontal lobe E. Thalamus Answer D. Is there any correlation between lesion location and the develoment of post-stroke neuropsychiatric sequelae? Possibly. In the case of post-stroke mania, it appears to occur most often with right hemispheric lesions especially when they occur in the right orbitofrontal region or the right thalamus. Treatment of post-stroke mania: controlled studies have not yet been completed, although case studies have suggested that Lithium, Depakote and Carbamazepine, Clonidine, and neuroleptics, may each be effective in such an entity. Given that anticonvulsant mood stabilizers have shown to be more effective in secondary mania, and given the propensity of convulsions in post-stroke patients, mood stabilizing anticonvulsants may be the agents of choice in post-stroke mania. Notes: Controvesy exists in correlating locations with post-stroke depression. It is suggested that it may be related to left frontal cortex, and left frontal basal ganglia. Treatment involves SSRI's (first line), TCA's (risk of ortho hypotension, and cardiac conduction abnormalities), Stimulants (May stimulate during post stroke rehab and stroke is NOT a contraindication) and ECT. Reference: Primary Care Companion J Clin Psych.2003;5(2) http://www.psychiatrist.com/pcc/pccpdf/v05n02/v05n0205.pdf Fragile X Syndrome
A- Background: Fragile X syndrome, also termed Martin-Bell syndrome or marker X syndrome, is the most common cause of inherited mental retardation and, after trisomy 21, is the second most common cause of genetically associated mental deficiencies. Two to four times as many females carry the gene abnormality as males, but only about one third of females carrying the abnormal gene show decreased intelligence. Males with the disorder are more likely to be sensitive to environmental factors. The pattern of inheritance most closely resembles X-linked dominant with variable penetrance. Occasionally, because the complex genetics of the disorder, a female will be affected severely. B- Pathophysiology: The genetic defect is dynamic and lies at the distal end of the long arm of the X chromosome. Careful examination of the karyotype of affected individuals' lymphocytes, reveals a constriction followed by a thin strand of genetic material extending beyond the long arm of chromosome X. This constriction and thin strand produces the appearance of a fragile portion of the X chromosome, leading to the term fragile X. The underlying pathology is an unusual high number of repeats of triplets CGG. Unaffected individuals have 5 to 55 CGG repeats. A span of 65 to 230 repeats is known as a premutation, whereas more than 230 repeats is a full mutation. The number of repeats is unstable from generation to generation, making the pattern of inheritance difficult to predict. • Males with a full mutation have fragile X syndrome. • Mothers of all males with fragile X syndrome have the premutation or fragile X syndrome themselves. • Males with fragile X syndrome pass a premutation to their daughters because sperm cells are mosaics. • Sons are unaffected because they receive the Y chromosome from their fathers. • Half of females with the full mutation on a single X chromosome are unaffected because of inactivation of the other X chromosome. The other half of females have fragile X syndrome, although with less severe mental retardation than males with the disorder. • Males with a premutation usually are unaffected to mildly affected and transmit the premutation to their daughters. The mutation is stable; thus, no increase in the CGG triplets exists, when it’s a male transmitting it. • Females with a premutation usually are unaffected to mildly affected. Unlike their male counterparts, the CGG triplets are unstable and increase in size during oogenesis. If the number of repeats exceeds 230 and the oocyte is fertilized, a male child will have fragile X syndrome, and a female child will have a 50% chance of having fragile X syndrome. The number of repeats is directly proportional to the risk of the disorder in an offspring. C- Clinically: Cognitive, behavioral, and neuropsychological difficulties predominate the clinical picture. These signs are especially important in alerting physicians, parents, and teachers to deficits exhibited by preschool and elementary school children—a time when the diagnosis of fragile X syndrome often is made or considered.
developmental delays after reaching early milestones (especially speech and language delays). and decreasing IQ with increasing age.emedicine. deficiency in abstract thinking. repeat evaluation may be necessary.Special Concerns: • Prenatal screening: Because fragile X syndrome is underdiagnosed. sinusitis. and neuropsychological findings. and occupational therapist is recommended to assess weaknesses and to identify areas where improvement is needed most. mental retardation with IQ typically 35-70. preconceptual and antenatal molecular genetic screening is encouraged for women as outlined below. scoliosis may be noted. It can be diagnostic and therapeutic by direct removal of common bile duct stones. They are sensitive (65%) and specific (6%) for chronic cholecystitis. physical therapist. and a prominent forehead and jaw. there are physical signs associated with fragile X syndrome. o Routine care involves treating the medical problems that these patients experience commonly. methylphenidate. F. attention deficits. o During infant and early childhood health care maintenance visits. o Stimulants (eg. depressed affect. As the patient matures. genital. and otitis media. the mouth has overcrowding and a high-arched palate.Work-up . focus examination on possible hip dislocations.A comprehensive developmental evaluation by a speech/language therapist.Problems include: mild-to-moderate autisticlike behavior (most notably. has a high prevalence. Responses are variable. and hypotonia. . behavioral. o Antiseizure and antireflux medications are useful for patients with these symptoms. In addition to the cognitive. They manifest in adolescence as a long thin face with prominent ears. and is inheritable.Complications: o Scoliosis o Mitral valve prolapse (most frequently encountered cardiac defect) G.com/ped/topic800. and musculoskeletal. pemoline) have been used for attention deficits in the doses prescribed for patients with ADHD.htm Updated March 2003 ERCP or HIDA Scan HIDA scans have sensitivity (94%) and specificity (65-85%) for acute cholecystitis. facial asymmetry.Emedicine: http://www. these signs are more obvious during adolescence or after puberty and rarely result in disabilities. the organ systems most frequently involved are craniofacial. however.Cytogenetics (Karyotype) is not as sensitive as molecular testing (Southern Blot and PCR). including gastroesophageal reflux. In addition. . dextroamphetamine. hand flapping and avoidance of eye contact). References: . hernias. D. E. aggressive tendencies.Medical Care: o Workup and diagnosis can be done on an outpatient basis. ERCP provides both endoscopic and radiographic visualization of the biliary tract. Sometimes. On the other hand. Macroorchidism is universal in adult males. In addition. a head circumference higher than the 50th percentile.
2)Dog. however.emedicine.128(19):1059-63. in general. Major complications of ERCP include pancreatitis and cholangitis. . in cases carrying a low risk of infection. Therefore. If a bite wound is infected. In this population. In patients who present early after the injury. Reference: http://www. since cholecystitis is caused by obstruction of the ducts. 3)Diagnosis and treatment of bites by cats. it appears prudent to leave the wounds open. bones and tendons. In patients with any of the risk factors. when a dilated common bile duct is found or elevated LFTs are present.com/emerg/topic98. and human bites: a review.87(21):716-8. people with any of the risk factors for common bile duct stones should undergo operative or ERCP evaluation of the common bile duct. The increased incidence of serious infections and complications associated with human bites to the hand warrants their consideration and management in three different categories: occlusional/simple. Furthermore. Debate exists as to when an ERCP should be performed.33(6):1019-29. References: 1)Dog. suspicion should remain high for common bile duct stones. The management of bite wounds consists of intensive irrigation with large volumes of normal saline and a cautions debridement of devitalized tissues. CT and HIDA scans are not better. J Am Acad Dermatol. and (3) a common bile duct diameter of less than 8 mm.Ultrasound is 50-75% sensitive for choledocholithiasis. and human bites Schweiz Rundsch Med Prax. a tetanus booster and in case of possible transfer of rabies. and occlusional bites to the hand. However. a primary surgical closure might be appropriate. the risk of common bile duct stones may be as low as 1%. Generally.htm Is a dog/cat's mouth cleaner than a human mouth? Animal and human bites carry a high risk of infectious complications. dogs and humans Dtsch Med Wochenschr. 1998 May 20. an antibiotic prophylaxis for 3-5 days is appropriate. cat. cat. recent data demonstrate that human bites occurring anywhere other than the hand present no more of a risk for infection than any other type of mammalian bite. Some studies have classified people as low risk for common bile duct stones based on (1) lack of jaundice. a rabies vaccination with immunoglobulins and inactivated virus preparation is recommended. clenched fist injuries. Human bite wounds have long had a bad reputation for severe infection and frequent complication. 2003 May 9. Human bites and in particular clenched-fist injuries as well as cat bites are highly prone to infection as are wounds that involve the hand or deep structures including joints. Q that remained unanswered about antiarrhythmics. In general. the rate of stones was 39%. an antibiotic course with amoxycillin/clavulanic acid (first choice) or tetracyclines (second choice) for 10-14 days is recommended. and an ERCP should be considered. (2) elevated transaminases. Therefore. 1995 Dec. the risk of common bile duct stones is approximately 10%. particularly when the risk for the development of infection is high.
Here is my input. trimethoprim. Dofetilide. Ic = Phase 0 = slow the rise of action potential/refractoriness but more than Ia. RANIDITINE. Prevention of VFib. They alter the electrophysiologic mechanisms responsible for arrhythmia. These agents are used only for chemical conversion. Examples: Quinidine. Procainamide (Lupus. Sotalol (noncardiac selective beta blocker). Examples: Verapamil. Relevant Indication: DOC for longterm control of A Fib (better than Dig if long term) Class V: . Fatal blood dyscrasias first 3 months!!). Neurotox!!!!!). Corneal and skin depostis. Symptomatic PVC's. These agents are used only in patients with structurally normal hearts (ie. They are classifed into: Class I: Blocks Na Channels Class II: are the beta-blockers Class III: Block K channels Class VI: Calcium channel blockers. Nifedipine. Examples: Amiodarone (Pulm Fibrosis. Phenytoin Indications: VTach.Ideal for use in patients at risk of complications from betablockade. Mexiletine(Leukopenia!!). Examples: Flecainide. and quinidine. Symptomatic PVC Ib = shorten action potential Examples: Lidocaine. amiodarone. beta-blockers. They pronlong action potential. Hyper/Hypothyroidism. Indications: SVT. Class V: Cardiac Glycosides. ClassI: * Ia = Phase 0 = Slow rhe rise of action potential = Make it longer thus more refractory. VTach. Propafenone (Weak CaBlock+BetaBlock) Indications: Life threatening VTach/VFib. Bretylium. absence of coronary artery disease or cardiomyopathy). They reduce rate of AV nodal conduction and control ventricular response in A Fib. Class IV: Block Calicum from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium. Class II: Beta Blockers: These agents slow the sinus rate in addition to decreasing AV nodal conduction. Disopyramide (Urinary retention!!). Side effects: bronchospasm. Note: Esmolol (Brevibloc) -. Moricizine Note: Can expect increased levels of procainamide metabolite NAPA in patients taking CIMETIDINE. Ibutilide. short half-life of 8 min Note: First line of treatment in Asthma secondary to beta blockers: ANTICHOLINERGICS/IPRATROPIUM (NOT BETA2 AGONISTS AS IN REGULAR ASTHMA). Refractory SVT. Prevention of VFib. Class III: Blocking K channels results in widened QRS and longer QT interval. Diltiazem.
. the most common brain tumors are: .Cerebellar Astrocytoma (15-20%) .Choroid Plexus papilloma (2-3%) . Visual changes.fpnotebook.#2: Astrocytoma . congenital mesoblastic nephroma. this question has to be classified by the location of the tumor: 1. Neuroblastoma. Digoxin (CI in idiopathic hypertrophic subaortic stenosis. constrictive pericarditis.Meningioma (<1%) Overall.Ependymoma (3-5%) .Pituitary tumor (<1%) . S brady!!!). Watch out for AV Block.Astrocytoma (8-12%) .Familypracticenotebook.#1: Medulloblastoma . AV Block.Meningioma (<1%) 2. weight loss). fever.htm Old Question on Neuroblastoma Vs Wilms: CT or IVP? Facts: .Wilms tumor commonly displaces and compresses vessels.Infratentorial (60%) .com/HEM147. PAT with a 2:1 block!!!!)hypercalcemia and hypercalcemia predisposes patient to digitalis toxicity predispose patient to digitalis toxicity. . References: .emedicine most common brain t/m in children To let you know why it gets confusing. They are used primarily in the setting of AF with CHF.Pineal tumor (2%) .com http://www. which commonly arises from the adrenal gland. and may represent Wilms tumor. Neuroblastoma also .Glioblastoma (<5%) . GI problems.Ependymoma (4-6%) .Wilms tumor arises from the kidney and most often is detected as a large asymptomatic abdominal mass. Examples: Adenosine (Flushing. such as malignant rhabdoid tumors. often presents with a mass and constitutional symptoms (eg.Supratentorial (40%) .Brain stem glioma (8-10%) .Schwannoma (<1%) . neuroblastoma. or other less common tumors.These drugs slow AV nodal conduction primarily by increasing vagal tone.Craniopharyngioma (5-8%) .Cardiac glycosides -.CMDT p363 .#3: Ependymoma Reference: . in peds.Medulloblastoma (18-25%) .Solid masses are ominous in a child as opposed to cystic ones.
he lies motionless.4= 162.40 yr M . pt. vascularity (1). care should be taken in children who are less than 1 year of age as a mesoblastic nephroma may have identical imaging characteristics (2).5 .50 yr M. to several days after event. presents with peritonitis.54(5):321-7. constant. other symptoms are not noted here due to the altered mentation. 1999 May.amylase. Additional Fact: In a recent study.html 2. wt loss+ a. 3. but ultrasound interpretation requires skilled expertise. r/o other causes of acute abd. rapid shallow breathing. identifies associated genitourinary abnormalities.emergency laparotomy . barium swallow b. confirms function of the contralateral kidney.pt. most likely has ARDS -. onset is acute several hrs. drinking+. however.displaces and compresses vessels but more often is infiltrative.hawaii. 1.CXR. - . ultrasound is useful for diagnosing intraabdominal tumors and can display calcifications.has hypoxemia refcractory to oxygen. ecg 2. Neuroblastoma Fact: At initial presentation. po2-65 on 40% o2. infections. CT scan is better at detecting subtle intraabdominal abnormalities such as tumor spread. nor in any theoretical review I found). . guar ding+. 2.Radiographic Evaluation of the Pediatric Urinary Tract http://www.emedicine. and indicates if there is extension to the inferior vena cava. ABG b.. Falsely negative studies are misleading for the clinician unless an alternate imaging study such as a CT scan is done to make the diagnosis (1). c-xray 3. lymph node enlargement. a. Wilms Tumor Fact: Ultrasound or CT helps localize the mass.in the 2 week of post-op for multiple gunshot wounds to the abdomen.edu/medicine/pediatrics/pedtext/s12c03..Ultrasound with Doppler can reveal inferior vena cava (IVC) invasion. severe. needs acute Mx. progressive machanical dysphagia. massive transfusions. tenderness to palpaion. like tachypnea. c-xray.com/ped/topic2751.Case Based Pediatrics For Medical Students and Residents http://www. to several days post injury but could be variable. h/o smoking+. References: 1. pt. endoscopy and biopsy Answers: 1. etc. is diaphoretic.characteristic for ARDS.With advances in medical imaging can the radiologist reliably diagnose Wilms' tumours? Clin Radiol. can have lethargy followed by obtundation. radiologists were accurate at diagnosing Wilms' tumors using modern imaging methods (IVP was not included in it. the most typical is several hrs. CT scan plays an important role in the management of Wilms tumor and neuroblastoma for staging (3).occurs in pts after trauma. plain x-ray b. come with pain from 1 hr. emergency laparotomy c. patient becomes unresponsive and progressively disoriented. 65/0.htm the next step in mgt in the below q.. pt.rigid abd. rebound tenderness+ a. p/e. the PaO2/FiO2 ratio < 200 mmHg.
Can last days .barrium swallow . In clinical scenarios. you step up the long term Rx from one level to the other when: . Treat as mild intermittent.Moderate persitent: * Symptoms daily * Night symptoms each week * Exacerbations affect activity >2x/week .. so then get ABG.Mild intermittent to moderate persistent WHEN Pt USES Beta2INHALER MORE THAN TWICE A WEEK . then CT scan to do staging .then do EGD .Mild intermittent: * Pt asymptomatic * Diurnal symptoms 1x or 2x/week * Nocturnal symptoms 2x/month . Classify Asthma first: . Steroids are used in the exacerbations that needs admission.Mild persistent to Moderate persistent WHEN PT USES INHALER DAILY.. .. . get ABG in either case after the CXR.Asthma variant cough: Cough without wheezing with atopic history. * OR!!!!!: Inhaled Cromolyn AND Salmeterol AND PO Steroids. can also Dx one of the most serious compl.Mild intermittent: * No long term Rx .correct me on this one if i am wrong 3..Moderate Persistent: * Inhaled steroids low/med dose AND Long acting beta adrenergic = SAlmeterol * OR!!!!!: Inhaled Cromolyn AND Salmeterol .Severe Persistent: * Inhaled Steroid high dose AND Salmeterol AND Steroids Tablets. if CXR is -ve .Moderate persistent to Severe persistent WHEN PT USES INHALER DAILY AND INCREASES DOSE (MORE THAN 2 PUFFS AT A TIME). .look for Mets Old Request about summary of treatment of Asthma Asthma is defined primarily as an INFLAMMATORY DISEASE with mostly MAST CELL degranulation. or normal then it could be PE.Mild persistent: * Diurnal symptoms >2x/week / <1x/day * Nocturnal symptoms >2x/month * Exacerbations affect activity .Severe persistent: * Continuing symptoms/exacb. CXR is fast to get.CA especially if they have symptoms of dysphagia. see the A-a gradient .. Long term use is the follwing: . .Mild persistent: * Inhaled Steroids OR Inhaled Cromolyn .usually the first Dx test in Pt w/ suspected esoph.. mostly at night * Limited activity Treat the acute episode with Ox and Beta2 adrenergic short acting. etc.TE fitule. infiltrates and/or consolidation.CXR will show bilateral pulm..
What is the likely diagnosis? How do you confirm the diagnosis? The culprit: what is mercury? Mercury is an elemental metal. Mercury use in diuretics. T = 99F. At room temperature it is a silvery. These properties have given it the common name quicksilver. erythematous rash – hands and feet.CMDT Mercury poisoning A 2 yo – peeling. Further history reveals child’s elder brothers have been playing with household thermometers. but no longer is. Mercury is purveyed by some herbal medicine or botanical shops to consumers unaware of the dangers of the substance. Ipratropium (anticholinergics) are first line of treatment of bronchospasm secondary to beta blockers. 2nd line of treatment out-pt after familure of beta2adrenergics Steroids systemic (PO) are first line in treating exacerbation in-patient and in control of severe persistent. Mercury was previously used in paint. Mercury's most well known use is in medical thermometers found in the home. and environmental control). Steroids Inhaled are first line in treatment of PERSISTENT ASTHMA. P=90. The ritual consists in the sprinkling of mercury about the home. Scenario of Pt undergoing accident or surgery and post-op clinical scnerio of adrenal insufficiency. however. Only 2-10% of the ingested mercury is absorbed from the gut. (2) inorganic salts. PE – irritable. Mercury exists in 3 forms: (1) elemental mercury.Swanson . Watch out for Adrnela insufficiency. RR = 23. and (3) organic compounds. perservatives and pesticides has greatly declined becuase effective substitutes have been found. New york State. adherence. pale child with photophobia. antiseptics. Puerto Rico. odorless liquid which vaporizes easily. (GIve Calicum and Vit D in chronic use.Note: Review treatment with Pt every 1 to 6 months and either step down or step up. 90% of any methyl mercury ingested is absorbed into the bloodstream from the gastrointestinal tract. Perhaps the most deadly form of mercury is methyl mercury. H/o of persistent asthma. Ritual Use of mercury: in haitian and carribean-american communities. particularly of spiritist faith such as Santeria. This causes intoxication by mercury vapor. Tremor of the tongue evident. but it is also used in electric switches. Amazon and virgin islands. New Jersey. North Carolina. This change will depend on the failure of other supporting measures (Technique of using inhaler. Mother says child has become ill tempered and refuses to walk. Or Pt with h/o of asthma who develops recurrent oral candidiasis). Note2: Beta2 adrenergics are first line in treatment of asthma. Mercury posoning by eating Fish: Japan. and ingested elemental mercury is not absorbed at all. or in CI of beta adrenergics. Some History: . propellant and fluorescent lamps. References: .
kidneys. mercury accumulates in the liver. ataxia. increased excitability or insomnia may occur after exposure to mercury vapors. and enzymes are all disrupted. The history of mercury and its toxic effects date back to the fifteenth century B. . Necrosis of the proximal tubules is a common direct renal toxic effect. numbness in the limbs and personality changes such as nervousness. brain and blood. Can mercury affect some people more than others? Age: Children are especially susceptible to the adverse effects of mercury. membranes. The setting: . The scenario: Children develop the symptoms of mercury poisoning more quickly and severely than adults. a body of water in Japan where.Mercury taken into the body through air. the babies’ exposure continued after birth. or exposing oneself through a hobby. in the early 1950s. caused by exposure to mercury vapor used in making felt hats. dizziness. because mercury was also discovered in the breast milk of the mothers. hearing loss. and ataxia. Because mercury binds to the body's ubiquitous sulfhydryl groups. but her child may be born with brain damage similar to cerebral palsy or autism. Unexplained renal abnormalities with neuropsychiatric disturbances should prompt the physician to consider Minamata disease or other forms of mercury poisoning. Methyl mercury is lipophilic and readily crosses the blood-brain and placentofetal barriers.When inhaled or absorbed through the skin.Exposure to mercury also may occur by moving into a mercury-contaminated home. mercury easily crosses the placental barrier and concentrates in the fetus more readily than in the mother. Criminals sentenced to work in mercury mines had a life expectancy of three years. causing both immediate and long term health effects. Furthermore. The major food sources of mercury are fish and shell fish. children playing with mercury. It is named for Minamata Bay. better known as Minamata disease. Pathophysiology: Mercury is an element and cannot be broken down into harmless components. toxicity involves multiple organ systems. Methyl mercury exerts its most devastating effect on the central nervous system by causing psychiatric disturbances. Mental instability. . Neurological symptoms are very similar to those seen in adults. Structural proteins. extremity numbness. Local villagers ate the fish and began to exhibit signs of neurologic damage such as visual loss. Children also may . Thus. is one of the most devastating forms of mercury exposure. a pregnant woman exposed to toxic levels of mercury may not exhibit any signs of mercury poisoning. hearing loss. Neurologic damage in the form of diffuse and widespread neuronal atrophy is most severe in patients exposed in utero.C. The effect: The most universal effect of mercury is damage to the nervous system. Babies exposed to the methyl mercury in utero were the most severely affected members of the village. The phrase "mad as a hatter" originated from the often strange behavior of hat makers. In pregnant women. visual loss.Methyl mercury poisoning. the fish contained high concentrations of methyl mercury from the polluted waste of a nearby industrial plant. and neuropathy. water and food is absorbed in varying amounts depending on the route of intake.
Ataxia .Dysarthria . The most damaging effect of ingested inorganic mercury (eg. and (sometimes) tissue analyses are required to confirm the diagnosis of mercury intoxication.Headache . Unexplained renal abnormalities with neuropsychiatric disturbances should prompt the physician to consider Minamata disease or other forms of mercury poisoning. Urinalysis . Ingested elemental mercury is considered nontoxic because of its poor absorption in the gut. Differential: Schizophrenia and Other Psychoses Substance Abuse: Cocaine Toxicity.Extremity numbness . Severe poisoning eventually causes the patient to lie in a mute semirigid posture that is broken only by episodes of crying or primitive reflexive movements. Visual loss.Labs: blood. The severity of mercury poisoning is not always correlated with the blood concentration because of the redistribution of mercury in the tissues. specifically those of the central nervous system.Memory loss . The normal range of mercury concentrations in whole blood is 0-10 mcg/L. a direct determination of the blood mercury concentrations is essential.problems in walking Methyl mercury exerts its most devastating effect on the central nervous system by causing the following: Psychiatric disturbances.Difficulty in hearing . Hearing loss. Ataxia. Symptoms include: . urine. Hallucinogens . Blood Analysis: Methyl mercury concentrates in red blood cells. mercuric chloride) is caustic gastroenteritis. Early signs and symptoms may occur with concentrations greater than 35 mcg/L. and Neuropathy Clinical examination typically reveals the following: * Deficits in the visual field relative to confrontation * Ataxia * Tremor * Psychiatric disturbances such as anxiety * Seizures * Respiratory distress and dermatitis can occur acutely.Perioral and facial paresthesias . it is most dangerous as a vapor because it can cause acute lung injury and respiratory failure.develop a bright red reash with sheets of peeling skin.PCP Autism: presents very many similarities (see 3) The Diagnosis: . Consequently. Neurotoxicity is the most damaging syndrome.Constriction of the visual fields .
the performance of baseline laboratory studies. Its toxicity is low. profound developmental delay. Outpatient follow-up: . Provide general supportive measures. tremor. the urinary excretion of mercury is minimal. activated charcoal should be administered even though it does not absorb heavy metals well in general. swordfish. * Gastric Lavage: Because of the high propensity for neurologic impairment. seizure disorders. it does not indicate the severity of mercury poisoning. After initial assessment and stabilization of the patient’s condition. Currently. incomplete visual loss (including tunnel . unfortunately. Extremity numbness eventually along with headache. Ataxia and dysarthria. Methyl mercury is primarily excreted through the feces.Neurological and Psych examinations Complications: Acute perioral and facial paresthesias. and animal trials have shown that it is superior to older chelating agents such as dimercaprol (BAL) and d-penicillamine (DPCN). the best agent for the treatment of Minamata disease is 2. Respiratory distress and nonspecific dermatitis. irreversible. chelating agents should be administered early in treatment. urinary assays are useful in monitoring chelation therapy. pregnant women and nursing mothers should avoid consuming larger fish (shark. Severe poisoning eventually causes the patient to lie in a mute semirigid posture that is broken only by episodes of crying or primitive reflexive movements. they are. DMSA is preferred over DPCN. The goal of medical management in Minamata disease is to reduce the total body burden of mercury and minimize further damage.Monitor Renal Function .3-dimercaptosuccinic acid (DMSA). Chelated mercury is excreted primarily through the kidneys. Even in cases of inorganic mercuric salt exposure. and the creation of a differential diagnosis. including monitoring. These agents are thought to competitively bind the mercury by using its thiol groups. especially in utero. In addition. Therefore.The detection of mercury in the urine demonstrates that exposure has occurred. fatigue.Monitor Mercury levels for months . and large tuna steaks ) because their mercury concentrations tend to be higher than those in smaller fish. eliminate the patient's exposure to the source of the mercury. however. Babies exposed in utero are the most severely affected (low birth weight. Diet: Because of the high morbidity and mortality rates associated with methyl mercury poisoning. Histologic Findings: Necrosis of the proximal tubules is a common direct renal toxic effect. Once the neurologic consequences of Minamata disease appear. patients with acute mercury ingestion should undergo gastric lavage with solutions containing proteins such as those from milk or egg whites. * Chelating agents (classified Category C = Safety for use during pregnancy has not been established): Because mercury binds to the body's ubiquitous cellular sulfhydryl groups. Medical Care: Medical Care: The general management measures in Minamata disease are the same as in those of any other toxicologic exposure.
In an emergency situation. remembering that the most common cause of Cushing syndrome is the use of exogenous glucocorticoids is important. Vacuuming causes mercury to vaporize and spread easily through the air. Do not put mercury down the drain or dispose of it in the house.whale. total blindness. place it in a sealed container and place it in the trash outside. because it will continue to vaporize. and during some manufacturing processes.html 3) http://www.htm 4) http://www. Reference: 1) http://www.Cushing disease = Pituitary adenoma ACTH secreting. Children so affected may have long-term stigmata. and seizure disorders.state. CUSHING SYNDROME/DISEASE.nc.us/epi/fish/mercuryhealthfacts.oh. during forest fires.Cushing syndrome is everything else with clinical features except etiology is NOT pituitary. Mercury is also released into the air. visual loss. and hearing loss). and memory. especially in utero. Answer to your question . pregnant women and nursing mothers should avoid consuming larger fish because their mercury concentrations tend to be higher than those in smaller fish. It displays clinical Cushing Syndrome.GENERAL REVIEW General Considerations: Cushing syndrome is caused by prolonged exposure to elevated levels of either endogenous or exogenous glucocorticoids. The correct way to dispose of small amounts of mercury is to pick it up with the sticky side of a piece of tape. soil and water throughout North Carolina.. Medicolegal pitfalls: * Consider mercury intoxication in the differential diagnosis when unexplained neuropsychiatric disturbances are coupled with renal abnormalities.epi. developmental delay. when municipal solid waste or medical waste is incinerated. * Because of the high morbidity and mortality rates associated with methyl mercury poisoning.state. language. Long-term studies indicate that even prenatal exposure at low concentrations can cause subtle but detectable decrements in the areas of motor function. IT SHOULD NOT BE VACUUMED.htm 2) http://www.to/a/table_a. .epa. water and land when fossil fuels (coal.vision). Mercury intoxication after eating fish: What is mercury and how does it get into the environment? Mercury is a metal that occurs naturally at low levels in rock.html What is the difference between Cushing Syndrome and Cushing Disease? First of all. oil and natural gas) are burned.us/pic/facts/mercury. Prevention: What should I do if I spill mercury in my house? If the mercury spills onto a surface.com/ped/topic1461. hearing loss. including motor impairment. Contact EPA when a spill of mercury would form a pool larger than a quarter.. Etiology: .emedicine. Exogenous steroids may cause suppression of the hypothalamic-pituitary-adrenal (HPA) axis that can last for as long as a year after exogenous steroid administration has ended. causing contamination.
- Adrenal Hyperplasia * Pituitary adenoma = Cushing Disease * ACTH or CRH secreting tumor = Ectopic (Oat cell CA - CA of thymus - PAncreatic CA - Bronchial Adenoma) - Adrenal Neoplasia - Exogenous/ Iatrogenic causes = MOST COMMON. Pathophysiology: Endogenous glucocorticoid overproduction or hypercortisolism that is independent of adrenocorticotropic hormone (ACTH) usually is due to a primary adrenocortical neoplasm. ACTH-secreting neoplasms cause ACTH-dependent Cushing syndrome. 80% are due to Classic Cushing disease = an anterior pituitary tumor. Ectopic sources of ACTH make up the balance of ACTH-dependent Cushing syndrome cases. Ectopic non pituitary = an oat cell, small-cell lung carcinoma, or carcinoid tumor. Rarely ectopic corticotropin-releasing hormone (CRH) secretion. Sex: female-to-male ratio is 5:1 for Cushing syndrome due to an adrenal or pituitary tumor. Ectopic ACTH production is more frequent in men than in women, due to the increased incidence of lung tumors in this population. Age: The peak incidence of Cushing syndrome due to either an adrenal or pituitary adenoma occurs between ages 25 and 40 years. Ectopic ACTH production due to lung cancer occurs later in life. History: - Weight gain, especially in the face, supraclavicular region, upper back, and torso. - Changes in skin= purple stretch marks, easy bruising, and other signs of skin thinning. - Irregular menses and hirsutism - Progressive proximal muscle weakness, patients may have difficulty climbing stairs, getting out of a low chair, and raising their arms. - Psychological problems (depression, cognitive dysfunction, and emotional lability) - New onset or worsening of hypertension and diabetes mellitus, difficulty with wound healing, increased infections, osteopenia, and osteoporotic fractures - Patients with an ACTH-producing pituitary tumor (Cushing disease) may develop headaches, polyuria and nocturia, visual problems, or galactorrhea. - Mass effect on the anterior pituitary (hyposomatotropism, hypothyroidism, and hypogonadism) Physical: - Obesity, moon facies, buffalo hump, and supraclavicular fat pads. - Central obesity with increased adipose tissue in the mediastinum and peritoneum, increased visceral fat is evident on CT. - Skin, Facial plethora, Violaceous striae over the abdomen, buttocks, lower back, upper thighs, upper arms, and breasts. Ecchymoses may be present. Patients may have telangiectasias and purpura. Cutaneous atrophy with exposure of subcutaneous vasculature tissue and tenting of skin may be evident. - Steroid acne - Acanthosis nigricans, which is associated with insulin resistance and hyperinsulinism, may be present. The most common sites are axilla and areas of frequent rubbing, such as
over elbows, around the neck, and under the breasts. - Cardiovascular/renal: Hypertension, Volume expansion (edema from sodium and water retention). - Atherosclerotic heart disease is caused by lipid abnormalities, while diabetes mellitus and hypertension are caused by Cushing syndrome. - Gastroenterologic: Peptic ulceration (rare in endogenous hypercortisolism). - Endocrine: Hypothyroidism may occur from anterior pituitary tumors, which can interfere with proper thyroid-releasing hormone (TRH) and thyroid-stimulating hormone (TSH) function. - Galactorrhea may occur when anterior pituitary tumors compress the pituitary stalk, leading to elevated prolactin levels. - Other pituitary function may be interrupted without obvious clinical findings. Possibilities include polyuria and nocturia from diabetes insipidus. - With severe hypercortisolism, hypokalemic metabolic alkalosis may occur. - Osteoporosis = incident fractures and kyphosis, height loss, and axial skeletal bone pain. Avascular necrosis of the hip also is possible from glucocorticoid excess. - Adrenal crisis Patients with cushingoid features may present to the emergency department in adrenal crisis. This may occur in patients on steroids who stop taking their glucocorticoids or neglect to increase their steroids during an acute illness. It also may occur in patients who have recently undergone resection of an ACTH-producing or cortisol-producing tumor. Physical findings that occur in a patient in adrenal crisis include hypotension, abdominal pain, vomiting, and mental confusion (secondary to low serum sodium or hypotension). Other findings include hypoglycemia, hyperkalemia, hyponatremia, and metabolic acidosis. Lab Studies: - WBC>11,000/mm3 - Hypokalemic (NA IS NORMAL) metabolic alkalosis may occur in patients with urinary free cortisol (UFC) levels higher than 1500 mcg/24-h. - 20% have Glucose intolerance/DM OVERVIEW OF EVALUATION OF PT WITH PRESUMED CUSHING SYNDROME: 1- CLINICAL SUSPICION 2- SCREENING TEST = OVERNIGHT DXM SUPPRESSION TEST (EXCLUDES CUSHING SYNDROME WITH 985 OF CERTAINTY). 3- IF ABOVE ABONORMAL = 24H URINE FREE CORTISOL + CREATININE 4- IF ABOVE ABNORMAL = CUSHING SYNDROME NEXT = HIGH DOSE DXM SUPPRESSION TEST 5- IF SUPPRESSION <50% CONTROL: CUSHING DISEASE (PITUITARY ADENOMA) IF NO SUPPRESSION: ADRENAL NEOPLASIA VS ECTOPIC TUMOR 6- NEXT = ACTH LEVEL IF HIGH = ACTH PRODUCING TUMOR => CT CHEST IG LOW = ADRENAL NEOPLASIA => URNIARY 17KS - DHEA-S - ABDOMINAL CT: ADRNEAL ADENOMA VS ADRENAL CARCINOMA. DETAILED EXPLANATION:
Diagnosis of excess endogenous cortisol production requires the demonstration of inappropriately high serum cortisol levels or its urinary metabolites. Because acute illness activates the HPA axis, resulting in increases in ACTH and cortisol, the laboratory workup for Cushing syndrome should not be performed when subjects are acutely ill. Two common screening tests for Cushing syndrome are the 24-hour UFC test and the overnight (ON) 1-mg dexamethasone suppression test. * The 24-hour UFC test is an excellent indicator of overall daily cortisol production. Values higher than 3- to 4-times the upper limit of normal are very suggestive of Cushing syndrome, whereas values 1- to 3-times normal are consistent with either pseudo-Cushing or Cushing syndrome. Ensuring that the 24-hour collection for this test was adequate, by simultaneously measuring urinary creatinine excretion on the same urine sample, is important. * The ON 1-mg dexamethasone suppression test calls for ingestion of 1 mg of dexamethasone at 11 PM, with measurement of an 8-AM serum cortisol the next morning. In healthy individuals, the serum cortisol should be less than 2-3 mcg/dL. Cushing syndrome may be excluded with a cortisol level less than 1.8 mcg/dL. Medications that increase corticosteroid-binding globulin, such as estrogen and tamoxifen, may cause appropriate increases in cortisol levels. Finally, medications that facilitate the metabolism of dexamethasone, such as phenobarbital, phenytoin, and rifampin, may cause false-positive results with the dexamethasone suppression test. In many instances, additional studies must be performed to establish the diagnosis of excess cortisol production. The 48-hour low-dose dexamethasone suppression test (0.5 mg dexamethasone PO q6h for 8 doses) has been used for many years. In healthy individuals, 24-hour urinary 17-hydroxycorticosteroids are suppressed to 4 mg or less during the second day of dexamethasone ingestion. Unfortunately, the sensitivity and specificity of this test are only approximately 70%. A promising new method of detecting mild glucocorticoid excess combines the 48-hour low-dose dexamethasone suppression test with CRH stimulation. Ovine CRH (1 mcg/kg IV) is given 2 hours after the eighth dose of 0.5 mg dexamethasone. Serum cortisol is measured 15 minutes after ovine CRH administration. A cortisol level of greater than 1.4 mg/dL is very suggestive of Cushing syndrome. Other tests that may be useful to identify Cushing syndrome are as follows: In order to institute appropriate therapy, the cause of excess cortisol secretion must be determined. The logical first step involves establishing the differential diagnosis between an ACTH-dependent or ACTH-independent disorder. A plasma ACTH (measured by an immunoradiometric assay) of less than 5 pg/mL is suggestive of a primary adrenal tumor. An ACTH greater than 10-20 pg/mL is consistent with ACTH-dependent Cushing syndrome. The 8-mg ON dexamethasone suppression test and the 48-hour high-dose dexamethasone test may be useful when baseline ACTH levels are indeterminate. These studies also help in determining whether a patient who has ACTH-dependent disease has pituitarydependent or ectopic ACTH disease. In the ON 8-mg dexamethasone suppression test, individuals ingest 8 mg dexamethasone orally at 11 PM, with measurement of an 8-AM cortisol the next day. A baseline 8-AM
Suppression of serum cortisol to less than 50% of baseline is suggestive of a pituitary source of ACTH rather than ectopic ACTH or primary adrenal disease.The treatment of choice for endogenous Cushing syndrome is surgical resection of the causative tumor. . control of hypercortisolism may be attempted with medication.Depression: High cortisol with no clinical features . . CTguided fine-needle aspiration then may have a role in management. as often occurs with ectopic ACTH or metastatic adrenal carcinoma.Alcoholics: high cortisol levels with clinical cushing . However. A decrease in UFC of greater than 50% is suggestive of an anterior pituitary adenoma.The primary therapy for adrenal tumors is adrenalectomy. Octreotide scintigraphy may be helpful in detecting ectopic ACTH tumors because neuroendocrine tumors typically have cell surface receptors for somatostatin. the diagnostic accuracy is only 70-80%. Differential Diagnosis: . When surgery is not successful or cannot be used. rather than ectopic ACTH or a primary adrenal tumor. measurement of 17-ketosteroid or other cortisol precursors (such as serum dehydroepiandrosterone sulfate [DHEAS]) is useful. . Unfortunately.Morbid obesity mimicks results of DXM suppression test but urine free cortisol is normal . The more stringent criterion of a 90% decrease in UFC levels excludes the diagnosis of ectopic ACTH and has 100% specificity for anterior pituitary disease. such as mitotane.cortisol measurement is required. with a specificity of 70-80%. Cushing syndrome Agents that inhibit steroidogenesis. If a pituitary source of excess ACTH is suspected. Imaging Studies: An abdominal CT scan is recommended if a primary adrenal problem is suspected. the sensitivity of this test is only 80%. ketoconazole. Pituitary radiation may be useful if surgery fails for Cushing disease.Anorexia Nervosa: Same wasting as in Cushing with extraordinary high levels of 24h urine cortisol . A culprit tumor should be removed if possible. . patients should undergo a contrastenhanced magnetic resonance imaging (MRI) study of the pituitary. patients ingest 2 mg dexamethasone every 6 hours for 8 doses. If concern for adrenal carcinoma exists. Medical Care: Overview Treatment of Cushing syndrome is directed by the primary cause of the syndrome. and adrenalectomy may be indicated in ACTHmediated Cushing syndrome.Pts on HAART for HIV-1 develop partial lipodystrophy with thin extremities and central obesity. metyrapone. With the 48-hour high-dose dexamethasone suppression test.The treatment for exogenous Cushing syndrome is gradual withdrawal of glucocorticoid. Chest and abdominal CT scans should be performed in patients with suspected ectopic ACTH production. medication failures are common.The primary therapy for Cushing disease is transsphenoidal surgery. However. buffalo hump. .
If enzymatic blockade is not complete. blocks 11-beta-hydroxylase. sedation. Ketoconazole probably is the most popular and effective of these agents for long-term use and usually is the agent of choice.aminoglutethimide. and hirsutism. Etomidate. decreased libido. ideally. and androstenedione. Ketoconazole is ineffective in patients on H2 blockers or proton-pump inhibitors because gastric acidity is required for metabolism. In rare cases. Adverse effects of ketoconazole include headache. a generalized pruritic rash. Patients receiving these medications may require glucocorticoid replacement to avoid adrenal insufficiency. If this agent is ineffective at controlling hypercortisolism. Ketoconazole and aminoglutethimide act at several sites. Aminoglutethimide increases the metabolism of dexamethasone but not cortisol. Because ACTH production may persist or increase in patients with Cushing disease. medical treatment should be initiated cautiously and. cholesterol side-chain cleavage. impotence. radiation therapy of the pituitary often is required after unsuccessful initial therapy. and elevated liver function tests. including hypertension. headache. either surgical or medical. is initiated. typically metyrapone. in conjunction with a specialist.5 g/d. It also may inhibit ACTH secretion when used at therapeutic doses (200-400 mg bid-tid). Aminoglutethimide is an anticonvulsant agent that blocks cholesterol side-chain cleavage to pregnenolone. and goiter. aldosterone. These agents have higher efficacy when used in combination because they may act synergistically. hypothyroidism. which decreases the synthesis of cortisol. Efficacy of these medical interventions can be assessed with serial measurements of 24-hour UFC. ACTH secretion overcomes the blockade so that hypercortisolism persists. including the first step in cortisol synthesis. It is . Adverse effects are from increases in androgen and mineralocorticoid precursors. may inhibit ACTH secretion. the dose may be maintained while another steroid enzyme inhibitor. Trilostane is not widely available and is not as well studied. Metyrapone blocks 11-beta-hydroxylase activity (the final step in cortisol synthesis) and. The drug is contraindicated during pregnancy. It is a relatively weak adrenal enzyme inhibitor at doses that patients can tolerate. irregular menses. Trilostane inhibits the conversion of pregnenolone to progesterone. causing a false elevation of cortisol measurements. trilostane interacts with some assays. have been used to cause medical adrenalectomy. and conversion of 11deoxycortisol to cortisol. trilostane.Adverse effects of aminoglutethimide include somnolence. acne. It acts on several of the P450 enzymes. It is not a first-choice agent because it is a weak inhibitor of steroidogenesis. Therapy is begun at 1 g/d divided into 4 doses and increased to a maximum dose of 4. and increased to 2 g four times daily. Aminoglutethimide typically is initiated at 250 mg twice daily. Thus. nausea. Metyrapone and trilostane are agents that competitively inhibit a single steroidogenic enzyme. it may cause bone marrow suppression. These medications are used rarely and often are toxic at the doses required to reduce cortisol secretion. . at high doses. gynecomastia. In addition. and etomidate. an imidazole-derivative anesthetic agent.
often with a laparoscopic approach. Its survival benefit is unclear. and medical therapy fail or if rapid normalization of cortisol levels is required. it is relatively contraindicated in women interested in remaining fertile. dizziness. mitotane is expensive. Its use is limited by the requirement for chronic administration by the intravenous route. * Adrenal source Adenomas may be removed with unilateral adrenalectomy. Medical therapy or bilateral adrenalectomy may be required. If unsuccessful. Nelson syndrome. use of these agents is investigational. The patient then requires lifelong glucocorticoid and mineralocorticoid therapy.Ectopic adrenocorticotropic production Surgical resection of the source of ACTH production may not always be possible. It is a potential teratogen and can cause abortion. arthralgias. It can be used in addition to radiation therapy for treatment of Cushing disease and in combination with metyrapone or aminoglutethimide for treatment of ectopic ACTH secretion. pituitary irradiation. including nausea. The procedure is less successful than surgery in adults. and its utility is limited by adverse gastrointestinal and neurological effects. and leukopenia. . and octreotide.3 mg/kg/h. cyproheptadine. . In individuals who undergo bilateral adrenalectomy. . Agents that decrease CRH or ACTH release have been studied for the treatment of Cushing disease. It currently is used only on an investigational basis for treatment of Cushing syndrome. Such agents include bromocriptine. competitively binds to the glucocorticoid and progesterone receptors. MRI-guided pituitary surgery. valproic acid. It is taken up by adipose tissues and persists in the circulation long after discontinuation. it is used in treatment of adrenal cancer. with a 45% cure rate in adults and 85% cure rate in children. diarrhea. may occur in one quarter to one half of adults not treated with pituitary irradiation and in as many as one quarter of patients pretreated with radiation therapy. therefore. This drug also leads to mitochondrial destruction and necrosis of adrenocortical cells in the zona fasciculata and reticularis. Both open and laparoscopic techniques are possible.Pituitary irradiation is employed when transsphenoidal surgery is not successful or not possible. Successful amelioration of hypercortisolism occurs in 60-80% of cases. For this reason. . Mitotane is an adrenolytic agent that acts by inhibiting 11-beta hydroxylase and cholesterol side-chain cleavage enzymes. Other adverse effects include rash. symptomatic enlargement of the pituitary gland and adenoma.Unfortunately. The goal of surgery is to remove the adenoma. preserving as much pituitary function as possible.Cushing disease Treatment of choice for classic Cushing disease is transsphenoidal surgery by an experienced neurosurgeon. .used intravenously at 0. a new procedure. Carcinomas should be resected for palliation.Bilateral adrenalectomy is an option if transsphenoidal surgery. which. Currently. Mifepristone (RU 486) is an antiprogestational agent. Late-onset adverse effects include hypopituitarism. at high doses. Surgical Care: . ie. and ataxia. may be indicated.
Unilateral or subtotal adrenalectomy may lead to recurrence. adrenal.Micronodular or macronodular hyperplasia causing Cushing syndrome may be treated effectively by bilateral adrenalectomy. Two catastrophic medical crises that occur in glucocorticoid excess states are perforated viscera and opportunistic fungal infections. References: 1) Emedicine: http://www. lifelong steroid replacement is necessary. Complications: Osteoporosis Increased susceptibility to infections Hirsutism Diabetes mellitus Hypertension Risk for adrenal crisis Panhypopituitarism Diabetes insipidus Medical/Legal Pitfalls: Patients with Cushing syndrome due to exogenous steroid use are at risk for having an adrenal crisis if they do not receive stress doses of steroids during acute illnesses. High levels of endogenous or exogenous glucocorticoids may mask the abdominal symptoms associated with catastrophic abdominal events such as perforated bowel. If the patient does well.htm 2) Kaplan notes 3) CMDT p1126-1128 Gotta go.gotta go. answer to your question: The actions of ADH are mediated through at least 2 receptors—V1 mediates .. either continuously or in boluses (60-100 mg every 8 h) starting prior to surgery and for the first 24 hours afterwards. intravenous glucocorticoid replacement may be tapered over 1-2 days and replaced with an oral formulation. or ectopic tumors should receive stress doses of glucocorticoid in the intraoperative and immediate postoperative period.com/MED/topic485. right now!! Diabetes insipidus Hypercalcemia/Hypokalemia: mechanism by which they provoke DI? First of all.Hormone replacement Patients with endogenous Cushing syndrome who undergo resection of pituitary.emedicine. The rate of steroid taper may be slowed if severe preoperative hypercortisolism was present. In the event of pituitary destruction or bilateral adrenalectomy. Typically. Untreated adrenal crises can lead to death. hydrocortisone at 200-300 mg is infused intravenously. ..
Canada. Normally. a gypsy woman traveling with her thirsty son is denied water by a housewife. AKA arginine vasopressin (AVP). as in urination. Nephrogenic DI (NDI) reached North America in 1761. Through a G protein–adenylate cyclase coupling. hypercalcemia. causing the housewife's sons to crave water while condemning her daughters to pass the curse on to future generations. surface of the tubule cell occurs. In contrast. exocytic insertion of aquaporin into the apical. NDI arises from defective or absent receptor sites at the cortical collecting duct segment of the nephron or defective or absent aquaporin. General Considerations: . A rare autosomal variant is caused by mutation in the aqua porin . lithium toxicity. supraoptic or paraventricular nuclei. that results in polyuria and polydipsia by diminishing the patient's ability to concentrate urine. and renal prostaglandin synthesis. In contrast to diabetes mellitus (DM). .Nephrogenic DI is characterized by a decrease in the ability to concentrate urine due to a resistance to ADH action in the kidney. causing inhibition of water uptake and polyuria. According to legend. resulting in a reversible nephrogenic DI. the ducts do not respond appropriately to vasopressin. Diminished or absent ADH can be the result of a defect in one or more sites involving the hypothalamic osmoreceptors. leading to increased recycling of the protein aquaporin in the plasma membrane. Next: The review Diabetes Insipidus Background: The word diabetes is derived from the Greek verb diabainein. As a consequence of one of these defects. or to go through. on a ship named Hopewell.Central diabetes insipidus (DI) is characterized by decreased secretion of antidiuretic hormone (ADH). In the presence of vasopressin stimulus. which means to stand with legs apart. V2 (Aquaporin) mediates the antidiuretic response. vasopressin is transported in the blood to receptor sites on the basolateral surface of the collecting duct membrane. carried by Ulster Scots who arrived in Nova Scotia.vasoconstriction. which describes the excretion of sweet urine. or the supraopticohypophyseal tract. enhancement of corticotrophin release. Insipidus comes from a Latin word meaning without taste. diabetes insipidus (DI) describes the passing of tasteless urine because of its relatively low sodium content. The gypsy woman curses the housewife. the protein that transports water at the collecting duct. or luminal. lesions of the posterior pituitary rarely cause permanent DI because ADH is produced in the hypothalamus and still can be secreted into the circulation. Hypokalemia and hypercalcemia have been shown to suppress cortical Aquaporin 1 (AQP2) as well as to downregulate medullary AQP2. Nephrogenic DI can be observed in chronic renal insufficiency. and tubulointerstitial disease. activation of the vasopressin receptor increases cyclic adenosine monophosphate (AMP) production and stimulates protein kinase A. Scottish folklore reports the existence of the disease in Scotland before 1761. The rare hereditary form of nephrogenic DI is transmitted as an X-linked genetic defect of the V2 receptor gene. hypokalemia. Absence of the vasopressin receptor does not allow this process to take place. Aquaporin enhances water entry into the cell from the lumen.
Ruling out secondary causes. a water-channel exclusively expressed in the collecting ducts of the kidney. urine Na. pyelonephritis. or triphasic. methicillin). Patients with a nontraumatic onset typically have a much more indolent course. demeclocycline. and ADH levels. crying. and nocturia (from 3-18 liters) are the predominant symptoms. IT IS OFTEN ASSOCIATED WITH OLIGOHYDRAMNIOS. an antidiuretic phase from release of stored hormone = urine osmolality rises. linear growth defects. 30% are idiopathic. and patient tolerance of dehydration also varies among individuals. such as diabetes mellitus. A circulating enzyme destroys native vasopressin. and fatigability typically predominate. a polyuric phase = fall in urine osmolality ** Second.Central: traumatic/surgery. foscarnet. OR HEPATIC DYSFUNCTION. . Uosm) ***Serum: electrolytes and glucose. neoplastic or infiltrative of the hypothalamus or pituitary (adenomas. Details: All water intake is withheld and urine osmolality and body weight are measured hourly. Physical Examination: Normal or signs of dehydration Causes: . It's called VASOPRESSINASEINDUCED DI. however synthetic desmopressin is unaffected. hypokalemia. It may exhibit 1 of 3 patterns—transient. glucose. Multiple Myeloma. When 2 sequential urine osmolalities vary by less than 30 mOsm or if the weight . enuresis. 2) The water deprivation test = compares Uosm after dehydration versus Uosm after vasopressin. polydipsia. hyperthermia. Clinically: . ** First. A urine specific gravity of 1.Mephrogenic: idiopathic. at a time when ADH release would be highest and urine would be most concentrated. In children. when stores of ADH are exhausted Polyuria. Radiation therapy. Note: Pregnancy is associated with increased risk of DI. Sickle Cell Disease. In infants. 1) USUALLY IN THE QUESTION STEM: *** 24h urine collection (volume. urine specific gravity. The triphasic pattern is observed more often clinically. leukemia. Random plasma osmolality generally is greater than 287 mOsm/kg.005 or less and a urine osmolality less than 200 mOsm/kg is the hallmark of DI. and weight loss may be the most apparent signs. irritability. THEREFORE RESPONDING TO DESMOPRESSIN THERAPY AND SUBSIDING SPONTANEOUSLY THEREAFTER. colchicine. The daily urine volume is highly variable (3-20 L/d).The most common form of DI is that which follows trauma or surgery to the region of the pituitary and hypothalamus. IT IS SEEN IN THIRD TRIMESTER AND PUERPERIUM. and meningitis. Workup: Perform testing with the patient maximally dehydrated as tolerated. also is important.gene AQP2. permanent. Sarcoidosis. or drugs (Lithium. hypercalcemia. creatinine. anorexia. ** The third phase can be permanent DI. HTN. sarcoid histiocytosis). PRE-ECLAMPSIA. ie. cranipharyngiomas. growth retardation. simultaneous serum and urine osmolality.
In healthy individuals. thirst can become an adequate guide. If on the right. Surgical Care: Postoperatively. clofibrate. In patients with central DI this signal is absent except in the rare familial form of central DI where the signal is still present. Patients may require hospitalization to establish fluid needs. and oral preparations of vasopressin analogues.C. as well as chlorpropamide. Compare with relationship betwen Posm and Uosm in normal individuals.005 with an increase in urine output. nasal.Nephrogenic DI may respond to combinations of indomethaci-hydrochlorothiazide or IDM-Desmopressin or IDM-amiloride. In case of inadequate thirst. it's DI. volume overload. thiazides. DESMOPRESSIN IS THE D. Avoid hyperglycemia. . water deprivation leads to a urine osmolality that is 2-4 times greater than plasma osmolality. A final urine specimen is obtained 60 minutes later for osmolality measurement. 5 U of aqueous vasopressin is administered subcutaneously. 3) Measuring Posm and Uosm at intervals and plotting them. with failure of the urine to be concentrated despite excessively concentrated serum. and indomethacin (limited efficacy). 4) Vasopressin challenge test: If injection of vasopressin normalizes response. Drug is not given to patients with Liver Disease because of mild elevation of liver enzymes. Water deficit may be calculated based on the assumption that body water is approximately 60% of body weight in kilograms. Pharmaceutical therapy for DI includes subcutaneous. diagnosis of Central DI is made. After pituitary surgery. carbamazepine. It is also useful for DI associated with pregnancy or puerperium (category B = Usually safe but benefits must outweigh the risks).008-1. Medical Care: ** In an emergency. Patients with nephrogenic DI have a normal-to-elevated serum ADH level and failure of the kidney to respond to exogenous ADH during the water deprivation test.O. 5) Consider MRI of pituitary/hypothalamus/skull: T1-weighted images of the healthy posterior pituitary yield a hyperintense signal. administer the usual dose of desmopressin to patients with DI and administer (hypotonic) IV fluids to match urine output. Replace losses with dextrose and water or IV fluid hyposmolar to the patient's serum. When the patient can tolerate oral intake. The time required to achieve maximal urine concentration ranges from 4-18 hours. and a correction of hypernatremia that is too rapid. . Follow the specific gravity of the urine and administer the next dose of desmopressin when the specific gravity has fallen to less than 1. Administration of vasopressin results in less than 9% increment in urine osmolality. along with adequate fluid to match losses. Generally. In complete central DI. most patients can drink enough fluid to replace their urine losses. testing reveals minimal ADH levels and activity. administer parenteral desmopressin every 12-24 hours. Medical Treatment: . urine osmolality increases by more than 50%. A good rule of thumb is to reduce serum sodium by 0. In response to exogenous vasopressin.Intranasal Desmopressin acetate (DDAVP)= DOC for Central DI.5 mmol/L/h. Frequent electrolyte monitoring is recommended. it can be administered 2-3 times per day.decreases by more than 3%.
Differential: .Frequent exacerbations due to chest infections.Psychogenic polydypsia .htm Clinically: Chronic Bronchitis Vs Emphysema Classicly.Blue Bloaters Pink Puffers: Emphysema predminant: . Am Soc Nephrol.Dyspnea is predominant.60(6):457-64 3. scant phlegm .Polyuria of Lithium Rx .com/PED/topic580. 1999 Dec. mouth almost closed to a puffing grimace to increase resistance to airway lost in the destruction of lung parenchyma.CMDT p1075-1077 5. Clofibrate. .Decreased aquaporin-2 expression and apical plasma membrane delivery in kidney collecting ducts of polyuric hypercalcemic rats.High V/Q areas (Dead space ventilation) Blue Bloaters: Chronic Bronchitis Predominant: .IVF administration .emedicine. . 1998 Dec.9(12):2181-93 4.CNS Sarcoidosis . O2Sat Normal. COPD patients have been categorized into: .Early polyuria and urinary concentrating defect in potassium deprivation Am J Physiol Renal Physiol 279: F655-F663. severe .Nephrogenic diabetes insipidus Ann Endocrinol (Paris).Polyuria of Cushing Syndrome .weight loss . . PaO2 normal.CXR= Hyperinflation + Flat Diaphragm . Special Precautions: Patients with DI also must take special precautions.emedicine..Cyanotic and mouth wide open to breathe more air.Pink puffers .Some drugs can be used to stimulate ADH secretion: Chlorpropamide.Emedicine http://www. .Chronic Cough is major complaint with mucopurrulent sputum .Kaplan Notes: 2002 6.com/med/topic543.Nocturnal Polyuria of Parkinson .Normal Hemoglobin.TLC increased . PaCO2 normal.R/O Diabetes Mellitus References: 1.DLco reduced . such as when traveling. 2000 2.Thin.Cough is rare. to be prepared to treat vomiting or diarrhea and to avoid dehydration with exertion or hot weather.Accessory muscles use. and Carbamezepine.htm http://author.Barrel chest .
- Hemoglobin elevated with PaO2 reduced and PaCO2 elevated. Severe O2 desaturation. - CXR= Interstitial markings - TLC normal, DLco normal. - Low V/Q areas (increased perfusion) - Progressive cardiac/respiratory failure over time, with edema and weight gain - Patients may be obese (Obstructive sleep apnea might be associated) Because they share many of the same physical signs, COPD may be difficult to distinguish from CHF. One crude bedside test for distinguishing COPD from CHF is peak expiratory flow. If patients blow 150-200 mL or less, they are probably having a COPD exacerbation; higher flows indicate a probable CHF exacerbation. Pharmacological therapy for COPD includes a number of agents, enthusiasm for which has waxed and waned as our understanding of this disease has evolved. Table 1 lists agents that have been used in COPD for 1) alleviation of symptoms, for 2) treatment of acute exacerbations and 3) for the management of its long term consequences. Bronchodilators in COPD Bronchodilator therapy in COPD is currently prescribed primarily for the relief of symptoms. There is no evidence that early regular use of these agents alters the progression of COPD. It is well established that both short acting beta-agonists and anticholinergic agents provide modest but significant relief for patients with COPD. Anticholinergics have been favored because they provide more consistent relief with fewer side effects (cardiovascular in particular) in this older population. For anticholinergic therapy, once a patient is found to suffer from daily symptoms, regular use of ipratropium bromide, the only currently available anticholinergic, is recommended on a regular basis, three or four times daily. Similarly, short acting beta-agonists, such as albuterol, pirbuterol or metaproterenol, are prescribed three to four times daily or before exercise. It is currently established that combined therapy with ipratopium and albuterol offer superior relief than mono-therapy Beta-2-agonists Salmeterol xinafoate, a long acting beta-2-agonist, initially introduced for the treatment of asthma is now FDA-approved for COPD. A new agent, tiotropium bromide, not yet approved for clinical use in the U.S., combines anticholinergic safety with long duration of action. Theophylline compounds have lost their popularity because of their frequent GI and CNS side effects. Nevertheless, now given at relatively lower doses than previously prescribed, they offer an important bronchodilatator alternative, since they can be administered once or twice daily in oral form. Such a regimen may improve compliance. Additional potential effects that may benefit the COPD patient include their anti-inflammatory effect and their ability to improve respiratory muscle function. Anti-inflammatory Therapy The role of corticosteroids in the management of COPD remains controversial. It is generally claimed that 15% of COPD patients can benefit from corticosteroid therapy. Corticosteroids are administered, both orally and parenterally, during acute exacerbation. Future Directions In spite of clear-cut evidence that current pharmacotherapy (other than drugs associated with smoking cessation) alters the course of COPD, common sense and pathologic
evidence of persistent inflammatory effects in the airways of patients with COPD suggest that anti-inflammatory therapy should be helpful in the secondary prevention and management of COPD. Unlike the findings in asthma patients, the broncho-alveolar lavage (BAL) fluid in patients with COPD demonstrates that neutrophils (and not eosinophils) are the primary airway inflammatory cell involved in this process. Primary prevention, by smoking cessation, of lung and other cigarette related diseases remains a priority in our approach to COPD. Nevertheless, enhanced understanding of the natural history of this disease, its underlying pathology and the genetic causes for susceptibility promise to open many new avenues for the treatment of this disorder. References: 1) emedicine: http://www.emedicine.com/emerg/topic99.htm 2) Cyberounds: http://www.cyberounds.com/conferences/pulmonary_medicine/ 3) CMDT: Please complete management p237-242 HOW TO DIFFERENTIATE BTW ALZHEIMER AND HIV Mr Smith goes to the doctor's office to collect his wife's test results. The lab tech says to him, "I'm sorry sir. There has been a bit of a mix-up and we've got a problem. When we sent the samples from your wife to the lab, the samples from another Mrs. Smith were sent as well, and now we are uncertain which one is your wife's. Frankly, it is either bad or terrible!!". "What do you mean?" "well, one Mrs smith has tested positive for Alzheimer's and the other one for HIV". "That's terrible!!!. Can we do the tests over again?" "Normally yes. But you have an HMO, and they won't pay for these expensive tests more than once". "Well, what am i supposed to do now?" "Well, the HMO recommends that you DROP YOUR WIFE OFF IN THE MIDDLE OF TOWN. IF SHE FINDS HER WAY HOME, DON'T SLEEP WITH HER!!!”. erectile dysfunction in a diabetic patient A 62 yo man complains of impotence& decreased libido for 2yr.His PMH significant for NIDDM of 10yr,controlled by diet& oral agents.He’s been otherwise well.On Ph.E,the skin is thin& pale,testes r both small& soft. Lab:Serum testosterone:114 ng/dl(normal:270-1070ng/dl) HbA1c:8% LH:7 IU/L(normal:2-12 IU/L) FSH:5 IU/L(normal:1-8 IU/L) The most appropriate next step of management is: A:measurement of serum estradiol B:measurement of serum prolactin C:referral for penile prosthesis D:referral for Doppler studies of penile blood flow E:to start treatment with insulin F:to initiate administration of trazodone G:to prescribe sildenafil H:to refer to a psychiatrist Answer is B.
The reported incidence of impotence in diabetic men at age 40 years is from 8-50%. The diabetes-related causes include: poor glycaemic control, autonomic neuropathy and atherosclerotic vascular disease. One is tempted to refer for Doppler studies of penile blood flow because of the longstanding diabetes where HbA1C is 8%. The cutoff point is 7.2% according to Swanson. However, Testosterone is important to erection. Testosterone is low in this patient along with normal gonadotrophins. This is suggestive of need for further assessment of hypothalamo-pituitary function. Prolactin level is the best option because of the effect of prolactin on the hypothalamic control of gonadotrophin. R/O Pituitary adenoma. References: - Swanson: DM - THE ASSESSMENT AND TREATMENT OF ERECTILE IMPOTENCE http://web.idirect.com/~ino/info18.htm A 35 yo woman currently taking maintenance fluoxetine following recovery from a depressive episode 3mo ago complains of markedly decreased llibido.What’s the best initial intervention? A:Advise the woman that her libido will likely return when fluoxetine is discontinued as scheduled in 3mo B:continue fluoxetine& add bupropion C:continue fluoxetine and add testosterone D:discontinue fluoxetine E:discontinue the fluoxetine& start bupropion Answer is E. Reference: 1- Improvement in fluoxetine-associated sexual dysfunction in patients switched to bupropion. J Clin Psychiatry. 1993 Dec;54(12):459-65. 2- http://www.socialaudit.org.uk/4200ACAM.htm Q on viral hepatitis An asymptoatic patient patient came with a h/o of exp to hepatitis C & serology came +ve.what shoud we do?Can we give interferon+ ribavarin? A patient came with a h/o exp to hepatitis A& serology came +ve.what shoud we do First, Answers to your questions: - Hepatitis A exposure with serology positive. No need for Immunoglobulin prophylaxis because it is then ineffective. It must be given right after exposure up to 2 weeks in the incubation period. No shown use if patient is Anti-HAV +. Similarly, patient already has serology positive, Vaccine is not recommended. Unless patient is symptomatic, only supportive measures are recommended for acute hepatitis. - Hepatitis C: Immunoglobulin Anti-C is no longer recommended. Treatment of Acute Hepatitis C involves Interferon 2b. The combination with Ribavirin results in increased response to treatment. - Hepatitis B: No antiviral treatment is established for Acute hepatitis B. Recommendations are for Immunoglobulins soon after exposure followed by Vaccine (see recommendations below).
Hospitalization is needed for patients whose nausea and vomiting places them at risk for dehydration. *Interferon alfa treatment for chronic hepatitis B Interferons have both antiviral and immunomodulatory effects. They must have evidence of active HBV replication. no antiviral therapy is available for healthy carriers who do not have actively replicating virus. Treatment is typically for 16 weeks. as marked by a positive HBeAg or a positive HBV DNA finding. The dose is 0. It also is recommended for contacts at daycare centers and institutions. Patients with acute liver failure require close monitoring to ensure that they do not develop FHF. Administration of hepatitis A immune globulin is an alternative to vaccination against HAV infection. * Prevention of hepatitis A virus infection The CDC now recommends vaccination against HAV for individuals traveling to endemic regions. or hospital). Treatment with alfa-interferon is appropriate for many patients with chronic hepatitis B. Typical dosing of immune globulin is 0. and to prevent or delay progression of chronic hepatitis to cirrhosis or HCC. * Treatment of chronic hepatitis B The goals of antiviral treatment of HBV infection are to reduce symptoms. Currently. who are very likely to be immune. Hepatitis B: *Treatment of acute hepatitis B As with the treatment of acute hepatitis A. Whether HAV vaccine administration should be mandated in children (as is HBV vaccination) remains unclear.06 mL/kg intramuscularly every 4-6 months if they are planning to spend more than 3 months in a region where HAV is endemic. no well-established antiviral therapy is available for acute HBV infection. .02 mL/kg. Postexposure prophylaxis with hepatitis A immune globulin is appropriate for household and intimate contacts of patients with HAV. Travelers should receive 0. Whether lamivudine and newer antiviral therapies have an impact on the natural history of severe cases of acute HBV infection remains unclear. Candidates for interferon therapy must have a clinical diagnosis of chronic HBV infection. if present. or for those known to have anti-HAV in their serum. Antiviral therapy infrequently leads to viral eradication. as marked by the loss of HBeAg and HBV DNA. to inhibit viral replication. factory. The author recommends that liver biopsy be performed prior to therapy to confirm the diagnosis and document the severity of disease. with an elevated level of alanine aminotransferase (ALT). It may be effective even when administered as late as 2 weeks after exposure. given intramuscularly as a single dose. Prophylaxis is not necessary for casual contacts (office. and vaccination is recommended for any patient with chronic liver disease.Review of Treatment guidelines for Hepatitis A/B/C/D/E: Hepatitis A * Treatment for acute of hepatitis A virus infection Treatment for acute hepatitis caused by HAV is supportive in nature because no antiviral therapy is available for HAV infection. A booster dose of the vaccine is recommended 6 months after initial vaccination. Supportive treatment recommendations are the same as for acute hepatitis A. as marked by the loss of HBsAg. for most elderly persons.02 mL/kg intramuscularly for individuals who anticipate spending fewer than 3 months in an endemic region. school.
followed by the usual two other doses at appropriate times (90% effective) . not in preventing infection. and another repeat vaccination at 6-18 months.Sexual contact with an acutely infected patient => HBIG within 14 days of exposure + . headache. neuropsychiatric symptoms (eg. irritability. This is explained by the development of a mutation at the YMDD locus in the HBV DNA polymerase gene. hematologic effects (eg. The possibility exists that combination therapy with nucleoside analogs. dyspepsia. with a greater than 95% rate of seroconversion. in order to prevent HBV-induced damage to the liver allograft. and its efficacy in populations generally not responsive to interferon therapy. Lamivudine for chronic hepatitis B Lamivudine is the negative enantiomer of 2’3'-dideoxy-3'-thiacytidine. pain at injection site. and lobucavir. Pregnancy is NOT a contraindication to vaccination. Reccomendations are as follows: . will result in improved suppression of HBV replication. The long-term impact of such mutations is unknown. thrombocytopenia). Its contribution appears to be in reducing the frequency of clinical illness. 16-32% of patients who are considered to have responded to lamivudine experience a recurrence of HBV DNA positivity.Adverse effects of interferon are common but lead to discontinuation of the drug in only 5-10% of patients. and other miscellaneous effects (eg. fatigue. The vaccines are highly effective. thyroid function abnormalities).Perinatal => HBIG immediately after birth + vaccination within the first 12 h. health care workers). It also has been used successfully in patients with decompensated cirrhosis and in the treatment of recurrent hepatitis B following liver transplantation. a repeat vaccination at 1 month. the virtual absence of adverse effects. * Hepatitis B virus vaccine: Pre-exposure prophylaxis: Plasma-derived and recombinant HBV vaccines use HBsAg to stimulate production of anti-HBs. including lamivudine. The recommended vaccination schedule for adults is an initial vaccination. It provides passive immunization for individuals who describe recent exposure to a patient infected with HBV. However. * Postexposure prophylaxis Hepatitis B immune globulin (HBIG) is derived from plasma. those on dialysis. fever. Such analogs include famciclovir. and another repeat vaccination at 6 months. HBIG also is administered following liver transplantation to those infected with HBV. depression. The latter 2 drugs are undergoing clinical trials for the treatment of both HIV disease and HBV infection and await FDA approval. somnolence). repeat vaccination at 1-2 months. The advantages of lamivudine over interferon include its ease of application. myalgia. Treatment also induces histologic improvement and a statistically significant reduction in the rate of development of hepatic fibrosis. adefovir. granulocytopenia. arthralgia). Vaccine administration is recommended for all infants and for adults at high risk of infection (eg. before hospital discharge). alopecia. It inhibits DNA polymerase–associated reverse transcriptase and can suppress HBV replication. Treatment with a dose of 100 mg orally once per day for 1 year results in loss of HBeAg in 32% of patients. Adverse effects include flulike symptoms (eg. The recommended vaccination schedule for infants is an initial vaccination at the time of birth (ie.
(4) natural interferon. as opposed to only 4% of untreated controls. Agents currently approved by the FDA for the treatment of HCV include (1) interferon alfa-2b (Intron. * Preexposure Prophylaxis: Genotype and quasispecies viral heterogeneity. (2) interferon alfa-2a (Roferon. When it is identified. and polymerases.Sexual contact with a chronic carrier => Vaccination . which is used in combination with interferon alfa-2b (Rebetol and Rebetron. or sexual exposure.g. Interferons are the backbone of antiviral strategies used against HCV. A recent meta-analysis showed that 41% of patients treated with interferon had negative HCV RNA findings at the end of treatment.vaccination . needle stick.Household contact with an acutely infected patient => None . (3) interferon-gamma. early therapy with interferon should be considered. Nutley. (4) to decrease the incidence of HCC. The combination of ribavirin. (5) ursodeoxycholic acid. Calif). (5) to ameliorate symptoms such as fatigue and joint pain. Amgen. dosed at 3 million units subcutaneously 3 times per week. and (6) to treat extrahepatic complications of HCV infection such as cryoglobulinemia or glomerulonephritis. Schering. (3) to decrease the incidence of cirrhosis. NJ). Agents under study include (1) pegylated interferons alfa-2b and alfa-2a. Currently. Kenilworth.: Needle Stick) => HBIG immediately after exposure + vaccination to begin within the first week after exposure When both HBIG and hepatitis B vaccine are recommended. was approved by the FDA in 1991 for the treatment of chronic HCV infection.Inadvertent percutaneous or permucosal exposure (e. they may be given at the same time but at separate sites. (2) to prevent progression of disease. NJ). Kenilworth.Household contact with an acutely infected person resulting in known exposure => HBIG +/. * Treatment of chronic hepatitis C Interferon alfa-2b. Schering. (2) interferonbeta. as well as rapid evasion of neutralizing . NJ). a nucleoside analog. Future medications may target the enzymes responsible for HCV replication. Roche. *Postexposure prophylaxis for Hepatitis C: IG has been shown to be ineffective in preventing hepatitis C and is no longer recommended for postexposure prophylaxis in cases of perinatal. These include (1) to decrease viral replication or eradicate HCV. (3) consensus interferon (Infergen. * Treatment of acute hepatitis C Acute hepatitis C is detected infrequently. They may have activity against viral helicases. and (6) silymarin (milk thistle).usual course of vaccination .Infant (<12 mo) primarily cared for by an acutely infected patient => HBIG +/vaccination . Thousand Oaks. with interferon alfa-2b has significantly improved patients' responses to treatment. proteases. Hepatitis C: * Treatment of hepatitis C virus infection Antiviral therapy has a number of major goals. and (4) ribavirin.
Glucocorticoid therapy has been shown in controlled trials to be ineffective.htm . correction of hypoglycemia.emedicine. * Prophylaxis for Hepatitis D Infection with hepatitis D can be prevented by vaccinating susceptible persons with hepatitis B vaccine Hepatitis E: *Treatment of hepatitis E The treatment of those infected with HEV is supportive in nature. and oral lactulose or neomycin administered. support of circulation and respiration. Meticulous intensive care is the one factor that does appear to improve survival.com/med/topic3180. lamivudine appears to be ineffective against HBV/HDV co-infection. Likewise. Hepatitis D: *Treatment of hepatitis D Patients co-infected with HBV and HDV are less responsive to interferon therapy than patients infected with HBV alone. Procedure: The treatment is carried out as follows: approximately 30 minutes before the scheduled treatment time. References: . Other agents used in ECT: Modified ECT use thiopentone sodium or methohexitol as anaesthetic. Orthotopic liver transplantation is resorted to with increasing frequency. The increase in systolic pressure is more than the diastolic pressure. To date. exchange transfusion. Next. and treatment of other complications of the comatose state in anticipation of liver regeneration and repair. Fulminant Hepatitis: In fulminant hepatitis. BP peaks during the ictal period.Emedicine http://www. the goal of therapy is to support the patient by maintenance of fluid balance. porcine liver cross-perfusion and hemoperfusion have not been proven to enhance survival. with excellent results. Protein intake should be restricted. control of bleeding. in patients with fulminant hepatitis.Harrisons 14th edition Electroconvulsive Therapy An acute response to unmodified ECT is bradyarrhythmia or even a cardiac asystole lasting for seconds followed by a transient tachycardia and increased blood pressure. conspire to render HCV a difficult target for immunoprophylaxis with a vaccine. the patient may receive an injection of a medication (such as atropine) that keeps the pulse rate from decreasing too much during the convulsion. human cross-circulation. Use of atropine as premedication increases RPP response. plasmapheresis. and succinyl choline as the muscle relaxant.antibodies by this rapidly mutating virus. the patient is placed on a cot and hooked up to a machine that automatically takes and . The BP drops sharply during the initial vagal hypertonic phase and then rapidly increased upto 40% over baseline. Rate pressure product a product of heart rate and systolic BP is one measure of cardiovascular response during ECT.
displays vital signs (temperature, pulse, respiration, and blood pressure) on a televisionlike monitor. A mild anesthetic is then injected into a vein, followed by a medication (such a Anectine) that relaxes all of the muscles in the body so that the seizure is mild, and the risk of broken bones is virtually eliminated. When the patient is both relaxed and asleep, an airway is placed in the mouth to aid with breathing. Electrodes are placed on the sides of the head in the temple areas. An electric current is passed through the brain by means of a machine specifically designed for this purpose. The usual dose of electricity is 70-150 volts for 0.1-0.5 seconds. In the first stage of the seizure (tonic phase), the muscles in the body that have not been paralyzed by medication contract for a period of five to 15 seconds. This is followed by the second stage (clonic phase) that is characterized by twitching movements, usually visible only in the toes or in a non-paralyzed arm or leg. These are caused by alternating contraction and relaxation of these same muscles. This stage lasts approximately 10-60 seconds. The entire procedure, from beginning to end, lasts about 30 minutes. Pre-care: Some medications, such as lithium (greater risk of cognitive side effects), benzodiazepines, and monoamine oxidase inhibitors, should be discontinued for some time before treatment. DO NOT DISCONTINUE ANTIEPILEPTICS USED TO TREAT EPILEPSY IN PT. SSRI's, Tricyclics, phenothiazines, are ok to continue Patients are instructed not to eat or drink for at least eight hours prior to the procedure in order to reduce the possibility of vomiting and choking. Aftercare After the treatment, patients are moved to a recovery area. Vital signs are recorded every five minutes until the patient is fully awake, which may take 15-30 minutes. Some initial confusion may be present but usually disappears in a matter of minutes. There may be complaints of headache, muscle pain, or back pain. Such discomfort is quickly relieved by mild medications such as aspirin. Risks Advanced medical technology has substantially reduced the complications associated with ECT. These include slow heart beat (bradycardia), rapid heart beat (tachycardia), memory loss, and confusion. Persons at high risk for ECT include those with recent heart attack, uncontrolled blood pressure, brain tumors, and previous spinal injuries. Normal results ECT often produces dramatic improvement in the signs and symptoms of major depression, especially in elderly individuals, sometimes during the first week of treatment. While it is estimated that 50% of these patients will experience a future return of symptoms, the prognosis for each episode of illness is good. Mania also often responds well to treatment. The picture is not as bright for schizophrenia, which is more difficult to treat and is characterized by frequent relapses. A few patients are placed on maintenance outpatient ECT. Special situations: - Patients with pacemakers: should be set to fixed mode. - Hypertension: Close control during procedure - Glaucoma: usually no problem. Consult ophthalmo. - Berry Aneurysm: No ECT until it is clipped.
- MI or CVA withint 3 months: Hyperoxygenate + Antihypertensives/antiarrhythmics PRN. - Cerebral Tumor: Ok to ECT if ICP normal. - COPD or respiratory limitations: Per anesthesiologist. Ok if can tolerate anesthesia. - Risk for retinal detachment: No ECT unless cleared by ophthalmo. - Pregnancy: Ok to ECT with close fetal monitoring only if high risk pregnancy. - Bone/Joint conditions (e.g.: joint prosthesis). Ok to ECT provided complete relaxation. - Deficiency of plasma pseudocholnesterase: leads to prolonged apnea after ECT. Guidelines are available. - Porphyrias: Avoid barbiturates during premedication. - Skull defect - Status post craniotomy: Avoid it when placing electrodes. - Dementia: Not a CI, but only if depression is a concomittent affective disorder will it respond to ECT. References: - ECT: http://home.iprolink.co.nz/~felicity/Ect_registrar_handout.pdf a 54 yo hospitalized woman who has severe recurrent MDD improves dramatically after her first 2Rx with bilateral ECT.after the 4th ECT she's disoriented to the date.The best choice for furthur Rx? a:administer 2more ECT and then initiate antidepressant medications b:discontinue ECT&treat with antidepressant medication c:discontinue ECT until her cognitive status improves and then resume ECT d:initiate a mood stabilizing medication and continue ECT e:switch to unilateral ECT for 4 additional Rx Answer is E ECT: Bilateral is preferred where there is urgency or where the patient has a high seizure threshold and good responses are hard to acheive. Once the inital urgency has passed, consider changing to unilateral placement after a few ECT's, as this DOES protect against both immediate and longer term cognitive problems post-ECT. It should always be tried if a patient has marked post-ECT confusion or memory deficit. If a patient has not responded to unilateral ECT after 6 treatments, abandon it and use bilateral. If a patient is strongly left-dominant, better to use bilateral not unlateral ECT. Reference: http://home.iprolink.co.nz/~felicity/Ect_registrar_handout.pdf A 43 yo woman has depressive rumination,hypersomnia,hyperphagia and a subjective sense of heaviness in her limbs that have not responded to trials of fluoxetine& nortriptyline.The most appropriate next step of management of this case is initiate: A:desipramine B:methylphenidate C:sertaline D:tanylcypromine E:trazodone Answer is D. This is atypical depression due to features of hyperphagia, and leaden paralysis, unresponsive to tricyclics and SSRI's. Drug of choice is MAOI. Hydrazines (e.g.: phenelzine) and non Hydrazines (e.g.: Tranylcypromine) are to be considered in this
patient. An 85yo widow who lives alone presents with weight loss,decreased energy,insomnia and a lack of interest in her usual activities.Her PMH is positive for HTN,AF,urge incontinence and contact dermatitis.She’s taking oxybutynin that she refuses to discontinue bcoz of its effectiveness.With diagnosis of depression and excluding other possible diagnosis,which drug is the best choice for this pt? a:thioridazine b:amitriptyline c:imipramine d:doxepine e:trazodone f:either d or e Answer is: E. Trazodone It is a weak SSRI Antidepressant. The main side effect is Priapism (obvisouly not the main concern in this patient). The other side effect to bear in mind is arrythmias in preexisiting cardiac disease for which it is recommended to closely monitor patient on it. Patient has Afib. Patient is presented with a combination of Urinary incontinence and depression. From a test-taking strategy point of view, Doxepine, amitryptiline, and imipramine are all Tricyclics so they can't be considered because they have similar effects. And Thioridazine is not indicated. Trazodone is left. From a medical point of view, Urge incontinence is due to detrusor instability for which patients take anticholinergics OR Tricyclics. Patient is stabilized on anticholinergic Oxybutyrin. Adding a Tricyclic will potentiate the anticholinergic side effects and may result in urinary prooblems such as OVERFLOW URINARY INCONTINENCE. SSRI's are under investigation as a treatment for urinary incontinence as well with fewer side effects than tricyclics. Consequently, Trazodone is the right answer. References: - http://www.mentalhealth.com/drug/p30-d03.html#Head_4 - http://www.healthandage.com/Home/gm=6!gid6=5013 Review on Hypersensitivity Pneumonitis Hypersensitivity Pneumonitis A- General Considerations: Farmer’s lung is the most common type of hypersensitivity pneumonitis. Hypersensitivity pneumonitis, also known as extrinsic allergic alveolitis, is an immunologically mediated inflammatory disease of the lung involving the terminal airways. The condition is associated with intense or repeated exposure to inhaled biologic dusts. The classic presentation of farmer’s lung results from inhalational exposure to thermophilic Actinomyces species and occasionally from exposure to various Aspergillus species. These organisms flourish in areas of high humidity and prefer temperatures of 40-60° (e.g.: contaminated ventilation systems and in decaying compost, hay, and sugar cane or bagasse). Farming is currently ranked as one of the top three most hazardous occupations, along with construction and mining. B- Pathophysiology: HP is characterized by diffuse inflammation of lung parenchyma and airways in previously sensitized patients. Based on the length and intensity of exposure and
it eliminates the possibility of active acute or chronic framer’s lung. Idiopathic • Rhinitis. C. HIV Neg: pulmonary MAC infection include cough. Rales. Acute farmer’s lung manifests as new onset of fever. D. Symptoms often spontaneously resolve within 12 hours to days if antigen exposure is eliminated or avoided.subsequent duration of illness. o Subacute: Nodular or reticulonodular pattern o Chronic: Linear radiodensities indicative of fibrosis. Allergic • Sarcoidosis E. Physical: • Acute farmer’s lung: Fever. subacute (intermittent). dyspnea. sputum production. Pulmonary apices are usually spared. • Subacute farmer’s lung: Normal examination findings between presentations. nonproductive cough. and impaired exercise tolerance. patients may develop acute respiratory failure. and shortness of breath.CXR: Normal findings between attacks. Subacute disease is insidious in onset and may occur over weeks to months. delayed-type hypersensitivity (type IV hypersensitivity) also plays a major role in the pathogenesis of this syndrome. headache.Clinically: ♣Acute farmer’s lung Acute farmer’s lung develops after large exposure to moldy hay or contaminated compost.High resolution CT Scan of chest: better than CXR. . weight loss. Death usually occurs 5 years after diagnosis. Clubbing .Differential: • Allergic and Environmental Asthma • Mycobacterium Avium-Intracellulare (HIV Pos: fever. o Acute: Diffuse air-space consolidation is typical of acute farmer’s lung (with acute antigen exposure). fatigue. The timing of development of symptoms after exposure supports this conclusion. Patients may have irreversible lung damage. dyspnea. chest tightness. Cell-mediated. Nonproductive cough. Abnormal findings are: . If the inhalational exposure is large. anorexia. and weight loss. clinical presentations of HP are categorized as acute. and chronic progressive.Labs and Imaging: . Patients may experience severe dyspnea at rest or with exertion. Strong evidence suggests the involvement of immune complex–induced tissue injury (type III hypersensitivity). lung♣Subacute farmer’s Subacute farmer’s lung manifests as chronic cough. Chronic farmer’s ♣lung Chronic farmer’s lung results from prolonged and continuous exposure to the antigen. and malaise. diarrhea. sweats. • Pneumonia • Pulmonary Fibrosis. weight loss. or chronic nonproductive cough • Chronic farmer’s lung: Bibasilar rales. and hemoptysis).More often observed in patients with chronic farmer’s lung with long-standing hypoxemia and parenchymal damage. If normal. fever. chills.
and Ground Glass Appearance. cromolyn. I. . and levels may be elevated in patients with farmer’s lung.Cor pulmonale . In a patient with acute farmer’s lung. .Failure to diagnose farmer’s lung in children living on farms .Treatment: . nedocromil) or systemic immune modulators are not indicated for treatment at this time.Special Concerns: .Pulmonary Function Tests: Restrictive . .Bronchoscopy: useful to rule out other diagnoses.Honeycombing (for pulm fibrosis). Note: Nonsteroidal anti-inflammatory drugs (NSAIDs) (eg. . . pulmonary function improves once antigen exposure is eliminated. This practice is not the criterion standard and should be considered only as the last resort with the understanding that it may not provide complete protection from the antigen. High ESR.Medical/Legal Pitfalls: .Diet: No dietary restrictions are needed. Between episodes of acute disease.Activity: Patients may decrease activity because of cough and dyspnea on exertion.Making the common mistake of misdiagnosing acute farmer’s lung as viral/bacterial pneumonia or acute infection.History of recurrent pneumonia should prompt consideration of hypersensitivity pneumonitis. .Failure to review a patient’s work and occupational history with emphasis on progression or improvement of symptoms when the patient is away from the farm . Positive IgG Precipitin . activity may be unlimited.Death H. and may be useful also for transbronchial biopsy which would show peri-bronchovascular granuloma.Hypoxemic respiratory failure .Pulmonary fibrosis . G.Failure to recognize the limits of transbronchial biopsy and serum precipitins: Interpretation of these tests is dependent on the size of the sample and proper testing with the correct antigen. .Encourage smoking cessation measures. .Medical Care: Systemic corticosteroid administration and avoidance measures constitute the primary treatment for farmer’s lung.CBC: Leukocytosis with neutrophilia (NOT EOSINOPHILIA).Failure to recognize farmer’s lung when pulmonary function test and radiographic findings are normal between exacerbations .Complications: . respectively. .Consider recommending the wear of filtration masks.Periodic episodes of acute respiratory symptoms without obvious triggers should also clue the clinician to evaluate for farmer’s lung. Glossary: . F.Krebs von den Lungen-6 (KL-6) has been recognized as a marker for the activity of diffuse interstitial lung diseases.A complete environmental and occupational history is the key to prompt diagnosis of farmer’s lung.
Because the clinical bleeding is severe in most patients. The FXIII zymogen circulates as a tetramer composed of 2 catalytic a subunits and 2 carrier b subunits (a2b2). B. „X Hemarthroses occur in 20% of cases „X Bleeding that is delayed (ie. .http://www.General Considerations: It is a rare autosomal recessive disease usually associated with a severe bleeding diathesis. Women with FXIII deficiency have spontaneous abortion rates of almost 100%. Malt worker’s lung. FXIII covalently binds fibronectin. Pigeon’s breeder’s lung. 12-36 h) after trauma or surgery is pathognomonic of FXIII deficiency. located on chromosome 6. as is bleeding into the mouth and gums during teething. Cheeseworker’s lung.http://www. Although acquired FXIII deficiency has been described in association with hepatic failure.Clinical Presentations: „X Bleeding from the stump of the umbilical cord within the first days to weeks of life is a characteristic sign that occurs in 80% of affected individuals. Inherited FXIII deficiency is usually due to mutations in the gene encoding the catalytic a subunit. Wheat weevil. resistance to fibrinolysis. „X Soft tissue bleeding and bruising are very common. the only significant association with bleeding in children is the inherited deficiency.com/med/topic771. and other molecules to the fibrin plug.htm updated january 2003 . bleeding from this specific site is uncommon in other inherited hemostatic diseases except afibrinogenemia. The mortality and morbidity are primarily related to bleeding.emedicine.htm updated March 2003 Review of Factor XIII deficiency Factor XIII Deficiency A. The b subunits are synthesized in hepatocytes.emedicine. „X CNS hemorrhage is frequent (25-30%) and may occur spontaneously or after minor trauma. and myeloid leukemia. the diagnosis is made at an early age. In addition. „X Recurrent spontaneous abortions are very common in women with FXIII deficiencies who do not receive FXIII replacement. intracranial hemorrhage can be life threatening. Grain Handler’s lung. this enhances adherence to the wound site. a2-plasmin inhibitor. usually during infancy. C. „X Wound healing is abnormal. Reference: Emedicine: . The a subunits are synthesized in hepatocytes in the liver and megakaryocytes and monocyte precursors in the bone marrow. a2 dimers are present in circulating platelets and monocytes. and wound healing.Hypersensitivity pneumonitis includes: Bagassosis. cross-linking the loose fibrin polymer into a highly organized structure.Pathogenesis: Factor XIII is a plasma transglutaminase that catalyzes the final step in the coagulation cascade.com/MED/topic1103. inflammatory bowel disease.
the clot dissolves in minutes to hours . and has the potential to reduce unplanned pregnancy by at least 75% (and. The development of autoantibodies to FXIII has been reported (Differentiate by mixing test.emedicine. EC is well-studied and safe. It has the advantage of working as an ongoing contraceptive for up to ten years. The Methods: There are two currently well accepted methods of emergency contraception. In addition. Reference: Emedicine: http://www. the formed clot is suspended in 5 mol/L of urea or 1% monochloroacetic acid. The patient's plasma is incubated with thrombin and calcium for a sufficient period to allow formation of a stable clot. most notably dysfibrinogenemia and decreased fibrinogen levels. derivatively. The hormonal method consists of various formulations of estrogen and progestins or progestins alone. and failure to implement prophylaxis as the treatment of choice. „X Consider other congenital coagulation factor deficiencies. a booster dose is recommended during labor to decrease the risk of bleeding in the mother. E.com/ped/topic3040.Functional and immunological assays available to confirm Ds F.htm Updated November 2002 Emergency Contraception Emergency Contraception Background: Unprotected sex will result in pregnancy about 8% of the time it occurs. Consequently. Its use is limited by the requirement for special training for insertion. „Ï Prior to surgery: patients should receive FXIII concentrate immediately before surgery to ensure optimal hemostasis and wound healing. intercourse with no contraception for any reason or forced intercourse. and cryoprecipitate have been used for replacement of FXIII but the treatment of Choice is plasma-derived Factor XIII concentrate. This can include failed contraception. induced abortions). the initial expense and the fact that some women are not candidates for IUDs.Work-up: . in its absence.PTT and PT are normal in FXIII deficiency . „Ï Patients requiring prophylaxis should be vaccinated for Hep A and B „Ï Medical/legal pitfall: failure to investigate family members for FXIII deficiency. According to different surveys. Plasma with inhibitor is still prolonged whereas that with true deficiency is corrected). and disseminated intravascular coagulation.Differential and associated diseases „X Acquired FXIII deficiency can be caused by liver disease. Emergency contraception is indicated in any situation in which a woman has had unprotected intercourse but does not wish to become pregnant.Measurement of clot stability is the most common screening test. inflammatory bowel disease. the clot is stable for more than 24 hours. treating pregnant patients requires more frequent prophylaxis (every 3 wk).Medical Care: „Ï Treatment of bleeding: Plasma. „Ï Prophylaxis in pregnant patients: Half-life is shorter. . In the presence of FXIII. the other is the emergency insertion of the coppercontaining IUD (intrauterine device).D. The latter can be used up to five days after unprotected coitus and is highly effective. „Ï Prophylaxis: Prophylactic therapy with FXIII concentrate 10-20 U/kg every 4-6 weeks provides adequate plasma levels in most patients.
75 mg taken 12 hours apart to a single dose of 1. will reduce the rate of pregnancy from 8% to 3. This medication is administered in two doses started within 72 hours after unprotected intercourse.5 times the amount of levonorgestrel than is in the Yuzpe regimen using levonorgestrel.1. If the woman is found to be pregnant. o A woman must be pregnant for several days before the test will turn positive. a pregnancy test should be done. the World Health Organization (WHO) changed the dose of levonorgestrel (Plan B) from 2 doses of 0. If a woman uses the test and it turns out negative.5 mg levonorgestrel (Plan B) o Five-day cut-off time for treatment. Note that this progestin dose is 1. particularly with the Yuzpe method. Undiagnosed vaginal bleeding is a CI of the Progestin-only method.2%. most prominently nausea and vomiting. H/O thromboembolism and migraine are two relative contraindications. Additional advice: WHO now makes the following recommendations: o One immediate dose of 1. When used correctly the progestin prevented 89% and Yuzpe prevented 76% expected pregnancies Contraindications: Same as with any OCP.When was the first day of your LMP (should be less than 4 weeks ago)? . it need not be used. The timing: It is very important to start EC as early as possible in the 72-hour window after intercourse.The Yuzpe Method = Preven® 100 mcg of ethinyl estradiol and 1 mg of norgestrel (2 pills immediately. If menses have not resumed 21 days after the administration of emergency contraception.Have you had sex within the last 72h? . o Even if a woman were to be pregnant and take the pills.The Progestin-only Method Levonorgestrel (LNG) = Plan B® has been shown to be equivalent to the Yuzpe method. so only half the milligrams.5 mg per dose. but rates so low that WHO only cites Current Pregnancy and hypersensitivity to any of the components as contraindications. They also extended the treatment period from 3 days (72 hours) to 5 days (120 hours). But it is also very important that the second dose be 12 hours later. which has twice the potency of norgestrel. The side effects: There are significant side effects to hormonal EC. Resumption of menses: 72% of patients resumed menses early or within three days of their expected date. 2. or 0. and the FDA required manufacturers to remove warnings about increased risk to the fetus several years ago. followed in 12 hours by 2 more pills). . she may feel that she took the pills when she didn't need to. The main concern is whether the vomiting will interfere with the absorption of the medication. The Preven® formulation is equivalent to the Yuzpe regimen but it contains levonorgestrel. Plan B® is the progestin-only formulation.5 mg. there should be no adverse effect on the pregnancy from taking EC. Treating more than 4000 women in 10 countries. is needed.Were your periods normal in time and length? Comparison of both methods: A large multicenter trial published in 1998 definitively showed that the progestin-only regimen was more effective than the Yuzpe. Birth control pills have frequently been taken in early pregnancy without adverse effects on the fetus. it would not cause spontaneous . rather than 3 days o Ongoing contraception started at time of emergency contraception Although the Preven kit comes with a pregnancy test. The screening prior to prescribing: three questions to which answer should be YES.
RU486. Remember. both products have a long shelf life: Preven®. Showing your outrage at the crime may cause victims even more trauma.com/conferences/womens_health/ Updated March 2003. Anal examination including proctoscopy should be performed if there is history of forced anal penetration with documentation of found injuries.abortion. it can be repeated without risk. Its efficacy as an emergency contraceptive is primarily due to its effect of delaying ovulation and possibly delaying maturation of the endometrium. only for medical abortions. 4) A full STD screen at presentation as research suggests a significant incidence of acquisition of STD's prior to rape event.S. the "Abortion Pill" and EC Mifepristone is a very effective emergency contraceptive. They should abstain from intercourse or use reliable back-up contraception until their next menstrual period.) 2. four years. Providing a prescription to be filled and kept at home is a wise precaution and will result in more immediate use and a higher success rate. it is preventing a pregnancy. Other considerations: Mifeprex®. Mifepristone is available in the U. . because if EC delayed ovulation. ovulation may yet occur for that cycle.Verify occurence of sexual assault. It presents an opportunity to review contraceptive needs and insure maintenance or initiation of effective contraception for women who wish it. Approach victims calmly. three years. Women should be cautioned to avoid unprotected coitus until their menses occur.History Taking: Unrushed and sensitive manner.cyberounds.emedicine. so off label use for emergency contraception would be difficult. and no harm would come to the fetus. In doing so. Oral contraception can be started immediately after EC. In this capacity. PMHcontraceptive history-Gynec History. so adrenal insufficiency and chronic treatment with corticosteroids are listed as contraindications in the insert. 3) Physical Examination: Injuries requiring immediate attention should take precedence. Mifepristone also blocks corticosteroid receptors. References: . Initial investigations: . Ask victims whether they would prefer a male or female physician. It is also a chance to educate and institute protection against STD’s. hemorrhagic disorders and anticoagulant medications are also listed.com/aaem/topic498. Porphyria. A follow up visit after successful EC is always advisable.htm Updated May 2003 Approach to a rape victim Approach to a rape victim 1. and Plan B®. avoid interpreting the victim's calmness or composure as evidence that a sexual assault did or did not occur. Use direct questioning to disclose forced oral or anal penetration by victim.Emedicine: http://www. Although EC is not a good method of contraception. (Note: False accusations of sexual assault are estimated to occur at the low rate of 2%—similar to the rate of false accusations for other violent crimes. It is not interrupting a pregnancy.Cyberounds: http://www. it is not causing an abortion. Ask about sexual history before rape. Its availability is restricted to health facilities doing medical abortions under strict protocols.
a meatal specimen discharge is an adequate substitute for an intraurethral swab specimen. Gonorrhea and Chlamydia Trachomatis cultures from specimens collected from any sites of penetration or attempted penetration. serologic. the vagina in girls. Isolates and specimens should be retained or preserved in case additional or . gonorrhoeae should be used. hepatitis B. . . . 7) Treat sexual partners if pt found to have STD.e. .Wet mount and culture of a vaginal swab specimen for Yeasts and Trichomonas Vaginalis.Collection of a serum sample for immediate evaluation for HIV. .. Cervical specimens are not recommended for pre-pubertal girls. or DNA probe methods).Hep B Vaccine up to three months after assault 3 doses. enzyme substrate.N.Offer Pregnancy prevention using Levonorgestrel (Ovral) 0. and the urethra in boys. Hepatitis B vaccine should be administered to sexual assault victims at the time of the initial examination if they have not been previously vaccinated. Special considerations: Sexual assault of a child: Specimen collection for culture for N. gonorrhoeae from the pharynx and anus in both boys and girls.. and syphilis. gonorrhoeae should be confirmed by at least two tests that involve different principles (i. and BV may be administered. 5) Treatment: Postexposure hepatitis B vaccination. If considered PEP should be given no later than 72h after event.75mg x1 dose only (recent guideline) or x2doses 12h apart no later than 73h after event. 0-1-6 months. For boys with a urethral discharge. biochemical. -------------------------------------------------------------------------------If patient pregnant or breast feeding: Amoxicillin 3g STAT + Probenecid ag STAT + Erythromycin 500mg BID x14days. 6) Offer ongoing counseling.Offer Post exposure Prophyaxis for HIV. Follow-up doses of vaccine should be administered 1--2 and 4--6 months after the first dose. FDA-approved nucleic acid amplification tests (as a substitute for culture). without HBIG. Recommended Regimen -------------------------------------------------------------------------------Ceftriaxone 125 mg IM in a single dose PLUS Metronidazole 2 g orally in a single dose PLUS Azithromycin 1 g orally in a single dose OR Doxycycline 100 mg orally twice a day for 7 days. trichomonas. should adequately protect against HBV. In addition. Only standard culture systems for the isolation of N. An empiric antimicrobial regimen for chlamydia. All presumptive isolates of N. gonorrhea. IUD copper-contraception can also be considered with ATB coverage.
even if the risk is perceived to be low by the healthcare provider. resulting in pain and tenderness. Epidermoid Cyst is more favored. Collection of a serum sample to be evaluated immediately. and bleeding have been reported.gov/std/treatment/8-2002TG. Rarely. However. but they may become inflamed or secondarily infected. some children or their parent(s) or guardian(s) may be concerned about the possibility of infection with an STD.CDC 2002 Guidelines: http://www. What is it? Epidermal Inclusion Cys Background: Also called Sebaceous cyst although not of sebaceous origin. To treat or not treat? Presumptive Treatment The risk of a child acquiring an STD as a result of sexual abuse or assault has not been determined. including basal cell carcinoma. the cysts can become inflamed or infected. Presumptive treatment for children who have been sexually assaulted or abused is not recommended because a) the prevalence of most STDs is low following abuse/assault. Cultures for C. vaginalis infection and BV.htm#AssaultSTDs . SCC.National guidelines for response to sexual assalut http://www. In the uncommon event of malignancy. History: Discharge of a foul-smelling cheeselike material is a common complaint. b) pre-pubertal girls appear to be at lower risk for ascending infection than adolescent or adult women. Biopsy reveals Cheese-like material. trachomatis from specimens collected from the anus in both boys and girls and from the vagina in girls. Less frequently. Bowen disease. Physical: Epidermoid cysts appear as firm. Gram stains are inadequate to evaluate pre-pubertal children for gonorrhea and should not be used to diagnose or exclude gonorrhea. and used as a baseline for comparison with follow-up serologic tests. Such concerns may be an appropriate indication for presumptive treatment in some settings and may be considered after all specimens for diagnostic tests relevant to the investigation have been collected. Epidermoid cysts are slow growing and usually asymptomatic. Extracts of this material have been shown to be chemotactic for polymorphonucleocytes. Epidermoid cysts result from the proliferation of epidermal cells within a circumscribed space of the dermis. Reference: . Agents for which suitable tests are available include T. and even mycosis fungoides. friability. mobile.PDF Question Question about Pt with picture of skin lesion showing nodule. preserved for subsequent analysis. resulting in pain and tenderness. rapid growth.mssvd. Culture and wet mount of a vaginal swab specimen for T.uk/PDF/CEG2001/sexassault%2006%2001.cdc. pallidum. HIV. malignancies.org. round. Inflammation is in part mediated by the horny material contained in epidermoid cysts. have developed in epidermoid cysts. and c) regular follow-up of children usually can be ensured. and HbsAg. flesh-colored to yellow or . Sera should be tested immediately for antibodies to sexually transmitted agents.repeated testing is needed.
FNA: Fine needle aspiration has been used to help diagnose epidermoid cysts. Biostats question With IQ test mean of 100 and SD 15. I was wrong in my reasoning just like Salil.What will be percentile of IQ if person IQ is 115 ? 50.com/derm/topic860. 68. Epidermoid cysts of the genitals are common in the general population and may appear as a mass in the breast.the most common presentation of submucosal fibroid is abnor. In turn. Squamous Cell carcinoma (MC cancer in this entity). A central pore or punctum is an inconsistent finding that may tether the cyst to the overlying epidermis and from which a thick cheesy material can sometimes be expressed. Therefore. . on the buccal mucosa. all excised cysts should be sent for pathologic analysis. and even on the uvula. the penis. Treatment: . or the perineum.So. and they demonstrate nucleated squames and wavy keratin material.Excision in toto = definitive treatment preventing recurrence by excising Keratin producing the lining of the cyst. . on the lips. You suspect uterine fibroids. Here's the exaplanation. removal is recommended for any cyst behaving in an unusual way (eg. the clitoris. Which work up is essential in determining the severity and therefore the treatment indication of this patient? From the hx. under the tongue. Smears of aspirated material can be stained with Wright-Giemsa.white subcutaneous nodules of variable size. USG is the best initial non-invasive investigation to do in this case.May be injected with triamcinolone if uninfected. Occasionally.The treatment of epidermoid cysts on the terminal phalanx is more complicated and may consist of curettage or chemical cautery followed by packing with bone chips. the vulva.htm Updated Feb 2003 Microbiology (if infected) and US Question 34 yo female patient presenting with heavy menstrual blood loss and elarged uterus. the scrotum. Medical/Legal Pitfalls: The major pitfall in managing epidermoid cysts is failure to diagnose an associated malignancy. and cysts have been reported on the palpebral conjunctivae.(enlarged uterus is very unlikely) Reg investigation.detect intramural/subserosal (as in this case)& vaginal sono .Abstinence . rapid growth). Physical examination reveals a large uterus with irregular consistency.vaginal bleeding.emedicine. Reference: emedicine: http://www. The ocular and oral mucosae can also be affected.the most likely diagnosis is either Subserosal fibroid or Intramural fibroid(as it is given as enlarged uterus).I&D if infected followed by antistaph ATB PO . 84.99 th ?? This question has been discussed in length before.Hysteroscopy will detect only the submucosal fibroids whereas USG can detect all types of fibroids.detect submucosal.Abd sono. 95 . .
consequence of long-standing PDA. If you add to it the new found number of between the mean (hump of the curve) and +1sd which is 34%. Another study concluded that psudotumor 1. In all instances healthy babies were delivered. Half of that area is 34% which is between the mean and +1sd. Similarly. Medical literature search: few articles describe two scenarios. Now from the hump of the curve to +1sd corresponds to half the area under the curve we talked about in the beggining. But that's the trick. The patients who already had the established diagnosis were treated medically.What we know from the bell-shaped curve is between +1SD and -1SD: the area under the curve consists in 68% of the population. Meaning. It has also been shown to increase pulmonary blood flow. therefy reducing the tendency to Pulmonary hypertension. 3/4 of patients responded to shunting the other 1/4 required optic nerve sheath decompression. the area between -2SD and +2SD is 95%. The question asks about the percentile. Usually one dose is enough. We already know that between 0 and the dome of the curve is 50 % because it's the mean. Read the explanation after drawing the bell shaped curve you'll understand it better. But if persist.5%. I wondered about the treatment in pregnancy. one in which a patient has pseudotumor and gets pregnant or the patients is pregnant and develops signs of increased intracranial pressures. Indomethacin either postnatally or sometimes prenatally as PDA prophylaxis inhibits Cyclo-oxygenase thereby inhibiting the production of Prostaglandins.5%. if the ICP became resistent to therapy (one study followed progressive visual loss) a shunt was placed. Avoid ergotamine. does not increase the risk of relapses 2. Half of it which is the area between the mean and +2SD is 47. What treatment would be best for her migraine during pregnancy? In general. it is a directional question. This area situated in the interval -1SD and +1sd which is 68%. Now let's join the two. it gives you 84%. Sometimes. however.5% are located below the +2SD point on the curve. The interpretation is a number AT +1sd is at the 84th percentile. does NOT affect the . It is not what is asked in the question. So the hump of the curve corresponds to the 50th percentile. Mechanism by which Indomethacin helps in the closure of PDA Patency of PDA is an active state maintained by the action of prostaglandins.5 = 97. Migraine and Pregnancy 26yo G1P0 with irregular menses and an LMP approximately 10 weeks ago is reffered to your clinic secondary to a positive pregnancy test. Therefore the percentile located AT +2sd is 50+47. and leading to closure of PDA in as many as 86% of the patients. it requires surgical intervention either because of failure to close or reopening after many treatments with Indomethacin. tx w/acetaminophen and antiemetics. (If severe use codene ormeperidine). Here's what I found. does not mean a worsening prognosis and 3. Pseudotumor Cerebri and Pregnancy I recall having read a question in which a pregnant woman came in with signs indicative of pseudotumor cerebri. It means of our population 97. We had calculated between 0 and the mean as being the 50th percentile. migrain HA normally improves in pregnancy. Her PMH is negative for anything other than migraine headaches that she suffered from regularly since high school. How much percent is between 0 and +1sd.
Avoid hyperglycemia. as well as chlorpropamide 100mg/d. 3) DI and pregnancy: Pregnancy increases risk for DI = Vasopressinase-induced DI.: at time when ADH should be highest and urine most concentrated). and rapid correction of hypernatremia. Uosm improves after administration of ADH. HCTZ 50-100 mg/d) induce mild salt depletion (block Na reabsorption in cortical diluting site) which results in volume contraction. Urine Na.005 . Thiazides (e. BP: normal. Lytes: Hypernatremia.g.e. Urine Specific Gravity. Volume depletion may decrease lithium excretion. May be combined with thiazide for additive antidiuretic effect and to balance potassium. The mechanism = circulating desmopressinase which destroys .developing child. The article listed 2 case studies . 1st step in management: 1)In ER: Hydrate IV dextrose and water or IV hyperosmolar fluid. Next step: Work up is done preferably with pt maximally dehydrated as tolerated (i. the latter being DOC for Lithium-indeuced Nephrogenic DI. In DI. in which elevated ICP occur during pregnacy is rare. volume overload. ADH levels.Amiloride: Agent of choice in lithium-induced nephrogenic DI since it may block lithium uptake in distal tubules and collecting ducts. thiazides. The latter results subsequently in decreased GFR. or hepatic dysfunction. See in 3rd Trimester and puerperium. 2) Central DI: DOC = Intranasal DDAVP Assess for drugs that potentiate effect of DDAVP: Chlorpropamide (patient IS DIABETIC AND ON CHLORPROPAMIDE).Thiazide diuretics combined with mild salt restriction is the most effective therapy for nephrogenic DI (can reduce polyuria as much as 50-70%). creatinine. She therefore started experiencing frequent urination. 2) Nephrogenic DI: Combination Indomethacin + HCTZ or Indomethacin-Desmopressin or Indomethacin-Amiloride. Uosm) 2) Serum: Electrolytes and Glucose. Allows lithium use to be continued. Main limitation is symptomatic volume depletion.Uosm < 200mOsm/kg 3)Differentiate bwteen Central and Nephrogenic: Water Deprivation Test: Compares Uosm after dehydration Vs Uosm after Vasopressin. hallmarok is: Urine Sp. pre-eclampsia. 1) 24h urine collection: volume. PE: no peripheral edema. and indomethacin. Salt restriction augments this effect. May also have thiazide-like action since it causes a negative Na balance. Carbamezepine. increased isotonic proximal fluid absorption and thus decreased delivery of fluid to the collecting duct. Must monitor for hyperkalemia and cannot use in renal insufficiency. . Grav=1. she reveals that she has been thirsty of late. Role of Thiazide in DI . and drinking lots of water. Upon further evaluation. Often associated with oligohydramnios. clofibrate. The second scenario. increasing risk of lithium toxicity. in both the baby was delivered vaginally without complications. Potassium should be given as needed to prevent hypokalemia. In Central. JB's got h/o of DM2 controlled by diet and exercise. clinical Scenario: JB a 57yo woman has been having recent epidoses of nocturnal enuresis.
The quickest response would be with IV immunoglobulin which is indicated in severe thrombocytopenia.so diagnostic test of choice Renal transplant rejection Vs Cyclosp.Diabetes Mellitus .edu/diabetes_insipidus.Multiple Myeloma Reference: .K:6. . and steroids (40-80%).endogenous ADH but not synthetic.HCO3-:16.Her PMH is positive only for hysterectomy 1mo earlier& chronic migraine headaches controlled with methysergide.No RBC fragmentation is noted on exam of peripheral blood smear.Sickle Cell Disease .Lab: Na:130.Plt count:2000. AZT (80-90% susteained positive response). A 54 yo woman presents with abrupt decline in urine output& RF.Endocrinology UCLA http://www.2.Sp. Urinary tract obstruction since it is abrupt onset? It is also a vasoconstrictor.Hypercalcemia .G=1. Methicillin). Demeclocycline(ATB tetracycline used for SIADH).Lithium.P:6.Emedicine . nephrotoxicity . this pt has a presentation typical of retroperitoneal fibrosis:clear association with methysergide CT generally confirms the Dx by showing medial deviation&extrinsic compression of the ureters.3.med.currentlt receiving no treatment.ucla.Pregnancy .2 U/A:PH:1.htm .protein&Hgb:trace.Pituitary surgery . Long-term treatment options would include spelectomy (increased risk for encapsulated organisms infections).glucose:101.010.develops the acute onset of petechiae and oropharyngeal bleeding.LINEAR GROWTH RETARDATION Note: Risk factors for DI: . Colchicine.Hypokalemia . Side effect of this drug: Retroperitoneal fibrosis.Albumin:4.Ca:7. Rx = DDAVP. Foscarnet.010.9.Cl:99. 4) DI in children: mostly ENURESIS .endocrinology.Cr:3.Kaplan notes 2002 Question A 24 yo man known to be HIV+.sediment:unremarkable Urine output over the past 12hr:60cc Next step of Mx? Stop offending drug and do CT. Also U.Rx? a:DDAVP b:plt transfusion c:aminocaproic acid d:IV gammaglobulin e:FFP IV immunoglobulin This is HIV-induced ITP. but the abrupt onset doesn't make it sound like ATN secondary to vasoconstriction.CMDT .
Normal t scores are above -1. bisphosphanates 3. Raloxifene significantly reduces the risk of vertebral fractures by approximately 30% but does not reduce the risk of hip or other nonvertebral fractures.Albumin:4. alcoholic. fever.2. Reference: . therefore protecting her against it is not necessarily warranted.9. MRI: loss of distinct cortico-medullary junction + swelling + density similar to that of Psoas and fat tissue. and oligouria.http://www.glucose:101. The risk she needs to be protected against is pathological fractures. she is a smoker.urine protein:6.pdf Question A 68 yo white man is reffered to u for evaluation of renal failure. According to CMDT Alendronate is the first agent to consider. . manometry: capsular pressure is<40mmHg.Lab: Na:135. hyalinosis. Bisphosphonates have the mechanism of action of inhibiting . US: increased graft cross-sectional area. Cyclosporine trough level>200ng/ml.stadtlander. including calcitonin. The evidence for reducing fracture risk is currently considered insufficient for most agents.past history of dvt. with sedentary lifestyle. endothelial vaculoization). Rsponds to decreasing cyclosporine.her bone density test [dexa scan[ shows t score of 0.Renal transplant patient on immunosuppressants among which cyclosporine.P:4. rapid rise in creatinine.Cl:109.Hct:29% Cr clearance:55ml/min.hrt 2. edema. calcitonin Answer is 2.Ca:10. and etidronate.2g/day Next step of Mx? this pt has multiple myeloma and his renal failure most likely is related to overproduction of Ig light chains. raloxifene 4.the pt has anemia.K:4.he has significant proteinuria WITH NORMAL serum albumin so nephrotic syndrome excluded!and the presence of LMW protein that's readily filterated at glomerulus such as Ig light chain. necrosis and sclerosis). what is best for her 1. US: unchanged graft corss-sectional area.cyclosporine toxicity: >6 weeks use. obese. This patient has no history or risk factor mentioned for breast cancer.HCO3-:24.com/content/transplant/Generic_Cyclo_PI. Is it graft rejection or cyclosporine nephrotoxicity? To differentiate the two: . Responds to increased steroids or antilymphocyte globulin. Manometry intracapsular pressure >40mmHg.9. Cyclosporine trough level <150ng/ml. estrogen(HRT).9. 4 weeks later: rapid rise of creatinine. So she's still not extremely depleted.Transplant rejection: <4weeks. oligouria after initial function.could explain the proteinuria first step of Mx:immunofixation electrophoresis of the serum&urine confirmation by BMA&biopsy&bone survey a 65 year old postmenopausal lady presents with bone pain. Bisphosphonates. Her t score is 0. Biopsy: arteriolopathy (intimal thickening. afebrile.3. fever and weight gain. The evidence of antifracture efficacy is most convincing for the 2 bisphosphonates alendronate and risedronate. Biopsy: endovaculitis (intimal arteritis. gradual rise in creatinine. According to CMDT the agents to use first are bisphosphonates.
It MAY BE GIVEN AT THE SAME TIME AS MMR. Should he be vaccinated? Yes. the vaccine should be repeated in 5 months. Shoul dhe get vaccine? YES. If the patient were to have mentioned any risk factor for breast cancer. This illness should be treated as regular chickenpox. Should he get vaccine if not immunized before? Yes within 3-5 days of exposure. then Raloxifene would be first choice. Immune globulin products should not be given for at least 2 to 3 weeks following the varicella vaccine. Most adults are immune." This is a mild case of chickenpox caused by the wild-type virus at least 6 weeks after vaccination. Inhaled steroids are not a ptoblem. If age is 6months old = DO NOT VACCINATE. in the household ARE NOT CONTRAINDICATIONS TO THE VACCINE WHEN IT'S DUE.Chickenpox developped after vaccine: 1% of vaccinated kida will have what is called "breakthrough disease. .PPD TEST MAY BE DONE AT THE SAME TIME AS VARICELLA VACCINE. however. There are usually less than 50 lesions and no severe symptoms. . . Asks you if she should be concerned and get the vaccine now? NO. . Was never vaccinated for chickenpox.The vaccine is not 100% protective. pregnant women. leukemic grandmother. Never vaccinated for chickenpox. DO NOT VACCINATE BABIES LESS THAN 1 YEAR. with no DEFINITE prior history of chickenpox or varicella vaccine.Pregnant woman 12 weeks. There is a possibility of rash 4-6 weeks after vaccine.HIV brother. Babies less than one year are perhaps considered immunocompromised?? At any rate it is not recommended IN THE USA. .The varicella vaccine should not be given for at least 5 months after receipt of an immune globulin preparation or a blood product (except washed red blood cells).Pregnant woman had a sever case of shingles. . He still has to get the vaccine.what will u tell the mother? Answer: If age is 6yo = give vaccine. Vaccine is contraindicated if ORAL STEROIDS. 15% of patients with get a mild rash. Now. . . Varicella Vaccine Facts 6 year old girl's mother is afraid the baby may get chicken pox becoz her friend got it. and it has been shown that this rash is more severe in immunocompromised patients. same patient with mild sore throat or diarreha. and Vaccine is contraindicated in pregnancy.Son is 8yo on inhaled steroids for asthma. .Vaccinate ANY child who is not immunocompromised and is more than one year old. . This baby's age is probably 6 months as opposed to six years old (probably a typo). they are given at the same time.Son had rash at 4 months of age. She asks you if her 1 yo son STILL has to get the vaccine or he's probably immune by now because of the exposure. . son is due for vaccination.Son exposed to chickenpox at school. Reference: . . MD said that it's "probably" chickenpox. If. NO.baby was not vaccinated . Since it's not a DEFINITE history of chickenpox.osteoclast activity this stopping calcium mobilization from the bones.
This sort of nerve injury may be associated with cervical spine fracture. What to do: Look for associated injuries. Construct a splint. Incomplete lesions may be satisfactorily referred for followup evaluation and physical therapy. usually by sleeping with his arm over the back of a chair. extending from proximal forearm to just beyond the metacarpophalyngeal joint (leaving the thumb free) which holds the wrist in 90 degree extension.Saturday night SYNDROME: USMLE Takers winding up forming a sorry newsgroup of DOCTORS without a date on a Saturday night. but when the hand is pronated (palm down) the wrist and hand will drop. hand function may appear normal. the importance of splinting and physical therapy for preservation of eventual function. thumb and finger joints.com/vacinfo_3-7.vaccinecheck. and of inability to extend his wrist. Most commonly it occurs when a person falls asleep. ignoring the growing . Less severe forms may befall the swain who keeps his arm on his date's chair back for an entire double feature. What not to do: Do not be misled by the patient's ability to extend the inter phalangeal joints of the fingers. Prognosis: short-term = very high likelyhood of sarcasm and irritability..already married. or fracture of the humerus. ligaments. and joint capsules which can result in loss of hand function after strength returns. which may be accomplished by the ulnar-innervated interosseus muscles. intoxicated.http://www. the slow rate of regeneration. complaining of decreased or absent sensation on the radial and dorsal side of his hand and wrist. held up by his arm thrown over the back of a chair. arrange for additional neurological evaluation and treatment right away. 2. Sometimes happens after humerus fracture since radial nerve trails down around humeral groove. Explain to the patient the nature of his nerve injury. Another presentation is a patient using crutches. Patient now presents holding the affected hand and wrist with his good hand. If there is complete paralysis or complete anesthesia. The rest was.Saturday night PALSY: Radial Neuropathy or Saturday Night Palsy or Wrist Drop: Basic Anatomy Stuff: The radial nerve contains axons contributed by the fifth and sixth cervical roots (C5-6). Discussion This neuropathy is produced by compression of the radial nerve as it spirals around the humerus.jsp?vac=3-7 What is Saturday night syndrome? Two aspects are to consider for this syndrome: 1. and arrange for followup. This and a sling will help protect the hand. also preventing edema and distortion of tendons. It forms the POSTERIOR CORD of the brachial plexus. Long-term = roughly 67% will end up with a date in the next three years.. With the hand supinated (palm up) and the extensors aided by gravity. injury to the brachial plexus in the axilla. Presentation The patient has injured his upper arm.
FANA e. The deficient groups will be the wrist ulnar extensors as well as the metacarpophalyngeal extensors. PALMS AND SOLES NOT INVOLVED (as opposed to roseola of secondary syphilis).zinc In an adolescent presenting with ptyriasis rosea.vit C d. No need to exclude child from school. confirm with treponemal FTA-ABS for ex. A high radial palsy in the axilla (e.emedicine .vit A b. and soap may cause irritation and should be avoided early in the disease. Questions: which of the following when given in excess would most likely cause pseudomotor cerebri? a. and challenging cases of pregnant wome. VDRL B.hepatitis A IgM d.vit B c. Reference: . 1-2 weeks later generalized rash which lasts approximately 6 weeks.glucose 1. so I thought I'd share what I had come across a while ago. sweat. Both are nontreponemal. Labs: RPR or VDRL to R/O secondary syphilis. The rash has a Christmas Tree appearance on the back. occurs in clusters among contacts. (Sensitivity for primary syphilis: RPR higher 86% (vs 78% for VDRL)=>use RPR first. including the triceps. from leaning on crutches) will involve all of the radial nerve innervations. Treatment: Self limited. Topical zinc oxide and calamine lotion are useful for pruritus.g.ca/pphb-dgspsp/std-mts/csg-ldcm/lab_e. Supportive measures: Water.High Yield..html Trauma in Pregnancy.Q#1 Many people came back from the exam with the common feedback that they have seen people that day flying through the windshield of their cars. salmon colored with darker periphery (primary plaque).. Cause: seasolnal predilection. Here goes. So if positive. If the injury to the radial nerve is at the elbow or just below.vit D e.pain and paresis.VDRL: Quick review on Pityriasis Rosea Presentation: Child with Herald patch 1-2 cm.. no organism involved.gc. .hc-sc. complete blood count c. This has been updated as of february 2003. there may be sparing of the wrist radial extensors as well as the radial nerve autonomous sensation. Secondary syphilis.Vit A (Typo: pseudoTUMOR cerebri) 2. both have 100% sensitivity and 98% specificity. so you can use either one of them).Lab Diagnosis of syphilis http://www.which f the following tests would be an appropriate blood test to order? a.
coned views aimed more than 10 cm away from the fetus result in very low exposure to the fetus. In addition. With modern radiographic machines. of course. the technique. You order intravenous fluids. An IVP causes 500-800 mrad exposure. it is positive. with a range between about 200 and 1200 mrad. pelvis. A quickly ordered quantitative bHCG shows that she is between 6 and 8 weeks pregnant.' The third patient -. So. CTs of the head result in about 50 mrad of exposure. She is complaining bitterly of low back pain. complaining of some low back pain and left upper quadrant abdominal pain.. She has no airway compromise. chest.is a 22-year-old female. but EMS is unable to perform this because of 'laryngeal spasm. chest and pelvis. (all of which were reported as 'normal'). She says that she was struck on the left side when the car hit the first pole and is tender in the left upper quadrant of the abdomen. intravenous pyelograms (IVP). Each of these examinations. while. as it can vary according to the equipment used. She is awake and aware. What did you forget to order specifically? Trauma in pregnancy.appear critically injured. urethrocystograms and the 'KUB' (or 'flat plate abdomen') are considered 'high dose'. pelvis and hip. She has never been pregnant before. given that she has had the x-rays ordered (cervical spine. You also order oral contrast for the CT of the abdomen and pelvis to be given as soon as the lumbar spine views are completed. CTs of the upper abdomen can produce up to 3000 mrad of exposure. 'High dose' examinations include lumbar spine. Examinations in the 'low dose' group include cervical spine.Q#2 A pregnancy test! Moreover. thoracic spine. Talking with the patient reveals that her last period was about 7 weeks earlier. The lumbar spine is the highest exposure. The pelvis and hip x-rays produce about 200 to 400 mrad each. Estimating exact exposure of any individual fetus is very difficult. EMS calls to say they are bringing in three patients from a rollover car wreck. bloods. When the patients arrive. lumbar spine) and has completed the CT of the abdomen and pelvis. maternal size and the age of the fetus. should result in less that 1 mrad exposure to the fetus. but has a respiration rate of 22 secondary to the pain on the left side of the chest inferiorly. understandably. together with lumbar spine views.. urinalysis. You quickly head off to deal with the other two victims. you quickly examine the 22-yearold. and an x-ray of the cervical spine. chest and all extremities.You are the only emergency physician in a well-equipped emergency department. CT of the pelvis produces a much higher exposure . Her pulse rate is 92 and her blood pressure is 110/75 mm Hg. It is an hour before handover in the morning. what would you tell her now? Trauma in pregnancy . Radiological exposures to the fetus can be divided into a 'low dose' group and a 'high dose' group. while a KUB is between 200 and 500 mrad. A urethrocystogram produces about 1500 mrad.Q#3 In general. Computerized tomography (CT) can produce more significant exposure levels. correctly performed.a restrained rear seat passenger -. They both require intubation. You are a little tired after a busy night. within minutes of each other. the fetus will be exposed to about 50-100 millirads (mrad) during the course of the 9-month pregnancy. OK this is an easy one given the title.. Two of the patients -an elderly couple -. while chest CT produces about 1000 mrad (significantly less if shielded).
even when in the emergency department if she wished -. The estimated mean initial radiation exposure of all patients was 4500 mrad. Another article1 quotes a risk of 1 adverse event/1000/1000 mrad of exposure (i. In this article. while malformations are greatest if radiation exposure occurs between 2 and 8 weeks gestational age. our patient has had some low risk examinations -. severe mental retardation and either temporary or permanent growth retardation.000 mrad. multiple types of congenital abnormalities.chest and cervical spine x-rays. exposures of less that 5000 mrad have negligible effects. as one might expect.000 mrad there appears to be a slight increase in the incidence of childhood cancers. equipment. At doses above 15. there may be an increased risk of carcinogenesis. I would counsel the patient about the slightly increased risk of fetal abnormality. Figures quoted indicate a 6% chance of mental retardation and about a 2-3% chance of developing childhood cancers. Mean gestational age was lower in this group.through shielding.e.level of between 3000 and 9000 mrad. at about 7 weeks. sterility and germ cell mutations. Thus.9%) of 3976 women admitted were pregnant. The take home message here should be that although we should take every precaution to reduce fetal exposure to radiation -. Thus.5 Between 5000 and 10. especially within the first two weeks. This is the period of maximum organogenesis in the developing fetus. there is one adverse event). minimizing numbers of x-rays or using alternative investigative techniques -. I would also caution her that the radiation dose is cumulative and she should be sure to mention that she has already had exposure should she require any further studies during the course of this pregnancy. fetal loss was significantly higher in the incidental pregnancy . depending upon exact technique.we should not deprive the mother of adequate investigation in the setting of trauma because of the theoretical risks from radiation. the pelvic CT. our patient probably did receive a dose that puts her fetus at a slightly increased risk for childhood cancer and at very low risk for fetal malformations. given this information. and some significant exposures from the pelvis and lumbar spine x-rays. Now. In the Japanese cohort.and arrange this for her if she lived in the catchment area of the hospital. In addition. and what are the risks? Trauma in pregnancy. especially. Abnormalities described include prenatal or neonatal death. 13(11%) were incidental pregnancies. A recent article addresses how often this scenario actually happens. the major congenital abnormality described has been microcephaly. Of these women. the abdominal CT and. Total dose could be between about 5000 and 13.. what is considered a 'dangerous' dose of radiation. The cumulative radiation exposure exceeded 5000 mrad in about 85% of patients.2 Bochicchio and colleagues studied trauma admissions over a four-year period and they found that 114(2. Additional information has been extrapolated from animal studies. there is a greater risk.000 mrad. In general. number of CT cuts and size of patient. for every 1000 infants exposed to 1000 mrad. The highest risk for fetal viability is in the earliest stages of pregnancy.Q#4 Information about radiation exposure of fetuses has been gathered from observational studies of radiation exposures from the use of nuclear weapons in Japan and from unintentional exposures to fetuses as a part of medical therapy. suggest she see an obstetrician as soon as possible -.
below the pregnant abdomen. She feels a little light headed. However. The patient is currently complaining of shortness of breath and has a cramping abdominal pain. Penetrating injury is less common than blunt injury. She has one intravenous line in place and has oxygen running via a facemask. Epidemiology of Trauma in Pregnancy Trauma is the leading cause of non-obstetric morbidity and mortality in the pregnant patient in the United States. when compared with belted pregnant females. The incidence of domestic violence in pregnancy is alarming and emergency physicians should be attuned to this as a possibility if they see a pregnant patient who has apparently been assaulted. Fetal mortality rates in penetrating trauma are as high as 70%. or wear it incorrectly. will often elicit the truth. accounting for up to 70% of blunt abdominal trauma. and to the side of the pregnant abdomen. up to one-half of all pregnant women do not wear their seat belt. she was wearing her seatbelt correctly. In America. she has been involved in a road crash where she was struck head-on by a truck that crossed the mid-line. After being given information about the risks of the pregnancy and discussing it with an obstetrician in the department. doctor?' What is your response? Trauma in pregnancy. She was lost to follow up. Instruction by health care workers in the wearing and the correct positioning of belts will result in a significant increase in the correct wearing of seat belts by patients (83% vs. She is lying flat on a stretcher immobilized in a neck collar. with the partner out of the room. between the breasts. gunshot wounds are the most frequently encountered cause of penetrating injury. fetal-maternal hemorrhage and fetal demise.Q#5 Your answer should be "YES. Because her primary care health worker had counseled her.5 times more likely to give birth within 2 days of the injury. there was significant damage to the patient's vehicle and she describes a momentary loss of consciousness. Her blood pressure is 100/60 mm Hg and the oxygen saturation is 99%.group when compared with the 'known' pregnancy group. The next leading cause is falls. ... A frequently asked question by pregnant patients is 'Should I wear my seat belt. our first patient elected to leave against medical advice to return to her home out of state.Q#6: Second Case The patient is a 27-year-old female who states that she is 28 weeks pregnant with her second child. the commonest cause of trauma in the United States is motor vehicle crashes. placental abruption. She is able to protect her airway. During pregnancy. It is estimated to occur in about 7% of pregnancies. Direct questioning. 65% for those not instructed Trauma in pregnancy. While driving to work. Her respiratory rate is 24 and shallow." Unfortunately. Very few women will admit to physical abuse and thus the physician must maintain a high index of suspicion for this problem. followed by direct assault. Domestic violence is thought to account for as much as 30% of all trauma seen in pregnancy. Complications peculiar to the pregnant patient as a result of trauma include preterm labor. with the shoulder belt placed over the mid point of the clavicle. Unbelted pregnant women are 4 times more likely to have a fetal demise and about 2... Correct placement of the belt is to wear the lap portion of the belt across the pelvis.
. The patient is now complaining of a cramping feeling in her abdomen.Q#10 The presence of a cramping sensation should raise the possibility of the development of a placental abruption.. What complication is a possibility now? Trauma in pregnancy... even if they appear hemodynamically stable.. The result of this movement is that the blood pressure is now 118/68 mm Hg.Q#7 The one immediate step that should be taken is that a wedge of some kind -. a number of physiological changes occur. An angle of about 15° is usually recommended. the use of lactated Ringer's solution is preferred.Q#9 In the pregnant patient.Q#11 Patients need to have at least four hours of external fetal monitoring if they are beyond 20 weeks gestation.. the presence of a normal blood pressure does not preclude the possibility of a significant bleed. then rises again in the third trimester almost back to pre-pregnancy levels. It is the reason why careful observation is required for pregnant women after trauma. Is this blood pressure 'normal'? And if it is normal. What monitoring modality is useful? Trauma in pregnancy.. The blood pressure recorded on our patient could be considered 'normal'. rises slightly in the second. with a baseline of 85 by the third trimester.. Among them. Saline appears more likely to cause a significant acidosis and should be avoided. what ONE measure could immediately help her and why? Trauma in pregnancy. Pregnant women suffering significant trauma should have two large bore IV lines established as a routine.should be placed under the right hip. moving the uterus over to the left side slightly. It results from the relatively inelastic placenta separating from the elastic uterine wall when the latter is distorted because of trauma.a rolled towel or other object -.. This is because the fluid is more physiologic and less acidotic that normal saline. The presence of 8 or more contractions in an hour is highly suggestive of the diagnosis of abruption. Compression of the vena cava can result in a significant reduction in venous return. ultrasound is not always reliable at spotting this problem.Q#8 During pregnancy. to levels about 50% or more above pre-pregnancy levels. The pulse rate gradually rises through pregnancy. The absence of any uterine activity over the four-hour period immediately following the trauma virtually excludes the possibility of an abruption. consideration should be given to warming the fluids.Given that her airway is protected and her breathing probably adequate currently. What fluid should be run through these lines. The result of this is that clinical signs of significant hypovolemia may be delayed because of the increased reserve. However. As is usual in the management of trauma victims. enough to appear that the patient is hypovolemic. does this indicate we don't have to worry about occult blood loss here? Trauma in pregnancy. and why? Trauma in pregnancy.. the blood pressure initially falls in the first trimester. Management then should be by an experienced obstetrician and will depend . This is a feared complication of trauma in pregnancy. This removes the uterus from the inferior vena cava and facilitates venous return. Unfortunately. It can occur after relatively minor trauma. Blood volume gradually increases through pregnancy.
The patient has no vaginal bleeding. The usual dose is 300 micrograms intramuscularly. In these cases.. using the fingers as a guide so as to keep the points away from the fetus. extended up to the top of the uterus. then abruption or another uterine abnormality is likely. Let us assume that examination of the abdomen in our patient now revealed a boggyfeeling uterus and you are sure you can easily palpate a foot through the abdominal wall. the abruption may be small enough to allow continuation of the pregnancy. In the remainder. Immediate delivery is paramount to save either life. The baby is delivered through the incision and the cord clamped. it is cut through.Q#12 The normal fetal heart rate is between 120 and 160 beats per minute.upon fetal gestational age. however. The uterus is opened in the lower section with a small vertical incision from a scalpel. A scissors is then inserted into the incision and..Q#14 The presence of a boggy uterus and easily palpable fetal parts are signs of a uterine rupture. hypoventilation or hypothermia does not improve the heart rate. it is devastating in that there is profuse bleeding and rapid deterioration of mother and fetus. We are also told that the patient is Rh negative. The technique of emergency department caesarian section is a little beyond this presentation. Patients who have an abruption have fetal distress obvious in at least 60% of cases on arrival in the emergency department. You are very suspicious that your patient has an abruption. with no pulse or blood pressure.. but the mother must be observed very closely. The patient has abruption. and the fetus is over 32 weeks.Q#13 Abruption is a risk factor for the development of disseminated intravascular coagulation. thus.. The technique involves a midline incision from the pubis to the umbilicus. not always available in the emergency department and is.. This incision is extended down through all layers to the uterus. and she must be given Rh immune globulin. If correction of maternal hypoperfusion. What devastating complication has now arisen? Trauma in pregnancy. many authorities would proceed to delivery. This test is. As little as 0. If there is a significant abruption. What is the normal fetal heart rate? What is the fetal response to stress? Trauma in pregnancy. so does this matter? Trauma in pregnancy. From what complication of the abruption is the mother at risk? You also find out that the mother is Rh negative. If the placenta is encountered on the anterior wall. Some authorities use the Kleihauer-Betke test to estimate the degree of fetal blood loss into the maternal circulation. for four minutes. Although this complication is very rare. Between 3 and 7 contractions in an hour require further observation and many would recommend 24 hours of continuous monitoring.5 ml of fetal blood is required to sensitize 70% of Rh negative women. and there is up to a 30% rate of fetal maternal hemorrhage. The normal fetal response to stress is bradycardia and the commonest cause of this is hypoxia. The management of pregnant trauma victims can be challenging and stressful for the . Assessment of the fetal heart tones are also vital and should be performed regularly while in the emergency department.. rarely useful in the emergency management of patients. secondary to the passage of placental products into the maternal circulation. immediate intervention is required. but it is indicated if there are signs of fetal life and resuscitative efforts on the mother have been unsuccessful.
The immediate resuscitation should follow well-established advanced trauma life support (ATLS) guidelines. Arteriogram after that.stop ocs Neurlogical localization Case 5 68 yo white female presents with inability to walk. What has happened to this patient and what is the appropriate management? DDx: TIA Labs: duplex (ateriogram if duplex not dx'ic) then tx w/aspirin and antiplatelets Neurological localization Case 3 A 60 year old man has a 15 minute episode in which he cannot express himself. Sometimes. he has difficulty swallowing. and is taking OCP. and her mouth was twisted. Her legs are diffusely weak. and he noticed he can do so if he moves it with his finger. and is not associated with back pain. together with obstetric.staff. pediatric and trauma surgical colleagues will result in the best outcome for our patient. Upon further questioning. . he complains having trouble eating and swallowing on one side of his mouth. His toes are equivocal. is short of breath. Neurological localization Case 4 26 yo female graduate student was conducting a philosphy seminar when she suddenly started stuttering and became incoherent. He becomes increasingly frustrated with this and suddenly stops talking. On exam. and the tone has changed.start heparin . Reflexes are brisk. Has has no sensory loss. She had a past hisotry of untreated rhematic heart disease. and good strength of the UE's. No CN deficits. but then progressing to both legs. including a jaw jerk. CT will most likely be normal. and all four proximal extremities. Language is intact. What is the most likely localization. One day later he comes to the emergency room for evaluation and at this time he is entirely neurologically normal and his speech is normal. Neurological localization Case 1 a 35yo black male is seen in clinic with a 3 month history of weakness and muscle cramps. and sometimes inappropriate. This persists for 15 minutes and then rapidly resolves. she is slightly inattentive. He remains unable to express himself and unwilling to talk for a period of 18 hours. An organized approach. arterial supply and next step in management? stroke localisation-frontal lobe hemisphere-dominant usually left arterial supply-middle cerebral artery management-give thrombolytic if not contraindicated. One arm hung limply. One year later. and she walked unsteadily. Fasciculations are present in the tongue at rest. 3 to 4 over 5. He has a completely normal neurological and ophthalmological examination. you find that this has progressed over a month or two. using the skills of the emergency department personnel. first felt in the left arm. and appears emaciated. hemisphere. Can you localize the lesion? Ans: ALS Neurlogical localization Case 2 A 55 year old normotensive man has an episode of sudden loss of vision in his right eye. His voice is not as loud as it used to be. She seemed confused. What distribution is it and what subsequent evaluation should be carried out? Broca's TIA.
General examination was unremarkable. triceps.proximally and distally. He gave a history of nocturia. and she has bilateral Babinski. There was a family history of diabetes His medications included hydrochlorthiazide and glyburide. and had recently been diagnosed with diabetes. with 4/5 strength in the deltoid. typically developing after the patient walked 300 to 400 yards. and coordination in lower limbs are normal. On neurological examination he was awake. He was oriented to person and place but was unsure of the month and day. peripheral arterial pulses both at rest and after exercise are normal. On cranial nerve examination the fundi were benign and there was a right sided facial palsy sparing the forehead. Symptoms were releived after a few minutes rest or when the patient sat down and stopped forward. Ans: The reason i posted this Q is that it didn't make sense to me. Art. non insulin dependent diabetic awoke with weakness of the left side of the body and was admitted to the hospital. hip flexors. and ipsilateral hemiplegia (before pyramidal decussation). He has had no sphincter disturbance and had low back pain for many years. the patient has experienced numbness in his thighs. they are absent). He was able to follow three step appendicular commands. Territory: Ant Cerb. He gave a history of a transient episode of mild weakness of the right side of the body occurring a week before that had resolved after 3-4 hours for which he did not seek medical attention. It has features of CONUS MEDULLARY SYNDROME: it is BILATERAL (Cauda Equina is unilat). Speech was fluent with good comprehension. you would find a sensory level. pulse 110. PE: loss of lumbar lordosis and reduced flexion and extension of lumbar spine. The right plantar reflex was extensor and the left was flexor. Reflexes are brisk in the legs. slightly brisker on the right side. power. UNILATERAL . If it were medullary. The symptoms started a few months ago. the blood pressure was 170/90. Neurlogical localization Case 7 70 yo male presenting with dull aching pain in bothcalves after moderate exercise. Problem chronic = Brain Tumor. Ipsilateral facial paralysis (fibers don't cross midline). temperature 36. Sensory examination was normal. Plantar reflexes are flexor. knee flexors and foot dorsiflexors. Neurlogical localization Case 6 A 40 year old male hypertensive. anxious. repetition and naming. Refelxes in LE symmetrical but reduced compared to upper limbs. Where is the lesion most likely? Ans: Lesion is at the pons at the level of VII. thirst and weight loss for the prior one year. Cerebellar testing was impaired by weakness on the right side but otherwise normal. In addition to the pain. On examination. DTRs were brisk throughout. DTR's are reduced but PRESENT (In Cauda Equina. Cauda Equina Syndrome has the Saddle Sensory Deficit but LATE SPHINCTER CHANGES. 2 hours after awakening.5 C. tone. On motor examination weakness was detected in the right upper and lower extremities. and poorly attentive. but then it SHOULD HAVE EARLY SPHINCTER PROBLEMS AND URINARY INCONTINENCE AS WELL AS IMPOTENCE. Where is the lesion? Alteration of mental status = cortical. as well as problem with GiI and continence. with no demarcated level. wrist and finger extensors. Sensory exam reveals questionable mild loss of light touch and pain sensation distally to LA's.
He throws it in all directions and claims he can't stop. thanks Among the problems associated with the 3 major nerves in the upper extremity. eyes deviated toward the left. Please give me 3 or 4.SYMPTOMS. but remainder of exam is normal. The patient upon further questioning reveals he like to taste things and is gaining weight because he is eating too much.there is hyperphagia. The patient feels fine. Neurlogical localization Case 9 15 yo male brought to you by his parents for a follow-up evaluation of herpes simplex encephalitis that he had a few months ago. He is a chronic smoker. In fact they all relate to the radial nerve: . but reassures you he's using condoms. AND ABSENT DTR's. He has been diagnoses with diabetes and HTN but has taken his medications intermittently.docility. On PE: patient is a known hypertensive and takes his meds irregularly. PE. Neurlogical localization Case 10 50yo male patient presents to the ER with uncontrollable wide movements with his left arm. I didn't find many of them. normal.. but the parents report a recent change in behavior from markedly agressive to extremely placid. right sided hemiplegia with fundoscopic examination revealing papilledema in addition to hypertensive retinopathy. Despite that he doesn't seem to have a problem getting dates since he noticed an increase in his sexual activities. Neurological localization Case 8 A 65 yo white male develops sudden severe headache and rightsided hemiplegia. right sided babinski.. There is no prior history of psychiatric illness. He now has both fecal and urinary incontinence. radial nerve entrapment is the least common.Radial Nerve Palsy: Most common cause is Fx of the humerus (holstein lewis fracture). Where is the lesion most likely? Ans: Hypertension. but I wanted to make the distinction in the explanation for more info. Carpal tunnel syndrome (median nerve compression at the wrist) and cubital tunnel syndrome (ulnar nerve compression at the elbow) are much more frequent. no meningeal signs present. Other cause is compression (in its course inside the triceps muscle or teres latissmus muscle). Diagnosis? Where is the lesion? Ans: hemiballismus-vascular lesion of the subthalmic nucleus-contraletral ballistic movemenets of one or both extremeties Question what are the differential diagnosis would you consider even if you suspect the patient has saturday night syndrome. In regards to Radial Nerve Syndromes. and that's the correct answer.hypersexuality and sometimes visual agnosia. no fever.most commonly affects Putamen because of rupture of penetrating arteries = This is putamenal infarct. Because of affected DTR's I would choose Cauda Equina Syndrome. BP210/180. Nerve injury secondary to compression or traction depends on intensity and duration . PE assesses the wild flailing movements of the left arm. Labs: elevated blood glucose of 190. Your diagnosis and localization of the lesion? Ans: kluver bucy syndrome involving anterior temporal lobe-amygdaloid nucleus.
and trauma." and she suffered from "ringing" in her left ear. reduced sensation on the left side of the face.Posterior Interosseous Nerve Syndrome: Compression is thought to occur after takeoff of the branches to the radial wrist extensors. . 4. Reference: emedicine http://www.horizontal nystagmus: left vestibular (VIII) nerve 3. This kind of tumor generally arises from the Schwann cells on the vestibular division of the VIIIth nerve and enlarges (often very slowly. . drooping of the left corner of the mouth.greatly reduced hearing acuity in the left ear: left cochlear (VIII) nerve 2.emedicine. weakness in biting down on the left side. since the trigeminal afferent axons of that reflex arc (unlike the other cranial nerves in the region) are particularly sensitive to the mechanical stresses imposed by the tumor. weaving gait. external compression. sometimes preceded by a period of tinnitus.htm Neurlogical localization Case 11 A 55 year-old restaurant manager complained to her physician that she had become increasingly unsteady on her feet to the point that now she "couldn't walk straight" and several times over the past few months had been embarrassed in public by people who assumed that she was intoxicated. Ans: This is a large acoustic neuroma in the cerebello-pontine angle on the left side of the brainstem which has begun to compress the cerebellum and brainstem. The symptoms above resulted from the following: 1.Radial tunnel syndrome: result of overuse. Other tumors of the cerebellopontine angle follow a different clinical sequence.reduced sensation on the left side of the face: sensory root of the left trigeminal (V) nerve. is essentially entrapment of the superficial sensory branch of the radial nerve. Other common causes include postsurgical injury. a broad-based. a dry. loss of the corneal reflex in the left eye. 6." In addition. tumors.20 years!) to put increasing pressure on the facial and trigeminal nerves. then on cerebellar peduncles.drooping of the left corner of the mouth: left facial (VII) nerve..weakness in biting down on the left side: motor root of the left trigeminal (V) nerve. In patients with de Quervain tendovaginitis. .Wartenberg syndrome.com/orthoped/topic549. but normal right eye. One of the most reliable symptoms is impairment of the corneal reflex. 5. over the past five years her hearing had become "difficult.. perhaps over 10 . The first symptoms detected are usually auditory and involve a progressive loss of hearing. and iatrogenic injuries. synovitis (rheumatoid). red left eye. horizontal nystagmus. cerebellum and underlying brainstem nuclei. Other possible etiologies for posterior interosseous nerve dysfunction include trauma (Monteggia fractures). She also said that she felt self-conscious that her face was "crooked. An examination revealed the following: greatly reduced hearing acuity in the left ear. secondary irritation of the Radial sensory nerve is frequent.loss of the corneal reflex in the left eye: left sensory V and left motor VII.
since pain is low level and can still be taken care of by analgesics. weaving gait: cerebellar peduncles and cerebellum and/or vestibular (VIII) nerve. but there is data suggesting they may still spontaneously descend until first year. helped with indigestion and nausea. pt had an ulstrasound that confirmed she has at least one very large stone (too large to pass. (Could be either side.Orchipexy after that is still indicated IF NOT TO RESTORE FERTLITY. After first year of life.By second year.a dry. Orchipexy does NOT decrease risk for Testicular cancer. After almost 2 years of recurrent gallbladder episodes (whereby severe pain was experienced but no visible sign of gallstones was detected in ultrasounds).) 2 cases of gallbladders disease and pregnancy Case 1 35 weeks pregnant with third child. will they still operate??? Ans: Case 1: Lap Chole is performed ideally in second trimester.a broad-based. red left eye.would it be a reasonable consideration to a) have it removed before the baby is due (and what sort of risks are involved?) b) request a cesarean section so that the gallbladder might be removed at the same time as the delivery? Case 2 16 weeks pregnant. will have virtually not a significantly elevated risk for testicular cancer. 8. they have a 32 fold increase of . The diet has. .Men who had their orchipexy done before 11 yo. and has had an abdominal ultrasound which shows no stones or sludge. REFER to UROLOGIST. irreversible changes might have already occured especially if intraabdominal.and therefore continue to present pain and possibly more problems -. but since other symptoms are on the left. Case 2: No surgical indications in this patient. . Most would descend by then. they hardly ever will on their own.Trial of hCG is indicated for some cases of BILATERAL undescended testes. For those who didn't. Pt has been on a low fat diet for about a week. Third trimerster cholecysitis with intractable pain may require OPEN CHOLE since gravid uterus may interfere with procedure. Compiled data about age of repair for cryptorchidism Medical Articles review showed the following: . C-Section may not be done since it is not an indication. 1) what are the indications for cholecystectomy in this patient if at all? 2) what if things get very bad in 3rd trimester. Not indicated for unilateral. If it continues to third trimester like Case 1. the left side should be the strongest suspect. and still experiencing low level pain in GB area as well as solar plexus and under right shoulder blade. I have found articles saying after 6 months of age. Success rate <10%.If by 6 months they haven't descended. but normal right eye: left facial (VII) nerve. according to the tech). Indications are intractable pain refractory to pain medication and diet. Most commonly orchiopexy would be done at the end of first year of life.Any infant with undescended testes should be monitored for 6 months. . AT LEAST TO MAKE TESTICLES READILY AVAILABLE FOR EXAMINATION. . OPEN CHOLE is to consider.7. Knowing that this stone will likely not go away -. . however.
Patients who have had orchipexy before may not have a clue what was done to them as children. If compliance and close follow-up cannot be ensured. If no clinical evidence of neurologic involvement. Obtain dark-field examination or direct fluorescent antibody (DFA) staining of exudate from suspicious lesions of primary syphilis. confirm allergy. Avoid trap of pneumonitis or cholangitis until seeing outcome of specific antitreponemal therapy.Cryptorchidism DOES NOT CAUSE TESTICULAR CANCER. IT MERELY INDICATES A TESTICULE IS AT RISK. And if they do know. Clinical evidence of neurologic involvement warrants CSF examination.A patient with suspicious lesions but negative serologic results. If patient is not pregnant and refuses desensitization. the same treatment regimen as for patients without HIV infection is recommended: 2. . 2 to 4 million units every 4 hours for 14 days). or selected secondary lesions. eg.VDRL and RPR titers are higher than in HIV neg population. such as condylomata. . because their mothers rarely tell them.Case Scenario: HIV patient with secondary syphilis was treated. . then desensitize.In penicillin-sensitive patients. . syphilis is a hot topic. ALWAYS INQUIRE SPECIFICALLY. Odd HIV case With the rise of syphilis as an STD in HIV populations.Serologic tests for syphilis are the cornerstone in diagnosing untreated syphilis infection--even in HIV-infected patients. they rarely bother to tell. . aqueous crystalline penicillin G is the treatment of choice (12 to 24 million units intravenously per day. . . carefully examine HIV-infected patients with syphilis for clinical evidence of neurologic involvement (eg. => JarischHerxheimer reaction. . on the efficacy of tetracyclines in treating syphilis in HIV-infected patients. In this patient.that risk compared to general population. . Facts: . .Before treating. or they rarely ask. however.CNS disease can occur during any stage of syphilis. cranial nerve palsies).ANY BOY WITH BILATERAL NON-PALPABLE TESTES SHOULD BE CONSIDERED FOR A DIFFERENTIAL OF CONGENITAL ADRENAL HYPERPLASIA UNTIL PROVEN OTHERWISE. it included a flare of hepatitis symptoms. resembling cholangitis. The diagnosis of syphilis may be more complicated in HIV-infected patients because of falsenegative and false-positive serologic results for T. then desensitization to penicillin and management in consultation with an infectious disease expert. optic and auditory symptoms. No data are available. . Desensitize penicillin-sensitive patients to penicillin. positive findings on dark-field examination or DFA stain can be diagnostic.For HIV-infected patients diagnosed with neurosyphilis (including ocular or auditory syphilis).A negative RPR or VDRL test result may not rule out syphilis in patients with HIV infection.4 million units of benzathine penicillin G administered intramuscularly at a single session. consider doxycycline (100 mg orally 2 times a day for 2 weeks). . then developed symptomatic hepatitis and subclinical reticulonodular pulmonary infiltrates. pallidum and atypical clinical presentations in the presence of HIV infection.
4 million units intramuscularly daily plus probenecid 500 mg by mouth 4 times daily for 14 days). . 12.ucsf.Motor symptoms are different between upper and lower extremities in Central.http://hivinsite. IV. Next: MRI: shows narrowing of the white column of CSF and impingement of the darker appearing spinal cord. paralysis below the injury with variable impairment of pain and temperature sensation is present. secondary. close follow-up: reexamine at 1 to 2 weeks and reteste with a quantitative nontreponemal test at 3. 18. Risk Factor: Cervical Spondylosis in older patients Mechanism: Hyperextension Trauma (minor bleeds in the tissue) Symptoms: Sensory deficit with level. Action: Since diagnosis is pretty much narrowed down. Spasticity. Methylprednisolone is thought to impact the biochemical cascade of injury that progresses after the initial injury for some hours. Pain of neuro etiology.Because of the possibility of recent clinical relapse following syphilis therapy in HIVinfected patients.Cavernous Sinus Cellulitis: Cavernous sinus contains internal carotid. and VI. More somber prognosis is after that. Prognosis: 97% completely recover if less than 50yo. hyperflexion. and early latent syphilis and at 6. Maintain a level of mild hypertension for spinal perfusion.Mechanism of injury is different .edu/InSite?page=kb-05-01-04#S7X What is the anterior and central cord syndrome? Central cord syndrome is the most common of incomplete Spinal Cord injury. 6. .. various degrees of motor involvement with paresis more pronounced in UE than LE. Difference with Central Cord Syndrome: . III. and 24 months after treatment for late latent syphilis or syphilis of unknown duration. and 12 months after treatment for primary. sympathetic fibers. or vascular injuries may play a role. Disc protrusion.. Patients generally have sinusitis or a midface infection (most commonly a furuncle) for 5-10 days 2. 1.Position and vibration modalities (posterior columns) are preserved. The anterior cord syndrome anatomically involves the anterior portion of the cord. Gabapentin for neuro pain. fever. Start Steroids: Solumedrol 30 mg/kg over 15 minutes then followed after 45 minutes by an infusion at 5. 9. PT/OT/Speech. Clinically. and malaise typically precede the development of ocular findings. V1 and V2. Hands are especially involved. May be tube feeding in acute phase because of adynamic ileus.4 mg / kg / hr is the typical regimen employed. Reference: . . Management: Admit to Neuro ICU.If intravenous administration is impossible. Orbital cellulitis and Cavernous Sinus Thrombosis How to differentiate between Cavernous sinus thrombosis and orbital cellulitis? . Other: Neurogenic bladder (retention). then aqueous procaine penicillin G is another option (2. DTR's below level are absent at first but return with level of spasticity once over Spinal shock. Bladder involvement common. Headache..
Without effective therapy.Preseptal: D/C only if adult with PO ATBx and close follow-up . This is pathognomonic for CST.Orbital abscess = collections of pus within the orbital soft tissue. 1. therefore.Preseptal (periorbital) cellulitis = inflammatory edema of the eyelids and periorbital skin with no involvement of the orbit. dentition. but the physical signs or papilledema on funduscopic examination. Sinusitis (60% patients. Increased INTRAOCULAR PRESSURE: sluggish pupillary response and decreased visual acuity 6. are suggestive. Lids cannot be opened because of edema. Classification: Group I . Death follows shortly thereafter.Cavernous sinus thrombosis + Bilateral symptoms: + Ophthalmoplegia. but it can be suspected based on physical examination + Orbital signs (see above) + Limitations of ocular motility = pain in globe movement toward the abcess. Increased RETROBULBAR PRESSURE: Exophthalmus and Ophthalmoplegia 5. complication of periorbital infection 2. This diagnosis is confirmed by CT scan. proptosis + Corneal hypesthesia with increased intraocular pressure Treatment: . CRANIAL NERVE PALSIES 7. Mainstay of therapy: Braod Spectrum Antibiotics (Staph Aureus Most common) Heparin therapy . extension from adjacent structures.3. dacryocysitis. The patient rapidly develops mental status changes from CNS involvement and/or sepsis. Group IV . + Fever and leukocytosis + Orbital signs Group III . + Lids cannot be opened because of paralysis secondary to III involvement. 8. . palsy of the pupillary and extraocular muscles) + CN V1 (forehead) anesthesia Group V . + Directional proptosis = Globe is looking away from the abcess. ethmoid most commonly).Orbital Cellulitis: Orbital infections develop via direct inoculation.Steroids (especially if progressed to pituitary insufficency to prevent adrenal crisis). and hematogenous spread. Group II . signs appear in the contralateral eye by spreading through the communicating veins to the contralateral cavernous sinus. . Diagnosis is confirmed by CT scan. orbital pain and fullness accompanied by periorbital edema and visual disturbances.Admit all children because children are deficient in IgG2 and are predisposed to bacteremia.Subperiosteal abscess = collections of purulent material between the orbital bony wall and periosteum. 4. + Severe unilateral ptosis + Severe ophthalmoplegia (ie.Orbital cellulitis = CT scan is not sensitive for diagnosing this entity. clinical examination guides therapy.
or chloramphenicol. elicited by palpation. cefotetan) can be used alone. Trauma "ABCDE" has been done. NSAID's contraindicated.ECG is next to r/o myocardial contusion: dysrhythmias. Your immediate DDx is a sternal fracture. If you know. The decision is finally made . Question Px comes in from a MVA.Surgical intervention if necessary (i. or ST segment changes. the decision is made based on what is thought WOULD BE that person’s choice. use meperidne or other Category B opiates. and r/o pneumothorax/Aortic disruption. There is no excuse for not doing so.. conduction disturbances. Palpation of the chest exquisitely tender over the sternum at a point where there is a gritty feeling of bone grating on bone. He is breathing well but obviously has mult bruises over the chest with the impression of a mercedes steering wheel (or yugo.: compromised vision) Oxacillin or nafcillin can be used with the addition of ampicillin and sulbactam in children to cover H influenzae. the patient knows. cefoxitin. clindamycin. No admission necessary if no associated conditions.CXR as procedure of choice to substantiate Sternal fracture. To pay attention to: If pregnant: shield abdomen and pelvis with lead apron before CXR.e. cefuroxime. Alternatively. what test is used for document osmotic diarreahea secondary to lactase deficinecy? 1.Orbital: Admit with IV ATBx +/. Patients who are allergic to penicillin can use vancomycin.Lactose elimination diet 2.Lactose Hydrogen breath test: 90% sensitive review of ethics by Valium RULES OF ETHICS HOW TO DEAL WITH A DYING PATIENT: 1) Tell the patient EVERYTHING. . NBS? Problems to be considered: Aortic Dissection Cardiac contusion or tamponade Flail chest Pulmonary contusion Thoracic spine injury To do: . To give: Adequate analgesia is treatment of choice as taping or splinting is contraindicated (risk of atelectasis and pulm insufficiency). 2) DO NOT GIVE FALSE HOPE 3) Allow the person to talk about his feelings 4) Kept he patient involved in social activities 5) Avoid social isolation GENERAL RULES: 1) “Substituted judgment”: when a patient cannot make a decision. a cephalosporin (eg. you add in your favorite car).
by who is most likely to represent the patient’s own wishes (not necessarily who is closest next of kin). -Drunk. Yet. DIAGNOSIS SAYS NOTHING ABOUT THE LEGAL COMPETENCE OF A PERSON!!! Competency can ONLY be decided by a COURT OF LAW: it is not a medical dg. It is not your personal preference is. When you are not clear about the patient’s wishes. 3) Patients decide over their own bodies: The patient ALWAYS MAKES THE DECISION. it is not a blood alcohol level! Clear behavioral evidence of incompetence: Attempted suicide Patient is grossly and evidently psychotic and dysfunctional Patient’s physical or mental state prevents communication However. You must set aside your personal preferences: like strong religious beliefs (that is considered irrelevant) As a general rule. the best interest standard rule was applied. you should make the decision as a dispassionate. without going to court. for example) 2) What would the patient want? : Substituted judgment 3) Best interest standard: what would most people want Rule #5: If patient is incompetent. they should use the following criteria and in this order: 1) Patient expressing wishes in the past: what historically did the patient say in the past? (wish for organ donation expressed to relative. Rule #2: Assume that the patient is competent unless clear behavioral evidence indicates otherwise. “What would a jury of 12 people do if they knew what I know?” Who makes the decision is not really important: anybody using the best interest standard should arrive to the same decision. and the only thing a doctor can do is lay out the possibilities. Alzheimer’s: these are all medical dg. physician may rely on advance directives Directives that a patient can leave for his doctor before becoming incompetent: . DO WHAT MOST PEOPLE WOULD WANT in this circumstance. This was decided over the ROE vs WADE case in 1973. the USMLE will want YOU to make the decision: try to avoid the answer that says “go to court”. In this case. when in doubt. assume competency! Rule #3: Decision-making should occur in clinical setting if possible. parents cannot withhold treatment from their children. no matter what. but it illustrates the principle that governs medicine in the US: the patient always decides. The issue will never be over abortion in the USMLE. rational observer: do what a rational person would do. SPECIFIC RULES: Rule #1: Competent patients have the right to refuse medical treatment. 2) “Best interest standard”: trying to determine what a never-competent patient would have wanted is practically impossible. Rule #4: When surrogates make decisions for a patient. And that is only if the case is not an emergency: if it can wait going to court. the case that made abortion legal. Normally. schizophrenia. they did. unless it is clearly stated that the guardian (ex: parent of a sick child) is NOT acting in the patient’s best interest. in Infant Doe’s case.
by the patient. In the case of anorexia nervosa: if the patient is a minor: not legally competent.Health powered attorney: person that was named by the patient to represent him. but on the exam this is accepted. THEY ARE ILLEGAL. ever threat to abandon your patient (not even if you are doing it to make sure they follow treatment). Rule #6: Feeding tube is a medical treatment and can be withdrawn at the patient's request. Do not ACTIVELY do anything (as opposed to number 6) Rule #8: the physician decides when the patient is dead. Rule #9: Never abandon a patient: even if they can’t pay you. even if you don’t like the patient. A competent patient has the right to refuse hydration and nutrition. Exceptions to informed consent: 1) Emergency situation 2) Waiver by the patient: the patient says it’s OK not to know what is going to happen (exploratory surgery. Period. The patient can revoke written consent orally. Rule #7: Do nothing to actively assist the patient to die sooner.Can be oral directive from patient to his doctor: does NOT necessarily have to be a written document. Futile treatment: means a treatment that is not AND WILL NOT improve anything. TREAT THIS PERSON AS THE PATIENT HIMSELF. at any moment Of the patient signs “consent” without reading it: it is NOT INFORMED CONSENT Informed consent: means that the patient understands: 1) Nature of the procedure 2) Purpose or rationale 3) Benefits of treatment or procedure 4) Risks 5) Availability of other alternatives “GAG CLAUSES”: you work for an institution that tells you not to discuss certain procedures or possibilities. Still. Refusing food and water: may seem close to euthanasia. If you simply CANNOT continue to be the doctor to this patient: you need to arrange that he will have care and make sure that they are getting it. In case of clear cortical death: even if the family is hoping for a special doctor to arrive. If NOT a minor: go to court. drug undergoing trial to know side effects) DO NOT ASSUME YOU HAVE A WAIVER UNLESS THE USMLE TELLS YOU. notarized. . 3) Patient is incompetent 4) Therapeutic privilege: doctors have the right and obligation to deprive the patient of . Never. if the patient or the family want the treatment to continue: it is not YOUR decision.Can be living will: expression in writing. it is the patient’s or the patient’s family.. IN TERMS OF DECISIONS: this person is the VOICE of the patient: a health powered attorney BEATS ALL OTHER CHOICES ON THE USMLE (it is the patient talking to you). . Rule #10: Always obtain informed consent: before you do ANYTHING!!! Informed consent can be oral. for a special treatment to come: CALL THE DEATH.
issues governed by laws that vary widely across states cannot be tested Rule #14: Good Samaritan Laws limit liability when physicians help at accidents Rule #15: Confidentiality is absolute Rule #16: Patients should be given the chance to state DNR (Do Not Resuscitate) orders. and will ALWAYS be the . BUT AS MOTHER THERESA WOULD.they can command a jury trial to determine sanity They lose only the civil liberty to come and go they retain their competence for everything UNLESS A COURT OF LAW DECIDES they are incompetent.or limb-saving treatment from their children Rule #13: For the purposes of the USMLE. Rule #19: Remove from patient contact health care professionals who pose risk to patients Rule #20: Focus on what is the best ethical conduct.talk to the collegue and REMOVE him from patient care . sued or that your hospital may go to shreds if you do the "right thing". rule # 17: Commited mentally ill adults legally are entitled to the following: .if there are no more treatment options (if the patient is cortically dead). Ex: patient on PCP. USMLE wants you to pick the answer where there are no doubts that it is the most ethical thing to do. The underlying rule here is that no matter what the psychiatric diagnosis is. treat the patient as you would any other competent person (unless they show signs of clear incompetence.if there is a direct employer or supervisor (like your residency program director) : TELL THE SUPERVISOR. There is also something interesting that they pointed out: what do you do if you find out a collegue or fellow resident is having a substance abuse problem? Who do you talk to? RULES: . but the patient (or surrogate) insists on continued treatment: then treatment must continue. (The USMLE wants you to be able to make decisions when the patient is DEAD) .their autonomy in the interest of the patient and other people. ACT NOT AS A LAWYER WOULD.if the physician thinks tratment is futile and the patient won't improve. don't worry about being fired. and physicians should follow them Rule #17: Committed mentally ill patients retain their rights Rule #18: Detain patients to protect them or others. In other words.they must have treatment available . not simply the letter of the law I looked it up: rule # 8 says this: . stated on #2) rule #20: Focus on what is most ethical. and the family insists in treatment?: if there are no options and there is nothing the physician can do. Failure to do so will endanger patients.they can refuse treatment . it is his duty to stop the treatment. violent and dangerous: put him on restraints! Rule #11: Special rules apply with children Rule #12: Parents cannot withhold life.
when cases like Previous COPD patient with COPD who comes with acute exabe. BP 60/40 and RR 40 6) 58yo African American man is treated with diuretics for HTN 7) a 34 yo IDDM patient is seen on his annual exam.34 -.34 -. and they won't authorize Home O2 for a patient with ONLY O2 Sat.38.50 -.5 1) 68 yo woman despondent about her disfiguring rheumatoid arthritis attempts suicide by ingesting a number of pills for a medication she has at home 2) 21 yo college senior is seen the morning of her finals complaining of palpitations. pCO2 = 43. we don't always look for ph. Ex: pH = 7.44 -.4.115 -.98 -.7.24 -.worong answer on the USMLE.98 -. pO2 = 68mmhg.2 E).K+ A)-7.--Cl.15 -.95 -.144 -.22 -.148 -.10 -.12 -. bicarb and pCO2 only. So don. HCO3 = 28 On exacerbation: pCO2 will go up pCO2 = 53 pO2 will go down pO2 = 55 O2 Sat= 84% HCO3. It's true.56 --20 --114 --138 -.70 -.5. but how about decreasing pO2? Think about it. anxiety.6 B)-7.0 F) -7.pCO2-. anion gap is important.136 -.25 -.3.12 -.14 -.108 --4.Will go up to compensate but not too much.29 --30 -.106 -. I posted some ABG's for your exercise.26 -.104-.110 -. Similarly.140 -. you look at other parameters depending on the clinical scenario. Let me know if you need more explanation ABG exercises #1 ---pH -.138 -. After all.24 -.52 -. If diarreha or vomiting.7.t waste time talking to the person or the family or anyone: go to the supervisor.112 -. What they meant was: the best way to get someone to treatment is if their employer forces them to: if they are afraid to lose their job.9 D). Home O2 indications guidlines for Medicare are based on O2Sat or pO2 and those of Medicaid REQUIRE ABG's where pO2 would be documented. His family reports that he has been this way for 2 days. If intoxication. U/A = 3+ proteinuria and serum creatinine 2.56 -. because the exacerbation is acute so it'll be probably 30.22 -. Exacerbation of COPD on ABG’s How can U interprete Acute exabe of COPD with Blood gas analysis esp.140 -. when talking about other Acid-Base disorders. and tingling in hre hands 3) an 18 yo man is left in the ER entrance and is found comatose 4) a 17yo high school student leaves summer camp and refuses to take his insulin for the first week of camp 5) a 29yo man with AIDS is brought to the ER lethargic and extremely tachypneic.8 C)-7.Na --HCO3. And so on and so forth. are given ? Ans: When interpreting ABG's.4 G) -7.110 -.1 mg/dl .3. All of you mentioned increasing pCO2.pO2 -.4. electrolytes come in handy.15 --111 --5.-.
138 -.43 -. Lactic Acidosis.144 -.25 -.94-.6 B)-7.34 -. 2) 21 yo college senior is seen the morning of her finals complaining of palpitations.--Cl. 3.2 E).52 -.-.114 -.34 -.0 1.24 -.44 -.7.= decreased (makes sense) => Metabolic Acidosis (Na+K+)-(Cl+HCO3)= Anion Gap: 22.140 -. it would have been increased.138 -.112 -.25 -.5 D).0 F) -7. Therefore.3.108 --4.Na --HCO3.106 -.98 -.56 --20 --114 --138 -.0 E).15 --111 --5.a 25yo develops severe watery diarrhea for 2 days while on vacation in MExico. Salicylates.pO2 -.104-. Hyperventiliating = Resp Alkalosis pH: Alkalosis Patient with no underlying pulm disease = No hypoxia pO2 expected to be normal to high pCO2 Low: Patient probably hyperventilating HCO3-: normal since no time for compensation.5 1) 68 yo woman despondent about her disfiguring rheumatoid arthritis attempts suicide by ingesting a number of pills for a medication she has at home B)-7.110 -.136 -.25 -. anxiety. 5. Uremia.70 -.98 -.30 --32 --96 --138 -.70 -.32 -.4.12 -.K+ A)-7.8 B)-7. His serum alcohol level is zero. 3) an 18 yo man is left in the ER entrance and is found comatose .140 -.52 -.3.108 -.49 -.-.95 -.7.pCO2-. 2.A 68yo with 40 year history of smoking and chronic cough.10 -. It is compensation) HCO3.10 --110 --5.112 -.26 --28 -.50 -.7. it's not respiratory. Paraldehyde.136 -.7.2 Panicking.24 -.140 -.138 -.#2: ---pH -.138 -.pCO2-.3.108 --3.56 -.22 -.A 19yo asthmatic presents to the ER with wheezing and tachypnea with RR 26 6.16 -.8 Salicylate Intoxication pH= Acid pCO2=decreased (If it were respiratory.96 -.110 -.4.29 --30 -.3.4.114 -.108 -.12 -.15 -.3.a 30yo develops severe vomiting 6 hours after a family picnic answers: ---pH -.--Cl.140 -.28 -.57 -.12 -.24 -.0 F) -7.56 --20 --114 --138 -.7. 4.148 -.78 -.50 -.4 G) -7.22 -.98 -.3.26 -.30 -.22 -.40 -. DKA.14 -.106 -. INH/Iron.4.16 -.8 C)-7.6 C)-7. and tingling in her hands D).A homeless man appears intoxicated and complains of blurry vision.5.Na --HCO3.A 23yo man with asthma with severe tachypnea and use of accessory muscles of respiration does not improve after 60min in ER.9 D).44 -.8 = Increased Anion Gap Anion Gap etiologies: MUDPILES: Methanol.K+ A)-7. Ethanol.24 -.115 -.pO2 -.
Lactic Acidosis.12 -. Uremia.108 -.5 .10 -.50 -.12 -. INH/Iron. Ethanol.78 -.136 -.106 -. Therefore.44 -.44 -.22 -.25 -. --------------------------------------------------------pH -.49 -.--Cl.98 -.56 -.115 -. it would have been increased. There is a major decrease in the number of tubule cells which can produce ammonia and this contributes to uremic acidosis.148 -.140 -.108 -. They enhance NaCl excretion in the distant tubule.140 -. which stimulates aldosterone secretion.3. DOC for African Americans is Thiazide diuretic.= decreased (makes sense) => Metabolic Acidosis (Na+K+)-(Cl+HCO3)= Anion Gap: 22.In Salicylates: Respiratory Alkalosis FOLLOWED by Metabloic Acidosis (mixed later on. think narcotics. Hypercholremia.4. The latter enhances reabsorption and increases hydrogen and to some extent K secretion.140 -.140 -. 7) a 34 yo IDDM patient is seen on his annual exam.98 -.52 -. Paraldehyde.22 -. and hypercarbia = Profound respiratory acidosis with hyperkalemia in response to the deep acidosis. ph will be NORMAL with Low pCO2 and High HCO3-). BP 60/40 and RR 40 E).0 Patient has Septic Shock.K+ A)-7.110 -.15 --111 --5.30 -. 6) 58yo African American man is treated with diuretics for HTN G) -7. Low Bicarb.70 -.24 -.8 = Increased Anion Gap Anion Gap etiologies: MUDPILES: Methanol. pCO2 is high to compensate. His family reports that he has been this way for 2 days.-.108 --3.57 -.6 C)-7.40 -. 4) a 17yo high school student leaves summer camp and refuses to take his insulin for the first week of camp DKA: Anion Gap Metabolic Acidosis B)-7. Difference between DKA and Salicylate acidosis: .110 -.7. there is inadequate perfusion with resultant secretion of stress hormones.4.24 -.8 pH= Acid pCO2=decreased (If it were respiratory. Comatose. 5) a 29yo man with AIDS is brought to the ER lethargic and extremely tachypneic.Bedside Blood sugar/Glucosuria . Borderline Anion Gap.4 Hyperkalemia.Na --HCO3.28 -.14 -. A)-7. Thiazide induced metabolic acidosis.3. It is compensation) HCO3. The acidosis occurring in uremic patients is due to failure of excretion of acid anions (particularly phosphate and sulphate) because of the decreased number of nephrons.4.1 mg/dl F) -7. it's not respiratory. DKA.pCO2-.Probably intoxication since he was "left in the ER entrance".6 Low respiratory drive : Hypoxia. Increase in glucocorticoids along with catecholamines causes Hypokalemia among other changes.138 -.pO2 -. U/A = 3+ proteinuria and serum creatinine 2.104-.70 -.8 B)-7.32 -. Salicylates.50 -. Metabolic acidosis with hypotension.29 --30 -.34 -.5.138 -.5 HTN in african american. In response to shock. Cl is high. Uremic Metabolic Acidosis.24 -.
138 -. generating a metabolic alkalosis. pO2 is normal.exam is .7.25 -. there is loss of Bicarb.A 23yo man with asthma with severe tachypnea and use of accessory muscles of respiration does not improve after 60min in ER. Explained before.0 Methanol Intoxication Anion Gap Metabolic Acidosis.32 -.30 --32 --96 --138 -.114 -.140 -.7.140 -. We just talked about this a few posts down.A 19yo asthmatic presents to the ER with wheezing and tachypnea with RR 26 This time.A homeless man appears intoxicated and complains of blurry vision.26 --28 -.70 -.138 -.10 --110 --5. Antidote: ethanol.52 -.40 -.44 -. as you would find for a COPD. 2.a 30yo develops severe vomiting 6 hours after a family picnic E). the hypokalemia is secondary to the alkalosis itself and to renal loss of potassium ions from the stimulation of aldosterone secretion.0 E). pCO2 is low to compensate. order Home O2.3.16 -.28 -. Potassium low to try to get as many hydrogen ions as possible in the extracellular compartment and compensate for the alkalosis. pCO2 normal.0 F) -7.wt is stable.108 --3. HCO3-: normal since no time for compensation. Chloride is high.0 1.108 -.78 -.138 -. Bicarb again normal because no time to compensate.108 -.16 -. 3. pH alkaline but normalizing.D).A 68yo with 40 year history of smoking and chronic cough. Volume depletion maintains alkalosis.3.57 -.3.3.138 -.138 -.94-.16 -. 5.43 -.114 -.114 -. for COPD patients. Hyperventilation = Respiratory Alkalosis.6 pO2 is low.3.30 -.43 -.30 --32 --96 --138 -. solids for one year)problems have not worsened at all. pancreatic secretions are not stimulated and a net gain of bicarbonate into the systemic circulation occurs. pO2 usually is around 50-60. pCO2 decreasing because of the hypoxia.52 -. it's Athma exacerbation Early response.0 Gastric secretions are rich in HCl. 4. GI question a 32 yr old woman with no past medical history comes with difficulty swallowing foods(esp. D).49 -.7.0 It's a metabolic acidosis but with NORMAL anion gap. and no net gain or loss of hydrogen ions or bicarbonate occurs.96 -. F) -7. When HCl is lost by vomiting or NG suction. these substances are neutralized. A)-7.96 -.8 This guy is retaining his CO2 = pCO2 high Result= pH low BUT pO2 is very low as well. 6. His serum alcohol level is zero.7. Ordinarily.24 -. C)-7. Below 55. In response to diarrhea.10 --110 --5. but not critically low.a 25yo develops severe watery diarrhea for 2 days while on vacation in MExico. In this case.16 -.4.5 Status Athmaticus.50 -.26 --28 -. B)-7.94-. The secretion of HCl by the stomach usually stimulates bicarbonate secretion by the pancreas once HCl reaches the duodenum.114 -.
Coagulopathy (drugs. what clinical markers would make you consider a gastroenterologist referral. given that this pt has no prior history of gi bleeding before. .Esophagus: Esophageal varices.CBC. a 46 yr old man is brought to emergency department after vomiting Bright red blood twice . Aortoenteric fistula (if previous aortic graft) . it's a differential. and MAllory weiss tear . .common causes celiac disease and pancreatic insuffiency. what qs do you ask pt.Esophageal web: plummer-vinson syndrome. liver disease).. the former is confirmed by trypsin level and secretin test and the latter by a biopsy. Follow Barium with CBC. EKG to look for infarct/ischemia ..Duodenum: Duodenal ulcer. she reports no constitutional symptoms. after stabilizing pt what do you do next. you consider diagnosis of malabsorption syndrome . more than 14gr per dl.ABC's : 2 large bore IV's + Fluid resuscitation (RL or NS) . Ans: once u suspect malabsorption then the next step would be to see whether it is with steatorrhea or without steatorrhea this done by sudan stain or fecal fat estimation.Esophagel Stricture following lye ingestion: but there is no history of major depression with suicidal thoughts and ingestion of caustic agents such as lye. that would help you consider your next step. pt does not have these alarming clinical markers. esophageal cancer.Type and cross match pRBC's x 2U in case needed later. if there is increased fat in the stool i.. then it is steatorrhea. a pt comes with new onset epigastric pain and dyspepsia.. what is the best next step in this case.what is the first step in management of this pt.what is the next step in evaluation of this pt? Ans: First test to order: Barium swallow Differential in dysphagia/Young patient/No med Hx: . next you do d-xylose test where you will have a normal test in pancreatic insuffiency and abnormal in celiac . her lab results show iron deficiency and low phosphorus. Most likely diagnosis: Shatzki ring a 27 yr old woman presents with complaint of diarrhea for 14 months. her examination is normal.. and endoscopy (r/o esophagel cancer associated with Plummer-vinson).Stomach: Gastric Ulcer. Gastritis. Nonetheless. esophagitis.Endoscopy (Barium studie are CI in the setting of an acute UGI bleed as it wil interfere with subsequent endoscopy or surgery if needed). . if there is no steatorrhea then you should exclude lactase def.but first things first: . Gastric Cancer . CBC= Because it's acute : Normocytic Normochromic Anemia Differential: . what type of anemia would you likely find while he is being evaluated in ER.but physical exam is normal and PV comes with long standing iron-deficiency anemia and glossitis.Mucosal or Shatzki ring: Follow UGI series with endoscopy both diagnostic and curative with attempt to dilate the ring. . and pernicious anemia. Next step to upper GI bleed = Endoscopy. renal disease.Keep NPO + PPI .unremarkable.e.
she has stopped taking milk. but no improvement. what is your next step in evaluation. ABG's pH normal and PCO2 borderline. as of 1997 asthma is DEFINED AS CHRONIC INFLAMMATION. Arachidonic acid metabolites Event 7: Activation of epithelial and endothelial cells enhancing inflammatory response Event 8: Release of IL3 thru Il10 and IL13. check gastrin levels 2.. diarrha occurs throughout the day with no blood or pus. Ans: Clues: PUD for last many yrs that has been resistant to medical treatment. Heparin Event 4: Smooth muscle bronchoconstriction Event 4: Recruitment of other inflammatory cells: Neutrophils.Bronchoconstriction .Answer to the Q . Proteolytic Enzymes.Is patient on any medications (NSAID's. diarrhea. Follow-up tests to screen for MEN I Status Asthmaticus Pt with classic scenario of Status Asthmaticus comes to ER tired. sensation of fullness post prandial. using accessory muscles. Ans: Clinical Markers: Weight loss. what is the first test to do. labs are normal except for a mild hypercalcemia. she has PUD for last many yrs that has been resistant to medical treatment.Endoscopy 42 yr old woman has diarrhea for 6 months.pt is not taking any medication. CT First line of treatment: PPI. hypercalcemia Zollinger-Ellison syndrome Labs: 1. Chemotactic factors. Result: + Increased bronchial hyper-responsiveness to stimuli + Reversible airflow obstruction by: Bronchoconstriction . IFNGamma.Sexually active/unprotected sex First test to do: . Antibiotics.Edema B.Muscle Fatigue Also others mentioned high yield: Mechanism of Asthma? Others: Management of Status Asthmaticus? A. IV secretion test 3.) . Dysphagia.Mucous Plug Formation . vasoactive factors. supraclavicular lymphadenopathy.. Event 1: Beggining of response of bronchial wall to the antigenic stimulation Event 2: EARLY PHASE RESPONSE: Mast Cell degranulation of preformed mediators Event 3: LATE PHASE RESPONSE = RELEASE OF SECONDARY MEDIATORS: Histamine. Mononuclear cells Event 6: Release of cytokines. oral thrush.Mechanism: Although BRONCHOCONSTRICTION and BRONCHIAL HYPERACTIVTY are components of asthma. Question to ask for next step: . Eosinophils. Whatis responsible for his respiratory "problem"? . Surgery follows if single gastrinoma that hadn't spread to adjacent structures. TNF. On PE: chest silent.
probably.... is bronchoconstricted. bcz pt. so pt. With INCREASING SEVERITY or RESPIRATORY MUSCLE FATIGUE . .. " the ABG analysis in pt's w/ mild attacks or early in the course of a severe attack shows hypoxemia ( a widened A-a gradiant) and hyperventilation ( a decreased PaCO2). was hyperventilating). as pt. over a period of time.. intubation with mechanical ventilation. is getting worse. w/ asthma is an ominous sign and may portend a medical emergency. gets fatigued.when a pt..the pt. pCO2 increases resulting in false-normal value for PCO2 and pH. is getting worse by the min. as they were low before ( when pt.. is breathing at this rate.... is bronchoconstricted. as that means the pt.CO2 decreases as they are blowing off CO2 and obviousely they are also hypoxic as they are not getting enough oxygen due to the bronchocostriction.. and.i. therefore CO2 levels begin to NORMALISE . here is quote from Cecil's essentials of medicine. they are STILL bronchoconstricted but muscle fatigued to keep breathing. as time goes on and the pt.therefore their ventilation is decreasing... breaths faster..e.. This is one of the indications of admission to the intensive care unit (ICU).that is a RED FLAG.. so he/she is retaining it... get. the pt. alkalosis b4 .. this mech. is hyperventilating.. pt.. the ref.. is hyperventilating. decrases ventilation.... and could be / is crashing... the PCO2 RETURNS to NORMAL and ultimately begins to rise. is not blowing off as much CO2.do not get full into thinking pt. and may require mechanical ventilation. not a drive mech ( meaning brain stem stimulation problem as it might be in COPD if you give them too much oxygen). as status asthmaticus ensues .as pt.as to bronchoconstriction ..A rising PaCo2 in a pt...not able to sustain this kind of ventilation.. and now is normalizing as CO2 is increasing... is having his bronchocontsriction resolving.how much more bronchocostricted can a pt. was in resp... a normalizing CO2 in acute exacerbation. as well as you will have "quiet chest" bcz pt. he/she does not have enough air coming into thier lungs." Cecil's More on the subject: The 4 stages of blood gas progression in persons with status asthmaticus are as follows: + First Stage: hyperventilation to maintain normal PO2. my little sidenote:. pt.. it simply comes down to the pt. these pt's require continued direct observation and monitoring.thus you will have normalization of the Ph as well.that is the whole pt.so muscle fatigue..... As the obstructed compartement (called the slow compartment) increases.... failure. + Third stage: Moderate = Unobstructed airways (called Fast Compartment) normally compensate.....the answer is --> muscle fatigue. . decreases breathing efforts and decreases ventilation.so you will not hear wheezes as much.. is in the first aid and also i looked it up in Cecil's and it is there as well. pt.. is fatigued to have to keep trying to breathe as he is very bronchoconstricted .he is already probably quiet constricted.. is strictly moreof a mechanical mech. + Second stage: hyperventilation accompanied by hypoxemia..'s breathing effort is decreased....to conpensate for that pt. most likley indicates fatigue of ventilatory muscles and impending resp.
exam otherwise is normal. This is an even more dangerous sign that mandates intubation and ventilatory support.History of medication intake which would provoke hyperprolactinemia .CMDT Approach to milk-like discharge 32 yr old woman has noticed milklike discharge from her breasts the past one month. . Potassium monitoring (as hypokalemia is a frequent side effect of the anti-asthma medication) .COMBINATION OF IPRATROPIUM AND ALBUTEROL nebulizer . NOT INDICATIED IN GER-INDUCED ASTHMA AS IT MAY EXACERBATE.Gynecological history: menses.TSH level . ANTI-REFLUX MEDS/H2 RECEPTOR BLOCKERS . fibrocystic breast disease.increased diaphragm function and CNS breathing stimulation.Pulse Ox Monitoring. infertility. High PRL: MRI of BRain +> Normal TSH and Normal PRL: Regular menses? .If non galactorrhea: consider intraductal breast cancer. Sources: .Hypoxemia is most common cause of death. MONITOR LEVELS.+ Fourth Stage: Severe : Slow compartment expands further and therefore removal of pCO2 decreases. pCO2 rising as well as Low PO2 (due to increased airway obstruction and atelectasis) will result in hypoxemic respiratory acidosis. C. h/o of excessive nipple stimulation .Emedicine .If PNT: CXR and Thoracocentesis (Other cause of silent chest) .History of illicit drugs: canabis. Therefore OXYGEN IS PRIMARY TREATMENT OF PATIENT.hCG Level . Decreased consciousness. etc.History of prior irradiation to the head. h/o of head injury .Swanson . . h/o encephalitis.PRL level .BUN and Creatinine +> High TSH and Low T4: Thyroid hormone replacement therapy +> Normal TSH. assess careful history taking and physical examination: .Start 2 IV lines. how should you approach this case Do pregnancy test first.INTUBATE IF: Apnea. One for CORTICOSTEROIDS .Management: Patient sitting up . ABG's.Caution: if ASTHMA AND NASAL POPYPS: DO NOT GIVE ASPIRIN. #1: Assess if it is GALACTORRHEA (microscopic examination).If Galactorrhea (Fat globules in discharge) => Labs #2: Labs: .History of headache and visual disturbances . . Warm humidified 100% via a non rebreather mask. Continued increase in pCO2 or hypoxemia despite treatment . Complete approach is: First of all.THEOPHYLLINE +/.FEV1 baseline and monitoring . amphetamines. .If GER-INDUCED. opioids.
SURGERY. etc. Prevention is mainstay of treatment........: Poison Ivy.html Anaphylaxis Usually a typical case of anaphylaxis. acids. Vesicles on erythematous base) . ON BENDS OF ELBOWS AND KNEES.. sometimes diaper. .... dyes. h/o of Atopy.Acute (Itchy Erosions + serous exudate. A.. around area of contact (e..). Saline... Not THAT itchy. 1) What if patient is on chronic beta blocker treatment for some reason (Refractoriness to adrenergic drugs)? What changes in the management? 2) What if the patient is on chronic ACE Inhibitor Treatment (More Severe Hypotension)? What changes in the management? Ans: 1) Give more higher doses of adrenergics plus Glucagon 2) Higher doses of pressors Review: ATOPIC Dermatitis Vs Allergic D/Irritant D I was always confused about the four of them.g.. OR RADIATION THERAPY.If Irregular menses: MRI of Brain IF PROLACTINOMA: BROMOCRIPTINE... D/c offending drug if applicable ..Main Differential for both: 1)Impetigo or Secondary infection (i.) .. Dyes. Poison Oak..If regular menses: Reassurance/Observe.. h/o of dry skin..org/afp/20010501/1763.... ASYMETRIC. CABERGOLINE (DOC OF CHOICE IF NOT WISHING TO CONCEIVE).. flexor areas of extremities...Antihistamine as an adjuvant. ERUPTION IS SYMETRIC.PHOTODERMATITIS: Sunexposed areas C.... 2)Other: . I looked them up for my own review so here goes.. etc.Vasopressors if remains hypotensive .... Reference: http://www...IVF Rapid infusion (LR. forehead.aafp.:impetiginization).. Red. Nickel. Gram stain will r/o it out.ATOPIC DERMATITIS (ATOPIC IS DIFFERENT FROM ALLERGIC): 1) Hallmarks: PRURITUS..Subacute (Scaling excoriated plaques) ..IRRITANT CONTACT DERMATITIS: Mostly Red and scaly.e. MONITOR FOR 24h because of Late-phase Anaphylaxis (Recrudescence 6-12h later after initial improvement).CONTACT URTICARIA: TYPE I HYPERSENSITIVITY!!!!=Wheal and Flare at contact area .Inhaled Terbutaline or Albuterol if severe bronchospasm .ALLERGIC CONTACT DERMATITIS: 1)Hallmarks: 1-3 days after exposure (TYPE IV HYPERSENSITIVITY).... 2)Variants: .IM or SQ Acqueous Epinephrine (Repeat Q15-30min PRN) .Management includes the following: . followed by vesicle/blotchy eruption weeping and crusting. Volume expanders) . Rarely with weeping and crusting (Contact with soaps.. solvents. B. Chronic (lichenification/Pigmentary changes with excoriated papules) 2)In infants: cheeks.
it will go away. What is the most likely diagnosis in this infant? A. or trauma.seborrheic dermatitis D. PAtient would be discharged a couple of weeks later if everything goes well. talcum powder. and DON'T CLOSE. You can take back to OR 2 days later and close abdomen correctly. oliguria starts which is refractive to fluid resuscitation. Distribution: Scalp.Impetigo = honey crusted lesions 2)Seborrheic Dermatitis: Dry scales and underlying erythema.hepatic and renal abnormalities are common in this condition . Some speculate xanthine oxidase. and three different prescribed corticosteroid creams from three different physicians as remedies. Drain. References: CMDT. and you'll find leakage of fluid (significant amounts) in the peritoneum. and body folds. Apparently. the result is the release of those toxic agents built up during the short ischemic episode creates increased permeability locally and significant edema which leads to increased pressure in the concerned compartment. Take back to the OR. Close using a "plastic-like" medium called silex I believ or something. Which of the following statements about this patient is (are) true? A. the more fluid you give.Candidal Diaper Dermatitis Compartment syndrome as a reperfusion injury: Mechanism Reperfusion syndrome is till being investigated as to where do the free radicals exactly come from. umbilicus. the more dangerous it is. vitamin E cream.allergic contact dermatitis C. One of the interesting questions to study about compartment syndrome is the abdominal one. interscapular. PAtient will improve dramatically. at approximately the eighteenth mile he fell to the ground in an unconscious state. Central face. the infant has an intensely erythematous diaper dermatitis that has a scalloped border and a sharply demarcated edge. There are numerous "satellite lesions" present on the lower abdomen and thighs. In fact. and allopurinol has been shown to reduce reperfusion effects experimentally. "Oh. His pulse is 128 bpm.this patient has heatstroke B.atopic dermatitis B." On examination. Question A 34-year-old male is brought to the Emergency Department by paramedics after having collapsed in a marathon. where ischemia took place. presternal. don't worry your pretty little head about it. 1 day after a major gut surgery for bypass.candidal diaper dermatitis Ans: E . Kaplan Center notes. She tells you that she went to three doctors because the first two said. On physical examination. His mother has tried cornstarch. his blood pressure is 90/60 mm Hg. just a little diaper rash. zinc oxide. Some say leukocytes through the NADPH oxidase. don't worry dear. Anyways.infectious eczematoid dermatitis E. The patient's temperature is 41° C. Emedicine Question An 8-month-old infant is brought to your office by his mother for assessment of a diaper rash.
GUNSHOT WOUNDS TO THE EXTREMITIES: A 25 yo man is shot with a .ABDOMINAL GUNSHOT WOUND 19yo gan member is shot in the abdomen with a . METABOLIC: Exam related are in my opinion . and culture tip of old one. Selenium (cardiomyopathy) Source: CMDT http://www. The bullet is lodged in the psaos muscle on the right.treatment should be directed at lowering the core temperature as quickly as possible D. and hollow viscera that will spill fluids in to the peritoneum. He is hemodynamically stable. lateral aspect of his thigh.Azotemia (Creatinine normal): Reduce protein . to the left of the midline. The abdomen is full of important strudtures that should not be penetrated.22 caliber reveolver. The rule of abdominal gunshot wounds is simple: They belong to the OR before any sign of peritonitis starts. CHANGE OF TASTE.gray-ink. .Close Observation B.CT abdomen D.Acalculous Cholecystitis: mostly from biliary stasis. .Emergency US C.Hyperglycemia: Caused by too rapid an infusion of dextrose. Increase Zinc intake. who develops fever without apparent source => Change line immediately.Arterial LAceration . Which of the ffg is most appropraite next step in management? A. The entrance wound is in the anterior. They can be divided into: CATHETER RELATED.38 caliber revolver. . add insulin if needed.Hyperchloremic nonketotic dehydration: reduce chloride.Other: Copper. and the abdomen is moderately tender. Reduce infusion rate. .Brachial Plexus Injury .Air Emboli ++++++ . or use of steroids. AND METABOLIC.Magnesium: muscle weakness and tremor.none of the above statements is true Ans: D. Decreased DTR and respiration.C. CATHETER RELATED: . and the bullet is seen on X-Ray films to be embedded in the . Give fat orally if possible .com/quillen/gi.Pneumothorax/Hemothorax . The entry wound is in the epigastrium.all of the above statements are true Quick Note on TPN .Zinc Deficiency: +++++ PATIENT DEVELOPS RASH.Catheter Thrombosis +++/ Catheter-related Sepsis +++ Patient with TPN using indwelling catheter. AND HAIR LOSS.Diagnostic Peritoneal Lavage E.High Yield Complications of TPN: Central Vein nutritional support occur in up to 50% of patients. Check for possible diarreha or bowel fitula.all of the above statements are true E. B.html Cases of Gunshot wounds and Facts of management A. solid organs that can bleed.Exploratory Laparotomy Ans: E.
He is again hemodynamically stable. arteriogram. It is NOT located in the lateral aspect where the bullet is located here.Formal surgical exploration of the area in the OR Ans: D. Tetanus prophylaxis is first. half way between the great trochanter and the knee. or surgical exploration. and eventually becomes central when it becomes the popliteal. Although absent pulses and an expanding hematoma make such injury virtually certain (and dictate the need for surgical exploration). and neurlogically stable. the main concern is the possibility of major vascular injuries. The entrance wound is in the anteromedial aspect of the upper thigh.Arteriogram E. Neurologic examination of the leg is normal. 5 cm below the groin crease. In wounds of the extremities.Doppler Studies C.Arteriogram D.Digital exploration of the wounds in the ED C.22 caliber revolver. There is no hematoma under the entrance wound. Anatomic proximity to major vessels is the main criterion to suspect vascular injury in gunshot wounds of the extremities.22 caliber revolver.Surgical Removal of the embedded bullet. but canno be felt by another. The popliteal pulse is reported normal by one examiner. A 25 yo man is shot with a . A steady trickle of blood flows from both wounds.Barium Swallow C. C. and it does not seem to responds to local pressure.Arteriogram D. Inspection of thew entrance and exit wounds indicates that the trajectory of the bullet is all above the levl of the angle of the mandible. the presence of normal pulses and the absence of a hematoma does NOT rule out vascular injury. is not necessary if it's not threatening to erode some vital structure. The ER departement MD cleans the wound thoroughly. Which of the following is the most appropriate next step in management? A.Discharge home B. He is fully conscious.Tetanus prophylaxis B. Arteriogram. but below the skull. and blood is oozing from both wounds. But one should know the femoral artery is located anteromedial in the upper thigh. They can be evaluated by Doppler.Surgical Explration of the femoral vessels E. X-ray films show the femur to be intact. In addition to local wound care and the appropriate tetanus prophylaxis. He has palpable pulses in the dorsum of his foot and in the posterior tibial artery behind the malleolus.GUNSHOT WOUNDS TO THE NECK: A young man is short in the upper part of the neck with a . which of the following is the most appropriate next step in management? A. although obligatory in movies. but not at an alarming rate. He is hemodynamically stable.Admit to observe for development of complications D.Continued Clinical observation B. Removing the bullet. Ans: A.muscles posterolateral to the femur. The exit wound is in the posterolateral aspect of the thigh.Endoscopy . Which of the following is the most appropraite next step in diagnosis? A. Only an arteriogram can provide the necessary reassurance.
two inches below the nipple. Sensory examination was intact for pin prick and light touch throughout. and his pulse is 145/min.Extrinsic Cardiogenic shock due to tension pneumothorax C. just to the left of the sternal border. There is no exit wound. He was taken immediately to the operating room. distended veins in his neck and forehead.Vasomotor Shock Ans: A. This is an absolute indication for neck exploration. A 25-year-old African American man arrived at the emergency room approximately 30 minutes after sustaining a single gunshot wound to the left posterior cervical region. and anxious. The hyoid bone was fractured and repaired. Neurologic examination showed intact cranial nerve (II through XII) functions. pericardial tamponade is the obvious mechanism. He is breathing adequately and has bilateral breath sounds.Surgical exploration Ans: C. and is asking for a blanket and a drink of water. What is the next step in management? Ans: Surgery. The area is too high to involve the aerodigestive tract.38 caliber revolver. The bullet entrance wound was in the left posterior cervical region. and there were no carotid bruits. He is neurlogically intact.Extrinsic cardiogenic shock due to pericardial tamponade B. above and medial to the left scapula. Surgical exploration of the left anterior cervical region revealed an extensive hematoma and a lacerated left external jugular vein. A bullet fragment was palpable in the left anterior aspect of the neck. with preserved bulbocavernosus reflex. and it is also rather difficult to explore surgically. He has large. lateral to the cricoid cartilage. Given the location of the injury. In gunshot wounds og the upper part of the neck. which was ligated. Rectal sphincter tone was decreased. resulting in hypotension and neck hematoma as well as cervical spine injury with an incomplete motor deficit at the C5 level.22 caliber revolver.Intrinsic cardiogenic shock due to Myocardial injury E. A large left anterior neck hematoma was present. His blood pressure is 65/40 mmHg. The entrance wound is in the anterior chest wall.E. Systolic blood pressure before his arrival was reported to be 90 mm Hg (palpatory). The exit wound was midline in the anterior aspect of the neck. and also provides a way for embolization of major arteries that might be bleeding significatnly. shivering. cold. Both carotid pulses were palpable. D. A 19yo gang member is shot once with a . with flaccid paralysis of all four extremities except for bilateral forearm flexion. Findings on the initial workup were consistent with a zone II neck injury (see below).Hemorrhagic shock D. Arteriograms offer the best way to assess the extent of the injuries. Which of the folloing is the most likely diagnosis? A.GUNSHOT WOUNDS TO THE CHEST: A 27 yo man is shot point blank with a . and barely perceptible. His chief complaints were neck pain and the inability to move any extremity. Deep tendon reflexes were absent bilaterally. which was possible against gravity. The bullet is lodged in the left . at the level of the 4th intercostal space. patient is in shock and the distended veins identify the type as cardiogenic. The entry wound in the left mid-clavicular line. He is diaphoretic. the main concern is the possibility of significant vascular injuries. Obviously.
Produced by high velocity projectiles (not from handguns). PE is diffult to do. Patients arriving shocked and bleeding are resuscitated and usually undergo urgent surgery with repair or ligation of the bleeding vessels.depends on the location.SOME FACTS AND REVIEW 1. The consequences are generally: +> Laceration and Crushing: projectile displacing the tissues in its track. Although it sounds like a chest wound. II and III. Belly and chest are stacked up and separated by a dome.Treatment of gunshot injuries Primary .resuscitative efforts as well as establishment of airway and restoration of hemodynamics Secondary .paraspinal muscles. +> Cavitation (permanent and temporary): also from even higher velocity projectiles. The point is to remind of the boundaries of the abodmen. and Exit wound is often considerably larger + Avulsive: Small entrance comparable to missile size Exit wound is usually gaping with large amount of tissue loss. E. Angle at impact. 3. and rarely lasts longer than a few milliseconds before collapsing into the permanent cavity or wound (bullet) track. Most institutions explore zone II injuries routinely. which can be obtained by endoscopy as well as . The temporary cavity may be considerably larger than the diameter of the bullet. What is the next step in management? (no choices) Ans: CXR (chest tube if needed) which is the usual for a chest injury. Bullet type. Entry wound is comparable to size of missile. but he is drunk and combative. +> Shock Waves: compression of tissues that lay ahead of the bullet. 2. The belly begins AT the nipple line. +> Zone I injuries are those that are below the cricoid cartilag +> zone II are above the cricoid cartelage but below the angle of the mandible +> zone III are above the angle of the mandible extending to the base of the skull. the kinetic energy imparted on the surrounding tissues forces them forward and radially producing a temporary cavity or temporary displacement of tissues. and Tissue Density. on the other hand. Progressive neurological deficit calls for rapid evaluation and management. In zone I and III more definite evidence of injury is required. can be subjected to whatever diagnostic modalities are required to diagnose the extent of injury accurately. The chest does NOT END AT THE NIPPLE line though. in addition to Exploratory laparotomy which is the usual for an abdominal injury. They are recognized as the primary wounding mechanism produced by handguns. Neck wounds are classified as zones I. Stable patients. NECK TRAUMA: A significant number of patients of neck trauma die at the scene and others on the way to hospital.The Wounding Capacity of a Bullet It is related to the following factors: Kinetic Energy. When a missile enters the body. He is hemodynamically stable. it is also abdominal.Classification of Gunshot Wounds + Penetrating : Missile is retained in tissue. Entry wound is typically small and ragged + Perforating: Missiles pass completely through the target.
HIV associated Nephropathy Pearls (HIVAN) . massive proteinuria in the nephrotic range with little to ne edema .medschool.Order Ultrasound: which in contrast with usual shrunken small kidneys of End-Stage Renal Disease.edu/depts/doms/rounds-6.rcsed. it is still highly controversial. asterixis etc. Direct injury is a consequence of the projectile crossing the spinal cord and/or canal causing compression. Please refer to the post: ODD HIV case posted on July18 for HIV and Syphilis association.edu/Nsurgery/GSWSp. contusion.S. Hemodialysis should also be started. as surgery has not been shown to improve much the neurological status. Overall most studies in the literature recommend a conservative (non-surgical) approach to GSWs to the spine.medscape.Confirm with Renal Biopsy: FOCAL SEGMENTAL GLOMERULAR SCLEROSIS is the most typical one. Indirect injury results from shock waves or secondary fragments damaging the neural elements. think of other diagnoses) .lsumc.ac. It not only slows the progression but may in fact reverse it. and if the patient is white.Patient may present with Uremic Encephalopathy with confusion. civilian population. .com/viewarticle/410823_4 Cases are from Kaplan Q book and Kaplan Surgery Notes HIV Associated Nephropathy With HIV being such a hot topic on the USMLE. GUNSHOT WOUND TO THE SPINE: Gunshot wounds (GSW) are the 3rd most common cause of traumatic spinal cord injuries in the U. in HIVAN. The injury from a gunshot wound could be either direct or indirect. but some authorities beleive that removing the bullet still gives the best chance to recovery. The firm indications for surgical intervention are usually: +> Progressive neurological deficits +> Persistent cerebrospinal (CSF) leaks +> Incomplete neurological deficits with radiographic evidence of neural compression (especially in the cervical spine and cauda equina). . that in the absence of renal biopsy. Indeed. Of note: Encephalopathy is a sign of rapidly changing nephro status either deteriorating ir improving (encephalopathy on first hemodialysis = Dialysis dysequilibrium Syndrome).uic. kidneys are ENLARGED!! . I post high-yield facts I encounter. ACE-I also have been used successfully to further slow progression. Corticosteroids have also been used but with caution because of the advanced stage of AIDS already for the patient. new-onset seizure (Management of seizure with subsequent treatment using phenytoin).html http://www.Mostly African Americans (So and so.uk/journal/vol43_2/4320019. Management: Antiretroviral Therapy is the most important feature.htm www.html http://www.angiography before exploration is embarked upon because of the difficulty in gaining access in zones I and III. Reference: www. with or without laceration of the dura.Labs: Uremia. or laceration of the spinal cord/ nerve roots.
Differential: Hep B and Hep C associated nephropathy. The problem is: since delivery of a set volume is not guaranteed. MD. air delivered under positive pressure is physiologically distinct from spontaneous breathing.Air is pushed in under POSITIVE PRESSURE. the art is to achieve this without damaging the lungs. the pressure starts from the PEEP and on up. . where air enters the lungs by virtue of a slight negative airway pressure. passive exhalation is physiologically the same as during spontaneous breathing. Indicated for conditions where risk of barotrauma can be instantly lifethreatening. The ventilator blows that volume at a certain FLOW. Olatinwo. where chapters on mechanical ventilation seem written more for the author's colleagues than for novices trying to learn the subject. WHAT'S THE DIFFERENCE BETWEEN CPAP AND PEEP? They virtually refer to the same thing. It will be delivered with increasing pressure until the set volume is given. Reference: . THE MECHANICAL RESPIRATORY CYCLE : . PEEP is the positive pressure you set for the end of expiration. both will be referred to as Mechanical Ventilation throughout the chapter.Medscape (posted from the AIDS reader) New Onset Seizures as an Initial Presentation of End-Stage Renal Failure in Patients With HIV/AIDS Toyin F. Hewitt. The problem is: barotrauma. . gas exchange can vary. Please find in the following my little rehashing of what I read about the subject. Heroin Associated Nephropathy. WHAT IS A VOLUME VENTILATOR? term used because you set a volume and the machine delivers that volume. to a degree far greater than the patient could deliver on his or her own. **************** MECHANICAL VENTILATION ************** The science of mechanical ventilation is to optimize pulmonary gas exchange.Mechanical ventilation: the ventilator is active and the patient passive . MD 8/2002 Mechanical Ventilation Lecture and Case Scenarios Inadequate teaching is not confined to medical or nursing schools.Assisted Ventilation: the patient initiates and may or may not participate in the breath. The concept of POSITIVE PRESSURE is that a baseline pressure is applied throughout the cycle to maintain alveolar recruitment. Continuing Positive pressure throughout the entire cycle instead of intermittently . CPAP refers to when inspiration starts.Exhalation is passive. Example: ARDS. but extends (sadly) to mainstream textbooks. Note: For general purposes. Ross G. Flow can be: . tidal volume will flow within that range. making dangerous hypercapnia or alkalosis possible. FIRST LET'S DIFFERENTIATE: . Mechanical Ventilation could be throughout intubation (invasive) or a tight-fit mask (non-invasive).Volume variable and pressure targeted: set the parameter of the inspiratory pressure. utilizing the recoil nature of the chest to let air be exhaled. at whatever pressure necessary (up to a limit).Volume targeted and pressure variable: set the parameter of the volume.
WHEN DO YOU INDICATED MECHANICAL VENTILATION IN ADDITION TO INTUBATION? Take home message: . Severely deranged pH that cannot otherwise be corrected (below 7. pH is 7. and PaO2 is 47 mm Hg while breathing 60% oxygen through a face mask. c.g. inhalation burn.Impairment of alveolar ventilation (assessed by PaCO2>50mmHg) and/or oxygenation (assessed by PaO2<50mmHg) are the only physiologic reasons for instituting mechanical ventilation. correlate with clinical setting.Low PaO2 (e. by secretions) 3. A 61-year-old woman who has severe emphysema is alert but is in moderate . less than 60 mm Hg): a. epiglottitis. WHEN DO YOU DECIDE THAT A PATIENT SHOULD BE INTUBATED? 1.1 is considered an indication for mechanical ventilation) e. Increasing fatigue c. A 29-year-old man is alert but in respiratory distress. IN CHRONIC LUNG DISEASE. 3..50.1 is an indication to mechanical ventilation). Either indication must be based SOLELY on the clinical examination.42.g.Apnea . Depressed mental status b. A 50-year-old man is comatose from drug overdose.Apnea 2. renal.31 while breathing room air. Reduced PaO2 that cannot otherwise be corrected d.g. although ABG's are often helpful to assure that mechanical ventilation is not necessary.Impaired alveolar ventilation (as assessed by PaCO2) when accompanied by one or more of the following: a. Loss of gag/cough reflex e. he is breathing 42 times/min. PaCO2 is 51 mm Hg. b. or cerebral function. that cannot be improved with an FIO2 less than 0. Airway obstruction: acute laryngeal edema – e.. and pH is 7.at the end of expiration is called Contiued Positive Airway Pressure CPAP.g. HIGH pCO2 IS SOMETIMES ACCEPTABLE BUT NOT CRITICALLY LOW pH (ph<7. Anticipated loss of control of the airway: anticipated laryngeal edema– e. head injury with GCS <8 (to prevent massive aspiration).g. that is causing symptoms or seriously impairing bodily function CLINICAL-BASED PROBLEM: WHICH (ONE OR MORE) OF THE FFG CASES SHOULD BE INTUBATED AND MECHANICALLY VENTILATED BASED ON THE ABOVE? a. neck trauma. Ludwig’s angina. Although mechanical ventilation can lead to better cardiac. Again. PaO2 is 76 mm Hg. acute stridor etc. rule of thumb. and b. 2. Treat the patient not the numbers. Official Criterias are: 1. the basic goal for its use must be to improve the PaO2 and/or the PaCO2 or TO REDUCE THE FiO2 OR THE MECHANICAL WORK needed to maintain blood gas values at an acceptable level. PaCO2 is 38 mm Hg. Compromise of upper airways (e.
38. PaO2 is 75 mm Hg while breathing nasal oxygen at 2 L/min. e. and usually patients are started on controlled modes (see below Modes of ventilation).If failure to ventilate or protect the airway was the problem. being careful not to damage the lung (be mindfull of the pressures generated).Is it failure to ventilate (is the PCO2 > 50mmHg). HOW DO WE INITIATE MECHANICAL VENTILATION? The ventilation strategy is determined by whether the patient has failure to ventilate or failure to oxygenate. and the pH is 7.If failure to oxygenate is the problem. Her chest x-ray is clear. Pressure Controlled. usually controlled pressure modes of ventilation are used. * Gas is unable to pass effectively from alveoli to capillaries – due to some obstruction in the interstitial space. PaCO2 is 31 mm Hg. HOW ARE MECHANICAL VENTILATORS CLASSIFIED? 1) How the ventilator knows how much flow to deliver = CONTROL = Volume Controlled . but is frequently easier to treat. and PaO2 is 89 mm Hg while breathing nasal oxygen at 3 L/min. which means adding pressure support to (S)IMV. Her pH is 7. A 31-year-old drug addict responds briefly to the administration of Narcan (a narcotic antagonist) by opening her eyes and crying out and then lapses back into a state of semistupor. * Ventilation is being wasted – alveoli are being ventilated but not perfused: dead space ventilation or more air than the blood can utilize (high ventilation/perfusion (V/Q) ratio). Every patient who is intubated is in need of a rest. PaCO2 is 26 mm Hg and PaO2 is 110 mm Hg while breathing room air.37. 2. to correct the respiratory acidosis. or failure to oxygenate (is the PO2 <50mmHg)? Remember that a low O2 is much more significant than a high PCO2.10.respiratory distress. pH is 7. . . PaCO2 is 59 mm Hg. 2) We determined how much flow and at what pressure. and carefully titrate the CPAP and the pressure control levels to set targets. HOW DO YOU EVALUATE? It is essential to deduce what part of the respiratory apparatus is malfunctioning. The first problem is managed by increasing the patients minute ventilation. it is important that the patient’s spontaneous breaths are supported. * Blood flow is inadequately utilized and blood is passing through the lungs without coming into contact with aerated alveoli: perfused but not ventilated – shunt or ventilation falls behind blood flow (low V/Q ratio). Now how long does it stay there? = CYCLING: how the ventilator switches from inspiration to expiration: . 1. * Air is not able to pass effectively from the upper to the lower airway – increased airway resistance. d.In essence the problem is one or more of the following: * The chest cage is not effective in guaranteeing adequate minute ventilation. controlled volume ventilation is used. or Dual Controlled. While the choice of control mode is probably irrelevant (assist control (AC) or intermittent mandatory ventilation (IMV)). WHEN FACED WITH A BORDERLINE ABG AND POSSIBLE MECHANICAL VENTILATION. A 29-year-old woman is suffering from diabetic ketoacidosis. her respiratory rate is 24/min. the second by recruiting collapsed lung units and controlling mean airway pressure.
But they were of little value since the disease was not inability to ventilate but that to oxygenate. but also breath controlled by ventilator is delivered. low PEEP. dynamic inspiration valves.Time cycled. Medical students were assigned to manually ventilate paralysis victims until restoration of neuromuscular activity occurred. +> AC: Assist-Control = Allows the trigger of the breath. have been developed. +> High Frequency Ventilation = where mean airway pressure is maintain constant and hundreds of tiny breaths are delivered per minute. WHY ARE THEY SO MANY DIFFERENT WAYS TO VENTILATE A PATIENT? . ventilators got smarter now with MODES OF VENTILATION: +> CMV = Controlled Mandatory Ventilation. OR Volume cycled. "old ventilators" called "iron lungs" used to provide negative pressure about the rib-cage allowing sucking up air. dOESN'T allow spontaneous breathing.During the 1990s widespread concern developed about ventilator induced lung injury. .respiratory muscle paralysis and failure to ventilate. .It all started in mid-1950's with the polio epidemic. . pressure support). This has led to the development of lung protective ventilator strategies (renewed interest in plateau pressure limitation and increasing mean airway pressures).During the 1970s and 1980s ventilators were developed which allowed patients breathe spontaneously. of course. rise time control. The solution? Breaths may also be synchronized to prevent "stacking". and the patient to make own effort but the flow/volume/pressure are controlled breaths. Assisted (as in assist control. initially with assisted breaths (assist control ventilation) and subsequently with spontaneous breathing limbs – (synchronized) intermittent mandatory ventilation (SIMV). Accumulating evidence revealed that larger tidal volume. The problem? "stacked breaths" where there is build-up of high-pressures and therefore alveolar stretching and damage.Dual modes. 4) We determined the volume.Then came the Pressure Controlled Ventilators. 3) What causes the ventilator to cycle to inspiration? = TRIGGERING = Ventilators may be time triggered. combining pressure limitation with guaranteed tidal volume. Now the questions is how is that breath going to be delivered to the alveoli? = BREATHS = Mandatory (controlled = which is determined by the respiratory rate). . Flow cycled. +> IMV: Intermittent Mandatory Ventilation = Patient initiate own breath and sucks up air. One type of ventilators to be familiar with is: FLOW-BY = FLOW-TRIGGERED RESPIRATOR (The patient's own breath triggers the breath to be delivered at set standards of volume and pressure). 5) Very much linked to the precedent. Patients suffering with this virus die from asphyxia . synchronized intermittent mandatory ventilation. ventilation strategies were damaging the lungs. pressure triggered or flow triggered (see next note). pressure. automatic tube compensation and. waveform analysis. Physicians are now demanding more control over gas flow than before hence the development of active exhalation valves.Modern ventilators deliver enhanced patient interactivity using better triggering sensors. trigger. . time. The latter was the first mode to allow partial ventilatory support and thus gradual liberation from the ventilator. . Many anesthesia ventilators operate in this way. or Spontaneous (patient sucks up his/her own breath).
If..PRACTICALLY? A. D.Minute ventilation is the product of tidal volume and rate.. the rate represents the minimal number of breaths. For patient for whic it is expected to have some sort of airway obstruction. . a patient who is intubated mainly for hypercapnia will usually be adequately oxygenated with an FIO2 under 0. ARDS) it may be permissible to allow the PCO2 to rise (permissive hypercapnia) to decrease injury from ventilation as long as the patient maintains hemodynamic stability and oxygenation. the respiratory rate is also the total number of ventilator breaths per minute. depending on the inspiratory sensitivity (also set by the machine). the patient may breathe spontaneously.Respiratory rate and Ventilation (Measured by minute ventilation = tidal volume x respiratory rate. HOW DO YOU GO BY MECHANICAL VENTILATION SETTING.00. for example. E.For controlled ventilation. C. the patient may initiate more than the minimal amount. or saturations at 90% or higher. An FiO2 of greater than 60% for over 24 hours has been associated with lung injury. Initial volume is 8 to 10 ml/kg.even in inverse ratio ventilation. . initiate mechanical ventilation with an FiO2 of 100%. A patient intubated because of severe hypoxemia or during cardiopulmonary resuscitation may need an initial FIO2 of 1.. the endotracheal tube slips into the patient's right main stem bronchus.For intermittent mandatory ventilation. A large Vt improves gas exchange and prevents atelectasis. and the peak inspiratory pressure will acutely rise.. Arterial oxygen content should be maintained at 60 mm Hg or higher.3-7. In certain situations (e. Goals of ventilations should be to maintain a pH (as determined by PCO2 and underlying diseases) of 7.For assist control ventilation. ARDS). Example: setting the tidal volume for delivery of 700 cc might achieve a peak airway pressure of 30 cm H2O. A smaller Vt may be required if PEEP is added. PEEP may be added to decrease the A-a gradient. Conceivably the elevated airway . between the machine breaths. the inspiratory pressure limit will protect patient from further complications. This has been shown to decrease mortality in some cases (e. Generally.Tidal volume (Vt) and Inspiratory Pressure limit. then taper 10% every 10 to 15 minutes to find the lowest FiO2 necessary to maintain adequate oxygenation.g. Increases in minute ventilation will cause a decrease of PCO2. and adjustments made to keep the PaO2 between 60 and 90 mm Hg at the lowest FIO2 possible.4.and more comfortable spontaneous breathing .. the rate equals the total number of ventilator breaths the patient will receive.Permissive hypercapnia. allowing a lower FiO2 while maintaining oxygenation.40. For all practical purposes.g. . and is reflected in the PCO2). the machine will attempt to deliver 700 cc to just one lung (half the previous lung volume). a pressure limit of 50 cm H2O can be set at the same time. The respiratory rate is set by using a dial on the machine. Blood gas measurements should be obtained in the first half hour after treatment. However. however. it is approximately 5 to 10 L/min or 100 ml/kg/min. it may decrease venous return higher volumes may increase risk of barotrauma. B.Oxygenation.
Immediate. For long. vecuronium.Inspiratory time and flow. is associated with prolonged (days to months) muscle weakness and ventilatory dependence. * Neuromuscular paralysis is occasionally necessary if sedation fails. decreased lung compliance. Adjust inspired flow rate to maintain a ratio of inhalation time (I:E ratio) to exhalation time of 1 to 1. It is usually begun at 3 to 5 cm H2O and increased in small increments. Cardiac output should be measured if there is an indication of problems because it may increase or decrease with increased PEEP. especially in continuous infusions. Use of nerve-stimulators can decrease the dose of paralyzing agents while maintaining adequate control. Dosages should be titrated to desired effect. consider nerve-stimulation testing to avoid over-medication. Instead. During the night she suffers acute pulmonary edema and requires cardiopulmonary resuscitation. G. or by decreasing respiratory rate. a neostigmine-atropine combination can be used to reverse the non-depolarizing agents. Patients with airway obstruction (asthma. The alarm will sound each time airway pressure reaches the preset inspiratory pressure limit.06. H. Prolonged use of these agents. Before the patient is intubated and mechanical ventilation is begun. Monitoring alarms must be functioning because ventilator malfunction is rapidly fatal if the patient is paralyzed. If repeated dosing or continuous drips are necessary. If the peak inspiratory pressure increases. but patients should still be sedated. This can be accomplished by decreasing inspiratory time. PaCO2 of 61 mm Hg. or cis-atracurium. the machine stops inspiration and an alarm sounds. F. and elevated intracranial pressure. Other negative consequences include overventilation. * Sedation and neuromuscular paralysis allow the patient to rest. Initial therapy includes midazolam.pressure could rupture the right lung or cause other damage. bronchospasm. perhaps after delivering only 400 cc. periodic interruption of sedation (if tolerated) reduces the total number of days on a ventilator. diazepam. However. when 50 cm H2O airway pressure is reached. With this warning.Positive end-expiratory pressure (PEEP) may increase compliance and decrease the work of breathing by preventing atelectasis. and ensure better compliance with the ventilator. The alarm limit should be set 10 cm H2O above this. or a pneumothorax from barotrauma. barotraumas. you need to consider obstruction in the ET tube. CLINICAL SCENARIO: A 60year old patient is in the hospital for treatment of a myocardial infarction.5 in most patients. and PaO2 of 50 mm Hg while . lorazepam and propofol. High levels may result in decreased venous return and severe hemodynamic compromise. The peak inspiratory flow rate determines how fast each breath will be delivered to the patient and is therefore a determinant of inspiratory time.Peak airway pressure reflects the pressure required to overcome airway resistance and is the peak pressure during the inspiratory cycle. and is usually achieved with a peak inspiratory flow rate between 40 and 70 L/min. the therapist or nurse can quickly investigate the problem. COPD) may require additional time for exhalation.term paralysis use nondepolarizing agents such as pancuronium. and thereby decreasing shunting. decrease anxiety. however. with monitoring of hemodynamic and respiratory status. short-term paralysis (3 to 7 minutes) can be achieved with succinylcholine 1 mg/kg IV. her blood gas measurements show pH of 7. If necessary.
Choose higher and readjust per subsequent ABG's. he is intubated and given mechanical ventilation. e. Tidal volume c. enough to correct acidosis 500 . FIO2 b. Vt= 500cc/min c.breathing 100% oxygen delivered by manual ventilation with an Ambu bag. Tidal volume c Inspiratory pressure limit d. 40% is a number to start with. . Tidal volume: Modest as well. W=55Kg. Would you provide PEEP? Answer: a. and he is almost unarousable. Respiratory rate e. FIO2: It is an oxygenation problem.5. The patient's estimated body weight is 50 kg (110 Lbs). A 72yearold man with severe chronic obstructive pulmonary disease is in the intensive care unit. Respiratory rate: Start with an empirical rate of 10-14/min. his blood gas measurements cannot be improved. Peak inspiratory flow rat: 40-70 L/min to acheive I:E ratio of 1 to 1. FIO2: 100% b. His estimated body weight is 70 kg (150 lbs). What initial ventilator settings would you choose for the following: a. FiO2 should be modest. What initial ventilator settings would you choose for the following: a. To ensure continued alveolar recruitment. Would you provide PEEP? Answer: Inability to Oxygenate secondary to Alveolar exchange problem (V/Q mismatch: high perfusion low ventilatin) a. Inspiratory pressure limit: empirically 40cmH2O since patient has pulomnary edema and is liekly to have airway obstruction and high airway pressure. FIO2 b. Tidal volume: 8-10cc/kg. d. Peak inspiratory flow rate f. Peak inspiratory flow rate 60-70 L/min since it's a COPD guy and should be allowed more time for expiration. Despite optimal drug therapy. To prevent respiratory arrest. f. Lung compliance is adequate but FiO2 is 100% at first so. PaCO2 is 84 mm Hg. Respiratory rate: 10-14 and readjust e. PEEP must be delivered. Respiratory rate e. Would you provide PEEP? Yes. PEEPis 15-20 cmH2O and readjust once you decrease FiO2.600cc/min with a RR of 10-14l/min c Inspiratory pressure limit: 50 is a good limit. b. d.24. His chest xray suggests severe emphysema. His pH is 7. Inspiratory pressure limit d. Peak inspiratory flow rate f. and PaO2 is 58 mm Hg while breathing 28% oxygen through a Venturi mask. Alveoles are full of fluid and will tend to collapse.
f. what settings would you choose? Decrease the FiO2 by 10% and redraw ABG's. Because of very shallow respirations and cyanosis. unless contraindicated (coagulopathy. to allow proper compliance to ventilatory oxygenation.PCO2 acceptable and a pH in normal range. . . . H2 blockers. Compression stockings and intermittent pneumatic devices (TEDS and Kendals) are also effective.VENTILATOR-ASSOCIATED PNEUMONIA: Continuous subglottic aspiration of secretions reduces the incidence of nosocomial pneumonia. .Patient is able to generate a peak negative inspiratory pressure of at least 20 cm H2O. WHEN DO YOU WEAN THE PATIENT OFF OF MECHANICAL VENTILATION? Guidelines for weaning from mechanical ventilation: . Otherwise: 1. and an FIO2 of 0. Heparin 5000 U SQ Q12h or LMW heparins (enox-aparin 40 mg SQ QD or 30 mg SQ Q12h) are preferred. No reason to change other settings. Gradually decrease the inspiratory pressure until 8-10 cm H20 above expiratory pressure.Stress ulcer prophylaxis. A bacteriologic diagnosis should be aggressively pursued in ventilator-associated pneumonia and will reduce mortality. However. C. with an FiO2 <50%. Initial ventilator settings include a tidal volume (VT) of 700 cc. If patient . the patient is intubated before his blood gas results are known. Sucralfate.An awake.50. a respiratory rate (RR) of 12/min. HOW DO YOU ACHEIVE WEANING OF MECHANICAL VENTILATION? The most effective method of weaning to discontinuation is spontaneous breathing trials (SBT).PEEP <8 cm H2O. or the respiratory rate'? If so. the tidal volume.Minute ventilation less than 10 L/min. Patient shows sings of improvement.25 56 117 50% oxygen 700 12 Following the second blood gas analysis. A semirecumbent position in bed also will minimize the risk of ventilator-associated pneumonia. WHAT ARE THE COMPLICATIONS OF MECHANICAL VENTILATION? A.Pressure-support method: Switch from an assisted mode of breathing to pressure support. Blood gas results obtained (1) before intubation and (2) 20 minutes later show the following: pH---PaCO2---PaO2 FIO2 VT RR (1) 7. . Would you provide PEEP? Lung compliance is increased. recent or future surgery).Patient is able to generate maximum voluntary ventilation without retractions. thrombocytopenia. alert patient. A comatose 20year old patient is brought to the emergency room following an overdose of sleeping pills. The patient has no spontaneous breathing. setting pressures to generate Vt similar to the assisted volumes with a ventilation rate less than 20.10 79 38 Room air 0 0 (2) 7. would you change the FIO2. . sucralfate may be associated with a lower rate of ventilator associated pneumonia.DVT prophylaxis. and proton-pump inhibitors have all been shown to be effective. 15-20 cmH2O still stands for this patient as well.PO2 >60. active bleeding. B.
to 90-minute intervals. . or develops significant arrhythmias or hemodynamic deterioration. He is switched to IMV at a rate of 12/min and within a half hour is noted to be in respiratory distress with a total respiratory rate (machine initiated plus spontaneous) of 20/min. Clinical Scenario: A decision is made to wean a 67 year old man from the ventilator.The single most traumatic event for the patient is conversion from positive pressure to negative pressure ventilation.40 IMV 12 (700 cc) 8 7. fatigued.39 47 65 0. . this is not in fact the case. the lungs. the machine is in the assist control (AC) mode. Gradually decrease the number of assisted respirations in 1 or 2 breath increments over 30. If the patient remains stable. since the ABG's are not yet critical. resume mechanical ventilation and consider IMV method (below) for weaning. consider a brief T-tube trial. Monitor ABGs and vital signs. How would you explain the changes? Should you D/C the weaning? Assist control 16 (700 cc) 0 7. There must be room in the abdomen . If the patient fails the attempt. HOW DO YOU KNOW WHEN TO D/C WEANING TRIALS AND RESUME MECHANICAL VENTILATION? When: .IMV method. the muscles themselves. . able to cough and protect their airway.The patient becomes anxious. Blood gas measurements obtained before and after the change to IMV are shown below. many body systems must be functioning: the cardiopulmonary apparatus. Before weaning is begun. the nerves that supply the diaphragm (including the neuromuscular junctions). For a patient to self ventilate. and hypoxia (inability to oxygenate)=> Give PEEP and increase FiO2. Moreover the patient must be willing to breath and maintain their own functional residual capacity (not if there is diaphragmatic splinting due to pain). consider extubation. No need to D/C weaning yet at this time. When an assisted rate of <4 breaths/min is achieved.Although the ventilator only appears to support on organ system.45 38 78 0. Switching to IMV caused both hypercapnia and acidosis (inability to ventilate)=> Increase minute ventilation. discontinue mechanical ventilation.To extubated a patient.T-tube method: (A T-tube allows the patient to breathe through an endotracheal tube without assistance from the ventilator. the central nervous system. increase assisted rate until patient stabilizes.) Have the patient use a T-tube with humidified oxygen. This decision should be supported by more thant those numbers: What are the consequences of Weaning? .40 Ans: Patient was in Assist Control with a controlled rate of 16 and a tidal volume of 700cc. discontinue mechanical ventilation. PO2 <60.pH <7. PCO2 >50. The patient is initiating 16 breaths/min and is receiving 700 cc/breath. 2.3. 3. If the patient tolerates this for 1 to 4 hours without deterioration. they need to be awake. demonstrates increasing respiratory distress. Repeat attempt the following day with a more gradual decrease in the rate of assisted breaths.can maintain adequate volumes with a ventilation rate of less than 20 for 30-60 minutes. If the trial fails.
as CO2 will displace O2 from the alveolus when it builds up (we know this from the alveolar gas equation: PAO2 = PiO2 – PaCO2/R). is the PO2 <50mmHg). where is the injury: is it in the blood supply. at least temporarily. then taper 10% every 10 to 15 minutes to find the lowest FiO2 necessary to maintain adequate oxygenation.for the diaphragm and lungs to move into. as you can see from his high CO2. PCO2 70mmHg. middle or lower airways? II. If it is ventilatory failure. and becomes acutely dyspneic: PCO2 is 47mmHg. PO2 60mmHg Hints: Is it ventilatory failure or oxygenation failure (is the PCO2 > 50mmHg. at the alveolar-capillary interface or in the upper. Start with RR 10-14. Now he is severely distressed and his chest is moving up and down in a seesaw manner. shortness of breath and weight loss. in the muscle itself or in the chest cage? If the problem is oxygenation failure. He has been short of breath all evening. BP 170/100mmHg. following a three week admission for sepsis following a perforated appendix. VII. with a PCO2 of 70mmHg and a PO2 of 50mmHg. This patient had a collapsed right lung on chest x-ray. 4 hours after admission you are called because he is hypoxemic. where is the injury – in the brain (the medulla). IV. which is not surprising.A 73 year old male is discharged from the intensive care unit. 36 hours post total abdominal hysterectomy. There must be adequate hemoglobin to deliver oxygen to the tissues. which can be reversed. at the neuromuscular junction. Inspiratory flow rate. his chest is hyperinflated and he is becoming hypercarbic. Remember that a low O2 is much more significant than a high PCO2. PCO2 is 29mmHg. CLINICAL SCENARIOS: I) A 22 year old male found collapsed in the street. but is frequently easier to treat. VI. FiO2 of 100% with CPAP. and many will do well in spite of poor mechanics (you must use clinical judgment). His forced vital capacity is 1 liter and his pCO2 is 70mmHg and pO2 60mmHg. pinpoint pupils. She is admitted through the ER in extremis. finds it difficult to get air in. Cheyne Stokes breathing pattern. exercise intolerance. and a tidal volume 7-10cc/kg. in the spinal cord. PO2 49mmHg.A 16 year old female presents with a two month history of severe fatigue. PO2 60mmHg. ANSWERS: I) This man has ventilatory failure. Intubate and ventilate in controlled mode.A 35 year old male with a history of asthma complains of acute severe left sided chest pain. Patients deserve a trial of extubation.A reintubation rate of 10% is acceptable. The combination of meiosis and bradypnea immediately suggests narcosis. generally set between 60 and 100 l/min (the faster the . V.A 67 year old male is admitted with an acute asthmatic attack. in the peripheral nerves. with naloxone. GCS 3. . III . VIII. respiratory rate of 5 and a PCO2 of 70 mmHg.A 74 year old female is admitted unconscious. becomes confused and hypotensive – PO2 is 45mmHg. The mechanism of his respiratory failure is thus loss of respiratory drive due to opioids reducing the sensitivity of the respiratory center to carbon dioxide.A 47 year old male with a two week history of upper respiratory tract infection is admitted with a history of bilateral lower limb weakness and shortness of breath. in atrial fibrillation. He is also somewhat hypoxemic.A 54 year old female.
The major concern here is that the patient has had an acute pneumothorax and there is a loss of hypoxic pulmonary vasoconstriction. causing further airway closure.flow rate. The patient is hypotensive.This patient has a ventilatory abnormality. The problem is failure of oxygenation due to a massive amount of wasted ventilation (dead space ventilation). in many ways the opposite to case 4. he attempts to actively exhale and this causes dynamic airways collapse. she should be intubated in IMV mode since patient can breathe on her own. VI. One thing to strongly consider is accumulation of secretions or inspissation of mucus. His diagnosis turns out to be Guillain-Barre syndrome.Patient has high pCO2 = Inability to Ventilate. increased FiO2. the larynx (laryngeal edema or stenosis) or below the larynx. along with Heparin therapy and other measures for PE management.This patient is acutely hypoxemic secondary to a barotrauma. and oxygen is not replenished – and there is a ventilation-perfusion mismatch. and thus effective neuromuscular blockade. sensory and autonomic neural demyelination and thus neuropathy. The low FVC is a sign of poor physiological reserve. Oxygenation is OK. and the patient feels uncomfortable. The diagnosis is Myasthenia Gravis. III. which indicates potentially a recent extubation. and paradoxical breathing. The main problem is an inability to ventilate (high pCO2) with an associated problem: inability to oxygenate (high pO2) due to shunt. which should be much lower in view of the degree of hypoxemia. is strongly suggestive of upper or middle airway obstruction. Intubate patient for pulmonary toilet and removal of impacted secretions. This suggests that there is a shunt present. which is characterized by anti-acetylcholine receptor antibodies.Failure to Ventilate due to outflow obstruction: the patient is attempting to ventilate at high lung volumes where the lungs are least compliant. and this patient requires controlled mechanical ventilation.The combination of recent discharge from ICU. V. He is not adequately clearing carbon dioxide. due to obstruction of blood flow. The most likely diagnosis is a massive pulmonary embolism from the pelvic veins. Due to the high resistance to ventilation. due to ineffective bronchial toilet (the patient probably has a very poor cough).This is. as evidenced by his inability to clear carbon dioxide. yet indicated if patient is full code. the quicker inspiration and the longer the patient has to exhale).This patient is failing to ventilate and failing to protect her airway. PEEP. This patient has severe outflow obstruction and gas trapping. A comatose patient with this breathing pattern is a brain stem stroke until otherwise proven. Mechanical Ventilation on IMV mode with increased minute ventilation. IV. This man is . Tidal volume 8-10cc/kg. The cause may be in the oropharynx (tongue or dentures obstructing breathing). which usually eventually reverses. Add PEEP to allow lower FiO2. hypoxemic and hypocarbic after pelvic surgery. Mechanical ventilation in this circumstance is invariably futile. VII. VIII. This patient has ventilatory failure. which is characterized by motor. Pneumothoraces are relatively common in young asthmatics. He requires urgent placement of a chest tube. She presents with a combination of fatigue. In view of her hypoxemia. suggesting muscle weakness. so FiO2 should be modest and readjusted until stabilization of O2 Sat and ABG's. Intubation is not necessary at this stage. II. The cause is either a bleed (hypertension) or an embolus (atrial fibrillation). and the inability to clear CO2. Some airways may remain closed during the entire ventilatory cycle. air is slow to exit the lungs.
what is the cause ? a. When the patient has less than 200 od CD4.hivdent.mtsinai.? A: It is 6wks of AZT irrespective of PCR(antibodies anyway can be from the mother and not of any diagnostic value).http://www. 1998c).should AZT be given for 6 weeks or 6 months.vh.. with repeated evaluations at one to two weeks and at one.http://www. BABY NOT TESTED FOR HIV ANTIBODIES AND CAME +VE PCR NOT DONE ? THANKS Ans: Upon checking more specific references: http://www.mycoplasma pneumoniae c.html My answer is: All three should have prophylaxis irrespectice of PCR.pcp e. chlamydia pnemoniae b. Small vessels rupturing and combined with phlegm gives the rusty look. References: . and six months (CDC.ccmtutorials. cough.org/pediatrics/reduce/ch4. 3. Otherwise they still have the same epidemiology as HIV.http://www.to be followed by PCP prophylaxis Q: to immunize a preterm baby.exhibiting signs of acute gas trapping (auto PEEP) and hypercarbia.htm .com/scenarios/intvent/index.strep pneumoniae d.com/rs/mv/ .should we administer vaccines based on the birth date? for example in a preterm 8 month(33-34 wk)baby. For the mother is it oral or IV AZT.Please clarify. aspergillus Ans: Rusty sputum = Strep Pneumonia.ccmtutorials. 25% to 30% of infected infants may be identified at birth and the remaining 70% to 75% of infected infants can be identified by one month of age.http://www.htm#introduction Question 30 yrs old hiv + man with fever.org/adult/provider/familymedicine/FPHandbook/Chapter04/03-4.. we start talking about PCP. Here's the reasoning: Using DNA PCR. the evaluation of the infants infection status should begin within 48 hours of birth. two.WHEN DO WE GIVE AZT PROPHYLAXIS? 1.people.BABY NOT TESTED FOR HIV ANTIBODIES AND CAME +VE PCR -VE. Patient is HIV+ Not AIDS patient. indicating worrisome loss of physiological reserve.In kaplan CD it says 6 months. According to the guidelines.html . cxr middle lobe infiltration & rusty sputum .BABY NOT TESTED FOR HIV ANTIBODIES OR VIRUS(PCR) 2.should we give the first DTaP at 2 . 20 Y/O GIRL WHO IS HIV + DELIVERED A BABY. Q: For the child.org/pulmonary/books/physiology/chap10a. He needs to be intubated and PEEP applied to his airway in excess of the auto-peep generated: he should be treated with pressure support ventilation: this mode provides limitless flow to match the patient's demands.
What's a normal Calcium level? 4.2-2. The effects of parathyroid hormone on serum calcium are mediated by : .2 mmol per L) of calcium for each gram per dL that the albumin is below 4 g per dL (1 mmol per L).Increasing release of calcium from bone. lymphoma and metastatic breast cancer) 5. kidney.12 The mechanism is analogous to the problem of neonatal hypoglycemia in newborns of mothers with diabetes.5-5. 4. Quick Review on Hyperparathyroidism: What is it? Elevated Parathormone. the suppressed neonatal parathyroid hormone and the abrupt halt of maternal calcium produce hypocalcemia. What causes it? Common causes of hypercalcemia 1.5 mEq/L. A negative feedback mechanism normally decreases production of parathyroid hormone as the ionized serum calcium level increases.month after birth or 3 months after birth? A: Immunize as he/she were term. Reference: .Vitamin D toxicity 4.Lithium use 3.Ectopic PTH: Humoral hypercalcemia of malignancy via parathyroid-related protein (especially malignancy of the lung.Milk alkali syndrome 6. Alternatively. including ectopic hyperparathyroidism 2.25-5.23-2. or 1.30 mmol/L. A low measured calcium with low albumin may be corrected by adding 0.25 mg/dL.57 mmol/L Disease states with altered protein binding require a correction factor to determine the ionized calcium level from the total calcium level.Malignancy via direct bone destruction (especially myeloma. Normal values are: 2.Increasing calcium absorption from the intestines (via vitamin D) .Increasing renal tubular resorption of calcium .Thiazide diuretics Uncommon causes of hypercalcemia 1.Hyperparathyroidism.Kaplan notes 2002 why maternal hyperpara causes hypocalcemia in neonate?? First answer to your question: Apparently the elevated maternal calcium levels suppress fetal production of parathyroid hormone until delivery occurs.Hyperthyroidism 5.Immobilization 2.15-1. Following delivery. the serum ionized calcium level can be measured directly.5 mEq/L 9-11mg/dL or 2.Renal failure 4. and esophagus) 3. head and neck.Multiple endocrine adenomatosis syndromes . ovary.8 mg per dL (0.
Mild acidosis If Hyperparathyroidism suspected on electrolytes => PTH LEVEL. via increased levels of 1.Polyuria and nephrolithiasis .If PTH level low or normal: Check 1.If PTH level elevated: PRIMARY HYPERPARATHYROIDISM 4.7. 3.Chloride > 102mEq/dl .25(OH)2D3 and high PTH-related peptide: HUMORAL HYPERCALCEMIA OF MALIGNANCY. How do you treat it? NON SURGICAL TREATMENT: Intravenous hydration !!! Intravenous hydration !!! Intravenous hydration is the most critical treatment for a patient with an acute presentation of hyperparathyroidism.Granulomatous diseases. together with polyuria and profound dehydration.25(OH)2D3 8. If positive => STOP MEDS AND RECHECK CALCIUM. What if it happens in pregnancy? Maternal hyperparathyroidism can lead to profound hypocalcemia and tetany in the newborn.Familial hypocalciuric hypercalcemia How do you diagnose it? ALGORITHM: * ELEVATED CALICUM LEVEL = 1st step: RECHECK CALCIUM * If still elevated.Chloride/Phosphate ratio > 33 is suggestive .Different ailments: myalgis.Calcium elevated but still less than 14.Depression . LITHIUM. tingling .25(OH)2D3 and PTH-related peptide + if High 1.Parathyroid storm or crisis: Nausea and vomiting.25(OH)2D3 and low PTH-related peptide: GRANULOMATOUS DISEASE + if Low 1. .This may be the first manifestation of maternal hyperparathyroidism. Untreated or medically treated hyperparathyroidism in pregnancy carries a higher rate of morbidity for both fetus and mother. This timing avoids the period of organogenesis in the first trimester and the risk of preterm labor that is present in the third trimester.Fam/h positive: URINE CALICUM LEVEL + If urine Calicum is low: FAMILIAL HYPOCALCIURIC HYPERCALCEMIA + If urine Calcium is high: CHECK FOR MEDICATION INTAKE: THIAZIDE.Constipation. 2. look for FAMILY HISTORY 1.5mg/dl (normal 9-11) . MILKALKALI (ANTACIDS). Hypercalcemia and cardiac arrhythmias. Nausea . especially sarcoidosis. CHF and HTN.If no meds => CHEM PANEL: Hyperparathyroidism suggested by the following: . The optimal time for maternal neck exploration is during the second trimester.Cardiovascular complications . How does it manifest in an individual? .Low phosphate .Osteoporosis .
Destruction of parathyroid glands with alcohol injected under ultrasound guidance has been successful. has been called the "hungry bone syndrome". present clinicians with the challenge of trying to decrease serum calcium levels while also trying to prevent osteoporosis.Avoid immobilization .Replacement of estrogen in postmenopausal women (in absence of contraindications) Reference: American Academy of Family Physicians Syphilis and PCN allergy male w/SY and allergies to Pen. Administration of pamidronate (Aredia) inhibits bone resorption and lowers serum calcium levels.Avoid dehydration . This technique of localization also has resulted in the discovery of parathyroid tumors in the mediastinal area. In fact. An externally palpable parathyroid gland should be considered malignant until proved otherwise. It has been suggested that the best way to localize an abnormal parathyroid gland is to let a good parathyroid surgeon look for it.what if it a post-menopausal woman? won't it aggravate her osteoporosis if you try to decrease serum calcium levels? Postmenopausal women. Such hypocalcemia responds to calcium supplementation and usually resolves spontaneously. A precipitous drop in the calcium level. In the absence of absolute contraindications. Transient hypocalcemia in the immediate postoperative period also is not unusual. the largest group of patients with hyperparathyroidism. accompanied by tetany and seizures.Use thiazide and loop diuretics cautiously . SURGICAL TREATMENT: In some studies. Localization of the pathology by computed tomographic (CT) scan. A recent trial demonstrated the protective effect of estrogen on bone in women with otherwise untreated hyperparathyroidism. ultrasonography or radionuclide scans has been used with varying degrees of success. Larger adenomas are easier to localize than smaller lesions.Treat Hypertension . parathyroid localization with technetium-99m sestamibi has been shown to have high sensitivity and specificity for single adenomas. and paralysis of the vocal cords. Thyroid nodules can be difficult to differentiate from parathyroid pathology on some imaging studies. magnetic resonance imaging (MRI). Are there other concerns in the follow-up of a patient? .Intravenous hydration is the most critical treatment for a patient with an acute presentation of hyperparathyroidism.. What is/are the potential complication(s) of this surgery? Parathyroid surgery has the potential complication of damage to the recurrent laryngeal nerve.. Recently. preoperative localization of adenomas decreased the time required for surgery and lowered the incidence of complications.Avoid high calcium diet and calcium-containing antacids . hormone replacement therapy with estrogen is indicated in these women. The addition of furosemide (Lasix) will increase urinary calcium loss. sometimes permanent. this approach is successful about 95 percent of the time. has occurred But. Multiple injections may be required. Tx? .
Azithromycin PO b.Babies may be breastfed until 3 hours before their own surgery .when a mother is an alcoholic .a mother is getting vaccine for RUBELLA . Increased RETROBULBAR PRESSURE: Exophthalmus and Ophthalmoplegia 5. .Active Hepatitis B: wait until baby is immunized .a.a baby has diarrhea . at least 2 weeks . III. 4. Cephalexin PO d. Increased INTRAOCULAR PRESSURE: sluggish pupillary response and decreased . Headache. Give neonate Zoster Immunoglobulin. sympathetic fibers.Maternal Chickenpox within 6 days of delivery or postpartum: Isolate mother and neonate. Only 1/2 of nenonates born to mothers who developed disease 5-15 days prior to delivery will develop the disease.Influenza .a baby is jaundiced . At that point. send them home together and start BF. IV. 3. If no lesions develop by time mother is noninfectious.a mother has breast augmentation implant . THEN DOXY 200mg PO x14 days.when a baby has galactosemia YES IT IS OK TO BREATFEED WHEN: .when a mother is HIV+ . ciprofloxacin PO e.HepB. and malaise typically precede the development of ocular findings. doxycycline PO Effectiveness of doxycycline has not been formally established in Syphilis.Cavernous Sinus Cellulitis: Cavernous sinus contains internal carotid.Mothers postoperatively may breastfeed if they can hold the baby unassisted. Desensitize.Active TB: Wait until Treatment established.a mother has breat infections . and VI. orbital pain and fullness accompanied by periorbital edema and visual disturbances. Desenssitize in allergy is first step. How to differentiate between Cavernous sinus thrombosis and orbital cellulitis? . Patients generally have sinusitis or a midface infection (most commonly a furuncle) for 5-10 days 2. IF PATIENT REFUSES.a baby is over 2 years . V1 and V2. fever. 1.a mother needs a mammogram .when a mother has HTLV-1 virus .a baby who has PKU (along with supervised phenyl-alanine free formula) Special Considerations: . Breast Feeding Facts Contra-indications to breastfeeding: .a mother is pregnant . then tx w/pen f.when a mother uses street drugs .Active Hepatitis A: Breastfeed when over acute state and after 24h treatment . enough of the sedative is out of the body and BF is safe. Pen IM c.
are suggestive. dacryocysitis.Cavernous sinus thrombosis + Bilateral symptoms: + Ophthalmoplegia. + Lids cannot be opened because of paralysis secondary to III involvement. signs appear in the contralateral eye by spreading through the communicating veins to the contralateral cavernous sinus.Admit all children because children are deficient in IgG2 and are predisposed to bacteremia. extension from adjacent structures. dentition. Lids cannot be opened because of edema. ethmoid most commonly). + Severe unilateral ptosis + Severe ophthalmoplegia (ie.Steroids (especially if progressed to pituitary insufficency to prevent adrenal crisis).: compromised vision) Oxacillin or nafcillin can be used with the addition of ampicillin and sulbactam in . Classification: Group I . This diagnosis is confirmed by CT scan. + Fever and leukocytosis + Orbital signs Group III . therefore. Mainstay of therapy: Braod Spectrum Antibiotics (Staph Aureus Most common) Heparin therapy . . + Directional proptosis = Globe is looking away from the abcess. This is pathognomonic for CST. .visual acuity 6. but the physical signs or papilledema on funduscopic examination.Preseptal (periorbital) cellulitis = inflammatory edema of the eyelids and periorbital skin with no involvement of the orbit. clinical examination guides therapy.Orbital cellulitis = CT scan is not sensitive for diagnosing this entity.Preseptal: D/C only if adult with PO ATBx and close follow-up .Orbital: Admit with IV ATBx +/. Without effective therapy. complication of periorbital infection 2.e. Group IV .Orbital Cellulitis: Orbital infections develop via direct inoculation. Diagnosis is confirmed by CT scan. but it can be suspected based on physical examination + Orbital signs (see above) + Limitations of ocular motility = pain in globe movement toward the abcess.Subperiosteal abscess = collections of purulent material between the orbital bony wall and periosteum.Surgical intervention if necessary (i. Sinusitis (60% patients. 1. 8. Death follows shortly thereafter. proptosis + Corneal hypesthesia with increased intraocular pressure Treatment: . CRANIAL NERVE PALSIES 7. and hematogenous spread.Orbital abscess = collections of pus within the orbital soft tissue. palsy of the pupillary and extraocular muscles) + CN V1 (forehead) anesthesia Group V . The patient rapidly develops mental status changes from CNS involvement and/or sepsis. Group II .
Start Steroids: Solumedrol 30 mg/kg over 15 minutes then followed after 45 minutes by an infusion at 5. hyperflexion. with or without administration of a parenteral antibiotic. accounting for 15% to 20% of cases. fever w/o a focus Fever in a 2months old child(>1 month). Other: Neurogenic bladder (retention). various degrees of motor involvement with paresis more pronounced in UE than LE. PT/OT/Speech. . If clear. Anterior Cord Syndrome The anterior cord syndrome anatomically involves the anterior portion of the cord. Guys. should be made only after carefully assessing the caregiver and . Clinically. Methylprednisolone is thought to impact the biochemical cascade of injury that progresses after the initial injury for some hours. or chloramphenicol. Hands are especially involved. The decision to observe a low-risk febrile infant at home.WBC=10000(5000<WBC<15000). a cephalosporin (eg. Prognosis: 97% completely recover if less than 50yo. clindamycin.. Central Cord Syndrome Central cord syndrome is the most common of incomplete Spinal Cord injury. Disc protrusion. no need to admit. or vascular injuries may play a role. cefotetan) can be used alone. Pain of neuro etiology. Management: Admit to Neuro ICU. Bladder involvement common. May be tube feeding in acute phase because of adynamic ileus. DTR's below level are absent at first but return with level of spasticity once over Spinal shock.well appear(not ill). cefuroxime. Next: MRI: shows narrowing of the white column of CSF and impingement of the darker appearing spinal cord. Spasticity. paralysis below the injury with variable impairment of pain and temperature sensation is present.but what about this case? Thanx in advance ANSWER: 2 MONTHS. Patients who are allergic to penicillin can use vancomycin. Risk Factor: Cervical Spondylosis in older patients Mechanism: Hyperextension Trauma (minor bleeds in the tissue) Symptoms: Sensory deficit with level. NO TOXIC MANIFESTATIONS Sepsis work up as UTI's are a frequent cause of fever in children under 3 months of age.4 mg / kg / hr is the typical regimen employed. Gabapentin for neuro pain.what should we do next? If he/she is less than 1 m of age or is ill we admit in hospital. Difference with Central Cord Syndrome: . Maintain a level of mild hypertension for spinal perfusion.Mechanism of injury is different . Action: Since diagnosis is pretty much narrowed down.Motor symptoms are different between upper and lower extremities in Central.if WBC is >15000 we give Abx(kaplan). cefoxitin. Give IM Rocephin x1 (not accepted by ALL authorities by recommended).Position and vibration modalities (posterior columns) are preserved. and observe outpatient. Alternatively... More somber prognosis is after that.children to cover H influenzae.
poor perfusion. marked hypoventilation or hyperventilation. <5 WBC/hpf REFERENCE: POST GRADUATE MEDICINE ONLINE http://www. *** Low-risk criteria for infants with fever without source *** 1) Clinical criteria Born at term (gestation >37 wk) Previously healthy No toxic manifestations No focal bacterial infection (except otitis media) on examination 2) Laboratory criteria WBC count 5. Q was about mechanism of action of Donepezil: A: The ChEIs are classified according to their duration of enzyme inhibition as shortacting. The ChEIs prolong the actions of the neurotransmitter acetylcholine (ACh) at the synaptic cleft. rivastigmine is hydrolyzed. Due to this longer duration of action. 4) over 90days: NO NEED TO ADMIT IF TEMP IS LESS THAN 39/102.caregiver reliable and taught what to expcet and when to bring patient back . which are decreased in patients with AD. which results in the prolonged inhibition of AChE. rivastigmine is classified as an intermediate-acting (pseudo-irreversible) agent.Rivastigmine fits into the enzyme's active site in a similar fashion to ACh. .making sure that a responsible physician will be available to provide follow-up evaluation. or long-acting inhibitors.fever without toxic signs: 1) 0-7days: admit 2) 7-28days: may follow as outpatient if: . GUILDELINES ARE AS FOLLOWS: .Fever with toxic signs: admit for workup . .000/mm3. or cyanosis). 3) 28 to 90days: allow to be treted as outpatient ONLY if low-risk group. stimulating presynaptic and postsynaptic muscarinic and nicotinic receptors.htm Q & A about Donepezil The foundation for the concept of Choline Esterase Inhibitors in AD treatment rests on the cholinergic hypothesis for the disease proposed over 20 years ago. Another term for this mechanism of action is reversible inhibition.500 band cells/mm3 Normal urinalysis (<5 WBC/hpf) or negative Gram's stain When diarrhea is present.postgradmed. <1. Like tacrine and donepezil. but unlike these two agents.2 AND NO TOXIC SYMPTOMS.patient belongs to low-risk grooup. lethargy. See below.000-15. . it can inhibit enzyme activity up to 10 hours.com/issues/2000/02_00/park.Tacrine and donepezil are short-acting agents that bind to AChE by hydrogen bonding and are hydrolyzed within minutes by the body's water. *** Toxic signs are: *** Clinical appearance consistent with the sepsis syndrome (ie. intermediate-acting.
#3: No creatinine level is given. Another example of mixed disorders is salycilate intoxication whereby the first change is respiratory alkalosis. anion gap 34 mmol/l Arterial Blood Gases pH 7.An example of a long-acting ChEI is the organophosphate compound metrifonate. #5: Why is it important to make those speculations? Stopping the offending drug and replacing it with another diuretic would probably correct some of the electrolyte imbalances. In addition. so we can concude that it is metabolic acidosis. In addition. She has hyperglycemia (67. Metrifonate is a prodrug that is converted to the active agent dichlorvos (DDVP). COMPENSATION NEVER "NORMALIZES" pH.. Overhydration is a concern in adults with compromised renal or cardiac functions and in elderly with incipient congestive heart failure. The . The most common side effects of thiazide diuretic is hypochloremic hypokalemic metabolic alkalosis. a New-Generation Cholinesterase Inhibitor. DDVP forms an extremely stable complex with a half-life of enzyme regeneration of 15 days. Hemodialysis may be needed in some occasions to treat acidosis in this situation. It's always close to normal.Article 2000 ABG Question A 55 year old insulin dependent diabetic woman was brought to Casualty by ambulance.. May be had an infection which precipitated DKA. Results include: K+ 2. aggravated by the possible renal failure the patient might have been experiencing. which corroborates it. Current medication was digoxin and a thiazide diuretic.41 pCO2 32 mmHg pO2 82 mmHg HCO3 19 mmol/l ANSWER: #1: Acid-Base disorder: IT's a mixed disorder.. The disorder usually starts with alkalosis and then acidosis ensues. glucose 67 mmols/l. One must rule out if patient is having some degree of renal failure due to long-standing diabetes which would aggravate the acidosis. Reference: Medcape: Rivastigmine. Past history of left ventricular failure.7. In the presence of renal failure administration of large amounts of fluid is unnecessary and generally is contra indicated. and no calcium level. which would explain the profound hypokalemia instead of the usual hyperkalemia you would have in a simple DKA episode. Normally it's below 6). no sodium level. hemodynamic assessments must be made in an intensive care setting in order to administer adequate quantities of fluid while avoiding overhydration that may complicate the condition. #4: The patient is on thiazide diuretic. The result is a "normal" pH. and the next is metabolic acidosis as the ASA accumulates. On binding to AChE. management of DKA differs in patients with renal failure. The anion gap is high. #2: PAtient has been sick for a while. dehydration probably increased plasma concentration of Thiazide. Consequently. She was semi-comatose and had been ill for several days.
Usually. Histologically. including dendritic cells (see below). and maybe by the development of donor-specific suppression of the recipient's immune response. Liver grafts seem to be less susceptible to such antibody-mediated hyperacute rejection. Cell-mediated rejection may be reversed in many cases by intensifying immunosuppressive therapy. Correct me if I am wrong.g. After resolution of acute rejection. It is a HYPERSENSITIVITY REACTION TYPE IV culminating in graft enlargement and tenderness.g: decreased clearance of creatinine for kidney transplant). It is irreversible.g: bone graft + SYNEGENEIC GRAFT: graft between identical twins. After successful reversal of an acute rejection episode. the allograft commonly survives for prolonged periods. or previous transplant) to HLA in the graft. vascular integrity is maintained. The pathological basis is anti-vascular antibodies that cause extensive proliferation of the arterial endothelium. te detect presensitization . and can be suspected on the basis of lowgrade fever with signs of graft insufficiency (e. resulting in ischemia and fibrinoid necrosis of the graft. Transplantation facts TYPES OF TRANSPLANTATIONS: + ORTHOTOPIC: organ graft transferred to an anatomically normal recipient site e. and graft infarction is unresponsive to known immunosuppressive therapies.: heart transplant. this rejection reaction is characterized by small vessel thrombosis. blood transfusion. + XENOGRAFT: graft between different species e. GRAFT REJECTION REACTIONS: Allografts may be rejected through either a cell-mediated or a humoral immune reaction of the recipient against transplantation (histocompatibility) antigens present on the membranes of the donor's cells . even though immunosuppressive drug dosages are reduced to very low levels. The role of humoral antibody in hyperacute graft rejection is evident when the recipient has been presensitized (by pregnancy.: porcine heart valves. although the arterial endothelium appears to be a primary target of the HVGR. There is no therapy for chronic rejection. 2) Chronic Rejection: Clinically less dramatic. + ALLOGRAFT: graft between genetically DISSIMILAR members of the same species. Pretransplantation evaluation usually includes a lymphocytotoxic test between recipient serum and donor lymphocytes in the presence of complement. + AUTOGRAFT: transfer of one's own tissue to another location of the body e. This process of graft adaptation is most likely explained by the loss of highly immunogenic passenger leukocytes. * HVGR = HOST-VS-GRAFT REJECTION: 1) Acute Rejection (4-60 DAYS POSTOP): Main mechanism is LYMPHOCYTEMEDIATED IMMUNE REACTION. severely damaged elements of the graft heal by fibrosis and the remainder of the graft appears normal. 3) Hyperacute rejection: Within hours or even minutes (intraoperatively). which may gradually occlude the vessel lumen. + HETEROTOPIC: organ transplant to an anatomically abnormal recipient site e. The reaction manifests as an Arthus Reaction (Type III hypersensitivity).result is a normal pH.g.g: kidney transplant to iliac fossa of recipient.
infertility.AZATHIOPRINE: Bone Marrow depression. weight gain. redistribution of fat tissue. and the patient returns to hemodialysis to await a subsequent transplant. cyclosporine. * GVHR = GRAFT VS HOST REJECTION: It is a major obstacle encountered in Bone Marrow transplants.Despite prophylaxis with immunosuppressants begun just before or at the time of transplantation. It occurs from the grafting of an immunocompetent donor tissue containing EFFECTOR T CELLS. drug-induced nephrotoxicity is sometimes difficult to differentiate from rejection. End-stage chronic hepatitis and biliary cirrhosis are the most frequent indications for liver transplantation in adults. . Acute Graft Rejection in 3 to 4 months (but they return to normal health and function with increased suppression and reversal). Intensified immunosuppressive therapy usually reverses rejection. and renal tubular cells. which respond to -allo-antigens expressed on host cells. If the diagnosis is unclear. Cadaveric donors of livers must be of previously healthy persons who are size. and appearance in the urine sediment of protein. do not stop immunosuppressants). sugar imbalance. etc. and hepatitis. II) LIVER TRANSPLANT: The advent of cyclosporine has permitted early reduction of corticosteroid dosage. as are biliary atresia and inborn metabolic deficiencies in children. osteoporosis. percutaneous needle biopsy is performed for histopathologic evaluation of tissue. Its adverse effects are similar to cyclosporine. . graft tenderness.CYCLOPHOSPHAMIDE: Hemorrhagic cystitis. most recipients undergo one or more acute rejection episodes in the early posttransplant period. If it cannot be reversed. SPECIFIC ORGAN TRANPLANTATIONS: I)KIDNEY TRANSPLANTATION ISSUES: . In cyclosporine-treated recipients. and B-cell lymphoproliferative disorders secondary to reactivation of EBV. IMMUNOSUPPRESSANTS AND COMMON ADVERSE EFFECTS: . Occasionally seen in intestinal grafts (lymphoid tissue). fever.TACROLIMUS: is an immunosuppressive drug for liver transplant recipients. hypertension.: renal artery vasoconstriction). lymphocytes. Nephrectomy of the transplanted kidney is necessary if hematuria. hirsutism. gum hypertrophy. and low-dose azathioprime. even with biopsy.and ABOmatched to the recipient. and risk of Epithelial Carcinoma and Lymphoma (in which case. tenderness and swelling of the graft. Major target organs are: SKIN (Dermatitis). immunosuppressive therapy is tapered. although gum hypertrophy and hirsutism are less prominent. Complications: Immunosuppressant toxicity. . Livers are stored in cold solutions generally for 8 to 16 h after . GASTROINTESTINAL TRACT (Diarrhea). It also may induce diabetes. resulting in better postoperative healing and greater resistance to overwhelming infection. and alopecia . Chronic Graft Rejection. or fever results from the rejection response with withdrawal of immunosuppressants. and LIVER.CYCLOSPORINE: Nephrotoxicity (ie. Rejection is suggested by deterioration of renal function. Therapy may be prolonged and usually consists of some combination of Steroids.in the recipient.PREDNISONE: adverse effects on growth in children.
but the incidence of graft nonfunction increases with prolonged storage. However. if necessary. hepatitis with hyperbilirubinemia. prolonged immunodeficiency.GVHR: Symptoms and signs of acute GVHD are fever. Jaundice and elevated serum levels of hepatic enzymes are corroborative findings. The vanishing bile duct syndrome.Immunology references (Compiled previous paper I had I don't recall from which references) . exfoliative dermatitis. Patients present with tachypnea. Rejection is suspected by development of hepatomegaly. Patients are also at risk of developing pneumocystis pneumonia. or monoclonal antibodies. antithymocyte globulin (ATG). rejection may be suggested by biopsy findings only. References: . diarrhea and abdominal pain. which generally occurs 40 to 60 days after transplantation. In milder cases. A worrisome late infection is cytomegalovirus interstitial pneumonitis. Arrhythmias may occur in more severe rejection episodes. but treatment with ganciclovir and passive immunity with immunoglobulin has decreased the mortality rate to about 25 to 40%. but prophylactic use of trimethoprim-sulfamethoxazole has dramatically decreased the incidence of this infection. hypoxemia.removal. Some grafts stored for > 24 h are successfully transplanted. With the use of cyclosporine. and disease recurrence. and weight loss. patients are very susceptible to infections. dyspnea. . Later complications include chronic GVHD. During this time. Rejection is treated with corticosteroid and ATG or OKT3. characterized by intrahepatic cholestasis with preserved hepatocellular function. and fever.Merck Manual . is a pattern of chronic rejection. and a chest x-ray with bilateral pulmonary infiltrates. patients continue to be immunocompromised and at risk for infections because of the drugs used to treat GVHD. The mortality rate of cytomegalovirus interstitial pneumonitis was 80 to 90%. acute GVHD. III) CARDIAC TRANSPLANTATION: Rejection onset may be heralded by fever. and infections. liver allografts are less aggressively rejected than other organ allografts. the WBC count can take 2 to 3 wk to recover. Acyclovir prophylaxis has dramatically decreased the risk of herpes simplex infections during this time. routine protocol transvenous endomyocardial biopsy has been used increasingly to diagnose rejection. retransplantation is the treatment. Surprisingly. IV) BONE MARROW TRANSPLANT: Early complications include rejection by the host of the marrow graft. and heart failure that is predominantly right-sided. malaise. tachycardia. hypotension. vomiting. Even after engraftment.Infection (See next post: Infections in Transplant patients): Following the preparative regimen for BMT. . Mild rejection by histologic criteria without detectable clinical sequelae requires no treatment. because other signs and symptoms are often absent and rejection may be detected before function of the graft deteriorates. light-colored bile (seen in Ttube drainage) or stools. and complaints of anorexia. right-sided pain. Suspected rejection episodes are treated with IV corticosteroids. Needle biopsy can provide pathologic confirmation. when either fulminant acute rejection or chronic rejection is refractory to immunosuppressive therapy. which may progress to an ileus.
Which one of the following agents is considered the drug of first choice in treating acute CMV infection in lung transplant recipients? A.After completing her course of antiviral therapy. In this situation. the patient was placed on oral ganciclovir. azathioprine.Because of suspicions that her CMV strain may have developed resistance to ganciclovir. One week after antiviral therapy finished.. she had a bronchial stent placed. the patient was discharged home to complete a 14day course of antiviral therapy. Biopsies were negative for CMV. Foscarnet IV. follow-up bronchoscopy was again positive for CMV. After four days of in-house monitoring for electrolyte disturbances (which did not occur).Ganciclovir C. The RSV infection was treated with ribavirin. 1998. the patient again reported shortness of breath (SOB). A BAL was positive for CMV. The patient did well for the next 10 weeks.Cidofovir 2. She underwent transbronchial biopsy.Foscarnet E. . but significant mucus plugging was present. 1 g TID. Both she and the donor were cytomegalovirus-(CMV) positive. despite continuing prophylaxis with oral ganciclovir. Postoperatively. Three weeks later. the patient was admitted to the hospital for treatment with a combination of foscarnet IV and ganciclovir IV. which disclosed CMV infection. Ganciclovir IV plus foscarnet IV 3. which was treated with antibiotics. Ganciclovir IV. as prophylaxis.Ayclovir B. She was discharged and placed on prophylactic oral ganciclovir for 3 months. the patient received 1 dose of CMV hyperimmune globulin (CMVIG) and was started on a standard immunosuppressive regimen with tacrolimus. lung cultures showed mucoid Pseudomonas. the patient underwent bronchoscopy because of decreasing pulmonary function on spirometry. until she again developed dyspnea. 120 mg/kg/day x 14 days D. Increased dosage of oral ganciclovir to 2 g TID B. Four weeks later. Repeat bronchoscopies done over the next 3 months were all negative for rejection and CMV.Harrison 14th edition Clinical Case in Lung Transplant I. At 6 months after transplantation and 3 months after the last dose of oral prophylactic ganciclovir. 10 mg/kg/day x 14 days C. Bronchoscopy showed no signs of rejection. which of the following alternatives would be most appropriate for treating this infection? A.Faqmciclovir D. and prednisone. but because of her history of CMV. after which she developed fevers and was found to have respiratory syncytial virus (RSV) on bronchoalveolar lavage (BAL). the patient was also treated with ganciclovir IV for 14 days.29-year-old woman with cystic fibrosis who underwent bilateral single lung transplantation on April 7. Two weeks after transplantation. The patient received a repeat course of foscarnet IV and ganciclovir IV for 14 days.
2.Which one of the following adverse effects associated with foscarnet is the most common serious toxicity? A. and avoidance of other nephrotoxic agents may also help to reduce the occurrence of renal impairment. However. early detection of CMV infection -except for which one? A. which may occur in more than 25% of patients. However. Most episodes of CMV pneumonia respond to a 2. neutropenia. but this response is delayed in immunosuppressed persons and often appears after the onset of disease. these drugs are associated with a significant risk for nephrotoxicity and other adverse events that limit their overall use. studies in AIDS patients with relapsing CMV retinitis have shown that combination therapy. Other common abnormalities associated with foscarnet include changes in serum electrolyte concentrations. 3. including phosphorus and particularly calcium. IgM antibodies may not be appropriately replaced by IgG antibodies. diarrhea. Nausea.to 3-week course of therapy. serologic monitoring of antibody levels . PCR for CMV DNA E. and headache. Seizures C.Answer is D. Adequate hydration and careful monitoring of renal function are critical in reducing the likelihood of this effect. Thus.Answer is C. using both ganciclovir and foscarnet.including infection due to ganciclovir-resistant strains. is superior to monotherapy with either agent alone.The correct answer is: B The appearance of anti-CMV IgM antibodies is the primary humoral response to CMV. the recurrence of CMV infection. dose modification. Less common side effects include seizures. suggests the possibility of ganciclovir resistance. despite ongoing ganciclovir prophylaxis. in organ-transplant recipients. CMV pp65 antigenemia D. Foscarnet and the new agent Cidofovir are effective therapies for treating CMV infection -. Nephrotoxicity D. fever. vomiting.Ganciclovir is the drug of choice for treating CMV infection. anemia. Foscarnet is approved for the treatment of CMV infections and represents an appropriate second-line agent for use in patients in whom ganciclovir treatment has failed. Serologic monitoring of IgM/IgG antibody levels C. Patients who have frequent relapses on ganciclovir may have their treatment augmented with IV CMV hyperimmune globulin (CMVIG). In this situation. Anemia E. and diarrhea 4. vomiting. The most common serious toxicity associated with foscarnet is nephrotoxicity. Electrolyte disturbance B.All of the following tests have been used for rapid. Saline loading. Shell vial assay with immunofluorescent staining B. Digene hybrid capture CMV DNA assay Answers: 1. 4. In addition. nausea.
thicker hair was noted on her hands and arms. Surgical reduction (gingivectomy) D. diltiazem was added to the treatment regimen after the patient developed new-onset hypertension.At this time. Discontinuation of cyclosporine 3.Which of the following methods is commonly used to treat advancing gingival hyperplasia? A. Approximately 2 months after transplantation. Oral examination showed generalized gingival enlargement involving the mandible and maxilla.43-year-old woman with a history of congestive heart failure secondary to a nonischemic dilated cardiomyopathy as well as hereditary protein S deficiency. The patient was extubated on the first postoperative day and weaned off vasopressors. Cyclosporine-induced hypertrichosis affects primarily females. Clinical manifestations of cyclosporine-induced hypertrichosis usually begin to appear approximately 4 to 6 months after initiation of cyclosporine therapy. cheeks. Which of the following statements about cyclosporine-induced hypertrichosis is/are correct? A. References: Interactive Grand Rounds in Immunology Clinical Case of Cyclosporine Adverse Effects 1. Meticulous dental hygiene. which had begun appearing 2 months previously. Short-term azithromycin C. There was no history of significant dental problems before transplantation. the patient also reported concern about aberrant hair growth involving her face. with twice-daily brushing and daily flossing B. Mild hemorrhage of the gingival tissue occurred on probing. diltiazem and warfarin. she was evaluated for cardiac transplantation. Because of progressive heart failure. Darker. Which one of the following strategies has been shown to prevent the development of gingival hyperplasia? A. Change antihypertensive medication from a calcium channel blocker to ACE inhibitor or other class of antihypertensive D. B. Initial immunosuppression included intravenous azathioprine and methylprednisolone. and orthotopic heart transplantation was performed without complications. The patient made satisfactory progress and was transferred out of the intensive care unit on the sixth postoperative day.is inadequate in screening for CMV infection. Cyclosporine-induced gingival hyperplasia was suspected. especially children and . the patient reported the development of "swollen gums" that tended to bleed when she brushed her teeth. and forehead regions. and prednisone. extending onto her shoulders. Subgingival scaling before initiation of cyclosporine E. Cyclosporine dosage reduction C. Approximately 1 week after transplantation. 2. Maintenance immunosuppression consisted of oral cyclosporine. None of the above is effectively preventive. Short-term dosage reduction of cyclosporine B. azathioprine. azathioprine. cyclosporine. Discharge medications included prednisone. A donor heart became available 15 days after the patient was admitted.
by hair follicles stimulated by cyclosporine. CMV infection may cause interstitial pneumonia. cervical lymphadenopathy). give Dapsone + Pyrimethamine. Prednisone B. 4. Low doses of Acyclovir PO have been traditionally given for prevention.Varicella Zoster Virus: Reactivation after several months (can be as early as 1 month). Hypertrichosis results from an increased production of 17-hydroxyprogesterone and DHEA sulfate.adolescents. 6 MONTHS AND BEYOND: ENCAPSULATED ORGANISMS (Pneumococcus and H. B-cell lymphoproliferative disease can be fatal (high fever.13 Clinical Cases I. Flu) AND VZV.Coli. . . HSV-2 = Anogenital Disease. C.EBV: 1-3 months. but they also inhibit development of VZV specific immunity => high risk when treatment stopped. If Allergic. . Diltiazem D.Herpes Simplex: 6 weeks in seropositive host or donor. Occurs between 2 weeks and 4 months. E. GN Organisms).BONE MARROW TRANSPLANT: FIRST MONTH: Give Prophylaxis TMP-SMX or CIPROFLOXACIN for GN bacteremia prevention. or graft failure.Answer : C Transplantation facts #2 . Prevent by Acyclovir in seropositives. Gondii.Besides cyclosporine. bone marrow suppression. II.Answer : D 4.Answer : C 3. Strep.Answer : E 2. . which one of the patient's current medications is associated with the induction of gingival hyperplasia? A. WBC recover in 2-4 weeks. Treatment includes combination of IV GANCICLOVIR AND CMV IG.CMV: Typically 30-60 days. . D. AND WOUND INFECTIONS (Due to surgery). Azathioprine C. Warfarin 1. HSV-1 = Esophagitis. OTHER: . they do have LONGER IMMUNOSUPPRESSION. Treatment with Ganciclovir and Immunotherapy. Treat with HIGH DOSES OF ACYCLOVIR. SECOND MONTH: CMV Disease is a major concern. Prophylaxis includes ORAL GANCICLOVIR. Risk only if donor is seropositive and recipient negative. Higher dosages and serum levels of cyclosporine are associated with an increased incidence and severity of hypertrichosis.SOLID ORGAN TRANSPLANT: The organisms are different from BMT recipients because solid organ recipients do not go through a period of neutropenia. E. Patient should still be on TMP-SMX up to one year. However. All of the above statements are correct. It also prevents T.<1 month: EXTRACELLULAR BACTERIA FROM SURGICAL WOUNDS OR ANASTOMOTIC SITES (Staph.
Influenza every year .Meningococcal Vaccine . . Neisseria Meningitidis and Inactivated Polio at 12 months.No Varicella Vaccine. Flu Vaccine . If contact with chickenpox => VZV IG ASAP (Within 96h).COLI. Tetanus.Japanese Encephalitis . and then 12 months thereafter. . OTHER .g. .Typhoid immunization (not the live one). Diphtheria.2 months (TO YEARS): EBV LYMPHOPROLIFERATIVE DISEASE = lung and heart transplants are most likely to develop EBV-induced B cell proliferation. If contact with measles => Immune Globulin Post-Exposure Prophylaxis (PEP). CANDIDA 1-6MONTHS: CMV LUNG INFECTION: * By Organism: <1 MONTH: LEGIONELLA. Meningitidis.No MMR before or after due to immunosuppression. Hepatitis B .>6 months: infections characteristic of patients with defects in cell-mediated immunity e.Varicella V.. various fungi. ENTEROCOCCUS. III.MMR at 24 months. KLEBSIELLA. H.TRAVEL VACCINATIONS FOR IMMUNOCOMPROMISED PATIENTS: ANYTHING APPROPRIATE TO THE AREA OTHER THAN LIVE VACCINES: 1.INFLUENZA Every year. Flu Vaccine. PSEUDOMONAS.1-6 months: CMV infection organ-specific + glomerulopathy in kidney transplant + bronchiolitis obliterans in lung transplant + premature atherosclerosis in heart transplant + vanishing bile duct syndrome in liver transplant (progressive cholestasis with normal LFT's).Hepatitis A. Nocardia.MMR . IV.. N.INFLUENZA 2. . SOLID ORGAN TRANSPLANT: BEFORE TRANSPLANTATION: . and other intracellular parasite. .Pneumovax. Repeat every 6 years. Household contacts should get IPV as well.Pneumovax before. .IPV .Live Typhoid .YES: .NO: .Live Yellow Fever .VACCINATION OF TRANSPLANT PATIENTS: BMT Patients: AFTER TRANSPLANTATION . infections with Listeria monocytogenes. H.TIMELINE AND COMMON CASE SCENARIOS AFTER TRANSPLANT: 1) UTI: <1 MONTH: E.
If no obvious infection site and patient febrile: AMPHOTERICIN B 2. PCP. Nocardia.Nodular Infiltrates: Fungi.LABS: Granulocye count<500 . Drug-induced. ASPERGILLUS.ANTIBIOTIC PROPHYLAXIS: + TRAVEL IN FUNGAL RISK AREAS (Coccidio. CHF. ASPERGILLUS. + HISTORY OF EXPOSURE TO TB: INH IF RECENT POSITIVE CXR. Gondii.(Sputum/Urine/Skin biopsy accordingly) NEXT: Initial Broad-based ATBx (GN and GP aerobes) FOLLOW-UP: 1. LISTERIA M.which statement is correct about immunization in this pt? a:influenza vaccine at 4mo following transplant and annually thereafter b:MMR at 24mo following transplant c:varicella at 6mo following transplant d:HBV at 12 mo following transplant e:Td at 6mo following transplant Case #2: Q 300 A 31yo man with diabetic nephropathy undergoes an uneventful renal transplant from his sister. Ganciclovir x 100days VII: ALGORITHM OF DIAGNOSIS AND TREATMENT OF FEBRILE NEUTROPENIC PATIENT: .steroids&cyclosporine. CMV. histoplasm) => Amphotericin B or imidazoles + LATENT VIRUSES: ACYCLOVIR AFTER BMT for HSV and VZV.Diffuse Infiltrates: CMV. TOXOPLASMOSIS >6MONTHS: CMV RETINITIS. Radiation Pneumonitis. 3. PCP.. Acyclovir x1 day prior -> Post-op: Bactrim x 1 year. ASPERGILLUS. Chlamydia. CNS: 1-6 MONTHS: LISTERIA MONOCYTOGENES. GANCICLOVIR IN CMV SEROPOSITIVE DONOR OR RECIPIENT + LATENT FUNGI/PARASITES: TMP/SMX or DAPSONE/PYRIMETHAMINE x 1 year for PCP and T. CLINICAL CASES: Case #1: Q309: U visit a 25 yo male pt who just received BM transplantation.CXR .on . Mycobacterium. CRYPTOCOCCUS.If no obvious infection site and patient afebrile: Con't ATBx. NOCARDIA VI. Diffuse Alveolar Hemorrhage. Recurrent tumor . + in BMT: -> Pre-op: Fluconazole x 1week before procedure.his immunosuppressive regimen includes azathioprine. LEGIONELLA > 6 MONTHS: NOCARDIA.If obvious infectious site found: CON'T BROAD-BASED SENSITIVITYORIENTED ATBx. Peri-rectal . IV Catheter.BCx . MUCOR * By CXR findings: . Toxo.1-6 MONTHS: CMV PNEUMONITIS.Localized infiltrates: Legionella .INITIAL EVAL: Skin Lesions.
He received a cadaveric renal allograft 1 yr ago&is now taking prednisone. a. fever.What’s the most likely diagnosis? Case #5: More prevalent in small bowel transplant than other transplants .8.T:37.urticaria 2wk after a heart transplant. e. Is it graft rejection or cyclosporine nephrotoxicity? Case #8: 60 year old man.chronic rejection.graft versus host disease. 4 weeks later: rapid rise of creatinine. 6 months after renal transplantation comes with cough. and oligouria.hyper acute rejection.The immunosuppressive agent most responsible is: a:azathioprine b:cyclosporine c:prednisone d:antitymocyte globulin Case #7: Renal transplant patient on immunosuppressants among which cyclosporine. c. SOB. edema.Serum Cr:1.azathioprine&cyclosporine.The allograft is not enlarged or tender.but Ph.What's the most appropriate next step of management? a:start gancyclovir b:start broad-spectrum Antibiotics c:Administer filgrastim d:Administer FK50 e:decrease cyclosporine f:increase cyclosporine g:decrease azathioprine h:increase azathioprine i:withhold stroids j:administer stroid boost k:obtain renal US Case #3: Q366: A 30 yo man on vacation has had symptoms of URI for 1 wk&persistent headache for 3days.fever.5mg/dl.E shows no abnormalities.acute tubular necrosis. b. acute rejection. .he now has a fever.WBC:5000. Which test should u do next to evaluate the pt’s condition? A:CT scan of the head B:LP C:xray of skull sinuses D:U/A E:Cxray F:serum cyclosporine measurement Case #4L Q373: A 32 yo man received an allogenic renal transplant 50 days ago&has been taking TMP-SMZ.malaise&evidence of hepatitis followed by progressive dyspnea&hypoxemia with a diffuse interstitial pulmonary infiltrate developing over 5-7days. Case #6: Q445: A 37 yo man develops arthralgias.but u notice on his routine lab tets that his WBC is 2000.related to the presence large amount of lymphoid tissue. d.there’s no nuchal rigidity&there r no focal neurologic findings.postoperative day3 the pt is doing well.
perivascular mononuclear infiltrate C. as well as repeated episodes of acute rejection and lung infection. At 2 weeks after transplantation. except for which one? A. The patient was CMV negative. the patient was started on standard immunosuppressive therapy with intravenous cyclosporine. Submucosal lymphocytic infiltrate with submucosal granulation tissue B. Which of the following histologic findings.fever 100. which was treated with intravenous methylprednisolone. Methylprednisolone plus antilymphocyte globulin C. with occasional foci of parenchymal or vascular necrosis D. Best step in treatment: a. Postoperatively. with intimal thickening and sclerosis of small airways. Which one of the following histologic descriptions best characterizes acute mild rejection? A. Methylprednisolone plus plasmapheresis with immunoglobulin replacement D. gancyclovir b. Approximately 3 months after successful treatment of her acute rejection episode with Methylprednisone. grade A3/4 rejection. azathioprine. Sputum is positive for Gomori coloration. For repeated recurrences of rejection. and the donor was CMV positive. treatment could include any of the following options. Her acute rejection episode resolved with this therapy. Lymphocytic bronchiolitis with CMV inclusion bodies . Dense perivascular lymphocytic infiltrates with extension into alveolar septae Case #10: . are indicative of chronic rejection? A. Infrequent perivascular mononuclear infiltrates B. Imipemen e. trimetoprim IV c. routine biopsy surveillance showed the development of acute mild rejection. Review of the biopsy specimen revealed findings suggestive of chronic rejection as well as acute rejection. The patient continued to manifest reduced FEV1. Conversion from cyclosporine to tacrolimus Case #11: The patient was treated with methylprednisolone and antilymphocyte globulin. Crackles were heard in the right lung base. extending to alveolar ducts and alveoli D. for which the patient remains under treatment. Other postoperative complications included diabetes mellitus. Histologic examination of a transbronchial biopsy specimen showed severe. Intravenous methylprednisolone alone B. Intraluminal plugs of granulation tissue in small airways. and prednisone. Frequent perivascular infiltrates around arterioles and venules. but she was left with reduced lung function (FEV1 reduced by approximately 25% compared to baseline). Submucosal fibrosis of terminal bronchioles. Acyclovir Case #9: The patient is a 28-year-old woman who 7 years previously underwent bilateral lung transplantation as treatment for cystic fibrosis. Frequent perivascular infiltrates around arterioles and venules C. Amphotericine d. the patient’s lung function began to deteriorate. Both were negative for hepatitis antibodies.
On POD7. Doppler ultrasonography (Doppler US) of portal vein and hepatic artery exclusively B. Case #3: the ANSWER is:B: doing LP to rule out cryptococal meningoencephalitis Chief complaint is heacache Case #4: CMV Pneumonitis. Crackles or wheezes at lung bases Case #13: A 45-year-old white male was transplanted for Child C alcoholic liver cirrhosis with portal thrombosis.IPV. Liver biopsy exclusively D. T-tube cholangiography. . T-tube cholangiography exclusively C. Chest X-ray was non contributive. Vascular catheters were exchanged and antibiotics (Ciprofloxacine-Ciproxine(r) and Vancomycine-Vancocin(r)) were instituted. All of these procedures (Doppler US. urine. Cold ischemia time was 10 hours and a peroperative thrombectomy had to be done.if he's immunocompotent 4-varicella not recommended CASE #2: the answer is g: Broad antibiotics and filgatrim are started only if the count falls below 500. The usual postoperative rise of aminotransferases (ALT and AST) was observed with a peak of 2.the schedule for this pts: 1-influenza vaccine>6mo following transplant&annual therafter 2-inactivated vaccines like Td.the pt’s decrease in WBCs is secondary to azathio toxicity and the most appropriate step is to decrease its dose. Firthermore. liver biopsy) step by step if the previous test does not give a definitive diagnosis ANSWERS TO CLINICAL SCENARIOS: Case #1: Answer is D: HBV at 12 mo following transplant Pts who recieved BMT. bile and transcutaneous portions of the catheters were sent to the bacteriological laboratory for direct examination and culture. Patient developed fever (38°C) on POD4. abdominal fluid. At that time echo-Doppler of the portal vein and hepatic artery was normal.HBV.both WBC&plts should be monitored in the immediate posttransplant period. Next step in diagnosis? A. which one of the following is most strongly associated with the diagnosis? A. Deteriorating expiratory airflow E.7 mg/dL together with alkaline phosphatase: 320 IU/L (N < 250 IU/L) whereas aminotransferases continued to drop. Orthotopic liver transplantation (LTX) was performed.Case #12: Although several nonspecific clinical signs and symptoms may be suggestive of bronchiolitis obliterans. bilirubin rose to 11.PPV after 12mo 3-MMR after 24mo. the major side effect of azathioprine is BM toxicity. Progressive dyspnea C.760 IU on POD2. Fever subsided whereas bacteriological work-up was negative. Blood.should be revaccinated. Nonproductive cough B. Fatigue/reduced exercise tolerance D. throat.
If inflammatory cells are present (characterized by a submucosal mononuclear infiltrate of lymphocytes. Case #10: The correct answer is A. Case #12: The correct answer is D. oligouria after initial function. the lesion is considered "active". endothelial vaculoization). to halt acute rejection or to treat potential bronchiolitis obliterans. Cyclosporine trough level>200ng/ml. manometry: capsular pressure is<40mmHg. necrosis and sclerosis). Case #11: The correct answer is B. reflecting declining expiratory airflow. Biopsy: arteriolopathy (intimal thickening. affecting a majority of transplant patients. hyalinosis. if inflammatory cells are absent. it is neither preventable nor treatable. Manometry intracapsular pressure >40mmHg.Transplant rejection: <4weeks. Case #9: Answer is B. Early acute rejection is a common occurrence. leading to the clinical manifestation of progressive expiratory airflow obstruction. the lesion is "inactive". US: unchanged graft corss-sectional area. acute mild rejection (grade A2) is characterized by the presence of frequent perivascular mononuclear infiltrates around the arterioles and venules.Case #5: d. which is characterized by lymphocytic bronchitis or bronchiolitis and may be related to infection or other causes. Biopsy: endovaculitis (intimal arteritis. Typical therapy consists of intravenous methylprednisolone in three successive daily doses. Chronic allograft rejection is characterized histologically by the findings of bronchiolitis obliterans. acute rejection can be prevented by immunosuppressants. Gomori offers best contrast for Pneumocystis Carinii (dark brown-black). the next option is usually to add treatment with a cytolytic drug. Rsponds to decreasing cyclosporine. antithymocyte globulin. . or antilymphocyte globulin. Case #6: d:antitymocyte globulin serum sickness Case #7: Cyclosporine Toxicity To differentiate the two: . This pattern of infiltrates must be differentiated from airway inflammation (B). Responds to increased steroids or antilymphocyte globulin. chronic rejection occurs after few years. IV Trimethoprim-Sulfamethoxazole. the antibodise that are already formed are resposible. has been shown to be a reliable and consistent indicator of impaired graft . hyper acute rejection occurs when there is serum incompatibility. rapid rise in creatinine. When corticosteroids alone fail to stem the decline in lung function. US: increased graft cross-sectional area. Case #8: PCP pneumonitis. MRI: loss of distinct cortico-medullary junction + swelling + density similar to that of Psoas and fat tissue. gradual rise in creatinine.cyclosporine toxicity: >6 weeks use. it resolves in few days or weeks. Patchy narrowing or obliteration of the small airways follows. such as OKT3 monoclonal antibody. and monocytes). The FEV1 score. it is chronic deterioration in organ function. acute tubular necrosis is a normal phenomenon after kidney transplant. graft versus host disease. fever and weight gain. Cyclosporine trough level <150ng/ml. afebrile. that occurs due to storage and handling etc. The hallmark sign is the proliferation of submucosal or intraluminal fibrous tissue in the terminal bronchioles. which in this patient was successful in resolving her rejection episode. plasma cells.
excluding bile leak) and then #3: CTscan.htm .Merck Manual: Transplantation .Harrison: Infections in Transplant Patients . step by step if the previous test does not give a definitive diagnosis": #1: Liver and Abdomen US as well as Doppler US (normal: excluding hepatic artery and portal vein thrombosis). which is based on biopsy results) is defined as a deterioration in FEV1 of more than 20% compared to the baseline FEV1.function. The diagnosis of bronchiolitis obliterans syndrome (as opposed to bronchiolitis obliterans.be/erasme/edu/gastrocd/Case35/C35r.net Forum: Previous posts Remembered Question on Transplantation Let's say you have a patient who recently received a renal transplant. the baseline score is an average of the two highest postoperative measurements taken 3 to 6 weeks apart. A biopsy of the kindey reveals rejection.ac. The decline in FEV1 must be present for at least 1 month and cannot be due to other factors such as infection. Case #13: The Algorithm in the presence of abnormal liver tests in a liver transplanted patient is "All of these three procedures. abundant councilman bodies (HCV) Ground glass hepatocytes.Liver dysfunction in a patient having liver transplant http://www. positive immunoperoxidase (HBV) Fibrous and inflammatory septa No bile duct loss * Acute rejection Interval < 2 months Triade: Activated lymphocytes. After a short time you notice a decline in renal function.USMLE. Because histologic proof of bronchiolitis obliterans cannot always be obtained. acute rejection.ulb. the International Society for Heart and Lung Transplantation in 1993 proposed using spirometric data to reach the diagnosis. or bronchial anastomatic complications. Differential diagnosis between hepatitis and rejection of the liver allograft * Hepatitis Interval > 2 months Lobular necro-inflammation Steatosis. Liver Biopsy and microbiological examinations. What do you do? . eosinophils. PMN > 50% bile duct lesions Endothelialitis * Chronic rejection Interval > 2 months > 50% loss of bile ducts Arteriopathy ± centrolobular necrosis/fibrosis Portal fibrosis References: . T#2: T-tube cholangiography (Normal.
and coumadin should b stop 48 h b4 surgery. The bacteremia with this agent is almost pathognomonic for the latter General Considerations: Streptococcus bovis is the main human pathogen among nonenterococcal group D streptococci..by the way hasan u r doing great job and valium u tooo. It usually takes care of the usual acute rejections in the post op period. If mechanical ventilation... A strong association exists between S bovis bacteremia with or without endocarditis and underlying malignancy or premalignant lesions of the colon. it is by default: 21%.a..i will post every day some qs or facts like u and valium do hasan bcz thats why this forum is. Some authors have found a similar relationship between bacteremia (or endocarditis) and liver diseases or nonmalignant diseases of the colon. they use infusion Methylprednisone alone.. The portal of entry for S bovis bacteremia is the GI tract. Work-up: . Whether S bovis plays a causative role in colon cancers or is only a marker of the disease is unclear.ifu dont have that book dont go for exam ..there.and so many others really nice ppl who post qs everyday ...believe me its a fact.. Bovis and colon CA? Ans: bacteremia with streptococcus bovis makes it mandatory to rule out the CA colon... increase the doses of the immunosuppresive drugs b. FiO2 has to be reset according to ABG's and different parameters discussed previously in my review: MEchanical Ventilation LEcture and Case Scenarios.to. Sometimes. When to d/c asprin or antiplatelets prior to surgery? asp we d/c befor i wk of surgery and heparin 4 h b4 goingto surgery its half lif is 90 minutes and it doesnt cause bad efefct during surgery like bleeding andocp we stop imonth b4 surgery bcz it cause dvt and smoke cessation should b done at least 6 wk.wish u all the best hasan and valium.. in solid organ transplant.. FiO2 simply put Inspiratory Fraction of Oxygen: That's how much percent of Oxygen is delivered in the air breathed by the patient in the mechanical ventilation. S bovis infection is a well-documented cause of infective endocarditis... remove the transplant surgically ANSWER: increase the dose of immunosuppressive drugs..this forum helped me alot so i will do som ething. The organism also has been isolated more frequently from the stools of patients with such malignancies.... In any event.21 (21%)..just follow valium advice dont read every book just finish what u have and read it coverto cover and it will b more than enough. wait for a week c. but the patient is breathing room air.thats what we do in common practice refrence would b crush and nail the board . every patient with S bovis bacteremia with or without endocarditis should be examined for a GI tract malignancy.goood luck to u and valium and every body else. -.8 wk b4 surgery.. FiO2 in standard atmosphere composition = .try to do recall qs bcz 70% come back to every one. That is if you are to calculate A-a gradient using FiO2 and you find out you don't have it....Gram Stain: Gram-positive cocci .excellent and easy book i will recomond to all..Blood cultures (BCs) are the most important tests.
DOWNS SYNDROME. al mothers have the same possibility of having a Turner girl. it is not anything we can avoid and it is not the result of something that has happened during the pregnancy. which may facilitate outpatient therapy. B. Are there possibilities to have another baby with Turner Syndrome? As previously commented. they are two independent facts. However. Reference: . Then why does Turner Syndrome Happen? There are two theories that try to explain this chromosomal anomaly (the loss of one of the sexual chromosomes): A. If the ovule or the sperm have suffered this chromosomal loss. Resistance mechanism (Van A) is identical to the one identified in most vancomycin-resistant enterococci (VRE).The “MEIOTIC” theory says that during the formation of the ovule or sperms (gametogenesis) some of them could have suffered an error and for this reason they carry a sexual chromosome less. therefore. it is one of every 5000.Emedicine . .The “MITOTIC” theory assures that the loss of one of the chromosomes is not produced in the gametes (ovule or sperm) but it is originated later. Complications for S bovis infection are similar to infective endocarditis caused by viridans streptococci. The most recent investigations support this last theory not the first. IN A PREGANANT LADY GIVING BIRTH TO A CHILD WITH THE DEFECT WHEN SHE ALREADY HAS A CHILD WITH THE DISORDER? TURNER SYNDROME: Can Turner Syndrome be inherited? NO.CMDT . .The barium enema should be performed on patients with S bovis bacteremia or endocarditis. i. The fact of having a Turner girl yet doesn’t increase the probability of having another one.in pairs or chains.: intravenous penicillin G for 4 weeks. if parents show a normal karyotype it is not inherited. Vancomycin is useful for patients with a history of major penicillin hypersensitivity (immunoglobulin E [IgE]-mediated).Medline Genetic Counseling TURNERS SYYDROME. 1 strain of S bovis has been isolated that is resistant to vancomycin. we can say it has happened by chance.. So. Treatment: The antimicrobial therapy for both Streptococcus viridans and S bovis endocarditis is identical. during the first period of the embryo growth (in the first gestation weeks). the person formed from the fertilisation will carry this chromosomal error.Liver ultrasound and CT scan should be performed in cases of associated hepatobiliary disease. Like any chromosomal syndrome. unless any of the parents suffer from an alteration in his/her sexual . Ceftriaxone is an alternative to penicillin and is administered once a day. Turner syndrome is not inherited.e..
if this happened they should consult their doctor. the mainstay of treatment for infertility in PCO is Clomiphene Citrate. Pergonal stimulates follicular maturation directly and therefore has no effect on dysmenorrhea either as far as I understand.restore menstrual cyclicity in 68 to 95 percent of patients treated for as short a time as four to six months.The most important longitudinal (prospective) study of lung function in smokers who have early COPD is the Lung Health Study (JAMA: 272:1497. The chance goes up quickly when the mother is over 34 years.improve insulin sensitivity .Decrease free testosterone levels. . DOWN SYNDROME: Are some people more likely than others to have a baby with Down syndrome? A young mother who has one child with Down syndrome has about a 2 in 100 chance of having another. but 40% will have a mosaic of 45X and 46XX. An alternative: Women who do not respond to clomiphene or are unable to conceive with clomiphene therapy may be treated with human menopausal gonadotropins such as follitropin alpha (Gonal-F). which drug answers her both infertlity and dysmenorrohea problem? Treatment with an insulin-sensitizing agent such as metformin (Glucophage). but the risks from ovarian hyperstimulation and multiple pregnancies remain of concern. Although insulin-sensitizing agents show promise in the treatment of polycystic ovary syndrome. However.decrease serum LH . Furthermore. 75% will result in spontaneous abortion. OCP does have effect on hirsutism by decreasing testosterone and increasing sex harmone binding globulin production in liver. OCP's in PCO inhibit the enogenous secretion of FSH and LH. The risk of Down syndrome increases with the age of the mother. It also goes up when the father is over 60 years of age. Ovulation is successful in approximately 75 percent of women treated with clomiphene. 50% will have a full monosomy. there are no studies of adequate power or design to allow them to be recommended as standard therapy. If the mother has been diagnosed with a chromosome abnormality. she has an increased risk of having a baby with Down syndrome. An older mother will continue to have about the same chance for her age. and restore the cyclicity of menses thereby taking care of the dysmenorrhea. Female with ah/o PCOD and dysmennorhoea wishes to get pregnant .html Smoking Cessation effects: Does it parallel non-smokers? . In addition. In addition.chromosomes. has been shown to: . Risk doesn't increase by maternal age.org/afp/20000901/1079. in a dosage of 500 mg two to three times daily. Of those who escape. In fact one of Clomiphene Citrate's side effects is Dysmenorrhea.aafp. especially in women with normal glucose function. This therapy has achieved pregnancy rates of 58 to 82 percent. 1994): Smoking cessation . Reference: American Association of Family Practice AAFP http://www. but subsequent pregnancy rates are only 30 to 40 percent.
Kronmal RA. hourly between midnight and 6 am. the risk of heart disease is decreased to about the level of never smokers. Smoking and lung function in elderly men and women: the Cardiovascular Health Study.Within three months of quitting. BP: 114/69 mm Hg. the smokers' cough disappears in most people. So by 5 years.e.The risk of having a stroke or a brain aneurysm go down by 30-50% in quitters. et al. et al.: INCREASE) in lung function during the first year.5 to 15 years. no detectable difference in lung function compared with non-smokers . . lansoprazole. The review of systems was notable only for skin allergies. The FEV1 DECLINE then was equal to that of non smokers (20-30 mL/year).e. a few ecchymoses. Morale of this: the earlier you quit the better.JAMA: +>Higgins MW. Lung function was equal to non-smokers older that then 2.postgradmed. due to reversal of nicotine's effects on inducing platelet aggregation and vasospasm. JAMA 1993. the FEV1 should be DECLINING!!!. JAMA 1994.272(19):1497-505 Postinfarction Ischemia Clinical Scenario: A 68-year-old Asian man with a previous cardiac history. He denied any arrhythmias or congestive heart failure.Quit after 60 yo => at 65yo.The risk of lung cancer is decreased by 80-90% after 15+ years of abstinence but never reaches levels of non-smokers. 9 days status-post inferior wall MI. Reference: . and under each eye. After 2 years of abstinence from tobacco. Previously active. There were no indications of diabetes. Episodes lasted 5-15 minutes.5 yo). lateral nose. atorvastatin.5 to 7. . THE RATIO SHOULD NOT BE DECLINING SINCE THE DECLINE IS IN BOTH FVC AND FEV1.The risk of heart attack is decreases by 50% within 24 hours of quitting smoking. Kiley JP. it started in the chest and spread to the throat. then a gradual decline thereafter. and atenelol. His medications included nitroglycerin.htm . and .5 years (i. Connett JE. Other studies revealed the following: .Post GRaduate MEdicine online http://www.: they have the lungs of a 67. Effects of smoking intervention and the use of an inhaled anticholinergic bronchodilator on the rate of decline of FEV1: the Lung Health Study.Quit between 40 and 60 => at 65yo.5 to 82. lung function is equal to that of older patients of 5. His medical history was significant for coronary artery bypass graft surgery twice. . . presented with the chief complaint of chest pain 6 times a night since MI.for more than a year leads a slight improvement (i. . 5 and 12 years ago. His skin showed evidence of excoriation. the man now spent most of his time in bed. Enright PL.269(21):2741-8 +>Anthonisen NR. jaw.com/issues/1998/12_98/hays.Quit before 40yo => at 65yo.Quitting decreases the overall risk of death (all causes combined) by 50% in 15 years as compared to continuing smokers. . The patient's chest pain was pressing and radiating.
If 4th dose given after 4 yo.Three doses of Polio . Lungs and heart were normal. BEta-blockers.Who'll get it?: Especially if pt had angina prior to the MI or non-ST Seg Elev MI. Despite numerous therapies including intra-aortic balloon angioplasty. repeat infarction. 4-8 weeks apart.CMDT . . . or sudden death. Hypercholesterolemia was also noted.DTaP: a five-dose series.What is it? Anginal pain at rest. reflecting an acute MI. POST INFARCTION ISCHEMIA . References: . . Angiography demonstrated multiple vessel occlusion and good motility. INQUIRING ABOUT CATCH UP IMMUNIZATION SCHEDULE +>CHILDREN 4 MONTHS TO 6YO: . People who do not get the vaccine until 13 years of age or older should get two doses. Cardiac enzymes confirmed this.What's the morbidity and mortality of this condition? It is associated with risk for infarct extension.How does it happen?: inadequate blood flow throuh a recanalized vessel /OR/ reocculsion. .Chickenpox (Varicella): at any age if they have never had chickenpox.How it is managed?: Nitrates. .cherry angiomata.and long-term mortality.4 doses of DPT (the last before 4 yo) . . On his chest was a well-healed sternotomy scar with a purple area at the inferior aspect. . 5th dose is NOT necessary. Heparin. REQUIRED VACCINATIONS? .New England Journal Of Medicine CATCH UP IMMUNIZATION SCHEDULE CHILD ABOUT TO ENTER SCHOOL. and plateletglycoprotein IIb/IIIa antagonists. EKG: changed from previously. Aspirin. . which develops within 2 weeks after Acute Myocardial Infarction episode. Trials of Calcium channel blockers for prevention didn't show results suggesting pathophysiology is different from that of Pre-MI angina. .Why is it important?: increased short.Does it happen in the same territory?: There are two forms of post-infarction angina: ischemia at a distance (angina with new electrocardiographic changes distant from the acute infarct) and ischemia in the infarct zone (angina with new electrocardiographic changes limited to the leads originally involved by the acute infarct). Lower extremities were cool with venous stasis. this condition remains associated with a poor prognosis.What if medical therapy contraindicated? Then take patient to Cath lab and do PTCA or CABG. 4 weeks should elapse between #1/#2/#3 then 6 months period elapse between 3rd/4th and 4th/5th dose. .Incidence: 30% of patients.Two doses of MMR OLDER CHILD NOT IMMUNIZED.
Who needs it? Adults born after 1957 (patient is >47years old now). 11 months between 2nd and 3rd doses. . 1 month between 1st and 2nd doses. only one is enough. Every ten years thereafter. • Illicitdrug users.Hepatitis B: 3 doses with 4 weeks between #1 and #2 and 8 weeks between #2 and #3 . If 1st dose given after 15 months old. . Who needs it? Travelers to endemic areas. College students and health care workers are advised to have a second dose (at least 4 weeks between doses). • Anyone on kidney dialysis. Anyone who has chronic heart. One dose for those with increased risk (travel to meningitis belt. sickle-cell disease.Lyme Disease: 3 doses. .Polio: IPV 3 doses 4 weeks apart.Influenza: 6 months or older. Patients should get boosters every 10 years.Hemophilus Influenzae: 4 doses with 4 weeks interval if started before 12 months old. endemic areas. Who needs it? Adults age 65 and up. Mumps and Rubella: Children should get two doses of MMR vaccine anytime provided 4 weeks have elsapsed between the two.Varicella: 2 doses. • Travelers to endemic areas.. .Who needs it? At risk populations: All adolescents ages 11-19. healthcare personel) . diabetes. lung.Hepatitis B: Hepatitis B 3 doses. 4-8 weeks between doses.Pneumococcal: If before 65yo. • Anyone with chronic liver disease or clotting-factor disorders. • Prisoners.MMR: 2 doses 4 weeks apart. at least 4 weeks between 1st and 2nd doses and at least 8 weeks between 2nd and 3rd. Stop giving it after ANY dose given >15 months old. or liver disease. alcoholism. repeast seconds shot 5 years later. • Sexual partners of and people who live with hepatitis B carriers. ADULT NOT VACCINATED AS A CHILD: .Hep B: 3 doses 4 weeks between #1 and #2 and 8 weeks between #2 and #3. . • Health-care workers. stop there (Total 2)!!!. One shot/year for designated population . Who needs it? Anyone who frequently spends time in tick-infested habitat in endemic areas should consider the vaccine. • Clients and workers in institutions for the mentally impaired. and so on. or compromised immunity or who has had spleen removed. and 6 months interval between #2 and #3. • Male homosexuals with multiple partners.Measles.MMR: 1 dose. should get one shot. • People who have multiple sex partners or abuse injectable drugs. dorms. who've never been immunized. . . Who needs it? Anyone who wasn't vaccinated with it before. 2 doses at least 6 months apart. only ONE dose is needed!!!! If second dose given after 15 months old.Varicella: 2 doses 4 weeks apart. +>CHLIDREN OF 7YO TILL 18 YEARS: . .Tetanus/Diphteria: If receiving for the first time. After 65yo. If third one is given after 4 yo. .Polio: 4 doses at 4 weeks interval each.Td: 3 doses with 4 weeks interval between #1 and #2. .Hepatitis A: 2 years or older. • Food handlers in high-incidence communities. patients should get a series of three shots: the second and third will follow two and six months (respectively) after the first.Meningococcus: 2 years or older. . . no need for a 4th dose!!!! .
DtaP: 4 doses .Multiple Sclerosis .Meniere B.Influenza: once a year if indicated ..CDC.Hemophilus Influenza: 1 dose .Behavioral Teratogen . Fusion of teeth .Hepatitis B: 3 doses if indicated .Polio Vaccine: 3 doses of IPV: The first dose at any time.com/health/vaccines/articles/0. Flat nose bridge.html Teratogenic effect of Isotretinoin WHAT KIND OF TERATOGENIC EFFECT DOES ISOTRETIONON CAUSE? Answer: .Polio: 3 doses (because >4yo) .http://www.Meningococcus: 1 dose if indicated .Cardiac and CNS abnormalities .MMR: 1 dose. Questions Transient sensiry symptom electric shock-like precipitated by neck flexion is a recognized feature of: A.10335.org/adultimmunizations. . .Varicella: 1dose (2 if she were 13yo) .Polio Vaccine Facts http://www.Polio: 3 doses if indicated. and health care workers treating patients who could have polio ANSWER TO PREVIOUS QUESTIONS FROM EXAM: So for example a 6 yo who wasn't immunized before and mother brings her in now for that should get: .giv/nip .Craniofacial anomalies: Cleft lip and Cleft Palate.00.xml .www. maxillary and mandibular hypoplasia. The third dose 6 to 12 months after the second.Td: 3 doses then every ten years get booster . Repeat once after 65yo.Thymus developmental abnormalities isoretinoin also increases triglycerides in the body . .aafp.Presbycusis C.Hepatitis B: 3 doses An 35yo adult who wants to catch up: . Who needs it? people traveling to areas of the world where polio is common.parentsplace.Pneumococcal: Once if indicated.166606_222430.MMR: 2 doses .Varicella: 2 doses . The second dose 1 to 2 months later. laboratory workers who might handle polio virus.Hepatitis A: 2 doses if indicated References: .
. the plasma water is approximately 93% with the reminaing 7% made of Lipids and proteins. and visual mostly in delirium. :) It's one of the remembered MCQ's Patient with classic retrosternal chest pain of GERD.immunization for pnemococci &H. Falletta JM.inf. but the measured sodium concentration in the total plasma volume will be reduced (since the specimen contains less plasma water). PE: thick skin of finger and toe pads. Prophylaxis with oral penicillin in children with sickle cell anemia: a randomized trial. Why does hyperlipidemia cause pseudohyponatremia Hyponatremia associated with normal plasma osmolality can occur when there is a reducation in the fraction of plasma that is water. . In normal subjects.Acoustic Neuroma This is Lhermitte sign beleive it or not. (source Medscape) "Penicillin prophylaxis of patients with sickle cell anemia significantly decreases the risk of septicemia and death due to encapsulated micro-organisms and is recommended for all children starting at 2 months of age. Woods G. Has multiple sex partners.. and sometimes painful bowel movements. Ans: Gonorrhea or the rectum. soreness. Verter JI.Aminoglycosides E. Discontinuing penicillin prophylaxis in children with sickle cell anemia.. bleeding..penicillin prophylaxis till 5yrs age. It's Multiple Sclerosis. Reference: the Prophylactic Penicillin Study (PROPS)multicenter. Verter JI.25:1593-99. the plasma water sodium concentration and plasma osmolality are unchanged. or hyperproteinemia (as in multiple myeloma).D.it was agreed that a 14-valent pneumococcal vaccine would be administered to all children at 1 year and 2 years of age. a normal plasma sodium concentration of 142mmol/L actually represents a concentration in the physiologically important plasma water of 154 mmol/L. -> delerium and schizo have what in common? waxing and waning memory impairment hallucination family hx of psychopathology social withdrawal ANS: Hallucinations.. et al. However. In a child with sickle cell disease 1. They're auditory in schizophrenia. In these settings. Thus. Gaston MH. 2. anal itching.". double-blind. Ds? Ans: Scleroderma Young man come to clinic with anal discharge. N Engl J Med 1986.127:685-90. J Pediatr 1995. the plasma fraction may fall below 80% in patients with marked hyperlipidemia (as with lactesent serum in uncontrolled diabetes mellitus). Do we have to give both or any specific indications for each? Thanks Ans: I would say both according to my review. Woods GM. placebo-controlled trial. since infants may not be protected by maternal antibodies beyond that time.
THAT'S THE ANTIBODY CIRCULATING IN THE PATIENT'S SERUM. the distal port measures pulmonary artery pressure (~ 30/15 mmHg) and the proximal port measures right atrial pressure (~ 0-2 mmHg). e. e. Patient's RBC's exposed to anti-D. Pulmonary Capillary Wedge Pressure REVEALED Pulmonary Capillary Wedge Pressure The measurement of pulmonary capillary wedge pressure (PCWP) provides an indirect measure of left atrial pressure and is particularly useful in the diagnosis of left ventricular failure and mitral valve disease. A balloon-tipped. The balloon is then deflated. When this occurs.Serum .g.mitral stenosis . These ports are connected to pressure transducers.g: Mother's serum to see if there are CIRCULATING ANTI-D ANTIBODIES.g.pdf Coombs test mystery REVEALED You take the patient's blood specimen and centrifuge it.g. e. #2: INDIRECT COOMBS: Take the patient's SERUM and add to it KNOWN RBC's. There is one opening (port) at the tip of the catheter (distal to the balloon) and a second port several centimeters proximal to the balloon.ANTIBODY SCREEN DETERMINED BY INDIRECT COOMBS TEST.TYPE AND RHESUS DETERMINED WITH DIRECT COOMBS TEST . acts as a long catheter which measures the blood pressures within the pulmonary veins (this pressure is virtually the same as mean left atrial pressure). The balloon is then inflated with air using a syringe (the balloon volume is about 1 ml) and this occludes the branch of the pulmonary artery. e.: BABY'S SERUM to see if there are CIRCULATING ANTI-D ANTIBODIES therefore COATING BABY's RBC's.: DIRECT COOMBS USED TO KNOW BABY'S RHESUS TYPE IF MOTHER IS RHESUS NEGATIVE. The measurement is made as follows. The recorded pressure during balloon inflation is similar to left atrial pressure because the occluded vessel. QUICK REVIEW: . reaches a stable lower value that is very similar to left atrial pressure (normally about 8-10 mmHg). e. and anti-AB. Wherever there is coagulation.kbsm.: ABO TYPING. Wherever there is coagulation. the pressure in the distal port rapidly falls. When properly positioned in a branch of the pulmonary artery. along with its distal branches which eventually form the pulmonary veins. A PCWP exceeding 15 mmHg suggests . Patient's RBC's exposed to anti-A. Separate: . the right ventricle.: RHESUS TYPING. and then positioned within a branch of the pulmonary artery. THAT'S THE ANTIGEN COATING THOSE RBC's. multi-lumen catheter (Swan-Ganz catheter) is advanced from a peripheral vein into the right atrium.g.acta-clinica. and after about 10 seconds.hr/Acta2002/ACTA2002_2/05RATK~1.Reference: Systematic approach to hyponatremia http://www.RBC's #1: DIRECT COOMBS: Take the RBC's and expose them to KNOWN ANTIBODIES. anti-B.
in order to permit. Nerve Section Clean wound cut w/laceration and incomplete section of the nerve.. CLOSED INJURY: USUALLY NOT EMERGENT REPAIR OF THE NERVE UNLESS SURGERY INDICATED FOR OTHER PURPOSES (E. not being able to recognizee the nervous lesion. • COMPLICATED = with contused lips. If there is a paralysis the nerve is usually interrupted and nerve suture must be done under operative microscope. bone.G. the lesion may be: • SIMPLE: = clean-cut lips and involvement limited to => the risk is to merely practice a skin suture. Other indications: . poli-tissutal involvement (nerve.aortic regurgitation . a suture will be practised.mitral insufficiency . If the lesion is clean. but it would be normal or low in non-cardiogenic shock. suture of wound immediately b. skin). SUMMARY AND USMLE TAKE HOME MESSAGE: OPEN LACERATION: SURGICAL EXPLORATION IMMEDIATELY. preferably without curarizing the patient. The wound exposure may be of various types: • Punctiform or minimum • Extended • With sub-amputation Moreover.: VASCULAR). the transmission of this pressure back into the pulmonary vasculature increases pulmonary capillary hydrostatic pressure which can lead to pulmonary congestion and edema.OPEN LESION: RULE OF THUMB: Surgical exploration is imperative in every case of open lesion.evaluating blood volume status when fluids are administered during hypotensive shock (maintain PCWP at 12-14) . vessel.) = > PCWP in caardiogenic will be elevated in the presence of pulmonary edema. a normal excitability of the motor endplate. Review of Emergency Nerve Surgery In this evaluation we have to distinguish two cases: • Open lesion • Closed lesion A.ventricular failure When the PCWP exceeds 20 mmHg. The operation must be done under general or peripheral anaesthesia. and contamination => In these cases the same principles mentioned above are valid .severe aortic stenosis .differentiating cardiogenic from non-cardiogenic (Septic shock . leave the wound open To answer your Q first: Surgical exploration immediately with suture of the nerve and the wound. with the obvious severe medical legal consequences. Nerve dissection must be limited to a few centimetres in order not to damage its vascular contributions. management? a.ARDS. etc. AND SUTURE OF THE NERVE IF INDICATED. during the operation. otherwise if the nerve is frayed for a .
The result is Factor V Leiden is inactivated at a rate approximately ten times slower than normal factor V and persists longer in the circulation. When one has factor V Leiden. Mechanism of action: The function of protein C is to inactivate factor Va and factor VIIIa. Epidemiology: Patients are mostly northern european: Swedish.tract. Reference: http://www-cdu. thus leading to a thrombophilic state by having increased activity of factor V in the blood. Factor Va is an essential cofactor for the factor Xa-catalyzed activation of prothrombin to the clotting enzyme thrombin. Some exceptions exist to this principle.htm factor V Leiden mutation General Considerations: Factor V Leiden is a genetically acquired trait that can result in a thrombophilic (hypercoaguable) state resulting in the phenomenon of activated protein C resistance (APCR). or there is a loss of nervous substance and it is not possible to practice a direct suture. protein C combines with thrombomodulin in order to produce activated Protein C. Subsequently. if the treatment has been correct. nervous grafts will be necessary (Secondary repair). Risk for DVT in case of mutation: 1 in 1000 If heterozygote allele: autosomal dominant If homozygote allele: autosomal recessive Diagnosis: Suspect it when you have: . when associated lesions (usually vascular and/or bone lesions) must be treated.unipi. The recovery of the nerve lesions is usually slow but. Having too much of it will generate too much thrombin and a hypercoagulable state. Activated protein C can then degrade factor Va and factor VIIIa.dc. mesenteric. The first step in this process is the activation of thrombomodulin by thrombin. greek.it/eates4/Invitedspeaker/Trauma/vigasio.med. The mutation refers to the specific G-to-A substitution at nucleotide level in the gene for factor V that predicts a single amino acid replacement (Arg) to (Gln) the cleavage sites for Protein C in the factor Va molecule.CLOSED LESION: usually it is not necessary to explore the nerve in emergency. ADJUVENT THERAPY: Rehabilitation treatment is absolutely necessary in these lesions to prevent and treat stiffness using even orthopaedic devices for hand or fingers. Electrotherapy of the denervated muscles is also suggested.A first venous thrombosis at less than 50 years of age . the factor Va is resistant to the normal effects of activated protein C.Venous thrombosis at unusual sites (such as cerebral.A first unprovoked venous thrombosis at any age Recurrent venous thrombosis . resulting in increased thrombin generation and a mild hypercoagulable state. it can be fairly good. Activated protein C then combines with protein S on the surface of a platelet. portal and hepatic veins) . etc. B.
. bilateral dysmetria. . weakness of his lower extremities. During the interview. uncontrollable trembling.html . He denies associated eye pain and discomfort. They also noted waxing and waning difficulties with speech..No h/o DVT: no prophylaxis needed . Examination of the patient demonstrates slight disorientation. or neurological or neurodegenerative disorders.Heterozygotes with only first episode: Coumadin hemorrhagic risk is 1-2%/year and is greater than <1%/yr DVT risk. an ataxic gait.Pregnancy: no consensus yet.Bleeding times and clotting times are consistently prolonged Important note: The presence of a factor V Leiden allele is not a major risk factor for arterial thrombosis.Venous thrombosis during pregnancy. the patient reveals that has been forcing himself to vomit after almost every meal over the last 6 weeks. Prophylaxis: . and prolonged immobilization. Management: . pregnancy. No prophylaxis needed.nih. and a tendency to doze off easily.Usual management of DVT (Coumadin f/u is 3 to 6 months out patient).A 57-year-old man is evaluated because of progressive memory problems and language disturbance. (Enoxaparin prophylaxis throughout pregnancy?) Reference: . His family states that he would repeatedly ask the same question and started forgetting easily. 2.ncbi.A first venous thrombosis and a strong family history of venous thrombosis The diagnosis of factor V Leiden thrombophilia is made either using a coagulation screening test or by DNA analysis of the F5 gene. turning left instead of right and getting lost in his own neighborhood.org/profiles/factor-v-leiden/details. which encodes the factor V protein. Several months ago. and gait difficulties. epilepsy. Laboratory analyses reveal mild dehydration and hypokalemia. he started noticing increasing difficulty with driving.gov/htbin-post/Omim/dispmim?227400 Dementia Qs 1.Evaluate for other inherited or acquired thrombophilic disorders .Prophylaxis in high risk settings: surgery. .National Library of medicine http://www3. There is no family history of psychiatric illness. . or dysphagia. 3.Prolonged PT. diffuse weakness of the lower extremities.Gene Reviews http://www.geneclinics.Old woman with rapidly developing decreased intellectual abilities with startle myoclonus.nlm. and hypothermia. PT correct by mizing test (adding deprothrombinized rabbit serum). the puerperium. particularly recent events. He has never experienced such symptoms in the past. Labs: . or in association with oral contraceptives or hormone replacement therapy . headache.A 45-year-old man is admitted to the hospital for the evaluation of diplopia. vertical nystagmus worse on downgaze.
and gradually became worse. The family states that he became aggressive. predominantly in the caudate and putamen. He has had problems with speech production. She says that her mother's symptoms began a year or two before. within a year of onset. Her medical history includes gall bladder surgery 10 years ago and hysterectomy 15 years ago for abnormal bleeding. myoclonic fasciculations. Testing reveals difficulties in naming common objects or pictures. astrogliosis and the lack of an inflammatory response. such as difficulty in naming familiar objects and verbal comprehension. MRI reveals enlargement of the ventricles without cortical atrophy 5. talked inappropriately to strangers. MRI typically shows bilateral areas of increased intensity.A 72-year-old man has impaired concentration and an inability to recollect names and appointments. The daughter tells the physician that her mother "walks oddly" and has been falling with increasing frequency. A neurologic examination confirms the presence of moderately severe short-term memory loss associated with disturbances in language. His neighbors caught him stealing things from their back yard. ataxia. with rapidly progressive dementia. The patient repeats the examiner's words and imitates the examiner's gestures.4. somnolence. As a result. starting with a changing gait. Spongiform changes . and his wife persuades him to see a physician. She does not have a tremor. Subsequently. and on neurologic examination. On physical examination. dysarthria. and has developed obsessional cravings for sweets. These memory problems have become increasingly worse over a period of months and begin to interfere with his social and financial activities. #2: CJD again. she is found to have normal strength and muscle tone. pathogenic isoform of the prion protein is designated PrPsc.A 68-year-old woman presents to her primary care physician complaining of clumsiness and urinary incontinence. More recently. Normal prion protein is termed PrPc (cellular). and does not drink alcohoI. while an abnormal. usually following pneumonia. the patient has gained 40 pounds over the past year. On light microscopy. using some phrases repeatedly. the physician notes that the patient has an ataxic gait. followed by urinary urgency and incontinence. ANSWERS: #1: CJD. aneurysms. MRI of the head reveals diffuse cerebral atrophy without focal lesions or tumors. He started to eat a great deaI. and showed insensitivity. She quit smoking fifteen years ago. 6. the patient becomes depressed. and showing a decreased vocabulary. contrary to his past consideration to others. It usually presents in late middle age (50-75 yr). the pathologic hallmarks of CJD are spongiform degeneration.A 56-year-old man is brought to the psychiatrist with a three-year history of progressive speech difficulties associated with altered social behavior. CJD is a degenerative disorder of the central nervous system that is caused by accumulation of abnormally folded protein (PrPsc) particles termed prions. she says her mother has had difficulty remembering things and has "ruined her credit rating" because she forgets to pay her bills. Family history is negative for strokes. or intracranial bleeds. and eventually death.
Mild to moderate depression is common in early stages. and cerebellum. #4: This patient has the classic triad of normal pressure hydrocephalus. However. initial personality change. emotional lability. and toilet functions. Circumscribed ('knife-like") lobar atrophy is the hallmark of Pick disease. Their sense of time and place are lost. In most cases of Pick disease. Some patients are aware of their difficulties. which leads to production of an abnormal tau protein. but spares the posterior part of the superior temporal gyrus and the pre. The common form of this disease typically affects people over age 60. spatial disorientation. mental status changes. and sometimes can be so severe that the postmortem brain weight can be as low as 800 g. bathing. impulse control. The CT makes the diagnosis likely because of the enlarged ventricles. Mental confusion is characterized by impaired awareness. hyperorality (overeating with obsessional craving for certain types of food). prolonged intravenous feeding.occur in the putamen. #5: Pick Disease. patients experience recent memory loss. Various apraxias are common. Presenile onset (under 65 years old). ataxia. #6: This patient has Alzheimer disease (AD). sociability may not be affected at this early stage. patients may have difficulties with sequential motor tasks. A common misconception about Wernicke encephalopathy is that it is seen exclusively in alcoholics. Classic symptoms and signs include "Wernicke's triad": acute mental confusion. thalamus. The symptoms of Pick disease occur because the frontal and temporal lobes are affected. and maintaining socially appropriate behavior. energy and enthusiasm. causing frustration and anxiety. and inability to concentrate. MRI scans may later show hippocampal atrophy. Most cases are idiopathic. Subarachnoid hemorrhage or meningitis are risk factors for the future development of NPH. leading to difficulties with dressing. leading to a . Prolonged vomiting and malnutrition. Compared to Alzheimer disease. the orbital frontal lobe. and diminished judgement. NPH is a disease usually found in older adults. consisting of urinary incontinence. progressive language dysfunction. eating. and ophthalmoplegia. and malabsorption syndrome can also be a potential cause of thiamine deficiency. #3: This is Wernicke encephalopathy caused by a nutritional deficiency of thiamine. and disinhibition are the key features of this disease. memory loss and impairment of intellect occur at later stages of the disease. hunger strikes. These lobes are important for language skills. The atrophy affects the anterior temporal and frontal lobes. In the early stage of AD. The wide-based ataxic gait results from cerebellar dysfunction. and gait disturbance. the cause cannot yet be determined. Horizontal or vertical nystagmus and paralysis of lateral rectus muscles are common. there is a strong genetic component in certain families. Pick disease is a rare form of neurodegenerative disorder characterized by a distinct progressive dementing process.and postcentral gyri. the most common cause of dementia in the Western world. either alone or in combination with vestibular dysfunction. and the medial temporal lobe. others are seemingly unaware of their symptoms. cerebral cortex. although not all the patients present with all of these. Ocular abnormalities are the hallmarks of this disease. eating disorders. and are due to impaired cerebrospinal fluid absorption. problem solving. language difficulties (especially word finding). personality changes. both recent and remote. caudate nucleus. A mutation on chromosome 17 has been identified. His symptoms are typical of early AD and the diffuse cerebral atrophy is also characteristic. Surprisingly. The intermediate stage is characterized by a worsening memory.
THEN I WILL DUPLICATE THE REVIEW OF CAT SCRATCH DISEASE.left axillary node. with resolution occurring over weeks to months. ----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------CAT SCRATCH DISEASE REVIEW: . but after 30 days there was no difference in lymph node volume. It is clear that for the majority of patients. In end-stage AD. Death generally results from malnutrition.8.is not correct? A:A scratch by a kitten is more likely to cause the disease than a scratch by an adult cat B:the presentation of skin nodules is a self-limited condition&corticostroids r not recommended C:boys r affected more often than girls D:Warthin-Starry silver stain useful to show the organisms E:azithromycin decreases the duration of disease in 50% of patients if prescribed during the first 30 days F:Incision and drainage of nonsuppurative nodes should be avoided because chronic draining sinuses may result FIRST THE ANSWER TO THE MCQ.She developed erythematous nodules and plaque over both shins 1 wk later.a red left eye without any pain&discharge&a left preauricular lymphadenopathy. 10days later she had a tender. secondary infections. the answer is:E:azithromycin decreases the duration of disease in 50% of patients if prescribed during the first 30 days A case of CSD with erythema nodusom(which is self-limited&corticostroids have no effect)&Parinaud's occuloglandular syndrome:the most common atypical presentation. clinical benefit. and uncooperative. but are at risk for accidents resulting from their confusion. the disease is self-limited.host of behavioral problems. Sometimes they can be quite aggressive.T:37. and that treatment affords minimal.from which no organism was grown on routine culture. The involved eye is usually not painful and has little or no discharge.Aspiration of the axillary node recovered pus. A conjunctival granuloma may be found at the inoculation site. which can alternate with being socially withdrawn and passive. Suppurative lymph nodes that become tense and extremely painful should be drained by needle aspiration. The typical duration of the disease is 8 to 10 years. Cat Scratch Disease Vs Cat bite This is an old MCQ from Orbit #360: A 6yo girl was scratched on the left hand by a cat. patients are unable to walk or perform tasks of daily living and their recent and remote memory is gone.Direct eye inoculation as a result of rubbing with the hands after cat contact is the presumed mode of spread. agitated. Which of the following statements regarding the most likely diagnosis. which may need to be repeated. No other clinical benefit was found. Incision and drainage of nonsuppurative nodes should be avoided because chronic draining sinuses may result. if any. and heart disease. but it may be quite red and swollen. including wandering and becoming lost.which is unilateral conjunctivitis followed by preauricular lymphadenopathy. They can still ambulate.noted in 2–17% of patients. A small prospective study of azithromycin shows decrease in initial lymph node volume in 50% of patients during the first 30 days.
may last for days to weeks. inguinal) is the predominant clinical feature of CSD. encephalopathy (2%).to 1-cm papule or pustule) at the site of a cat scratch or bite. Perinaud's oculoglandular syndrome is manifested by conjunctival granuloma. figurate erythemas. non-selective blood agar incubated over a prolonged period in a CO2 atmosphere. scratch. This agent has requirements necessary for growth in vitro. or petting. .In addition. short-lived. 2) development of lymphadenopathy approximately 2 weeks after the primary inoculation. periauricular lymphadenopathy.Unusual manifestations of CSD. anorexia. and the CBC is normal or shows mild leukocytosis. hepatic granulomas (0. non-specific maculopapular eruptions. Fleas and ticks have also been associated with the transmission of CSD. .3%). erythema nodosum. sore throat. and pulmonary disease (0. weight loss. .Regional lymphadenopathy (axillary. and thrombocytopenic purpura have been observed. The bacterium is most frequently isolated in young. and nonsuppurative conjunctivitis. . nausea and vomiting. The saliva is deposited on an infected cat’s fur and claws from self-grooming. including enriched. The skin lesions typically develop 3 to 10 days after injury and precede the onset of lymphadenopathy by 1 to 2 weeks. male kittens that are not ill and require no treatment. Encephalopathy. although more evidence is required to establish ticks as vectors. The erythrocyte sedimentation rate is usually elevated during the initial stages of lymphadenopathy. osteomyelitis (0. and splenomegaly may develop. these complications resolve without sequelae.Between 25% and 60% of patients report a primary cutaneous inoculation lesion (0. Optic neuritis with transient blindness may also occur.Answer is E. . with the exclusion of other causes of lymphadenopathy. affected nodes are often tender and occasionally suppurate.5. and 4) histopathologic findings on lymph node biopsy specimens showing a granulomatous process with stellate necrosis and pleomorphic bacilli visualized by Warthin-Starry silver staining. A basic laboratory evaluation of CSD should also include a CBC with differential to rule out other causative conditions and a TB skin test to rule out tuberculosis. manifested as fever and coma that progress to convulsions. as a result of direct contact with the cat’s saliva. Transmission of CSD occurs from a bite. Bartonella henselae is now regarded as the etiologic agent of CSD. 3) a positive CSD skin test. head and neck. Historically the diagnosis of CSD is confirmed by three of the four following criteria: 1) history of cat contact and the presence of a primary lesion. In general. cerebrospinal fluid is unremarkable. include Perinaud's oculoglandular syndrome (6%). but that serve as passive vectors in transmitting the disease to humans. . Please Read following: We are trying hard to keep up with all the name changes for the culprit organism of CSD! As if any of them are easy to pronounce! We’ve gone from Rochalimaea to Afipia and now to Bartonella henselae! CSD is typically a benign and self-limited illness lasting 6 to 12 weeks in the absence of antibiotic therapy.Low-grade fever and malaise accompany lymphadenopathy in up to 50% of patients. which occur in up to 14% of patients.5.3%). headache.8).2%) (4.
mesenteric lymphadenitis. and it may present as fever of unknown origin with or without lymphadenopathy. urethritis. In AIDS patients and in other people who have suppressed immune systems (chemo. Margileth (1992) suggested the efficacy of oral rifamin (87%). arthralgia. toxoplasmosis. which has 91% positive predictive value. and cervical adenitis caused by mycobacteria. The most common diagnoses in a series of patients with adenopathy and negative CSD skin test were pyogenic lymphadenitis or abscess. and an 84% sensitivity. thrombocytopenic purpura. It has been associated with CSD in both children and adults. a 96% specificity. management should include conservative symptomatic care and observation. Tularemia. the test is not standardized.). and the enzyme immunoassay (EIA) test. epitrochlear and preauricular nodes. and treatment with antibiotics is recommended. and is no longer recommended. For the majority of patients with CSD. henselae infection recently. and Kawasaki disease must be considered because of the need for specific therapy. benign of malignant neoplasms. headache and muscle weakness. regardless of antibiotic treatment. is not available commercially. Recovery has occurred without residua in most cases. unilateral occurrence. henselae. and intramuscular gentamicin . has been serologically and microbiologically linked to B. inguinal and generalized lymph node involvement is less specific for CSD and necessitates more care in differential diagnosis. ciprofloxacin (84%) TMP/SMX (58%). stellate macular exudates. femoral. neuroretinitis. iritis. Complete resolution of lymphadenopathy usually occurs after 2 to 6 months. The CSF is normal or shows minimal pleocytosis or elevated protein content. Neuroretinitis one of the most frequently reported neurologic syndromes. Treatment: CSD is almost uniformly a self-limiting illness.Currently available for diagnostic purposes are the serum immunofluorescent-antibody (IFA) test for B. such as the axillary. In a retrospective study of uncontrolled data. Osteolytic bone lesions far from the inoculated site have been noted in several well-documented cases. As a general rule the diagnosis is favored by chronicity. Cervical. High fever and convulsions develop within 6 weeks of the onset of lymphadenopathy followed by alteration in the level of consciousness. Other rare complications include erythema multiforme.. but choice of antibiotics is unclear. Granulomatous hepatitis is another newly recognized systemic manifestation of CSD. Diabetes. neuroretinitis) may have a shortened course and thus benefit from antibiotic therapy. plague. Differential: It can include virtually all known causes of lymphadenopathy. pneumonia. cat scratch disease is not benign. Complications: The most serious complication of CSD is involvement of the CNS in the form of encephalitis or encephalopathy. and optic disc edema. EEGs reveal diffuse slowing or focal abnormalities. suggesting hematogenous spread. thyroiditis and non-traumatic atlanto-axial dislocation (Grisel syndrome). tenderness and characteristic sites of involvement. which is thought to be the most accurate. Patients with severe CSD (encephalopathy. ESRD. The syndrome of Leber’s idiopathic stellate neuroretinitis is characterized by visual loss. Although the CSD skin test has a high degree of specificity and has been used for over 40 years to confirm a diagnosis of CSD.
(73%) for improving clinical symptoms. In the same 1992 study. oral rifampin was prescribed using 10 to 20 mg/kg two to three times daily for 7 to 14 days. and most patients with CSD recover fully with no permanent sequalae in a variable period of time from 2 to 4 months.edu/oto/grand/12592. and there is no evidence that CSD is transmitted by humans. and abscesses). Periods of transmission are thought to be limited (possibly 2 to 3 weeks).Medline . Incision and drainage carries the reported risk of sinus tract formation and formal node excision may be preferable. (f) handle cats and all animals gently.bcm. they are relatively rare.Grand Rounds Archives: http://www. boney lesions. and (i) ensure routine veterinary care for all pets. Although the complication of CSD can be serious (central nervous involvement. or bites immediately. and oral ciprofloxacin using 20 to 30 mg/kg twice daily for 7 to 14 days. (b) treat animals for fleas and ticks. (c) wash cat scratches. and the cats do not appear ill in any way. cuts. hematological disorders. Consistent with the 1994 CDC guidelines. prescribed over several weeks or months. Reference: . even though others may have been scratched by the same cat. parents and cat owners should consider the following recommendations: (a) wash hands after petting or playing with cats.CDC . Warm moist compresses to affected nodes may decrease swelling and tenderness.html -----------------------------------------------------------------------------------------------------------------------------------------------Second MCQ is also an old one Q404: . when handling cats. (e) declaw cats if possible. In addition. Aspiration may be helpful for those cases in which suppuration occurs. Relapsing Bartonella is rare.tmc. Paradoxically. and one episode of CSD appears to confer lifelong immunity in children and young adults. children who are immunocompromised appear to respond quite well to common antibiotics. in vitro and in vivo antibiotic susceptibilities to Bartonella species often do not correlate and cannot be used to guide antibiotic recommendations. Cats seldom infect more than one family member. Intramuscular gentamicin was prescribed for severely ill patients using 5 mg/kg in divided doses every 8 hours for 72 hours. Families become concerned about the transmission of CSD to other family members by infected cats. Young cats and kittens may be most frequently implicated in CSD transmission because they are held more often than are older cats and are less experienced in getting away. but using good judgment when handling cats and kittens is essential. but failures also have been reported after treatment with gentamicin and TMS-SMX. such as erythromycin and doxycycline. Collipp (1992) reported improvement in 101 children with CSD by treating with 20 mg/kg of TMP/SMX twice per day for 7 days. especially toddlers. oral TMP/SMX using 6 to 8 mg/kg two to three times daily for 7 days. Isolation of the affected individual is not required. (h) supervise young children. (g) instruct children to avoid contact with stray animals. (d) never allow cats to lick open wounds. Disposal of the offending cat is not recommended.
an attempt to contact the dog owner is a reasonable first step to determine the pet's vaccination status.HR:63. :provide local wound care without antibiotic & vaccination Only 5-20% of dog bites become infected.If rabies is suspected.provide local wound care without ABX & vaccination.On Ph. Human bites and in particular clenched-fist injuries as well as cat bites are highly prone to infection as are wounds that involve the hand or deep structures including joints.Hand bites should also be treated with antibiotics since infection can be devastating to a patient.suspicion might be higher.ABX not necessary.A 20 yo man comes to ur office with a dog bite to his left thigh received after he and a friend taunted a neighbor's dog. Rabies vaccination is not indicated now.Amoxicillin-clavulanic acid and clindamycin would both be acceptable antibiotics since they have broad spectrums covering likely infectious organisms such as Pasteurella multocida. the neighbor's dog is a domestic dog. which is mildly tender.no erythema.Also. Streptococci. which probably indicates that it was vaccinated in the past. if not sure you can check w/ public health dept. and anaerobes. the dog was a household pet. pt.E you notice a shallow abrasion on his left thigh. shallow abrasion. Antibiotics would be indicated for pts with signs of local or systemic infection. it appears prudent to . Generally. most likely dog is not rabid.In this case.BP:110/70 mm Hg.Vaccination for rabies should be considered only when you have a strong suspicion of rabies. If the dog spontaneously bit the patient. has small .This pt does not seem to have any systemic signs of infection and his wound doesn't appear to be infected. before vaccinating the pt.There is no surrounding edema or erythema.He reports that the bite occurred about 36 hrs ago and only came to your office after coworkers informed him that dog bites frequently become infected. ADDENDUM: IS A DOG/CAT'S MOUTH CLEANER THAN A HUMAN MOUTH? Animal and human bites carry a high risk of infectious complications. the dog did not seem rabid (the dog bite occurred only after being provoked). no edema.and irrigation are essential. bones and tendons.RR:13. The most appropriate management of this patient is to: a:administer 5 doses of Rabies vaccines within 28days b:administer RIG&4 doses of Rabis vaccine within 28days c:prescribe amoxicillin-clavulanate d:prescribe clindamycin e:prescribe penicillin f:administer RIG& penicillin g:administer 5 doses of Rabies vaccines within 28days& amoxi-clavulanate h: administer 5 doses of Rabies vaccines within 28days& clindamycin i:provide local wound care without antibiotic & vaccination ANSWER: I.His temperature is 37. Staphylococcus.Local wound care including debridement.. Local wound care remains important.Puncture wounds become infected more often than abrasion and this pt doesn't have any skin punctures.cleaning. Penicillin is a well studied choice for prophylaxis of hand bites but concerns about narrow spectrum of activity have caused many physicians to use alternative antibiotics. most likely vaccinated. The management of bite wounds consists of intensive irrigation with large volumes of normal saline and a cautions debridement of devitalized tissues.
leave the wounds open, however, in cases carrying a low risk of infection, a primary surgical closure might be appropriate. If a bite wound is infected, an antibiotic course with amoxycillin/clavulanic acid (first choice) or tetracyclines (second choice) for 10-14 days is recommended. In patients who present early after the injury, an antibiotic prophylaxis for 3-5 days is appropriate, particularly when the risk for the development of infection is high. Furthermore, a tetanus booster and in case of possible transfer of rabies, a rabies vaccination with immunoglobulins and inactivated virus preparation is recommended. Human bite wounds have long had a bad reputation for severe infection and frequent complication. However, recent data demonstrate that human bites occurring anywhere other than the hand present no more of a risk for infection than any other type of mammalian bite. The increased incidence of serious infections and complications associated with human bites to the hand warrants their consideration and management in three different categories: occlusional/simple, clenched fist injuries, and occlusional bites to the hand. References: 1)Dog, cat, and human bites Schweiz Rundsch Med Prax. 1998 May 20;87(21):716-8. 2)Dog, cat, and human bites: a review. J Am Acad Dermatol. 1995 Dec;33(6):1019-29. 3)Diagnosis and treatment of bites by cats, dogs and humans Dtsch Med Wochenschr. 2003 May 9;128(19):1059-63. Imp... Tips On Diabetes and Surgery For non–insulin–dependent diabetes: perioperative Intravenous solutions containing glucose should be avoided unless hypoglycemia is a risk. If the operation is major, treatment should be the same as for insulin–dependent diabetes until the stress response of surgery is finished . For insulin–dependent diabetes: preoperative Preoperative admission for stabilization may be needed to achieve a blood glucose concentration of 100–180 mg/dL. If control is good, the insulin regimen need not be changed until the day of surgery; if control is poor before a meal, short–acting insulin achieves rapid metabolic control. Blood glucose concentration must be monitored. The main side effect is hypoglycemia. For insulin–dependent diabetes: perioperative Short–acting insulin, 50 units in 50mL normal saline solution with an infusion pump; 500mL 10% dextrose with 10mEq/L potassium chloride through a separate infusion pump infused 5–hourly. Blood glucose concentration must be maintained at 100–180 mg/dL; 1–4 units of insulin may be needed hourly via an infusion pump Alternatively, glucose–potassium–insulin infusion: 10% dextrose, 500 mL, with potassium chloride, 10 mEq/L, and short–acting insulin, 15 units infused as a mixture 5– hourly. Premixed insulins are unsuitable when insulin need changes rapidly.
If blood glucose is >200 mg/dL, 20 units insulin should be added; if blood glucose is <100 mg/dL, 10 units should be added; other parameters should not be changed. The insulin infusion must be continued until the patient's first meal, when s.c. insulin should be started 30 min prior to cessation of insulin infusion; insulin needs will probably be higher than usual. please explain "dicrotic pulse, pulsus bigeminus, pulsus alternans?" - Normal Arterial pulse: The normal arterial wave form has a smooth, fairly sharp upstroke, a momentarily sustained peak and a quick downstroke. - Dicrotic pulse: A dicrotic pulse is one in which two impulses are felt for each heartbeat; the second small upstroke appearing in the blood pressure wave during the diastolic phase. It literally means twice beating pulse. It is only clinically apparent in pyrexic patients, and some valvulopathies. - Pulsus Alternans: also called pressure alternans. This is the situation where the amplitude of a regular pulse is large and small alternately. Pressure Alternans is a sign of a failing ventricle. - Pulsus bigeminus consists of groups of two beats close together, followed by a longer pause. It is associated with every contraction and is an alternate contraction produced by the extra systolic PVC. - Pulsus paradoxus is caused by a greater than normal decrease in systolic pressure and pulse wave amplitude during inspiration. It is associated with circumstances in which respiration is labored and often accompanies such conditions as emphysema, pulmonary embolus, cardiac tamponade or lung cancer. Questions 8yo child by stander with gun shot wound in the epigastric region..stable..next step..choices exploratory lap,usg,tetanus prophy, xray abdomen many qs on localisation of lesion... with some weakness in the body and where possibly could be the problem... copd abg compensated.. next step.. psychiatry- all diagnosis...direct sympotms.. skin - case of pityriasis rosea.. diagnosis.. classic presentation.. GI many qs on pain next best step.. details could not remember.. hep Bpositive pregnant women... what do you do??? HUS, ITP,. urology- many on all the membrano proliferative,all those conditions.. mix and match ... told me to read that well one day before the exam... sorry this is really hotch potch but this is the info i could gather so far Answers: #1: Rule for gunshot wounds to the abdomen = Always exploratory lap. Not so much to exctract the bullet but to explore solid and hollow organs for any perforation. #2: First nebulizer= Treatment of choice anticholinergic lately has been coupled to betaadrenergics (duoneb). Treat underlying infection if indicated. Mucolytics and pulmo-aid to help clear secretions. #3: Pityriasis Rosea = Herald patch then erythema in Christmas Tree distribution in the back. Differential with Syphilis. #4: Hep +ve pregnant. Baby should be vaccinated at birth with HepB IG, then vaccine at 1 month then at 6 months. Monitor LFT's.
#5: HUS. post-diarrheal episode in a child (E.Coli-Shigella). Develops thrombocytopenia, hemolytic anemia (shistocytes, Helmet cells), acute renal failure, hematuria. Treatment is supportive. May dialyse and/or transfuse. It is the same as TTP without the neurological symptoms and in a child rather than adult. Treatment to TTP: Plasmapheresis and NSAID's NO PLATELETS. #6: ITP: It could be child or adult. The trigger infection is viral, and it causes autoimmune (Antiplatelet antibodies) thrombocytopenia without hemolysis and kidney's not affected. Treatment is steroids and if it fails resots to splenectomy with subsequent H.Flu and Pneumovac Vaccine. Repeat Pneumovac after 65yo. #6: For completion: Henoch-Shonlein Purpura. In a child, after an URI. Purpura with hematuria, arthritis, melena and abdominal pain (if intususception). No thrombocytopenia. Treatment supportive. #7: Next post – Nephropathies Nephropathies Glomerular Pathology: - NEPHR"I"TIC SYNDROME: Hematuria, HTN, Oliguria, Azotemia +>Acute Post Streptococcal Glomerulonephritis - Lumpy Bumpy + Granular pattern on IF +>Crescentic Glomerulonephritis (i.e.:Rapidly progressive) - Crescent moon shape +>Good Pasture Syndrome - Linear pattern deposits +> Membranoproliferative Glomerulonephritis - Subendothelial humps + Tram Tracks +> IgA Nephropathy (Berger's Disease) - Mesandial deposits of IgA NEPHR"O"TIC SYNDROME: Massive proteinuria, hypoalbuminemia, generalized edema, hyperlipidemia. +> Membranous Glomerulonephritis - Spike and dome + Diffuse capillary and basement membrane thickening (MCC in adults) +> Minimal Change disease - Foot process Effacement (MCC in children) +> Focal Segmental Glomerular Sclerosis - Segmental Sclerosis and hyalinosis +> Diabetic Nephropathy - Kimmelstielwilson Disease +> Lupus Nephritis - 5 patterns: Wire-loop appearance with extensive subendothelial/Basement Mb granular deposits. --------------------------------------------------------------------------------------------------------------------------------------------- #1: MINIMAL CHANGE DISEASE = LIPID NEPHROSIS Most common cuase of nephrotic syndrome in children. Associated with URI's, immunizations, hypersensitivity to drugs (NSAID's), or allergic reactions (Bee stings). May be paraneoplastic for Hodgkin. Treatment: Predisone induces remission in 90% children and 50% adults. Add Cyclophosphamide or Chlorambucil for relapses. Complications: Incrased susceptibility to bacterial infections, spontaneous bacterial peritonitis, thromboembolic events, svere hyperlipidemia, and protein malnutrition. Case: 10 YO BOY WITH 2 MONTH HISTORY OF LOWER EXT EDEMA AND PROGRESSIVE ABDOMINAL DISTENTION. PRIOT TO THAT, H/O "BAD COLD" FOR SEVERAL WEEKS. PE/ ABDOMEN DISTENDED WITH SHIFTING DULLNESS. PEDAL EDEMA 2+. U/A PROTEINURIA 3+, SERUM ALBUMIN AND
CAN BE CRESCENTIC. RENAL BIOPSY SHOWS THICKENED GLOMERULAR BASEMENT MEMBRANE AND "SPIKE AND DOME" PATTERN WITH SILVER STAIN. FROTHY URINE (from protein). NO PRIOR HISTORY. INCREASED IgA. Renal Biopsy = IgA DEPOSITS. U/A = Protein and fatty casts. CASE: 22YO WHITE MALE COMPLAINS OF RECURRENT EPISODES OF BLOODY URINE FOR SEVERAL DAYS IN CONJUNCTION WITH URI.PROTEIN DECREASED. stomach. FOCAL SEGMENTAL. BS: 234MG/DL. PE: HTN (160/110). ABDOMEN ASCITIC WITH 3+EDEMA. U/A 3+ PROTEIN AND GLUCOSE. PITTING EDEMA. CASE: 52YO WITH RHEUMATOID ARTHRITIS AND BORDERLINE DIABETES PRESENTS TO THE OUTPATIENT CLINIC COMPLAINING OF ABDOMINAL BLOATING AND BILATERAL ANKLE SWELLING OF SEVERAL MONTHS. U/A 3+ PROTEIN AND NEPHROTIC RANGE PROTEINURIA. Chronically progresses to glomerulosclerosis after about 10 years. Penicillamine. H/O DM1. IT IS THE SAME GLOMERULAR PATHOLOGY SEEN IN HENOCH-SHONLEIN IN KIDS. it then presents with HEMATURIA. #2: MEMBRANOUS GLOMERULONEPHRITIS It's the most common cause of primary nephrotic syndrome in adults. IT IS ALSO SEEN IN CELIAC DISEASE AND LIVER DISEASE because of decreased IgA clearance. Case: 48YO WHITE FEMALE ADMITTED BECAUSE OF WORSENING GENERALIZED EDEMA AND WEAKNESS ALONG WITH HYPERTENSION. BUN AND C ELEVATED. U/A= Protein and Red Cell Casts. #3: DIABETIC NEPHROPATHY: Insidious proteinuria secondary to diabetic microangiopathy. ANA -VE. NO LATENCY PERIOD (AS OPPOSED TO POST-STREPTOCOCCAL). RENAL BIOPSY: FOCAL GLOMERULONEPHRITIS INVOLVING ONLY SELECTED GLOMERULI WITH MESANGIAL PROLIFERATION AND . and Captopril). BROAD AND FATTY CASTS. IF: GRANULAR DEPOSITS OF IgG AND C3. PATIENT HAS BEEN USING GOLD THERAPYF FOR HIS RA FOR 2 YEARS NOW. Protein restriction. #4: Iga NEPHROPATHY = BERGER'S DISEASE Idiopathic Glomerulonephritis associated with URI or GI infections. NEITHER KIDNEY IS PALPABLE. NEPHROTIC SD ON LABS. OR MESANGIOPROLIFERATIVE. Complications: progressive loss of renal function over 3-10years in 10% of cases. Increased incidence of occult neoplasms: lung. EM: fusion of epithelial foot processes. asymptomatic at first. Hb A1C= 10%. Treat with ACE-Inhibitors. IF: -VE FOR Ig. RENAL BIOPSY: LIGHT MICROSCOPY UNREMARKABLE. ANASARCA. GROSS HEMATURIA. U/A RED CELL CASTS IN URINE. AND HYPERTENSION. NO EVIDENCE OF PLEURISY/ASCITES. NO EFFECTIVE TREATMENT. strict Glucose control with Insulin if necessary. FUNDOSCOPY: PROLIFERATIVE DIABETIC RETINOPATHY. DECREASED ALBUMIN. Associated with autoimmune disorders and use of medications (Gold. Treat with Prednisone with ot without cytotoxic agents for 3 months. Renal Biopsy = KIMMELSTILL-WILSON = INCREASED MESANGIAL MATRIX AND THINKENED BASEMENT MEMBRANES. Presents with HEMATURIA. ELEVATED IgA. and colon in patients >50yo. 1/2 of patients progress to renal failure.
AND OLIGURIA X24H. Minimal hematuria or proteinuria. . CXR=BILAT ALV INFILTRATES. STEROIDS.Class V: MEMBRANOUS GLOMERULONEPHRITIS. IgG. IgA DEPOISTS REAPPEAR. IF: MESANGIAL IgA DEPOSITS WITH SOME IgM.Class III: FOCAL PROLIFERATIVE GLOMERULONEPHRITIS. . RED CELL CASTS. HE ALSO DESCRIBES EPISODES OF DARK ORANGE URINE. HEMATURIA. #7: Lupus Nephritis: There are five patterns to Lupus Nephritis: . SERUN: ELEVATED BUN AND C. PROTEINURIA. HOWEVER IT IS METABOLIZED TO CYANIDE AND THIOCYANITE SO MONITOR BLOOD LEVELS.Class IV: by far the most common as in the folling case. . SEVERE OCCIPITAL HEADACHE. PATIENT IS A HEAVY SMOKER. ASSOCIATED: NECROTOZING HEMORRHAGIC ALVEOLITIS ON LUNG BIOPSY = TYPE II HYPERSENSITIVITY. TREAT BY REDUCING DIASTOLIC BLOOD PRESSURE TO AT LEAST 100 AND MAINTAIN URINE OUTPUT AT LEAST 20CC/HR. DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS. EVEN AFTER RENAL TRANSPLANTS. #5: CRESCENTIC GLOMERULONEPHRITIS CASE: 36YO WHITE MALE COMPLAINS OF CHRONIC COUGH OF SEVERAL MONTHS WITH LIGHTHEADEDNESS. FUNDOSCOPY REVEALS PRESENCE OF PAPILLEDEMA WITH HYPERTENSIVE RETINOPATHY. THERE IS CHARACTERISTIC IgG LINEAR DEPOSITS ON BASEMENT MEMBRANE AND ALVEOLAR SEPTA ON IF. #6: HYPERTENSIVE RENAL DISEASE: CASE: 45YO BLACK MALE PRESENTS WITH UNCONTROLLED HYPERTENSION. AND MALAISE. . HYPERPLASTIC ARTERIOLOSCLEROSIS (ONION SKINNING).Class II: MESANGIAL LUPUS GLOMERULONEPHRITIS.Class I: NORMAL in light/immunofluorescence microscopy. U/A OLIGURIA. AND NECROTIZING GLOMERULITIS WITH THROMBOTIC MICROANGIOPATHY. and mild renal insufficiency. YESTERDAY. CBC: SHISTOCYTES. Nephrotic syndrome. AND C3.SEGMENTAL NECROSIS WITH CRESCENTS. TREAT GOOD PASTURE'S SYNDROME WITH PLASMAPHERESIS. . GIVE NITROPRUSSIDE BECAUSE IT DOESN'T IMPAIR MYOCARDIAL BLOOD FLOW. Recurrent hematuria. RENAL BIOPSY: FIBRINOID CHANGES OF ARTERIOLES (NECROTIZING ARTERIOLITIS). HE COUGHED UP BLOOD. ABG'S: HYPOXEMIA. HEMOLYTIC ANEMIA. FATIGUE. AND IMMUNOSUPPRESSIVE THERAPY. IN SERUM = ANTIGLOMERULAR BASEMENT MEMBRANE ANTIBODIES +VE. U/A: PROTEINURIA. RENAL BIOPSY: KIDNEYS' ENLARGED AND PROLIFERATIVE NECROTIZING GLOMERULONEPHITIS IN CRESCENTS WITH ACCUMULATION OF NEUTROPHILS AND MACROPHAGES IN BOWMAN'S CAPSULE. TREAT SUPPORTIVELY. VISUAL BLURRING.
LABS: ELEVATED RUN/C. ANA-VE. Minimal change disease (MCC in children). AND LOSS OF HAIR. SHE ALSO HAS HEMATURIA. #8: MEMBRANOUS GLOMERULONEPHRITIS Nephrotic Syndrome may be idiopathic or caused by membranous glomerulonephritis (the most common cause in adults). or membranoproliferative GNitis. CHEST PALPITATIONS. Case: 11YO WHITE FEMALE BROUGHT BECAUSE OF HEADACHE. RENAL BIOPSY: DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS WITH IMMUNE COMPLEX DEPOSITS TYPICALLY SUBENDOTHELIAL AND FORMING "WIRE-LOOPS". NO PAST MED H/O. PERIORBITAL EDEMA. HYPOALBUMENIMA. PE: PERIORBITAL EDEMA. Activation of only alternate complement pathway. ON PAS OR SILVER: SPLITTING OF BASEMENT MEMBRANE CAUSING RAILRAOD TRACK APPEARANCE. There is a high recurrence rate following renal transplantation. SUBENDOTHELIAL DEPOSITS OF IgG AND C3 ALONG BASEMENT MEMBRANE SEEN IN "SPIKE AND DOME" PATTERN ON SILVER STAIN. ELEVATED BUN AND C. HYPERTENSION 140/110. PROGRESSIVE SOB. ANA +VE. AND ASCITES. WEIGHT LOSS. TypeI MPGN: both classic and alternative complement pathways are activated TypeII MPGN: Dense Deposit disease. VDRL +VE. #7: MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS Idiopathic. .Case: 30YO BLACK WOMAN WITH PAIN IN BOTH KNEE JOINTS AND SMALL JOINTS OF HANDS TOGETHER WITH MILD FEVER. SHE ALSO HAS RECURRENT ORAL ULCERS AND PHOTOSENSITIVE SKIN RASH. It may be associated with inherited diseases of complement components and partial lipodystrophy. SHE IS HYPERTENSIVE WITH BUTTERFLY RASH OVER MALAR AREA. focal glomerulosclerosis. ANTI-DS DNA +VE. 50% progress to renal failure. LABS: NORMO/NORMO ANEMIA U/A MICROSCOPIC HEMATURIA WITH RBC CASTS IN ADDITION TO PROTEINURIA. HYPERLIPIDEMIA. UA/ PROTEINURIA. RENAL BIOPSY: DIFFUSE GLOMERULAR INVOLVEMENT WITH THICKENED CAPILLARY WALLS AND LOBULAR MESANGIAL PROLIFERATION ON LIGHT MICROSCOPY. NORMAL ASO TITERS. AND RINGING IN HER EARS TOGETHER WITH GENERALIZED EDEMA. LONG-TERM HEMODIALYSIS OR TRANSPLANT. Case: 47YO BLACK DIABETIC FEMALE COMPLAINS OF WEIGHT LOSS. Patients with nephrotic syndrome have hypercoagulability secondary to loss of ANTITHROMBIN III in the urine. TREAT WITH STEROIDS AND CYCLOPHOSPHAMIDE/AZATHIOPRINE/CHLORAMBUCIAL. HYPOCOMPLEMENTEMIA. U/A FATTY CASTS AND OVAL BODIES ALONG WITH PROTEINS. AND SWELLING OF BOTH LEGS AND ARMS. RENAL BIOPSY: THICKENED BASEMENT MEMBRANE. IF: PROMINENT MESANGIAL AND SUBENDOTHELIAL DEPOSITS OF IMMUNE-COMPLEXES. HYPOALBUMINEMIA. NO EVIDENCE OF PLEURAL EFFUSION/ASCITES. TREAT WITH STEROIDS AND RENAL TRANSPLANT. THE IMMUNE DEPOSITS ARE IN A "LUMPY-BUMPY" = DISCONTINUOUS PATTERN ON IMMUNOFLURESCENCE.
ACE-I REDUCE PROTEIN LOSS. C3 AND TOTAL COMPLEMENT CH50 LOW. PE: HTN. #9: POST-STREPTOCOCCAL GLOMERULONEPHRITIS: It's an immune complex disease that is usually caused by beta-hemolytic streptococcus type 12 and 49. AND BUN/C. Tuberculosis. #10: PRIMARY AMYLOIDOSIS Primary Amyloidosis commonly presents with nephrotic syndrome. NO P. MORNING SWELLING OF THE EYES. it occurs 10-14 DAYS AFTER URI. LEADING TO NARROWING OF LUMEN AND ISCHEMIA. Multiple Myeloma. RENAL BIOPSY: APPLE-GREEN BIREFRINGENCE IN POLARIZED LIGHT WHEN STAINED WITH CONGO RED. Resolution may take 6-12 months. CASE: 45YO WHITE FEMALE COMPLAINS OF PALPITATIONS AND SOB. H/O THROAT INFECTION TEN DAYS AGO FROM WHICH HE REOVERED UNEVENTFULLY. and chronic glomerulonephritis. severe headache. and scarlet fever. PROTEINURIA. U/A: PROTEINURIA. CBC. uremia. Case: 5YO MALE PRESENTS WITH MALAISE. WITH NUMBENESS OF THE LOWER LEGS TOGETHER WITH WEIGHT LOSS AND FATIGUE. skin infections. LEUKOCYTOSIS. visual disturbances). Occurs after URI. LABS: HYPERLIPIDEMIA. or secondary (Rheumatoid Arthritis. Treat Renal and Cardiac Failure with peritoneal dialysis. Pregnancy where it's beta2microglobulin). INCREASED ASO TITER.MED. PE: MILD CARDIOMEGALY.TREAT WITH STEROIDS. Diet high in carbohydrates and low in protein. RENAL BIOPSY: ELECTRON-DENSE HUMPS ON THE EPITHELIAL SIDE OF THE GLOMERULAR BASEMENT MEMBRANE.H/O. TONSILS CRYPTIC BUT NO EXUDATE. #11: RENAL TUBULAR ACIDOSIS It results from: . CXR: BIVENTRICULAR CARDIAC ENLARGEMENT. ABDOMINAL PAIN WITH VOMITING. CYCLOPHOSPHAMIDE. DNASE TITER HIGH. ASCITES. MACROGLOSSIA. It is the most common childhood nephritis and affects preschool and school-age children. followed by activation of complement leading to inflammation. INCREASED ESR. AMYLOID DEPOSITION IN MESANGIUM AND ENDOTHELIUM SURROUNDING HEPATIC SINUSOIDS AND IN SPLEEN. HYALINE THICKENING OF ARTERIOLAR WALLS. sodium. ANEMIA. Hypertensive Encephalopathy (vomiting. Complications: Cardiac Failure. AND ARMS/LEGS. convulsions. acute pulmonary edema. IF: GRANULAR PATTERN OF Ig DEPOSITION. PITTING EDEMA. U/A RBC'S AND RBC CASTS. ABG'S=METABOLIC ACIDOSIS. potassium and water. PERIORBITAL EDEMA. Pathogenesis may be related to the deposition of strep antigen-antibody complexes in the glomeruli. EKG: LOW-VOLTAGE. Treat with Penicillin for 10 days to prevant spread of nephrogenic strain (erythromycin if allergic). ANKLE EDEMA. HYPOPROTENEMIA. ANA -VE. SMOKY COLORED URINE (HEMATURIA). Amyloidosis may be primary (monoclonal Ig light chains). AND CARDIAC ARRYTHMIA. AND MILD FEVER.
and it is seen in patients with renal insufficiency and chronic medical illnesses such as DM with nephropathy..BONE LESIONS (OSTEOMALACIA and RICKETS). Serum Bicarb is 10. Patients may require higher doses because of resistance. Renal Insufficiency. CHRONIC HEPATITIS. Sickle CEll Disease. zero/positive urine anion gap. There is Nephrocalcinosis and Nephrolithiasis. HTNm and AIDS. TREAT WITH ORAL BICARB (proximal tubule reabsorption still works)AND POTASSIUM REPLACEMENT. . Loop diuretics and exchange resins can also be used. or other acids. which normally stimulate Aldosterone secretion. and exclusion of presence of diarrhea. Acidosis usually corrects as soon as hyperkalemia contributing to decreased ammonia production. Lithium. ACE-I. Sjogren).Diagnosis: ORAL SALT RESTRICTION => CON'T HIGH URINE SODIUM. . .IV sodium bicarb = ph urine still basic. If RTA I. Addision. lab evidence of primary hyperchloremic hyperkalemic metabolic acidosis. SERUM BICARB 1820. tubular interstitial renal disease. This results in defective secretion of both potassium and H+ in the distal nephron. . These patients secrete it but do not reabsorb it. and D/C aldosterone antagonists drugs (NSAIDS. Type IV is the most common. whereas Type I get Kidney Stones. NSAID's and HEPARIN. or other (Nephrocalcinosis. paresthesias. Wilson Disease.: Sjogren) or drugs (Amphotericin. These patients produce acidic urine despite reduced H+ secretion because of inadequate ammonia to buffer the protons in the distal tubule. and Chronic Infection). Treat by restricting potassium. Also with drugs: ACE-I. Secondary Hyperaldosteronism and HYPOKALEMIA.Etiology: Diabetes. .Inability to absorb bicarb. Amyloidosis Myeloma. CHRONIC HYPOCALCEMIA.Diagnosis: Bicarb Loading Test . Normal individuals do not excrete bicarb until serum >24. Analgesics). AUTOIMMUNE DISEASE (SLE. Urine pH is basic HYPOKALEMIA. Urine pH>5. Complications: metabolic acidosis.Type III: Supressed renal generation of ammonia secondary to reduced GFR. . hyperkalemia (confusion. HEPARIN). Sickel Cell. VIT D DEFICIENCY. ETIOLOGY: Fanconi Syndrome.Type IV: Aldosterone Deficiency of any cause. Both are hypokalemic. . . . which should lower urine pH secondary to increase H+ production.Type II: Defective bicarbonate reabsorption in the proximal tubule. leading to inadequate excretion of the acid load.Treat with potassium. Urine pH remains elevated. Can be secondary to auto-immune disease (e.4. calcium chloride. Give thiazides and very large amounts of bicarbs.g. or Adrenal Insensitivity to Angiotensin II. weakness. Mineralocorticoid replacement with Fludrocortisone usually improves hyperkalemiaand acidosis but may worsen HTN. So they are also Acidemic.TypeI: Deficient H+ secretion in the distal tubule. is corrected. HEAVY METALS. The resulting hyperkalemia decreases proximal tubule ammonia production and reduces H+ secretion. RTA is ALSO diagnosed by asymptomatic hyperkalemia. Mild volume depletion enhance proximal reabsorption of bicarb. . DIAGNOSIS: ACID LOAD TEST: Give ammonium chloride. normal anion gap.
Pathophysiology. Olatinwo.Medscape (posted from the AIDS reader) New Onset Seizures as an Initial Presentation of End-Stage Renal Failure in Patients With HIV/AIDS Toyin F.Kaplan notes . U/A URINE PH ACID<5. CALICUM CHANNEL BLOCKER FOR HTN. Differential: Hep B and Hep C associated nephropathy.First Aid Step 1 Causes of Abdominal pain in Different Quadrants Causes of abdominal pain in different quadrants: . Internal Medicine . new-onset seizure (Management of seizure with subsequent treatment using phenytoin). AND RHEUMATOID ARTHRITIS PRESENTS WITH A DECLINE IN MENTAL STATUS AND DECREASED URINE OUTPUT. DM WAS POORLY CONTROLLED DESPITE INSULIN AND ORAL AGENTS. URINARY ANION GAP+VE. MD 8/2002 . asterixis etc.5. THIAZIDE. ACE-I also have been used successfully to further slow progression. PE: HTN. kidneys are ENLARGED!! . Corticosteroids have also been used but with caution because of the advanced stage of AIDS already for the patient.paralysis.Confirm with Renal Biopsy: FOCAL SEGMENTAL GLOMERULAR SCLEROSIS is the most typical one. AND TAKES NSAIDS FOR PERSISTENT RA.Labs: Uremia. massive proteinuria in the nephrotic range with little to ne edema . and if the patient is white. Hewitt. REFERENCES: . MD.Patient may present with Uremic Encephalopathy with confusion. HE IS CURRENTLY ON ACE-I.UNDERGROUND CLINICAL VIGNETTES: Pediatrics. HTN. ELEVATED BUN/C. Ross G. ABG: NONANION GAP METABOLIC ACIDOSIS.Order Ultrasound: which in contrast with usual shrunken small kidneys of End-Stage Renal Disease. CASE: 73YO MALE WITH ADULT ONSET DM FOR 30Y. arrythmias. in HIVAN. Management: Antiretroviral Therapy is the most important feature. think of other diagnoses) . Hemodialysis should also be started. Of note: Encephalopathy is a sign of rapidly changing nephro status either deteriorating ir improving (encephalopathy on first hemodialysis = Dialysis dysequilibrium Syndrome). LABS: HYPERKALEMIA. and even cardiac arrest). It not only slows the progression but may in fact reverse it. Heroin Associated Nephropathy. LETHARGY. .Mostly African Americans (So and so. HE HAS HAD OCULAR DISEASE AND RENAL INSUFFICIENCY FOR >5Y. DIFFERENTIAL: DIABETIC NEPHROPATHY WHICH SHOULD BE TREATED WITH ACE-I AS OPPOED TO TUBULAR ACIDOSIS WHERE THEY HAVE TO BE D/C'ED. HYPERCHLOREMIA. #12: HIV-ASSOCIATED NEPHROPATHY HIV associated Nephropathy Pearls (HIVAN) . that in the absence of renal biopsy..
ECTOPIC pregnancy. Budd chiari(esp if pt. Switch dugs to which one? Erythromycin. Developed Autonomic neuropathy of gastroparesis.Lower lobe pneumonia. Tuboovarian abscess(PID) GIT-rarely diverticulitis(usually occurs on left side). Spleen.re looking for answer using the least invasive most cost effective procedure.hepatitis. Fatigue. Developed Tardive dyskinesia despite reducing dosage.think of Zolinger Ellison) Lung base. ERCP when you want to investigate the Common Bile Duct rather than the gallbladder. . has Nephrotic/paroxysmal nocturnal hemoglobinuria). Ovary. 2002 Oct. Confusion.Gallstone colic Duodenum-ulcer (on exams. Stomach. Others: Anorexia. Perihepatitis(eg Fitz-Hugh-Curtis syndrome-chlamydia or gonococcus). Encourage fiber in diet. Gall bladder.calculous or non calculous(esp in pt in ICU or on cephalosporins) cholecystitis.red degeneration.25(8):483-6. pancreas. ruptured hepatic adenoma(young female on oral contraceptives). Weight loss Reference: CMDT Question Diabetic for many years. Appendix-Appendicitis-acute or chronic Caecum-Typhilitis esp in post chemotherapy patient . Given Meoclopramide. hydration-PO or IV and stool softening. fibroid. They're pretty good about this. Side effects of interferon therapy in Hep C: Is it depression or irritability or hallucinations or delirium. LUQ: Spleen and structures around it. It's beyond the scope to talk about each one regarding each diagnosis.especially diverticulitis that is seen in elderly population and is treated with antibiotics. Somnolence. pleuritis Diaphragm-irritation due to blood in peritoneum(also pain in Right shoulder when patient is in head low position-esp seen in splenic rupture-inspite of spleen being left sided) RLQ: Structures around caecum and thse on right side of uterus. Orient youself with the differential above and study each condition on CMDT . colon-splenic flexure LLQ: Sigmoid colon. DEPRESSION Reference: Acute hepatitis C: response to treatment with interferon-alpha plus ribavirin Gastroenterol Hepatol. Abdominal Us is almost always right answer is you. hepatic trauma.cyst rupture or torsion. Uterine structures-as in LLQ area. RUQ-perihepatic structures Liver.For differential diagnosis purposes let us see the abdomen in 4 anterior quadrants and the left and right flanks.occurs with Pseudomonas and Clostridium septicum with approximately equal frequency.
. What if it is constipation? Laxatives such as senna. Malingering Factitious disorder.. History typical of hypochondriasis but what differentiates is the obvious secondary gain.. WHAT ARE THE ODDS . OR HOW MANY MORE CASES WERE ATTRIBUTABLE TO SMOKING. and then there were various options to interpretation.PPV senstivity and specificity. like the values were given. Now on the inpatient floor. No known etiology has been found for this pain despite an intensive metabolic. or Demerol addiction). Factitious disorder D. It would have been malingering if there hadn't been surgery involved as it would be less likely she would resort deliberately to surgery just to have the pain medication or her mother take the kinds in.. or kids at mom's.like the OR.INCIDENCE IN NON EXPOSED GROUP => MEANS HOW MANY MORE CASES WERE THERE OF LUNG CANCER IN SMOKERS COMPARED TO NON SMOKERS. A social work consult is called and reveals that the patient is a single mother with 2 small children who stay at her mother's house when she is hospitalized. If not responding => associated with impaired sphincter control and fecal incontinence : Use Loperamide QD or Combination Diphenoxylate/Atropine. Conversion disorder C. Body dysmorphic disorder B. Which of the following is the most likely diagnosis? A..Improves gastric emptying by binding to motilin receptors in stomach.IN A COHORT STUDY FOR SMOKING AND RISK OF LUNG CANCER: RELATIVE RISK = INCIDENCE IN EXPOSED GROUP/INCIDENCE IN UNEXPOSED GROUP => IT MEANS HOW MUCH MORE RISK WOULD A SMOKER HAVE TO DEVELOP LUNG CANCER COMPARED TO A NON SMOKER ATTRIBUTABLE RISK = INCIDENCE IN EXPOSED GROUP . She comes to the emergency department complaining of similar pain and is admitted to the hospital for management. Hypochondriasis E. Refernce: CMDT Question A 20-year-old woman has a history of repeated admissions for sudden abdominal pain. RR attributable risk. Answers to some BIOSTATS MCQ's there were lot os interpretation qs of case control and cohort studies. The patient has also had repeated imaging studies of her abdomen and 1 exploratory laparotomy. Extensive imaging and laboratory studies are all normal.IN CASE-CONTROL STUDIES: ODDS RATIO = ODD OF EXPOSURE FOR CASES/ODDS OF EXPOSURE FOR CONTROLS = AD/BC => IF YOU HAVE LUNG CANCER.. infectious. and the conclusion after the end of the study were asked. . What if it was Diarrhea in Autonomic Neuropathy setting? Ans: Often self-limited but use broad-based Antibiotic therapy. It is of psyhological nature (20yo singe mother needs attention... . the patient is relaxed. and endocrine evaluation.
5 cases. #2. what is the odds ratio? Interpret it in a sentence. It means if the baby has a feta. #2: I. It's in the past because the study is retrospective case-control.(520/695)(80/305) G. the risk factor exposed to in this study accounted for 0.YOU HAVE BEEN EXPOSED TO SMOKING IN THE PAST? Q: A research study investigated the relationship btw mean blood values in pregestational diabetic women and major fetal malformations: Major fetal malf--------->130----------<130------Total Present------------------10---------------2-------350 Absent-------------------50-------------300-------350 total--------------------60-------------302-------362 What is the odds ratio? How would you put it in a sentence to interpret? Ans: Odds ratio = ad/bc = 10x300/50x2 = 30.520/695 B. The relative risk is = Incidence of Exposed/ Incidence of non exposed.(520/695)/(80/305) Ans: #1: H => Incidence of exposed . Q: Match with the correct value: ------------Disease------Well Exposed------520----------175-----------695 Non exposed---80----------225-----------305 -------------600----------400----------1000 #1. there is 30-fold likelihood the woman HAD a pre-gestational diabetes.5 Incidence of exposed= New/Total = 520/695 Incidence of non exposed = New/total = 80/305 Of every thousand cases observed. what is the attributable risk? Interpret it in a sentence. then we would not use the Odds ratio. it cannot be determined.695/1000 E. With that said. #3.(520x225)/(175x80) H.80/305 F. malformation. Choices: A. If it were prospective.Incidence of nonexposed = approximately 0. but the relative and attributale risk (see below).600/1000 c. what is the relative risk? Interpret it in a sentence.Assume the table is a cohort study. = J = approximately 2.Cannot be determined by this type of study J. The attributable risk is happens in cohort studies not crosssectional.Assume the table represents a case-control study.Assume the table represents a cross-sectional study.(520/695)-(80/305) I.87 .520/600 D. Let's assume it's a cohort.
If a test comes back negative.It means people exposed to the risk factor studied are 2. #2: In clinical settings where prevalence is higher: . What happens to Incidence and Prevalence? Ans: Incidence is unchanged.36 This means the odds of having a history of exposure IN THE PAST to the risk factor is 8. If it is negative. If test X retunrs positive in a person who is randomly selected in this population under study. If a test has a specificity of 100%. IN SCREENING TESTS: #1: In general population screening where the prevalence is low: . the question to ask is is it a True positive or a False Positive? That's the PPV of a test. But it still doesn.t say anything if it is negative. If the test has 100% specificity.NEGATIVE PREDICTIVE VALUE = TRUE NEGATIVES/ALL NEGATIVES. However if it is positive. that means. it rules out the disease.36 times greater in those who have the disease than in those who do not. they're asking for the Positive predictive value. you ask yourself is your negative a true negative or a false negative? Of course if it is a test with 100% sensitivity. . it confirms the disease. Prevalence increases. we resort to positive and negative predictive value. If it is positive.87 more likely to develop the disease IN THE FUTURE than non exposed people. If a test has 100% sensitivity.SPECIFICITY = TRUE NEGATIVES/ALL WELL (tn+fp) => How often the test is negative if people who do NOT have the disease. Q: Test X for SLE is positive in 60 out of 100 patients with known SLE and is normal in 80 out a 100 controls. Q: A recently dicovered treatment for leukemia extends the lifespan but does not prevent the diseas or lead to its cure. IN DISEASE STATISTICS: . then there are no false negatives and therefore NPV=100% too.PREVALENCE = PERSONS WITH DISEASE/PERSON AT RISK => HOW MANY EXIST AT A GIVEN TIME . the Positive Predictive Value will always be 100% too because there is no False Positives. what is the percent chance that the person has SLE? Ans: In other words. if it is a True Negative or False Negative.Odds ratio=AD/BC = (520x225)/(80x175)= approximately 8. that means it has no false positives. .SENSITIVITY = TRUE POSITIVES/ALL SICK (tp+fn) => How often is the test positive in patients who have the disease. ------------------------------Test+ve------Test(-ve) Patients with SLE--------------TP60--------FN40 . we still don't know if it is True Postive or False Positive. Therefore. that means it has no false negatives. #3: G .INCIDENCE = PERSONS WITH DISEASE ONSET/PERONS AT RISK => HOW MANY NEW CASES. It would be easier to redistribute the information in a visual way. For both those reasons.POSITIVE PREDICTIVE VALUE = TRUE POSITIVES/ALL POSITIVES => HOW POSITIVE IS A POSITIVE? When a test returns positive. sensitivity is for screening random asymptomatic people.
SO BEFORE WE START OUR STUDY. TP/TP+FP = 75% ... IF WE ACCEPT IT (IN THE STATISTICIANS LANGUAGE THEY SAY "FAIL TO REJEC" INSTEAD OF "ACCEPT"). THE IDEAL WOULD BE IF A TEST COULD BE BOTH. THEN IT'S NOTSTATISTICALLY SIGNIFICANT.. THEN WE HAVE REJECTED OUR GOAL. THERE IS INCREASED RISK.0. CHOOSE A SAMPLE AND GET RESULTS OF A STUDY. WE WILL EITHER CONFIRM IT (ACCEPT IT) OR DENY IT (REJECT IT).0.. WE NEED TO KNOW IF WE . WE WILL MAKE THE START POINT HYPOTHESIS (NULL HYPOTHESIS) THE OPPOSITE OF WHAT WE WANT TO PROVE.EXTRAPOLATE OR IF OUR RSULTS WERE ONLY OBTAINED BY CHANCE. HOWEVER. . IF IT'S ABOVE 1.CAN. PRECISION (or reliability) IS HOW CONSISTENT AND CLOSE TOGETHER THE RESULTS OF THE TEST ON THE SAME PERSON IN THE SAME CONDITION WOULD BE.5 (5%). THEN WE HAVE PROVEN OUR GOAL. IT IS THE 84TH PERCENTILE.G: SMOKING CAUSE CANCER. WE WOULD INSTEAD OF STUDYING THE ENTIRE POPULATION OF THE EARTH.0 VALUE IN ITS CONFIDENCE INTERVAL. It is a population with a 50% pervalence (100 controls and 100 sick with total 200). THERE IS DECREASED RISK. THAT'S THE HYPOTHESIS WE WANT TO TEST. BUT THEN AGAIN. P VALUE IS PART OF WHAT WE CALL INFERENTIAL STATISTICS. WE WILL DO A .ACCURACY = TRUE POSITIVES + TRUE NEGATIVES / ALL => HOW MUCH PERCENT IS THIS TEST ACCURATE? . SINCE IT IS IN REAL LIFE EASIER TO REJECT THAN TO ACCEPT. IF WE REJECT IT. IF IT'S BELOW 1. IF IT IS AT 1SD. IT IS SO CONFUSING COMTIMES BUT KEEP IN MIND THESE NOTIONS. A TEST COULD BE PRECISE (REPRODUCIBLE) BUT NOT ACCURATE. IT MEANS OUR RESULT IS ACCURATE AT A 95% CONFIDENCE IF P-VALUE IS 0. A TEST COULD ALSO BE ACCURATE BUT NOT PRECISE. WE WOULD CALL IT HYPOTHESIS ZERO OR NULL. THEN EXTRAPOLATE AND DRAW CONCLUSIONS ABOUT THE ENTIRE POPULATION OF THE PLANET. THATS WHY WE CHOOSE THE CONFIDENCE INTERVAL WHICH IS THE P VALUE. . CONVENTIONALLY. also there was some q about interval analysis which my friend said that he did not understand at all. IT MEANS WE LEFT 5% CHANCE FOR PURE COINCIDENCE TO HAVE BEEN THE CAUSE OF OUR RESULTS. oUR NULL HYPOTHESIS IS "SMOKING DOES NOT CAUSE CANCER".STATISTICAL SIGNIFICANCE: RELATIVE RISK AND CONFIDENCE INTERVAL (THIS ONE I LEARNED IT LIKE THIS)=> IF THE RELATIVE RISK CONTAINS 1.ACCURACY VS PRECISION: ACCURACY (also called Validity) IS HOW CLOSE TO THE NORM. which is why we use the PPV.Control Population-------------FP20--------TN80 Totals---------------------------80---------120 Now we see it clearly. WE HAD ALREADY DISCUSSED AT LENGTH THE PERCENTILES WITH REGARDS TO THE MEAN. WE DECIDE WHAT IS OUR STATEMENT? E. SO FOR THE EXAMPLE OF "SMOKING CAUSES CANCER".ANOTHER NOTION IS THE P-VALUE.
:P VALUE OF 0.05 => Chance of Type I error is 5%.important to know about minors and when . What type of error did the resreacher make? A. Type I error (Alpha) is rejecting the null hypothesis when it actually true.% OF PATIENTS WHO WILL BENEFIT . if Pvalue if 0.The chance that an individual would benefit from a low-salt diet is less than 0. Q. This difference is significant at a p value less than 0.An experimental error E. IN DOING SO.Type II error is failing to reject the null hypothesis when it is actually false.NO TELLING IF AN INDIVIDUAL WILL BENEFIT (SEE BELOW) .Type I error B.Blood pressure difference is clinically significant B.05. The chance to do that is set by the criterion alpha (with is the same as p-value). Ans: C.TELLS STATISTICAL SIGNIFICANCE = STATISTICALLY SIGNIFICANT AT P VALUE=0. It can't tell if patient can benefit from salt diet or not and to what degree. he had 5-6 qs on ethics which were standard. WE WILL ACCEPT OUR ALTERNATIVE HYPOTHESIS WHICH WAS WHAT WE WANTED IN THE VERY BEGGINING WHICH IS" SMOKING CAUSES CANCER".Type II error C.5).E.QUANTIFIES CHANCES FOR ERROR (5% CHANCE IT'S AN ERROR = BY RANDOM) . THIS ACCEPTANCE WOULD BE AT 95% CONFIDENCE (I.05 C. you need to increase the sample size. Beta = 1-Power Power of a test is the capacity to detect a difference when it exists.Increasing the number of subjects would tend to change the p value from significant to non-significant. To increase the power of a test.STUDY AND REJECT IT WITH A P VALUE OF 0. Q: The difference in mean diastolic pressure among 150 subjects in a low-salt diet group and 150 subjects in a no-added-salt group is 10mmHg.. SO: ..It is unlikely that random variation accounted for the difference in diastolic blood pressure between the two groups D. p value is part of inferential statistics and merely reflects if a result occured by chance or not.5 WHAT P VALUE DOESNT DO: .An inferential error Ans: B.P-VALUE IS A CRITERION FOR MAKING DECISIONS ABOUT THE NULL HYPOTHESIS (SEE ABOVE)= ACCEPT OR REJECT .DEGREE OF BENEFIT EXPECTED.5 (ONLY 5% CHANCE OUR RESULTS OF REJECTION OCCURED BY RANDOM COINCIDENCE). A cancer researcher conducted a medical experiment and failed to reject the null hypothesis although the experiment was successful.Type II error D. Which of the following statements about the two groups is true? Which of the following is true? A.
etc. failure to thrive. Sundden Bilateral Painless blindness first associated with severe head or blunt thoracic trauma.html what is Purtscher's retinopathy? Barter's syndrome? Purtscher Retinopathy: is a hemorrhagic and vasoocclusive vasculopathy. Reference: American Association of Family Physicians Thyroid nodules Feb 2003 http://www. and chest compression. and it is a "hot" nodule. you skin the Radionuclide scan because it is contraindicated in pregnancy. If it is indterminate or clinical suspicon. you do a FNAC as well. amniotic fluid embolization. . then thyroid lobectomy. This results in the follinwg: . Aetiology is unknown. If it is malignant.Na wasting results in a chronically low plasma volume reflected by a NORMAL BP despite high renin and angiotensin levels and by an impaired pressor response to angiotensin infusion. Subtotal Thyroidectomy only in 2nd trimester pregnancy or in children. Na.). References: .Metabolic alkalosis often develops.org/afp/20030201/559. then you treat with radioiodine or surgery.NMSR Tests . SLE. REFER TO PREVIOUS QUESTIONS LABELED ETHICS. If it is non-functioning. it should warrant investigating a battered child syndrome with intracranial hemorrhage (Subdural).K. It usually occurs in children and growth retardation is frequently associated. . There is usually no provem treatment for it except that of the underlying condition (Pancreatitis. Barter Syndrome: A syndrome characterised by deranged NaCl transport in the ascending thick limb of the loop of Henle and the distal tubule. If you do the thyronuclide scan. and Cl wasting contributing to the stimulation of renin release accompanied by juxtaglomerular cell hyperplasia. then Surgery with Radioiodine. polydipsia.aafp. . polyuria and muscle weakness. Hyperuricemia and hypomagnesemia may occur. and vasculitic diseases. then it is FNAC. If it is thyrotoxic. and intraretinal hemorrhage. then radionuclide scan..K depletion is not eliminated by correction of the hyperaldosteronism. Obviously. The kinin-prostaglandin axis is stimulated. trauma. Mental retardation may be a feature. If it is "cold". and urinary excretion of prostaglandins and kallikrein is increased. . retinal microinfarcts at the level of the nerve fiber layer).Aldosterone levels are elevated.. Platelet aggregation is inhibited. It appears on the fundoscopy as cotton-wool spots around the optic nerve (ie. Clinical features present in infancy or childhood and include anorexia. fat embolization. If it is bening.Kaplan notes . repeat FNAC in 6 months. .they can make decisions on there own and when they need parental consent. but then described with a number of conditions such as acute pancreatitis. ALREADY DISCUSSED PREVIOUSLY IN THE FORUM. In a child.High Yield Biostatistics Complete Approach Thyroid Nodule First: TSH.
Indomethacin 1 to 2 mg/kg/day usually maintains the plasma K level close to the lower limit of normal. 12 MONTHS FOLLOWUP IS ON AN AS-NEEDED BASIS.09%. tHIRD AGENT CAN BE INDINAVIR AS PREVIOUSLY RECOMMENDED OR MORE RECENTLY NELFINAVIR. and zalcitabine. K supplementation plus spironolactone. amiloride. OTHER AGENTS ARE AVAILABLE. PREGNANCY SHOULD NOT PRECLUDE SAME RECOMMENDATIONS. MORE ON THE SUBJECT: Risk: The average risk for HIV transmission after a percutaneous exposure to HIV-infected blood is approximately 0. NO DATA ABOUT TERATOGENICITY OF ANTIRETROVIRALS EXCEPT EFAVIRENZ IN ANIMALS. #2: NRTIs that can be considered for use with ZDV for PEP are lamivudine (3TC). HIV seroconversion: the estimated median interval from exposure to seroconversion was 46 days (mean: 65 days). the urinary chloride is usually low (< 20 mmol/L). nonnuceloside reverse transcriptase inhibitors (NNRTIs). nelfinavir (NEL) was approved for use by FDA and is now included in regimens recommended for the treatment of primary HIV infection. Think of Bartter syndrome. CHOICE OF ANTIRETROVIRALS DEPENDS ON THEIR TOXICITY AND UNDERLYING CONDITIONS OF PATIENT. In summary: Child with growth delay. IF UNCLEAR WHAT TO START WITH ZDZ/3TC IS A GOOD START SINCE 3TC (lAMIVUDINE) IS GOOD FOR ZDV RESISTANCE. didanosine (ddI). indinavir (IDV) was recommended as the PI for PEP because of its increased bioavailability when compared with saquinavir and its more favorable immediate toxicity profile compared with ritonavir. #1: ZDV (an NRTI) is the only agent shown to prevent HIV transmission in humans. #3: The addition of a PI as a third drug for PEP following high-risk exposures : Previously. FOLLOW-UP IS 6 WEEKS. or indomethacin will correct most features. triamterene. Antiretrovirals in prophylaxis: Several antiretroviral agents from at least three classes of drugs are available for the treatment of HIV disease. In adult patients. each of which has been included in recommended regimens that include ZDV. SEVERE HYPOKALEMIA. an ACE inhibitor. 12 WEEKS AND 6 MONTHS. In these conditions.3% and after a mucous membrane exposure is 0.Inheritance is autosomal recessive. who presents with normal BP. Since the 1996 PEP recommendations were published. but no drug completely eliminates K wasting. and Metabolic alkalosis. vomiting. Antiretrovirals in pregnancy: . Postexposure Prophylaxis to HIV-Patient (Source: CDC) SUMMARY AND USMLE TAKE HOME MESSAGE: TESTING AND PEP ARES RECOMMENDED ASAP AFTER EXPOSURE. and protease inhibitors (PIs). or surreptitious diuretic or laxative abuse must be excluded as a cause. bulimia nervosa. an estimated 95% seroconverted within 6 months after the exposur. These include the nucleoside analogue reverse transcriptase inhibitors (NRTIs).
change to Phenobarbital 3. old man brought to er and complained of both auditory & visual hallicination on ph/exa. usually a PI (i. The one that has most antimuscarinic is imipramine which is why it is used for Urinary incontinence and Enuresis along with desipramine. T3 and T4 total are low. or tuning the dosage of medication (Lithium. what to do? She is on phenytoin. TAKE IT. epileptic woman want to have a baby. HIV-antibody testing should be performed for at least 6 months postexposure (e. IDV or NEL). his skin is dry &pupil dilated What is the drug a)amitriptyline b)atropin c)risperidone d)Imipramine Ans: Tricyclics.advice abortion SWITCH TO PHENOBARBITAL. it is unknown whether the use of these agents during pregnancy will exacerbate the risk for pregnancy-associated hyperglycemia. The addition of a third drug. IF CHOICE IS GIVEN TO STOP PHENYTOIN FIRST TRIMESTER (AND NO OTHER CHOICE . and medical evaluation regardless of whether they receive PEP. and 6 months).htm Updated March 2003 "atropin psychosis” in is old men? A 72yr.g. should be considered for exposures that pose an increased risk for transmission or where resistance to the other drugs used for PEP is known or suspected.). but TSH is slightly high. Choice of agents: Most HIV exposures will warrant only a two-drug regimen.. ON THE OTHER HAND. They have antimuscarinic effects which would contribute to an atropinelike effect of psychosis. but for purposes of USMLE: Setting = Chronic illness (very sick patient). Checking Free T3 and T4 (mostly T4) would show normal range.stop phenytoin in first trimester of pregnany b. with not many symptoms as far as hypothroidism. So I would go for that one what is "sick euthyroid syndrome?" It's a much talked about syndrome still being investigated. No treatment is necessary except for tht of underlying chronic illness.cdc. Postexposure follow-up: HCWs with occupational exposure to HIV should receive follow-up counseling. usually ZDV and 3TC.e.gov/mmwr/preview/mmwrhtml/00052722.. IF CHOICE IS GIVEN NOT TO STOP DRUG (STICK WITH PHENYTOIN). Reference: http://www. a. at 6 weeks.change to valproicacid 4. using two NRTIs. postexposure testing.ZDV appears safe and well tolerated in both women and their infants who have had a follow-up period of several years. Amiodarone etc. 12 weeks. The use of PIs in HIV-infected persons has been associated with hyperglycemia.
One dose before 65yo. water source. II.HIV negative: ERHZ or SRHZ for 2 months then RH for 4 months . Bronchoalveolar Lavage => Bactrim. Elderly). IF HOSPITAL ACQUIRED (after 5-7days inpatient) : GNB Resistant: 3rd Cephalo (Ceftazidime/Cefotaxime). H. Flu and Strep B in neonatal. O2 Sat <94%. If life threatening = Amphotericin B). Endocarditis. Pneumonia: 1.LIKE IN THIS CASE TO SWITCH TO PHENOBARBITAL). Or new Fluoroquinolones. Inpatient: Fluoroquinolones alone if it’s CAP (Levo-Moxi-Gati) /or /3rd Cephalo. Otitis Media: Strep Pneumoniae most common. DHA. Hepatitis => Doxycycline). If pregnant: ERH higher doses same period as PZA and Streptomycin are contraindicated). then Amox/Clavulanate. CD4<200. Accompanying Diarrhea). Atovaquone for prophylaxis if G6PD deficient). Listeria. FIRST STEP = CXR. carbapenems. CT of scan if Papilledema. treat with ERHZ or SRHZ for 2 months then RH for 7 months (total 9 months. IV. or no response. Klebsiella (Current Jelly. There is no treatment currently proven for viral/aseptic meningitis. Ampicillin if Listeria suspected (Neonates.Viral 4. immunocompromised esp T cell. Cryptococcus in HIV. Ds with physical examination (bulging tympanic membrane in setting of ear pain and fever and decreased hearing). Coccidiomycosis (Arizona. Heamophilus (smoker COPD). COMORBIDITY. then Heamophilus Influenzae. Southwest desert => Fluconazole or Itraconazole.Other: PCP (HIV. If h/o of MRSA: Vanco. Otherwise. TRIAL OF STOPPING THE DRUG ON THE FIRST TRIMESTER IS ATTEMPTED++ Most commonly asked Infections: Focus on Management Most commonly asked infectious disease questions I. If Cryptococcus suspected: Amphotericin B followed by fluconazole therapy lifelong. (Ceftriaxone or cefuroxime) + erythromycin or doxycycline. . Meatpacking. ). Same as in bronchitis and sinusitis. Staph Aureus in neurosurgery. Mycoplasma (Bullous myringitis. If TB meningitis. Cold Agglutinins). RR>20-24). Dapsone for prophylaxis is sulfa resistant. or zosyn (Piperacillin/tazobactam) PNEUMOVAC if increased susceptibility. Give antibiotics prior to CT scan. If PCN allergy: azithromycin or clarithromycin. If resistance is a concern: ERH x 9months. Tuberculosis: . Pentamidine or Atovaquone if sulfa resistant. If recent Amoxicillin use. Cattle. then RH twice Qweek x 7months. ERH (increased doses) for 48weeks.Atypical: Legionella (older smoker. Empirically: Ceftriaxone or cefotaxime. I HAD VERIFIED IT.Pregnant and lactating woman: PZA and Streptmycin CI. Then Sputum if indicated. HSMG. and another one after.Typical: Strep Pneumoniae (rusty sputum). Best initial therapy: AMOXICILLIN. Chlamydia Psittaci (Birds). Meningitis:: Strep Pneumoniae most common in adults. Alcoholics => 3rd Cephalo. LP. Moraxella 2. and Moraxella Catarrhalis. III. Chlamydia 3. Neisseria Meningitides in adolescents. Q Fever (Coxiella Burnetti. ADMIT IF: HYPOXIA (pO2<70. Outpatient: Azithromycin or Clarithromycin.
. If bloody with fever and pain. VitB6 mandatory with INH to reduce side effects.Undercooked hamburger meat. Breastfeeding is not contraindicated despite presence of small amounts of meds in milk. If bone: early surgical drainage and debridement of necrotic bone. Infectious Diarrhea: . Vulnificus (if seawater contamination and underlying liver disease) . Coli or Shigella. MC protozoan with blood = Entamoeba Histolytica . Cyclospora.Blood => Enteroinvasive : Salmonella. Coli 0157:H7 . Difficile. If gas. . 3) Rifampin x 4 months (Side Effect: Red Man Syndrome). hemolysis and uremia=> Enterohemorrhagic E. Shigella (HUS). and contaminated water source. bloating. screen for prior TB Rx and current contraindications.Most common agent: CAMPYLOBACTER (Acute in healthy patient. Rifampin interaction with anti-HIV meds. Cryptosporidium. directly-observed TB therapy should be used for all HIV pts.Steriod use in TB Rx: only in TB meningitis and TB pericarditis. or contaminated water source Giardia or Cryptosporidiosis. E. Give Vit B6 if at risk to develop neuropathy (Pregnant. Others require expert intervention. Rotavirus second. Canned food => C. . Viruses. or joint TB.: Healthcare worker with high % of multiresistant TB patients. bloody diarrhea). Steriod therapy prevents cardiac constriction and neurologic complications from meningitis. Perfringens. bone.Antibiotic use => C. think Entamoeaba Histolytica.Travler’s watery diarrhea => Enterotoxic E. Coli most common.Acute onset diarrhea with RUQ pain => Yersinia .Add Vit B6 with INH use. think Giardia.Friend rice => Bacillus Cereus .Ship diarrhea => Most common Norwalk virus.Poultry/Eggs => Salmonella . high volume watery diarrhea => Cryptosporidium . V. meningeal. CI if immune deficiency/impairement. . . If immunocompromised. Protozoans. HIV. 2) RZ x 2 months. and Campylobacter (Guillain-barre). Seizure disorder). . uremia. . Also in children. Yersinia. DM.Contaminated shellfish => Vibrio Parahaemolyticus or V. along with RUQ pain and Jaundice.Latent TB: targeted testing to identify candidates. Diarrhea. Vomiting and WHEEZING => Scrombroid (histamine reaction) FIRST STEP: Is there blood or not? . Three regimens are considered: 1) Ideally: INH for 9months. weight loss.Extrapulmonary TB: 9months with same drugs if miliary. alcoholic. If Pregnant or lactating: INH QD or BID + Vit B6. .Immunocompromised (CD4<50). test for HIV. . Unrefrigerated meat => C. steatorrhea. NEXT STEP: NO BLOOD => WBC in Stools (Methylene Blue Testing) => WBC+ = .Pruritic rash.Camping trip => either Staph aureus if around 4hrs with UGI symptoms.g.Immunocompromised and bloody diarrhea => CMV .No blood => Giardia. Care must be taken if HIV patients on Nonnucleoside RT Inhibitors or Protease inhibitors. . Botulium.HIV Positive: Same treatment with additional considerations: longer duration.BCG Vaccine: recommended only on individual basis: e. Coli (HUS). think Enteroinvasive E.Drug-resistant patient: Resistance only to INH => RZ with E or S x 6months or E/R x 12 months. .
Mycoplasma Hominis.Secondary: Benzathine Penicillin Q week x 3 weeks same dose . TREAT: DOXYCYCLINE OR ERYTHROMYCIN . . IV Fluids if severe. Coli => 3rd Cephalosporins VI.Chronic Hepatitis C: Interferon combined with Ribavirin . Diagnose clinically and rising titers of complement fixing antibodies.Non Gonococcal Urethritis: Chlamydia.C. Serology for Chlamydia or Ligase chain reaction test.Needlestick: HBIg and Hep B vaccine if Hep B. Diff Toxin in stool TREATMENT: Oral fluid and electrolyte replacement (hypokalemic metabolic acidosis).If allergy to penicillin: desensitize or give doxycycline.Chronic Hepatitis B: Interferon or Lamivudine 3TC. Herpes Simplex. culture and PCR if needed. Desensitize first in Tertiary and Pregnancy D.E. IM Ceftriaxone Single dose and PO doxycycline x7days or PO Azithromycin Single dose. TREAT : Azithromycin single dose or IM rocephin single dose. E. Isolate organism in pus of buboes.Scrombroid => Antihistamine . No PEP for Hep C VII.Stool culture .4 million .C.Urethritis/Cervicitis: . (We add treatment for Chlamydia) . Laparoscopy is definitive test. Hepatitis: .Syphilis: .Campylobacter => Erythromycin .Cryptosporidium => Control of HIV with HAART . Diff => Metronidazole. Diagnose clinically along with Gram stain.Tertiary: IV Penicillin 10-20 million U/day x10 days . Trichomonas.PID: cervical motion tenderness. NEXT: US Pelvis (R/O Ovarian cyst or TOA). diplococci coffeebean intracellular. Alternatives: Ciprofloxacin x 3 days or Erythromycin x 7 days. . Treat: Admit when high WBC or high fever • Inpatient – IV CEFOXITIN (or Cefotetan) + Doxycycline • Outpatient – IV CEFTRIAXONE single dose + Doxycycline x14d C.Lymphogranuloma Venereum: Chlamydia Trachomatis – transitory primary lesion with suppurative lymphangitis. STD’s: A.Ova/parasites: Giardia and Cryptosporidia .invasive NEXT STEP: .Primary: Benzathine-Penicillin single dose IM 2.Chancroid: Heamophilus Ducreyi = Gram –ve B.Gonococcal: Gram –ve.Giardia => Metronidazole . B. . Culture for Gonorrhea on Thayer-Martin. Ureaplasma.
IV VANCO. If non gonococcal. Klebsiella. Urinary Tract Infections: A. TMP/SMX • Inpatient: IV Quinolones. If Chronic Osteomyelitis: IV x 12weeks then PO x 8-12 weeks.If allergic: Cephalexin.Granuloma Inguinale: Donovania Granulomatis – painless red nodule. Osteomyelitis FIRST: X-Ray+++ Takes two to three weeks before we see signs NEXT: Technecium bone scan or MRI NEXT: Blood Culture.Non gonococcal: IV Semi-synthetic Penicillin + Genta or 3rd Ceph. vaginal delivery.F. Infective endocarditis: FIRST: Blood Cultures + Transesophageal Echocardiogram .Cystitis: E. Septic Joint: FIRST: TAP IT + CULTURE – XRAY TREAT: . BONE BIOPSY AND CULTURE if BCx are sterile TREAT: IV Semisynthetic Penicillin + Genta or 3rd Ceph until culture results obtained.Gonococcal: IV Ceftriaxone XII.If allergic = IV Cefazolin if minor or IV Vanco if major allergy If oral therapy only: . If mother has disease but no vesicles apparent (not active). Diagnose with Giemsa or Wright stain = Donovan bodies – Punch biopsy if necessary TREAT: DOXYCYCLINE OR TMP/SMX. IV ATBx x 6-12 weeks. XI. If allergic. Coli. And S Aureus (Bullous impetigo).DOC = IV Peni 2 million Q4h . Staph Saprophyticus (Honeymoon cystitis). Enterococci. Enterobacter. FIRST: U/A (nitrites = Gram –ve) TREAT: • Uncomplicated: 3 days of TMP/SMX or Quinolone • Diabetic: 7 days • Pregnant: Amoxicillin or Nitrofurantoin B. C-section if active disease in pregnant. IV Ampicillin/Genta.Genital Herpes: Herpes Simples II – Tzanck test and culture TREAT: ACYCLOVIR – famcyclovir – valacyclovir. then Proteus. then elevated granulomatous mass in perineal area. Impetigo/Erysipela: Group A BetaHemol. OR ERYTHROMYCIN G.Amoxicillin twice daily for 7 -10 days . VIII. Clindamycin. 3rd cephalosporins IX. TREAT: If blood cultures +ve or facial erysipelas => IV ATBx . Healing and scar formation.Pyelonephritis: FIRST: U/A and US to r/o obstruction TREAT: • Outpatient: 10-14 days fluoroquinolones. or macrolides (Clarithromycin or Azithromycin) are alternatives: X. .
Bronchoscopy rigid only . . or Cephalexin) . Flu-like syndrome. Eikenella Corrodens. LABOR WITH ONLY MVP. Transesophageal Echocardiography. malaise. Flexible bronchoscopy. .DENTAL PROCEDURES: AMOXICILLIN OR CLINDA IF ALLERGIC (azithromycin. Recurrence of infection despite ATBx. Hemophilus parainfluenzae. If amp/amox given because of Cx+ve for Strep. systemic emboli. Hypertrophic cardiomyopathy.TREAT: IV Semi synthetic Penicillin + IV Ampicillin + Genta. and NEURO WITH IV CEFTRIAXONE XIV. ASD ostium secundum. circumcision. . may cause maculopapular rash. . Clarithromycin. Then alter according to cultures x 4-6 weeks. XIII.NO PROPHYLAXIS IN CARDIAC CATH+++. MITRAL VALVE PROLAPSE W/O REGURGITATION. C-section. Intubation.95% recover without intervention. Actinobacillus Actinomycetemocomitans. Cardiobacterium hominis. Fungal etiology.Ixodes scapularis (dammini) tick.Other: MYOCARDITIS. Hysterectomy. MENINGOENCEPHALITIS. Kingella Kingae): DOC = CEFTRIAXONE x 4 weeks.Symptoms 3-30days after bite.FIRST: Monospot (heterophil agglutination test) – Atypical lymphocytes on blood smear . Congenital Malformation except in ASD only Primum. SMG. Extravalvular infection. TREAT CARDIAC AND FACIAL PALSY WITH PO DOXY TREAT JOINTS WITH A MONTH OF ORAL DOXY TREAT MYOCARDITIS.Weeks later: NEUROLOGIC SYMPTOMS – FACIAL PARALYSIS. 8 weeks if it’s prosthetic valve. TAKE TO OR IF: CHF.CARDIAC CONDITIONS: Mitral Valve prolapse (WITH REGURGITATION).Fever. Headache. and occasionally.ERYTHEMA MIGRANS resolving in a few weeks.Bite often not remembered may be missing in the question stem . GIVE PROPHYLAXIS IF: . Do nothing. IV VANCO IF PENI RESISTANT. . H/O Bacterial Endocarditis. Prosthetic valve obstruction. lymphadenopathy. Lyme Disease: . maculopapular rash. . PERICARDITIS .Months: JOINT INVOLVEMENT DIAGNOSE: Clinical (ERYTHEMA + ONE LATE MANIF) + LAB (ELISA +WB) TREAT MINOR SYMPTOMS WITH DOXYCYCLINE OR AMOXICILLIN.URINARY OR GI PROCEDURES: AMP/GENTA OR VANCO/GENTA IF ALLERGIC . persistent bacteremia despite ATBx. Memory . sore throat. IF HACEK organisms (Hemophilus aphrophilus. Self-limited. Needs 24h of attachment to transmit borrelia burgdorefri. OTHER: 1) Infectious Mononucleosis: .
headache. Pneumonitis (usual cause of death).IF PREGNANT: CHLORAMPHENICOL. The capsule allows host defense evasion. . then painless black eschar.Exposure to the woodtick Dermacentor Andersoni EASTERN USA . FLUSHED FACE AND INJECTED CONJUNCTIVA .day 2-6: RASH WRITS AND ANKLES SPREADS CENTRALLY – PALMS AND SOLES+++ . horses.TREAT WITH PO or IV DOXYCYCLINE++ .Naturally occurring: exposure to sheep. .MAJOR COMPLICATION: CORONARY ARTERITIS = 1 OUT OF 4 => AMI .2-14days: Flu-like.Differentiate from Meningococcemia . TREAT WITH BOTULINUS ANTITOXIN FROM AUTHORITIES AFTER REPORTING TREAT RESPIRATORY FAILURE WITH INTUBATION AND MECHANICAL VENTILATION. tick-repellant. goats . .MUCOCUTANEOUS LYMPH NODE SYNDROME . then vesiculates.Infant: ingestion of organisms with elaboration or toxin in vivo (e.FEVER AND 4 OF: ♣BILATERAL CONJUNCTIVITIS MUCOUS MEMBRANE CHANGES: STRAWBERRY♣ TONGUE desquamation.B.COUMADIN FOR CORONARY ARTERY ANEURYSMS > 6.: honey-related = floppy-baby syndrome). removal of ticks at frequent intervals. 5) ANTHRAX: .g.Labs: Thrombocytopenia.Adult: ingestion of pre-formed toxin from canned food . nausea. Regional lymphadenopathy ++. CERVICAL ♣LYMPHADENOPATHY .5mm 4) BOTULISM: Difference between adult and infant botulism: .Transmission: DIRECT INOCULATION OR INHALATION .DIAGNOSE WITH SKIN BIOPSY OR SEROLOGY (not until 2 weeks later) .PROPHLAXY AFTER TICK BITE IS NOT CURRENTLY RECOMMENDED. erythematous papule. erythema)♣EXTREMITY CHANGES (edema.Hepatitis. 3) KAWASAKI Syndrome: . Steroids in refractory disease. Splenic rupture => Emergency Splenectomy 2) Rocky Mountain Spotted Fever: . .TREAT with ASIPIRIN AND IV Ig in high doses.Asian Chilren at higher risk . Mycoarditis.Bioterrorism .. . First.Complicated cases: ARDS – DELIRIUM – HSMG/JAUNDICE – MYOCARDITIS . then ulcerates. Encephalitis are managed symptomatically. High LFT’s . vomiting => self-limited or may spread with meningitis. Anthracis = Gram+ve Bacillus aerobic spore-forming. and generates edema.Cutaneous Anthrax within 2 weeks of exposure provokes toxin which impairs neutrophils.Prevent with protective clothing.
Throat Swab for SARS Test – CXR – CBC/Diff – GOT/GPT – LDH – CPK . . dysphagia. TREAT: No specific treatment recommendations can be made at this time.. Catarrhal stage. Imminzation available. Empiric therapy should include coverage for organisms associated with any community-acquired pneumonia of unclear etiology. Pertussis. or Platelet<150K YES: Respiratory distress? If yes => Suspect case of SARS. Within hours. AND ACCOMMODATION. rhinitis. recheck in 3 days. Infectious disease consultation is recommended. NO: Respiratory distress? If yes => Suspect case of SARS. GRAM STAIN CUTANEOUS LESION =>BOXCAR SHAPE CAPSULE ORGANISM – CULTURE – PCR . . h/o travel or contact. REACTIVITY.History of contact or travel . Can be only oropharyngeal: regional lymphadenopathy. DIAGNOSE BY ISOLATING ORGANISM FROM NASOPHARYNGEAL CULTURE (Bordet-gengou agar).TREAT WITH: DOC = CIPROFLOXACIN X 7-10DAYS (IF NATURALLY OCCURING – 60 DAYS IF BIOTERRORISM). etc. and convalescent stage. MANAGEMENT: . diarrhea. sore throat.GI anthrax: 2-5 days after ingestion. spores germinate in macrophages in lungs or multiply in lymphatics causing hemorrhagic lymphadenitis – overwhelming sepsis.Inhalational Anthrax: 10 days after exposure. even bowel perforation.Kaplan notes . .WHO PUPIL SIZE. rebound tenderness. coffeeground emesis.DIAGNOSE WITH PLEURAL FLUID. cervical edema. If no => Quarantine but no need for reverse isolation.CMDT . 6) Whooping Cough: B. ASSESS PUPIL SIZE. If no => Home rest with quarantine. REACTIVITY. Flu-like symptoms. abdominal pain.PROPHYLAXIS AFTER EXPOSURE TO SPORES: SINGLE-DRUG THERAPY.Add rifampin if inhalational/systemic X 2 WEEKS . SHAPE. 7) SARS = coronavirus DIAGNOSE: Fever 38deg. References: . Fever. DOXYCYCLINE = FIRST-LINE ALTERNATIVE. Treatment choices may be influenced by severity of the illness. TREAT WITH ERYTHROMYCIN x 10 days. paroxysmal stage (whoop cough). and URI. then mediastinitis.CDC .Does CXR show Pneumonia? ♣YES: Send to negative pressurized quarantine + report online to CDC ♣NO: Lymphocyte < 1000 or Inc GOT/GPT or Inc LDH or CPK. including agents with activity against both typical and atypical respiratory pathogens.ADMIT and ISOLATE (Universal Precautions for now) . . CSF. CXR IS FIRST STEP (Mediastinal widening = hallmark).
This is due to poor transmission of the light to the brain via a damaged optic nerve. more pronounced in darkness.(The parasymp system controls constriction -dilatation is controlled by the symp system. aneurysms of the carotid or subclavian arteries.significant possibility that there is an underlying malignancy Adie’s tonic pupil. ipsilateral anhidrosis may be secondary to lung cancer.heterochromia of the iris may occur (affected side being less pigmented). B) Equal Pupils: Argyl Robertson pupil –miosis. slow dilatation in prolonged darkness. bilateral. Syringomyelia if newly acquired in an adult --must be thoroughly investigated -. The brain perceives the same stimulus as having a decreased intensity and dilates both pupils. spinal cord. no response).-. . Parasympathetic dysfunction at or distal to ciliary ganglion. parasymp system is dominant because the iris sphincter is a stronger muscle. Pupil must be small . pupil is hypersensitive to weak pilocarpine 0. but fail to dilate a postganglionic lesion. Lyme disease . CVA. demyelinating disease. There is a segmental palsy of the iris sphincter muscle. diabetes (ischemia due to narrowing of small vessels that supply nerve). topical cocaine which will fail to dilate the miotic pupil relative to the larger pupil. Mostly in young females & unilateral .a slow redilatation after completion of accommodation (the near stimulus is removed). A) Unequal Pupils . mediastinal tumors. If both eyes are functioning poorly. relative mydriasis in bright illumination. hydroxyampthetamine 1% will dilate a pre-ganglionic lesion. migraine variants and apical lobe bronchogenic carcinoma. Pupil contracts with Physostigmine (agonist). dilated pupil is not indicative of pending herniation unless the patient is comatose. Miosis can also be seen in the early stages of coma and Due to drugs like Morphine and Pilocarpine. If longstanding--. Retina is light sensitive Cause lesions in Edinger Westphal nucleus associated with neurosyphilis. Horner’s syndrome – occulo-sympathetic paralysis-..Anisocoria: 20% of the population have perceptible anisocoria. C) Relative Afferent Pupil Defect The afferent pupil defect is the dilation of the pupil in the both eyes when the light is swung from the normal eye over to the defective one. but Atropine (antagonist) produces poor dilatation. ptosis. There may be transient dilation of conjunctival vessels and increased accommodation. preganglionic lesion is more serious.idiopathic benign internal ophthalmoplegia. or peripheral sympathetic trunk) causing miosis. poor to absent light reaction. a slow contraction to prolonged accommodation-. poor responsiveness to light good response to accommodation.125%. If associated with altered deep tendon reflexes (hypo. slow constriction in prolonged light.interruption of sympathetic innervation of eye (interruption of sympathetic pathways in the medulla.) Two most common pupillary problems: anisocoria and decreased pupillary constriction to light. etc. Causes are vertebral fractures. MS and midbrain tumors. (in Pharmacological mydriasis.or areflexia) is called Holmes-Adie syndrome.
5%. 0.5%. and 1. chiasmal tumors. Miosis. must be used TID or QID to maintain mydriasis. CVA. Destructive lesions result in ocular deviation to the same side but inability to turn to the opposite side. unilateral mydriasis via Hippocampal herniation through the Tentorium with compression of CN III as it exits brainstem. These cause corneal toxicity with repeated use--NEVER prescribe for home use. Mydriasis.total gaze palsy (ie inability to move both eyes together in a certain direction). Thalamus. OCULAR MOVEMENTS: If supranuclear control is lacking -. Irritative lesions cause the eyes to deviate to the opposite side acutely. acute angle-closure glaucoma.25%. histamine Pinpoint Pupils: Pontine hemorrhage or infarct. such as pinealomas . interruption of ascending Sympathetic pupillodilator fibers Large Pupil: Causes: Traumatic irridioplegia. thalamic pathology and transiently in newborns. Downward deviations occur in patients with hydrocephalus (setting sun). Anesthesia. Oculogyric crises are spasms of upward gaze typical of post-encephalitic states. Parkinson’s disease and Phenothiazine toxicity. May be caused by optic neuritis. morphine. Pilocarpine in 0. There has to be extensive retinal or optic nerve damage for an RAPD to be demonstrable. etc. limitation of gaze excursion. Drugs. class of drugs which cause pupillary dilatation: Alpha adrenoceptor agonists (sympathomimetics) such as epinephrine Small Pupil: Cause: Meningitis. scopolamine: dilatation at about 1 hour. ischemic optic neuropathy. homatropine: maximal dilatation is rapid. proparacaine 0. retinal detachment. See section on acute glaucoma for exception. Occipital lesions cause impairment of the pursuit movement to the same side and a homonymous field defect to the opposite side. temporal Arteritis. coma.0%. Cyclopentolate: maximal dilatation at 25 to 75 minutes. Apart from atropine.there will not be an relative afferent pupillary defect. must be used TID to QID. Frontal lobe lesions prevent conjugate movements to the opposite side on demand but normal movements on pursuit. Tetracaine 1%. deviation with coarse nystagmus or internuclear ophthalmoplegia can result. Generally needed only once per day. Patients with congenital achromatopsia and congenital stationary night blindness have been known to show a transient pupillary constriction to darkness. Vertical gaze paresis is classical for dorsal midbrain lesions. retinal artery or vein occlusion. lesions in the Subthalamus. pilocarpine instillation. Brain stem pathology is associated with multiple cranial nerve palsies and contralateral hemiplegia. lasting 6 to 24 hours. Media opacities like cataracts or vitreous hemorrrhages alone would not be sufficient.
Both ankle reflexes were absent and the right knee jerk was diminished. AV malformations. the index and. loss of the medial rectus adduction in the contralateral eye and a jerky nystagmus in the abducting eye. how should the arm be treated? #2: A 45-year-old man was recovering from a mild upper respiratory tract infection when he suddenly noticed weakness in both legs while walking up the stairs. with the exception of the flexor carpi ulnaris and the medial half of the flexor digitorum profundus. The latter two fingers were weakened by the loss of the flexor digitorum superficialis. The muscles of the thenar eminence were paralyzed and the right thumb was laterally rotated and adducted. In younger patients up to 25% have a thymoma. No flexion was possible at the interphalangeal joints of the index and middle fingers. he noticed a weakness of the muscles on the right side of his face. gliomas. He had sensory deficits for touch and pain sensations in the distribution of the stocking area of both feet and lower legs. All ocular muscle palsies and ptosis may be mimicked by myasthenia gravis. On physical examination the patient did not appear to be ill. Here a Tensilon test is diagnostic. Motor loss consisted of paralysis of the pronator muscles of the forearm and the long flexor muscles of the wrist and fingers. Two days later. while the ring and little fingers flexed. Examination of his leg muscles showed obvious signs of muscle weakness involving both legs. He also developed a numb sensation over the lower part of both legs and the feet. As a result of this. brain) or peripheral? Why? Would you request that an MRI be done? . AV malformations or hydrocephalus. Flexion of the terminal phalanx of the thumb was lost due to paralysis of the flexor pollicis longus.(Parinaud’s). The latter deviation was due to the paralysis of the flexor carpi radialis and the strength of both the flexor carpi ulnaris and the medial half of the flexor digitorum profundus. to a lesser extent. Internuclear ophthalmoplegia results from lesions in the medial longitudinal fasciculus connecting the ipsilateral CN VI and the contralateral CN III nuclei. often indicative of MS. the right forearm was kept in the supine position. He had no pyrexia. but can also be the result of head trauma. Sensory loss of the skin of the right hand involved the lateral half of the palm and the palmar aspect of the lateral three and one-half fingers. Would you expect damage to be central (spinal cord. MS and 3rd ventricle tumours. especially below the knees. When the patient was asked to make a fist of his right hand. There was also sensory loss of the skin of the distal parts of the dorsal surfaces of the lateral three and one-half fingers. What steps should the surgeon take in the repair of the wound? Is there a crucial time factor in repairing the nerve? How long would it take until function returns? What will be the first sign? Until recovery of function. Try yourselves at this: Neuro Cases #1: A 26-year-old man was involved in a street brawl and received a knife wound of the right arm at about the midhumeral level. brain stem neoplasms. and a mild form of facial nerve palsy involving the right side of the face. although weak flexion of the metacarpophalangeal joints of these fingers was attempted by the interossei. wrist flexion was weak and was accompanied by adduction. the middle fingers tended to remain straight. while shaving.
he complained to his wife of a left-sided headache. along a strip on her thigh on the right side. there was Babinsky response on the right. She complains of numbness on her right leg and especially on her thigh. She found him 1/2 hour later. How do you explain that? The CT scan showed that the infarct included the territory of the middle cerebral artery but the occlusion involved the internal carotid artery. but did not take his blood pressure medications. canceled the appointment. When her right toe is moved up or down. Although she can feel that she is touched on the right leg (except where noted above). he was unable to produce any intelligible speech and appeared to understand only very simple phrases. fine discrimination and vibration? There was no loss of pain and temperature. Upon examination you find the following. including pin pricks and touch. "like a shade coming down. She has a knife wound low on her right side in the back. What type of lesion would result in absence of sensation of a narrow strip on her thigh? Which sensory tracts are damaged to explain the lack of proprioception. slumped in a chair apparently confused and paralyzed on the right side. she has no reflex response when the tendon of the quadriceps is tapped (knee jerk) on the right side. Motor problems on the left. What's the territory? Headache and Visual problems on the right. She can tell the difference between the sharp point versus the dull point of the safety pin on the right leg. the patient cannot tell in which direction it is moved. when he developed several episodes of blurred vision. The leg was only mildly affected. . she cannot discriminate whether she is touched with two objects close together or just one object. the patient also complains that her left leg is numb and she has lost voluntary movements of her right leg. Her left side is totally normal. She has a reflex response when her Achilles tendon is tapped (ankle reflex). Several weeks later. Which sensory tract was spared? Explain the results of the Achilles and quatricepes reflex tests." involving his left eye. a middle-aged lady was brought to the emergency room. She has normal sensation above her pelvic region on both sides. He was referred for neurologic evaluation but because of a busy schedule. became hyperactive. Deep tendon reflexes were initially depressed on the right side. but within several days.Would you hospitalize the patient? #3: A successful 48-year old attorney was told he was hypertensive. She cannot feel when the tuning fork stops vibrating. These attacks each lasted less than an hour. Her sensory findings for her right leg are the same as during the previous examination. She has no sensation when stimulated. Where is the lesion? #5: Now it's the same case. Neurologic examination in the hospital revealed total paralysis of the right arm and severe weakness of the right face. Why was the territory of the anterior cerebral artery not infarcted? #4: After a fight in a bar. But this time. The patient was globally aphasic. He was apparently well until 4 days after his birthday.
foot and leg on the right side upon command. All reflexes appeared within normal range. a right pupil that was smaller than the left. The headaches began approximately 2 years previously.200 µL. the left side of her face appeared drier than . In addition. There were right motor problems and problems with especially the left eye. What is this due to? Would you request a lumbar puncture? What might it show? What is the diagnosis? #7: A 36-year old school teacher was evaluated for headaches and left arm weakness. However. Cranial nerve testing revealed a pupillary asymmetry (left. there is also some resistance to movement of the foot and lower leg. Six months ago she noted the onset of progressive numbness and weakness of the left hand and she reports that she is now unable to distinguish the temperature of bath water with her left hand. especially on the right side. The right plantar extensor response was equivocal. She was still unresponsive to spoken commands and had a rigid neck. and right nasolabial droop. the patient cannot tell the difference whether she is touched with the dull part or the sharp part of the needle --> they both feel dull to her. the Achilles tendon reflex is much more brisk on the right side than the left side. When quickly dorsoflexing her right foot. right 3 mm). following an episode of severe coughing. but the left was normal. she can accurately identify when the tunning fork stops and whether you move her toe up or down. with a right facial droop. Other findings included bilateral papilledema. you note some twitching of the muscle fibers. and the erythrocyte sedimentation rate was 30 mm/h. pulse rate and temperature were in the normal range. in addition.On the left leg. A CT scan showed a high-density area in the cisterns. right hemiparesis. decreased right corneal reflex." There have been no bowel or bladder abnormalities and her general health is otherwise well. She is unable to move her toes. A few days later. you can feel a rhythmic oscillation. she had noted dull pain in the left hand during the past year. incomplete extraocular movements on the left side. What does the twitching of the muscle fibers tell you about the area included in the lesion? Where is the lesion and which areas are included? #6:A 44-year-old woman was admitted after having a seizure. Examination was remarkable for mild thoracic kyphoscoliosis. on her left leg. she seemed slightly more alert and made purposeful movements with her left hand--but not her right hand. What sensory tract is now affected to give the absence of pain sensation on the left side? What structure is included in the lesion to give the plantar extension (Babinsky sign)? Explain the results of the reflex tests and the resistance felt when dorsoflexing the foot. and right hyperreflexia. Over the area of the right quadriceps. The blood pressure. During the past month she also has found that her walking is "stiffer than usual. but the other extremities were normal. When stroking the bottom of her feet. There was. 1 mm. the white blood count was 11. Dull occipital pain had persisted on and off since that time. She was lethargic. She complained of headache and a painful neck. however. You test reflexes: the knee jerk is still absent on the right side. The patient's right arm was hypertonic and paretic. a left ptosis. the right one has the plantar extension. Both pupils were round and reactive.
only the left one responds with an eye blink. There was marked atrophy of all muscle groups in the left arm. however. nausea and vomiting? Vibration and position sense impaired on left arm. and vomiting. When the left or right corneas are lightly touched. She can accurately detect. was admitted to the hospital because of a sudden onset of facial numbness. although no abnormalities could be detected on examination. On the right side of the body. Upon examination the following are noted. What's your diagnosis? Why was sensation impaired over the face? Why were the arm and leg on the left described as clumsy? There is also an intention tremor. she cannot distinguish the sharp one from the dull one--both stimuli feel dull to her. When the right side of her face is touched with a sharp or a dull object. with moderate spacticity of both legs. Why? Pain and temperature were impaired on the right side of the body. the patient can draw the lips back on the left side and she can wrinkle her forehead on that side. Examination revealed impaired sensation over the left half of the face. There was subjective numbness of the right arm. but otherwise unremarkable. What could be the cause for the unequal size of pupils and ptosis? Why would one side of her face be drier? Which area in the spinal cord could be involved to give the above symptoms? #8: A 49-year old landscape artist. on both sides of the body. and the gag reflex was diminished. There was complete loss of pain and temperature perception from C5 to T1 on the left and patchy abnormalities of pain and temperature sensation in the right forearm.on the right. How would you explain the motor problems to her face? Would you expect that sounds appear louder on the right side? Why? . there was impaired pain and temperature sensibility. A leftsided Horner's syndrome (miosis. vertigo. he developed difficulty swallowing and complained of intractable hiccups. She complains about numbness on the right half of her face and loss of motor control also on the right side of the face. on the left side both stimuli appear dull to her (on her body and upper and lower limbs). Vibratory and position sense were now impaired in the left arm. and there was an intention tremor on the left. Why? #9: A 53-year old woman is referred to the neurologist. Over the ensuing 12 hours. however. had paralyzed vocal cords and a diminished gag reflex. she makes accurate responses when touched on the right side. ataxia. She can accurately localize where she is touched on her body and all limbs. ptosis. Why was there a Horner's syndrome? The patient had difficulty in swallowing. who had traveled to many countries. Gait was mildly stiff legged. The arm and leg on the left side were clumsy. nausea. She has no motor problems involving her body and upper or lower limbs. When asked to smile. She is numb on the left side of her body. Touching various parts of her body with dull and sharp objects. She was areflexic in the left arm and hyperreflexic in the right arm and in both legs. Position and vibration perception were normal throughout. anhydrosis) was apparent. Why? What caused the vertigo. the right side shows little motility. the vocal cord was paralyzed. when the tuning fork stops vibrating and if the toes are moved up or down.
there were exaggerated biceps. Gait was stable.How do you explain the lack of pain discrimination on the right side of her face versus the left side of her body? How do you explain the results when testing the corneal reflex? Where would you expect the lesion to be? #10: A 67-year old man suddenly could no longer move his left arm and leg. Testing the sensory system. the only finding was that the right eye did not constrict in response to light. he could wrinkle his forehead. Testing for eye movements: when asked to look to the left. Sensory examination was normal. he could not pull his lips back on command. The landlady remembered that 2 months earlier he . Although he was apparently in good health. There was a left facial asymmetry. however. Although the headaches typically disappeared shortly after arising from bed. Which structure was involved to give you the exaggerated reflexes on the left upper and lower limb? What caused the problems with the facial muscles? What did the tests for eye movements show? Is that consistent with the pupillary response? What would an MRI show? #11: A 59-year-old man was well until 2 months prior to admission. The neurological examination found the following. knee and ankle reflexes on the left limbs but normal on the right. at rest. The remainder of the cranial nerves were normal. On examination. His family took him to the emergency room. he had also bitten his lip. Testing the motor system. although the patient had a tendency to fall when turning rapidly. On the left side of his face. What is the most likely cause of the patient's symptoms? What is the significance of the papilledema and headaches (especially early morning ones)? What tests would you recommend? #12: A 55-year-old professional exhibiting signs of confusion was brought to the hospital. Reflexes were increased on the left and plantar responses were extensor bilaterally. the right eye tended to move laterally. Past medical history was notable for a malignant melanoma which was discovered on his right arm 2 years previously and treated with local resection and a radical axillary lymph node dissection. Two days earlier he developed progressive weakness of his left hand and an unstable gait. although confused and unable to give a coherent history. his landlady had entered the apartment on the day of admission because he did not respond to her calls. when he developed early morning headaches which would awaken him from sleep. Fundoscopic examination revealed bilateral papilledema. incontinent of urine and appearing bewildered. the patient was alert. The plantar response was extensor on the left (Babinsky sign) and flexor on the right. All other sensory systems were intact. the left eye moved laterally but the right eye looked straight ahead. triceps. Review of systems revealed weight loss of 15 pounds over the past month. on the way there he also complained that he was seeing double. There was nearly complete paralysis of the left arm and mild weakness of the proximal left leg. the severity of the headaches was increasing with time. She found him lying on the floor. The history gathered from his landlady disclosed that he had been separated from his family because he drank too much.
Vital signs.5 mm per day is the average rate of regeneration. 4/µL. The patient recovered only minimally. #2: Would you expect damage to be central (spinal cord. normal extraocular movements. and urinalysis were within normal limits. Neurologic examination showed normal optic fundi.had been involved in a fight in a bar. A CT scan of the head was obtained. The reflexes were either diminished or absent-central problems would cause hyperreflexia. and dirty. touch and tactile sensation are the last to return. complete blood count. On what area would you have them focus the MRI? Would you hospitalize the patient? Yes. Motor problems on the left because the motor fibers crossed therefore the symptoms were . 3 weeks previously he had fractured his wrist falling down stairs. sensory and motor systems were equally affected on both legs-indicating most likely peripheral involvement Would you request that an MRI be done? No. On examination. The wound has to be cleaned and be free of infection. Angiography revealed occlusion of the internal carotid artery. The peripheral nerves dealing with breathing and/or swallowing could become involved. Sensation returns before voluntary movement. Cell counts in all tubes showed red blood cells. Pain caused by deep pressure is the first sign of recovery. and a glucose level of 70mg/dL. and polymorphonuclear neutrophils. probably Gullain-Barré syndrome. and there was a left sided plantar extensor response. brain) or peripheral? Why? The damage would involve the peripheral nervous system. xanthochromia. #3: A CT scan revealed an infarct in the territory of the middle cerebral artery of the left side. this segment becomes sensitive to mechanical stimulation (Tinel’s sign). the patient became deeply obtunded and seemed to develop a left-sided hemiparesis. the patient was unconcerned. Could the patient's problems be due to recent trauma? What is the most likely diagnosis? What do the findings from the lumbar puncture indicate? ANSWERS: ----------------------------------------------------------------------------------------------------------------------------Answers: #1: Median nerve. how should the arm be treated? Paralyzed muscles should be protected with a splint and joints exercised daily to maintain circulation and preserve motility. How long will it takes for recovery and how will the patient know? 1. and no abnormalities that would result from dysfunction of other cranial nerves. Bruises on his head and legs were consistent with recent trauma from a fall. disheveled. The patient appeared to fall asleep when left alone. The nerve can be repaired up to 12 months post-trauma. Until recovery of function. lymphocytes. Over the next 36 hours. The reflexes were normal and symmetric. Patient has polyneuropathy. A lumbar puncture showed an opening pressure of 180 mm of water. 800/µL. vasomotor control return at this time. 20/µL. Once the nerve has entered the distal segment. a protein level of 80 mg/dL.
dorsal root) or the posterolateral area in the spinal cord where the fibers enter (i. the posterior columns are intact on the left side. The Achilles tendon reflex is hyperreflexic. Damage to posterior column on the right side could explain the lack of proprioception. blood supply from the right internal carotid system supplied the blood to the left anterior cerebral artery. indicates that the lesion is at the L2 level. zone of Lissauer). Where is the lesion and which areas are included? This is a lateral hemisection of the spinal cord (Brown-Sequard syndrome) at L2 level. indicate an upper motor problem = damage to the corticospinal tract. Why was the territory of the anterior cerebral artery not infarcted? There was collateral circulation via the anterior communicating artery. i. What is the diagnosis? . anesthesia. Explain the results of the reflex tests and the resistance felt when dorsoflexing the foot. The knee jerk is absent which means either the sensory or motor component is absent. the finding would be blood in the CSF. The Achilles reflex is normal therefore sensory and motor root segments of S1-2 are intact. If done. The anterolateral system was spared. a lumbar puncture is not advisable. together with the hyperreflexia. the problem with the eye is caused by involvement of the cranial nerve III. # 6: The sudden onset suggests involvement of blood vessels.e. the incoming sensory information (proprioception) is absent on the right side (L2-4). fine discrimination and vibration. Would you request a lumbar puncture? What might it show? The bilateral papilledema suggests increased intracranial pressure. There were right motor problems and problems with especially the left eye. the proximal portions of the dorsal root and zone of Lissauer was damaged. What does the twitching of the muscle fibers tell you about the area included in the lesion? The twitching indicates that a motor neuron has been damaged (lower motor neuron sign). The visual problems are called "amaurosis fugax" = transient monocular blindness due to interruption of blood flow from the ophthalmic artery to the retinal artery. In this case. In this case.e. What is this due to? These alternating signs are due to damage to the motor tract carrying information for the opposite side of the body.opposite to the lesion. The spasticity and clonus.e. This area as well as the level of anesthesia and other sensory losses. What structure is included in the lesion to give the plantar extension (Babinsky sign)? The corticospinal tract on the right side. The lesion therefore is at the posterolateral quadrant of the spinal cord at level L2. However. however. #5: What sensory tract is now affected to give the absence of pain sensation on the left side? The anterolateral system is damaged on the right side. therefore there is no loss of discriminatory touch or vibration on that side. The CT scan showed that the infarct included the territory of the middle cerebral artery but the occlusion involved the internal carotid artery. It could be an aneurysm. the damage must occur either to the incoming afferents (i. it does not appear to be due to hypertension. #4: To have absence of all sensation.
carried out on an emergency basis. Which area in the spinal cord could be involved to give the above symptoms? Syringomyelia: cavitation within the spinal cord around the area of the central canal. arms and hands). presumably infarction. usually in the cervical spinal cord. Therefore . most likely one of the cerebellar peduncles was involved. Arteriography. Why would one side of her face be drier? Interruption of sympathetic ANS. #8: MRI demonstrated an abnormality. revealed occlusion of the posterior inferior cerebellar artery with "beading" (evidence of inflammation) of vertebral arteries and anterior inferior cerebellar arteries. loss of some eye movements). Over the ensuing six months. Brainstem = Crossed signs: Ipsilateral Nerve Palsy (Left). Why? The lower motor neurons innervating the pharynx and larynx were damaged. and a presumptive diagnosis of Wallenberg's syndrome (lateral medullary plate syndrome) on the basis of occlusion of the posterior inferior cerebellar artery was made. #7: What could be the cause for the unequal size of pupils and ptosis? Left eye: miosis. Together with the intention tremor. this is called Horner's syndrome. this is also part of Horner's syndrome. had paralyzed vocal cords and a diminished gag reflex. The initial symptoms are loss of pain and temperature bilaterally but only for arm and shoulder regions. the posterior columns might be involved (with loss of discriminatory touch) as well as the anterior horn (causing paralysis of muscles in shoulders. Why was there a Horner's syndrome? There is a descending tract dealing with sympathetic information going to the upper thoracic spinal cord. there was greater involvement of the left portion of the spinal cord. It often affects only the crossing pain and temperature fibers (these are second order fibers: cell bodies are in the dorsal horn and the axons are crossing near the central canal to join the contralateral anterolateral system (ALS). Why was sensation impaired over the face? The trigeminal nerve. the sign for the latter are decreased corneal reflex and nasolabial droop) and the CN III (signs are small pupil. Most likely. The patient was treated with intravenous penicillin. many of his deficits resolved and he resumed his activities including his painting. putting pressure on the medial portion of the left cerebral peduncle (especially motor pathways to the arm and face. this is ataxia. Lumbar puncture revealed 40 white blood cells (mostly lymphocytes) per cc of CSF. Serologic testing of the CSF and serum was positive for syphilis. the intermediolateral cell column was affected giving the Horner's syndrome. ptosis and anhydrosis due to interruption of sympathetic innervation of the face including the eye. Why were the arm and leg on the left described as clumsy? There is also an intention tremor.Subarachnoid hemorrhage on the left side of the midbrain. and contralateral motor sings (right). The patient had difficulty in swallowing. As the cavity expands. In this case. tract or nuclei must be involved. in the lateral medulla on the left side. In this case. this indicates damage to tracts or areas associated with the cerebellum. the tract is located in the lateral portion of the medulla and was damaged.
Pain and temperature were impaired on the right side of the body. Note: The corticobulbar tract also involves other cranial nerves. Why? ALS damage gives contralateral signs. sparing the medial lemniscus and the corticospinal tract. the damage is either to the nerve or nucleus of CN VII on the right. #9: How would you explain the motor problems to her face? Since there is little motility in both the upper and lower portion of the right half of the face. What did the tests for eye movements show? Is that consistent with the pupillary response? The right eye could not move medially and at rest tended to move laterally--these are sign of CNIII damage. which has crossed.the vagal nerve complex and/or nucleus ambiguus were damaged. the information has not yet crossed. Where would you expect the lesion to be? At the level of the pons but the caudal portion. only the lateral tegmental portion is involved. on the right was also damaged. the spinal component dealing with pain and temperature. this is an upper-motor-neuron sign and the corticospinal tract (or motor cortex) is damaged. This suggests damage to the contralateral (right) corticobulbar tract. #10: Which structure was involved to give you the exaggerated reflexes on the left upper and lower limb? This is hyperreflexia. which dampens incoming sounds. is innervated by CN VII. the loss of pain on the body is due to damage of the ALS. How do you explain the lack of pain discrimination on the right side of her face versus the left side of her body? Loss of pain discrimination on the face is due to damage of the spinal trigeminal nerve. The plantar extension on the left is also indicative of this type of damage. The innervation of the cornea does consist primarily of pain fibers but there is sufficient touch innervation to get the corneal response. left face. CN V. How do you explain the results when testing the corneal reflex? CN VII is responsible for the motor component of the corneal reflex. the innervation of cranial nerve motor nucleus is bilateral (except for the motor neurons innervating the lower portion of the face) and damage to one corticobulbar tract gives minimal signs if any. . What caused the problems with the facial muscles? The problem was only with movement of the lower. The stapedius muscle. However. What caused the vertigo. although it may be sluggish. Why? Only the gracilis nucleus/tract were damaged. cuneate nucleus is more rostral and was not damaged. It is therefore absent on the right. Vibration and position sense impaired on left arm. Would you expect that sounds appear louder on the right side? Why? The sounds would be louder in the right ear. the medial rectus is required to move the eye medially and oppose the lateral rectus muscle. Note: CN V is responsible for the sensory component of this reflex. however. nausea and vomiting? Damage to the vestibular area.
What do the findings from the lumbar puncture indicate? The findings indicate subdural hemorrhage. His level of consciousness had deteriorated and he seemed to have had a seizure (incontinence and a bitten lip). #11: What is the most likely cause of the patient's symptoms? Metastic tumor in the right frontal lobe. The fight in the bar could have caused arachnoid tearing which was aggravated by his fall. the drop in CSF pressure associated with lumbar puncture or both. triggered by the blood mass. The medial portion of the cerebral peduncle contains corticopontine fibers which do not give a symptom.html OLD REQUEST: Next step in of Cholesterol/LDL labs Basically. References: http://www.indiana. FIRST OF ALL: RISK FACTORS: .low HDL<35 Note: TG are NOT A RISK FACTOR YET.] What is the most likely diagnosis? Right-sided subdural hemorrhage confirmed by CT. Now: after assessing your patient: . in this patient chest X-ray revealed metastic lesions of lung and bone. #12: Could the patient's problems be due to recent trauma? Yes. What is the significance of the papilledema and headaches (especially early morning ones)? Both signs are due to increased intracranial pressure What tests would you recommend? CT: would expect to find multiple areas of increased density in both hemispheres = gliomas. Prognosis is poor.HTN>140/90 . Cerebral metastes usually occur in the setting of widely disseminated cancer therefore one should investigate the extent of cancer spread. increased protein and glucose. TYPE A PERSONALITY IS NOT RISK FACTOR. HDL>60 IS PROTECTIVE AND NEGATES ONE RISK FACTOR.CURRENT SMOKING .AGE MEN>45 WOMEN>55 (If you give male gender as a risk factor don't add age and vice versa) . both findings suggesting cerebral involvement. think of it this way. spread via blood supply. The worsening of the patient's condition was caused by imminent herniation of the brain.FAM/H FIRST DEGREE RELATIVES CAD<55 MEN <65WOMEN . [xanthochromia = old and fresh blood.edu/~m555/cases/cases. The majority of patients with brain metastasis die of complications from systemic cancer rather than from direct effects of the brain tumor. Patient has less than 2 risk factors or more than 2. Treatment is surgical removal of blood and closure of bleeding veins. Compromised were the CNIII and portions of the cerebral peduncle involving the corticospinal and corticobulbar tracts. increased pressure.What would an MRI show? An infarct to the right ventromedial quadrant of the mesencephalon.DM .
Playing with her blood sugar medications in hope to reduce the TG will not do much since she is already borederline. so primary prevention has a goal for LDL of < 100. and thyroxine. CAD S/P Inf MI 8 years ago. Reference: -CTB -Swanson . She is a lifelong NONsmoker. Lipid Panel: Total Chol=288 TG= 262 HDL 37 LDL=199 This guy also has more than 2 risk factors. LDL >190 => START MEDICATION. Sternum). His uncle had an MI at 58. Usually HMG CoA is first line in high cholesterol. but according to CTB.Less than 2RF: Cholesterol<200 => remeasure in 5 years Cholesterol 200-240 => remeasure in 1-2 years Choesterol >400 => MOVE TO NEXT STEP =>LDL LDL<160 => Remeasure in 1 year LDL 160-190 => DIET 3 months step1 then 3 months step2 before moving to meds. Cholesterol: 240 HDL 46 LDL 167 TG 135 HBA1C 7% Glucose 128 Next step in managing her lipid panel? Introduce medication HMG CoA Reductase with goal LDL<100. NIACIN AND GEMFIBROZIL ARE FIRST LINE UNLESS CHOLESTEROL IS REAL HIGH. and hypothyroidism. CXR is First step If Wide Mediastinum = NONINVASIVE TESTS: Spiral CT or Transesophageal Echo. . ASpirin. Niacin would increase her BS. . He never had an MI. She is on Glyburide. A 51 yo male comes to ur office for yearly visit.Blueprints medicine Rupture Thoracic Aorta Suspect with Deceleration injury of Fx of hard to break bone (Scapula.More than 2 risk factors: Cholesterol<200 : Remeasure in 5 years Cholesterol >200 : => LDL LDL<130 : Remeasure in 1 year LDL 130-160 : DIET (same as above) LDL >160: Medication Cases: 72yo woman presents with Type 2 diabetes history. Chol >200 and LDL>160. She denies any sympptoms. Introduce Diet and Medications HMG CoA Reductase. BP 170/100. Atenolol.. and brother at 55yo. body mass index 31.
5-1%/year Other: .PSA is ordered . THEN Surgical Repair Bistats Q A 55 yr old man visits his physician with a complaint of urinary infrequency.commonly PSA greater than 4 is considered abnormal. Let's draw that in a table shall we? -------POSITIVE-----NEGATIVE SICK---80(TP)--------20(FN) WELL---90(FP)--------810(TN) We use the numbers of positive predictive and negative predictive value = Meaning How positive is positive and how negative is a negative. Endometrial cancer screening (endom aspiration or transvaginal US) at 2535yo for women. yearly sigmoidoscopy at 12 yo. The best estimate that the patient is ACTUALLY HAVING CA PROSTATE = Positive Predictive Value. If diag +ve = surgery before 20yo.what is ur best estimate that this man is actually having ca prostate. 100 will have the disease and 900 wil be well.Barium Enema Q5-10 years FAM/H OR 1ST DEGREE RELATIVE WITH COLORECTAL CA: . . And 90 are NEGATIVE AND SICK (False Negatives).using this standard this test has a sensitivity of 80 and specificity of 90. Frequency: every 1-2 years – multiple biopsies each time (@least 32). 80 are positive AND sick (True Positives).Colonoscopy Q 10years . The prevalence in this population is 10%. If not possible. and 20 are negative AND sick (FAlse Positives) . If +ve => Family colonoscopy q1-2y starting from 25yo or 5 years younger than the earliest diagnosed in the family.Examination finds a 1cm nodule in his prostate. If low-grade dysplasia => every 3-6 months to confirm presence of dysplasia before performing colectomy Risk of colon carcinoma after 10 years of disease = increases 0.the pt's test result is 7.the prevelance of prostate ca in this age group is 10. the answer is 47%.The specificity is 90%. Means out of the 900 well population . 2> at what age is FOBT recommended? AVERAGE RISK: . can anyone plz explain how u arrive at this. . Means out of the 100 people sick.HNPCC = suspect after colonic adenoma => Genetic screening. when shud we start colonoscopy/sigmoidoscopy? START COLONOSCOPY 8-10 YEARS AFTER DIAGNOSIS.FOBT annually >50yo in average risk individuals . 90% (810)are NEGATIVE AND WELL (True negatives).familial polyposis = genetic screen at 10yo. PPV = True positive/all positives = 80/80+90 x100 = 47%. Means if we assume a number of 1000 people. Random Q & A from exam 1>in UC.FOBT + Flex Sig Q 5 y .IF non-conclusive THEN AORTOGRAM.The sensitivity is 80%.
BETA-BLOCKER. But remains awake if short episode) = TRICYCLIC ANTIDEPRESSANTS . 7> IF A ASTHAMAA AND HTN IN A PT GIVE CA CHANEEL BLOCK SAME IS WITH ACHALSIA ND HYPERTENTION. IV VERAPAMIL.Begin at 40yo or 10 years younger than diagnosis of youngest relative => Colonoscopy q3-5y 3>what is the first step in cushing disease LOW-DOSE OVERNIGHT DEXAMETHASONE SUPPRESSION TEST (excludes Cushing in 98% cases). most common = campylobacter. drug abuse and somatization disorder. Salmonella. (Montezuma’s revenge). OR DILTIAZEM. If no history of travel. CAREFUL IF THAT’S WPW. tortured animals when kids. 10>drug of first choice in depression SSRI = FLUOXETINE 11>what the adult form of conduct disorder ANTISOCIAL PD = Long criminal record. AVOID VERAPAMIL/DIG…USE PROCAINAMIDE/QUINIDINE 9>diarrhea in mexico with no blood and wbc in stool. THEN Surgical Repair 6>what is the clinical association for ADHD genetically? TOURETTE SYNDROME. TRAVELER = E. Other invasive: Shigella. Liars with no remorse. 13>drug of choice for eclampsia MAGNESIUM SULFATE 14>drug for narcolepsy FORCED NAPS AT REGULAR TIMES IS TREAMENT OF CHOICE. DIGOXIN. Yersinia. and set fires. EXCEPT ANTISOCIAL WHICH BEFORE 18YO WOULD BE CONDUCT DISORDER. CLINICAL ASSOCIATION. COLI. 12>can we diagnose a pt of 15 yrs with personality disorder YES.. strong association with alcoholism. DRUG: PSYCHOSTIMULANTS IF CATAPLEXY PRESENT (sudden loss of muscle tone precipitated by loud noise or emotion = pathognomonic. Sternum). 4>gold standard test for aortic dissection? AORTOGRAM 5> first step in aortic dissection if the pt is stable => CXR Suspect with Deceleration injury of Fx of hard to break bone (Scapula. IF non-conclusive THEN AORTOGRAM.most common cause: NO BLOOD/ WBC +VE => INVASIVE. OCD. 8>drug of choice for VF and AF V-FIB IMMEDIATE DEFIBRILLATION A-FIB SYNCHRONIZED CARDIOVERSION IF UNSTABLE. CXR is First step If Wide Mediastinum = NONINVASIVE TESTS: Spiral CT or Transesophageal Echo. GENETICALLY REALTED = STILL UNDER INVESTIGATION.
good academics. THEN STARTS DECLINING SEMIPHYSIOLOGICALLY MORE THAN NON-SMOKERS.WEATHER ITS BCZ KIDNEY IS BEING REJECTED BY THE PT OR ITS DUE TO CYCLOSPORIN U HAV ETO DO BIOPSY. poor impulse control).. OTHER: RISK OF HEART ATTACK IS DECREASED BY 50% WITHIN 24H OF QUITTING. RISK OF LUNG CANCER DECREASES BY 80-90% AFTER 15YEARS BUT NEVER REACHES LEVELS OF NON-SMOKERS. USUALLY . 20>effects of malignany on psychological state I CAN’T FIGURE OUT THIS QUESTION. NEEDS MORE EXPLICIT. Risk of having a stroke and brain aneurysm declines by 30-50%. purging. HE ALSO SAID THAT FOR EXAM POINT OF VIEW THEY WILL ASK U THAT AFTER 7 DAYS OF KIDNEY TRANSPALNT PTS CRETINE WENT SKY HIGH . RATIO SHOULD NOT BE DECLINING SINCE FEV1 AND FVC ARE DECLINING “PHYSIOLOGICALLY” AT SAME RATE.…. . exercise. fasting.BUT B4 THAT U HAVE TO C WEATHER THERE IS ANY TENDERNESS AT TH E GRAFT SITE OR FEVER IS . 21> IN A PATIENT WITH ACUTE LUNG INJURY BREATHING SPONTANEOUSLY. Joins level of non-smokers after 2 years.. INTUBATION AND THE APPLICATION OF BOTH AN ENRICHED FiO2 AND PEEP SUFFICIENT TO RECRUIT COLLAPSE ALVEOLAR UNITS SHOULD DO WHAT TO PULMONARY VASCULAR RESISTANCE? Decrease it by reversing hypoxic pulmonary vasoconstriction.15>pt with wt loss.female.HTN which drug to administer THIAZIDE DIURETIC 19>smoking cessation. exercise. purging etc. 16>most common case of suicide? UNTREATED DEPRESSION 17>which drug to administer first to a pt of thyroid storm? PROPRANOLOL OTHER: PTU (=THIOUREA DRUG) – POTASSIUM IODIDE (1H AFTER FIRST ANTITHROID DRUG) – Ipodate sodium (1h after PTU) – DXM.AN= WEIGHT LOSS – SPORTS – AMENORRHEA – MAJOR DEPRESSIVE DISORDER with atypical features (leaden paralysis.HTN AND NEPHROTOXICITY....15 yrs:diagnosis? MAIN QUESTION is it Anorexia or Bulimia? Both have fasting.. BUT LESS THAN CURRENT SMOKERS...effect on lung changes FEV1 IMPROVES FIRST YEAR. how do you treat Cyclosporine induced HTN? ACCORDING TO DR SAKALA HE SAID CYCLOSPORIN IS MUST FOR POST TRANSPLANT PT BCZ WE DONT WANT TH E PT TO REJECT KIDNEY BUT WE HAVE TWOMAIN PROB . overeating). HE ALSO SAID NEVER D/C CYCLOSPORIN BUT JUST DEC TH EDOSE AND GIVE PT ACE INHIBITERS... Definitive treatment with radioactive iodine or surgery is delayed until euthyroid.... 18>black male.BN = RELATIVE GOOD WEIGHT FOR AGE – BORDERLINE PERSONALITY DISORDER (body image.30s....
html My review of the exam I had one of those days. the government may step in. However..? START HER ON SYNTHYROID. Reference: http://www. the rate of relapse declines during pregnancy.. the minor's parents are NOT legally obligated to support the baby... SLOW DEEP TENDON REFLEXES WITHDRWAL..NEVER EVER DO TAHT THEY TEST U WITH AMIDIARON AND OTHER MEDS IN SAME WAY BCZ IF U WILL D/C PRIMARY PT WILL RELAPS AND THEN U WILL HAV ETWO PROBLEMS INSTAED OF I.WHAT U WILL DO. Postpartum IVIg treatment is beneficial in preventing acute childbirth-associated exacerbations in patients with Relapsing/Remitting Multiple Sclerosis.. D/C LITHIUM AND START HER ON SYNTHYAROID .albany.. and increases during the first three months post partum before returning to the prepregnancy rate. long-term disability is not higher in pregnant women or even women experiencing relapses during the pregnancy year.. I REMMBER IN MY ACTUAL TEST THEY ASK THAT THIS PT IS ON LITHIUM FROM LAST 3 YRS BCZ OF BIPOLAR SHE IS OKAY NOW S/S FREE FROMLAST SIX MONTHS AND NOW SHE IS SO DEP AND FEEL WEAK AND GAINING WEIGHT AND HAIR R CANGING IN TEXTURE BARDYCARDIAC ... Unique Ethics case: Minor patient doesn’t want to abort but mother wants her to It's depending on the states.. This could result in the baby becoming Dependent. Some Dependent children live with birth parents or other relatives but are subject to government monitoring.. On the other hand. although patients with severe MS may have difficulty fully caring for their newborns..CHECK LITHIUMMM LEVEL . I took a break at the end of every block.. but generally: the parents of a pregnant minor cannot legally force their child to have an abortion. the lifetime risk rate does not appear to change because of pregnancy. If the minor and the baby's father and any other willing relatives cannot or will not support or care for the baby... Other Dependent babies are placed in foster care.... Multiple Sclerosis and Pregnancy In women with Multiple Sclerosis.JUST CHECK TH E LEVEL AND DEC THE DOSE AND START PT ON THE MEDICATION THEN SLOWLY INC THE MEDCIATION IN A THERAPETIC RANGE.net/~tjc/pregnancy.HIGH BCZ INFECTIONIS MOST COMON CAUSE OF DEATH IN ALL TRANSPLANT PTS JUST LIKE AMI IS TH EMOST C C IN EVERY VASCULAR SURGERY THAT THERE IS. and on the basis of current retrospective studies.... It had given me the opportunity to take a whole day . SO THANKS PHARMAA GOOOD Q... if the minor chooses to give birth and not place the baby with adoptive parents. And it's over. SO POINT THAT I AM MAKING HERE IS THEY WILL ALWAYS MAKE U FOOOL THAT PT IS SYMPTOM FREE SO SINCE U KNOW THAT LITHIUM CAUSE HYPOTHYROIDSM U WILL THINK PT IS OKAYS LETS D/C MEDICATION SO PT WILLL B OKAY. That's when the CD of Kaplan was useful. especially in the third trimester... MS has little or no effect on the course of pregnancy or delivery...
I made observations when was my score coming down (After lunch. . It started with "easy" questions. TWO YEARS AGO. THE CHEST PAIN EXACERBATES ON EXERTION. MI . but two hours answering questions is not good. USE YOUR HANDS ON THE SCREEN MONITOR. you get a little impatient and you tend to want to do it without a break. Now about the topics: The usual: . Ten minutes between the 7th and 8th one. I always finished ontime.. I made my "break plan". I had learned som much from doing questions. Before I went this morning. So I made a point to take longer breaks on those times.Multiple Sclerosis and Pregnancy. X-rays of Fractures. 10 min for "lunch" which was a turkey sandwich. you miss the clues easily if you don't read it that way. You'd know the answer right off the bat.I had the usual ATHMA treatment changes . And 2 graphs for Arrest of descent. The examples I had posted before SHOULD BE MORE THAN ENOUGH.EKG: VERY EASY ones: V Fib.exam. HE REFUSED TO CHECK HIS BLOOD CHOLESTEROL. their strategy is to put the Cheif complaint. A 30 TO WITH CHEST PAIN AND EKG CHANGES IN THE SETTING OF 2 RISK FACTORS AMONG WHICH FAMILY HISTORY . READ THE QUESTION STEM LIKE IF YOUR LIFE DEPENDED IN IT.Gynecomastia in male with infertility . When reading the questions.Blah blah blah.Risk factors for Breast Cancer .. Power of attorney = Treat like if it's patient talking to you.OB-GYN usual OB complications: Arrest of Descent .. HE STATES HIS FATHER DIED OF HEART ATTACK AT 55YO.Hirsutism . and the other hand hiding the choices. If your mind is not trained to filter the parasites.Mechanism of alcohol-induced hypoglycemia (Inhibition of gluconeogenesis). VERY EASY ONES.doesn't read the same as 30YO PRESENTS TO THE CLINIC WITH BURNING SENSATION IN LEFT SHOULDER AND UPPER LEFT CHEST. and 90% of management with about 40% treatment.I had about 4 ABG Questions. You have to rearrange it in your mind. Because I would be feeling sleep y by then.HTN + Hypokalemia = Think Hyperaldosteronism even if positive family history of essential hypertension . There is ALWAYS something to look for. 10 min on the block after lunch. then a piece of history which may be relevant but it distracts you. . . 5 min after each block. last block). The questions were NOT tricky as much as I expected. and explaining the methods to my students that it was SO easy to pick on the clues. PATIENTS UnDERWENT APPENDECTOMY. Beleive me. then something about family history. It was pretty easy. And reconstruc the scenario in your mind. . I had definitely just about 1% of pathophysiology.. Type on the search button ABG and it'll take you to them.Placenta Previa . I helped myself with my finger following each and every word. coz you're cutting yourself short on the questions at the end of the last block. Obvious. AT THAT TIME. And when I did it. PATIENT'S LABS ARE. then putting again something relevant to the present. Effect of the latter on the first. 2 Q. I used the scratch laminated paper to SUMMARIZE the questions stem. Because.LOTS OF ETHICS. . I had time to read the Question stem twice.Derma: the mundane ones.
with a touch of care from me:) THANKS TO EVERYBODY WHO SUPPORTED ME ALL THROUGHOUT.Didn't have much of the nephropathies. which will have to go to reprocessing and paying for the test again with ECFMG. I don't know if I will get it.Neuro: again very easy ones.. but tricky. . . I SHALL REMAIN HELPING FOR WHOMEVER NEEDS HELP.Achilles Tendon rupture is also called Hell Cord rupture hehehe .Transplantation: Very easy: Increase the steroids if acute rejection at 30 days for ex.CSF findings in Antisocial PD. IF I DON'T KNOW I WILL POINT YOU TO THE RIGHT RESOURCE. But I feel releived I took the test. MS. I specifically asked. Splint. ? . Usual stroke.Zenkel Diverticulum: 2 Q. For the colleague who asked about not sholwing up to the test today please follow with us and tell us what happened. I am bound not to say much about the specific questions as Dr Carl reminded us again that this site is being monitored which is why I posted mostly topics.2 Q on Mechanical Ventilation: Recognize indication for weaning (Type Mechanical Ventilation notes #2: don't read everything. So let us know your experience. SINCERELY HASSAN . GUIDANCE OR SPECIFIC MEDICAL QUESTIONS. Finally: I will be available for any questions. I KNOW AND HAVE BEEN THROUGH A LOT.Alzheimer and genetic testing for iff-spring possible? What is it? What does it predict? . . . . They don't name it Zenkel. The guy said at the end of each day they send the data to ECFMG including NO SHOWS.Fractures of children = Treatment: Cast. I WISH AND HOPE IT'LL BE THE LAST WITH STEP2. as they would appear on the Step2 outline. . I CAN'T NAME PEOPLE BUT I'M SURE THOSE WHO I HAVE BEEN IN CONTACT WITH THROUGH THE WEBSITE OR EMAIL KNOW ME AND KNOW HOW WEL THEY CONTRIBUTED TO WHERE I AM NOW. I am available for questions or more details. and when to wean patient off).Prevention of Rheumatic Fever: What antibiotic and for how long. USE ME PLEASE. Know about permissive hypercapnia in ARDS. Only the modes of ventilation. Meningomyelocele. . Also Complications of MEch Ventilation: Barotrauma if pressurecontrolled ventilator.Down and Alzheimer.
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