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The complete compilation of Hassan’s posts on July

Tuberculosis pearls Tuberculosis TB treatment: - HIV negative: ERHZ or SRHZ for 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. Breatfeding 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.

. a head circumference higher than the 50th percentile. scoliosis may be noted. and otitis media. focus examination on possible hip dislocations. these signs are more obvious during adolescence or after puberty and rarely result in disabilities. has a high prevalence. depressed affect.Special Concerns: • Prenatal screening: Because fragile X syndrome is underdiagnosed. In addition.Complications: o Scoliosis o Mitral valve prolapse (most frequently encountered cardiac defect) G. E. and musculoskeletal. On the other hand. pemoline) have been used for attention deficits in the doses prescribed for patients with ADHD. and hypotonia. D. methylphenidate. As the patient matures.Medical Care: o Workup and diagnosis can be done on an outpatient basis. They manifest in adolescence as a long thin face with prominent ears. and decreasing IQ with increasing age. genital. ERCP provides both endoscopic and radiographic visualization of the biliary tract. sinusitis. hand flapping and avoidance of eye contact). In addition.Emedicine: http://www. physical therapist. Responses are variable. In addition to the cognitive. o Stimulants (eg. there are physical signs associated with fragile X syndrome. It can be diagnostic and therapeutic by direct removal of common bile duct stones. and is inheritable. and a prominent forehead and jaw. They are sensitive (65%) and specific (6%) for chronic cholecystitis. Macroorchidism is universal in adult males. and neuropsychological findings. mental retardation with IQ typically 35-70. the organ systems most frequently involved are craniofacial.Problems include: mild-to-moderate autisticlike behavior (most notably. attention deficits. dextroamphetamine. deficiency in abstract thinking.com/ped/topic800.Work-up . and occupational therapist is recommended to assess weaknesses and to identify areas where improvement is needed most. facial asymmetry. developmental delays after reaching early milestones (especially speech and language delays).A comprehensive developmental evaluation by a speech/language therapist. F. hernias.Cytogenetics (Karyotype) is not as sensitive as molecular testing (Southern Blot and PCR). preconceptual and antenatal molecular genetic screening is encouraged for women as outlined below. Sometimes. o Antiseizure and antireflux medications are useful for patients with these symptoms. . o Routine care involves treating the medical problems that these patients experience commonly. the mouth has overcrowding and a high-arched palate. behavioral. References: . aggressive tendencies. repeat evaluation may be necessary. however. including gastroesophageal reflux.htm Updated March 2003 ERCP or HIDA Scan HIDA scans have sensitivity (94%) and specificity (65-85%) for acute cholecystitis. o During infant and early childhood health care maintenance visits.emedicine.

Major complications of ERCP include pancreatitis and cholangitis. the rate of stones was 39%. In patients with any of the risk factors. 1995 Dec. In this population. If a bite wound is infected. and human bites Schweiz Rundsch Med Prax. people with any of the risk factors for common bile duct stones should undergo operative or ERCP evaluation of the common bile duct. however. particularly when the risk for the development of infection is high. and (3) a common bile duct diameter of less than 8 mm. Generally. 3)Diagnosis and treatment of bites by cats. in general. and human bites: a review. dogs and humans Dtsch Med Wochenschr.com/emerg/topic98. it appears prudent to leave the wounds open. Reference: http://www. 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. Therefore.Ultrasound is 50-75% sensitive for choledocholithiasis.87(21):716-8. cat. the risk of common bile duct stones is approximately 10%.33(6):1019-29. 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. an antibiotic prophylaxis for 3-5 days is appropriate. CT and HIDA scans are not better. when a dilated common bile duct is found or elevated LFTs are present. Some studies have classified people as low risk for common bile duct stones based on (1) lack of jaundice. a tetanus booster and in case of possible transfer of rabies. Q that remained unanswered about antiarrhythmics.emedicine. 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. However. clenched fist injuries.128(19):1059-63. In general. in cases carrying a low risk of infection. bones and tendons. J Am Acad Dermatol. . Human bite wounds have long had a bad reputation for severe infection and frequent complication. and an ERCP should be considered. References: 1)Dog. The management of bite wounds consists of intensive irrigation with large volumes of normal saline and a cautions debridement of devitalized tissues. the risk of common bile duct stones may be as low as 1%. suspicion should remain high for common bile duct stones. an antibiotic course with amoxycillin/clavulanic acid (first choice) or tetracyclines (second choice) for 10-14 days is recommended.htm Is a dog/cat's mouth cleaner than a human mouth? Animal and human bites carry a high risk of infectious complications. cat. Debate exists as to when an ERCP should be performed. 2003 May 9. In patients who present early after the injury. (2) elevated transaminases. 1998 May 20. and occlusional bites to the hand. a rabies vaccination with immunoglobulins and inactivated virus preparation is recommended. Therefore. Furthermore. since cholecystitis is caused by obstruction of the ducts. 2)Dog. a primary surgical closure might be appropriate.

Phenytoin Indications: VTach. Examples: Quinidine. trimethoprim. Hyper/Hypothyroidism. They alter the electrophysiologic mechanisms responsible for arrhythmia.Here is my input. Mexiletine(Leukopenia!!). Indications: SVT. beta-blockers. Diltiazem. Propafenone (Weak CaBlock+BetaBlock) Indications: Life threatening VTach/VFib. Symptomatic PVC Ib = shorten action potential Examples: Lidocaine. Examples: Amiodarone (Pulm Fibrosis. amiodarone. Examples: Flecainide. Ibutilide. Moricizine Note: Can expect increased levels of procainamide metabolite NAPA in patients taking CIMETIDINE. 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. 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). Side effects: bronchospasm. and quinidine. Procainamide (Lupus. These agents are used only in patients with structurally normal hearts (ie. They pronlong action potential. Corneal and skin depostis. These agents are used only for chemical conversion. Note: Esmolol (Brevibloc) -. Class II: Beta Blockers: These agents slow the sinus rate in addition to decreasing AV nodal conduction. Class III: Blocking K channels results in widened QRS and longer QT interval. Bretylium.Ideal for use in patients at risk of complications from betablockade. Class IV: Block Calicum from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium. Ic = Phase 0 = slow the rise of action potential/refractoriness but more than Ia. Relevant Indication: DOC for longterm control of A Fib (better than Dig if long term) Class V: . Refractory SVT. Neurotox!!!!!). Dofetilide. Class V: Cardiac Glycosides. Prevention of VFib. Prevention of VFib. VTach. Sotalol (noncardiac selective beta blocker). They reduce rate of AV nodal conduction and control ventricular response in A Fib. Disopyramide (Urinary retention!!). Fatal blood dyscrasias first 3 months!!). Nifedipine. Symptomatic PVC's. RANIDITINE. absence of coronary artery disease or cardiomyopathy). ClassI: * Ia = Phase 0 = Slow rhe rise of action potential = Make it longer thus more refractory. Examples: Verapamil.

Examples: Adenosine (Flushing.Medulloblastoma (18-25%) . S brady!!!). PAT with a 2:1 block!!!!)hypercalcemia and hypercalcemia predisposes patient to digitalis toxicity predispose patient to digitalis toxicity.CMDT p363 .Wilms tumor arises from the kidney and most often is detected as a large asymptomatic abdominal mass. Neuroblastoma.Glioblastoma (<5%) .Pineal tumor (2%) .Infratentorial (60%) . or other less common tumors. which commonly arises from the adrenal gland. in peds.Ependymoma (3-5%) . AV Block. Digoxin (CI in idiopathic hypertrophic subaortic stenosis.Schwannoma (<1%) . such as malignant rhabdoid tumors.htm Old Question on Neuroblastoma Vs Wilms: CT or IVP? Facts: . Watch out for AV Block.Cardiac glycosides -.Meningioma (<1%) 2.Familypracticenotebook. References: . They are used primarily in the setting of AF with CHF. congenital mesoblastic nephroma.#3: Ependymoma Reference: .#2: Astrocytoma . Neuroblastoma also . Visual changes.Ependymoma (4-6%) . the most common brain tumors are: .Astrocytoma (8-12%) . .Brain stem glioma (8-10%) . neuroblastoma.com/HEM147.Choroid Plexus papilloma (2-3%) .Cerebellar Astrocytoma (15-20%) .Meningioma (<1%) Overall.Craniopharyngioma (5-8%) .Supratentorial (40%) . constrictive pericarditis. often presents with a mass and constitutional symptoms (eg.emedicine most common brain t/m in children To let you know why it gets confusing. GI problems.#1: Medulloblastoma .Pituitary tumor (<1%) . this question has to be classified by the location of the tumor: 1. weight loss). and may represent Wilms tumor. . fever.Wilms tumor commonly displaces and compresses vessels.com http://www.fpnotebook.Solid masses are ominous in a child as opposed to cystic ones.These drugs slow AV nodal conduction primarily by increasing vagal tone.

plain x-ray b.50 yr M. 3.Case Based Pediatrics For Medical Students and Residents http://www.html 2. he lies motionless. to several days after event. is diaphoretic. 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). pt. . lymph node enlargement.Radiographic Evaluation of the Pediatric Urinary Tract http://www. infections. the most typical is several hrs. confirms function of the contralateral kidney. 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). pt. and indicates if there is extension to the inferior vena cava. etc.in the 2 week of post-op for multiple gunshot wounds to the abdomen. guar ding+. identifies associated genitourinary abnormalities. h/o smoking+.rigid abd.occurs in pts after trauma. constant. ultrasound is useful for diagnosing intraabdominal tumors and can display calcifications.hawaii.com/ped/topic2751. c-xray 3.characteristic for ARDS. emergency laparotomy c. presents with peritonitis. - .edu/medicine/pediatrics/pedtext/s12c03. drinking+. r/o other causes of acute abd. patient becomes unresponsive and progressively disoriented.amylase. like tachypnea. to several days post injury but could be variable. rebound tenderness+ a. endoscopy and biopsy Answers: 1. progressive machanical dysphagia. c-xray.pt. ABG b. radiologists were accurate at diagnosing Wilms' tumors using modern imaging methods (IVP was not included in it. tenderness to palpaion. onset is acute several hrs. come with pain from 1 hr.. Additional Fact: In a recent study. Wilms Tumor Fact: Ultrasound or CT helps localize the mass. 1. pt.CXR.has hypoxemia refcractory to oxygen.. however. most likely has ARDS -. the PaO2/FiO2 ratio < 200 mmHg. other symptoms are not noted here due to the altered mentation. 1999 May.htm the next step in mgt in the below q.. but ultrasound interpretation requires skilled expertise.With advances in medical imaging can the radiologist reliably diagnose Wilms' tumours? Clin Radiol. severe. ecg 2. massive transfusions. wt loss+ a. can have lethargy followed by obtundation.40 yr M . needs acute Mx. barium swallow b.4= 162. CT scan is better at detecting subtle intraabdominal abnormalities such as tumor spread.Ultrasound with Doppler can reveal inferior vena cava (IVC) invasion. Neuroblastoma Fact: At initial presentation. 65/0. a.displaces and compresses vessels but more often is infiltrative.emergency laparotomy . rapid shallow breathing.5 . nor in any theoretical review I found). po2-65 on 40% o2.54(5):321-7. p/e. References: 1.emedicine. 2. CT scan plays an important role in the management of Wilms tumor and neuroblastoma for staging (3).

Long term use is the follwing: ..Asthma variant cough: Cough without wheezing with atopic history.Mild persistent: * Inhaled Steroids OR Inhaled Cromolyn .TE fitule.Moderate persitent: * Symptoms daily * Night symptoms each week * Exacerbations affect activity >2x/week . Treat as mild intermittent. see the A-a gradient . In clinical scenarios..Mild persistent to Moderate persistent WHEN PT USES INHALER DAILY. . .Severe persistent: * Continuing symptoms/exacb.CXR will show bilateral pulm. get ABG in either case after the CXR.. infiltrates and/or consolidation.Mild intermittent to moderate persistent WHEN Pt USES Beta2INHALER MORE THAN TWICE A WEEK . . . can also Dx one of the most serious compl..Moderate Persistent: * Inhaled steroids low/med dose AND Long acting beta adrenergic = SAlmeterol * OR!!!!!: Inhaled Cromolyn AND Salmeterol . etc.Mild intermittent: * Pt asymptomatic * Diurnal symptoms 1x or 2x/week * Nocturnal symptoms 2x/month . then CT scan to do staging .Severe Persistent: * Inhaled Steroid high dose AND Salmeterol AND Steroids Tablets.usually the first Dx test in Pt w/ suspected esoph. if CXR is -ve .barrium swallow . Classify Asthma first: . or normal then it could be PE. mostly at night * Limited activity Treat the acute episode with Ox and Beta2 adrenergic short acting..Moderate persistent to Severe persistent WHEN PT USES INHALER DAILY AND INCREASES DOSE (MORE THAN 2 PUFFS AT A TIME).Mild persistent: * Diurnal symptoms >2x/week / <1x/day * Nocturnal symptoms >2x/month * Exacerbations affect activity .then do EGD . * OR!!!!!: Inhaled Cromolyn AND Salmeterol AND PO Steroids.Mild intermittent: * No long term Rx .look for Mets Old Request about summary of treatment of Asthma Asthma is defined primarily as an INFLAMMATORY DISEASE with mostly MAST CELL degranulation. CXR is fast to get. you step up the long term Rx from one level to the other when: . Steroids are used in the exacerbations that needs admission.Can last days ..CA especially if they have symptoms of dysphagia.. so then get ABG.correct me on this one if i am wrong 3.

propellant and fluorescent lamps. but it is also used in electric switches. pale child with photophobia. This change will depend on the failure of other supporting measures (Technique of using inhaler. Perhaps the most deadly form of mercury is methyl mercury. 90% of any methyl mercury ingested is absorbed into the bloodstream from the gastrointestinal tract. H/o of persistent asthma. These properties have given it the common name quicksilver. but no longer is. and (3) organic compounds. Scenario of Pt undergoing accident or surgery and post-op clinical scnerio of adrenal insufficiency. Puerto Rico. RR = 23. Amazon and virgin islands. PE – irritable. At room temperature it is a silvery.Swanson . antiseptics. Further history reveals child’s elder brothers have been playing with household thermometers. New Jersey. What is the likely diagnosis? How do you confirm the diagnosis? The culprit: what is mercury? Mercury is an elemental metal. or in CI of beta adrenergics. Only 2-10% of the ingested mercury is absorbed from the gut. Watch out for Adrnela insufficiency. Ritual Use of mercury: in haitian and carribean-american communities. Ipratropium (anticholinergics) are first line of treatment of bronchospasm secondary to beta blockers. (2) inorganic salts. adherence. T = 99F. particularly of spiritist faith such as Santeria. This causes intoxication by mercury vapor.Note: Review treatment with Pt every 1 to 6 months and either step down or step up. Some History: . P=90. Mother says child has become ill tempered and refuses to walk. odorless liquid which vaporizes easily. Mercury is purveyed by some herbal medicine or botanical shops to consumers unaware of the dangers of the substance. Mercury posoning by eating Fish: Japan. perservatives and pesticides has greatly declined becuase effective substitutes have been found. New york State. Note2: Beta2 adrenergics are first line in treatment of asthma. and ingested elemental mercury is not absorbed at all. Mercury's most well known use is in medical thermometers found in the home. erythematous rash – hands and feet. Tremor of the tongue evident. however. 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. and environmental control). (GIve Calicum and Vit D in chronic use. References: . Mercury use in diuretics. Steroids Inhaled are first line in treatment of PERSISTENT ASTHMA.CMDT Mercury poisoning A 2 yo – peeling. North Carolina. Or Pt with h/o of asthma who develops recurrent oral candidiasis). Mercury was previously used in paint. Mercury exists in 3 forms: (1) elemental mercury. The ritual consists in the sprinkling of mercury about the home.

.When inhaled or absorbed through the skin. hearing loss. Criminals sentenced to work in mercury mines had a life expectancy of three years. The phrase "mad as a hatter" originated from the often strange behavior of hat makers. visual loss. dizziness. mercury accumulates in the liver. Unexplained renal abnormalities with neuropsychiatric disturbances should prompt the physician to consider Minamata disease or other forms of mercury poisoning. Methyl mercury exerts its most devastating effect on the central nervous system by causing psychiatric disturbances. Can mercury affect some people more than others? Age: Children are especially susceptible to the adverse effects of mercury. the babies’ exposure continued after birth. Structural proteins. The setting: . in the early 1950s. caused by exposure to mercury vapor used in making felt hats. Necrosis of the proximal tubules is a common direct renal toxic effect. better known as Minamata disease. Local villagers ate the fish and began to exhibit signs of neurologic damage such as visual loss. The scenario: Children develop the symptoms of mercury poisoning more quickly and severely than adults. and enzymes are all disrupted.Mercury taken into the body through air. Children also may . Mental instability. a pregnant woman exposed to toxic levels of mercury may not exhibit any signs of mercury poisoning. mercury easily crosses the placental barrier and concentrates in the fetus more readily than in the mother. Because mercury binds to the body's ubiquitous sulfhydryl groups. Furthermore. numbness in the limbs and personality changes such as nervousness. In pregnant women. Methyl mercury is lipophilic and readily crosses the blood-brain and placentofetal barriers. Thus. a body of water in Japan where. extremity numbness. causing both immediate and long term health effects. The history of mercury and its toxic effects date back to the fifteenth century B. Neurologic damage in the form of diffuse and widespread neuronal atrophy is most severe in patients exposed in utero. but her child may be born with brain damage similar to cerebral palsy or autism. or exposing oneself through a hobby.Methyl mercury poisoning. ataxia. toxicity involves multiple organ systems. and neuropathy. Neurological symptoms are very similar to those seen in adults. water and food is absorbed in varying amounts depending on the route of intake. children playing with mercury. increased excitability or insomnia may occur after exposure to mercury vapors. The effect: The most universal effect of mercury is damage to the nervous system. . the fish contained high concentrations of methyl mercury from the polluted waste of a nearby industrial plant. It is named for Minamata Bay. because mercury was also discovered in the breast milk of the mothers. Pathophysiology: Mercury is an element and cannot be broken down into harmless components.C.Exposure to mercury also may occur by moving into a mercury-contaminated home. brain and blood. hearing loss. membranes. kidneys. and ataxia. The major food sources of mercury are fish and shell fish. is one of the most devastating forms of mercury exposure. Babies exposed to the methyl mercury in utero were the most severely affected members of the village.

Ingested elemental mercury is considered nontoxic because of its poor absorption in the gut.problems in walking Methyl mercury exerts its most devastating effect on the central nervous system by causing the following: Psychiatric disturbances. Early signs and symptoms may occur with concentrations greater than 35 mcg/L. Urinalysis .Constriction of the visual fields . 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.Labs: blood. Differential: Schizophrenia and Other Psychoses Substance Abuse: Cocaine Toxicity. The normal range of mercury concentrations in whole blood is 0-10 mcg/L.PCP Autism: presents very many similarities (see 3) The Diagnosis: .Dysarthria . Symptoms include: . mercuric chloride) is caustic gastroenteritis. 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 .Extremity numbness .develop a bright red reash with sheets of peeling skin. Unexplained renal abnormalities with neuropsychiatric disturbances should prompt the physician to consider Minamata disease or other forms of mercury poisoning. Hearing loss. 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. Hallucinogens .Headache .Memory loss . Ataxia.Difficulty in hearing . a direct determination of the blood mercury concentrations is essential. it is most dangerous as a vapor because it can cause acute lung injury and respiratory failure. Consequently. and (sometimes) tissue analyses are required to confirm the diagnosis of mercury intoxication. Neurotoxicity is the most damaging syndrome. The most damaging effect of ingested inorganic mercury (eg. Visual loss.Ataxia . Blood Analysis: Methyl mercury concentrates in red blood cells. urine.

and the creation of a differential diagnosis. especially in utero. profound developmental delay. irreversible. and large tuna steaks ) because their mercury concentrations tend to be higher than those in smaller fish. Therefore. seizure disorders. the best agent for the treatment of Minamata disease is 2.3-dimercaptosuccinic acid (DMSA). 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. DMSA is preferred over DPCN. Methyl mercury is primarily excreted through the feces. Its toxicity is low. Respiratory distress and nonspecific dermatitis. These agents are thought to competitively bind the mercury by using its thiol groups. * 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. Ataxia and dysarthria. activated charcoal should be administered even though it does not absorb heavy metals well in general.The detection of mercury in the urine demonstrates that exposure has occurred.Monitor Renal Function . incomplete visual loss (including tunnel . Extremity numbness eventually along with headache. tremor. unfortunately. Currently. Babies exposed in utero are the most severely affected (low birth weight. Chelated mercury is excreted primarily through the kidneys. After initial assessment and stabilization of the patient’s condition. 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. they are. it does not indicate the severity of mercury poisoning. Outpatient follow-up: . * Gastric Lavage: Because of the high propensity for neurologic impairment. Medical Care: Medical Care: The general management measures in Minamata disease are the same as in those of any other toxicologic exposure.Monitor Mercury levels for months . In addition. including monitoring. the urinary excretion of mercury is minimal. pregnant women and nursing mothers should avoid consuming larger fish (shark. Diet: Because of the high morbidity and mortality rates associated with methyl mercury poisoning. the performance of baseline laboratory studies. however. eliminate the patient's exposure to the source of the mercury. urinary assays are useful in monitoring chelation therapy.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). chelating agents should be administered early in treatment. swordfish. Even in cases of inorganic mercuric salt exposure. Provide general supportive measures. fatigue. The goal of medical management in Minamata disease is to reduce the total body burden of mercury and minimize further damage. Histologic Findings: Necrosis of the proximal tubules is a common direct renal toxic effect.

vision).state. Answer to your question . * Because of the high morbidity and mortality rates associated with methyl mercury poisoning. total blindness. hearing loss. when municipal solid waste or medical waste is incinerated. language. Contact EPA when a spill of mercury would form a pool larger than a quarter. oil and natural gas) are burned. remembering that the most common cause of Cushing syndrome is the use of exogenous glucocorticoids is important. The correct way to dispose of small amounts of mercury is to pick it up with the sticky side of a piece of tape.Cushing disease = Pituitary adenoma ACTH secreting. Long-term studies indicate that even prenatal exposure at low concentrations can cause subtle but detectable decrements in the areas of motor function. .GENERAL REVIEW General Considerations: Cushing syndrome is caused by prolonged exposure to elevated levels of either endogenous or exogenous glucocorticoids..emedicine. Medicolegal pitfalls: * Consider mercury intoxication in the differential diagnosis when unexplained neuropsychiatric disturbances are coupled with renal abnormalities. visual loss. In an emergency situation.epi.epa. causing contamination. 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.to/a/table_a. and hearing loss).com/ped/topic1461. place it in a sealed container and place it in the trash outside.htm 2) http://www. Children so affected may have long-term stigmata. and during some manufacturing processes.html What is the difference between Cushing Syndrome and Cushing Disease? First of all. IT SHOULD NOT BE VACUUMED. developmental delay. CUSHING SYNDROME/DISEASE. Vacuuming causes mercury to vaporize and spread easily through the air.htm 4) http://www. pregnant women and nursing mothers should avoid consuming larger fish because their mercury concentrations tend to be higher than those in smaller fish.us/epi/fish/mercuryhealthfacts.whale.oh. and memory. water and land when fossil fuels (coal. during forest fires. soil and water throughout North Carolina.us/pic/facts/mercury. Reference: 1) http://www.nc. because it will continue to vaporize. It displays clinical Cushing Syndrome. especially in utero. Etiology: . Mercury is also released into the air. 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. and seizure disorders.Cushing syndrome is everything else with clinical features except etiology is NOT pituitary. Prevention: What should I do if I spill mercury in my house? If the mercury spills onto a surface. Do not put mercury down the drain or dispose of it in the house.. including motor impairment.html 3) http://www.state.

- 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

control of hypercortisolism may be attempted with medication. metyrapone.cortisol measurement is required. and adrenalectomy may be indicated in ACTHmediated Cushing syndrome. However.The primary therapy for adrenal tumors is adrenalectomy. A decrease in UFC of greater than 50% is suggestive of an anterior pituitary adenoma. Chest and abdominal CT scans should be performed in patients with suspected ectopic ACTH production. buffalo hump. Unfortunately.Pts on HAART for HIV-1 develop partial lipodystrophy with thin extremities and central obesity. However.Anorexia Nervosa: Same wasting as in Cushing with extraordinary high levels of 24h urine cortisol . CTguided fine-needle aspiration then may have a role in management. . With the 48-hour high-dose dexamethasone suppression test. rather than ectopic ACTH or a primary adrenal tumor. . Octreotide scintigraphy may be helpful in detecting ectopic ACTH tumors because neuroendocrine tumors typically have cell surface receptors for somatostatin.The treatment of choice for endogenous Cushing syndrome is surgical resection of the causative tumor. . A culprit tumor should be removed if possible. . as often occurs with ectopic ACTH or metastatic adrenal carcinoma. measurement of 17-ketosteroid or other cortisol precursors (such as serum dehydroepiandrosterone sulfate [DHEAS]) is useful. with a specificity of 70-80%. Pituitary radiation may be useful if surgery fails for Cushing disease. patients should undergo a contrastenhanced magnetic resonance imaging (MRI) study of the pituitary. 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. Cushing syndrome Agents that inhibit steroidogenesis. the sensitivity of this test is only 80%. Medical Care: Overview Treatment of Cushing syndrome is directed by the primary cause of the syndrome. When surgery is not successful or cannot be used. Differential Diagnosis: . such as mitotane.Depression: High cortisol with no clinical features . patients ingest 2 mg dexamethasone every 6 hours for 8 doses.The treatment for exogenous Cushing syndrome is gradual withdrawal of glucocorticoid. .Morbid obesity mimicks results of DXM suppression test but urine free cortisol is normal . ketoconazole. 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 primary therapy for Cushing disease is transsphenoidal surgery.Alcoholics: high cortisol levels with clinical cushing . Imaging Studies: An abdominal CT scan is recommended if a primary adrenal problem is suspected. If a pituitary source of excess ACTH is suspected. If concern for adrenal carcinoma exists. medication failures are common. the diagnostic accuracy is only 70-80%.

causing a false elevation of cortisol measurements. and androstenedione. Etomidate. including the first step in cortisol synthesis. In addition. Trilostane is not widely available and is not as well studied. an imidazole-derivative anesthetic agent. These medications are used rarely and often are toxic at the doses required to reduce cortisol secretion. decreased libido. and increased to 2 g four times daily. Metyrapone and trilostane are agents that competitively inhibit a single steroidogenic enzyme. Ketoconazole probably is the most popular and effective of these agents for long-term use and usually is the agent of choice. These agents have higher efficacy when used in combination because they may act synergistically.5 g/d. the dose may be maintained while another steroid enzyme inhibitor. Adverse effects of ketoconazole include headache. gynecomastia. either surgical or medical. sedation. acne. radiation therapy of the pituitary often is required after unsuccessful initial therapy. headache. in conjunction with a specialist. aldosterone. and goiter. Aminoglutethimide typically is initiated at 250 mg twice daily. Ketoconazole and aminoglutethimide act at several sites. Ketoconazole is ineffective in patients on H2 blockers or proton-pump inhibitors because gastric acidity is required for metabolism. and hirsutism. It acts on several of the P450 enzymes. ideally. cholesterol side-chain cleavage. Trilostane inhibits the conversion of pregnenolone to progesterone. ACTH secretion overcomes the blockade so that hypercortisolism persists. is initiated. trilostane. and conversion of 11deoxycortisol to cortisol. Patients receiving these medications may require glucocorticoid replacement to avoid adrenal insufficiency. . a generalized pruritic rash. In rare cases. irregular menses. It is a relatively weak adrenal enzyme inhibitor at doses that patients can tolerate. The drug is contraindicated during pregnancy. It is . medical treatment should be initiated cautiously and. It also may inhibit ACTH secretion when used at therapeutic doses (200-400 mg bid-tid). Because ACTH production may persist or increase in patients with Cushing disease.Adverse effects of aminoglutethimide include somnolence. Aminoglutethimide is an anticonvulsant agent that blocks cholesterol side-chain cleavage to pregnenolone. have been used to cause medical adrenalectomy. may inhibit ACTH secretion. and elevated liver function tests. Adverse effects are from increases in androgen and mineralocorticoid precursors. Aminoglutethimide increases the metabolism of dexamethasone but not cortisol. If this agent is ineffective at controlling hypercortisolism. It is not a first-choice agent because it is a weak inhibitor of steroidogenesis. impotence. and etomidate. it may cause bone marrow suppression. at high doses. Metyrapone blocks 11-beta-hydroxylase activity (the final step in cortisol synthesis) and. nausea. typically metyrapone. which decreases the synthesis of cortisol. If enzymatic blockade is not complete. Efficacy of these medical interventions can be assessed with serial measurements of 24-hour UFC.aminoglutethimide. blocks 11-beta-hydroxylase. Therapy is begun at 1 g/d divided into 4 doses and increased to a maximum dose of 4. Thus. including hypertension. hypothyroidism. trilostane interacts with some assays.

The patient then requires lifelong glucocorticoid and mineralocorticoid therapy. . It currently is used only on an investigational basis for treatment of Cushing syndrome. Mifepristone (RU 486) is an antiprogestational agent. Both open and laparoscopic techniques are possible. It is a potential teratogen and can cause abortion. and its utility is limited by adverse gastrointestinal and neurological effects. Agents that decrease CRH or ACTH release have been studied for the treatment of Cushing disease. competitively binds to the glucocorticoid and progesterone receptors. it is relatively contraindicated in women interested in remaining fertile. 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. . Other adverse effects include rash. Successful amelioration of hypercortisolism occurs in 60-80% of cases. Late-onset adverse effects include hypopituitarism. valproic acid. MRI-guided pituitary surgery.Cushing disease Treatment of choice for classic Cushing disease is transsphenoidal surgery by an experienced neurosurgeon. may be indicated. a new procedure. 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. If unsuccessful. and leukopenia.Unfortunately. it is used in treatment of adrenal cancer. diarrhea. Its survival benefit is unclear. Carcinomas should be resected for palliation. This drug also leads to mitochondrial destruction and necrosis of adrenocortical cells in the zona fasciculata and reticularis. and medical therapy fail or if rapid normalization of cortisol levels is required. which. ie. mitotane is expensive. Currently. Nelson syndrome.3 mg/kg/h.Ectopic adrenocorticotropic production Surgical resection of the source of ACTH production may not always be possible. preserving as much pituitary function as possible. and octreotide. cyproheptadine. including nausea. and ataxia. . Surgical Care: . For this reason. In individuals who undergo bilateral adrenalectomy. dizziness. at high doses. Medical therapy or bilateral adrenalectomy may be required. pituitary irradiation.used intravenously at 0. with a 45% cure rate in adults and 85% cure rate in children. therefore. Its use is limited by the requirement for chronic administration by the intravenous route. Mitotane is an adrenolytic agent that acts by inhibiting 11-beta hydroxylase and cholesterol side-chain cleavage enzymes. . Such agents include bromocriptine. The goal of surgery is to remove the adenoma. The procedure is less successful than surgery in adults.Bilateral adrenalectomy is an option if transsphenoidal surgery. often with a laparoscopic approach. . It is taken up by adipose tissues and persists in the circulation long after discontinuation. symptomatic enlargement of the pituitary gland and adenoma. * Adrenal source Adenomas may be removed with unilateral adrenalectomy. arthralgias.Pituitary irradiation is employed when transsphenoidal surgery is not successful or not possible. use of these agents is investigational.

Hormone replacement Patients with endogenous Cushing syndrome who undergo resection of pituitary. adrenal. The rate of steroid taper may be slowed if severe preoperative hypercortisolism was present. Unilateral or subtotal adrenalectomy may lead to recurrence. . or ectopic tumors should receive stress doses of glucocorticoid in the intraoperative and immediate postoperative period.emedicine. either continuously or in boluses (60-100 mg every 8 h) starting prior to surgery and for the first 24 hours afterwards. Typically. intravenous glucocorticoid replacement may be tapered over 1-2 days and replaced with an oral formulation.htm 2) Kaplan notes 3) CMDT p1126-1128 Gotta go. In the event of pituitary destruction or bilateral adrenalectomy. 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. answer to your question: The actions of ADH are mediated through at least 2 receptors—V1 mediates . 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.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.com/MED/topic485. References: 1) Emedicine: http://www. Untreated adrenal crises can lead to death. hydrocortisone at 200-300 mg is infused intravenously... right now!! Diabetes insipidus Hypercalcemia/Hypokalemia: mechanism by which they provoke DI? First of all.gotta go. lifelong steroid replacement is necessary.

enhancement of corticotrophin release. or to go through. causing inhibition of water uptake and polyuria. as in urination. The gypsy woman curses the housewife. or luminal. the ducts do not respond appropriately to vasopressin. hypercalcemia. a gypsy woman traveling with her thirsty son is denied water by a housewife. which describes the excretion of sweet urine. hypokalemia. V2 (Aquaporin) mediates the antidiuretic response. surface of the tubule cell occurs. Normally. which means to stand with legs apart. According to legend. Through a G protein–adenylate cyclase coupling. NDI arises from defective or absent receptor sites at the cortical collecting duct segment of the nephron or defective or absent aquaporin. and renal prostaglandin synthesis. Hypokalemia and hypercalcemia have been shown to suppress cortical Aquaporin 1 (AQP2) as well as to downregulate medullary AQP2. causing the housewife's sons to crave water while condemning her daughters to pass the curse on to future generations. Scottish folklore reports the existence of the disease in Scotland before 1761. that results in polyuria and polydipsia by diminishing the patient's ability to concentrate urine. In the presence of vasopressin stimulus.Central diabetes insipidus (DI) is characterized by decreased secretion of antidiuretic hormone (ADH). Absence of the vasopressin receptor does not allow this process to take place. carried by Ulster Scots who arrived in Nova Scotia. supraoptic or paraventricular nuclei. Insipidus comes from a Latin word meaning without taste. activation of the vasopressin receptor increases cyclic adenosine monophosphate (AMP) production and stimulates protein kinase A. A rare autosomal variant is caused by mutation in the aqua porin . or the supraopticohypophyseal tract.vasoconstriction.Nephrogenic DI is characterized by a decrease in the ability to concentrate urine due to a resistance to ADH action in the kidney. . lithium toxicity. Next: The review Diabetes Insipidus Background: The word diabetes is derived from the Greek verb diabainein. General Considerations: . lesions of the posterior pituitary rarely cause permanent DI because ADH is produced in the hypothalamus and still can be secreted into the circulation. The rare hereditary form of nephrogenic DI is transmitted as an X-linked genetic defect of the V2 receptor gene. AKA arginine vasopressin (AVP). leading to increased recycling of the protein aquaporin in the plasma membrane. Diminished or absent ADH can be the result of a defect in one or more sites involving the hypothalamic osmoreceptors. exocytic insertion of aquaporin into the apical. on a ship named Hopewell. diabetes insipidus (DI) describes the passing of tasteless urine because of its relatively low sodium content. In contrast. the protein that transports water at the collecting duct. Canada. vasopressin is transported in the blood to receptor sites on the basolateral surface of the collecting duct membrane. Aquaporin enhances water entry into the cell from the lumen. Nephrogenic DI can be observed in chronic renal insufficiency. and tubulointerstitial disease. Nephrogenic DI (NDI) reached North America in 1761. resulting in a reversible nephrogenic DI. In contrast to diabetes mellitus (DM). As a consequence of one of these defects.

also is important.The most common form of DI is that which follows trauma or surgery to the region of the pituitary and hypothalamus. enuresis. neoplastic or infiltrative of the hypothalamus or pituitary (adenomas. however synthetic desmopressin is unaffected. and weight loss may be the most apparent signs. . and fatigability typically predominate. leukemia. HTN. ie.gene AQP2. or drugs (Lithium. at a time when ADH release would be highest and urine would be most concentrated. demeclocycline. when stores of ADH are exhausted Polyuria. simultaneous serum and urine osmolality. such as diabetes mellitus. PRE-ECLAMPSIA. OR HEPATIC DYSFUNCTION. colchicine. A urine specific gravity of 1. When 2 sequential urine osmolalities vary by less than 30 mOsm or if the weight . The triphasic pattern is observed more often clinically. glucose. 1) USUALLY IN THE QUESTION STEM: *** 24h urine collection (volume. The daily urine volume is highly variable (3-20 L/d).Central: traumatic/surgery. a polyuric phase = fall in urine osmolality ** Second. pyelonephritis. Patients with a nontraumatic onset typically have a much more indolent course. growth retardation. sarcoid histiocytosis). hypokalemia. urine specific gravity. Sickle Cell Disease. urine Na. methicillin). IT IS SEEN IN THIRD TRIMESTER AND PUERPERIUM. Multiple Myeloma. polydipsia. Ruling out secondary causes. IT IS OFTEN ASSOCIATED WITH OLIGOHYDRAMNIOS. foscarnet. Random plasma osmolality generally is greater than 287 mOsm/kg. anorexia. It may exhibit 1 of 3 patterns—transient. and meningitis. 2) The water deprivation test = compares Uosm after dehydration versus Uosm after vasopressin. A circulating enzyme destroys native vasopressin. THEREFORE RESPONDING TO DESMOPRESSIN THERAPY AND SUBSIDING SPONTANEOUSLY THEREAFTER. Details: All water intake is withheld and urine osmolality and body weight are measured hourly. Workup: Perform testing with the patient maximally dehydrated as tolerated. an antidiuretic phase from release of stored hormone = urine osmolality rises. cranipharyngiomas. and ADH levels. It's called VASOPRESSINASEINDUCED DI.005 or less and a urine osmolality less than 200 mOsm/kg is the hallmark of DI. hypercalcemia. crying. a water-channel exclusively expressed in the collecting ducts of the kidney. Clinically: . Physical Examination: Normal or signs of dehydration Causes: . In children. linear growth defects. and patient tolerance of dehydration also varies among individuals. ** First. Note: Pregnancy is associated with increased risk of DI. Uosm) ***Serum: electrolytes and glucose. and nocturia (from 3-18 liters) are the predominant symptoms. In infants. Radiation therapy.Mephrogenic: idiopathic. ** The third phase can be permanent DI. permanent. 30% are idiopathic. creatinine. hyperthermia. irritability. or triphasic. Sarcoidosis.

Water deficit may be calculated based on the assumption that body water is approximately 60% of body weight in kilograms. After pituitary surgery. Pharmaceutical therapy for DI includes subcutaneous. Follow the specific gravity of the urine and administer the next dose of desmopressin when the specific gravity has fallen to less than 1. 5 U of aqueous vasopressin is administered subcutaneously. water deprivation leads to a urine osmolality that is 2-4 times greater than plasma osmolality. and oral preparations of vasopressin analogues. it's DI. Frequent electrolyte monitoring is recommended. A final urine specimen is obtained 60 minutes later for osmolality measurement. urine osmolality increases by more than 50%. 5) Consider MRI of pituitary/hypothalamus/skull: T1-weighted images of the healthy posterior pituitary yield a hyperintense signal. along with adequate fluid to match losses. 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. carbamazepine.Nephrogenic DI may respond to combinations of indomethaci-hydrochlorothiazide or IDM-Desmopressin or IDM-amiloride. as well as chlorpropamide. . 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. Medical Treatment: . and indomethacin (limited efficacy). The time required to achieve maximal urine concentration ranges from 4-18 hours. In healthy individuals. 3) Measuring Posm and Uosm at intervals and plotting them. Generally. A good rule of thumb is to reduce serum sodium by 0. If on the right. Surgical Care: Postoperatively. Medical Care: ** In an emergency. Drug is not given to patients with Liver Disease because of mild elevation of liver enzymes. In response to exogenous vasopressin.O. Patients may require hospitalization to establish fluid needs. thirst can become an adequate guide. administer the usual dose of desmopressin to patients with DI and administer (hypotonic) IV fluids to match urine output.Intranasal Desmopressin acetate (DDAVP)= DOC for Central DI. When the patient can tolerate oral intake. In case of inadequate thirst.005 with an increase in urine output.decreases by more than 3%. It is also useful for DI associated with pregnancy or puerperium (category B = Usually safe but benefits must outweigh the risks). administer parenteral desmopressin every 12-24 hours. Replace losses with dextrose and water or IV fluid hyposmolar to the patient's serum. with failure of the urine to be concentrated despite excessively concentrated serum. it can be administered 2-3 times per day. Avoid hyperglycemia. 4) Vasopressin challenge test: If injection of vasopressin normalizes response.008-1.C. . DESMOPRESSIN IS THE D. and a correction of hypernatremia that is too rapid. testing reveals minimal ADH levels and activity. diagnosis of Central DI is made. Compare with relationship betwen Posm and Uosm in normal individuals. In complete central DI. thiazides. volume overload.5 mmol/L/h. nasal. most patients can drink enough fluid to replace their urine losses. Administration of vasopressin results in less than 9% increment in urine osmolality.

Barrel chest .Psychogenic polydypsia .emedicine.High V/Q areas (Dead space ventilation) Blue Bloaters: Chronic Bronchitis Predominant: .Normal Hemoglobin. such as when traveling. . PaCO2 normal.IVF administration . severe . scant phlegm .htm Clinically: Chronic Bronchitis Vs Emphysema Classicly.Dyspnea is predominant.Blue Bloaters Pink Puffers: Emphysema predminant: . . PaO2 normal. Special Precautions: Patients with DI also must take special precautions.. to be prepared to treat vomiting or diarrhea and to avoid dehydration with exertion or hot weather. .Decreased aquaporin-2 expression and apical plasma membrane delivery in kidney collecting ducts of polyuric hypercalcemic rats. Am Soc Nephrol. mouth almost closed to a puffing grimace to increase resistance to airway lost in the destruction of lung parenchyma.Thin.Nocturnal Polyuria of Parkinson .com/med/topic543. Differential: .TLC increased . 1998 Dec.Early polyuria and urinary concentrating defect in potassium deprivation Am J Physiol Renal Physiol 279: F655-F663.htm http://author.Emedicine http://www.com/PED/topic580.Frequent exacerbations due to chest infections. Clofibrate.CXR= Hyperinflation + Flat Diaphragm .Cough is rare.Cyanotic and mouth wide open to breathe more air.Some drugs can be used to stimulate ADH secretion: Chlorpropamide.Accessory muscles use.Polyuria of Lithium Rx .Nephrogenic diabetes insipidus Ann Endocrinol (Paris).CMDT p1075-1077 5.CNS Sarcoidosis . 1999 Dec. O2Sat Normal.R/O Diabetes Mellitus References: 1.Pink puffers .DLco reduced .Chronic Cough is major complaint with mucopurrulent sputum . .Polyuria of Cushing Syndrome .weight loss . COPD patients have been categorized into: .9(12):2181-93 4.Kaplan Notes: 2002 6. 2000 2. and Carbamezepine.emedicine.60(6):457-64 3.

- 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).

Whether HAV vaccine administration should be mandated in children (as is HBV vaccination) remains unclear. given intramuscularly as a single dose.02 mL/kg. for most elderly persons. and to prevent or delay progression of chronic hepatitis to cirrhosis or HCC. factory.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. Hospitalization is needed for patients whose nausea and vomiting places them at risk for dehydration. no antiviral therapy is available for healthy carriers who do not have actively replicating virus. who are very likely to be immune. Supportive treatment recommendations are the same as for acute hepatitis A. The dose is 0. Treatment with alfa-interferon is appropriate for many patients with chronic hepatitis B. Postexposure prophylaxis with hepatitis A immune globulin is appropriate for household and intimate contacts of patients with HAV. It may be effective even when administered as late as 2 weeks after exposure. no well-established antiviral therapy is available for acute HBV infection. Administration of hepatitis A immune globulin is an alternative to vaccination against HAV infection.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. Candidates for interferon therapy must have a clinical diagnosis of chronic HBV infection. Prophylaxis is not necessary for casual contacts (office. as marked by the loss of HBeAg and HBV DNA. Patients with acute liver failure require close monitoring to ensure that they do not develop FHF.02 mL/kg intramuscularly for individuals who anticipate spending fewer than 3 months in an endemic region. as marked by a positive HBeAg or a positive HBV DNA finding. to inhibit viral replication. . It also is recommended for contacts at daycare centers and institutions. Travelers should receive 0. or hospital). with an elevated level of alanine aminotransferase (ALT). *Interferon alfa treatment for chronic hepatitis B Interferons have both antiviral and immunomodulatory effects. The author recommends that liver biopsy be performed prior to therapy to confirm the diagnosis and document the severity of disease. * Prevention of hepatitis A virus infection The CDC now recommends vaccination against HAV for individuals traveling to endemic regions. * Treatment of chronic hepatitis B The goals of antiviral treatment of HBV infection are to reduce symptoms. if present. Treatment is typically for 16 weeks. Hepatitis B: *Treatment of acute hepatitis B As with the treatment of acute hepatitis A. Typical dosing of immune globulin is 0. or for those known to have anti-HAV in their serum. Antiviral therapy infrequently leads to viral eradication. They must have evidence of active HBV replication. Whether lamivudine and newer antiviral therapies have an impact on the natural history of severe cases of acute HBV infection remains unclear. and vaccination is recommended for any patient with chronic liver disease. as marked by the loss of HBsAg. school. Currently.

and its efficacy in populations generally not responsive to interferon therapy. pain at injection site. The latter 2 drugs are undergoing clinical trials for the treatment of both HIV disease and HBV infection and await FDA approval. Its contribution appears to be in reducing the frequency of clinical illness. The long-term impact of such mutations is unknown. * Postexposure prophylaxis Hepatitis B immune globulin (HBIG) is derived from plasma. granulocytopenia.Adverse effects of interferon are common but lead to discontinuation of the drug in only 5-10% of patients. The advantages of lamivudine over interferon include its ease of application. before hospital discharge). The recommended vaccination schedule for infants is an initial vaccination at the time of birth (ie. fever. The recommended vaccination schedule for adults is an initial vaccination. in order to prevent HBV-induced damage to the liver allograft. Treatment also induces histologic improvement and a statistically significant reduction in the rate of development of hepatic fibrosis. Lamivudine for chronic hepatitis B Lamivudine is the negative enantiomer of 2’3'-dideoxy-3'-thiacytidine. a repeat vaccination at 1 month. and another repeat vaccination at 6-18 months. It provides passive immunization for individuals who describe recent exposure to a patient infected with HBV. fatigue. health care workers). including lamivudine. Such analogs include famciclovir. However. arthralgia). the virtual absence of adverse effects. neuropsychiatric symptoms (eg. Adverse effects include flulike symptoms (eg. will result in improved suppression of 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. those on dialysis. * Hepatitis B virus vaccine: Pre-exposure prophylaxis: Plasma-derived and recombinant HBV vaccines use HBsAg to stimulate production of anti-HBs. This is explained by the development of a mutation at the YMDD locus in the HBV DNA polymerase gene. followed by the usual two other doses at appropriate times (90% effective) . thyroid function abnormalities). and another repeat vaccination at 6 months. irritability. myalgia. dyspepsia. somnolence). repeat vaccination at 1-2 months. The possibility exists that combination therapy with nucleoside analogs. Reccomendations are as follows: .Sexual contact with an acutely infected patient => HBIG within 14 days of exposure + . and other miscellaneous effects (eg.Perinatal => HBIG immediately after birth + vaccination within the first 12 h. adefovir. thrombocytopenia). depression. It also has been used successfully in patients with decompensated cirrhosis and in the treatment of recurrent hepatitis B following liver transplantation. alopecia. and lobucavir. not in preventing infection. 16-32% of patients who are considered to have responded to lamivudine experience a recurrence of HBV DNA positivity. It inhibits DNA polymerase–associated reverse transcriptase and can suppress HBV replication. headache. The vaccines are highly effective. HBIG also is administered following liver transplantation to those infected with HBV. hematologic effects (eg. Pregnancy is NOT a contraindication to vaccination. Vaccine administration is recommended for all infants and for adults at high risk of infection (eg. with a greater than 95% rate of seroconversion.

Kenilworth. (2) to prevent progression of disease. (5) ursodeoxycholic acid. Nutley. proteases. which is used in combination with interferon alfa-2b (Rebetol and Rebetron. * Preexposure Prophylaxis: Genotype and quasispecies viral heterogeneity.g. (3) interferon-gamma. Hepatitis C: * Treatment of hepatitis C virus infection Antiviral therapy has a number of major goals. (4) natural interferon. *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.Household contact with an acutely infected person resulting in known exposure => HBIG +/. they may be given at the same time but at separate sites.: Needle Stick) => HBIG immediately after exposure + vaccination to begin within the first week after exposure When both HBIG and hepatitis B vaccine are recommended. When it is identified. (4) to decrease the incidence of HCC. NJ). The combination of ribavirin. (3) consensus interferon (Infergen.usual course of vaccination . and (6) silymarin (milk thistle). as opposed to only 4% of untreated controls.Household contact with an acutely infected patient => None . Thousand Oaks. with interferon alfa-2b has significantly improved patients' responses to treatment.Infant (<12 mo) primarily cared for by an acutely infected patient => HBIG +/vaccination . NJ).vaccination . (2) interferonbeta. or sexual exposure. * Treatment of chronic hepatitis C Interferon alfa-2b. and polymerases. NJ). and (6) to treat extrahepatic complications of HCV infection such as cryoglobulinemia or glomerulonephritis. Currently. They may have activity against viral helicases. Roche. (3) to decrease the incidence of cirrhosis. (5) to ameliorate symptoms such as fatigue and joint pain. needle stick. and (4) ribavirin. as well as rapid evasion of neutralizing . (2) interferon alfa-2a (Roferon. These include (1) to decrease viral replication or eradicate HCV. Schering. * Treatment of acute hepatitis C Acute hepatitis C is detected infrequently.Sexual contact with a chronic carrier => Vaccination .Inadvertent percutaneous or permucosal exposure (e. Future medications may target the enzymes responsible for HCV replication. a nucleoside analog. A recent meta-analysis showed that 41% of patients treated with interferon had negative HCV RNA findings at the end of treatment. Schering. was approved by the FDA in 1991 for the treatment of chronic HCV infection. dosed at 3 million units subcutaneously 3 times per week. early therapy with interferon should be considered. Agents currently approved by the FDA for the treatment of HCV include (1) interferon alfa-2b (Intron. Amgen. Calif). Agents under study include (1) pegylated interferons alfa-2b and alfa-2a. Kenilworth. Interferons are the backbone of antiviral strategies used against HCV.

com/med/topic3180. in patients with fulminant hepatitis. Other agents used in ECT: Modified ECT use thiopentone sodium or methohexitol as anaesthetic. the patient may receive an injection of a medication (such as atropine) that keeps the pulse rate from decreasing too much during the convulsion. Procedure: The treatment is carried out as follows: approximately 30 minutes before the scheduled treatment time. with excellent results.Emedicine http://www. Rate pressure product a product of heart rate and systolic BP is one measure of cardiovascular response during ECT. lamivudine appears to be ineffective against HBV/HDV co-infection. exchange transfusion.antibodies by this rapidly mutating virus. and treatment of other complications of the comatose state in anticipation of liver regeneration and repair. 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. conspire to render HCV a difficult target for immunoprophylaxis with a vaccine. correction of hypoglycemia. Fulminant Hepatitis: In fulminant hepatitis. Glucocorticoid therapy has been shown in controlled trials to be ineffective. Protein intake should be restricted.htm . plasmapheresis.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.emedicine. the patient is placed on a cot and hooked up to a machine that automatically takes and . human cross-circulation. Likewise. Orthotopic liver transplantation is resorted to with increasing frequency. BP peaks during the ictal period. Next. and succinyl choline as the muscle relaxant. The BP drops sharply during the initial vagal hypertonic phase and then rapidly increased upto 40% over baseline. Use of atropine as premedication increases RPP response. The increase in systolic pressure is more than the diastolic pressure. * 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. the goal of therapy is to support the patient by maintenance of fluid balance. Meticulous intensive care is the one factor that does appear to improve survival. References: . and oral lactulose or neomycin administered. porcine liver cross-perfusion and hemoperfusion have not been proven to enhance survival. To date. support of circulation and respiration. control of bleeding.

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

and weight loss. . patients may develop acute respiratory failure.More often observed in patients with chronic farmer’s lung with long-standing hypoxemia and parenchymal damage. Idiopathic • Rhinitis. The timing of development of symptoms after exposure supports this conclusion. delayed-type hypersensitivity (type IV hypersensitivity) also plays a major role in the pathogenesis of this syndrome. • Pneumonia • Pulmonary Fibrosis. Physical: • Acute farmer’s lung: Fever. weight loss. Patients may experience severe dyspnea at rest or with exertion. or chronic nonproductive cough • Chronic farmer’s lung: Bibasilar rales.Clinically: ♣Acute farmer’s lung Acute farmer’s lung develops after large exposure to moldy hay or contaminated compost. dyspnea. Cell-mediated. sweats. Pulmonary apices are usually spared. dyspnea. it eliminates the possibility of active acute or chronic framer’s lung. HIV Neg: pulmonary MAC infection include cough. and shortness of breath. Allergic • Sarcoidosis E. and malaise. Symptoms often spontaneously resolve within 12 hours to days if antigen exposure is eliminated or avoided. clinical presentations of HP are categorized as acute.subsequent duration of illness. nonproductive cough. fatigue. Clubbing .CXR: Normal findings between attacks. Patients may have irreversible lung damage. and impaired exercise tolerance. anorexia. Subacute disease is insidious in onset and may occur over weeks to months.Differential: • Allergic and Environmental Asthma • Mycobacterium Avium-Intracellulare (HIV Pos: fever. Death usually occurs 5 years after diagnosis. If the inhalational exposure is large. Nonproductive cough. diarrhea.Labs and Imaging: . chest tightness. Abnormal findings are: .High resolution CT Scan of chest: better than CXR. If normal. chills. o Acute: Diffuse air-space consolidation is typical of acute farmer’s lung (with acute antigen exposure). and chronic progressive. weight loss. C. • Subacute farmer’s lung: Normal examination findings between presentations. Chronic farmer’s ♣lung Chronic farmer’s lung results from prolonged and continuous exposure to the antigen. headache. Acute farmer’s lung manifests as new onset of fever. Strong evidence suggests the involvement of immune complex–induced tissue injury (type III hypersensitivity). fever. lung♣Subacute farmer’s Subacute farmer’s lung manifests as chronic cough. o Subacute: Nodular or reticulonodular pattern o Chronic: Linear radiodensities indicative of fibrosis. subacute (intermittent). sputum production. D. Rales. and hemoptysis).

A complete environmental and occupational history is the key to prompt diagnosis of farmer’s lung.Krebs von den Lungen-6 (KL-6) has been recognized as a marker for the activity of diffuse interstitial lung diseases.Medical/Legal Pitfalls: . .Pulmonary fibrosis .Cor pulmonale . . nedocromil) or systemic immune modulators are not indicated for treatment at this time. pulmonary function improves once antigen exposure is eliminated. G.Failure to diagnose farmer’s lung in children living on farms . F. Note: Nonsteroidal anti-inflammatory drugs (NSAIDs) (eg. activity may be unlimited. cromolyn.Consider recommending the wear of filtration masks.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.Special Concerns: .Failure to recognize farmer’s lung when pulmonary function test and radiographic findings are normal between exacerbations .Complications: . Glossary: .Hypoxemic respiratory failure .Medical Care: Systemic corticosteroid administration and avoidance measures constitute the primary treatment for farmer’s lung. In a patient with acute farmer’s lung. . and may be useful also for transbronchial biopsy which would show peri-bronchovascular granuloma. 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. .Treatment: .Activity: Patients may decrease activity because of cough and dyspnea on exertion. .Bronchoscopy: useful to rule out other diagnoses. .Death H. Positive IgG Precipitin .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 . . High ESR.Diet: No dietary restrictions are needed.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.Pulmonary Function Tests: Restrictive .Periodic episodes of acute respiratory symptoms without obvious triggers should also clue the clinician to evaluate for farmer’s lung. and levels may be elevated in patients with farmer’s lung. and Ground Glass Appearance. .CBC: Leukocytosis with neutrophilia (NOT EOSINOPHILIA).Encourage smoking cessation measures. I. respectively.Honeycombing (for pulm fibrosis). Between episodes of acute disease.

General Considerations: It is a rare autosomal recessive disease usually associated with a severe bleeding diathesis. resistance to fibrinolysis. Wheat weevil. B. cross-linking the loose fibrin polymer into a highly organized structure. The b subunits are synthesized in hepatocytes. Reference: Emedicine: . and other molecules to the fibrin plug.htm updated january 2003 . a2 dimers are present in circulating platelets and monocytes.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. Cheeseworker’s lung. 12-36 h) after trauma or surgery is pathognomonic of FXIII deficiency. . The a subunits are synthesized in hepatocytes in the liver and megakaryocytes and monocyte precursors in the bone marrow. intracranial hemorrhage can be life threatening. bleeding from this specific site is uncommon in other inherited hemostatic diseases except afibrinogenemia. „X Wound healing is abnormal. Pigeon’s breeder’s lung. the diagnosis is made at an early age. and myeloid leukemia. Although acquired FXIII deficiency has been described in association with hepatic failure. The mortality and morbidity are primarily related to bleeding. as is bleeding into the mouth and gums during teething. Grain Handler’s lung. Women with FXIII deficiency have spontaneous abortion rates of almost 100%.http://www. usually during infancy. Because the clinical bleeding is severe in most patients. located on chromosome 6. Inherited FXIII deficiency is usually due to mutations in the gene encoding the catalytic a subunit.http://www. „X Hemarthroses occur in 20% of cases „X Bleeding that is delayed (ie.com/MED/topic1103. the only significant association with bleeding in children is the inherited deficiency. a2-plasmin inhibitor.emedicine. FXIII covalently binds fibronectin.Pathogenesis: Factor XIII is a plasma transglutaminase that catalyzes the final step in the coagulation cascade. Malt worker’s lung. and wound healing. The FXIII zymogen circulates as a tetramer composed of 2 catalytic a subunits and 2 carrier b subunits (a2b2). „X Soft tissue bleeding and bruising are very common. In addition. „X CNS hemorrhage is frequent (25-30%) and may occur spontaneously or after minor trauma. „X Recurrent spontaneous abortions are very common in women with FXIII deficiencies who do not receive FXIII replacement.com/med/topic771.Hypersensitivity pneumonitis includes: Bagassosis. this enhances adherence to the wound site.htm updated March 2003 Review of Factor XIII deficiency Factor XIII Deficiency A. C.emedicine. inflammatory bowel disease.

treating pregnant patients requires more frequent prophylaxis (every 3 wk). This can include failed contraception. induced abortions).Work-up: . in its absence. Reference: Emedicine: http://www. In the presence of FXIII. „X Consider other congenital coagulation factor deficiencies. the other is the emergency insertion of the coppercontaining IUD (intrauterine device). most notably dysfibrinogenemia and decreased fibrinogen levels.Differential and associated diseases „X Acquired FXIII deficiency can be caused by liver disease.PTT and PT are normal in FXIII deficiency .D. The latter can be used up to five days after unprotected coitus and is highly effective. and has the potential to reduce unplanned pregnancy by at least 75% (and. the clot dissolves in minutes to hours . a booster dose is recommended during labor to decrease the risk of bleeding in the mother. the clot is stable for more than 24 hours. derivatively. The hormonal method consists of various formulations of estrogen and progestins or progestins alone.Medical Care: „Ï Treatment of bleeding: Plasma. inflammatory bowel disease. and disseminated intravascular coagulation.Measurement of clot stability is the most common screening test. Consequently. the formed clot is suspended in 5 mol/L of urea or 1% monochloroacetic acid. The development of autoantibodies to FXIII has been reported (Differentiate by mixing test. and cryoprecipitate have been used for replacement of FXIII but the treatment of Choice is plasma-derived Factor XIII concentrate. According to different surveys. In addition. The patient's plasma is incubated with thrombin and calcium for a sufficient period to allow formation of a stable clot. and failure to implement prophylaxis as the treatment of choice. intercourse with no contraception for any reason or forced intercourse. Emergency contraception is indicated in any situation in which a woman has had unprotected intercourse but does not wish to become pregnant. „Ï Prophylaxis: Prophylactic therapy with FXIII concentrate 10-20 U/kg every 4-6 weeks provides adequate plasma levels in most patients. „Ï Prior to surgery: patients should receive FXIII concentrate immediately before surgery to ensure optimal hemostasis and wound healing. „Ï Prophylaxis in pregnant patients: Half-life is shorter. Plasma with inhibitor is still prolonged whereas that with true deficiency is corrected). the initial expense and the fact that some women are not candidates for IUDs.emedicine. The Methods: There are two currently well accepted methods of emergency contraception. Its use is limited by the requirement for special training for insertion. It has the advantage of working as an ongoing contraceptive for up to ten years.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.com/ped/topic3040. . „Ï Patients requiring prophylaxis should be vaccinated for Hep A and B „Ï Medical/legal pitfall: failure to investigate family members for FXIII deficiency. E. EC is well-studied and safe.

it would not cause spontaneous .5 times the amount of levonorgestrel than is in the Yuzpe regimen using levonorgestrel. The side effects: There are significant side effects to hormonal EC. o A woman must be pregnant for several days before the test will turn positive. If menses have not resumed 21 days after the administration of emergency contraception. it need not be used.Have you had sex within the last 72h? . 2. The timing: It is very important to start EC as early as possible in the 72-hour window after intercourse.5 mg per dose. followed in 12 hours by 2 more pills).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. there should be no adverse effect on the pregnancy from taking EC. will reduce the rate of pregnancy from 8% to 3. is needed.When was the first day of your LMP (should be less than 4 weeks ago)? . Resumption of menses: 72% of patients resumed menses early or within three days of their expected date. the World Health Organization (WHO) changed the dose of levonorgestrel (Plan B) from 2 doses of 0. When used correctly the progestin prevented 89% and Yuzpe prevented 76% expected pregnancies Contraindications: Same as with any OCP. o Even if a woman were to be pregnant and take the pills. The screening prior to prescribing: three questions to which answer should be YES. which has twice the potency of norgestrel.2%. Birth control pills have frequently been taken in early pregnancy without adverse effects on the fetus. .75 mg taken 12 hours apart to a single dose of 1. particularly with the Yuzpe method.1. Undiagnosed vaginal bleeding is a CI of the Progestin-only method. The Preven® formulation is equivalent to the Yuzpe regimen but it contains levonorgestrel. Treating more than 4000 women in 10 countries. Plan B® is the progestin-only formulation.5 mg levonorgestrel (Plan B) o Five-day cut-off time for treatment. The main concern is whether the vomiting will interfere with the absorption of the medication.5 mg. H/O thromboembolism and migraine are two relative contraindications. They also extended the treatment period from 3 days (72 hours) to 5 days (120 hours). she may feel that she took the pills when she didn't need to. but rates so low that WHO only cites Current Pregnancy and hypersensitivity to any of the components as contraindications. If a woman uses the test and it turns out negative. But it is also very important that the second dose be 12 hours later. or 0. so only half the milligrams. and the FDA required manufacturers to remove warnings about increased risk to the fetus several years ago. Additional advice: WHO now makes the following recommendations: o One immediate dose of 1.The Yuzpe Method = Preven® 100 mcg of ethinyl estradiol and 1 mg of norgestrel (2 pills immediately. This medication is administered in two doses started within 72 hours after unprotected intercourse. Note that this progestin dose is 1.The Progestin-only Method Levonorgestrel (LNG) = Plan B® has been shown to be equivalent to the Yuzpe method. a pregnancy test should be done. rather than 3 days o Ongoing contraception started at time of emergency contraception Although the Preven kit comes with a pregnancy test. most prominently nausea and vomiting. If the woman is found to be pregnant.

ovulation may yet occur for that cycle. 4) A full STD screen at presentation as research suggests a significant incidence of acquisition of STD's prior to rape event. Its availability is restricted to health facilities doing medical abortions under strict protocols. only for medical abortions.Cyberounds: http://www.com/conferences/womens_health/ Updated March 2003. the "Abortion Pill" and EC Mifepristone is a very effective emergency contraceptive. three years. Initial investigations: . Remember. Porphyria. so off label use for emergency contraception would be difficult. . Mifepristone is available in the U. In doing so.htm Updated May 2003 Approach to a rape victim Approach to a rape victim 1. Although EC is not a good method of contraception. it can be repeated without risk. Mifepristone also blocks corticosteroid receptors. It is also a chance to educate and institute protection against STD’s. both products have a long shelf life: Preven®. Approach victims calmly. It presents an opportunity to review contraceptive needs and insure maintenance or initiation of effective contraception for women who wish it. A follow up visit after successful EC is always advisable. 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.) 2. RU486. hemorrhagic disorders and anticoagulant medications are also listed. Its efficacy as an emergency contraceptive is primarily due to its effect of delaying ovulation and possibly delaying maturation of the endometrium. Women should be cautioned to avoid unprotected coitus until their menses occur. Ask victims whether they would prefer a male or female physician. it is not causing an abortion. (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.Emedicine: http://www. References: . Anal examination including proctoscopy should be performed if there is history of forced anal penetration with documentation of found injuries. and Plan B®. Ask about sexual history before rape. In this capacity. because if EC delayed ovulation. it is preventing a pregnancy. four years. so adrenal insufficiency and chronic treatment with corticosteroids are listed as contraindications in the insert. It is not interrupting a pregnancy. They should abstain from intercourse or use reliable back-up contraception until their next menstrual period.Verify occurence of sexual assault. avoid interpreting the victim's calmness or composure as evidence that a sexual assault did or did not occur.S. and no harm would come to the fetus.com/aaem/topic498. 3) Physical Examination: Injuries requiring immediate attention should take precedence. Oral contraception can be started immediately after EC. PMHcontraceptive history-Gynec History.emedicine.cyberounds.History Taking: Unrushed and sensitive manner. Showing your outrage at the crime may cause victims even more trauma.abortion. Use direct questioning to disclose forced oral or anal penetration by victim. Other considerations: Mifeprex®.

IUD copper-contraception can also be considered with ATB coverage. . In addition.. hepatitis B. trichomonas.75mg x1 dose only (recent guideline) or x2doses 12h apart no later than 73h after event. enzyme substrate. 7) Treat sexual partners if pt found to have STD. Follow-up doses of vaccine should be administered 1--2 and 4--6 months after the first dose.Collection of a serum sample for immediate evaluation for HIV. . For boys with a urethral discharge. Hepatitis B vaccine should be administered to sexual assault victims at the time of the initial examination if they have not been previously vaccinated.Hep B Vaccine up to three months after assault 3 doses. FDA-approved nucleic acid amplification tests (as a substitute for culture). 0-1-6 months. . serologic. All presumptive isolates of N. Special considerations: Sexual assault of a child: Specimen collection for culture for N. and BV may be administered. and the urethra in boys. Isolates and specimens should be retained or preserved in case additional or . and syphilis. Gonorrhea and Chlamydia Trachomatis cultures from specimens collected from any sites of penetration or attempted penetration.Wet mount and culture of a vaginal swab specimen for Yeasts and Trichomonas Vaginalis.Offer Post exposure Prophyaxis for HIV. Only standard culture systems for the isolation of N. 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.N. gonorrhoeae should be confirmed by at least two tests that involve different principles (i. the vagina in girls. -------------------------------------------------------------------------------If patient pregnant or breast feeding: Amoxicillin 3g STAT + Probenecid ag STAT + Erythromycin 500mg BID x14days. 6) Offer ongoing counseling. a meatal specimen discharge is an adequate substitute for an intraurethral swab specimen.. If considered PEP should be given no later than 72h after event. should adequately protect against HBV. 5) Treatment: Postexposure hepatitis B vaccination. . . gonorrhoeae from the pharynx and anus in both boys and girls.e. gonorrhea. An empiric antimicrobial regimen for chlamydia. without HBIG. or DNA probe methods). Cervical specimens are not recommended for pre-pubertal girls. biochemical. gonorrhoeae should be used.Offer Pregnancy prevention using Levonorgestrel (Ovral) 0.

CDC 2002 Guidelines: http://www. trachomatis from specimens collected from the anus in both boys and girls and from the vagina in girls.cdc. Physical: Epidermoid cysts appear as firm. Epidermoid Cyst is more favored. 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.org.htm#AssaultSTDs . Less frequently. pallidum. mobile. In the uncommon event of malignancy. Sera should be tested immediately for antibodies to sexually transmitted agents. have developed in epidermoid cysts. rapid growth. and HbsAg. HIV. the cysts can become inflamed or infected. and bleeding have been reported. Rarely. and even mycosis fungoides. Extracts of this material have been shown to be chemotactic for polymorphonucleocytes. flesh-colored to yellow or .mssvd. Reference: . Agents for which suitable tests are available include T. 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.PDF Question Question about Pt with picture of skin lesion showing nodule. History: Discharge of a foul-smelling cheeselike material is a common complaint. SCC. and used as a baseline for comparison with follow-up serologic tests. Bowen disease. Epidermoid cysts result from the proliferation of epidermal cells within a circumscribed space of the dermis. friability. Inflammation is in part mediated by the horny material contained in epidermoid cysts. round. including basal cell carcinoma. Epidermoid cysts are slow growing and usually asymptomatic. but they may become inflamed or secondarily infected.uk/PDF/CEG2001/sexassault%2006%2001. Culture and wet mount of a vaginal swab specimen for T. Gram stains are inadequate to evaluate pre-pubertal children for gonorrhea and should not be used to diagnose or exclude gonorrhea. Collection of a serum sample to be evaluated immediately. even if the risk is perceived to be low by the healthcare provider. However.National guidelines for response to sexual assalut http://www. some children or their parent(s) or guardian(s) may be concerned about the possibility of infection with an STD. vaginalis infection and BV. and c) regular follow-up of children usually can be ensured. b) pre-pubertal girls appear to be at lower risk for ascending infection than adolescent or adult women. 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. What is it? Epidermal Inclusion Cys Background: Also called Sebaceous cyst although not of sebaceous origin. Biopsy reveals Cheese-like material.gov/std/treatment/8-2002TG.repeated testing is needed. resulting in pain and tenderness. resulting in pain and tenderness. preserved for subsequent analysis. malignancies. Cultures for C.

the vulva. or the perineum.Hysteroscopy will detect only the submucosal fibroids whereas USG can detect all types of fibroids. Biostats question With IQ test mean of 100 and SD 15. USG is the best initial non-invasive investigation to do in this case. Which work up is essential in determining the severity and therefore the treatment indication of this patient? From the hx. Smears of aspirated material can be stained with Wright-Giemsa. 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.htm Updated Feb 2003 Microbiology (if infected) and US Question 34 yo female patient presenting with heavy menstrual blood loss and elarged uterus. The ocular and oral mucosae can also be affected. . Squamous Cell carcinoma (MC cancer in this entity).What will be percentile of IQ if person IQ is 115 ? 50. FNA: Fine needle aspiration has been used to help diagnose epidermoid cysts. all excised cysts should be sent for pathologic analysis. Treatment: .Abstinence . on the buccal mucosa. and they demonstrate nucleated squames and wavy keratin material.Abd sono. 84. the penis. In turn.white subcutaneous nodules of variable size. Therefore.the most common presentation of submucosal fibroid is abnor.May be injected with triamcinolone if uninfected. .vaginal bleeding. Reference: emedicine: http://www.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. rapid growth).99 th ?? This question has been discussed in length before.So.emedicine. Physical examination reveals a large uterus with irregular consistency. the clitoris.the most likely diagnosis is either Subserosal fibroid or Intramural fibroid(as it is given as enlarged uterus). Occasionally. under the tongue.detect submucosal. 68. 95 . I was wrong in my reasoning just like Salil. the scrotum.Excision in toto = definitive treatment preventing recurrence by excising Keratin producing the lining of the cyst. Medical/Legal Pitfalls: The major pitfall in managing epidermoid cysts is failure to diagnose an associated malignancy.com/derm/topic860. and even on the uvula. Epidermoid cysts of the genitals are common in the general population and may appear as a mass in the breast. removal is recommended for any cyst behaving in an unusual way (eg. and cysts have been reported on the palpebral conjunctivae. You suspect uterine fibroids. .detect intramural/subserosal (as in this case)& vaginal sono . Here's the exaplanation.I&D if infected followed by antistaph ATB PO . on the lips.(enlarged uterus is very unlikely) Reg investigation.

it gives you 84%. migrain HA normally improves in pregnancy. and leading to closure of PDA in as many as 86% of the patients. What treatment would be best for her migraine during pregnancy? In general. Mechanism by which Indomethacin helps in the closure of PDA Patency of PDA is an active state maintained by the action of prostaglandins. Indomethacin either postnatally or sometimes prenatally as PDA prophylaxis inhibits Cyclo-oxygenase thereby inhibiting the production of Prostaglandins. Read the explanation after drawing the bell shaped curve you'll understand it better. Pseudotumor Cerebri and Pregnancy I recall having read a question in which a pregnant woman came in with signs indicative of pseudotumor cerebri. consequence of long-standing PDA. Sometimes. We had calculated between 0 and the mean as being the 50th percentile. It means of our population 97. I wondered about the treatment in pregnancy.5 = 97.What we know from the bell-shaped curve is between +1SD and -1SD: the area under the curve consists in 68% of the population. does NOT affect the . But that's the trick. it requires surgical intervention either because of failure to close or reopening after many treatments with Indomethacin. Similarly. It has also been shown to increase pulmonary blood flow. one in which a patient has pseudotumor and gets pregnant or the patients is pregnant and develops signs of increased intracranial pressures. The interpretation is a number AT +1sd is at the 84th percentile. Half of that area is 34% which is between the mean and +1sd. therefy reducing the tendency to Pulmonary hypertension. tx w/acetaminophen and antiemetics. does not increase the risk of relapses 2. Meaning. But if persist. if the ICP became resistent to therapy (one study followed progressive visual loss) a shunt was placed. Now from the hump of the curve to +1sd corresponds to half the area under the curve we talked about in the beggining. This area situated in the interval -1SD and +1sd which is 68%. (If severe use codene ormeperidine). Half of it which is the area between the mean and +2SD is 47.5% are located below the +2SD point on the curve. Therefore the percentile located AT +2sd is 50+47.5%. The patients who already had the established diagnosis were treated medically. Here's what I found. Medical literature search: few articles describe two scenarios. Another study concluded that psudotumor 1. Usually one dose is enough. The question asks about the percentile. So the hump of the curve corresponds to the 50th percentile. however.5%. the area between -2SD and +2SD is 95%. does not mean a worsening prognosis and 3. We already know that between 0 and the dome of the curve is 50 % because it's the mean. Now let's join the two. In all instances healthy babies were delivered. How much percent is between 0 and +1sd. Her PMH is negative for anything other than migraine headaches that she suffered from regularly since high school. 3/4 of patients responded to shunting the other 1/4 required optic nerve sheath decompression. Avoid ergotamine. It is not what is asked in the question. If you add to it the new found number of between the mean (hump of the curve) and +1sd which is 34%. 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. it is a directional question.

Allows lithium use to be continued.g. May be combined with thiazide for additive antidiuretic effect and to balance potassium. clinical Scenario: JB a 57yo woman has been having recent epidoses of nocturnal enuresis. Potassium should be given as needed to prevent hypokalemia. the latter being DOC for Lithium-indeuced Nephrogenic DI. Thiazides (e. The article listed 2 case studies . Uosm improves after administration of ADH. In Central.Uosm < 200mOsm/kg 3)Differentiate bwteen Central and Nephrogenic: Water Deprivation Test: Compares Uosm after dehydration Vs Uosm after Vasopressin. In DI. Upon further evaluation. 2) Nephrogenic DI: Combination Indomethacin + HCTZ or Indomethacin-Desmopressin or Indomethacin-Amiloride. pre-eclampsia. Salt restriction augments this effect. Often associated with oligohydramnios. as well as chlorpropamide 100mg/d. ADH levels. See in 3rd Trimester and puerperium. BP: normal. Must monitor for hyperkalemia and cannot use in renal insufficiency. Carbamezepine. 3) DI and pregnancy: Pregnancy increases risk for DI = Vasopressinase-induced DI. Grav=1. she reveals that she has been thirsty of late. . creatinine. The second scenario. 1st step in management: 1)In ER: Hydrate IV dextrose and water or IV hyperosmolar fluid. 1) 24h urine collection: volume. volume overload. Urine Specific Gravity. Avoid hyperglycemia.Thiazide diuretics combined with mild salt restriction is the most effective therapy for nephrogenic DI (can reduce polyuria as much as 50-70%). Uosm) 2) Serum: Electrolytes and Glucose. increased isotonic proximal fluid absorption and thus decreased delivery of fluid to the collecting duct.005 . 2) Central DI: DOC = Intranasal DDAVP Assess for drugs that potentiate effect of DDAVP: Chlorpropamide (patient IS DIABETIC AND ON CHLORPROPAMIDE). She therefore started experiencing frequent urination. and indomethacin. or hepatic dysfunction. and drinking lots of water. PE: no peripheral edema. The mechanism = circulating desmopressinase which destroys . thiazides. Next step: Work up is done preferably with pt maximally dehydrated as tolerated (i. Urine Na. and rapid correction of hypernatremia. increasing risk of lithium toxicity.developing child. Volume depletion may decrease lithium excretion. Role of Thiazide in DI .e. JB's got h/o of DM2 controlled by diet and exercise. in both the baby was delivered vaginally without complications.Amiloride: Agent of choice in lithium-induced nephrogenic DI since it may block lithium uptake in distal tubules and collecting ducts. hallmarok is: Urine Sp.: at time when ADH should be highest and urine most concentrated). HCTZ 50-100 mg/d) induce mild salt depletion (block Na reabsorption in cortical diluting site) which results in volume contraction. May also have thiazide-like action since it causes a negative Na balance. Main limitation is symptomatic volume depletion. clofibrate. Lytes: Hypernatremia. The latter results subsequently in decreased GFR. in which elevated ICP occur during pregnacy is rare.

Sp.Rx? a:DDAVP b:plt transfusion c:aminocaproic acid d:IV gammaglobulin e:FFP IV immunoglobulin This is HIV-induced ITP.Endocrinology UCLA http://www.3.K:6. .Diabetes Mellitus .2 U/A:PH:1.Multiple Myeloma Reference: . nephrotoxicity .Kaplan notes 2002 Question A 24 yo man known to be HIV+.so diagnostic test of choice Renal transplant rejection Vs Cyclosp.Ca:7. AZT (80-90% susteained positive response).Cl:99.Pituitary surgery . 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.010.endocrinology.Hypokalemia . Side effect of this drug: Retroperitoneal fibrosis.HCO3-:16.Pregnancy . Also U. Urinary tract obstruction since it is abrupt onset? It is also a vasoconstrictor.glucose:101.ucla.Plt count:2000.Sickle Cell Disease . The quickest response would be with IV immunoglobulin which is indicated in severe thrombocytopenia. Long-term treatment options would include spelectomy (increased risk for encapsulated organisms infections).protein&Hgb:trace. and steroids (40-80%). Colchicine.CMDT .Hypercalcemia . Demeclocycline(ATB tetracycline used for SIADH). Rx = DDAVP.9. 4) DI in children: mostly ENURESIS .endogenous ADH but not synthetic.2.LINEAR GROWTH RETARDATION Note: Risk factors for DI: .med.Emedicine .P:6.develops the acute onset of petechiae and oropharyngeal bleeding.edu/diabetes_insipidus. A 54 yo woman presents with abrupt decline in urine output& RF. Foscarnet.Her PMH is positive only for hysterectomy 1mo earlier& chronic migraine headaches controlled with methysergide. but the abrupt onset doesn't make it sound like ATN secondary to vasoconstriction.G=1.htm .Albumin:4.010.Cr:3.currentlt receiving no treatment.No RBC fragmentation is noted on exam of peripheral blood smear.Lithium.sediment:unremarkable Urine output over the past 12hr:60cc Next step of Mx? Stop offending drug and do CT. Methicillin).Lab: Na:130.

Cyclosporine trough level <150ng/ml. and oligouria. MRI: loss of distinct cortico-medullary junction + swelling + density similar to that of Psoas and fat tissue. oligouria after initial function. The evidence for reducing fracture risk is currently considered insufficient for most agents. endothelial vaculoization).Hct:29% Cr clearance:55ml/min. Bisphosphonates. . According to CMDT Alendronate is the first agent to consider. Cyclosporine trough level>200ng/ml.Ca:10.K:4.HCO3-:24. US: unchanged graft corss-sectional area.9. obese. therefore protecting her against it is not necessarily warranted. So she's still not extremely depleted. Normal t scores are above -1.hrt 2.Albumin:4. The risk she needs to be protected against is pathological fractures. what is best for her 1. bisphosphanates 3.her bone density test [dexa scan[ shows t score of 0. fever. Manometry intracapsular pressure >40mmHg. calcitonin Answer is 2.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. rapid rise in creatinine.glucose:101. Is it graft rejection or cyclosporine nephrotoxicity? To differentiate the two: .P:4. necrosis and sclerosis).http://www. Rsponds to decreasing cyclosporine. estrogen(HRT).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. manometry: capsular pressure is<40mmHg. Reference: .2. and etidronate. 4 weeks later: rapid rise of creatinine.3. Responds to increased steroids or antilymphocyte globulin.9. alcoholic.9.pdf Question A 68 yo white man is reffered to u for evaluation of renal failure. The evidence of antifracture efficacy is most convincing for the 2 bisphosphonates alendronate and risedronate. afebrile. Bisphosphonates have the mechanism of action of inhibiting . Biopsy: endovaculitis (intimal arteritis. US: increased graft cross-sectional area. fever and weight gain.com/content/transplant/Generic_Cyclo_PI. Biopsy: arteriolopathy (intimal thickening.Transplant rejection: <4weeks.past history of dvt. she is a smoker. edema. with sedentary lifestyle. raloxifene 4.2g/day Next step of Mx? this pt has multiple myeloma and his renal failure most likely is related to overproduction of Ig light chains.Cl:109. Her t score is 0.the pt has anemia. Raloxifene significantly reduces the risk of vertebral fractures by approximately 30% but does not reduce the risk of hip or other nonvertebral fractures.Renal transplant patient on immunosuppressants among which cyclosporine.Lab: Na:135. including calcitonin. According to CMDT the agents to use first are bisphosphonates. This patient has no history or risk factor mentioned for breast cancer.urine protein:6.stadtlander. gradual rise in creatinine.cyclosporine toxicity: >6 weeks use. hyalinosis.

Vaccine is contraindicated if ORAL STEROIDS. If the patient were to have mentioned any risk factor for breast cancer." This is a mild case of chickenpox caused by the wild-type virus at least 6 weeks after vaccination.Son is 8yo on inhaled steroids for asthma. This illness should be treated as regular chickenpox. Reference: .Son exposed to chickenpox at school. then Raloxifene would be first choice.The vaccine is not 100% protective.Pregnant woman 12 weeks. . Most adults are immune. He still has to get the vaccine. with no DEFINITE prior history of chickenpox or varicella vaccine.Vaccinate ANY child who is not immunocompromised and is more than one year old. DO NOT VACCINATE BABIES LESS THAN 1 YEAR. Should he be vaccinated? Yes. son is due for vaccination. Immune globulin products should not be given for at least 2 to 3 weeks following the varicella vaccine. .Son had rash at 4 months of age. Shoul dhe get vaccine? YES. Was never vaccinated for chickenpox. Never vaccinated for chickenpox.what will u tell the mother? Answer: If age is 6yo = give vaccine. .Chickenpox developped after vaccine: 1% of vaccinated kida will have what is called "breakthrough disease. . If age is 6months old = DO NOT VACCINATE. . This baby's age is probably 6 months as opposed to six years old (probably a typo). NO. If.PPD TEST MAY BE DONE AT THE SAME TIME AS VARICELLA VACCINE. Varicella Vaccine Facts 6 year old girl's mother is afraid the baby may get chicken pox becoz her friend got it. leukemic grandmother. There is a possibility of rash 4-6 weeks after vaccine. they are given at the same time. the vaccine should be repeated in 5 months. 15% of patients with get a mild rash. Babies less than one year are perhaps considered immunocompromised?? At any rate it is not recommended IN THE USA. however. Since it's not a DEFINITE history of chickenpox. . same patient with mild sore throat or diarreha. . Asks you if she should be concerned and get the vaccine now? NO.osteoclast activity this stopping calcium mobilization from the bones. pregnant women. .It MAY BE GIVEN AT THE SAME TIME AS MMR. MD said that it's "probably" chickenpox. and Vaccine is contraindicated in pregnancy.HIV brother. 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.Pregnant woman had a sever case of shingles.baby was not vaccinated . Should he get vaccine if not immunized before? Yes within 3-5 days of exposure.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). and it has been shown that this rash is more severe in immunocompromised patients. There are usually less than 50 lesions and no severe symptoms. in the household ARE NOT CONTRAINDICATIONS TO THE VACCINE WHEN IT'S DUE. . . Now. . Inhaled steroids are not a ptoblem. .

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. Patient now presents holding the affected hand and wrist with his good hand. injury to the brachial plexus in the axilla.http://www. also preventing edema and distortion of tendons. Discussion This neuropathy is produced by compression of the radial nerve as it spirals around the humerus. intoxicated. Prognosis: short-term = very high likelyhood of sarcasm and irritability. Construct a splint. It forms the POSTERIOR CORD of the brachial plexus. hand function may appear normal. ligaments. held up by his arm thrown over the back of a chair. Incomplete lesions may be satisfactorily referred for followup evaluation and physical therapy. ignoring the growing . If there is complete paralysis or complete anesthesia. Explain to the patient the nature of his nerve injury.jsp?vac=3-7 What is Saturday night syndrome? Two aspects are to consider for this syndrome: 1. 2.already married. This sort of nerve injury may be associated with cervical spine fracture. complaining of decreased or absent sensation on the radial and dorsal side of his hand and wrist. which may be accomplished by the ulnar-innervated interosseus muscles.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). What to do: Look for associated injuries. Sometimes happens after humerus fracture since radial nerve trails down around humeral groove. and arrange for followup. This and a sling will help protect the hand. Presentation The patient has injured his upper arm. What not to do: Do not be misled by the patient's ability to extend the inter phalangeal joints of the fingers.. thumb and finger joints. and of inability to extend his wrist. and joint capsules which can result in loss of hand function after strength returns. the slow rate of regeneration. usually by sleeping with his arm over the back of a chair.vaccinecheck. Another presentation is a patient using crutches. Long-term = roughly 67% will end up with a date in the next three years. the importance of splinting and physical therapy for preservation of eventual function.. Most commonly it occurs when a person falls asleep. Less severe forms may befall the swain who keeps his arm on his date's chair back for an entire double feature. or fracture of the humerus. The rest was. but when the hand is pronated (palm down) the wrist and hand will drop. arrange for additional neurological evaluation and treatment right away. With the hand supinated (palm up) and the extensors aided by gravity.com/vacinfo_3-7.

both have 100% sensitivity and 98% specificity. so you can use either one of them). So if positive.vit C d. from leaning on crutches) will involve all of the radial nerve innervations.. . Labs: RPR or VDRL to R/O secondary syphilis. No need to exclude child from school.hc-sc.. no organism involved.hepatitis A IgM d. (Sensitivity for primary syphilis: RPR higher 86% (vs 78% for VDRL)=>use RPR first. including the triceps. PALMS AND SOLES NOT INVOLVED (as opposed to roseola of secondary syphilis). Both are nontreponemal.vit D e.ca/pphb-dgspsp/std-mts/csg-ldcm/lab_e.Lab Diagnosis of syphilis http://www. 1-2 weeks later generalized rash which lasts approximately 6 weeks. Cause: seasolnal predilection.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. If the injury to the radial nerve is at the elbow or just below.emedicine .pain and paresis. confirm with treponemal FTA-ABS for ex. Treatment: Self limited. The deficient groups will be the wrist ulnar extensors as well as the metacarpophalyngeal extensors.vit A b.zinc In an adolescent presenting with ptyriasis rosea. The rash has a Christmas Tree appearance on the back.. Here goes.gc. Secondary syphilis. occurs in clusters among contacts.FANA e.vit B c. Reference: . Supportive measures: Water.Vit A (Typo: pseudoTUMOR cerebri) 2. Questions: which of the following when given in excess would most likely cause pseudomotor cerebri? a. VDRL B. Topical zinc oxide and calamine lotion are useful for pruritus.High Yield.glucose 1. salmon colored with darker periphery (primary plaque). This has been updated as of february 2003.g. so I thought I'd share what I had come across a while ago. and challenging cases of pregnant wome. there may be sparing of the wrist radial extensors as well as the radial nerve autonomous sensation. and soap may cause irritation and should be avoided early in the disease. sweat. A high radial palsy in the axilla (e. complete blood count c.html Trauma in Pregnancy.VDRL: Quick review on Pityriasis Rosea Presentation: Child with Herald patch 1-2 cm.which f the following tests would be an appropriate blood test to order? a.

but EMS is unable to perform this because of 'laryngeal spasm. She has no airway compromise. Examinations in the 'low dose' group include cervical spine. You order intravenous fluids. it is positive. She is awake and aware. Radiological exposures to the fetus can be divided into a 'low dose' group and a 'high dose' group. but has a respiration rate of 22 secondary to the pain on the left side of the chest inferiorly. together with lumbar spine views. 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. thoracic spine.Q#2 A pregnancy test! Moreover. So. while chest CT produces about 1000 mrad (significantly less if shielded). within minutes of each other. With modern radiographic machines. of course. what would you tell her now? Trauma in pregnancy . Estimating exact exposure of any individual fetus is very difficult.. 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. What did you forget to order specifically? Trauma in pregnancy. CTs of the upper abdomen can produce up to 3000 mrad of exposure. She has never been pregnant before.You are the only emergency physician in a well-equipped emergency department.Q#3 In general. Each of these examinations. An IVP causes 500-800 mrad exposure. the fetus will be exposed to about 50-100 millirads (mrad) during the course of the 9-month pregnancy. The lumbar spine is the highest exposure. 'High dose' examinations include lumbar spine. understandably. It is an hour before handover in the morning. while. maternal size and the age of the fetus. A quickly ordered quantitative bHCG shows that she is between 6 and 8 weeks pregnant. You quickly head off to deal with the other two victims. complaining of some low back pain and left upper quadrant abdominal pain. The pelvis and hip x-rays produce about 200 to 400 mrad each. OK this is an easy one given the title. urethrocystograms and the 'KUB' (or 'flat plate abdomen') are considered 'high dose'. with a range between about 200 and 1200 mrad. They both require intubation. urinalysis. intravenous pyelograms (IVP). A urethrocystogram produces about 1500 mrad. (all of which were reported as 'normal'). EMS calls to say they are bringing in three patients from a rollover car wreck. the technique. given that she has had the x-rays ordered (cervical spine. pelvis and hip. lumbar spine) and has completed the CT of the abdomen and pelvis. correctly performed.appear critically injured. When the patients arrive. CTs of the head result in about 50 mrad of exposure. You are a little tired after a busy night.' The third patient -. bloods. Talking with the patient reveals that her last period was about 7 weeks earlier. coned views aimed more than 10 cm away from the fetus result in very low exposure to the fetus. and an x-ray of the cervical spine. as it can vary according to the equipment used. you quickly examine the 22-yearold.. pelvis.is a 22-year-old female. Two of the patients -an elderly couple -. Her pulse rate is 92 and her blood pressure is 110/75 mm Hg. chest. She is complaining bitterly of low back pain. should result in less that 1 mrad exposure to the fetus.a restrained rear seat passenger -.. while a KUB is between 200 and 500 mrad. chest and pelvis. In addition. CT of the pelvis produces a much higher exposure . chest and all extremities. Computerized tomography (CT) can produce more significant exposure levels.

our patient has had some low risk examinations -. there is one adverse event). Thus. In addition. In this article. suggest she see an obstetrician as soon as possible -. Figures quoted indicate a 6% chance of mental retardation and about a 2-3% chance of developing childhood cancers. 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. 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. while malformations are greatest if radiation exposure occurs between 2 and 8 weeks gestational age. sterility and germ cell mutations.we should not deprive the mother of adequate investigation in the setting of trauma because of the theoretical risks from radiation. at about 7 weeks. The take home message here should be that although we should take every precaution to reduce fetal exposure to radiation -.000 mrad there appears to be a slight increase in the incidence of childhood cancers.chest and cervical spine x-rays. Abnormalities described include prenatal or neonatal death.2 Bochicchio and colleagues studied trauma admissions over a four-year period and they found that 114(2. number of CT cuts and size of patient. Mean gestational age was lower in this group. severe mental retardation and either temporary or permanent growth retardation. the major congenital abnormality described has been microcephaly.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. and some significant exposures from the pelvis and lumbar spine x-rays. 13(11%) were incidental pregnancies. as one might expect. what is considered a 'dangerous' dose of radiation. the abdominal CT and. Another article1 quotes a risk of 1 adverse event/1000/1000 mrad of exposure (i. the pelvic CT.000 mrad. fetal loss was significantly higher in the incidental pregnancy .and arrange this for her if she lived in the catchment area of the hospital. equipment. The cumulative radiation exposure exceeded 5000 mrad in about 85% of patients. there is a greater risk. At doses above 15. A recent article addresses how often this scenario actually happens. In general.even when in the emergency department if she wished -. exposures of less that 5000 mrad have negligible effects.9%) of 3976 women admitted were pregnant. In the Japanese cohort. The highest risk for fetal viability is in the earliest stages of pregnancy.level of between 3000 and 9000 mrad. depending upon exact technique. Thus..5 Between 5000 and 10.e. especially within the first two weeks. I would counsel the patient about the slightly increased risk of fetal abnormality. Total dose could be between about 5000 and 13. multiple types of congenital abnormalities. and what are the risks? Trauma in pregnancy.through shielding. This is the period of maximum organogenesis in the developing fetus. for every 1000 infants exposed to 1000 mrad. minimizing numbers of x-rays or using alternative investigative techniques -. The estimated mean initial radiation exposure of all patients was 4500 mrad. Of these women.000 mrad. there may be an increased risk of carcinogenesis. especially. Additional information has been extrapolated from animal studies. Now. given this information.

Q#5 Your answer should be "YES. Domestic violence is thought to account for as much as 30% of all trauma seen in pregnancy. However. Complications peculiar to the pregnant patient as a result of trauma include preterm labor.. She is lying flat on a stretcher immobilized in a neck collar. will often elicit the truth. she was wearing her seatbelt correctly. In America. It is estimated to occur in about 7% of pregnancies. there was significant damage to the patient's vehicle and she describes a momentary loss of consciousness.. The patient is currently complaining of shortness of breath and has a cramping abdominal pain. Her blood pressure is 100/60 mm Hg and the oxygen saturation is 99%. Correct placement of the belt is to wear the lap portion of the belt across the pelvis. During pregnancy. Because her primary care health worker had counseled her. doctor?' What is your response? Trauma in pregnancy. gunshot wounds are the most frequently encountered cause of penetrating injury. Fetal mortality rates in penetrating trauma are as high as 70%. with the partner out of the room. or wear it incorrectly. accounting for up to 70% of blunt abdominal trauma. followed by direct assault. After being given information about the risks of the pregnancy and discussing it with an obstetrician in the department. Very few women will admit to physical abuse and thus the physician must maintain a high index of suspicion for this problem. Unbelted pregnant women are 4 times more likely to have a fetal demise and about 2. placental abruption. Her respiratory rate is 24 and shallow. Penetrating injury is less common than blunt injury. below the pregnant abdomen. with the shoulder belt placed over the mid point of the clavicle. the commonest cause of trauma in the United States is motor vehicle crashes.5 times more likely to give birth within 2 days of the injury. She has one intravenous line in place and has oxygen running via a facemask. up to one-half of all pregnant women do not wear their seat belt. She was lost to follow up.group when compared with the 'known' pregnancy group. when compared with belted pregnant females. . She is able to protect her airway. 65% for those not instructed Trauma in pregnancy. she has been involved in a road crash where she was struck head-on by a truck that crossed the mid-line." Unfortunately. She feels a little light headed.. A frequently asked question by pregnant patients is 'Should I wear my seat belt. fetal-maternal hemorrhage and fetal demise. between the breasts. our first patient elected to leave against medical advice to return to her home out of state. While driving to work.Q#6: Second Case The patient is a 27-year-old female who states that she is 28 weeks pregnant with her second child. 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.. Epidemiology of Trauma in Pregnancy Trauma is the leading cause of non-obstetric morbidity and mortality in the pregnant patient in the United States. and to the side of the pregnant abdomen. The next leading cause is falls. Direct questioning. 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.

ultrasound is not always reliable at spotting this problem.Q#11 Patients need to have at least four hours of external fetal monitoring if they are beyond 20 weeks gestation. It results from the relatively inelastic placenta separating from the elastic uterine wall when the latter is distorted because of trauma. the presence of a normal blood pressure does not preclude the possibility of a significant bleed.Q#8 During pregnancy.Q#9 In the pregnant patient. and why? Trauma in pregnancy.Q#7 The one immediate step that should be taken is that a wedge of some kind -. The absence of any uterine activity over the four-hour period immediately following the trauma virtually excludes the possibility of an abruption.a rolled towel or other object -.Q#10 The presence of a cramping sensation should raise the possibility of the development of a placental abruption. Saline appears more likely to cause a significant acidosis and should be avoided. The patient is now complaining of a cramping feeling in her abdomen. consideration should be given to warming the fluids. This is a feared complication of trauma in pregnancy.. The pulse rate gradually rises through pregnancy. Unfortunately. Management then should be by an experienced obstetrician and will depend ... What fluid should be run through these lines. the use of lactated Ringer's solution is preferred. What complication is a possibility now? Trauma in pregnancy.Given that her airway is protected and her breathing probably adequate currently. It can occur after relatively minor trauma. what ONE measure could immediately help her and why? Trauma in pregnancy. This removes the uterus from the inferior vena cava and facilitates venous return. It is the reason why careful observation is required for pregnant women after trauma. However. The presence of 8 or more contractions in an hour is highly suggestive of the diagnosis of abruption. even if they appear hemodynamically stable. Blood volume gradually increases through pregnancy. An angle of about 15° is usually recommended. rises slightly in the second.. Pregnant women suffering significant trauma should have two large bore IV lines established as a routine. the blood pressure initially falls in the first trimester. This is because the fluid is more physiologic and less acidotic that normal saline.. What monitoring modality is useful? Trauma in pregnancy. Is this blood pressure 'normal'? And if it is normal. Among them.. The result of this movement is that the blood pressure is now 118/68 mm Hg. with a baseline of 85 by the third trimester. moving the uterus over to the left side slightly. a number of physiological changes occur. Compression of the vena cava can result in a significant reduction in venous return... The result of this is that clinical signs of significant hypovolemia may be delayed because of the increased reserve. enough to appear that the patient is hypovolemic.should be placed under the right hip.. The blood pressure recorded on our patient could be considered 'normal'. does this indicate we don't have to worry about occult blood loss here? Trauma in pregnancy. then rises again in the third trimester almost back to pre-pregnancy levels. As is usual in the management of trauma victims. to levels about 50% or more above pre-pregnancy levels..

The patient has no vaginal bleeding. This incision is extended down through all layers to the uterus. Although this complication is very rare.Q#12 The normal fetal heart rate is between 120 and 160 beats per minute. The normal fetal response to stress is bradycardia and the commonest cause of this is hypoxia.5 ml of fetal blood is required to sensitize 70% of Rh negative women. The usual dose is 300 micrograms intramuscularly. Between 3 and 7 contractions in an hour require further observation and many would recommend 24 hours of continuous monitoring. and there is up to a 30% rate of fetal maternal hemorrhage. extended up to the top of the uterus. rarely useful in the emergency management of patients. If the placenta is encountered on the anterior wall. What is the normal fetal heart rate? What is the fetal response to stress? Trauma in pregnancy. thus. then abruption or another uterine abnormality is likely.. If there is a significant abruption. From what complication of the abruption is the mother at risk? You also find out that the mother is Rh negative. If correction of maternal hypoperfusion. but it is indicated if there are signs of fetal life and resuscitative efforts on the mother have been unsuccessful. The patient has abruption. Some authorities use the Kleihauer-Betke test to estimate the degree of fetal blood loss into the maternal circulation. immediate intervention is required.upon fetal gestational age. many authorities would proceed to delivery. We are also told that the patient is Rh negative. hypoventilation or hypothermia does not improve the heart rate. the abruption may be small enough to allow continuation of the pregnancy. for four minutes. 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. Immediate delivery is paramount to save either life. In the remainder.. A scissors is then inserted into the incision and. The baby is delivered through the incision and the cord clamped. with no pulse or blood pressure. You are very suspicious that your patient has an abruption. and she must be given Rh immune globulin. so does this matter? Trauma in pregnancy. secondary to the passage of placental products into the maternal circulation. however.. In these cases.Q#13 Abruption is a risk factor for the development of disseminated intravascular coagulation. The uterus is opened in the lower section with a small vertical incision from a scalpel. not always available in the emergency department and is.. The technique involves a midline incision from the pubis to the umbilicus. it is cut through. The technique of emergency department caesarian section is a little beyond this presentation. and the fetus is over 32 weeks. Patients who have an abruption have fetal distress obvious in at least 60% of cases on arrival in the emergency department.. As little as 0. it is devastating in that there is profuse bleeding and rapid deterioration of mother and fetus.Q#14 The presence of a boggy uterus and easily palpable fetal parts are signs of a uterine rupture. This test is. What devastating complication has now arisen? Trauma in pregnancy. 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. using the fingers as a guide so as to keep the points away from the fetus. but the mother must be observed very closely.

but then progressing to both legs.stop ocs Neurlogical localization Case 5 68 yo white female presents with inability to walk.start heparin . and her mouth was twisted. and is taking OCP. using the skills of the emergency department personnel. together with obstetric. He remains unable to express himself and unwilling to talk for a period of 18 hours. This persists for 15 minutes and then rapidly resolves. On exam. She seemed confused. Language is intact. first felt in the left arm. One arm hung limply. He has a completely normal neurological and ophthalmological examination. Fasciculations are present in the tongue at rest.staff. One year later. and all four proximal extremities. 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. What distribution is it and what subsequent evaluation should be carried out? Broca's TIA. and she walked unsteadily. She had a past hisotry of untreated rhematic heart disease. An organized approach. His voice is not as loud as it used to be. and appears emaciated. she is slightly inattentive. and he noticed he can do so if he moves it with his finger. No CN deficits. and sometimes inappropriate. including a jaw jerk. and the tone has changed. CT will most likely be normal. Neurological localization Case 4 26 yo female graduate student was conducting a philosphy seminar when she suddenly started stuttering and became incoherent. Reflexes are brisk. he complains having trouble eating and swallowing on one side of his mouth. Her legs are diffusely weak. 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. pediatric and trauma surgical colleagues will result in the best outcome for our patient. The immediate resuscitation should follow well-established advanced trauma life support (ATLS) guidelines. . Has has no sensory loss. He becomes increasingly frustrated with this and suddenly stops talking. and good strength of the UE's. 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. is short of breath. Sometimes. you find that this has progressed over a month or two. hemisphere. His toes are equivocal. he has difficulty swallowing. Arteriogram after that. and is not associated with back pain. Neurological localization Case 1 a 35yo black male is seen in clinic with a 3 month history of weakness and muscle cramps. What is the most likely localization. 3 to 4 over 5. Upon further questioning. 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.

On cranial nerve examination the fundi were benign and there was a right sided facial palsy sparing the forehead. you would find a sensory level. Where is the lesion? Alteration of mental status = cortical. with 4/5 strength in the deltoid. UNILATERAL . slightly brisker on the right side. Cerebellar testing was impaired by weakness on the right side but otherwise normal. triceps. General examination was unremarkable. repetition and naming. peripheral arterial pulses both at rest and after exercise are normal. There was a family history of diabetes His medications included hydrochlorthiazide and glyburide. Refelxes in LE symmetrical but reduced compared to upper limbs. anxious. Territory: Ant Cerb. Sensory examination was normal. they are absent). He was oriented to person and place but was unsure of the month and day. typically developing after the patient walked 300 to 400 yards. In addition to the pain. hip flexors. On motor examination weakness was detected in the right upper and lower extremities. PE: loss of lumbar lordosis and reduced flexion and extension of lumbar spine. Neurlogical localization Case 6 A 40 year old male hypertensive. non insulin dependent diabetic awoke with weakness of the left side of the body and was admitted to the hospital. Sensory exam reveals questionable mild loss of light touch and pain sensation distally to LA's. Neurlogical localization Case 7 70 yo male presenting with dull aching pain in bothcalves after moderate exercise. thirst and weight loss for the prior one year. and ipsilateral hemiplegia (before pyramidal decussation). Plantar reflexes are flexor. but then it SHOULD HAVE EARLY SPHINCTER PROBLEMS AND URINARY INCONTINENCE AS WELL AS IMPOTENCE. The symptoms started a few months ago. power. Cauda Equina Syndrome has the Saddle Sensory Deficit but LATE SPHINCTER CHANGES. wrist and finger extensors. the patient has experienced numbness in his thighs. DTRs were brisk throughout. It has features of CONUS MEDULLARY SYNDROME: it is BILATERAL (Cauda Equina is unilat). Symptoms were releived after a few minutes rest or when the patient sat down and stopped forward. as well as problem with GiI and continence. Problem chronic = Brain Tumor. Reflexes are brisk in the legs. 2 hours after awakening.proximally and distally. Where is the lesion most likely? Ans: Lesion is at the pons at the level of VII. The right plantar reflex was extensor and the left was flexor. On examination. temperature 36. and poorly attentive. If it were medullary. tone. Ans: The reason i posted this Q is that it didn't make sense to me. He was able to follow three step appendicular commands. knee flexors and foot dorsiflexors. DTR's are reduced but PRESENT (In Cauda Equina. and had recently been diagnosed with diabetes. On neurological examination he was awake. and coordination in lower limbs are normal. and she has bilateral Babinski. Art. Speech was fluent with good comprehension. with no demarcated level. Ipsilateral facial paralysis (fibers don't cross midline). He has had no sphincter disturbance and had low back pain for many years.5 C. the blood pressure was 170/90. He gave a history of nocturia. pulse 110. 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.

He throws it in all directions and claims he can't stop. Despite that he doesn't seem to have a problem getting dates since he noticed an increase in his sexual activities.docility. BP210/180. There is no prior history of psychiatric illness. I didn't find many of them.Radial Nerve Palsy: Most common cause is Fx of the humerus (holstein lewis fracture).there is hyperphagia. no fever. and that's the correct answer. normal. In fact they all relate to the radial nerve: . Nerve injury secondary to compression or traction depends on intensity and duration . Other cause is compression (in its course inside the triceps muscle or teres latissmus muscle).most commonly affects Putamen because of rupture of penetrating arteries = This is putamenal infarct. right sided babinski. no meningeal signs present.hypersexuality and sometimes visual agnosia. The patient feels fine. On PE: patient is a known hypertensive and takes his meds irregularly. thanks Among the problems associated with the 3 major nerves in the upper extremity. right sided hemiplegia with fundoscopic examination revealing papilledema in addition to hypertensive retinopathy.SYMPTOMS. 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. 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. PE assesses the wild flailing movements of the left arm. radial nerve entrapment is the least common. Neurological localization Case 8 A 65 yo white male develops sudden severe headache and rightsided hemiplegia. He now has both fecal and urinary incontinence. Carpal tunnel syndrome (median nerve compression at the wrist) and cubital tunnel syndrome (ulnar nerve compression at the elbow) are much more frequent.. He is a chronic smoker. PE. but I wanted to make the distinction in the explanation for more info. but the parents report a recent change in behavior from markedly agressive to extremely placid. He has been diagnoses with diabetes and HTN but has taken his medications intermittently. but reassures you he's using condoms. Because of affected DTR's I would choose Cauda Equina Syndrome. Where is the lesion most likely? Ans: Hypertension. AND ABSENT DTR's. Please give me 3 or 4. In regards to Radial Nerve Syndromes.. Your diagnosis and localization of the lesion? Ans: kluver bucy syndrome involving anterior temporal lobe-amygdaloid nucleus. 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. Labs: elevated blood glucose of 190. Neurlogical localization Case 10 50yo male patient presents to the ER with uncontrollable wide movements with his left arm. eyes deviated toward the left.

then on cerebellar peduncles.com/orthoped/topic549. The first symptoms detected are usually auditory and involve a progressive loss of hearing. horizontal nystagmus. external compression. Other common causes include postsurgical injury.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. This kind of tumor generally arises from the Schwann cells on the vestibular division of the VIIIth nerve and enlarges (often very slowly.Wartenberg syndrome.horizontal nystagmus: left vestibular (VIII) nerve 3.20 years!) to put increasing pressure on the facial and trigeminal nerves. but normal right eye. perhaps over 10 . is essentially entrapment of the superficial sensory branch of the radial nerve. drooping of the left corner of the mouth. cerebellum and underlying brainstem nuclei. Reference: emedicine http://www." and she suffered from "ringing" in her left ear. She also said that she felt self-conscious that her face was "crooked.greatly reduced hearing acuity in the left ear: left cochlear (VIII) nerve 2. 6. secondary irritation of the Radial sensory nerve is frequent. weaving gait.drooping of the left corner of the mouth: left facial (VII) nerve. Other tumors of the cerebellopontine angle follow a different clinical sequence.Posterior Interosseous Nerve Syndrome: Compression is thought to occur after takeoff of the branches to the radial wrist extensors. sometimes preceded by a period of tinnitus. 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. In patients with de Quervain tendovaginitis. synovitis (rheumatoid). reduced sensation on the left side of the face. 4. An examination revealed the following: greatly reduced hearing acuity in the left ear.weakness in biting down on the left side: motor root of the left trigeminal (V) nerve. . 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. Other possible etiologies for posterior interosseous nerve dysfunction include trauma (Monteggia fractures). a dry. and iatrogenic injuries.emedicine.loss of the corneal reflex in the left eye: left sensory V and left motor VII. . weakness in biting down on the left side. The symptoms above resulted from the following: 1.Radial tunnel syndrome: result of overuse. 5. red left eye.reduced sensation on the left side of the face: sensory root of the left trigeminal (V) nerve. tumors. over the past five years her hearing had become "difficult. . a broad-based.. loss of the corneal reflex in the left eye. One of the most reliable symptoms is impairment of the corneal reflex. and trauma.." In addition.

a dry. they have a 32 fold increase of . irreversible changes might have already occured especially if intraabdominal. Case 2: No surgical indications in this patient.7. . .Trial of hCG is indicated for some cases of BILATERAL undescended testes. If it continues to third trimester like Case 1. 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). weaving gait: cerebellar peduncles and cerebellum and/or vestibular (VIII) nerve. Not indicated for unilateral.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. Pt has been on a low fat diet for about a week. but normal right eye: left facial (VII) nerve. since pain is low level and can still be taken care of by analgesics.If by 6 months they haven't descended. (Could be either side. After first year of life. but there is data suggesting they may still spontaneously descend until first year. OPEN CHOLE is to consider. 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. Success rate <10%. will they still operate??? Ans: Case 1: Lap Chole is performed ideally in second trimester. but since other symptoms are on the left. pt had an ulstrasound that confirmed she has at least one very large stone (too large to pass. according to the tech). . Third trimerster cholecysitis with intractable pain may require OPEN CHOLE since gravid uterus may interfere with procedure. C-Section may not be done since it is not an indication.Men who had their orchipexy done before 11 yo. Most commonly orchiopexy would be done at the end of first year of life. red left eye. Most would descend by then. 8. I have found articles saying after 6 months of age. however. Indications are intractable pain refractory to pain medication and diet. REFER to UROLOGIST.) 2 cases of gallbladders disease and pregnancy Case 1 35 weeks pregnant with third child.and therefore continue to present pain and possibly more problems -.Orchipexy after that is still indicated IF NOT TO RESTORE FERTLITY. will have virtually not a significantly elevated risk for testicular cancer. AT LEAST TO MAKE TESTICLES READILY AVAILABLE FOR EXAMINATION. For those who didn't. helped with indigestion and nausea.Any infant with undescended testes should be monitored for 6 months. and has had an abdominal ultrasound which shows no stones or sludge. 1) what are the indications for cholecystectomy in this patient if at all? 2) what if things get very bad in 3rd trimester. Compiled data about age of repair for cryptorchidism Medical Articles review showed the following: .By second year. . they hardly ever will on their own. The diet has. Knowing that this stone will likely not go away -.a broad-based.

If patient is not pregnant and refuses desensitization. Clinical evidence of neurologic involvement warrants CSF examination. Avoid trap of pneumonitis or cholangitis until seeing outcome of specific antitreponemal therapy. then developed symptomatic hepatitis and subclinical reticulonodular pulmonary infiltrates. 2 to 4 million units every 4 hours for 14 days).CNS disease can occur during any stage of syphilis.A negative RPR or VDRL test result may not rule out syphilis in patients with HIV infection. then desensitize. Obtain dark-field examination or direct fluorescent antibody (DFA) staining of exudate from suspicious lesions of primary syphilis. And if they do know.4 million units of benzathine penicillin G administered intramuscularly at a single session. resembling cholangitis. or selected secondary lesions.Patients who have had orchipexy before may not have a clue what was done to them as children. syphilis is a hot topic. Facts: .Case Scenario: HIV patient with secondary syphilis was treated. or they rarely ask.Serologic tests for syphilis are the cornerstone in diagnosing untreated syphilis infection--even in HIV-infected patients.In penicillin-sensitive patients. they rarely bother to tell.A patient with suspicious lesions but negative serologic results. eg. IT MERELY INDICATES A TESTICULE IS AT RISK. positive findings on dark-field examination or DFA stain can be diagnostic. . then desensitization to penicillin and management in consultation with an infectious disease expert. cranial nerve palsies). consider doxycycline (100 mg orally 2 times a day for 2 weeks). it included a flare of hepatitis symptoms. however. aqueous crystalline penicillin G is the treatment of choice (12 to 24 million units intravenously per day.Before treating. No data are available. carefully examine HIV-infected patients with syphilis for clinical evidence of neurologic involvement (eg. because their mothers rarely tell them. . . If no clinical evidence of neurologic involvement. .ANY BOY WITH BILATERAL NON-PALPABLE TESTES SHOULD BE CONSIDERED FOR A DIFFERENTIAL OF CONGENITAL ADRENAL HYPERPLASIA UNTIL PROVEN OTHERWISE. the same treatment regimen as for patients without HIV infection is recommended: 2. .Cryptorchidism DOES NOT CAUSE TESTICULAR CANCER. . .For HIV-infected patients diagnosed with neurosyphilis (including ocular or auditory syphilis).that risk compared to general population. ALWAYS INQUIRE SPECIFICALLY. Desensitize penicillin-sensitive patients to penicillin. => JarischHerxheimer reaction. . pallidum and atypical clinical presentations in the presence of HIV infection. confirm allergy. such as condylomata. . Odd HIV case With the rise of syphilis as an STD in HIV populations. If compliance and close follow-up cannot be ensured. . The diagnosis of syphilis may be more complicated in HIV-infected patients because of falsenegative and false-positive serologic results for T. .VDRL and RPR titers are higher than in HIV neg population. optic and auditory symptoms. on the efficacy of tetracyclines in treating syphilis in HIV-infected patients. . In this patient.

sympathetic fibers. V1 and V2. Methylprednisolone is thought to impact the biochemical cascade of injury that progresses after the initial injury for some hours. Difference with Central Cord Syndrome: . Prognosis: 97% completely recover if less than 50yo. The anterior cord syndrome anatomically involves the anterior portion of the cord. fever. Orbital cellulitis and Cavernous Sinus Thrombosis How to differentiate between Cavernous sinus thrombosis and orbital cellulitis? .Position and vibration modalities (posterior columns) are preserved. III. Reference: .If intravenous administration is impossible. hyperflexion. or vascular injuries may play a role. 18. Patients generally have sinusitis or a midface infection (most commonly a furuncle) for 5-10 days 2.Mechanism of injury is different . secondary. .4 million units intramuscularly daily plus probenecid 500 mg by mouth 4 times daily for 14 days).4 mg / kg / hr is the typical regimen employed. IV. Risk Factor: Cervical Spondylosis in older patients Mechanism: Hyperextension Trauma (minor bleeds in the tissue) Symptoms: Sensory deficit with level.Motor symptoms are different between upper and lower extremities in Central. Management: Admit to Neuro ICU. 12. More somber prognosis is after that. Pain of neuro etiology. Hands are especially involved. and 24 months after treatment for late latent syphilis or syphilis of unknown duration. various degrees of motor involvement with paresis more pronounced in UE than LE.Cavernous Sinus Cellulitis: Cavernous sinus contains internal carotid. .Because of the possibility of recent clinical relapse following syphilis therapy in HIVinfected patients. close follow-up: reexamine at 1 to 2 weeks and reteste with a quantitative nontreponemal test at 3...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. 9. Next: MRI: shows narrowing of the white column of CSF and impingement of the darker appearing spinal cord. DTR's below level are absent at first but return with level of spasticity once over Spinal shock. Clinically. paralysis below the injury with variable impairment of pain and temperature sensation is present. Spasticity. . PT/OT/Speech. May be tube feeding in acute phase because of adynamic ileus. Start Steroids: Solumedrol 30 mg/kg over 15 minutes then followed after 45 minutes by an infusion at 5. and VI. Action: Since diagnosis is pretty much narrowed down. Other: Neurogenic bladder (retention). 1. Bladder involvement common.http://hivinsite. and early latent syphilis and at 6. and 12 months after treatment for primary. Headache. Maintain a level of mild hypertension for spinal perfusion. Disc protrusion. Gabapentin for neuro pain.ucsf. and malaise typically precede the development of ocular findings. then aqueous procaine penicillin G is another option (2. 6..

Mainstay of therapy: Braod Spectrum Antibiotics (Staph Aureus Most common) Heparin therapy .Subperiosteal abscess = collections of purulent material between the orbital bony wall and periosteum. signs appear in the contralateral eye by spreading through the communicating veins to the contralateral cavernous sinus. 4. but the physical signs or papilledema on funduscopic examination. 1. CRANIAL NERVE PALSIES 7. . extension from adjacent structures. Classification: Group I . . Diagnosis is confirmed by CT scan. 8. The patient rapidly develops mental status changes from CNS involvement and/or sepsis. dacryocysitis. Group II . + Lids cannot be opened because of paralysis secondary to III involvement. palsy of the pupillary and extraocular muscles) + CN V1 (forehead) anesthesia Group V . Sinusitis (60% patients. dentition. Increased RETROBULBAR PRESSURE: Exophthalmus and Ophthalmoplegia 5. + Fever and leukocytosis + Orbital signs Group III .Orbital Cellulitis: Orbital infections develop via direct inoculation. + Severe unilateral ptosis + Severe ophthalmoplegia (ie. complication of periorbital infection 2. Without effective therapy. Death follows shortly thereafter.Orbital cellulitis = CT scan is not sensitive for diagnosing this entity.Preseptal: D/C only if adult with PO ATBx and close follow-up .Steroids (especially if progressed to pituitary insufficency to prevent adrenal crisis). are suggestive. Increased INTRAOCULAR PRESSURE: sluggish pupillary response and decreased visual acuity 6. and hematogenous spread. therefore.Orbital abscess = collections of pus within the orbital soft tissue. Group IV .Cavernous sinus thrombosis + Bilateral symptoms: + Ophthalmoplegia. ethmoid most commonly). This diagnosis is confirmed by CT scan. + Directional proptosis = Globe is looking away from the abcess. This is pathognomonic for CST.Preseptal (periorbital) cellulitis = inflammatory edema of the eyelids and periorbital skin with no involvement of the orbit. but it can be suspected based on physical examination + Orbital signs (see above) + Limitations of ocular motility = pain in globe movement toward the abcess.3. proptosis + Corneal hypesthesia with increased intraocular pressure Treatment: . Lids cannot be opened because of edema. clinical examination guides therapy.Admit all children because children are deficient in IgG2 and are predisposed to bacteremia. orbital pain and fullness accompanied by periorbital edema and visual disturbances.

Orbital: Admit with IV ATBx +/. a cephalosporin (eg. Patients who are allergic to penicillin can use vancomycin. cefoxitin. The decision is finally made .Surgical intervention if necessary (i. the decision is made based on what is thought WOULD BE that person’s choice. or ST segment changes. clindamycin. Question Px comes in from a MVA. the patient knows.CXR as procedure of choice to substantiate Sternal fracture. If you know.e. Palpation of the chest exquisitely tender over the sternum at a point where there is a gritty feeling of bone grating on bone. No admission necessary if no associated conditions. . cefotetan) can be used alone. and r/o pneumothorax/Aortic disruption. 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. conduction disturbances. you add in your favorite car). Your immediate DDx is a sternal fracture.ECG is next to r/o myocardial contusion: dysrhythmias. Trauma "ABCDE" has been done.. Alternatively. elicited by palpation. or chloramphenicol. There is no excuse for not doing so. To give: Adequate analgesia is treatment of choice as taping or splinting is contraindicated (risk of atelectasis and pulm insufficiency).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. NSAID's contraindicated. use meperidne or other Category B opiates. He is breathing well but obviously has mult bruises over the chest with the impression of a mercedes steering wheel (or yugo. cefuroxime.Lactose elimination diet 2. To pay attention to: If pregnant: shield abdomen and pelvis with lead apron before CXR.: compromised vision) Oxacillin or nafcillin can be used with the addition of ampicillin and sulbactam in children to cover H influenzae. NBS? Problems to be considered: Aortic Dissection Cardiac contusion or tamponade Flail chest Pulmonary contusion Thoracic spine injury To do: . what test is used for document osmotic diarreahea secondary to lactase deficinecy? 1.

without going to court. parents cannot withhold treatment from their children. “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. This was decided over the ROE vs WADE case in 1973. And that is only if the case is not an emergency: if it can wait going to court. but it illustrates the principle that governs medicine in the US: the patient always decides. Rule #2: Assume that the patient is competent unless clear behavioral evidence indicates otherwise. the case that made abortion legal. the USMLE will want YOU to make the decision: try to avoid the answer that says “go to court”.by who is most likely to represent the patient’s own wishes (not necessarily who is closest next of kin). they did. DO WHAT MOST PEOPLE WOULD WANT in this circumstance. the best interest standard rule was applied. and the only thing a doctor can do is lay out the possibilities. 2) “Best interest standard”: trying to determine what a never-competent patient would have wanted is practically impossible. Yet. It is not your personal preference is. 3) Patients decide over their own bodies: The patient ALWAYS MAKES THE DECISION. Rule #4: When surrogates make decisions for a patient. in Infant Doe’s case. when in doubt. 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. schizophrenia. Normally. You must set aside your personal preferences: like strong religious beliefs (that is considered irrelevant) As a general rule. When you are not clear about the patient’s wishes. rational observer: do what a rational person would do. 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. SPECIFIC RULES: Rule #1: Competent patients have the right to refuse medical treatment. In this case. no matter what. Alzheimer’s: these are all medical dg. assume competency! Rule #3: Decision-making should occur in clinical setting if possible. you should make the decision as a dispassionate. The issue will never be over abortion in the USMLE. 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. -Drunk. 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. physician may rely on advance directives Directives that a patient can leave for his doctor before becoming incompetent: . unless it is clearly stated that the guardian (ex: parent of a sick child) is NOT acting in the patient’s best interest.

by the patient. In case of clear cortical death: even if the family is hoping for a special doctor to arrive. 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). If NOT a minor: go to court. Rule #10: Always obtain informed consent: before you do ANYTHING!!! Informed consent can be oral. Never. it is the patient’s or the patient’s family. 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. drug undergoing trial to know side effects) DO NOT ASSUME YOU HAVE A WAIVER UNLESS THE USMLE TELLS YOU. for a special treatment to come: CALL THE DEATH. Refusing food and water: may seem close to euthanasia. Rule #9: Never abandon a patient: even if they can’t pay you.Can be oral directive from patient to his doctor: does NOT necessarily have to be a written document. but on the exam this is accepted.Health powered attorney: person that was named by the patient to represent him. Rule #7: Do nothing to actively assist the patient to die sooner. A competent patient has the right to refuse hydration and nutrition. even if you don’t like the patient.Can be living will: expression in writing. THEY ARE ILLEGAL. .. 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. In the case of anorexia nervosa: if the patient is a minor: not legally competent. TREAT THIS PERSON AS THE PATIENT HIMSELF. 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. if the patient or the family want the treatment to continue: it is not YOUR decision. The patient can revoke written consent orally. Still. . Rule #6: Feeding tube is a medical treatment and can be withdrawn at the patient's request. notarized. 3) Patient is incompetent 4) Therapeutic privilege: doctors have the right and obligation to deprive the patient of . Period. Do not ACTIVELY do anything (as opposed to number 6) Rule #8: the physician decides when the patient is dead. Futile treatment: means a treatment that is not AND WILL NOT improve anything. ever threat to abandon your patient (not even if you are doing it to make sure they follow treatment).

In other words. sued or that your hospital may go to shreds if you do the "right thing". 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: .if there are no more treatment options (if the patient is cortically dead).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.if the physician thinks tratment is futile and the patient won't improve. and the family insists in treatment?: if there are no options and there is nothing the physician can do. and physicians should follow them Rule #17: Committed mentally ill patients retain their rights Rule #18: Detain patients to protect them or others. ACT NOT AS A LAWYER WOULD. Failure to do so will endanger patients. The underlying rule here is that no matter what the psychiatric diagnosis is. USMLE wants you to pick the answer where there are no doubts that it is the most ethical thing to do. and will ALWAYS be the .if there is a direct employer or supervisor (like your residency program director) : TELL THE SUPERVISOR.they can refuse treatment .talk to the collegue and REMOVE him from patient care . Ex: patient on PCP. don't worry about being fired. treat the patient as you would any other competent person (unless they show signs of clear incompetence. but the patient (or surrogate) insists on continued treatment: then treatment must continue. BUT AS MOTHER THERESA WOULD.or limb-saving treatment from their children Rule #13: For the purposes of the USMLE.they must have treatment available . it is his duty to stop the treatment. rule # 17: Commited mentally ill adults legally are entitled to the following: . not simply the letter of the law I looked it up: rule # 8 says this: . (The USMLE wants you to be able to make decisions when the patient is DEAD) . stated on #2) rule #20: Focus on what is most ethical. 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. violent and dangerous: put him on restraints! Rule #11: Special rules apply with children Rule #12: Parents cannot withhold life. Rule #19: Remove from patient contact health care professionals who pose risk to patients Rule #20: Focus on what is the best ethical conduct.their autonomy in the interest of the patient and other people.

4. because the exacerbation is acute so it'll be probably 30. HCO3 = 28 On exacerbation: pCO2 will go up pCO2 = 53 pO2 will go down pO2 = 55 O2 Sat= 84% HCO3. electrolytes come in handy.34 -.70 -. you look at other parameters depending on the clinical scenario.29 --30 -.7.56 -.34 -.10 -. U/A = 3+ proteinuria and serum creatinine 2.144 -. And so on and so forth. when talking about other Acid-Base disorders.108 --4.24 -.110 -.t waste time talking to the person or the family or anyone: go to the supervisor.140 -. Let me know if you need more explanation ABG exercises #1 ---pH -. we don't always look for ph.115 -.K+ A)-7. Home O2 indications guidlines for Medicare are based on O2Sat or pO2 and those of Medicaid REQUIRE ABG's where pO2 would be documented. pCO2 = 43.138 -.110 -. anion gap is important.22 -.14 -. 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. If diarreha or vomiting.148 -.52 -.5.95 -.25 -.Na --HCO3.pCO2-.--Cl.24 -.104-.38. All of you mentioned increasing pCO2.22 -.44 -. I posted some ABG's for your exercise.12 -.106 -.Will go up to compensate but not too much.50 -.12 -. 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. bicarb and pCO2 only. are given ? Ans: When interpreting ABG's.98 -. but how about decreasing pO2? Think about it.3.98 -.1 mg/dl .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.7.pO2 -. and they won't authorize Home O2 for a patient with ONLY O2 Sat.15 -. So don.56 --20 --114 --138 -.9 D). It's true.-.0 F) -7. His family reports that he has been this way for 2 days. After all.26 -. pO2 = 68mmhg.140 -. Ex: pH = 7.8 C)-7.6 B)-7. Exacerbation of COPD on ABG’s How can U interprete Acute exabe of COPD with Blood gas analysis esp. anxiety.4. 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.worong answer on the USMLE.4 G) -7.3.2 E).112 -.136 -. when cases like Previous COPD patient with COPD who comes with acute exabe. If intoxication. Similarly.15 --111 --5.

#2: ---pH -.43 -.34 -.3.140 -.70 -.7.70 -.pO2 -. 2) 21 yo college senior is seen the morning of her finals complaining of palpitations.52 -.12 -.138 -.5 D).112 -.0 F) -7.96 -.4 G) -7.115 -.106 -.140 -.98 -.136 -. 5.16 -.2 E).8 = Increased Anion Gap Anion Gap etiologies: MUDPILES: Methanol. Lactic Acidosis.24 -.108 -.pCO2-.24 -.K+ A)-7.0 E).50 -.10 --110 --5. it's not respiratory.K+ A)-7.25 -. Therefore.A 19yo asthmatic presents to the ER with wheezing and tachypnea with RR 26 6.7.5.57 -.44 -. Salicylates.110 -.32 -.6 C)-7.5 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)-7.6 B)-7.114 -. 3) an 18 yo man is left in the ER entrance and is found comatose .30 --32 --96 --138 -.a 25yo develops severe watery diarrhea for 2 days while on vacation in MExico.12 -. anxiety.98 -.7.29 --30 -.a 30yo develops severe vomiting 6 hours after a family picnic answers: ---pH -.Na --HCO3.108 -.--Cl.34 -.112 -.4.95 -.26 --28 -.148 -.25 -.A 68yo with 40 year history of smoking and chronic cough.22 -. His serum alcohol level is zero.4. 4.136 -.0 1.15 -.-.10 -.--Cl.104-.14 -.25 -.98 -.A homeless man appears intoxicated and complains of blurry vision.24 -. and tingling in her hands D).= decreased (makes sense) => Metabolic Acidosis (Na+K+)-(Cl+HCO3)= Anion Gap: 22.7.12 -.9 D). DKA.138 -.3.24 -.15 --111 --5.16 -.3.8 C)-7. 2. 3. Ethanol. INH/Iron.56 --20 --114 --138 -.138 -.144 -.3.108 --4.2 Panicking.22 -.50 -.44 -.140 -.3.114 -.78 -.8 Salicylate Intoxication pH= Acid pCO2=decreased (If it were respiratory.28 -.Na --HCO3.52 -. it would have been increased.7.106 -.3. 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.30 -.110 -.108 --3.56 --20 --114 --138 -.40 -.49 -. It is compensation) HCO3.8 B)-7. Uremia.56 -.4.A 23yo man with asthma with severe tachypnea and use of accessory muscles of respiration does not improve after 60min in ER.pCO2-.0 F) -7.140 -.138 -.26 -.-.pO2 -. Paraldehyde.94-.22 -.4.

Difference between DKA and Salicylate acidosis: .25 -.5 . Lactic Acidosis.115 -. 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.K+ A)-7.70 -. ph will be NORMAL with Low pCO2 and High HCO3-). Salicylates. it's not respiratory. Comatose. Hypercholremia. Uremia.34 -.106 -.8 B)-7. think narcotics.140 -. His family reports that he has been this way for 2 days.136 -.24 -.32 -.108 -. and hypercarbia = Profound respiratory acidosis with hyperkalemia in response to the deep acidosis.3.50 -.49 -. The latter enhances reabsorption and increases hydrogen and to some extent K secretion.0 Patient has Septic Shock.44 -. Uremic Metabolic Acidosis. pCO2 is high to compensate.70 -.44 -. DOC for African Americans is Thiazide diuretic.= decreased (makes sense) => Metabolic Acidosis (Na+K+)-(Cl+HCO3)= Anion Gap: 22.12 -. 6) 58yo African American man is treated with diuretics for HTN G) -7.4. A)-7. 5) a 29yo man with AIDS is brought to the ER lethargic and extremely tachypneic. Paraldehyde.15 --111 --5.8 pH= Acid pCO2=decreased (If it were respiratory. They enhance NaCl excretion in the distant tubule.52 -.10 -.In Salicylates: Respiratory Alkalosis FOLLOWED by Metabloic Acidosis (mixed later on. 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. it would have been increased.5.--Cl.3. It is compensation) HCO3.5 HTN in african american.78 -. Metabolic acidosis with hypotension. Low Bicarb.56 -.-.Na --HCO3. In response to shock.Probably intoxication since he was "left in the ER entrance".138 -. BP 60/40 and RR 40 E).138 -. there is inadequate perfusion with resultant secretion of stress hormones.104-.98 -.12 -.4. Increase in glucocorticoids along with catecholamines causes Hypokalemia among other changes. --------------------------------------------------------pH -.30 -.140 -. INH/Iron.pO2 -. There is a major decrease in the number of tubule cells which can produce ammonia and this contributes to uremic acidosis.148 -.108 -.24 -.4.1 mg/dl F) -7. Ethanol.8 = Increased Anion Gap Anion Gap etiologies: MUDPILES: Methanol.pCO2-.Bedside Blood sugar/Glucosuria . which stimulates aldosterone secretion. Borderline Anion Gap.50 -.6 Low respiratory drive : Hypoxia.29 --30 -. 7) a 34 yo IDDM patient is seen on his annual exam.140 -.110 -.28 -.110 -.140 -.4 Hyperkalemia.40 -. Cl is high. Therefore.98 -. DKA.108 --3.22 -. U/A = 3+ proteinuria and serum creatinine 2.6 C)-7.7. Thiazide induced metabolic acidosis.24 -.14 -.57 -.22 -.

108 --3.7.70 -. Volume depletion maintains alkalosis.3.57 -.138 -.49 -. Bicarb again normal because no time to compensate.140 -. The secretion of HCl by the stomach usually stimulates bicarbonate secretion by the pancreas once HCl reaches the duodenum.4. Explained before.114 -.94-.a 25yo develops severe watery diarrhea for 2 days while on vacation in MExico. pCO2 is low to compensate. In this case. and no net gain or loss of hydrogen ions or bicarbonate occurs.3.0 Gastric secretions are rich in HCl.30 -.5 Status Athmaticus.114 -. In response to diarrhea.96 -.138 -.3. Below 55. D). When HCl is lost by vomiting or NG suction.16 -. generating a metabolic alkalosis. Chloride is high.50 -.6 pO2 is low. Antidote: ethanol.94-.26 --28 -. Hyperventilation = Respiratory Alkalosis.A 68yo with 40 year history of smoking and chronic cough. order Home O2. A)-7. Ordinarily. pO2 is normal. 4. pH alkaline but normalizing. pCO2 normal.24 -. as you would find for a COPD. but not critically low.16 -.52 -.D).16 -.3.A 23yo man with asthma with severe tachypnea and use of accessory muscles of respiration does not improve after 60min in ER. pCO2 decreasing because of the hypoxia.26 --28 -.0 Methanol Intoxication Anion Gap Metabolic Acidosis.114 -. His serum alcohol level is zero. 3.108 -.10 --110 --5. F) -7. 2.78 -.32 -.114 -. for COPD patients.44 -.52 -. We just talked about this a few posts down.108 -. Potassium low to try to get as many hydrogen ions as possible in the extracellular compartment and compensate for the alkalosis.7. C)-7.0 E).7.0 F) -7.wt is stable. it's Athma exacerbation Early response.40 -.43 -.3.16 -. these substances are neutralized.a 30yo develops severe vomiting 6 hours after a family picnic E).0 It's a metabolic acidosis but with NORMAL anion gap. pancreatic secretions are not stimulated and a net gain of bicarbonate into the systemic circulation occurs.43 -. solids for one year)problems have not worsened at all. GI question a 32 yr old woman with no past medical history comes with difficulty swallowing foods(esp. 6.exam is .7.8 This guy is retaining his CO2 = pCO2 high Result= pH low BUT pO2 is very low as well.30 --32 --96 --138 -. the hypokalemia is secondary to the alkalosis itself and to renal loss of potassium ions from the stimulation of aldosterone secretion. B)-7.A homeless man appears intoxicated and complains of blurry vision.10 --110 --5.A 19yo asthmatic presents to the ER with wheezing and tachypnea with RR 26 This time. 5.138 -.138 -.96 -.140 -. HCO3-: normal since no time for compensation. pO2 usually is around 50-60.0 1.28 -.138 -.30 --32 --96 --138 -. there is loss of Bicarb.25 -.

her examination is normal.Esophagus: Esophageal varices. Gastritis..e. what qs do you ask pt. Next step to upper GI bleed = Endoscopy.ABC's : 2 large bore IV's + Fluid resuscitation (RL or NS) .Esophageal web: plummer-vinson syndrome. liver disease). pt does not have these alarming clinical markers.unremarkable. . Follow Barium with CBC. a pt comes with new onset epigastric pain and dyspepsia. if there is no steatorrhea then you should exclude lactase def.what is the first step in management of this pt.Keep NPO + PPI .. CBC= Because it's acute : Normocytic Normochromic Anemia Differential: .Coagulopathy (drugs. Gastric Cancer . esophageal cancer.. more than 14gr per dl. if there is increased fat in the stool i. what clinical markers would make you consider a gastroenterologist referral. given that this pt has no prior history of gi bleeding before.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 . . that would help you consider your next step. esophagitis. and endoscopy (r/o esophagel cancer associated with Plummer-vinson). she reports no constitutional symptoms. . then it is steatorrhea. it's a differential. and MAllory weiss tear . and pernicious anemia. 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. . what is the best next step in this case.Stomach: Gastric Ulcer. Most likely diagnosis: Shatzki ring a 27 yr old woman presents with complaint of diarrhea for 14 months. the former is confirmed by trypsin level and secretin test and the latter by a biopsy.but first things first: . Nonetheless.Mucosal or Shatzki ring: Follow UGI series with endoscopy both diagnostic and curative with attempt to dilate the ring.. EKG to look for infarct/ischemia .Esophagel Stricture following lye ingestion: but there is no history of major depression with suicidal thoughts and ingestion of caustic agents such as lye.Type and cross match pRBC's x 2U in case needed later. what type of anemia would you likely find while he is being evaluated in ER. a 46 yr old man is brought to emergency department after vomiting Bright red blood twice ..Endoscopy (Barium studie are CI in the setting of an acute UGI bleed as it wil interfere with subsequent endoscopy or surgery if needed). Aortoenteric fistula (if previous aortic graft) .Duodenum: Duodenal ulcer.but physical exam is normal and PV comes with long standing iron-deficiency anemia and glossitis. renal disease. after stabilizing pt what do you do next. you consider diagnosis of malabsorption syndrome . her lab results show iron deficiency and low phosphorus.CBC.common causes celiac disease and pancreatic insuffiency.

Mononuclear cells Event 6: Release of cytokines. sensation of fullness post prandial. vasoactive factors. supraclavicular lymphadenopathy. labs are normal except for a mild hypercalcemia. oral thrush. check gastrin levels 2. Ans: Clues: PUD for last many yrs that has been resistant to medical treatment. using accessory muscles.Mucous Plug Formation . CT First line of treatment: PPI.. IV secretion test 3.Answer to the Q . what is the first test to do. TNF. Heparin Event 4: Smooth muscle bronchoconstriction Event 4: Recruitment of other inflammatory cells: Neutrophils. what is your next step in evaluation.Is patient on any medications (NSAID's. but no improvement. diarrha occurs throughout the day with no blood or pus. she has PUD for last many yrs that has been resistant to medical treatment.Edema B. Follow-up tests to screen for MEN I Status Asthmaticus Pt with classic scenario of Status Asthmaticus comes to ER tired. Antibiotics.Bronchoconstriction .Mechanism: Although BRONCHOCONSTRICTION and BRONCHIAL HYPERACTIVTY are components of asthma. On PE: chest silent. she has stopped taking milk. Eosinophils. hypercalcemia Zollinger-Ellison syndrome Labs: 1.Sexually active/unprotected sex First test to do: . diarrhea. Dysphagia.Muscle Fatigue Also others mentioned high yield: Mechanism of Asthma? Others: Management of Status Asthmaticus? A.Endoscopy 42 yr old woman has diarrhea for 6 months. Ans: Clinical Markers: Weight loss.) .pt is not taking any medication. Proteolytic Enzymes. Arachidonic acid metabolites Event 7: Activation of epithelial and endothelial cells enhancing inflammatory response Event 8: Release of IL3 thru Il10 and IL13. as of 1997 asthma is DEFINED AS CHRONIC INFLAMMATION. 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. Question to ask for next step: . Whatis responsible for his respiratory "problem"? . ABG's pH normal and PCO2 borderline. Chemotactic factors. IFNGamma.. Surgery follows if single gastrinoma that hadn't spread to adjacent structures. Result: + Increased bronchial hyper-responsiveness to stimuli + Reversible airflow obstruction by: Bronchoconstriction .

not a drive mech ( meaning brain stem stimulation problem as it might be in COPD if you give them too much oxygen). is having his bronchocontsriction resolving.that is the whole pt. and could be / is crashing. it simply comes down to the pt.. is fatigued to have to keep trying to breathe as he is very bronchoconstricted .. pt. this mech. is in the first aid and also i looked it up in Cecil's and it is there as well..how much more bronchocostricted can a pt.. gets fatigued. as well as you will have "quiet chest" bcz pt.. " 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). most likley indicates fatigue of ventilatory muscles and impending resp.. they are STILL bronchoconstricted but muscle fatigued to keep breathing.. and may require mechanical ventilation.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.... the pt. .to conpensate for that pt. the PCO2 RETURNS to NORMAL and ultimately begins to rise. + Second stage: hyperventilation accompanied by hypoxemia. as they were low before ( when pt. so pt.. decreases breathing efforts and decreases ventilation... is bronchoconstricted.. so he/she is retaining it.A rising PaCo2 in a pt.. here is quote from Cecil's essentials of medicine..... and..when a pt.e. decrases ventilation. is bronchoconstricted.. is getting worse by the min.... is hyperventilating... a normalizing CO2 in acute exacerbation.. get.. he/she does not have enough air coming into thier lungs. probably. is breathing at this rate. is hyperventilating.. is getting worse... failure. and now is normalizing as CO2 is increasing. pt. over a period of time. was hyperventilating).. as pt. + Third stage: Moderate = Unobstructed airways (called Fast Compartment) normally compensate..as to bronchoconstriction ..thus you will have normalization of the Ph as well. This is one of the indications of admission to the intensive care unit (ICU). .. is not blowing off as much CO2..therefore their ventilation is decreasing.so you will not hear wheezes as much. therefore CO2 levels begin to NORMALISE ... these pt's require continued direct observation and monitoring. as time goes on and the pt... As the obstructed compartement (called the slow compartment) increases..not able to sustain this kind of ventilation." 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...the answer is --> muscle fatigue.. breaths faster. as that means the pt.do not get full into thinking pt. was in resp. w/ asthma is an ominous sign and may portend a medical emergency.that is a RED FLAG. bcz pt.... as status asthmaticus ensues . is strictly moreof a mechanical mech. pt.i. intubation with mechanical ventilation.. alkalosis b4 . the ref.the pt....'s breathing effort is decreased.so muscle fatigue. my little sidenote:.as pt. With INCREASING SEVERITY or RESPIRATORY MUSCLE FATIGUE ... pCO2 increases resulting in false-normal value for PCO2 and pH..he is already probably quiet constricted.

exam otherwise is normal. .BUN and Creatinine +> High TSH and Low T4: Thyroid hormone replacement therapy +> Normal TSH. . pCO2 rising as well as Low PO2 (due to increased airway obstruction and atelectasis) will result in hypoxemic respiratory acidosis. NOT INDICATIED IN GER-INDUCED ASTHMA AS IT MAY EXACERBATE.If PNT: CXR and Thoracocentesis (Other cause of silent chest) . High PRL: MRI of BRain +> Normal TSH and Normal PRL: Regular menses? .THEOPHYLLINE +/.hCG Level .If Galactorrhea (Fat globules in discharge) => Labs #2: Labs: .History of prior irradiation to the head. infertility.Management: Patient sitting up . This is an even more dangerous sign that mandates intubation and ventilatory support.PRL level . assess careful history taking and physical examination: . how should you approach this case Do pregnancy test first.If GER-INDUCED. fibrocystic breast disease. Continued increase in pCO2 or hypoxemia despite treatment . ABG's.+ Fourth Stage: Severe : Slow compartment expands further and therefore removal of pCO2 decreases. Decreased consciousness. Warm humidified 100% via a non rebreather mask.CMDT Approach to milk-like discharge 32 yr old woman has noticed milklike discharge from her breasts the past one month.History of headache and visual disturbances . h/o of excessive nipple stimulation .Gynecological history: menses.If non galactorrhea: consider intraductal breast cancer. opioids. Complete approach is: First of all. etc.History of medication intake which would provoke hyperprolactinemia .increased diaphragm function and CNS breathing stimulation. h/o of head injury . ANTI-REFLUX MEDS/H2 RECEPTOR BLOCKERS .Swanson . C. One for CORTICOSTEROIDS .FEV1 baseline and monitoring .INTUBATE IF: Apnea.TSH level . amphetamines. #1: Assess if it is GALACTORRHEA (microscopic examination). Sources: . .Emedicine . h/o encephalitis.Start 2 IV lines. MONITOR LEVELS.History of illicit drugs: canabis.Pulse Ox Monitoring. .Hypoxemia is most common cause of death. Potassium monitoring (as hypokalemia is a frequent side effect of the anti-asthma medication) .Caution: if ASTHMA AND NASAL POPYPS: DO NOT GIVE ASPIRIN. Therefore OXYGEN IS PRIMARY TREATMENT OF PATIENT.COMBINATION OF IPRATROPIUM AND ALBUTEROL nebulizer .

. etc. h/o of Atopy.. Rarely with weeping and crusting (Contact with soaps.. h/o of dry skin. Dyes..If Irregular menses: MRI of Brain IF PROLACTINOMA: BROMOCRIPTINE.Management includes the following: .e... around area of contact (e.. 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..aafp.. Gram stain will r/o it out.IM or SQ Acqueous Epinephrine (Repeat Q15-30min PRN) .ATOPIC DERMATITIS (ATOPIC IS DIFFERENT FROM ALLERGIC): 1) Hallmarks: PRURITUS. ... A.Subacute (Scaling excoriated plaques) .. OR RADIATION THERAPY. Not THAT itchy. ASYMETRIC.... I looked them up for my own review so here goes. SURGERY.Main Differential for both: 1)Impetigo or Secondary infection (i..html Anaphylaxis Usually a typical case of anaphylaxis... MONITOR FOR 24h because of Late-phase Anaphylaxis (Recrudescence 6-12h later after initial improvement)....Inhaled Terbutaline or Albuterol if severe bronchospasm ... ON BENDS OF ELBOWS AND KNEES.... 2)Variants: . acids. etc... B. Vesicles on erythematous base) . 2)Other: ..Vasopressors if remains hypotensive .Antihistamine as an adjuvant. Chronic (lichenification/Pigmentary changes with excoriated papules) 2)In infants: cheeks. Volume expanders) .. flexor areas of extremities..If regular menses: Reassurance/Observe.: Poison Ivy.IRRITANT CONTACT DERMATITIS: Mostly Red and scaly.. Nickel.. Prevention is mainstay of treatment. CABERGOLINE (DOC OF CHOICE IF NOT WISHING TO CONCEIVE)....org/afp/20010501/1763. forehead. dyes.PHOTODERMATITIS: Sunexposed areas C.. Poison Oak.IVF Rapid infusion (LR. followed by vesicle/blotchy eruption weeping and crusting..). Reference: http://www..ALLERGIC CONTACT DERMATITIS: 1)Hallmarks: 1-3 days after exposure (TYPE IV HYPERSENSITIVITY).) .. sometimes diaper.Acute (Itchy Erosions + serous exudate.. Saline.:impetiginization). solvents...CONTACT URTICARIA: TYPE I HYPERSENSITIVITY!!!!=Wheal and Flare at contact area .g. Red... D/c offending drug if applicable . ERUPTION IS SYMETRIC.

On physical examination. don't worry your pretty little head about it. Question A 34-year-old male is brought to the Emergency Department by paramedics after having collapsed in a marathon. vitamin E cream. where ischemia took place. 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. Drain. interscapular. at approximately the eighteenth mile he fell to the ground in an unconscious state. just a little diaper rash. 1 day after a major gut surgery for bypass. don't worry dear. and DON'T CLOSE. umbilicus. talcum powder.infectious eczematoid dermatitis E.atopic dermatitis B. and body folds. Close using a "plastic-like" medium called silex I believ or something. His mother has tried cornstarch." On examination. Some speculate xanthine oxidase.hepatic and renal abnormalities are common in this condition . She tells you that she went to three doctors because the first two said.Impetigo = honey crusted lesions 2)Seborrheic Dermatitis: Dry scales and underlying erythema. "Oh. Distribution: Scalp.allergic contact dermatitis C. References: CMDT. In fact. One of the interesting questions to study about compartment syndrome is the abdominal one. and three different prescribed corticosteroid creams from three different physicians as remedies. his blood pressure is 90/60 mm Hg. There are numerous "satellite lesions" present on the lower abdomen and thighs. the more fluid you give.seborrheic dermatitis D. Some say leukocytes through the NADPH oxidase. oliguria starts which is refractive to fluid resuscitation. Emedicine Question An 8-month-old infant is brought to your office by his mother for assessment of a diaper rash. it will go away. and allopurinol has been shown to reduce reperfusion effects experimentally. presternal. What is the most likely diagnosis in this infant? A. Which of the following statements about this patient is (are) true? A. or trauma. Anyways.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. PAtient will improve dramatically. Central face. Apparently. the more dangerous it is. and you'll find leakage of fluid (significant amounts) in the peritoneum. Kaplan Center notes.candidal diaper dermatitis Ans: E . You can take back to OR 2 days later and close abdomen correctly. the infant has an intensely erythematous diaper dermatitis that has a scalloped border and a sharply demarcated edge. Take back to the OR. The patient's temperature is 41° C. His pulse is 128 bpm. zinc oxide. PAtient would be discharged a couple of weeks later if everything goes well.this patient has heatstroke B.

CT abdomen D.Arterial LAceration . METABOLIC: Exam related are in my opinion .none of the above statements is true Ans: D. or use of steroids. He is hemodynamically stable.Other: Copper. Reduce infusion rate. and hollow viscera that will spill fluids in to the peritoneum. Check for possible diarreha or bowel fitula.C.Pneumothorax/Hemothorax .Air Emboli ++++++ . CHANGE OF TASTE. They can be divided into: CATHETER RELATED.Catheter Thrombosis +++/ Catheter-related Sepsis +++ Patient with TPN using indwelling catheter. Decreased DTR and respiration.Brachial Plexus Injury . and the bullet is seen on X-Ray films to be embedded in the .Zinc Deficiency: +++++ PATIENT DEVELOPS RASH.Azotemia (Creatinine normal): Reduce protein .38 caliber revolver. The abdomen is full of important strudtures that should not be penetrated.Hyperglycemia: Caused by too rapid an infusion of dextrose. Which of the ffg is most appropraite next step in management? A. The rule of abdominal gunshot wounds is simple: They belong to the OR before any sign of peritonitis starts. lateral aspect of his thigh.22 caliber reveolver. AND HAIR LOSS. The entry wound is in the epigastrium. to the left of the midline.Diagnostic Peritoneal Lavage E.Exploratory Laparotomy Ans: E. and culture tip of old one.html Cases of Gunshot wounds and Facts of management A. solid organs that can bleed. The entrance wound is in the anterior.all of the above statements are true Quick Note on TPN .all of the above statements are true E. . AND METABOLIC. B.High Yield Complications of TPN: Central Vein nutritional support occur in up to 50% of patients. and the abdomen is moderately tender. The bullet is lodged in the psaos muscle on the right. add insulin if needed. Give fat orally if possible . .Close Observation B. who develops fever without apparent source => Change line immediately.Emergency US C.gray-ink.Acalculous Cholecystitis: mostly from biliary stasis.com/quillen/gi. . . Selenium (cardiomyopathy) Source: CMDT http://www.Hyperchloremic nonketotic dehydration: reduce chloride.Magnesium: muscle weakness and tremor. Increase Zinc intake.treatment should be directed at lowering the core temperature as quickly as possible D.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 . CATHETER RELATED: .

A 25 yo man is shot with a .Surgical Explration of the femoral vessels E.Tetanus prophylaxis B. although obligatory in movies. but below the skull.Formal surgical exploration of the area in the OR Ans: D.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 appropraite next step in diagnosis? A.Admit to observe for development of complications D. Tetanus prophylaxis is first. Only an arteriogram can provide the necessary reassurance.Discharge home B. arteriogram. and eventually becomes central when it becomes the popliteal. But one should know the femoral artery is located anteromedial in the upper thigh. Anatomic proximity to major vessels is the main criterion to suspect vascular injury in gunshot wounds of the extremities.Arteriogram E. In wounds of the extremities. 5 cm below the groin crease. He is hemodynamically stable. Arteriogram. the presence of normal pulses and the absence of a hematoma does NOT rule out vascular injury. They can be evaluated by Doppler. Although absent pulses and an expanding hematoma make such injury virtually certain (and dictate the need for surgical exploration). In addition to local wound care and the appropriate tetanus prophylaxis.Surgical Removal of the embedded bullet.Continued Clinical observation B.muscles posterolateral to the femur. Which of the following is the most appropriate next step in management? A. which of the following is the most appropriate next step in management? A.Digital exploration of the wounds in the ED C. and blood is oozing from both wounds. There is no hematoma under the entrance wound. half way between the great trochanter and the knee. Ans: A. He has palpable pulses in the dorsum of his foot and in the posterior tibial artery behind the malleolus.Arteriogram D. or surgical exploration.Barium Swallow C. and it does not seem to responds to local pressure. The ER departement MD cleans the wound thoroughly. Neurologic examination of the leg is normal.Doppler Studies C.22 caliber revolver. He is again hemodynamically stable. is not necessary if it's not threatening to erode some vital structure. X-ray films show the femur to be intact. It is NOT located in the lateral aspect where the bullet is located here. He is fully conscious. and neurlogically stable. but not at an alarming rate.Arteriogram D. The exit wound is in the posterolateral aspect of the thigh. Removing the bullet. The entrance wound is in the anteromedial aspect of the upper thigh. but canno be felt by another. The popliteal pulse is reported normal by one examiner. the main concern is the possibility of major vascular injuries.Endoscopy . 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.22 caliber revolver. C. A steady trickle of blood flows from both wounds.

Deep tendon reflexes were absent bilaterally.Extrinsic cardiogenic shock due to pericardial tamponade B.22 caliber revolver. and his pulse is 145/min. two inches below the nipple. In gunshot wounds og the upper part of the neck. which was ligated. patient is in shock and the distended veins identify the type as cardiogenic. pericardial tamponade is the obvious mechanism. Rectal sphincter tone was decreased. There is no exit wound.Vasomotor Shock Ans: A. just to the left of the sternal border. A large left anterior neck hematoma was present. His blood pressure is 65/40 mmHg. resulting in hypotension and neck hematoma as well as cervical spine injury with an incomplete motor deficit at the C5 level. What is the next step in management? Ans: Surgery. at the level of the 4th intercostal space. A bullet fragment was palpable in the left anterior aspect of the neck. with flaccid paralysis of all four extremities except for bilateral forearm flexion. He was taken immediately to the operating room. D. His chief complaints were neck pain and the inability to move any extremity.Hemorrhagic shock D. and is asking for a blanket and a drink of water. The bullet entrance wound was in the left posterior cervical region. Obviously. 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. with preserved bulbocavernosus reflex. The exit wound was midline in the anterior aspect of the neck. Both carotid pulses were palpable. Findings on the initial workup were consistent with a zone II neck injury (see below). lateral to the cricoid cartilage. above and medial to the left scapula. A 19yo gang member is shot once with a . which was possible against gravity. and barely perceptible. This is an absolute indication for neck exploration. distended veins in his neck and forehead. Sensory examination was intact for pin prick and light touch throughout. He is diaphoretic.Surgical exploration Ans: C.Intrinsic cardiogenic shock due to Myocardial injury E. Neurologic examination showed intact cranial nerve (II through XII) functions. The bullet is lodged in the left . Given the location of the injury. He is neurlogically intact. Systolic blood pressure before his arrival was reported to be 90 mm Hg (palpatory). and it is also rather difficult to explore surgically.GUNSHOT WOUNDS TO THE CHEST: A 27 yo man is shot point blank with a .38 caliber revolver. the main concern is the possibility of significant vascular injuries. Which of the folloing is the most likely diagnosis? A. The hyoid bone was fractured and repaired. and also provides a way for embolization of major arteries that might be bleeding significatnly. Surgical exploration of the left anterior cervical region revealed an extensive hematoma and a lacerated left external jugular vein. He has large. He is breathing adequately and has bilateral breath sounds. and anxious.Extrinsic Cardiogenic shock due to tension pneumothorax C.E. cold. The area is too high to involve the aerodigestive tract. The entry wound in the left mid-clavicular line. Arteriograms offer the best way to assess the extent of the injuries. shivering. and there were no carotid bruits. The entrance wound is in the anterior chest wall.

When a missile enters the body. Bullet type. it is also abdominal. +> 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. Entry wound is typically small and ragged + Perforating: Missiles pass completely through the target. The chest does NOT END AT THE NIPPLE line though. E. Stable patients.paraspinal muscles. the kinetic energy imparted on the surrounding tissues forces them forward and radially producing a temporary cavity or temporary displacement of tissues. Produced by high velocity projectiles (not from handguns). Patients arriving shocked and bleeding are resuscitated and usually undergo urgent surgery with repair or ligation of the bleeding vessels. +> Shock Waves: compression of tissues that lay ahead of the bullet. and rarely lasts longer than a few milliseconds before collapsing into the permanent cavity or wound (bullet) track. 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. Most institutions explore zone II injuries routinely. in addition to Exploratory laparotomy which is the usual for an abdominal injury.SOME FACTS AND REVIEW 1. The belly begins AT the nipple line. The consequences are generally: +> Laceration and Crushing: projectile displacing the tissues in its track. and Tissue Density. 3. What is the next step in management? (no choices) Ans: CXR (chest tube if needed) which is the usual for a chest injury. can be subjected to whatever diagnostic modalities are required to diagnose the extent of injury accurately. Although it sounds like a chest wound. Entry wound is comparable to size of missile. The temporary cavity may be considerably larger than the diameter of the bullet.The Wounding Capacity of a Bullet It is related to the following factors: Kinetic Energy. He is hemodynamically stable. PE is diffult to do. on the other hand. +> Cavitation (permanent and temporary): also from even higher velocity projectiles. II and III. but he is drunk and combative. which can be obtained by endoscopy as well as .depends on the location.Treatment of gunshot injuries Primary . Progressive neurological deficit calls for rapid evaluation and management. Neck wounds are classified as zones I.resuscitative efforts as well as establishment of airway and restoration of hemodynamics Secondary . They are recognized as the primary wounding mechanism produced by handguns. The point is to remind of the boundaries of the abodmen. NECK TRAUMA: A significant number of patients of neck trauma die at the scene and others on the way to hospital. Belly and chest are stacked up and separated by a dome. Angle at impact. 2.Classification of Gunshot Wounds + Penetrating : Missile is retained in tissue. In zone I and III more definite evidence of injury is required.

in HIVAN. contusion. . new-onset seizure (Management of seizure with subsequent treatment using phenytoin).Labs: Uremia. think of other diagnoses) .html http://www. asterixis etc. with or without laceration of the dura. but some authorities beleive that removing the bullet still gives the best chance to recovery. Direct injury is a consequence of the projectile crossing the spinal cord and/or canal causing compression. Management: Antiretroviral Therapy is the most important feature. .ac. that in the absence of renal biopsy. Indirect injury results from shock waves or secondary fragments damaging the neural elements.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.htm www. Of note: Encephalopathy is a sign of rapidly changing nephro status either deteriorating ir improving (encephalopathy on first hemodialysis = Dialysis dysequilibrium Syndrome). Corticosteroids have also been used but with caution because of the advanced stage of AIDS already for the patient.Patient may present with Uremic Encephalopathy with confusion.uk/journal/vol43_2/4320019.rcsed.S.html http://www. GUNSHOT WOUND TO THE SPINE: Gunshot wounds (GSW) are the 3rd most common cause of traumatic spinal cord injuries in the U.Confirm with Renal Biopsy: FOCAL SEGMENTAL GLOMERULAR SCLEROSIS is the most typical one. I post high-yield facts I encounter. as surgery has not been shown to improve much the neurological status. or laceration of the spinal cord/ nerve roots.edu/depts/doms/rounds-6. kidneys are ENLARGED!! .medschool.medscape. it is still highly controversial. HIV associated Nephropathy Pearls (HIVAN) . ACE-I also have been used successfully to further slow progression. Reference: www. and if the patient is white.lsumc.uic. Indeed. Please refer to the post: ODD HIV case posted on July18 for HIV and Syphilis association.edu/Nsurgery/GSWSp. civilian population.Order Ultrasound: which in contrast with usual shrunken small kidneys of End-Stage Renal Disease. Hemodialysis should also be started. It not only slows the progression but may in fact reverse it. The injury from a gunshot wound could be either direct or indirect.angiography before exploration is embarked upon because of the difficulty in gaining access in zones I and III. massive proteinuria in the nephrotic range with little to ne edema . Overall most studies in the literature recommend a conservative (non-surgical) approach to GSWs to the spine. 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).Mostly African Americans (So and so.

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. Note: For general purposes.Differential: Hep B and Hep C associated nephropathy. but extends (sadly) to mainstream textbooks. It will be delivered with increasing pressure until the set volume is given. Olatinwo.Volume targeted and pressure variable: set the parameter of the volume. Heroin Associated Nephropathy. Continuing Positive pressure throughout the entire cycle instead of intermittently . WHAT'S THE DIFFERENCE BETWEEN CPAP AND PEEP? They virtually refer to the same thing. The problem is: barotrauma. . Hewitt. Ross G. utilizing the recoil nature of the chest to let air be exhaled. Mechanical Ventilation could be throughout intubation (invasive) or a tight-fit mask (non-invasive). Please find in the following my little rehashing of what I read about the subject. where air enters the lungs by virtue of a slight negative airway pressure.Volume variable and pressure targeted: set the parameter of the inspiratory pressure. where chapters on mechanical ventilation seem written more for the author's colleagues than for novices trying to learn the subject. . Example: ARDS. FIRST LET'S DIFFERENTIATE: . **************** MECHANICAL VENTILATION ************** The science of mechanical ventilation is to optimize pulmonary gas exchange.Assisted Ventilation: the patient initiates and may or may not participate in the breath. gas exchange can vary.Exhalation is passive. PEEP is the positive pressure you set for the end of expiration. the pressure starts from the PEEP and on up. The ventilator blows that volume at a certain FLOW. CPAP refers to when inspiration starts.Air is pushed in under POSITIVE PRESSURE. MD. to a degree far greater than the patient could deliver on his or her own. making dangerous hypercapnia or alkalosis possible.Mechanical ventilation: the ventilator is active and the patient passive . passive exhalation is physiologically the same as during spontaneous breathing. Indicated for conditions where risk of barotrauma can be instantly lifethreatening. Reference: . at whatever pressure necessary (up to a limit). THE MECHANICAL RESPIRATORY CYCLE : . The problem is: since delivery of a set volume is not guaranteed. MD 8/2002 Mechanical Ventilation Lecture and Case Scenarios Inadequate teaching is not confined to medical or nursing schools. The concept of POSITIVE PRESSURE is that a baseline pressure is applied throughout the cycle to maintain alveolar recruitment. air delivered under positive pressure is physiologically distinct from spontaneous breathing. tidal volume will flow within that range. WHAT IS A VOLUME VENTILATOR? term used because you set a volume and the machine delivers that volume. the art is to achieve this without damaging the lungs. Flow can be: . both will be referred to as Mechanical Ventilation throughout the chapter.

Depressed mental status b. PaCO2 is 38 mm Hg. WHEN DO YOU INDICATED MECHANICAL VENTILATION IN ADDITION TO INTUBATION? Take home message: . epiglottitis. 3.Impaired alveolar ventilation (as assessed by PaCO2) when accompanied by one or more of the following: a.Apnea . Reduced PaO2 that cannot otherwise be corrected d. Severely deranged pH that cannot otherwise be corrected (below 7. 2. renal. correlate with clinical setting. WHEN DO YOU DECIDE THAT A PATIENT SHOULD BE INTUBATED? 1. head injury with GCS <8 (to prevent massive aspiration).g.g.31 while breathing room air.Low PaO2 (e. A 61-year-old woman who has severe emphysema is alert but is in moderate .. Treat the patient not the numbers. or cerebral function. Either indication must be based SOLELY on the clinical examination. PaO2 is 76 mm Hg. 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.g. A 29-year-old man is alert but in respiratory distress.Apnea 2. Anticipated loss of control of the airway: anticipated laryngeal edema– e. acute stridor etc. HIGH pCO2 IS SOMETIMES ACCEPTABLE BUT NOT CRITICALLY LOW pH (ph<7.1 is considered an indication for mechanical ventilation) e.Impairment of alveolar ventilation (assessed by PaCO2>50mmHg) and/or oxygenation (assessed by PaO2<50mmHg) are the only physiologic reasons for instituting mechanical ventilation. that cannot be improved with an FIO2 less than 0. he is breathing 42 times/min. pH is 7.50. and PaO2 is 47 mm Hg while breathing 60% oxygen through a face mask. Official Criterias are: 1.g. c. Ludwig’s angina.g. A 50-year-old man is comatose from drug overdose. although ABG's are often helpful to assure that mechanical ventilation is not necessary. Increasing fatigue c. Loss of gag/cough reflex e. Compromise of upper airways (e. PaCO2 is 51 mm Hg. by secretions) 3. and b.1 is an indication to mechanical ventilation). less than 60 mm Hg): a. IN CHRONIC LUNG DISEASE. Airway obstruction: acute laryngeal edema – e. Again.42.at the end of expiration is called Contiued Positive Airway Pressure CPAP. inhalation burn. 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. b. and pH is 7. Although mechanical ventilation can lead to better cardiac. rule of thumb.

respiratory distress. Pressure Controlled. PaCO2 is 26 mm Hg and PaO2 is 110 mm Hg while breathing room air. PaCO2 is 59 mm Hg. or failure to oxygenate (is the PO2 <50mmHg)? Remember that a low O2 is much more significant than a high PCO2. * 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). to correct the respiratory acidosis. While the choice of control mode is probably irrelevant (assist control (AC) or intermittent mandatory ventilation (IMV)).37.If failure to oxygenate is the problem. * 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). but is frequently easier to treat. PaO2 is 75 mm Hg while breathing nasal oxygen at 2 L/min. Her pH is 7. Now how long does it stay there? = CYCLING: how the ventilator switches from inspiration to expiration: . the second by recruiting collapsed lung units and controlling mean airway pressure. * Gas is unable to pass effectively from alveoli to capillaries – due to some obstruction in the interstitial space. e. 2) We determined how much flow and at what pressure. and usually patients are started on controlled modes (see below Modes of ventilation).In essence the problem is one or more of the following: * The chest cage is not effective in guaranteeing adequate minute ventilation.38. pH is 7.10. and carefully titrate the CPAP and the pressure control levels to set targets. Every patient who is intubated is in need of a rest. 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. being careful not to damage the lung (be mindfull of the pressures generated).Is it failure to ventilate (is the PCO2 > 50mmHg). PaCO2 is 31 mm Hg. usually controlled pressure modes of ventilation are used. and PaO2 is 89 mm Hg while breathing nasal oxygen at 3 L/min. controlled volume ventilation is used. . * Air is not able to pass effectively from the upper to the lower airway – increased airway resistance. A 29-year-old woman is suffering from diabetic ketoacidosis. 2. WHEN FACED WITH A BORDERLINE ABG AND POSSIBLE MECHANICAL VENTILATION. HOW DO WE INITIATE MECHANICAL VENTILATION? The ventilation strategy is determined by whether the patient has failure to ventilate or failure to oxygenate. her respiratory rate is 24/min. .If failure to ventilate or protect the airway was the problem. d. which means adding pressure support to (S)IMV. HOW DO YOU EVALUATE? It is essential to deduce what part of the respiratory apparatus is malfunctioning. 1. it is important that the patient’s spontaneous breaths are supported. Her chest x-ray is clear. The first problem is managed by increasing the patients minute ventilation. HOW ARE MECHANICAL VENTILATORS CLASSIFIED? 1) How the ventilator knows how much flow to deliver = CONTROL = Volume Controlled . and the pH is 7. or Dual Controlled.

pressure triggered or flow triggered (see next note). dOESN'T allow spontaneous breathing. +> IMV: Intermittent Mandatory Ventilation = Patient initiate own breath and sucks up air. The latter was the first mode to allow partial ventilatory support and thus gradual liberation from the ventilator. .It all started in mid-1950's with the polio epidemic. initially with assisted breaths (assist control ventilation) and subsequently with spontaneous breathing limbs – (synchronized) intermittent mandatory ventilation (SIMV). ventilation strategies were damaging the lungs. This has led to the development of lung protective ventilator strategies (renewed interest in plateau pressure limitation and increasing mean airway pressures). . automatic tube compensation and. time. Many anesthesia ventilators operate in this way. pressure support). But they were of little value since the disease was not inability to ventilate but that to oxygenate. +> 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? . .respiratory muscle paralysis and failure to ventilate. "old ventilators" called "iron lungs" used to provide negative pressure about the rib-cage allowing sucking up air. The solution? Breaths may also be synchronized to prevent "stacking".Modern ventilators deliver enhanced patient interactivity using better triggering sensors. 4) We determined the volume. Patients suffering with this virus die from asphyxia . OR Volume cycled. rise time control. low PEEP.During the 1970s and 1980s ventilators were developed which allowed patients breathe spontaneously. 3) What causes the ventilator to cycle to inspiration? = TRIGGERING = Ventilators may be time triggered. ventilators got smarter now with MODES OF VENTILATION: +> CMV = Controlled Mandatory Ventilation. . 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. synchronized intermittent mandatory ventilation. Accumulating evidence revealed that larger tidal volume. trigger. . of course. have been developed. 5) Very much linked to the precedent. combining pressure limitation with guaranteed tidal volume. or Spontaneous (patient sucks up his/her own breath).Time cycled.Dual modes. Medical students were assigned to manually ventilate paralysis victims until restoration of neuromuscular activity occurred. The problem? "stacked breaths" where there is build-up of high-pressures and therefore alveolar stretching and damage. Assisted (as in assist control. and the patient to make own effort but the flow/volume/pressure are controlled breaths. waveform analysis. +> AC: Assist-Control = Allows the trigger of the breath. .Then came the Pressure Controlled Ventilators. pressure. 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). Physicians are now demanding more control over gas flow than before hence the development of active exhalation valves. dynamic inspiration valves. but also breath controlled by ventilator is delivered.During the 1990s widespread concern developed about ventilator induced lung injury.

For controlled ventilation. 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. however. Increases in minute ventilation will cause a decrease of PCO2. ARDS). HOW DO YOU GO BY MECHANICAL VENTILATION SETTING.Oxygenation.g. Generally. C.PRACTICALLY? A. A large Vt improves gas exchange and prevents atelectasis. E. a patient who is intubated mainly for hypercapnia will usually be adequately oxygenated with an FIO2 under 0. The respiratory rate is set by using a dial on the machine. This has been shown to decrease mortality in some cases (e. or saturations at 90% or higher. and is reflected in the PCO2). Arterial oxygen content should be maintained at 60 mm Hg or higher. If.. the respiratory rate is also the total number of ventilator breaths per minute. For patient for whic it is expected to have some sort of airway obstruction. the patient may breathe spontaneously.For assist control ventilation. for example.Tidal volume (Vt) and Inspiratory Pressure limit. it is approximately 5 to 10 L/min or 100 ml/kg/min.and more comfortable spontaneous breathing . the rate represents the minimal number of breaths.even in inverse ratio ventilation..4. initiate mechanical ventilation with an FiO2 of 100%. B. For all practical purposes. A smaller Vt may be required if PEEP is added.3-7.00. D. the endotracheal tube slips into the patient's right main stem bronchus. However. it may decrease venous return higher volumes may increase risk of barotrauma. . between the machine breaths. A patient intubated because of severe hypoxemia or during cardiopulmonary resuscitation may need an initial FIO2 of 1. and adjustments made to keep the PaO2 between 60 and 90 mm Hg at the lowest FIO2 possible..For intermittent mandatory ventilation. a pressure limit of 50 cm H2O can be set at the same time. . the machine will attempt to deliver 700 cc to just one lung (half the previous lung volume). An FiO2 of greater than 60% for over 24 hours has been associated with lung injury. then taper 10% every 10 to 15 minutes to find the lowest FiO2 necessary to maintain adequate oxygenation.Respiratory rate and Ventilation (Measured by minute ventilation = tidal volume x respiratory rate. . Initial volume is 8 to 10 ml/kg.Permissive hypercapnia. PEEP may be added to decrease the A-a gradient.Minute ventilation is the product of tidal volume and rate. the inspiratory pressure limit will protect patient from further complications.40. In certain situations (e. and the peak inspiratory pressure will acutely rise. Goals of ventilations should be to maintain a pH (as determined by PCO2 and underlying diseases) of 7. depending on the inspiratory sensitivity (also set by the machine).g. allowing a lower FiO2 while maintaining oxygenation... Blood gas measurements should be obtained in the first half hour after treatment. the rate equals the total number of ventilator breaths the patient will receive. the patient may initiate more than the minimal amount. Example: setting the tidal volume for delivery of 700 cc might achieve a peak airway pressure of 30 cm H2O. Conceivably the elevated airway .

Peak airway pressure reflects the pressure required to overcome airway resistance and is the peak pressure during the inspiratory cycle. lorazepam and propofol. Monitoring alarms must be functioning because ventilator malfunction is rapidly fatal if the patient is paralyzed. you need to consider obstruction in the ET tube. but patients should still be sedated. High levels may result in decreased venous return and severe hemodynamic compromise. bronchospasm. With this warning. The alarm limit should be set 10 cm H2O above this. G. barotraumas. decreased lung compliance. F. Instead. perhaps after delivering only 400 cc. Prolonged use of these agents. * Sedation and neuromuscular paralysis allow the patient to rest. H. especially in continuous infusions.Positive end-expiratory pressure (PEEP) may increase compliance and decrease the work of breathing by preventing atelectasis. Initial therapy includes midazolam. when 50 cm H2O airway pressure is reached. Use of nerve-stimulators can decrease the dose of paralyzing agents while maintaining adequate control. Adjust inspired flow rate to maintain a ratio of inhalation time (I:E ratio) to exhalation time of 1 to 1. and thereby decreasing shunting. The alarm will sound each time airway pressure reaches the preset inspiratory pressure limit. It is usually begun at 3 to 5 cm H2O and increased in small increments. If necessary. For long. the therapist or nurse can quickly investigate the problem. If repeated dosing or continuous drips are necessary. Immediate. Cardiac output should be measured if there is an indication of problems because it may increase or decrease with increased PEEP.Inspiratory time and flow. is associated with prolonged (days to months) muscle weakness and ventilatory dependence. If the peak inspiratory pressure increases. or cis-atracurium. and ensure better compliance with the ventilator. Other negative consequences include overventilation. * Neuromuscular paralysis is occasionally necessary if sedation fails. the machine stops inspiration and an alarm sounds. Before the patient is intubated and mechanical ventilation is begun.06. CLINICAL SCENARIO: A 60year old patient is in the hospital for treatment of a myocardial infarction. however. a neostigmine-atropine combination can be used to reverse the non-depolarizing agents.term paralysis use nondepolarizing agents such as pancuronium. periodic interruption of sedation (if tolerated) reduces the total number of days on a ventilator. or by decreasing respiratory rate. her blood gas measurements show pH of 7. During the night she suffers acute pulmonary edema and requires cardiopulmonary resuscitation. consider nerve-stimulation testing to avoid over-medication. or a pneumothorax from barotrauma. diazepam. with monitoring of hemodynamic and respiratory status. The peak inspiratory flow rate determines how fast each breath will be delivered to the patient and is therefore a determinant of inspiratory time. and PaO2 of 50 mm Hg while . However. decrease anxiety. and elevated intracranial pressure.pressure could rupture the right lung or cause other damage. COPD) may require additional time for exhalation. and is usually achieved with a peak inspiratory flow rate between 40 and 70 L/min. PaCO2 of 61 mm Hg. Dosages should be titrated to desired effect. This can be accomplished by decreasing inspiratory time. vecuronium. Patients with airway obstruction (asthma.5 in most patients. short-term paralysis (3 to 7 minutes) can be achieved with succinylcholine 1 mg/kg IV.

FIO2: 100% b. Tidal volume: Modest as well. FIO2 b. A 72yearold man with severe chronic obstructive pulmonary disease is in the intensive care unit. b. Would you provide PEEP? Answer: Inability to Oxygenate secondary to Alveolar exchange problem (V/Q mismatch: high perfusion low ventilatin) a. FIO2: It is an oxygenation problem. Would you provide PEEP? Yes. What initial ventilator settings would you choose for the following: a. Would you provide PEEP? Answer: a. enough to correct acidosis 500 . To ensure continued alveolar recruitment. Tidal volume c. FiO2 should be modest. Vt= 500cc/min c. 40% is a number to start with. His chest xray suggests severe emphysema.24. Tidal volume c Inspiratory pressure limit d. e. Respiratory rate e. PEEP must be delivered.600cc/min with a RR of 10-14l/min c Inspiratory pressure limit: 50 is a good limit. Tidal volume: 8-10cc/kg. and he is almost unarousable. Peak inspiratory flow rat: 40-70 L/min to acheive I:E ratio of 1 to 1. Peak inspiratory flow rate f. and PaO2 is 58 mm Hg while breathing 28% oxygen through a Venturi mask. His pH is 7. Alveoles are full of fluid and will tend to collapse. Inspiratory pressure limit d.breathing 100% oxygen delivered by manual ventilation with an Ambu bag. Choose higher and readjust per subsequent ABG's. Lung compliance is adequate but FiO2 is 100% at first so. d. His estimated body weight is 70 kg (150 lbs). To prevent respiratory arrest. he is intubated and given mechanical ventilation. PEEPis 15-20 cmH2O and readjust once you decrease FiO2. Peak inspiratory flow rate 60-70 L/min since it's a COPD guy and should be allowed more time for expiration. . Peak inspiratory flow rate f. What initial ventilator settings would you choose for the following: a. The patient's estimated body weight is 50 kg (110 Lbs). Respiratory rate: Start with an empirical rate of 10-14/min. Inspiratory pressure limit: empirically 40cmH2O since patient has pulomnary edema and is liekly to have airway obstruction and high airway pressure. Respiratory rate e. f. Despite optimal drug therapy.5. his blood gas measurements cannot be improved. W=55Kg. d. PaCO2 is 84 mm Hg. Respiratory rate: 10-14 and readjust e. FIO2 b.

. Sucralfate. . . setting pressures to generate Vt similar to the assisted volumes with a ventilation rate less than 20. Gradually decrease the inspiratory pressure until 8-10 cm H20 above expiratory pressure. thrombocytopenia. A bacteriologic diagnosis should be aggressively pursued in ventilator-associated pneumonia and will reduce mortality.PCO2 acceptable and a pH in normal range.f. or the respiratory rate'? If so. Initial ventilator settings include a tidal volume (VT) of 700 cc. WHEN DO YOU WEAN THE PATIENT OFF OF MECHANICAL VENTILATION? Guidelines for weaning from mechanical ventilation: . would you change the FIO2.An awake. the patient is intubated before his blood gas results are known. alert patient. A comatose 20year old patient is brought to the emergency room following an overdose of sleeping pills.50. . WHAT ARE THE COMPLICATIONS OF MECHANICAL VENTILATION? A. Patient shows sings of improvement. active bleeding. unless contraindicated (coagulopathy. Compression stockings and intermittent pneumatic devices (TEDS and Kendals) are also effective. C.Minute ventilation less than 10 L/min. However. and proton-pump inhibitors have all been shown to be effective.DVT prophylaxis. HOW DO YOU ACHEIVE WEANING OF MECHANICAL VENTILATION? The most effective method of weaning to discontinuation is spontaneous breathing trials (SBT). the tidal volume. and an FIO2 of 0. Blood gas results obtained (1) before intubation and (2) 20 minutes later show the following: pH---PaCO2---PaO2 FIO2 VT RR (1) 7. . what settings would you choose? Decrease the FiO2 by 10% and redraw ABG's. Would you provide PEEP? Lung compliance is increased.10 79 38 Room air 0 0 (2) 7. recent or future surgery).25 56 117 50% oxygen 700 12 Following the second blood gas analysis.Patient is able to generate a peak negative inspiratory pressure of at least 20 cm H2O.Patient is able to generate maximum voluntary ventilation without retractions. The patient has no spontaneous breathing. A semirecumbent position in bed also will minimize the risk of ventilator-associated pneumonia.PO2 >60.Stress ulcer prophylaxis. If patient . . Because of very shallow respirations and cyanosis. Otherwise: 1. with an FiO2 <50%. Heparin 5000 U SQ Q12h or LMW heparins (enox-aparin 40 mg SQ QD or 30 mg SQ Q12h) are preferred. sucralfate may be associated with a lower rate of ventilator associated pneumonia.VENTILATOR-ASSOCIATED PNEUMONIA: Continuous subglottic aspiration of secretions reduces the incidence of nosocomial pneumonia.Pressure-support method: Switch from an assisted mode of breathing to pressure support. No reason to change other settings.PEEP <8 cm H2O. a respiratory rate (RR) of 12/min. B. 15-20 cmH2O still stands for this patient as well. H2 blockers. to allow proper compliance to ventilatory oxygenation.

and hypoxia (inability to oxygenate)=> Give PEEP and increase FiO2. many body systems must be functioning: the cardiopulmonary apparatus. . demonstrates increasing respiratory distress. The patient is initiating 16 breaths/min and is receiving 700 cc/breath. increase assisted rate until patient stabilizes. HOW DO YOU KNOW WHEN TO D/C WEANING TRIALS AND RESUME MECHANICAL VENTILATION? When: . . For a patient to self ventilate.IMV method. discontinue mechanical ventilation. the nerves that supply the diaphragm (including the neuromuscular junctions). Clinical Scenario: A decision is made to wean a 67 year old man from the ventilator. Repeat attempt the following day with a more gradual decrease in the rate of assisted breaths. Before weaning is begun. this is not in fact the case. Monitor ABGs and vital signs. Blood gas measurements obtained before and after the change to IMV are shown below. If the patient remains stable. There must be room in the abdomen .To extubated a patient. 2. 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.to 90-minute intervals.40 IMV 12 (700 cc) 8 7. the lungs. discontinue mechanical ventilation. If the patient tolerates this for 1 to 4 hours without deterioration.pH <7. or develops significant arrhythmias or hemodynamic deterioration.45 38 78 0.39 47 65 0. since the ABG's are not yet critical. How would you explain the changes? Should you D/C the weaning? Assist control 16 (700 cc) 0 7.can maintain adequate volumes with a ventilation rate of less than 20 for 30-60 minutes.The single most traumatic event for the patient is conversion from positive pressure to negative pressure ventilation. consider extubation. . Moreover the patient must be willing to breath and maintain their own functional residual capacity (not if there is diaphragmatic splinting due to pain). able to cough and protect their airway.40 Ans: Patient was in Assist Control with a controlled rate of 16 and a tidal volume of 700cc. 3.) Have the patient use a T-tube with humidified oxygen. No need to D/C weaning yet at this time. When an assisted rate of <4 breaths/min is achieved. resume mechanical ventilation and consider IMV method (below) for weaning. the central nervous system. This decision should be supported by more thant those numbers: What are the consequences of Weaning? . the muscles themselves.T-tube method: (A T-tube allows the patient to breathe through an endotracheal tube without assistance from the ventilator.Although the ventilator only appears to support on organ system. PCO2 >50. PO2 <60. Gradually decrease the number of assisted respirations in 1 or 2 breath increments over 30. consider a brief T-tube trial.The patient becomes anxious. Switching to IMV caused both hypercapnia and acidosis (inability to ventilate)=> Increase minute ventilation.3. If the trial fails. the machine is in the assist control (AC) mode. fatigued. If the patient fails the attempt. they need to be awake.

PCO2 is 29mmHg. 4 hours after admission you are called because he is hypoxemic. VIII. Patients deserve a trial of extubation. as you can see from his high CO2. in the peripheral nerves. There must be adequate hemoglobin to deliver oxygen to the tissues.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.A 35 year old male with a history of asthma complains of acute severe left sided chest pain. 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. 36 hours post total abdominal hysterectomy. GCS 3. IV. then taper 10% every 10 to 15 minutes to find the lowest FiO2 necessary to maintain adequate oxygenation. Inspiratory flow rate. She is admitted through the ER in extremis. III . The combination of meiosis and bradypnea immediately suggests narcosis. Now he is severely distressed and his chest is moving up and down in a seesaw manner. becomes confused and hypotensive – PO2 is 45mmHg. his chest is hyperinflated and he is becoming hypercarbic. in the muscle itself or in the chest cage? If the problem is oxygenation failure. He has been short of breath all evening. PCO2 70mmHg. which can be reversed. middle or lower airways? II. where is the injury – in the brain (the medulla). which is not surprising.A 16 year old female presents with a two month history of severe fatigue.A reintubation rate of 10% is acceptable. at the neuromuscular junction. pinpoint pupils. with naloxone. VII.for the diaphragm and lungs to move into. He is also somewhat hypoxemic. and becomes acutely dyspneic: PCO2 is 47mmHg. . is the PO2 <50mmHg). CLINICAL SCENARIOS: I) A 22 year old male found collapsed in the street. where is the injury: is it in the blood supply. finds it difficult to get air in. PO2 49mmHg. respiratory rate of 5 and a PCO2 of 70 mmHg. at the alveolar-capillary interface or in the upper. This patient had a collapsed right lung on chest x-ray.A 74 year old female is admitted unconscious. in the spinal cord. generally set between 60 and 100 l/min (the faster the . with a PCO2 of 70mmHg and a PO2 of 50mmHg. but is frequently easier to treat. Intubate and ventilate in controlled mode. Remember that a low O2 is much more significant than a high PCO2.A 67 year old male is admitted with an acute asthmatic attack. PO2 60mmHg.A 73 year old male is discharged from the intensive care unit. ANSWERS: I) This man has ventilatory failure. following a three week admission for sepsis following a perforated appendix. VI. shortness of breath and weight loss. exercise intolerance. V. at least temporarily. His forced vital capacity is 1 liter and his pCO2 is 70mmHg and pO2 60mmHg. FiO2 of 100% with CPAP. If it is ventilatory failure. BP 170/100mmHg. as CO2 will displace O2 from the alveolus when it builds up (we know this from the alveolar gas equation: PAO2 = PiO2 – PaCO2/R).A 54 year old female. and many will do well in spite of poor mechanics (you must use clinical judgment). and a tidal volume 7-10cc/kg. Start with RR 10-14. in atrial fibrillation. Cheyne Stokes breathing pattern. PO2 60mmHg Hints: Is it ventilatory failure or oxygenation failure (is the PCO2 > 50mmHg.

in many ways the opposite to case 4. She presents with a combination of fatigue. Intubation is not necessary at this stage. which usually eventually reverses. the quicker inspiration and the longer the patient has to exhale). A comatose patient with this breathing pattern is a brain stem stroke until otherwise proven. the larynx (laryngeal edema or stenosis) or below the larynx. hypoxemic and hypocarbic after pelvic surgery. and the inability to clear CO2. which is characterized by anti-acetylcholine receptor antibodies. VII. so FiO2 should be modest and readjusted until stabilization of O2 Sat and ABG's. V. The diagnosis is Myasthenia Gravis. This man is . Intubate patient for pulmonary toilet and removal of impacted secretions. III. This suggests that there is a shunt present.This patient has a ventilatory abnormality. Oxygenation is OK. which indicates potentially a recent extubation. along with Heparin therapy and other measures for PE management. is strongly suggestive of upper or middle airway obstruction. yet indicated if patient is full code. and oxygen is not replenished – and there is a ventilation-perfusion mismatch. she should be intubated in IMV mode since patient can breathe on her own.The combination of recent discharge from ICU. He is not adequately clearing carbon dioxide. The most likely diagnosis is a massive pulmonary embolism from the pelvic veins. Mechanical Ventilation on IMV mode with increased minute ventilation. Add PEEP to allow lower FiO2. The major concern here is that the patient has had an acute pneumothorax and there is a loss of hypoxic pulmonary vasoconstriction.flow rate. increased FiO2. PEEP. which is characterized by motor. In view of her hypoxemia. Tidal volume 8-10cc/kg. IV. One thing to strongly consider is accumulation of secretions or inspissation of mucus. The main problem is an inability to ventilate (high pCO2) with an associated problem: inability to oxygenate (high pO2) due to shunt. and this patient requires controlled mechanical ventilation.Patient has high pCO2 = Inability to Ventilate. due to ineffective bronchial toilet (the patient probably has a very poor cough). as evidenced by his inability to clear carbon dioxide. Pneumothoraces are relatively common in young asthmatics.Failure to Ventilate due to outflow obstruction: the patient is attempting to ventilate at high lung volumes where the lungs are least compliant. The cause is either a bleed (hypertension) or an embolus (atrial fibrillation). VI. and thus effective neuromuscular blockade. This patient has ventilatory failure. sensory and autonomic neural demyelination and thus neuropathy.This is. Mechanical ventilation in this circumstance is invariably futile. and paradoxical breathing. Due to the high resistance to ventilation. The patient is hypotensive. suggesting muscle weakness.This patient is acutely hypoxemic secondary to a barotrauma. air is slow to exit the lungs. His diagnosis turns out to be Guillain-Barre syndrome. The cause may be in the oropharynx (tongue or dentures obstructing breathing). The problem is failure of oxygenation due to a massive amount of wasted ventilation (dead space ventilation). II. Some airways may remain closed during the entire ventilatory cycle. due to obstruction of blood flow. He requires urgent placement of a chest tube. he attempts to actively exhale and this causes dynamic airways collapse.This patient is failing to ventilate and failing to protect her airway. and the patient feels uncomfortable. which should be much lower in view of the degree of hypoxemia. This patient has severe outflow obstruction and gas trapping. VIII. The low FVC is a sign of poor physiological reserve. causing further airway closure.

com/scenarios/intvent/index. When the patient has less than 200 od CD4. with repeated evaluations at one to two weeks and at one. For the mother is it oral or IV AZT. 3..mtsinai. chlamydia pnemoniae b.http://www. cough. Here's the reasoning: Using DNA PCR.? A: It is 6wks of AZT irrespective of PCR(antibodies anyway can be from the mother and not of any diagnostic value).BABY NOT TESTED FOR HIV ANTIBODIES AND CAME +VE PCR -VE.vh.hivdent. 1998c).org/adult/provider/familymedicine/FPHandbook/Chapter04/03-4. Small vessels rupturing and combined with phlegm gives the rusty look.BABY NOT TESTED FOR HIV ANTIBODIES OR VIRUS(PCR) 2.Please clarify. References: .com/rs/mv/ . 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.mycoplasma pneumoniae c. and six months (CDC.http://www. aspergillus Ans: Rusty sputum = Strep Pneumonia. what is the cause ? a. Patient is HIV+ Not AIDS patient. we start talking about PCP.people.In kaplan CD it says 6 months.exhibiting signs of acute gas trapping (auto PEEP) and hypercarbia.htm .WHEN DO WE GIVE AZT PROPHYLAXIS? 1. Q: For the child. 20 Y/O GIRL WHO IS HIV + DELIVERED A BABY. Otherwise they still have the same epidemiology as HIV.. the evaluation of the infants infection status should begin within 48 hours of birth. BABY NOT TESTED FOR HIV ANTIBODIES AND CAME +VE PCR NOT DONE ? THANKS Ans: Upon checking more specific references: http://www.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.htm#introduction Question 30 yrs old hiv + man with fever.should we give the first DTaP at 2 .org/pediatrics/reduce/ch4.http://www.ccmtutorials.should AZT be given for 6 weeks or 6 months. According to the guidelines.org/pulmonary/books/physiology/chap10a.html . cxr middle lobe infiltration & rusty sputum .html My answer is: All three should have prophylaxis irrespectice of PCR.pcp e. two. indicating worrisome loss of physiological reserve.to be followed by PCP prophylaxis Q: to immunize a preterm baby.should we administer vaccines based on the birth date? for example in a preterm 8 month(33-34 wk)baby.strep pneumoniae d.http://www.

the suppressed neonatal parathyroid hormone and the abrupt halt of maternal calcium produce hypocalcemia. Normal values are: 2. or 1.Vitamin D toxicity 4. including ectopic hyperparathyroidism 2.Increasing renal tubular resorption of calcium . What's a normal Calcium level? 4.Ectopic PTH: Humoral hypercalcemia of malignancy via parathyroid-related protein (especially malignancy of the lung. The effects of parathyroid hormone on serum calcium are mediated by : .5-5.Milk alkali syndrome 6.Hyperparathyroidism.month after birth or 3 months after birth? A: Immunize as he/she were term. and esophagus) 3.5 mEq/L 9-11mg/dL or 2. lymphoma and metastatic breast cancer) 5. head and neck.23-2.30 mmol/L.Thiazide diuretics Uncommon causes of hypercalcemia 1.5 mEq/L.Malignancy via direct bone destruction (especially myeloma. What causes it? Common causes of hypercalcemia 1.25-5. 4. the serum ionized calcium level can be measured directly. ovary.57 mmol/L Disease states with altered protein binding require a correction factor to determine the ionized calcium level from the total calcium level.Multiple endocrine adenomatosis syndromes .2-2.8 mg per dL (0.Renal failure 4.Hyperthyroidism 5.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.25 mg/dL.Increasing calcium absorption from the intestines (via vitamin D) . Quick Review on Hyperparathyroidism: What is it? Elevated Parathormone.Immobilization 2.Lithium use 3. kidney. A negative feedback mechanism normally decreases production of parathyroid hormone as the ionized serum calcium level increases.12 The mechanism is analogous to the problem of neonatal hypoglycemia in newborns of mothers with diabetes.2 mmol per L) of calcium for each gram per dL that the albumin is below 4 g per dL (1 mmol per L).15-1. Reference: . Alternatively.Increasing release of calcium from bone. A low measured calcium with low albumin may be corrected by adding 0. Following delivery.

Mild acidosis If Hyperparathyroidism suspected on electrolytes => PTH LEVEL.Cardiovascular complications .7. How does it manifest in an individual? . 3.Depression .25(OH)2D3 and low PTH-related peptide: GRANULOMATOUS DISEASE + if Low 1.Calcium elevated but still less than 14.5mg/dl (normal 9-11) .25(OH)2D3 and high PTH-related peptide: HUMORAL HYPERCALCEMIA OF MALIGNANCY.Polyuria and nephrolithiasis . tingling .Low phosphate . Hypercalcemia and cardiac arrhythmias.Different ailments: myalgis.If no meds => CHEM PANEL: Hyperparathyroidism suggested by the following: . together with polyuria and profound dehydration. MILKALKALI (ANTACIDS). This timing avoids the period of organogenesis in the first trimester and the risk of preterm labor that is present in the third trimester. If positive => STOP MEDS AND RECHECK CALCIUM.Chloride/Phosphate ratio > 33 is suggestive . look for FAMILY HISTORY 1.25(OH)2D3 8.Constipation.This may be the first manifestation of maternal hyperparathyroidism. . LITHIUM. What if it happens in pregnancy? Maternal hyperparathyroidism can lead to profound hypocalcemia and tetany in the newborn.If PTH level elevated: PRIMARY HYPERPARATHYROIDISM 4.Fam/h positive: URINE CALICUM LEVEL + If urine Calicum is low: FAMILIAL HYPOCALCIURIC HYPERCALCEMIA + If urine Calcium is high: CHECK FOR MEDICATION INTAKE: THIAZIDE.25(OH)2D3 and PTH-related peptide + if High 1. 2. The optimal time for maternal neck exploration is during the second trimester.If PTH level low or normal: Check 1.Familial hypocalciuric hypercalcemia How do you diagnose it? ALGORITHM: * ELEVATED CALICUM LEVEL = 1st step: RECHECK CALCIUM * If still elevated. Nausea .Parathyroid storm or crisis: Nausea and vomiting. via increased levels of 1. CHF and HTN. 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.Chloride > 102mEq/dl . especially sarcoidosis.Osteoporosis . Untreated or medically treated hyperparathyroidism in pregnancy carries a higher rate of morbidity for both fetus and mother.Granulomatous diseases.

. this approach is successful about 95 percent of the time. In fact. SURGICAL TREATMENT: In some studies. A precipitous drop in the calcium level. Such hypocalcemia responds to calcium supplementation and usually resolves spontaneously.Intravenous hydration is the most critical treatment for a patient with an acute presentation of hyperparathyroidism. A recent trial demonstrated the protective effect of estrogen on bone in women with otherwise untreated hyperparathyroidism.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. Localization of the pathology by computed tomographic (CT) scan. Recently. Thyroid nodules can be difficult to differentiate from parathyroid pathology on some imaging studies.what if it a post-menopausal woman? won't it aggravate her osteoporosis if you try to decrease serum calcium levels? Postmenopausal women. Tx? . ultrasonography or radionuclide scans has been used with varying degrees of success. Larger adenomas are easier to localize than smaller lesions. The addition of furosemide (Lasix) will increase urinary calcium loss.Use thiazide and loop diuretics cautiously . What is/are the potential complication(s) of this surgery? Parathyroid surgery has the potential complication of damage to the recurrent laryngeal nerve. preoperative localization of adenomas decreased the time required for surgery and lowered the incidence of complications. has occurred But. sometimes permanent.Avoid high calcium diet and calcium-containing antacids . parathyroid localization with technetium-99m sestamibi has been shown to have high sensitivity and specificity for single adenomas. It has been suggested that the best way to localize an abnormal parathyroid gland is to let a good parathyroid surgeon look for it. and paralysis of the vocal cords. present clinicians with the challenge of trying to decrease serum calcium levels while also trying to prevent osteoporosis.Avoid immobilization . Administration of pamidronate (Aredia) inhibits bone resorption and lowers serum calcium levels.Treat Hypertension . magnetic resonance imaging (MRI).. hormone replacement therapy with estrogen is indicated in these women. An externally palpable parathyroid gland should be considered malignant until proved otherwise. accompanied by tetany and seizures. In the absence of absolute contraindications. Destruction of parathyroid glands with alcohol injected under ultrasound guidance has been successful. Are there other concerns in the follow-up of a patient? . the largest group of patients with hyperparathyroidism. This technique of localization also has resulted in the discovery of parathyroid tumors in the mediastinal area. Multiple injections may be required. has been called the "hungry bone syndrome".Avoid dehydration . Transient hypocalcemia in the immediate postoperative period also is not unusual.

Active Hepatitis B: wait until baby is immunized .when a mother is an alcoholic . Patients generally have sinusitis or a midface infection (most commonly a furuncle) for 5-10 days 2. Desensitize. IV. IF PATIENT REFUSES. Only 1/2 of nenonates born to mothers who developed disease 5-15 days prior to delivery will develop the disease. ciprofloxacin PO e. send them home together and start BF.a mother is pregnant .Babies may be breastfed until 3 hours before their own surgery . At that point.a mother has breat infections .when a mother uses street drugs . enough of the sedative is out of the body and BF is safe. Desenssitize in allergy is first step.a baby is over 2 years . 1.Maternal Chickenpox within 6 days of delivery or postpartum: Isolate mother and neonate. How to differentiate between Cavernous sinus thrombosis and orbital cellulitis? .HepB. Azithromycin PO b.when a mother has HTLV-1 virus . If no lesions develop by time mother is noninfectious.a.a mother is getting vaccine for RUBELLA . and VI. orbital pain and fullness accompanied by periorbital edema and visual disturbances. fever.when a mother is HIV+ .Active Hepatitis A: Breastfeed when over acute state and after 24h treatment .a baby has diarrhea . Give neonate Zoster Immunoglobulin. 3. Breast Feeding Facts Contra-indications to breastfeeding: .a baby is jaundiced . and malaise typically precede the development of ocular findings.a mother needs a mammogram .when a baby has galactosemia YES IT IS OK TO BREATFEED WHEN: . THEN DOXY 200mg PO x14 days. at least 2 weeks . 4. doxycycline PO Effectiveness of doxycycline has not been formally established in Syphilis. .Active TB: Wait until Treatment established. sympathetic fibers.a baby who has PKU (along with supervised phenyl-alanine free formula) Special Considerations: .Mothers postoperatively may breastfeed if they can hold the baby unassisted.Influenza . III. Pen IM c. Headache. V1 and V2. then tx w/pen f. Increased INTRAOCULAR PRESSURE: sluggish pupillary response and decreased .Cavernous Sinus Cellulitis: Cavernous sinus contains internal carotid. Cephalexin PO d. Increased RETROBULBAR PRESSURE: Exophthalmus and Ophthalmoplegia 5.a mother has breast augmentation implant .

clinical examination guides therapy. 8.Admit all children because children are deficient in IgG2 and are predisposed to bacteremia. Sinusitis (60% patients. + Fever and leukocytosis + Orbital signs Group III . therefore. but the physical signs or papilledema on funduscopic examination. . are suggestive. and hematogenous spread. CRANIAL NERVE PALSIES 7.Orbital Cellulitis: Orbital infections develop via direct inoculation.Orbital abscess = collections of pus within the orbital soft tissue.Surgical intervention if necessary (i. ethmoid most commonly).Subperiosteal abscess = collections of purulent material between the orbital bony wall and periosteum. Mainstay of therapy: Braod Spectrum Antibiotics (Staph Aureus Most common) Heparin therapy . . Classification: Group I . signs appear in the contralateral eye by spreading through the communicating veins to the contralateral cavernous sinus. dacryocysitis. Lids cannot be opened because of edema. but it can be suspected based on physical examination + Orbital signs (see above) + Limitations of ocular motility = pain in globe movement toward the abcess. Group IV . Diagnosis is confirmed by CT scan. This is pathognomonic for CST. + Severe unilateral ptosis + Severe ophthalmoplegia (ie. 1.e. + Lids cannot be opened because of paralysis secondary to III involvement.visual acuity 6. Death follows shortly thereafter. This diagnosis is confirmed by CT scan. complication of periorbital infection 2. proptosis + Corneal hypesthesia with increased intraocular pressure Treatment: . + Directional proptosis = Globe is looking away from the abcess.Preseptal: D/C only if adult with PO ATBx and close follow-up .: compromised vision) Oxacillin or nafcillin can be used with the addition of ampicillin and sulbactam in . The patient rapidly develops mental status changes from CNS involvement and/or sepsis.Cavernous sinus thrombosis + Bilateral symptoms: + Ophthalmoplegia.Steroids (especially if progressed to pituitary insufficency to prevent adrenal crisis). extension from adjacent structures.Preseptal (periorbital) cellulitis = inflammatory edema of the eyelids and periorbital skin with no involvement of the orbit. palsy of the pupillary and extraocular muscles) + CN V1 (forehead) anesthesia Group V . Group II . Without effective therapy.Orbital: Admit with IV ATBx +/. dentition.Orbital cellulitis = CT scan is not sensitive for diagnosing this entity.

DTR's below level are absent at first but return with level of spasticity once over Spinal shock. Start Steroids: Solumedrol 30 mg/kg over 15 minutes then followed after 45 minutes by an infusion at 5. no need to admit. Bladder involvement common. Give IM Rocephin x1 (not accepted by ALL authorities by recommended). fever w/o a focus Fever in a 2months old child(>1 month).Motor symptoms are different between upper and lower extremities in Central.Mechanism of injury is different . Disc protrusion. Risk Factor: Cervical Spondylosis in older patients Mechanism: Hyperextension Trauma (minor bleeds in the tissue) Symptoms: Sensory deficit with level. Hands are especially involved. Patients who are allergic to penicillin can use vancomycin. a cephalosporin (eg. Prognosis: 97% completely recover if less than 50yo. cefoxitin. More somber prognosis is after that. Difference with Central Cord Syndrome: . Action: Since diagnosis is pretty much narrowed down. Methylprednisolone is thought to impact the biochemical cascade of injury that progresses after the initial injury for some hours. or chloramphenicol.well appear(not ill). Central Cord Syndrome Central cord syndrome is the most common of incomplete Spinal Cord injury. May be tube feeding in acute phase because of adynamic ileus. Spasticity. Maintain a level of mild hypertension for spinal perfusion.what should we do next? If he/she is less than 1 m of age or is ill we admit in hospital. Alternatively. If clear. should be made only after carefully assessing the caregiver and . cefuroxime. and observe outpatient. clindamycin. with or without administration of a parenteral antibiotic..children to cover H influenzae. Next: MRI: shows narrowing of the white column of CSF and impingement of the darker appearing spinal cord. Gabapentin for neuro pain. Clinically. various degrees of motor involvement with paresis more pronounced in UE than LE. The decision to observe a low-risk febrile infant at home. hyperflexion.. cefotetan) can be used alone.but what about this case? Thanx in advance ANSWER: 2 MONTHS. paralysis below the injury with variable impairment of pain and temperature sensation is present. or vascular injuries may play a role. accounting for 15% to 20% of cases. Other: Neurogenic bladder (retention). Guys. Pain of neuro etiology. Anterior Cord Syndrome The anterior cord syndrome anatomically involves the anterior portion of the cord. PT/OT/Speech.WBC=10000(5000<WBC<15000).. .4 mg / kg / hr is the typical regimen employed.Position and vibration modalities (posterior columns) are preserved. Management: Admit to Neuro ICU. NO TOXIC MANIFESTATIONS Sepsis work up as UTI's are a frequent cause of fever in children under 3 months of age.if WBC is >15000 we give Abx(kaplan).

. Due to this longer duration of action.com/issues/2000/02_00/park. .500 band cells/mm3 Normal urinalysis (<5 WBC/hpf) or negative Gram's stain When diarrhea is present. marked hypoventilation or hyperventilation. Q was about mechanism of action of Donepezil: A: The ChEIs are classified according to their duration of enzyme inhibition as shortacting. it can inhibit enzyme activity up to 10 hours. or long-acting inhibitors.Fever with toxic signs: admit for workup . which results in the prolonged inhibition of AChE.000-15. 4) over 90days: NO NEED TO ADMIT IF TEMP IS LESS THAN 39/102. See below. rivastigmine is hydrolyzed. lethargy.fever without toxic signs: 1) 0-7days: admit 2) 7-28days: may follow as outpatient if: . rivastigmine is classified as an intermediate-acting (pseudo-irreversible) agent. <1. . intermediate-acting.caregiver reliable and taught what to expcet and when to bring patient back . The ChEIs prolong the actions of the neurotransmitter acetylcholine (ACh) at the synaptic cleft.postgradmed. Another term for this mechanism of action is reversible inhibition. which are decreased in patients with AD. poor perfusion.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.Rivastigmine fits into the enzyme's active site in a similar fashion to ACh. Like tacrine and donepezil.Tacrine and donepezil are short-acting agents that bind to AChE by hydrogen bonding and are hydrolyzed within minutes by the body's water.patient belongs to low-risk grooup. or cyanosis). GUILDELINES ARE AS FOLLOWS: . stimulating presynaptic and postsynaptic muscarinic and nicotinic receptors.000/mm3. *** 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. but unlike these two agents. *** Toxic signs are: *** Clinical appearance consistent with the sepsis syndrome (ie.2 AND NO TOXIC SYMPTOMS.making sure that a responsible physician will be available to provide follow-up evaluation. 3) 28 to 90days: allow to be treted as outpatient ONLY if low-risk group. <5 WBC/hpf REFERENCE: POST GRADUATE MEDICINE ONLINE http://www.

She was semi-comatose and had been ill for several days. #4: The patient is on thiazide diuretic. no sodium level. Another example of mixed disorders is salycilate intoxication whereby the first change is respiratory alkalosis. On binding to AChE. so we can concude that it is metabolic acidosis. management of DKA differs in patients with renal failure. COMPENSATION NEVER "NORMALIZES" pH.. Results include: K+ 2. aggravated by the possible renal failure the patient might have been experiencing. dehydration probably increased plasma concentration of Thiazide.Article 2000 ABG Question A 55 year old insulin dependent diabetic woman was brought to Casualty by ambulance. Reference: Medcape: Rivastigmine. May be had an infection which precipitated DKA.7. Normally it's below 6). One must rule out if patient is having some degree of renal failure due to long-standing diabetes which would aggravate the acidosis. The result is a "normal" pH. It's always close to normal. She has hyperglycemia (67. a New-Generation Cholinesterase Inhibitor. In addition. which would explain the profound hypokalemia instead of the usual hyperkalemia you would have in a simple DKA episode. The anion gap is high.An example of a long-acting ChEI is the organophosphate compound metrifonate. The disorder usually starts with alkalosis and then acidosis ensues.. #2: PAtient has been sick for a while. Past history of left ventricular failure. Consequently. The most common side effects of thiazide diuretic is hypochloremic hypokalemic metabolic alkalosis. anion gap 34 mmol/l Arterial Blood Gases pH 7. and the next is metabolic acidosis as the ASA accumulates. In addition.. #3: No creatinine level is given. The . Metrifonate is a prodrug that is converted to the active agent dichlorvos (DDVP). #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. Current medication was digoxin and a thiazide diuretic. In the presence of renal failure administration of large amounts of fluid is unnecessary and generally is contra indicated. Hemodialysis may be needed in some occasions to treat acidosis in this situation. glucose 67 mmols/l. DDVP forms an extremely stable complex with a half-life of enzyme regeneration of 15 days. and no calcium 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. which corroborates it.41 pCO2 32 mmHg pO2 82 mmHg HCO3 19 mmol/l ANSWER: #1: Acid-Base disorder: IT's a mixed disorder. Overhydration is a concern in adults with compromised renal or cardiac functions and in elderly with incipient congestive heart failure.

and maybe by the development of donor-specific suppression of the recipient's immune response. Histologically. which may gradually occlude the vessel lumen. + ALLOGRAFT: graft between genetically DISSIMILAR members of the same species.: heart transplant. The role of humoral antibody in hyperacute graft rejection is evident when the recipient has been presensitized (by pregnancy.g: bone graft + SYNEGENEIC GRAFT: graft between identical twins. Cell-mediated rejection may be reversed in many cases by intensifying immunosuppressive therapy. Pretransplantation evaluation usually includes a lymphocytotoxic test between recipient serum and donor lymphocytes in the presence of complement. blood transfusion. It is a HYPERSENSITIVITY REACTION TYPE IV culminating in graft enlargement and tenderness. 3) Hyperacute rejection: Within hours or even minutes (intraoperatively). The pathological basis is anti-vascular antibodies that cause extensive proliferation of the arterial endothelium. including dendritic cells (see below). * HVGR = HOST-VS-GRAFT REJECTION: 1) Acute Rejection (4-60 DAYS POSTOP): Main mechanism is LYMPHOCYTEMEDIATED IMMUNE REACTION. Liver grafts seem to be less susceptible to such antibody-mediated hyperacute rejection. Usually. severely damaged elements of the graft heal by fibrosis and the remainder of the graft appears normal. After resolution of acute rejection.result is a normal pH.g: kidney transplant to iliac fossa of recipient. 2) Chronic Rejection: Clinically less dramatic. vascular integrity is maintained.g. te detect presensitization . Correct me if I am wrong. + XENOGRAFT: graft between different species e.g: decreased clearance of creatinine for kidney transplant). After successful reversal of an acute rejection episode. It is irreversible. resulting in ischemia and fibrinoid necrosis of the graft. This process of graft adaptation is most likely explained by the loss of highly immunogenic passenger leukocytes.: porcine heart valves. + AUTOGRAFT: transfer of one's own tissue to another location of the body e. The reaction manifests as an Arthus Reaction (Type III hypersensitivity). although the arterial endothelium appears to be a primary target of the HVGR. and can be suspected on the basis of lowgrade fever with signs of graft insufficiency (e.g. the allograft commonly survives for prolonged periods. even though immunosuppressive drug dosages are reduced to very low levels. There is no therapy for chronic rejection. or previous transplant) to HLA in the graft. this rejection reaction is characterized by small vessel thrombosis. Transplantation facts TYPES OF TRANSPLANTATIONS: + ORTHOTOPIC: organ graft transferred to an anatomically normal recipient site e. + HETEROTOPIC: organ transplant to an anatomically abnormal recipient site 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 . and graft infarction is unresponsive to known immunosuppressive therapies.

redistribution of fat tissue. osteoporosis. and hepatitis. do not stop immunosuppressants). SPECIFIC ORGAN TRANPLANTATIONS: I)KIDNEY TRANSPLANTATION ISSUES: . drug-induced nephrotoxicity is sometimes difficult to differentiate from rejection. It also may induce diabetes. graft tenderness. Its adverse effects are similar to cyclosporine. Occasionally seen in intestinal grafts (lymphoid tissue). . cyclosporine.CYCLOPHOSPHAMIDE: Hemorrhagic cystitis. weight gain. * GVHR = GRAFT VS HOST REJECTION: It is a major obstacle encountered in Bone Marrow transplants. hypertension.: renal artery vasoconstriction). If the diagnosis is unclear. Complications: Immunosuppressant toxicity. although gum hypertrophy and hirsutism are less prominent. immunosuppressive therapy is tapered. and alopecia . and B-cell lymphoproliferative disorders secondary to reactivation of EBV.and ABOmatched to the recipient. tenderness and swelling of the graft. Livers are stored in cold solutions generally for 8 to 16 h after . resulting in better postoperative healing and greater resistance to overwhelming infection. gum hypertrophy. If it cannot be reversed. II) LIVER TRANSPLANT: The advent of cyclosporine has permitted early reduction of corticosteroid dosage. as are biliary atresia and inborn metabolic deficiencies in children. sugar imbalance. and the patient returns to hemodialysis to await a subsequent transplant. fever. It occurs from the grafting of an immunocompetent donor tissue containing EFFECTOR T CELLS. infertility. Major target organs are: SKIN (Dermatitis). hirsutism. Intensified immunosuppressive therapy usually reverses rejection. and renal tubular cells. and risk of Epithelial Carcinoma and Lymphoma (in which case. most recipients undergo one or more acute rejection episodes in the early posttransplant period. End-stage chronic hepatitis and biliary cirrhosis are the most frequent indications for liver transplantation in adults. and appearance in the urine sediment of protein. Cadaveric donors of livers must be of previously healthy persons who are size. IMMUNOSUPPRESSANTS AND COMMON ADVERSE EFFECTS: . Therapy may be prolonged and usually consists of some combination of Steroids. GASTROINTESTINAL TRACT (Diarrhea). which respond to -allo-antigens expressed on host cells.Despite prophylaxis with immunosuppressants begun just before or at the time of transplantation.AZATHIOPRINE: Bone Marrow depression. and LIVER. or fever results from the rejection response with withdrawal of immunosuppressants.TACROLIMUS: is an immunosuppressive drug for liver transplant recipients. . lymphocytes. . etc. Acute Graft Rejection in 3 to 4 months (but they return to normal health and function with increased suppression and reversal). percutaneous needle biopsy is performed for histopathologic evaluation of tissue. and low-dose azathioprime.CYCLOSPORINE: Nephrotoxicity (ie. Rejection is suggested by deterioration of renal function. Chronic Graft Rejection.PREDNISONE: adverse effects on growth in children.in the recipient. Nephrectomy of the transplanted kidney is necessary if hematuria. In cyclosporine-treated recipients. even with biopsy.

dyspnea. vomiting. hepatitis with hyperbilirubinemia.Immunology references (Compiled previous paper I had I don't recall from which references) . but prophylactic use of trimethoprim-sulfamethoxazole has dramatically decreased the incidence of this infection. The vanishing bile duct syndrome. Acyclovir prophylaxis has dramatically decreased the risk of herpes simplex infections during this time. characterized by intrahepatic cholestasis with preserved hepatocellular function. IV) BONE MARROW TRANSPLANT: Early complications include rejection by the host of the marrow graft. The mortality rate of cytomegalovirus interstitial pneumonitis was 80 to 90%. or monoclonal antibodies. Rejection is suspected by development of hepatomegaly. malaise. acute GVHD. which generally occurs 40 to 60 days after transplantation. and weight loss. Jaundice and elevated serum levels of hepatic enzymes are corroborative findings.removal. Rejection is treated with corticosteroid and ATG or OKT3. if necessary. prolonged immunodeficiency. tachycardia. Arrhythmias may occur in more severe rejection episodes. With the use of cyclosporine. is a pattern of chronic rejection. Surprisingly. antithymocyte globulin (ATG). and disease recurrence. light-colored bile (seen in Ttube drainage) or stools. exfoliative dermatitis. the WBC count can take 2 to 3 wk to recover. retransplantation is the treatment. and infections. and a chest x-ray with bilateral pulmonary infiltrates. Some grafts stored for > 24 h are successfully transplanted. and complaints of anorexia. Later complications include chronic GVHD. Suspected rejection episodes are treated with IV corticosteroids. However. rejection may be suggested by biopsy findings only. but treatment with ganciclovir and passive immunity with immunoglobulin has decreased the mortality rate to about 25 to 40%. and fever. hypoxemia. liver allografts are less aggressively rejected than other organ allografts. because other signs and symptoms are often absent and rejection may be detected before function of the graft deteriorates. A worrisome late infection is cytomegalovirus interstitial pneumonitis. diarrhea and abdominal pain. . when either fulminant acute rejection or chronic rejection is refractory to immunosuppressive therapy.Infection (See next post: Infections in Transplant patients): Following the preparative regimen for BMT. patients are very susceptible to infections. Mild rejection by histologic criteria without detectable clinical sequelae requires no treatment. Even after engraftment. . III) CARDIAC TRANSPLANTATION: Rejection onset may be heralded by fever. In milder cases. patients continue to be immunocompromised and at risk for infections because of the drugs used to treat GVHD. During this time. right-sided pain. but the incidence of graft nonfunction increases with prolonged storage. hypotension. Needle biopsy can provide pathologic confirmation. routine protocol transvenous endomyocardial biopsy has been used increasingly to diagnose rejection. References: .GVHR: Symptoms and signs of acute GVHD are fever. Patients are also at risk of developing pneumocystis pneumonia. Patients present with tachypnea. and heart failure that is predominantly right-sided. which may progress to an ileus.Merck Manual .

A BAL was positive for CMV. After four days of in-house monitoring for electrolyte disturbances (which did not occur). the patient received 1 dose of CMV hyperimmune globulin (CMVIG) and was started on a standard immunosuppressive regimen with tacrolimus. Ganciclovir IV plus foscarnet IV 3. Two weeks after transplantation. lung cultures showed mucoid Pseudomonas.Because of suspicions that her CMV strain may have developed resistance to ganciclovir. 1 g TID. Biopsies were negative for CMV. She underwent transbronchial biopsy. Three weeks later. follow-up bronchoscopy was again positive for CMV. the patient was admitted to the hospital for treatment with a combination of foscarnet IV and ganciclovir IV. Both she and the donor were cytomegalovirus-(CMV) positive. Repeat bronchoscopies done over the next 3 months were all negative for rejection and CMV. The RSV infection was treated with ribavirin. azathioprine. but significant mucus plugging was present. . but because of her history of CMV. She was discharged and placed on prophylactic oral ganciclovir for 3 months. Bronchoscopy showed no signs of rejection. she had a bronchial stent placed. until she again developed dyspnea.29-year-old woman with cystic fibrosis who underwent bilateral single lung transplantation on April 7.Cidofovir 2. At 6 months after transplantation and 3 months after the last dose of oral prophylactic ganciclovir.. Foscarnet IV. and prednisone.Ganciclovir C.Harrison 14th edition Clinical Case in Lung Transplant I. after which she developed fevers and was found to have respiratory syncytial virus (RSV) on bronchoalveolar lavage (BAL). One week after antiviral therapy finished. Postoperatively. the patient was also treated with ganciclovir IV for 14 days. 120 mg/kg/day x 14 days D. Four weeks later. 1998. The patient received a repeat course of foscarnet IV and ganciclovir IV for 14 days.After completing her course of antiviral therapy.Ayclovir B. which disclosed CMV infection. the patient again reported shortness of breath (SOB).Foscarnet E. Which one of the following agents is considered the drug of first choice in treating acute CMV infection in lung transplant recipients? A. the patient was discharged home to complete a 14day course of antiviral therapy. the patient was placed on oral ganciclovir. The patient did well for the next 10 weeks. despite continuing prophylaxis with oral ganciclovir. 10 mg/kg/day x 14 days C.Faqmciclovir D. In this situation. as prophylaxis. which was treated with antibiotics. Increased dosage of oral ganciclovir to 2 g TID B. Ganciclovir IV. which of the following alternatives would be most appropriate for treating this infection? A. the patient underwent bronchoscopy because of decreasing pulmonary function on spirometry.

However. Most episodes of CMV pneumonia respond to a 2.to 3-week course of therapy. and headache. However. using both ganciclovir and foscarnet. neutropenia.including infection due to ganciclovir-resistant strains. including phosphorus and particularly calcium. and avoidance of other nephrotoxic agents may also help to reduce the occurrence of renal impairment. In this situation.Answer is D. vomiting.All of the following tests have been used for rapid. In addition. Other common abnormalities associated with foscarnet include changes in serum electrolyte concentrations. Serologic monitoring of IgM/IgG antibody levels C. Saline loading. Foscarnet and the new agent Cidofovir are effective therapies for treating CMV infection -. dose modification. but this response is delayed in immunosuppressed persons and often appears after the onset of disease. studies in AIDS patients with relapsing CMV retinitis have shown that combination therapy. despite ongoing ganciclovir prophylaxis. Adequate hydration and careful monitoring of renal function are critical in reducing the likelihood of this effect. PCR for CMV DNA E. anemia. Electrolyte disturbance B. IgM antibodies may not be appropriately replaced by IgG antibodies. Thus. Nephrotoxicity D. the recurrence of CMV infection. Patients who have frequent relapses on ganciclovir may have their treatment augmented with IV CMV hyperimmune globulin (CMVIG).Answer is C. 3. diarrhea. CMV pp65 antigenemia D.The correct answer is: B The appearance of anti-CMV IgM antibodies is the primary humoral response to CMV. Nausea. serologic monitoring of antibody levels . 4. Anemia E. is superior to monotherapy with either agent alone. suggests the possibility of ganciclovir resistance. and diarrhea 4. The most common serious toxicity associated with foscarnet is nephrotoxicity. Less common side effects include seizures. 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.Which one of the following adverse effects associated with foscarnet is the most common serious toxicity? A. vomiting. which may occur in more than 25% of patients. Seizures C. fever. these drugs are associated with a significant risk for nephrotoxicity and other adverse events that limit their overall use. Shell vial assay with immunofluorescent staining B. nausea. in organ-transplant recipients. 2.Ganciclovir is the drug of choice for treating CMV infection. early detection of CMV infection -except for which one? A. Digene hybrid capture CMV DNA assay Answers: 1.

Initial immunosuppression included intravenous azathioprine and methylprednisolone. Which of the following statements about cyclosporine-induced hypertrichosis is/are correct? A. azathioprine. thicker hair was noted on her hands and arms. Mild hemorrhage of the gingival tissue occurred on probing. References: Interactive Grand Rounds in Immunology Clinical Case of Cyclosporine Adverse Effects 1. the patient reported the development of "swollen gums" that tended to bleed when she brushed her teeth. B. Cyclosporine dosage reduction C. Change antihypertensive medication from a calcium channel blocker to ACE inhibitor or other class of antihypertensive D. diltiazem and warfarin.Which of the following methods is commonly used to treat advancing gingival hyperplasia? A. Short-term azithromycin C. cheeks. which had begun appearing 2 months previously. and orthotopic heart transplantation was performed without complications. and prednisone. Because of progressive heart failure. and forehead regions. Approximately 1 week after transplantation. azathioprine. Subgingival scaling before initiation of cyclosporine E. the patient also reported concern about aberrant hair growth involving her face. especially children and . Cyclosporine-induced hypertrichosis affects primarily females. Maintenance immunosuppression consisted of oral cyclosporine. Discharge medications included prednisone. Darker. There was no history of significant dental problems before transplantation.is inadequate in screening for CMV infection. 2. diltiazem was added to the treatment regimen after the patient developed new-onset hypertension. cyclosporine. Short-term dosage reduction of cyclosporine B. Approximately 2 months after transplantation. Discontinuation of cyclosporine 3. Oral examination showed generalized gingival enlargement involving the mandible and maxilla. with twice-daily brushing and daily flossing B. The patient made satisfactory progress and was transferred out of the intensive care unit on the sixth postoperative day. extending onto her shoulders. Meticulous dental hygiene. None of the above is effectively preventive. A donor heart became available 15 days after the patient was admitted.43-year-old woman with a history of congestive heart failure secondary to a nonischemic dilated cardiomyopathy as well as hereditary protein S deficiency.At this time. she was evaluated for cardiac transplantation. Cyclosporine-induced gingival hyperplasia was suspected. Which one of the following strategies has been shown to prevent the development of gingival hyperplasia? A. Surgical reduction (gingivectomy) D. Clinical manifestations of cyclosporine-induced hypertrichosis usually begin to appear approximately 4 to 6 months after initiation of cyclosporine therapy. The patient was extubated on the first postoperative day and weaned off vasopressors.

Risk only if donor is seropositive and recipient negative. Treatment with Ganciclovir and Immunotherapy. Prevent by Acyclovir in seropositives. OTHER: .Answer : C Transplantation facts #2 .Answer : C 3.<1 month: EXTRACELLULAR BACTERIA FROM SURGICAL WOUNDS OR ANASTOMOTIC SITES (Staph.Coli. Prednisone B. or graft failure. Hypertrichosis results from an increased production of 17-hydroxyprogesterone and DHEA sulfate. Treatment includes combination of IV GANCICLOVIR AND CMV IG. Prophylaxis includes ORAL GANCICLOVIR.Varicella Zoster Virus: Reactivation after several months (can be as early as 1 month).SOLID ORGAN TRANSPLANT: The organisms are different from BMT recipients because solid organ recipients do not go through a period of neutropenia. 6 MONTHS AND BEYOND: ENCAPSULATED ORGANISMS (Pneumococcus and H. Gondii. . 4.CMV: Typically 30-60 days. SECOND MONTH: CMV Disease is a major concern. HSV-2 = Anogenital Disease. cervical lymphadenopathy).Answer : D 4. WBC recover in 2-4 weeks.EBV: 1-3 months. CMV infection may cause interstitial pneumonia. Higher dosages and serum levels of cyclosporine are associated with an increased incidence and severity of hypertrichosis.adolescents. Flu) AND VZV. D. Strep. Low doses of Acyclovir PO have been traditionally given for prevention. II. Patient should still be on TMP-SMX up to one year. GN Organisms). they do have LONGER IMMUNOSUPPRESSION. All of the above statements are correct. C. B-cell lymphoproliferative disease can be fatal (high fever. bone marrow suppression.Herpes Simplex: 6 weeks in seropositive host or donor. . which one of the patient's current medications is associated with the induction of gingival hyperplasia? A. However. Azathioprine C. give Dapsone + Pyrimethamine. . .13 Clinical Cases I. Diltiazem D.BONE MARROW TRANSPLANT: FIRST MONTH: Give Prophylaxis TMP-SMX or CIPROFLOXACIN for GN bacteremia prevention. Occurs between 2 weeks and 4 months. If Allergic. but they also inhibit development of VZV specific immunity => high risk when treatment stopped. E. AND WOUND INFECTIONS (Due to surgery). HSV-1 = Esophagitis. E. Warfarin 1. It also prevents T.Answer : E 2. by hair follicles stimulated by cyclosporine. Treat with HIGH DOSES OF ACYCLOVIR. .Besides cyclosporine.

Live Typhoid . . PSEUDOMONAS. Nocardia. CANDIDA 1-6MONTHS: CMV LUNG INFECTION: * By Organism: <1 MONTH: LEGIONELLA. and other intracellular parasite.VACCINATION OF TRANSPLANT PATIENTS: BMT Patients: AFTER TRANSPLANTATION .g. Hepatitis B .IPV . III. Tetanus. If contact with measles => Immune Globulin Post-Exposure Prophylaxis (PEP). Meningitidis. . Household contacts should get IPV as well. H. .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). OTHER .. If contact with chickenpox => VZV IG ASAP (Within 96h). N.COLI.>6 months: infections characteristic of patients with defects in cell-mediated immunity e.Live Yellow Fever . . and then 12 months thereafter. Repeat every 6 years.Japanese Encephalitis .Pneumovax before.No Varicella Vaccine.TIMELINE AND COMMON CASE SCENARIOS AFTER TRANSPLANT: 1) UTI: <1 MONTH: E. .Pneumovax.TRAVEL VACCINATIONS FOR IMMUNOCOMPROMISED PATIENTS: ANYTHING APPROPRIATE TO THE AREA OTHER THAN LIVE VACCINES: 1.MMR . ENTEROCOCCUS.2 months (TO YEARS): EBV LYMPHOPROLIFERATIVE DISEASE = lung and heart transplants are most likely to develop EBV-induced B cell proliferation. SOLID ORGAN TRANSPLANT: BEFORE TRANSPLANTATION: . various fungi. Diphtheria.Hepatitis A.INFLUENZA Every year.Typhoid immunization (not the live one).Influenza every year . Neisseria Meningitidis and Inactivated Polio at 12 months.YES: . KLEBSIELLA. Flu Vaccine . infections with Listeria monocytogenes.Meningococcal Vaccine .. Flu Vaccine.No MMR before or after due to immunosuppression. IV.INFLUENZA 2.MMR at 24 months.NO: .Varicella V. H. .

CMV. CNS: 1-6 MONTHS: LISTERIA MONOCYTOGENES. Toxo. Gondii. GANCICLOVIR IN CMV SEROPOSITIVE DONOR OR RECIPIENT + LATENT FUNGI/PARASITES: TMP/SMX or DAPSONE/PYRIMETHAMINE x 1 year for PCP and T. + HISTORY OF EXPOSURE TO TB: INH IF RECENT POSITIVE CXR. CRYPTOCOCCUS. Drug-induced. Diffuse Alveolar Hemorrhage.Localized infiltrates: Legionella . NOCARDIA VI. Acyclovir x1 day prior -> Post-op: Bactrim x 1 year.INITIAL EVAL: Skin Lesions. MUCOR * By CXR findings: .Nodular Infiltrates: Fungi.ANTIBIOTIC PROPHYLAXIS: + TRAVEL IN FUNGAL RISK AREAS (Coccidio. LEGIONELLA > 6 MONTHS: NOCARDIA. LISTERIA M. CHF.If no obvious infection site and patient afebrile: Con't ATBx.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: . CLINICAL CASES: Case #1: Q309: U visit a 25 yo male pt who just received BM transplantation. Mycobacterium.his immunosuppressive regimen includes azathioprine. PCP..Diffuse Infiltrates: CMV. histoplasm) => Amphotericin B or imidazoles + LATENT VIRUSES: ACYCLOVIR AFTER BMT for HSV and VZV.1-6 MONTHS: CMV PNEUMONITIS.CXR . 3.steroids&cyclosporine. Radiation Pneumonitis. Nocardia.on . Peri-rectal . Chlamydia. PCP.BCx . Recurrent tumor .If no obvious infection site and patient febrile: AMPHOTERICIN B 2. + in BMT: -> Pre-op: Fluconazole x 1week before procedure. ASPERGILLUS.(Sputum/Urine/Skin biopsy accordingly) NEXT: Initial Broad-based ATBx (GN and GP aerobes) FOLLOW-UP: 1. IV Catheter. ASPERGILLUS.If obvious infectious site found: CON'T BROAD-BASED SENSITIVITYORIENTED ATBx. TOXOPLASMOSIS >6MONTHS: CMV RETINITIS.LABS: Granulocye count<500 . ASPERGILLUS.

fever.related to the presence large amount of lymphoid tissue. 6 months after renal transplantation comes with cough.E shows no abnormalities. edema.What’s the most likely diagnosis? Case #5: More prevalent in small bowel transplant than other transplants . and oligouria. e.hyper acute rejection.WBC:5000. SOB.there’s no nuchal rigidity&there r no focal neurologic findings. .5mg/dl.but u notice on his routine lab tets that his WBC is 2000. Is it graft rejection or cyclosporine nephrotoxicity? Case #8: 60 year old man. 4 weeks later: rapid rise of creatinine.fever.he now has a fever.graft versus host disease.acute tubular necrosis.but Ph. Case #6: Q445: A 37 yo man develops arthralgias. d. a.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.urticaria 2wk after a heart transplant.8.chronic rejection.Serum Cr:1.malaise&evidence of hepatitis followed by progressive dyspnea&hypoxemia with a diffuse interstitial pulmonary infiltrate developing over 5-7days.He received a cadaveric renal allograft 1 yr ago&is now taking prednisone.The allograft is not enlarged or tender. c. acute rejection.postoperative day3 the pt is doing well. b.azathioprine&cyclosporine.T:37. 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.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.

the patient was started on standard immunosuppressive therapy with intravenous cyclosporine. for which the patient remains under treatment. Crackles were heard in the right lung base. as well as repeated episodes of acute rejection and lung infection. Imipemen e. Best step in treatment: a. routine biopsy surveillance showed the development of acute mild rejection. Conversion from cyclosporine to tacrolimus Case #11: The patient was treated with methylprednisolone and antilymphocyte globulin. Methylprednisolone plus plasmapheresis with immunoglobulin replacement D. Methylprednisolone plus antilymphocyte globulin C. Review of the biopsy specimen revealed findings suggestive of chronic rejection as well as acute rejection. Frequent perivascular infiltrates around arterioles and venules. Sputum is positive for Gomori coloration. with intimal thickening and sclerosis of small airways. treatment could include any of the following options. are indicative of chronic rejection? A. Submucosal fibrosis of terminal bronchioles. Frequent perivascular infiltrates around arterioles and venules C. Lymphocytic bronchiolitis with CMV inclusion bodies . Histologic examination of a transbronchial biopsy specimen showed severe. Her acute rejection episode resolved with this therapy. azathioprine. Other postoperative complications included diabetes mellitus. Dense perivascular lymphocytic infiltrates with extension into alveolar septae Case #10: . Submucosal lymphocytic infiltrate with submucosal granulation tissue B. except for which one? A. The patient was CMV negative. Which of the following histologic findings. The patient continued to manifest reduced FEV1. Both were negative for hepatitis antibodies. Amphotericine d. For repeated recurrences of rejection.fever 100. Intravenous methylprednisolone alone B. but she was left with reduced lung function (FEV1 reduced by approximately 25% compared to baseline). and prednisone. gancyclovir b. grade A3/4 rejection. trimetoprim IV c. perivascular mononuclear infiltrate C. Postoperatively. At 2 weeks after transplantation. which was treated with intravenous methylprednisolone. the patient’s lung function began to deteriorate. and the donor was CMV positive. Approximately 3 months after successful treatment of her acute rejection episode with Methylprednisone. Which one of the following histologic descriptions best characterizes acute mild rejection? A. with occasional foci of parenchymal or vascular necrosis D. extending to alveolar ducts and alveoli D. Infrequent perivascular mononuclear infiltrates B. Intraluminal plugs of granulation tissue in small airways. Acyclovir Case #9: The patient is a 28-year-old woman who 7 years previously underwent bilateral lung transplantation as treatment for cystic fibrosis.

Patient developed fever (38°C) on POD4.IPV. The usual postoperative rise of aminotransferases (ALT and AST) was observed with a peak of 2.Case #12: Although several nonspecific clinical signs and symptoms may be suggestive of bronchiolitis obliterans. throat.PPV after 12mo 3-MMR after 24mo. which one of the following is most strongly associated with the diagnosis? A. Cold ischemia time was 10 hours and a peroperative thrombectomy had to be done. Vascular catheters were exchanged and antibiotics (Ciprofloxacine-Ciproxine(r) and Vancomycine-Vancocin(r)) were instituted.760 IU on POD2. Fever subsided whereas bacteriological work-up was negative. On POD7.both WBC&plts should be monitored in the immediate posttransplant period. Deteriorating expiratory airflow E. bile and transcutaneous portions of the catheters were sent to the bacteriological laboratory for direct examination and culture. Fatigue/reduced exercise tolerance D. Nonproductive cough B. T-tube cholangiography exclusively C. Orthotopic liver transplantation (LTX) was performed.the pt’s decrease in WBCs is secondary to azathio toxicity and the most appropriate step is to decrease its dose. Next step in diagnosis? A.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. bilirubin rose to 11. T-tube cholangiography. 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.the schedule for this pts: 1-influenza vaccine>6mo following transplant&annual therafter 2-inactivated vaccines like Td. Doppler ultrasonography (Doppler US) of portal vein and hepatic artery exclusively B. Progressive dyspnea C. 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. At that time echo-Doppler of the portal vein and hepatic artery was normal. Chest X-ray was non contributive. Firthermore.7 mg/dL together with alkaline phosphatase: 320 IU/L (N < 250 IU/L) whereas aminotransferases continued to drop.should be revaccinated. the major side effect of azathioprine is BM toxicity. abdominal fluid. Case #3: the ANSWER is:B: doing LP to rule out cryptococal meningoencephalitis Chief complaint is heacache Case #4: CMV Pneumonitis. urine. . Blood.HBV. Liver biopsy exclusively D. All of these procedures (Doppler US.

Chronic allograft rejection is characterized histologically by the findings of bronchiolitis obliterans. Case #10: The correct answer is A. If inflammatory cells are present (characterized by a submucosal mononuclear infiltrate of lymphocytes. antithymocyte globulin. Biopsy: arteriolopathy (intimal thickening. acute tubular necrosis is a normal phenomenon after kidney transplant. the lesion is considered "active". . Case #9: Answer is B.cyclosporine toxicity: >6 weeks use. Rsponds to decreasing cyclosporine. the antibodise that are already formed are resposible. or antilymphocyte globulin. US: increased graft cross-sectional area. the next option is usually to add treatment with a cytolytic drug. The hallmark sign is the proliferation of submucosal or intraluminal fibrous tissue in the terminal bronchioles. it resolves in few days or weeks. rapid rise in creatinine. hyalinosis. endothelial vaculoization). Biopsy: endovaculitis (intimal arteritis. oligouria after initial function. hyper acute rejection occurs when there is serum incompatibility. has been shown to be a reliable and consistent indicator of impaired graft . plasma cells. and monocytes). fever and weight gain. graft versus host disease. Manometry intracapsular pressure >40mmHg. reflecting declining expiratory airflow. that occurs due to storage and handling etc.Transplant rejection: <4weeks.Case #5: d. which in this patient was successful in resolving her rejection episode. manometry: capsular pressure is<40mmHg. The FEV1 score. Cyclosporine trough level>200ng/ml. leading to the clinical manifestation of progressive expiratory airflow obstruction. acute rejection can be prevented by immunosuppressants. if inflammatory cells are absent. Patchy narrowing or obliteration of the small airways follows. it is neither preventable nor treatable. Typical therapy consists of intravenous methylprednisolone in three successive daily doses. such as OKT3 monoclonal antibody. Case #12: The correct answer is D. When corticosteroids alone fail to stem the decline in lung function. the lesion is "inactive". it is chronic deterioration in organ function. Case #8: PCP pneumonitis. to halt acute rejection or to treat potential bronchiolitis obliterans. Case #11: The correct answer is B. US: unchanged graft corss-sectional area. necrosis and sclerosis). afebrile. Gomori offers best contrast for Pneumocystis Carinii (dark brown-black). which is characterized by lymphocytic bronchitis or bronchiolitis and may be related to infection or other causes. Responds to increased steroids or antilymphocyte globulin. Cyclosporine trough level <150ng/ml. This pattern of infiltrates must be differentiated from airway inflammation (B). acute mild rejection (grade A2) is characterized by the presence of frequent perivascular mononuclear infiltrates around the arterioles and venules. Early acute rejection is a common occurrence. affecting a majority of transplant patients. chronic rejection occurs after few years. IV Trimethoprim-Sulfamethoxazole. MRI: loss of distinct cortico-medullary junction + swelling + density similar to that of Psoas and fat tissue. gradual rise in creatinine. Case #6: d:antitymocyte globulin serum sickness Case #7: Cyclosporine Toxicity To differentiate the two: .

which is based on biopsy results) is defined as a deterioration in FEV1 of more than 20% compared to the baseline FEV1. positive immunoperoxidase (HBV) Fibrous and inflammatory septa No bile duct loss * Acute rejection Interval < 2 months Triade: Activated lymphocytes.htm .net Forum: Previous posts Remembered Question on Transplantation Let's say you have a patient who recently received a renal transplant. abundant councilman bodies (HCV) Ground glass hepatocytes. The diagnosis of bronchiolitis obliterans syndrome (as opposed to bronchiolitis obliterans.ac.Harrison: Infections in Transplant Patients . The decline in FEV1 must be present for at least 1 month and cannot be due to other factors such as infection. excluding bile leak) and then #3: CTscan. A biopsy of the kindey reveals rejection. Differential diagnosis between hepatitis and rejection of the liver allograft * Hepatitis Interval > 2 months Lobular necro-inflammation Steatosis. eosinophils.function.USMLE. or bronchial anastomatic complications.ulb.Liver dysfunction in a patient having liver transplant http://www.Merck Manual: Transplantation . Liver Biopsy and microbiological examinations. the International Society for Heart and Lung Transplantation in 1993 proposed using spirometric data to reach the diagnosis. 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). T#2: T-tube cholangiography (Normal. Case #13: The Algorithm in the presence of abnormal liver tests in a liver transplanted patient is "All of these three procedures. acute rejection. What do you do? . Because histologic proof of bronchiolitis obliterans cannot always be obtained.be/erasme/edu/gastrocd/Case35/C35r. After a short time you notice a decline in renal function. the baseline score is an average of the two highest postoperative measurements taken 3 to 6 weeks apart. PMN > 50% bile duct lesions Endothelialitis * Chronic rejection Interval > 2 months > 50% loss of bile ducts Arteriopathy ± centrolobular necrosis/fibrosis Portal fibrosis References: .

.excellent and easy book i will recomond to all. 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.. A strong association exists between S bovis bacteremia with or without endocarditis and underlying malignancy or premalignant lesions of the colon.. It usually takes care of the usual acute rejections in the post op period.. wait for a week c.. FiO2 in standard atmosphere composition = . Work-up: . but the patient is breathing room air.by the way hasan u r doing great job and valium u tooo.8 wk b4 surgery....wish u all the best hasan and valium.i will post every day some qs or facts like u and valium do hasan bcz thats why this forum is. 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. Bovis and colon CA? Ans: bacteremia with streptococcus bovis makes it mandatory to rule out the CA colon. Some authors have found a similar relationship between bacteremia (or endocarditis) and liver diseases or nonmalignant diseases of the colon.goood luck to u and valium and every body else....try to do recall qs bcz 70% come back to every one..to. If mechanical ventilation....believe me its a fact. Whether S bovis plays a causative role in colon cancers or is only a marker of the disease is unclear. In any event. remove the transplant surgically ANSWER: increase the dose of immunosuppressive drugs. S bovis infection is a well-documented cause of infective endocarditis. it is by default: 21%.and so many others really nice ppl who post qs everyday . The organism also has been isolated more frequently from the stools of patients with such malignancies. increase the doses of the immunosuppresive drugs b.. they use infusion Methylprednisone alone.a...ifu dont have that book dont go for exam . -. The portal of entry for S bovis bacteremia is the GI tract.Gram Stain: Gram-positive cocci .thats what we do in common practice refrence would b crush and nail the board . 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.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. every patient with S bovis bacteremia with or without endocarditis should be examined for a GI tract malignancy. FiO2 has to be reset according to ABG's and different parameters discussed previously in my review: MEchanical Ventilation LEcture and Case Scenarios.this forum helped me alot so i will do som ething... in solid organ transplant. Sometimes..21 (21%)....Blood cultures (BCs) are the most important tests.. and coumadin should b stop 48 h b4 surgery.there. That is if you are to calculate A-a gradient using FiO2 and you find out you don't have it.

The most recent investigations support this last theory not the first. DOWNS SYNDROME.. Turner syndrome is not inherited. Like any chromosomal syndrome. Resistance mechanism (Van A) is identical to the one identified in most vancomycin-resistant enterococci (VRE).: intravenous penicillin G for 4 weeks. . Ceftriaxone is an alternative to penicillin and is administered once a day.Emedicine . B.e. unless any of the parents suffer from an alteration in his/her sexual . So.in pairs or chains. they are two independent facts. Complications for S bovis infection are similar to infective endocarditis caused by viridans streptococci.The barium enema should be performed on patients with S bovis bacteremia or endocarditis. therefore. it is not anything we can avoid and it is not the result of something that has happened during the pregnancy.Medline Genetic Counseling TURNERS SYYDROME.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.. Treatment: The antimicrobial therapy for both Streptococcus viridans and S bovis endocarditis is identical. The fact of having a Turner girl yet doesn’t increase the probability of having another one. If the ovule or the sperm have suffered this chromosomal loss. However. if parents show a normal karyotype it is not inherited.CMDT . i.Liver ultrasound and CT scan should be performed in cases of associated hepatobiliary disease. Are there possibilities to have another baby with Turner Syndrome? As previously commented. Vancomycin is useful for patients with a history of major penicillin hypersensitivity (immunoglobulin E [IgE]-mediated).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. al mothers have the same possibility of having a Turner girl. . 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. the person formed from the fertilisation will carry this chromosomal error. which may facilitate outpatient therapy. 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. during the first period of the embryo growth (in the first gestation weeks). it is one of every 5000. Reference: . we can say it has happened by chance. 1 strain of S bovis has been isolated that is resistant to vancomycin.

. OCP's in PCO inhibit the enogenous secretion of FSH and LH. but subsequent pregnancy rates are only 30 to 40 percent.The most important longitudinal (prospective) study of lung function in smokers who have early COPD is the Lung Health Study (JAMA: 272:1497. In addition.restore menstrual cyclicity in 68 to 95 percent of patients treated for as short a time as four to six months. but 40% will have a mosaic of 45X and 46XX. This therapy has achieved pregnancy rates of 58 to 82 percent. she has an increased risk of having a baby with Down syndrome. 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. The risk of Down syndrome increases with the age of the mother.improve insulin sensitivity .Decrease free testosterone levels.chromosomes. in a dosage of 500 mg two to three times daily. and restore the cyclicity of menses thereby taking care of the dysmenorrhea. Furthermore. 1994): Smoking cessation . If the mother has been diagnosed with a chromosome abnormality. if this happened they should consult their doctor. has been shown to: . An older mother will continue to have about the same chance for her age. Ovulation is successful in approximately 75 percent of women treated with clomiphene. It also goes up when the father is over 60 years of age. In fact one of Clomiphene Citrate's side effects is Dysmenorrhea. 75% will result in spontaneous abortion. In addition. 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.aafp. Reference: American Association of Family Practice AAFP http://www. but the risks from ovarian hyperstimulation and multiple pregnancies remain of concern. However. OCP does have effect on hirsutism by decreasing testosterone and increasing sex harmone binding globulin production in liver. Although insulin-sensitizing agents show promise in the treatment of polycystic ovary syndrome. Of those who escape.html Smoking Cessation effects: Does it parallel non-smokers? .decrease serum LH . Risk doesn't increase by maternal age. The chance goes up quickly when the mother is over 34 years. Female with ah/o PCOD and dysmennorhoea wishes to get pregnant .org/afp/20000901/1079. 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). especially in women with normal glucose function. there are no studies of adequate power or design to allow them to be recommended as standard therapy. 50% will have a full monosomy. which drug answers her both infertlity and dysmenorrohea problem? Treatment with an insulin-sensitizing agent such as metformin (Glucophage).

it started in the chest and spread to the throat.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. and under each eye. a few ecchymoses. JAMA 1993. then a gradual decline thereafter. Lung function was equal to non-smokers older that then 2.: INCREASE) in lung function during the first year. et al.Within three months of quitting. and .Post GRaduate MEdicine online http://www. His medical history was significant for coronary artery bypass graft surgery twice. 5 and 12 years ago. Enright PL.htm .Quit before 40yo => at 65yo. . Other studies revealed the following: . the man now spent most of his time in bed.The risk of heart attack is decreases by 50% within 24 hours of quitting smoking. Morale of this: the earlier you quit the better. hourly between midnight and 6 am. lung function is equal to that of older patients of 5. Effects of smoking intervention and the use of an inhaled anticholinergic bronchodilator on the rate of decline of FEV1: the Lung Health Study.The risk of having a stroke or a brain aneurysm go down by 30-50% in quitters. Kronmal RA. lansoprazole. Smoking and lung function in elderly men and women: the Cardiovascular Health Study. .JAMA: +>Higgins MW. . et al. the FEV1 should be DECLINING!!!. So by 5 years. THE RATIO SHOULD NOT BE DECLINING SINCE THE DECLINE IS IN BOTH FVC AND FEV1. lateral nose. Previously active.5 yo). .272(19):1497-505 Postinfarction Ischemia Clinical Scenario: A 68-year-old Asian man with a previous cardiac history. After 2 years of abstinence from tobacco. BP: 114/69 mm Hg. the smokers' cough disappears in most people.269(21):2741-8 +>Anthonisen NR.for more than a year leads a slight improvement (i. His skin showed evidence of excoriation.5 to 15 years.e.e.5 to 82. .Quitting decreases the overall risk of death (all causes combined) by 50% in 15 years as compared to continuing smokers. and atenelol.5 years (i. jaw.postgradmed.5 to 7.Quit between 40 and 60 => at 65yo. presented with the chief complaint of chest pain 6 times a night since MI. no detectable difference in lung function compared with non-smokers .: they have the lungs of a 67. Episodes lasted 5-15 minutes. the risk of heart disease is decreased to about the level of never smokers. 9 days status-post inferior wall MI. The review of systems was notable only for skin allergies. The patient's chest pain was pressing and radiating. His medications included nitroglycerin. JAMA 1994. Connett JE. Reference: . Kiley JP.com/issues/1998/12_98/hays. . He denied any arrhythmias or congestive heart failure. due to reversal of nicotine's effects on inducing platelet aggregation and vasospasm. The FEV1 DECLINE then was equal to that of non smokers (20-30 mL/year). There were no indications of diabetes. atorvastatin.

and long-term mortality.What if medical therapy contraindicated? Then take patient to Cath lab and do PTCA or CABG. or sudden death.How does it happen?: inadequate blood flow throuh a recanalized vessel /OR/ reocculsion. . Trials of Calcium channel blockers for prevention didn't show results suggesting pathophysiology is different from that of Pre-MI angina.New England Journal Of Medicine CATCH UP IMMUNIZATION SCHEDULE CHILD ABOUT TO ENTER SCHOOL.Chickenpox (Varicella): at any age if they have never had chickenpox. People who do not get the vaccine until 13 years of age or older should get two doses.What is it? Anginal pain at rest.DTaP: a five-dose series. . 4-8 weeks apart.Incidence: 30% of patients. References: . . .How it is managed?: Nitrates.Three doses of Polio . Aspirin. . REQUIRED VACCINATIONS? .Two doses of MMR OLDER CHILD NOT IMMUNIZED. Angiography demonstrated multiple vessel occlusion and good motility. Cardiac enzymes confirmed this. .Why is it important?: increased short.4 doses of DPT (the last before 4 yo) . Heparin. Hypercholesterolemia was also noted.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).cherry angiomata. . If 4th dose given after 4 yo.CMDT . INQUIRING ABOUT CATCH UP IMMUNIZATION SCHEDULE +>CHILDREN 4 MONTHS TO 6YO: . EKG: changed from previously. which develops within 2 weeks after Acute Myocardial Infarction episode. POST INFARCTION ISCHEMIA .Who'll get it?: Especially if pt had angina prior to the MI or non-ST Seg Elev MI. this condition remains associated with a poor prognosis. 5th dose is NOT necessary. 4 weeks should elapse between #1/#2/#3 then 6 months period elapse between 3rd/4th and 4th/5th dose. . .What's the morbidity and mortality of this condition? It is associated with risk for infarct extension. On his chest was a well-healed sternotomy scar with a purple area at the inferior aspect. Lungs and heart were normal. and plateletglycoprotein IIb/IIIa antagonists. Despite numerous therapies including intra-aortic balloon angioplasty. repeat infarction. Lower extremities were cool with venous stasis. . BEta-blockers. reflecting an acute MI.

only one is enough. +>CHLIDREN OF 7YO TILL 18 YEARS: . Mumps and Rubella: Children should get two doses of MMR vaccine anytime provided 4 weeks have elsapsed between the two.Td: 3 doses with 4 weeks interval between #1 and #2. 2 doses at least 6 months apart. • People who have multiple sex partners or abuse injectable drugs. stop there (Total 2)!!!. or compromised immunity or who has had spleen removed. at least 4 weeks between 1st and 2nd doses and at least 8 weeks between 2nd and 3rd. College students and health care workers are advised to have a second dose (at least 4 weeks between doses). . repeast seconds shot 5 years later. • Male homosexuals with multiple partners. alcoholism.Polio: IPV 3 doses 4 weeks apart. Who needs it? Anyone who wasn't vaccinated with it before.Measles. who've never been immunized. . If third one is given after 4 yo.Hepatitis B: Hepatitis B 3 doses. • Anyone on kidney dialysis. Who needs it? Adults age 65 and up. . . or liver disease.Hepatitis B: 3 doses with 4 weeks between #1 and #2 and 8 weeks between #2 and #3 . .Meningococcus: 2 years or older. After 65yo. • Health-care workers.Varicella: 2 doses 4 weeks apart. Every ten years thereafter. only ONE dose is needed!!!! If second dose given after 15 months old. • Prisoners. ADULT NOT VACCINATED AS A CHILD: . One shot/year for designated population . 4-8 weeks between doses. . • Food handlers in high-incidence communities. . and 6 months interval between #2 and #3.Influenza: 6 months or older. • Travelers to endemic areas. and so on. Anyone who has chronic heart.Lyme Disease: 3 doses. should get one shot.Who needs it? At risk populations: All adolescents ages 11-19.Hep B: 3 doses 4 weeks between #1 and #2 and 8 weeks between #2 and #3.Pneumococcal: If before 65yo. • Clients and workers in institutions for the mentally impaired. healthcare personel) . lung. . One dose for those with increased risk (travel to meningitis belt. sickle-cell disease. diabetes.. dorms. . Who needs it? Anyone who frequently spends time in tick-infested habitat in endemic areas should consider the vaccine. patients should get a series of three shots: the second and third will follow two and six months (respectively) after the first. • Sexual partners of and people who live with hepatitis B carriers. 1 month between 1st and 2nd doses. • Anyone with chronic liver disease or clotting-factor disorders. If 1st dose given after 15 months old.Hepatitis A: 2 years or older. Who needs it? Travelers to endemic areas. • Illicitdrug users. endemic areas. Who needs it? Adults born after 1957 (patient is >47years old now). .MMR: 2 doses 4 weeks apart.Varicella: 2 doses. .Polio: 4 doses at 4 weeks interval each. no need for a 4th dose!!!! . Patients should get boosters every 10 years.Tetanus/Diphteria: If receiving for the first time.MMR: 1 dose. Stop giving it after ANY dose given >15 months old. 11 months between 2nd and 3rd doses. .Hemophilus Influenzae: 4 doses with 4 weeks interval if started before 12 months old.

html Teratogenic effect of Isotretinoin WHAT KIND OF TERATOGENIC EFFECT DOES ISOTRETIONON CAUSE? Answer: . Fusion of teeth .Varicella: 2 doses . 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: .CDC. maxillary and mandibular hypoplasia. .parentsplace..aafp.xml . laboratory workers who might handle polio virus.Presbycusis C. .DtaP: 4 doses .Hemophilus Influenza: 1 dose .Multiple Sclerosis .www.Meniere B. The third dose 6 to 12 months after the second.giv/nip .Cardiac and CNS abnormalities .Hepatitis A: 2 doses if indicated References: .Polio: 3 doses if indicated.Pneumococcal: Once if indicated.Craniofacial anomalies: Cleft lip and Cleft Palate.10335. The second dose 1 to 2 months later.MMR: 2 doses . Flat nose bridge.Polio: 3 doses (because >4yo) .http://www.Behavioral Teratogen .166606_222430.Meningococcus: 1 dose if indicated . Questions Transient sensiry symptom electric shock-like precipitated by neck flexion is a recognized feature of: A.Polio Vaccine: 3 doses of IPV: The first dose at any time.Polio Vaccine Facts http://www.Influenza: once a year if indicated .com/health/vaccines/articles/0.Td: 3 doses then every ten years get booster .Varicella: 1dose (2 if she were 13yo) .Hepatitis B: 3 doses if indicated . .MMR: 1 dose.org/adultimmunizations.Thymus developmental abnormalities isoretinoin also increases triglycerides in the body . Repeat once after 65yo.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.00.

soreness. and sometimes painful bowel movements. In normal subjects. PE: thick skin of finger and toe pads. Reference: the Prophylactic Penicillin Study (PROPS)multicenter. Prophylaxis with oral penicillin in children with sickle cell anemia: a randomized trial. the plasma water sodium concentration and plasma osmolality are unchanged. N Engl J Med 1986. Falletta JM. Gaston MH. Discontinuing penicillin prophylaxis in children with sickle cell anemia. bleeding.. Has multiple sex partners. since infants may not be protected by maternal antibodies beyond that time. -> delerium and schizo have what in common? waxing and waning memory impairment hallucination family hx of psychopathology social withdrawal ANS: Hallucinations.Aminoglycosides E. . a normal plasma sodium concentration of 142mmol/L actually represents a concentration in the physiologically important plasma water of 154 mmol/L. In a child with sickle cell disease 1. They're auditory in schizophrenia. and visual mostly in delirium.127:685-90.immunization for pnemococci &H. (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... 2. Verter JI.Acoustic Neuroma This is Lhermitte sign beleive it or not. Woods G. Do we have to give both or any specific indications for each? Thanks Ans: I would say both according to my review. :) It's one of the remembered MCQ's Patient with classic retrosternal chest pain of GERD..25:1593-99. It's Multiple Sclerosis. et al.penicillin prophylaxis till 5yrs age. anal itching.". Verter JI. Ans: Gonorrhea or the rectum.D. the plasma water is approximately 93% with the reminaing 7% made of Lipids and proteins. or hyperproteinemia (as in multiple myeloma). In these settings. the plasma fraction may fall below 80% in patients with marked hyperlipidemia (as with lactesent serum in uncontrolled diabetes mellitus).inf. double-blind. Thus. However. Ds? Ans: Scleroderma Young man come to clinic with anal discharge. placebo-controlled trial. but the measured sodium concentration in the total plasma volume will be reduced (since the specimen contains less plasma water). 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. Woods GM.it was agreed that a 14-valent pneumococcal vaccine would be administered to all children at 1 year and 2 years of age. J Pediatr 1995..

Serum . THAT'S THE ANTIBODY CIRCULATING IN THE PATIENT'S SERUM. Patient's RBC's exposed to anti-D. the pressure in the distal port rapidly falls. THAT'S THE ANTIGEN COATING THOSE RBC's. #2: INDIRECT COOMBS: Take the patient's SERUM and add to it KNOWN RBC's. QUICK REVIEW: . and then positioned within a branch of the pulmonary artery. e.: ABO TYPING.: BABY'S SERUM to see if there are CIRCULATING ANTI-D ANTIBODIES therefore COATING BABY's 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. e. Patient's RBC's exposed to anti-A.kbsm. anti-B.Reference: Systematic approach to hyponatremia http://www. 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. the distal port measures pulmonary artery pressure (~ 30/15 mmHg) and the proximal port measures right atrial pressure (~ 0-2 mmHg).: DIRECT COOMBS USED TO KNOW BABY'S RHESUS TYPE IF MOTHER IS RHESUS NEGATIVE.acta-clinica. along with its distal branches which eventually form the pulmonary veins. When properly positioned in a branch of the pulmonary artery. e. The balloon is then deflated. the right ventricle. reaches a stable lower value that is very similar to left atrial pressure (normally about 8-10 mmHg).TYPE AND RHESUS DETERMINED WITH DIRECT COOMBS TEST . Wherever there is coagulation. multi-lumen catheter (Swan-Ganz catheter) is advanced from a peripheral vein into the right atrium. Wherever there is coagulation. These ports are connected to pressure transducers. 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. The recorded pressure during balloon inflation is similar to left atrial pressure because the occluded vessel. A balloon-tipped.pdf Coombs test mystery REVEALED You take the patient's blood specimen and centrifuge it. A PCWP exceeding 15 mmHg suggests .g. Separate: .hr/Acta2002/ACTA2002_2/05RATK~1. The measurement is made as follows.ANTIBODY SCREEN DETERMINED BY INDIRECT COOMBS TEST.: RHESUS TYPING. 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). and after about 10 seconds.g: Mother's serum to see if there are CIRCULATING ANTI-D ANTIBODIES. e.g. e. and anti-AB.mitral stenosis .g. When this occurs.g.RBC's #1: DIRECT COOMBS: Take the RBC's and expose them to KNOWN ANTIBODIES.

) = > PCWP in caardiogenic will be elevated in the presence of pulmonary edema. AND SUTURE OF THE NERVE IF INDICATED. with the obvious severe medical legal consequences. not being able to recognizee the nervous lesion. The operation must be done under general or peripheral anaesthesia.. Nerve Section Clean wound cut w/laceration and incomplete section of the nerve.ventricular failure When the PCWP exceeds 20 mmHg.ARDS. The wound exposure may be of various types: • Punctiform or minimum • Extended • With sub-amputation Moreover. otherwise if the nerve is frayed for a . Review of Emergency Nerve Surgery In this evaluation we have to distinguish two cases: • Open lesion • Closed lesion A. • COMPLICATED = with contused lips. a suture will be practised. skin).mitral insufficiency . a normal excitability of the motor endplate.OPEN LESION: RULE OF THUMB: Surgical exploration is imperative in every case of open lesion. management? a. during the operation. etc. SUMMARY AND USMLE TAKE HOME MESSAGE: OPEN LACERATION: SURGICAL EXPLORATION IMMEDIATELY. If there is a paralysis the nerve is usually interrupted and nerve suture must be done under operative microscope. If the lesion is clean. CLOSED INJURY: USUALLY NOT EMERGENT REPAIR OF THE NERVE UNLESS SURGERY INDICATED FOR OTHER PURPOSES (E. leave the wound open To answer your Q first: Surgical exploration immediately with suture of the nerve and the wound.G. Nerve dissection must be limited to a few centimetres in order not to damage its vascular contributions. suture of wound immediately b. bone. the transmission of this pressure back into the pulmonary vasculature increases pulmonary capillary hydrostatic pressure which can lead to pulmonary congestion and edema.severe aortic stenosis .differentiating cardiogenic from non-cardiogenic (Septic shock . vessel. and contamination => In these cases the same principles mentioned above are valid . the lesion may be: • SIMPLE: = clean-cut lips and involvement limited to => the risk is to merely practice a skin suture. but it would be normal or low in non-cardiogenic shock. Other indications: . poli-tissutal involvement (nerve.aortic regurgitation .: VASCULAR). in order to permit.evaluating blood volume status when fluids are administered during hypotensive shock (maintain PCWP at 12-14) . preferably without curarizing the patient.

when associated lesions (usually vascular and/or bone lesions) must be treated. portal and hepatic veins) . protein C combines with thrombomodulin in order to produce activated Protein C. Subsequently. mesenteric. Electrotherapy of the denervated muscles is also suggested. thus leading to a thrombophilic state by having increased activity of factor V in the blood.A first venous thrombosis at less than 50 years of age . 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. Factor Va is an essential cofactor for the factor Xa-catalyzed activation of prothrombin to the clotting enzyme thrombin. The first step in this process is the activation of thrombomodulin by thrombin.A first unprovoked venous thrombosis at any age Recurrent venous thrombosis .CLOSED LESION: usually it is not necessary to explore the nerve in emergency.it/eates4/Invitedspeaker/Trauma/vigasio. Having too much of it will generate too much thrombin and a hypercoagulable state. greek. or there is a loss of nervous substance and it is not possible to practice a direct suture. Epidemiology: Patients are mostly northern european: Swedish. the factor Va is resistant to the normal effects of activated protein C.dc. if the treatment has been correct. 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: . resulting in increased thrombin generation and a mild hypercoagulable state. 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. it can be fairly good.unipi.tract.med. nervous grafts will be necessary (Secondary repair). Some exceptions exist to this principle. Activated protein C can then degrade factor Va and factor VIIIa.Venous thrombosis at unusual sites (such as cerebral. When one has factor V Leiden. etc. ADJUVENT THERAPY: Rehabilitation treatment is absolutely necessary in these lesions to prevent and treat stiffness using even orthopaedic devices for hand or fingers. The recovery of the nerve lesions is usually slow but. Reference: http://www-cdu.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). Mechanism of action: The function of protein C is to inactivate factor Va and factor VIIIa. Activated protein C then combines with protein S on the surface of a platelet. B.

Examination of the patient demonstrates slight disorientation.A 45-year-old man is admitted to the hospital for the evaluation of diplopia. the patient reveals that has been forcing himself to vomit after almost every meal over the last 6 weeks. or neurological or neurodegenerative disorders. bilateral dysmetria. which encodes the factor V protein. He has never experienced such symptoms in the past. and a tendency to doze off easily.nih.No h/o DVT: no prophylaxis needed . He denies associated eye pain and discomfort.Prolonged PT. . uncontrollable trembling. 3.Venous thrombosis during pregnancy. turning left instead of right and getting lost in his own neighborhood. epilepsy. an ataxic gait. Labs: .html .org/profiles/factor-v-leiden/details. weakness of his lower extremities.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. During the interview.nlm. and hypothermia. and prolonged immobilization.ncbi. .Gene Reviews http://www. (Enoxaparin prophylaxis throughout pregnancy?) Reference: .geneclinics. or dysphagia. Prophylaxis: . or in association with oral contraceptives or hormone replacement therapy . Management: . Laboratory analyses reveal mild dehydration and hypokalemia.National Library of medicine http://www3. vertical nystagmus worse on downgaze. and gait difficulties. They also noted waxing and waning difficulties with speech. headache. No prophylaxis needed.Prophylaxis in high risk settings: surgery.Pregnancy: no consensus yet. particularly recent events.Heterozygotes with only first episode: Coumadin hemorrhagic risk is 1-2%/year and is greater than <1%/yr DVT risk. . the puerperium. Several months ago.gov/htbin-post/Omim/dispmim?227400 Dementia Qs 1. PT correct by mizing test (adding deprothrombinized rabbit serum). His family states that he would repeatedly ask the same question and started forgetting easily. . diffuse weakness of the lower extremities.Old woman with rapidly developing decreased intellectual abilities with startle myoclonus.Usual management of DVT (Coumadin f/u is 3 to 6 months out patient). 2..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.Evaluate for other inherited or acquired thrombophilic disorders . There is no family history of psychiatric illness.A 57-year-old man is evaluated because of progressive memory problems and language disturbance. pregnancy. he started noticing increasing difficulty with driving.

Subsequently. It usually presents in late middle age (50-75 yr). such as difficulty in naming familiar objects and verbal comprehension. dysarthria. As a result. she says her mother has had difficulty remembering things and has "ruined her credit rating" because she forgets to pay her bills. A neurologic examination confirms the presence of moderately severe short-term memory loss associated with disturbances in language. and on neurologic examination. MRI of the head reveals diffuse cerebral atrophy without focal lesions or tumors. myoclonic fasciculations. Her medical history includes gall bladder surgery 10 years ago and hysterectomy 15 years ago for abnormal bleeding. ataxia. MRI typically shows bilateral areas of increased intensity.A 72-year-old man has impaired concentration and an inability to recollect names and appointments. predominantly in the caudate and putamen. astrogliosis and the lack of an inflammatory response. usually following pneumonia. These memory problems have become increasingly worse over a period of months and begin to interfere with his social and financial activities. aneurysms. while an abnormal. Normal prion protein is termed PrPc (cellular). and his wife persuades him to see a physician. using some phrases repeatedly. talked inappropriately to strangers. the physician notes that the patient has an ataxic gait. and eventually death. the patient becomes depressed. 6. His neighbors caught him stealing things from their back yard. starting with a changing gait. More recently. The daughter tells the physician that her mother "walks oddly" and has been falling with increasing frequency. MRI reveals enlargement of the ventricles without cortical atrophy 5. and showing a decreased vocabulary. with rapidly progressive dementia. within a year of onset. and showed insensitivity. followed by urinary urgency and incontinence. and has developed obsessional cravings for sweets. or intracranial bleeds. On physical examination. Family history is negative for strokes. She says that her mother's symptoms began a year or two before. and does not drink alcohoI.A 56-year-old man is brought to the psychiatrist with a three-year history of progressive speech difficulties associated with altered social behavior. Testing reveals difficulties in naming common objects or pictures. the pathologic hallmarks of CJD are spongiform degeneration. She quit smoking fifteen years ago. She does not have a tremor. He has had problems with speech production. He started to eat a great deaI. contrary to his past consideration to others. and gradually became worse. Spongiform changes . #2: CJD again. pathogenic isoform of the prion protein is designated PrPsc. The patient repeats the examiner's words and imitates the examiner's gestures. The family states that he became aggressive.4. somnolence. ANSWERS: #1: CJD. CJD is a degenerative disorder of the central nervous system that is caused by accumulation of abnormally folded protein (PrPsc) particles termed prions.A 68-year-old woman presents to her primary care physician complaining of clumsiness and urinary incontinence. the patient has gained 40 pounds over the past year. she is found to have normal strength and muscle tone. On light microscopy.

These lobes are important for language skills. Pick disease is a rare form of neurodegenerative disorder characterized by a distinct progressive dementing process. and maintaining socially appropriate behavior. and cerebellum. Some patients are aware of their difficulties. and gait disturbance. NPH is a disease usually found in older adults. emotional lability. Surprisingly. and are due to impaired cerebrospinal fluid absorption. sociability may not be affected at this early stage. memory loss and impairment of intellect occur at later stages of the disease. A common misconception about Wernicke encephalopathy is that it is seen exclusively in alcoholics. causing frustration and anxiety. and ophthalmoplegia. either alone or in combination with vestibular dysfunction. prolonged intravenous feeding. Most cases are idiopathic. Prolonged vomiting and malnutrition. patients experience recent memory loss. In most cases of Pick disease. The CT makes the diagnosis likely because of the enlarged ventricles. eating disorders. The atrophy affects the anterior temporal and frontal lobes. mental status changes. initial personality change. eating. #4: This patient has the classic triad of normal pressure hydrocephalus. but spares the posterior part of the superior temporal gyrus and the pre. His symptoms are typical of early AD and the diffuse cerebral atrophy is also characteristic. the most common cause of dementia in the Western world. spatial disorientation. and inability to concentrate. The wide-based ataxic gait results from cerebellar dysfunction. Compared to Alzheimer disease. consisting of urinary incontinence. problem solving. The intermediate stage is characterized by a worsening memory. progressive language dysfunction. Classic symptoms and signs include "Wernicke's triad": acute mental confusion. leading to difficulties with dressing. and disinhibition are the key features of this disease. Presenile onset (under 65 years old). The common form of this disease typically affects people over age 60. MRI scans may later show hippocampal atrophy. Circumscribed ('knife-like") lobar atrophy is the hallmark of Pick disease. and the medial temporal lobe. although not all the patients present with all of these. #5: Pick Disease. #3: This is Wernicke encephalopathy caused by a nutritional deficiency of thiamine. In the early stage of AD. personality changes. which leads to production of an abnormal tau protein. Mild to moderate depression is common in early stages.occur in the putamen. others are seemingly unaware of their symptoms. patients may have difficulties with sequential motor tasks. there is a strong genetic component in certain families. hunger strikes. ataxia. Mental confusion is characterized by impaired awareness. impulse control. The symptoms of Pick disease occur because the frontal and temporal lobes are affected. Ocular abnormalities are the hallmarks of this disease. However. both recent and remote. Subarachnoid hemorrhage or meningitis are risk factors for the future development of NPH. the orbital frontal lobe. hyperorality (overeating with obsessional craving for certain types of food). the cause cannot yet be determined. thalamus.and postcentral gyri. caudate nucleus. and diminished judgement. Their sense of time and place are lost. and malabsorption syndrome can also be a potential cause of thiamine deficiency. and sometimes can be so severe that the postmortem brain weight can be as low as 800 g. #6: This patient has Alzheimer disease (AD). language difficulties (especially word finding). A mutation on chromosome 17 has been identified. leading to a . cerebral cortex. Horizontal or vertical nystagmus and paralysis of lateral rectus muscles are common. energy and enthusiasm. and toilet functions. Various apraxias are common. bathing.

Suppurative lymph nodes that become tense and extremely painful should be drained by needle aspiration. agitated. but it may be quite red and swollen.a red left eye without any pain&discharge&a left preauricular lymphadenopathy. but are at risk for accidents resulting from their confusion. and heart disease.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. if any.Direct eye inoculation as a result of rubbing with the hands after cat contact is the presumed mode of spread. The typical duration of the disease is 8 to 10 years.which is unilateral conjunctivitis followed by preauricular lymphadenopathy. and that treatment affords minimal.8. including wandering and becoming lost. 10days later she had a tender.Aspiration of the axillary node recovered pus.She developed erythematous nodules and plaque over both shins 1 wk later. with resolution occurring over weeks to months. the disease is self-limited. and uncooperative.left axillary node. The involved eye is usually not painful and has little or no discharge. It is clear that for the majority of patients. clinical benefit.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. Incision and drainage of nonsuppurative nodes should be avoided because chronic draining sinuses may result. Which of the following statements regarding the most likely diagnosis. secondary infections. Sometimes they can be quite aggressive.from which no organism was grown on routine culture. ----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------CAT SCRATCH DISEASE REVIEW: . No other clinical benefit was found.T:37. 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. which may need to be repeated.host of behavioral problems. but after 30 days there was no difference in lymph node volume. which can alternate with being socially withdrawn and passive. Death generally results from malnutrition. In end-stage AD. 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. THEN I WILL DUPLICATE THE REVIEW OF CAT SCRATCH DISEASE. patients are unable to walk or perform tasks of daily living and their recent and remote memory is gone. A conjunctival granuloma may be found at the inoculation site. They can still ambulate.

Fleas and ticks have also been associated with the transmission of CSD. This agent has requirements necessary for growth in vitro. sore throat. hepatic granulomas (0.Regional lymphadenopathy (axillary. and nonsuppurative conjunctivitis. which occur in up to 14% of patients.Unusual manifestations of CSD. In general. 2) development of lymphadenopathy approximately 2 weeks after the primary inoculation. and the CBC is normal or shows mild leukocytosis. 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. head and neck. nausea and vomiting. 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. these complications resolve without sequelae. .8). affected nodes are often tender and occasionally suppurate. . including enriched. although more evidence is required to establish ticks as vectors.to 1-cm papule or pustule) at the site of a cat scratch or bite. The bacterium is most frequently isolated in young. or petting. The skin lesions typically develop 3 to 10 days after injury and precede the onset of lymphadenopathy by 1 to 2 weeks. inguinal) is the predominant clinical feature of CSD. figurate erythemas. headache. erythema nodosum.Answer is E. Perinaud's oculoglandular syndrome is manifested by conjunctival granuloma. with the exclusion of other causes of lymphadenopathy. short-lived. osteomyelitis (0. . The erythrocyte sedimentation rate is usually elevated during the initial stages of lymphadenopathy.In addition. 3) a positive CSD skin test.Low-grade fever and malaise accompany lymphadenopathy in up to 50% of patients. and pulmonary disease (0. 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. Transmission of CSD occurs from a bite. Optic neuritis with transient blindness may also occur. . anorexia. periauricular lymphadenopathy. Encephalopathy.Between 25% and 60% of patients report a primary cutaneous inoculation lesion (0. . but that serve as passive vectors in transmitting the disease to humans. and splenomegaly may develop.3%). as a result of direct contact with the cat’s saliva. weight loss. Bartonella henselae is now regarded as the etiologic agent of CSD.2%) (4. male kittens that are not ill and require no treatment. manifested as fever and coma that progress to convulsions.3%). 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.5. non-specific maculopapular eruptions. non-selective blood agar incubated over a prolonged period in a CO2 atmosphere.5. include Perinaud's oculoglandular syndrome (6%). . may last for days to weeks. cerebrospinal fluid is unremarkable. scratch. and thrombocytopenic purpura have been observed. encephalopathy (2%). The saliva is deposited on an infected cat’s fur and claws from self-grooming.

thrombocytopenic purpura. Margileth (1992) suggested the efficacy of oral rifamin (87%). epitrochlear and preauricular nodes. neuroretinitis. pneumonia. benign of malignant neoplasms. toxoplasmosis. which is thought to be the most accurate. urethritis. such as the axillary. unilateral occurrence. It has been associated with CSD in both children and adults. henselae. and optic disc edema. In AIDS patients and in other people who have suppressed immune systems (chemo. thyroiditis and non-traumatic atlanto-axial dislocation (Grisel syndrome). headache and muscle weakness. Granulomatous hepatitis is another newly recognized systemic manifestation of CSD. In a retrospective study of uncontrolled data. henselae infection recently. suggesting hematogenous spread. EEGs reveal diffuse slowing or focal abnormalities. inguinal and generalized lymph node involvement is less specific for CSD and necessitates more care in differential diagnosis. mesenteric lymphadenitis. Patients with severe CSD (encephalopathy. and is no longer recommended. and cervical adenitis caused by mycobacteria. stellate macular exudates. The syndrome of Leber’s idiopathic stellate neuroretinitis is characterized by visual loss. The most common diagnoses in a series of patients with adenopathy and negative CSD skin test were pyogenic lymphadenitis or abscess. iritis. regardless of antibiotic treatment. Recovery has occurred without residua in most cases. and an 84% sensitivity. and it may present as fever of unknown origin with or without lymphadenopathy. which has 91% positive predictive value. ciprofloxacin (84%) TMP/SMX (58%). management should include conservative symptomatic care and observation. neuroretinitis) may have a shortened course and thus benefit from antibiotic therapy. and intramuscular gentamicin . The CSF is normal or shows minimal pleocytosis or elevated protein content. and treatment with antibiotics is recommended. As a general rule the diagnosis is favored by chronicity. tenderness and characteristic sites of involvement. Diabetes. 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. Other rare complications include erythema multiforme. Treatment: CSD is almost uniformly a self-limiting illness. For the majority of patients with CSD. Differential: It can include virtually all known causes of lymphadenopathy. arthralgia. Neuroretinitis one of the most frequently reported neurologic syndromes. cat scratch disease is not benign. femoral. Complete resolution of lymphadenopathy usually occurs after 2 to 6 months. Osteolytic bone lesions far from the inoculated site have been noted in several well-documented cases. but choice of antibiotics is unclear.). and Kawasaki disease must be considered because of the need for specific therapy. the test is not standardized. is not available commercially. and the enzyme immunoassay (EIA) test. ESRD. Tularemia.Currently available for diagnostic purposes are the serum immunofluorescent-antibody (IFA) test for B. Complications: The most serious complication of CSD is involvement of the CNS in the form of encephalitis or encephalopathy. High fever and convulsions develop within 6 weeks of the onset of lymphadenopathy followed by alteration in the level of consciousness. has been serologically and microbiologically linked to B. a 96% specificity. plague. Cervical..

(b) treat animals for fleas and ticks. and (i) ensure routine veterinary care for all pets. oral rifampin was prescribed using 10 to 20 mg/kg two to three times daily for 7 to 14 days.Grand Rounds Archives: http://www. 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. Warm moist compresses to affected nodes may decrease swelling and tenderness.Medline . and most patients with CSD recover fully with no permanent sequalae in a variable period of time from 2 to 4 months. Families become concerned about the transmission of CSD to other family members by infected cats. (d) never allow cats to lick open wounds. Reference: . such as erythromycin and doxycycline. (f) handle cats and all animals gently. parents and cat owners should consider the following recommendations: (a) wash hands after petting or playing with cats. and there is no evidence that CSD is transmitted by humans.CDC . and one episode of CSD appears to confer lifelong immunity in children and young adults. Periods of transmission are thought to be limited (possibly 2 to 3 weeks). Disposal of the offending cat is not recommended.(73%) for improving clinical symptoms. Collipp (1992) reported improvement in 101 children with CSD by treating with 20 mg/kg of TMP/SMX twice per day for 7 days. or bites immediately. in vitro and in vivo antibiotic susceptibilities to Bartonella species often do not correlate and cannot be used to guide antibiotic recommendations. Consistent with the 1994 CDC guidelines. In the same 1992 study.html -----------------------------------------------------------------------------------------------------------------------------------------------Second MCQ is also an old one Q404: .bcm. Although the complication of CSD can be serious (central nervous involvement. (g) instruct children to avoid contact with stray animals. (h) supervise young children.tmc. Relapsing Bartonella is rare. even though others may have been scratched by the same cat. cuts. prescribed over several weeks or months. Cats seldom infect more than one family member. (c) wash cat scratches. Aspiration may be helpful for those cases in which suppuration occurs. children who are immunocompromised appear to respond quite well to common antibiotics. Paradoxically. Isolation of the affected individual is not required. In addition.edu/oto/grand/12592. (e) declaw cats if possible. they are relatively rare. and oral ciprofloxacin using 20 to 30 mg/kg twice daily for 7 to 14 days. boney lesions. Intramuscular gentamicin was prescribed for severely ill patients using 5 mg/kg in divided doses every 8 hours for 72 hours. when handling cats. Incision and drainage carries the reported risk of sinus tract formation and formal node excision may be preferable. and the cats do not appear ill in any way. oral TMP/SMX using 6 to 8 mg/kg two to three times daily for 7 days. but using good judgment when handling cats and kittens is essential. but failures also have been reported after treatment with gentamicin and TMS-SMX. hematological disorders. and abscesses). especially toddlers.

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. Streptococci.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. most likely dog is not rabid.Vaccination for rabies should be considered only when you have a strong suspicion of rabies. the dog did not seem rabid (the dog bite occurred only after being provoked).If rabies is suspected. 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. if not sure you can check w/ public health dept.cleaning.Hand bites should also be treated with antibiotics since infection can be devastating to a patient. 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.provide local wound care without ABX & vaccination.Puncture wounds become infected more often than abrasion and this pt doesn't have any skin punctures.Local wound care including debridement.E you notice a shallow abrasion on his left thigh.His temperature is 37. and anaerobes.suspicion might be higher.On Ph. it appears prudent to .RR:13.no erythema. The management of bite wounds consists of intensive irrigation with large volumes of normal saline and a cautions debridement of devitalized tissues. which probably indicates that it was vaccinated in the past. no edema. :provide local wound care without antibiotic & vaccination Only 5-20% of dog bites become infected. most likely vaccinated. 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. which is mildly tender.This pt does not seem to have any systemic signs of infection and his wound doesn't appear to be infected. the neighbor's dog is a domestic dog. Staphylococcus.In this case. has small . If the dog spontaneously bit the patient.HR:63. Rabies vaccination is not indicated now. ADDENDUM: IS A DOG/CAT'S MOUTH CLEANER THAN A HUMAN MOUTH? Animal and human bites carry a high risk of infectious complications. bones and tendons.and irrigation are essential.ABX not necessary. Local wound care remains important.Also.BP:110/70 mm Hg. before vaccinating the pt.There is no surrounding edema or erythema. pt.Amoxicillin-clavulanic acid and clindamycin would both be acceptable antibiotics since they have broad spectrums covering likely infectious organisms such as Pasteurella multocida. Antibiotics would be indicated for pts with signs of local or systemic infection. an attempt to contact the dog owner is a reasonable first step to determine the pet's vaccination status.. shallow abrasion. Generally. the dog was a household pet.

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

U/A 3+ PROTEIN AND GLUCOSE. #4: Iga NEPHROPATHY = BERGER'S DISEASE Idiopathic Glomerulonephritis associated with URI or GI infections. AND HYPERTENSION. FROTHY URINE (from protein). Associated with autoimmune disorders and use of medications (Gold. Presents with HEMATURIA. RENAL BIOPSY: FOCAL GLOMERULONEPHRITIS INVOLVING ONLY SELECTED GLOMERULI WITH MESANGIAL PROLIFERATION AND . NO LATENCY PERIOD (AS OPPOSED TO POST-STREPTOCOCCAL). RENAL BIOPSY SHOWS THICKENED GLOMERULAR BASEMENT MEMBRANE AND "SPIKE AND DOME" PATTERN WITH SILVER STAIN. U/A 3+ PROTEIN AND NEPHROTIC RANGE PROTEINURIA. ABDOMEN ASCITIC WITH 3+EDEMA. NO EFFECTIVE TREATMENT. U/A = Protein and fatty casts. #2: MEMBRANOUS GLOMERULONEPHRITIS It's the most common cause of primary nephrotic syndrome in adults. FOCAL SEGMENTAL. asymptomatic at first. BROAD AND FATTY CASTS. Increased incidence of occult neoplasms: lung. #3: DIABETIC NEPHROPATHY: Insidious proteinuria secondary to diabetic microangiopathy. it then presents with HEMATURIA. Hb A1C= 10%. stomach.PROTEIN DECREASED. Renal Biopsy = IgA DEPOSITS. NO EVIDENCE OF PLEURISY/ASCITES. FUNDOSCOPY: PROLIFERATIVE DIABETIC RETINOPATHY. ELEVATED IgA. Treat with Prednisone with ot without cytotoxic agents for 3 months. IT IS ALSO SEEN IN CELIAC DISEASE AND LIVER DISEASE because of decreased IgA clearance. BS: 234MG/DL. Case: 48YO WHITE FEMALE ADMITTED BECAUSE OF WORSENING GENERALIZED EDEMA AND WEAKNESS ALONG WITH HYPERTENSION. Renal Biopsy = KIMMELSTILL-WILSON = INCREASED MESANGIAL MATRIX AND THINKENED BASEMENT MEMBRANES. U/A RED CELL CASTS IN URINE. Penicillamine. and colon in patients >50yo. CASE: 22YO WHITE MALE COMPLAINS OF RECURRENT EPISODES OF BLOODY URINE FOR SEVERAL DAYS IN CONJUNCTION WITH URI. IF: -VE FOR Ig. and Captopril). ANA -VE. 1/2 of patients progress to renal failure. Protein restriction. IF: GRANULAR DEPOSITS OF IgG AND C3. PITTING EDEMA. GROSS HEMATURIA. Treat with ACE-Inhibitors. Chronically progresses to glomerulosclerosis after about 10 years. Complications: progressive loss of renal function over 3-10years in 10% of cases. CASE: 52YO WITH RHEUMATOID ARTHRITIS AND BORDERLINE DIABETES PRESENTS TO THE OUTPATIENT CLINIC COMPLAINING OF ABDOMINAL BLOATING AND BILATERAL ANKLE SWELLING OF SEVERAL MONTHS. INCREASED IgA. NO PRIOR HISTORY. PATIENT HAS BEEN USING GOLD THERAPYF FOR HIS RA FOR 2 YEARS NOW. CAN BE CRESCENTIC. PE: HTN (160/110). ANASARCA. NEPHROTIC SD ON LABS. RENAL BIOPSY: LIGHT MICROSCOPY UNREMARKABLE. EM: fusion of epithelial foot processes. BUN AND C ELEVATED. H/O DM1. OR MESANGIOPROLIFERATIVE. strict Glucose control with Insulin if necessary. U/A= Protein and Red Cell Casts. DECREASED ALBUMIN. IT IS THE SAME GLOMERULAR PATHOLOGY SEEN IN HENOCH-SHONLEIN IN KIDS. NEITHER KIDNEY IS PALPABLE.

SEGMENTAL NECROSIS WITH CRESCENTS. HOWEVER IT IS METABOLIZED TO CYANIDE AND THIOCYANITE SO MONITOR BLOOD LEVELS.Class III: FOCAL PROLIFERATIVE GLOMERULONEPHRITIS. TREAT SUPPORTIVELY. VISUAL BLURRING. AND NECROTIZING GLOMERULITIS WITH THROMBOTIC MICROANGIOPATHY.Class IV: by far the most common as in the folling case. #7: Lupus Nephritis: There are five patterns to Lupus Nephritis: . IgG. RED CELL CASTS.Class V: MEMBRANOUS GLOMERULONEPHRITIS. HYPERPLASTIC ARTERIOLOSCLEROSIS (ONION SKINNING). HEMATURIA. . IN SERUM = ANTIGLOMERULAR BASEMENT MEMBRANE ANTIBODIES +VE. SERUN: ELEVATED BUN AND C. . . and mild renal insufficiency. TREAT GOOD PASTURE'S SYNDROME WITH PLASMAPHERESIS. AND IMMUNOSUPPRESSIVE THERAPY. CBC: SHISTOCYTES. PROTEINURIA. YESTERDAY. GIVE NITROPRUSSIDE BECAUSE IT DOESN'T IMPAIR MYOCARDIAL BLOOD FLOW. AND OLIGURIA X24H. TREAT BY REDUCING DIASTOLIC BLOOD PRESSURE TO AT LEAST 100 AND MAINTAIN URINE OUTPUT AT LEAST 20CC/HR. RENAL BIOPSY: KIDNEYS' ENLARGED AND PROLIFERATIVE NECROTIZING GLOMERULONEPHITIS IN CRESCENTS WITH ACCUMULATION OF NEUTROPHILS AND MACROPHAGES IN BOWMAN'S CAPSULE. ABG'S: HYPOXEMIA. . HE COUGHED UP BLOOD. Recurrent hematuria. U/A: PROTEINURIA. HEMOLYTIC ANEMIA.Class I: NORMAL in light/immunofluorescence microscopy. FATIGUE. AND MALAISE. THERE IS CHARACTERISTIC IgG LINEAR DEPOSITS ON BASEMENT MEMBRANE AND ALVEOLAR SEPTA ON IF. FUNDOSCOPY REVEALS PRESENCE OF PAPILLEDEMA WITH HYPERTENSIVE RETINOPATHY. #5: CRESCENTIC GLOMERULONEPHRITIS CASE: 36YO WHITE MALE COMPLAINS OF CHRONIC COUGH OF SEVERAL MONTHS WITH LIGHTHEADEDNESS. RENAL BIOPSY: FIBRINOID CHANGES OF ARTERIOLES (NECROTIZING ARTERIOLITIS). IF: MESANGIAL IgA DEPOSITS WITH SOME IgM. CXR=BILAT ALV INFILTRATES. DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS. HE ALSO DESCRIBES EPISODES OF DARK ORANGE URINE. PATIENT IS A HEAVY SMOKER. U/A OLIGURIA. Nephrotic syndrome. #6: HYPERTENSIVE RENAL DISEASE: CASE: 45YO BLACK MALE PRESENTS WITH UNCONTROLLED HYPERTENSION.Class II: MESANGIAL LUPUS GLOMERULONEPHRITIS. IgA DEPOISTS REAPPEAR. STEROIDS. Minimal hematuria or proteinuria. SEVERE OCCIPITAL HEADACHE. EVEN AFTER RENAL TRANSPLANTS. ASSOCIATED: NECROTOZING HEMORRHAGIC ALVEOLITIS ON LUNG BIOPSY = TYPE II HYPERSENSITIVITY. AND C3. .

Activation of only alternate complement pathway. There is a high recurrence rate following renal transplantation. PERIORBITAL EDEMA. #8: MEMBRANOUS GLOMERULONEPHRITIS Nephrotic Syndrome may be idiopathic or caused by membranous glomerulonephritis (the most common cause in adults). THE IMMUNE DEPOSITS ARE IN A "LUMPY-BUMPY" = DISCONTINUOUS PATTERN ON IMMUNOFLURESCENCE. RENAL BIOPSY: THICKENED BASEMENT MEMBRANE. HYPERLIPIDEMIA. Case: 47YO BLACK DIABETIC FEMALE COMPLAINS OF WEIGHT LOSS. SHE ALSO HAS RECURRENT ORAL ULCERS AND PHOTOSENSITIVE SKIN RASH. Minimal change disease (MCC in children).Case: 30YO BLACK WOMAN WITH PAIN IN BOTH KNEE JOINTS AND SMALL JOINTS OF HANDS TOGETHER WITH MILD FEVER. LABS: NORMO/NORMO ANEMIA U/A MICROSCOPIC HEMATURIA WITH RBC CASTS IN ADDITION TO PROTEINURIA. TypeI MPGN: both classic and alternative complement pathways are activated TypeII MPGN: Dense Deposit disease. AND ASCITES. CHEST PALPITATIONS. or membranoproliferative GNitis. LABS: ELEVATED RUN/C. Patients with nephrotic syndrome have hypercoagulability secondary to loss of ANTITHROMBIN III in the urine. . AND RINGING IN HER EARS TOGETHER WITH GENERALIZED EDEMA. ON PAS OR SILVER: SPLITTING OF BASEMENT MEMBRANE CAUSING RAILRAOD TRACK APPEARANCE. AND SWELLING OF BOTH LEGS AND ARMS. U/A FATTY CASTS AND OVAL BODIES ALONG WITH PROTEINS. WEIGHT LOSS. SUBENDOTHELIAL DEPOSITS OF IgG AND C3 ALONG BASEMENT MEMBRANE SEEN IN "SPIKE AND DOME" PATTERN ON SILVER STAIN. focal glomerulosclerosis. NORMAL ASO TITERS. ANA +VE. RENAL BIOPSY: DIFFUSE GLOMERULAR INVOLVEMENT WITH THICKENED CAPILLARY WALLS AND LOBULAR MESANGIAL PROLIFERATION ON LIGHT MICROSCOPY. VDRL +VE. TREAT WITH STEROIDS AND RENAL TRANSPLANT. #7: MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS Idiopathic. SHE IS HYPERTENSIVE WITH BUTTERFLY RASH OVER MALAR AREA. UA/ PROTEINURIA. RENAL BIOPSY: DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS WITH IMMUNE COMPLEX DEPOSITS TYPICALLY SUBENDOTHELIAL AND FORMING "WIRE-LOOPS". HYPERTENSION 140/110. PE: PERIORBITAL EDEMA. SHE ALSO HAS HEMATURIA. Case: 11YO WHITE FEMALE BROUGHT BECAUSE OF HEADACHE. NO EVIDENCE OF PLEURAL EFFUSION/ASCITES. ANA-VE. HYPOALBUMINEMIA. ELEVATED BUN AND C. IF: PROMINENT MESANGIAL AND SUBENDOTHELIAL DEPOSITS OF IMMUNE-COMPLEXES. TREAT WITH STEROIDS AND CYCLOPHOSPHAMIDE/AZATHIOPRINE/CHLORAMBUCIAL. LONG-TERM HEMODIALYSIS OR TRANSPLANT. ANTI-DS DNA +VE. AND LOSS OF HAIR. 50% progress to renal failure. HYPOALBUMENIMA. PROGRESSIVE SOB. It may be associated with inherited diseases of complement components and partial lipodystrophy. NO PAST MED H/O. HYPOCOMPLEMENTEMIA.

#10: PRIMARY AMYLOIDOSIS Primary Amyloidosis commonly presents with nephrotic syndrome. followed by activation of complement leading to inflammation.H/O. U/A: PROTEINURIA. or secondary (Rheumatoid Arthritis. uremia. Case: 5YO MALE PRESENTS WITH MALAISE. It is the most common childhood nephritis and affects preschool and school-age children. MACROGLOSSIA. C3 AND TOTAL COMPLEMENT CH50 LOW. LEUKOCYTOSIS. Pathogenesis may be related to the deposition of strep antigen-antibody complexes in the glomeruli. DNASE TITER HIGH. CXR: BIVENTRICULAR CARDIAC ENLARGEMENT. and chronic glomerulonephritis. Amyloidosis may be primary (monoclonal Ig light chains). Treat Renal and Cardiac Failure with peritoneal dialysis. ACE-I REDUCE PROTEIN LOSS. INCREASED ASO TITER. #11: RENAL TUBULAR ACIDOSIS It results from: . Diet high in carbohydrates and low in protein. ANEMIA. HYPOPROTENEMIA. CBC. potassium and water. H/O THROAT INFECTION TEN DAYS AGO FROM WHICH HE REOVERED UNEVENTFULLY. ABG'S=METABOLIC ACIDOSIS.MED. sodium. SMOKY COLORED URINE (HEMATURIA). convulsions. Tuberculosis. LABS: HYPERLIPIDEMIA. CASE: 45YO WHITE FEMALE COMPLAINS OF PALPITATIONS AND SOB. AND MILD FEVER. and scarlet fever. RENAL BIOPSY: APPLE-GREEN BIREFRINGENCE IN POLARIZED LIGHT WHEN STAINED WITH CONGO RED. LEADING TO NARROWING OF LUMEN AND ISCHEMIA. PE: MILD CARDIOMEGALY. ASCITES. IF: GRANULAR PATTERN OF Ig DEPOSITION. ANKLE EDEMA. Treat with Penicillin for 10 days to prevant spread of nephrogenic strain (erythromycin if allergic). RENAL BIOPSY: ELECTRON-DENSE HUMPS ON THE EPITHELIAL SIDE OF THE GLOMERULAR BASEMENT MEMBRANE.TREAT WITH STEROIDS. Multiple Myeloma. NO P. it occurs 10-14 DAYS AFTER URI. severe headache. #9: POST-STREPTOCOCCAL GLOMERULONEPHRITIS: It's an immune complex disease that is usually caused by beta-hemolytic streptococcus type 12 and 49. ANA -VE. CYCLOPHOSPHAMIDE. INCREASED ESR. visual disturbances). U/A RBC'S AND RBC CASTS. ABDOMINAL PAIN WITH VOMITING. HYALINE THICKENING OF ARTERIOLAR WALLS. AMYLOID DEPOSITION IN MESANGIUM AND ENDOTHELIUM SURROUNDING HEPATIC SINUSOIDS AND IN SPLEEN. AND BUN/C. EKG: LOW-VOLTAGE. acute pulmonary edema. Complications: Cardiac Failure. Occurs after URI. WITH NUMBENESS OF THE LOWER LEGS TOGETHER WITH WEIGHT LOSS AND FATIGUE. skin infections. AND ARMS/LEGS. TONSILS CRYPTIC BUT NO EXUDATE. Resolution may take 6-12 months. PERIORBITAL EDEMA. Hypertensive Encephalopathy (vomiting. Pregnancy where it's beta2microglobulin). AND CARDIAC ARRYTHMIA. PROTEINURIA. PE: HTN. PITTING EDEMA. MORNING SWELLING OF THE EYES.

Urine pH>5. whereas Type I get Kidney Stones. and it is seen in patients with renal insufficiency and chronic medical illnesses such as DM with nephropathy. .Type IV: Aldosterone Deficiency of any cause. lab evidence of primary hyperchloremic hyperkalemic metabolic acidosis.: Sjogren) or drugs (Amphotericin. If RTA I. Patients may require higher doses because of resistance. CHRONIC HEPATITIS. HTNm and AIDS. normal anion gap. which should lower urine pH secondary to increase H+ production.Diagnosis: Bicarb Loading Test . tubular interstitial renal disease. Amyloidosis Myeloma.Treat with potassium. VIT D DEFICIENCY. SERUM BICARB 1820. . weakness. which normally stimulate Aldosterone secretion. Acidosis usually corrects as soon as hyperkalemia contributing to decreased ammonia production.Type III: Supressed renal generation of ammonia secondary to reduced GFR. Renal Insufficiency. Loop diuretics and exchange resins can also be used. DIAGNOSIS: ACID LOAD TEST: Give ammonium chloride. Type IV is the most common. and exclusion of presence of diarrhea.g.Inability to absorb bicarb. Give thiazides and very large amounts of bicarbs. Sickel Cell. . . Also with drugs: ACE-I. NSAID's and HEPARIN.TypeI: Deficient H+ secretion in the distal tubule. paresthesias. ETIOLOGY: Fanconi Syndrome. Addision. Urine pH remains elevated. leading to inadequate excretion of the acid load. .. Sjogren).Diagnosis: ORAL SALT RESTRICTION => CON'T HIGH URINE SODIUM. Mild volume depletion enhance proximal reabsorption of bicarb. TREAT WITH ORAL BICARB (proximal tubule reabsorption still works)AND POTASSIUM REPLACEMENT. The resulting hyperkalemia decreases proximal tubule ammonia production and reduces H+ secretion. Can be secondary to auto-immune disease (e. This results in defective secretion of both potassium and H+ in the distal nephron. There is Nephrocalcinosis and Nephrolithiasis.Etiology: Diabetes.Type II: Defective bicarbonate reabsorption in the proximal tubule. or Adrenal Insensitivity to Angiotensin II. Lithium. Normal individuals do not excrete bicarb until serum >24. . . CHRONIC HYPOCALCEMIA. calcium chloride. or other (Nephrocalcinosis. is corrected. . zero/positive urine anion gap. and Chronic Infection). These patients secrete it but do not reabsorb it. So they are also Acidemic. . HEAVY METALS. Treat by restricting potassium. Complications: metabolic acidosis. or other acids. RTA is ALSO diagnosed by asymptomatic hyperkalemia. hyperkalemia (confusion. Analgesics). Both are hypokalemic.IV sodium bicarb = ph urine still basic. Mineralocorticoid replacement with Fludrocortisone usually improves hyperkalemiaand acidosis but may worsen HTN.4. Secondary Hyperaldosteronism and HYPOKALEMIA. These patients produce acidic urine despite reduced H+ secretion because of inadequate ammonia to buffer the protons in the distal tubule. AUTOIMMUNE DISEASE (SLE. Serum Bicarb is 10. Wilson Disease. HEPARIN). . Sickle CEll Disease. Urine pH is basic HYPOKALEMIA.BONE LESIONS (OSTEOMALACIA and RICKETS). ACE-I. and D/C aldosterone antagonists drugs (NSAIDS.

ACE-I also have been used successfully to further slow progression.Order Ultrasound: which in contrast with usual shrunken small kidneys of End-Stage Renal Disease. Heroin Associated Nephropathy. Corticosteroids have also been used but with caution because of the advanced stage of AIDS already for the patient. and even cardiac arrest). ELEVATED BUN/C. LABS: HYPERKALEMIA.First Aid Step 1 Causes of Abdominal pain in Different Quadrants Causes of abdominal pain in different quadrants: . Hemodialysis should also be started. massive proteinuria in the nephrotic range with little to ne edema .. URINARY ANION GAP+VE. Pathophysiology. HE IS CURRENTLY ON ACE-I. It not only slows the progression but may in fact reverse it.Labs: Uremia. . LETHARGY.Confirm with Renal Biopsy: FOCAL SEGMENTAL GLOMERULAR SCLEROSIS is the most typical one.Patient may present with Uremic Encephalopathy with confusion. DM WAS POORLY CONTROLLED DESPITE INSULIN AND ORAL AGENTS. kidneys are ENLARGED!! . Olatinwo. AND RHEUMATOID ARTHRITIS PRESENTS WITH A DECLINE IN MENTAL STATUS AND DECREASED URINE OUTPUT. DIFFERENTIAL: DIABETIC NEPHROPATHY WHICH SHOULD BE TREATED WITH ACE-I AS OPPOED TO TUBULAR ACIDOSIS WHERE THEY HAVE TO BE D/C'ED. arrythmias. Internal Medicine . CALICUM CHANNEL BLOCKER FOR HTN. AND TAKES NSAIDS FOR PERSISTENT RA.UNDERGROUND CLINICAL VIGNETTES: Pediatrics. in HIVAN.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. Management: Antiretroviral Therapy is the most important feature. THIAZIDE. U/A URINE PH ACID<5. Of note: Encephalopathy is a sign of rapidly changing nephro status either deteriorating ir improving (encephalopathy on first hemodialysis = Dialysis dysequilibrium Syndrome). HYPERCHLOREMIA. #12: HIV-ASSOCIATED NEPHROPATHY HIV associated Nephropathy Pearls (HIVAN) . MD 8/2002 . CASE: 73YO MALE WITH ADULT ONSET DM FOR 30Y. and if the patient is white. think of other diagnoses) . HTN. REFERENCES: . Ross G.5.paralysis. new-onset seizure (Management of seizure with subsequent treatment using phenytoin).Kaplan notes . HE HAS HAD OCULAR DISEASE AND RENAL INSUFFICIENCY FOR >5Y. Hewitt. that in the absence of renal biopsy. asterixis etc.Mostly African Americans (So and so. MD. Differential: Hep B and Hep C associated nephropathy. ABG: NONANION GAP METABOLIC ACIDOSIS. PE: HTN.

LUQ: Spleen and structures around it. colon-splenic flexure LLQ: Sigmoid colon.Gallstone colic Duodenum-ulcer (on exams.Lower lobe pneumonia. . Given Meoclopramide. Confusion. pancreas.occurs with Pseudomonas and Clostridium septicum with approximately equal frequency. Weight loss Reference: CMDT Question Diabetic for many years. Perihepatitis(eg Fitz-Hugh-Curtis syndrome-chlamydia or gonococcus).think of Zolinger Ellison) Lung base. Orient youself with the differential above and study each condition on CMDT . has Nephrotic/paroxysmal nocturnal hemoglobinuria). Encourage fiber in diet.For differential diagnosis purposes let us see the abdomen in 4 anterior quadrants and the left and right flanks. Stomach.calculous or non calculous(esp in pt in ICU or on cephalosporins) cholecystitis. 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. It's beyond the scope to talk about each one regarding each diagnosis. Fatigue.red degeneration. Appendix-Appendicitis-acute or chronic Caecum-Typhilitis esp in post chemotherapy patient . Switch dugs to which one? Erythromycin. Budd chiari(esp if pt. Side effects of interferon therapy in Hep C: Is it depression or irritability or hallucinations or delirium. Tuboovarian abscess(PID) GIT-rarely diverticulitis(usually occurs on left side). fibroid. ECTOPIC pregnancy.especially diverticulitis that is seen in elderly population and is treated with antibiotics.cyst rupture or torsion.re looking for answer using the least invasive most cost effective procedure. DEPRESSION Reference: Acute hepatitis C: response to treatment with interferon-alpha plus ribavirin Gastroenterol Hepatol. Developed Tardive dyskinesia despite reducing dosage. Spleen. Uterine structures-as in LLQ area.25(8):483-6. ERCP when you want to investigate the Common Bile Duct rather than the gallbladder. Gall bladder. Abdominal Us is almost always right answer is you. They're pretty good about this. Others: Anorexia. RUQ-perihepatic structures Liver. Developed Autonomic neuropathy of gastroparesis. 2002 Oct. ruptured hepatic adenoma(young female on oral contraceptives). hydration-PO or IV and stool softening. Somnolence. Ovary.hepatitis. hepatic trauma.

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 .. 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. No known etiology has been found for this pain despite an intensive metabolic. History typical of hypochondriasis but what differentiates is the obvious secondary gain.. . or kids at mom's. Body dysmorphic disorder B.. and endocrine evaluation. . Refernce: CMDT Question A 20-year-old woman has a history of repeated admissions for sudden abdominal pain.like the OR. 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. OR HOW MANY MORE CASES WERE ATTRIBUTABLE TO SMOKING. and the conclusion after the end of the study were asked.. RR attributable risk.INCIDENCE IN NON EXPOSED GROUP => MEANS HOW MANY MORE CASES WERE THERE OF LUNG CANCER IN SMOKERS COMPARED TO NON SMOKERS. Which of the following is the most likely diagnosis? A. like the values were given.Improves gastric emptying by binding to motilin receptors in stomach. Extensive imaging and laboratory studies are all normal.. Malingering Factitious disorder. the patient is relaxed. WHAT ARE THE ODDS . What if it is constipation? Laxatives such as senna... Now on the inpatient floor.IN CASE-CONTROL STUDIES: ODDS RATIO = ODD OF EXPOSURE FOR CASES/ODDS OF EXPOSURE FOR CONTROLS = AD/BC => IF YOU HAVE LUNG CANCER. She comes to the emergency department complaining of similar pain and is admitted to the hospital for management. What if it was Diarrhea in Autonomic Neuropathy setting? Ans: Often self-limited but use broad-based Antibiotic therapy. or Demerol addiction). Conversion disorder C. Answers to some BIOSTATS MCQ's there were lot os interpretation qs of case control and cohort studies. infectious..PPV senstivity and specificity. It is of psyhological nature (20yo singe mother needs attention. Hypochondriasis E. If not responding => associated with impaired sphincter control and fecal incontinence : Use Loperamide QD or Combination Diphenoxylate/Atropine. Factitious disorder D. The patient has also had repeated imaging studies of her abdomen and 1 exploratory laparotomy. and then there were various options to interpretation.

there is 30-fold likelihood the woman HAD a pre-gestational diabetes. The attributable risk is happens in cohort studies not crosssectional. #2.520/600 D. what is the attributable risk? Interpret it in a sentence. = J = approximately 2. #3.5 cases. #2: I.520/695 B. malformation.600/1000 c. what is the relative risk? Interpret it in a sentence.Assume the table is a cohort study. It's in the past because the study is retrospective case-control.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.Incidence of nonexposed = approximately 0.Assume the table represents a cross-sectional study. it cannot be determined. Choices: A. Q: Match with the correct value: ------------Disease------Well Exposed------520----------175-----------695 Non exposed---80----------225-----------305 -------------600----------400----------1000 #1. It means if the baby has a feta.Cannot be determined by this type of study J. but the relative and attributale risk (see below). With that said.87 .(520x225)/(175x80) H.(520/695)/(80/305) Ans: #1: H => Incidence of exposed .695/1000 E. Let's assume it's a cohort. the risk factor exposed to in this study accounted for 0.80/305 F. what is the odds ratio? Interpret it in a sentence.(520/695)-(80/305) I. If it were prospective. then we would not use the Odds ratio. The relative risk is = Incidence of Exposed/ Incidence of non exposed.Assume the table represents a case-control study.5 Incidence of exposed= New/Total = 520/695 Incidence of non exposed = New/total = 80/305 Of every thousand cases observed.(520/695)(80/305) G.

PREVALENCE = PERSONS WITH DISEASE/PERSON AT RISK => HOW MANY EXIST AT A GIVEN TIME . However if it is positive. the question to ask is is it a True positive or a False Positive? That's the PPV of a test.SENSITIVITY = TRUE POSITIVES/ALL SICK (tp+fn) => How often is the test positive in patients who have the disease. If a test has a specificity of 100%.SPECIFICITY = TRUE NEGATIVES/ALL WELL (tn+fp) => How often the test is negative if people who do NOT have the disease. we still don't know if it is True Postive or False Positive.87 more likely to develop the disease IN THE FUTURE than non exposed people. 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. sensitivity is for screening random asymptomatic people. IN SCREENING TESTS: #1: In general population screening where the prevalence is low: . it confirms the disease. What happens to Incidence and Prevalence? Ans: Incidence is unchanged. that means it has no false positives. If test X retunrs positive in a person who is randomly selected in this population under study.t say anything if it is negative.It means people exposed to the risk factor studied are 2. If a test comes back negative. that means.INCIDENCE = PERSONS WITH DISEASE ONSET/PERONS AT RISK => HOW MANY NEW CASES. Prevalence increases. IN DISEASE STATISTICS: . #3: G . . Therefore. It would be easier to redistribute the information in a visual way.Odds ratio=AD/BC = (520x225)/(80x175)= approximately 8. that means it has no false negatives. what is the percent chance that the person has SLE? Ans: In other words.NEGATIVE PREDICTIVE VALUE = TRUE NEGATIVES/ALL NEGATIVES. If it is positive. If it is negative. they're asking for the Positive predictive value.36 This means the odds of having a history of exposure IN THE PAST to the risk factor is 8. you ask yourself is your negative a true negative or a false negative? Of course if it is a test with 100% sensitivity. ------------------------------Test+ve------Test(-ve) Patients with SLE--------------TP60--------FN40 . it rules out the disease. the Positive Predictive Value will always be 100% too because there is no False Positives. . If a test has 100% sensitivity. But it still doesn. Q: A recently dicovered treatment for leukemia extends the lifespan but does not prevent the diseas or lead to its cure. we resort to positive and negative predictive value. For both those reasons.36 times greater in those who have the disease than in those who do not.POSITIVE PREDICTIVE VALUE = TRUE POSITIVES/ALL POSITIVES => HOW POSITIVE IS A POSITIVE? When a test returns positive. If the test has 100% specificity. #2: In clinical settings where prevalence is higher: . then there are no false negatives and therefore NPV=100% too. if it is a True Negative or False Negative.

THAT'S THE HYPOTHESIS WE WANT TO TEST. HOWEVER.Control Population-------------FP20--------TN80 Totals---------------------------80---------120 Now we see it clearly. P VALUE IS PART OF WHAT WE CALL INFERENTIAL STATISTICS. THERE IS INCREASED RISK. .ACCURACY VS PRECISION: ACCURACY (also called Validity) IS HOW CLOSE TO THE NORM. WE NEED TO KNOW IF WE .STATISTICAL SIGNIFICANCE: RELATIVE RISK AND CONFIDENCE INTERVAL (THIS ONE I LEARNED IT LIKE THIS)=> IF THE RELATIVE RISK CONTAINS 1. CHOOSE A SAMPLE AND GET RESULTS OF A STUDY. WE WILL EITHER CONFIRM IT (ACCEPT IT) OR DENY IT (REJECT IT).EXTRAPOLATE OR IF OUR RSULTS WERE ONLY OBTAINED BY CHANCE. IT MEANS OUR RESULT IS ACCURATE AT A 95% CONFIDENCE IF P-VALUE IS 0. . IF IT IS AT 1SD. THEN IT'S NOTSTATISTICALLY SIGNIFICANT. THEN WE HAVE REJECTED OUR GOAL. SINCE IT IS IN REAL LIFE EASIER TO REJECT THAN TO ACCEPT. IF IT'S BELOW 1.ACCURACY = TRUE POSITIVES + TRUE NEGATIVES / ALL => HOW MUCH PERCENT IS THIS TEST ACCURATE? . A TEST COULD BE PRECISE (REPRODUCIBLE) BUT NOT ACCURATE. THATS WHY WE CHOOSE THE CONFIDENCE INTERVAL WHICH IS THE P VALUE. SO BEFORE WE START OUR STUDY. WE HAD ALREADY DISCUSSED AT LENGTH THE PERCENTILES WITH REGARDS TO THE MEAN. oUR NULL HYPOTHESIS IS "SMOKING DOES NOT CAUSE CANCER"... WE WOULD INSTEAD OF STUDYING THE ENTIRE POPULATION OF THE EARTH.G: SMOKING CAUSE CANCER.. WE WILL MAKE THE START POINT HYPOTHESIS (NULL HYPOTHESIS) THE OPPOSITE OF WHAT WE WANT TO PROVE.0 VALUE IN ITS CONFIDENCE INTERVAL. which is why we use the PPV.0. WE WILL DO A STUDY AND REJECT IT WITH A P VALUE OF 0.. BUT THEN AGAIN. TP/TP+FP = 75% . THE IDEAL WOULD BE IF A TEST COULD BE BOTH. IT MEANS WE LEFT 5% CHANCE FOR PURE COINCIDENCE TO HAVE BEEN THE CAUSE OF OUR RESULTS. WE DECIDE WHAT IS OUR STATEMENT? E.0. THEN WE HAVE PROVEN OUR GOAL.5 (5%).ANOTHER NOTION IS THE P-VALUE. IT IS THE 84TH PERCENTILE. also there was some q about interval analysis which my friend said that he did not understand at all.CAN.5 (ONLY 5% CHANCE OUR . It is a population with a 50% pervalence (100 controls and 100 sick with total 200). A TEST COULD ALSO BE ACCURATE BUT NOT PRECISE. PRECISION (or reliability) IS HOW CONSISTENT AND CLOSE TOGETHER THE RESULTS OF THE TEST ON THE SAME PERSON IN THE SAME CONDITION WOULD BE. IT IS SO CONFUSING COMTIMES BUT KEEP IN MIND THESE NOTIONS. IF WE ACCEPT IT (IN THE STATISTICIANS LANGUAGE THEY SAY "FAIL TO REJEC" INSTEAD OF "ACCEPT"). CONVENTIONALLY. THERE IS DECREASED RISK. IF IT'S ABOVE 1. IF WE REJECT IT. SO FOR THE EXAMPLE OF "SMOKING CAUSES CANCER". WE WOULD CALL IT HYPOTHESIS ZERO OR NULL. THEN EXTRAPOLATE AND DRAW CONCLUSIONS ABOUT THE ENTIRE POPULATION OF THE PLANET.

Blood pressure difference is clinically significant B.:P VALUE OF 0. This difference is significant at a p value less than 0.RESULTS OF REJECTION OCCURED BY RANDOM COINCIDENCE).. p value is part of inferential statistics and merely reflects if a result occured by chance or not..Type II error C.% OF PATIENTS WHO WILL BENEFIT . What type of error did the resreacher make? A. To increase the power of a test.05.important to know about minors and when they can make decisions on there own and when they need parental consent.5 WHAT P VALUE DOESNT DO: .05 C. WE WILL ACCEPT OUR ALTERNATIVE HYPOTHESIS WHICH WAS WHAT WE WANTED IN THE VERY BEGGINING WHICH IS" SMOKING CAUSES CANCER".. you need to increase the sample size. Which of the following statements about the two groups is true? Which of the following is true? A.Increasing the number of subjects would tend to change the p value from significant to non-significant.TELLS STATISTICAL SIGNIFICANCE = STATISTICALLY SIGNIFICANT AT P VALUE=0. The chance to do that is set by the criterion alpha (with is the same as p-value). THIS ACCEPTANCE WOULD BE AT 95% CONFIDENCE (I. Ans: C. 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.Type II error D. It can't tell if patient can benefit from salt diet or not and to what degree.05 => Chance of Type I error is 5%. A cancer researcher conducted a medical experiment and failed to reject the null hypothesis although the experiment was successful.An inferential error Ans: B.5).It is unlikely that random variation accounted for the difference in diastolic blood pressure between the two groups D.DEGREE OF BENEFIT EXPECTED.NO TELLING IF AN INDIVIDUAL WILL BENEFIT (SEE BELOW) . IN DOING SO.The chance that an individual would benefit from a low-salt diet is less than 0.QUANTIFIES CHANCES FOR ERROR (5% CHANCE IT'S AN ERROR = BY RANDOM) . if Pvalue if 0.P-VALUE IS A CRITERION FOR MAKING DECISIONS ABOUT THE NULL HYPOTHESIS (SEE ABOVE)= ACCEPT OR REJECT .. Beta = 1-Power Power of a test is the capacity to detect a difference when it exists. . Q. he had 5-6 qs on ethics which were standard. Type I error (Alpha) is rejecting the null hypothesis when it actually true.E.Type I error B. SO: .An experimental error E.Type II error is failing to reject the null hypothesis when it is actually false.

then radionuclide scan. References: .html what is Purtscher's retinopathy? Barter's syndrome? Purtscher Retinopathy: is a hemorrhagic and vasoocclusive vasculopathy. It appears on the fundoscopy as cotton-wool spots around the optic nerve (ie.Aldosterone levels are elevated. If it is thyrotoxic.Kaplan notes .aafp. Hyperuricemia and hypomagnesemia may occur. If it is non-functioning. If it is indterminate or clinical suspicon. then you treat with radioiodine or surgery.K. . Inheritance is autosomal recessive.NMSR Tests . you do a FNAC as well. Subtotal Thyroidectomy only in 2nd trimester pregnancy or in children. If it is malignant.). If it is bening. and intraretinal hemorrhage. repeat FNAC in 6 months. . There is usually no provem treatment for it except that of the underlying condition (Pancreatitis.org/afp/20030201/559.ALREADY DISCUSSED PREVIOUSLY IN THE FORUM.High Yield Biostatistics Complete Approach Thyroid Nodule First: TSH. Clinical features present in infancy or childhood and include anorexia. then thyroid lobectomy. The kinin-prostaglandin axis is stimulated. and vasculitic diseases. but then described with a number of conditions such as acute pancreatitis. and chest compression. If you do the thyronuclide scan.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. fat embolization. and it is a "hot" nodule. and urinary excretion of prostaglandins and kallikrein is increased.Metabolic alkalosis often develops. Aetiology is unknown. retinal microinfarcts at the level of the nerve fiber layer). you skin the Radionuclide scan because it is contraindicated in pregnancy. This results in the follinwg: . Barter Syndrome: A syndrome characterised by deranged NaCl transport in the ascending thick limb of the loop of Henle and the distal tubule. It usually occurs in children and growth retardation is frequently associated. Platelet aggregation is inhibited. Sundden Bilateral Painless blindness first associated with severe head or blunt thoracic trauma. . If it is "cold". then it is FNAC. Na. REFER TO PREVIOUS QUESTIONS LABELED ETHICS. and Cl wasting contributing to the stimulation of renin release accompanied by juxtaglomerular cell hyperplasia.K depletion is not eliminated by correction of the hyperaldosteronism. failure to thrive. then Surgery with Radioiodine. . it should warrant investigating a battered child syndrome with intracranial hemorrhage (Subdural). etc. trauma. SLE. polydipsia. polyuria and muscle weakness. Reference: American Association of Family Physicians Thyroid nodules Feb 2003 http://www. amniotic fluid embolization. In a child. . Mental retardation may be a feature. Obviously.

#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).09%. the urinary chloride is usually low (< 20 mmol/L).In adult patients. SEVERE HYPOKALEMIA. CHOICE OF ANTIRETROVIRALS DEPENDS ON THEIR TOXICITY AND UNDERLYING CONDITIONS OF PATIENT. bulimia nervosa. Indomethacin 1 to 2 mg/kg/day usually maintains the plasma K level close to the lower limit of normal. each of which has been included in recommended regimens that include ZDV. didanosine (ddI). or indomethacin will correct most features. an ACE inhibitor. 12 MONTHS FOLLOWUP IS ON AN AS-NEEDED BASIS. 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. FOLLOW-UP IS 6 WEEKS. NO DATA ABOUT TERATOGENICITY OF ANTIRETROVIRALS EXCEPT EFAVIRENZ IN ANIMALS. but no drug completely eliminates K wasting. nelfinavir (NEL) was approved for use by FDA and is now included in regimens recommended for the treatment of primary HIV infection. tHIRD AGENT CAN BE INDINAVIR AS PREVIOUSLY RECOMMENDED OR MORE RECENTLY NELFINAVIR. triamterene. and protease inhibitors (PIs). or surreptitious diuretic or laxative abuse must be excluded as a cause. an estimated 95% seroconverted within 6 months after the exposur. MORE ON THE SUBJECT: Risk: The average risk for HIV transmission after a percutaneous exposure to HIV-infected blood is approximately 0. nonnuceloside reverse transcriptase inhibitors (NNRTIs). Since the 1996 PEP recommendations were published. PREGNANCY SHOULD NOT PRECLUDE SAME RECOMMENDATIONS. 12 WEEKS AND 6 MONTHS. IF UNCLEAR WHAT TO START WITH ZDZ/3TC IS A GOOD START SINCE 3TC (lAMIVUDINE) IS GOOD FOR ZDV RESISTANCE. Postexposure Prophylaxis to HIV-Patient (Source: CDC) SUMMARY AND USMLE TAKE HOME MESSAGE: TESTING AND PEP ARES RECOMMENDED ASAP AFTER EXPOSURE. Antiretrovirals in prophylaxis: Several antiretroviral agents from at least three classes of drugs are available for the treatment of HIV disease. and Metabolic alkalosis. In summary: Child with growth delay. In these conditions.3% and after a mucous membrane exposure is 0. who presents with normal BP. Antiretrovirals in pregnancy: ZDV appears safe and well tolerated in both women and their infants who have had a . OTHER AGENTS ARE AVAILABLE. and zalcitabine. Think of Bartter syndrome. vomiting. K supplementation plus spironolactone. #3: The addition of a PI as a third drug for PEP following high-risk exposures : Previously. amiloride. #1: ZDV (an NRTI) is the only agent shown to prevent HIV transmission in humans. These include the nucleoside analogue reverse transcriptase inhibitors (NRTIs).

at 6 weeks.. and medical evaluation regardless of whether they receive PEP. 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. IDV or NEL).follow-up period of several years. They have antimuscarinic effects which would contribute to an atropinelike effect of psychosis. Checking Free T3 and T4 (mostly T4) would show normal range. his skin is dry &pupil dilated What is the drug a)amitriptyline b)atropin c)risperidone d)Imipramine Ans: Tricyclics. and 6 months). No treatment is necessary except for tht of underlying chronic illness. T3 and T4 total are low.htm Updated March 2003 "atropin psychosis” in is old men? A 72yr. but TSH is slightly high. usually a PI (i. Choice of agents: Most HIV exposures will warrant only a two-drug regimen. Postexposure follow-up: HCWs with occupational exposure to HIV should receive follow-up counseling. I HAD VERIFIED IT.advice abortion SWITCH TO PHENOBARBITAL. IF CHOICE IS GIVEN NOT TO STOP DRUG (STICK WITH PHENYTOIN). The use of PIs in HIV-infected persons has been associated with hyperglycemia. but for purposes of USMLE: Setting = Chronic illness (very sick patient). HIV-antibody testing should be performed for at least 6 months postexposure (e.e. epileptic woman want to have a baby. usually ZDV and 3TC. So I would go for that one what is "sick euthyroid syndrome?" It's a much talked about syndrome still being investigated. The one that has most antimuscarinic is imipramine which is why it is used for Urinary incontinence and Enuresis along with desipramine.gov/mmwr/preview/mmwrhtml/00052722.cdc. a.change to valproicacid 4.. Reference: http://www.). it is unknown whether the use of these agents during pregnancy will exacerbate the risk for pregnancy-associated hyperglycemia. Amiodarone etc.g. using two NRTIs. 12 weeks. old man brought to er and complained of both auditory & visual hallicination on ph/exa. IF CHOICE IS GIVEN TO STOP PHENYTOIN FIRST TRIMESTER (AND NO OTHER CHOICE LIKE IN THIS CASE TO SWITCH TO PHENOBARBITAL). ON THE OTHER HAND. or tuning the dosage of medication (Lithium. postexposure testing. .stop phenytoin in first trimester of pregnany b. The addition of a third drug. with not many symptoms as far as hypothroidism.change to Phenobarbital 3. what to do? She is on phenytoin. TAKE IT.

If pregnant: ERH higher doses same period as PZA and Streptomycin are contraindicated). IV. then Amox/Clavulanate. Pentamidine or Atovaquone if sulfa resistant. CD4<200. Add Vit B6 with INH use. If h/o of MRSA: Vanco. Elderly). Ds with physical examination (bulging tympanic membrane in setting of ear pain and fever and decreased hearing).Typical: Strep Pneumoniae (rusty sputum). O2 Sat <94%. then RH twice Qweek x 7months. If resistance is a concern: ERH x 9months. COMORBIDITY. Best initial therapy: AMOXICILLIN. Alcoholics => 3rd Cephalo. H. II. ). Atovaquone for prophylaxis if G6PD deficient). immunocompromised esp T cell. or zosyn (Piperacillin/tazobactam) PNEUMOVAC if increased susceptibility. If PCN allergy: azithromycin or clarithromycin. Ampicillin if Listeria suspected (Neonates. If recent Amoxicillin use. Accompanying Diarrhea). If TB meningitis. Dapsone for prophylaxis is sulfa resistant. IF HOSPITAL ACQUIRED (after 5-7days inpatient) : GNB Resistant: 3rd Cephalo (Ceftazidime/Cefotaxime). Southwest desert => Fluconazole or Itraconazole. Neisseria Meningitides in adolescents. then Heamophilus Influenzae. Cold Agglutinins). (Ceftriaxone or cefuroxime) + erythromycin or doxycycline. Chlamydia 3. FIRST STEP = CXR. DHA. One dose before 65yo. Cattle. ERH (increased doses) for 48weeks. LP. Pneumonia: 1. Moraxella 2. Empirically: Ceftriaxone or cefotaxime.Other: PCP (HIV. Give antibiotics prior to CT scan. Same as in bronchitis and sinusitis. and Moraxella Catarrhalis. and another one after. Q Fever (Coxiella Burnetti. III. Meatpacking. Meningitis:: Strep Pneumoniae most common in adults. Flu and Strep B in neonatal.Atypical: Legionella (older smoker. Chlamydia Psittaci (Birds). Staph Aureus in neurosurgery. Mycoplasma (Bullous myringitis. Otherwise. Endocarditis. Tuberculosis: . Then Sputum if indicated. HSMG. Coccidiomycosis (Arizona. ADMIT IF: HYPOXIA (pO2<70.Pregnant and lactating woman: PZA and Streptmycin CI.Viral 4. Inpatient: Fluoroquinolones alone if it’s CAP (Levo-Moxi-Gati) /or /3rd Cephalo. Listeria. There is no treatment currently proven for viral/aseptic meningitis. water source. Breastfeeding is not contraindicated despite presence of small .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. Otitis Media: Strep Pneumoniae most common. RR>20-24). Hepatitis => Doxycycline). Cryptococcus in HIV. Heamophilus (smoker COPD). Or new Fluoroquinolones. treat with ERHZ or SRHZ for 2 months then RH for 7 months (total 9 months.HIV negative: ERHZ or SRHZ for 2 months then RH for 4 months . CT of scan if Papilledema. Outpatient: Azithromycin or Clarithromycin. or no response. If life threatening = Amphotericin B). Klebsiella (Current Jelly. carbapenems. Bronchoalveolar Lavage => Bactrim. If Cryptococcus suspected: Amphotericin B followed by fluconazole therapy lifelong.

Latent TB: targeted testing to identify candidates. think Entamoeaba Histolytica. If Pregnant or lactating: INH QD or BID + Vit B6. Shigella (HUS). Steriod therapy prevents cardiac constriction and neurologic complications from meningitis.g. E. Infectious Diarrhea: . . weight loss. V. If immunocompromised. alcoholic. 2) RZ x 2 months. Coli (HUS). . Vulnificus (if seawater contamination and underlying liver disease) . Rotavirus second. Three regimens are considered: 1) Ideally: INH for 9months. Coli most common. along with RUQ pain and Jaundice. Give Vit B6 if at risk to develop neuropathy (Pregnant.Ship diarrhea => Most common Norwalk virus. Difficile. Coli or Shigella.: Healthcare worker with high % of multiresistant TB patients.No blood => Giardia. Yersinia. 3) Rifampin x 4 months (Side Effect: Red Man Syndrome). Also in children. screen for prior TB Rx and current contraindications. . If gas. DM. Perfringens. . . .Acute onset diarrhea with RUQ pain => Yersinia . Viruses. . NEXT STEP: NO BLOOD => WBC in Stools (Methylene Blue Testing) => WBC+ = invasive . CI if immune deficiency/impairement. uremia. .BCG Vaccine: recommended only on individual basis: e. Diarrhea. and contaminated water source. hemolysis and uremia=> Enterohemorrhagic E. HIV. think Giardia.Extrapulmonary TB: 9months with same drugs if miliary.Antibiotic use => C. Coli 0157:H7 . Vomiting and WHEEZING => Scrombroid (histamine reaction) FIRST STEP: Is there blood or not? .Most common agent: CAMPYLOBACTER (Acute in healthy patient. or contaminated water source Giardia or Cryptosporidiosis. Care must be taken if HIV patients on Nonnucleoside RT Inhibitors or Protease inhibitors. bloody diarrhea). MC protozoan with blood = Entamoeba Histolytica . directly-observed TB therapy should be used for all HIV pts.HIV Positive: Same treatment with additional considerations: longer duration. Cryptosporidium. bone. Botulium.amounts of meds in milk. Cyclospora.Blood => Enteroinvasive : Salmonella. If bloody with fever and pain. Rifampin interaction with anti-HIV meds. .Friend rice => Bacillus Cereus .Contaminated shellfish => Vibrio Parahaemolyticus or V.Steriod use in TB Rx: only in TB meningitis and TB pericarditis. bloating.Poultry/Eggs => Salmonella .Camping trip => either Staph aureus if around 4hrs with UGI symptoms. Protozoans. high volume watery diarrhea => Cryptosporidium .Drug-resistant patient: Resistance only to INH => RZ with E or S x 6months or E/R x 12 months. or joint TB. If bone: early surgical drainage and debridement of necrotic bone. Seizure disorder). Others require expert intervention.Undercooked hamburger meat.Immunocompromised and bloody diarrhea => CMV . VitB6 mandatory with INH to reduce side effects. steatorrhea. . Canned food => C. and Campylobacter (Guillain-barre). .Immunocompromised (CD4<50). meningeal.Travler’s watery diarrhea => Enterotoxic E.Pruritic rash. Unrefrigerated meat => C. think Enteroinvasive E. test for HIV.

Serology for Chlamydia or Ligase chain reaction test.Cryptosporidium => Control of HIV with HAART .Giardia => Metronidazole .Primary: Benzathine-Penicillin single dose IM 2. STD’s: A.Scrombroid => Antihistamine . NEXT: US Pelvis (R/O Ovarian cyst or TOA).Ova/parasites: Giardia and Cryptosporidia . . Alternatives: Ciprofloxacin x 3 days or Erythromycin x 7 days. Diagnose clinically along with Gram stain.Campylobacter => Erythromycin .C.Granuloma Inguinale: .Needlestick: HBIg and Hep B vaccine if Hep B.Urethritis/Cervicitis: . Isolate organism in pus of buboes.PID: cervical motion tenderness.C. No PEP for Hep C VII.Syphilis: . Diagnose clinically and rising titers of complement fixing antibodies.E.Chronic Hepatitis C: Interferon combined with Ribavirin . (We add treatment for Chlamydia) . E. Herpes Simplex. .Tertiary: IV Penicillin 10-20 million U/day x10 days . Ureaplasma.Chronic Hepatitis B: Interferon or Lamivudine 3TC. Desensitize first in Tertiary and Pregnancy D.If allergy to penicillin: desensitize or give doxycycline. . TREAT : Azithromycin single dose or IM rocephin single dose. culture and PCR if needed. Hepatitis: . IV Fluids if severe. Trichomonas. B. Laparoscopy is definitive test. Diff => Metronidazole. Diff Toxin in stool TREATMENT: Oral fluid and electrolyte replacement (hypokalemic metabolic acidosis). Culture for Gonorrhea on Thayer-Martin.Stool culture . diplococci coffeebean intracellular.NEXT STEP: .4 million . TREAT: DOXYCYCLINE OR ERYTHROMYCIN F.Non Gonococcal Urethritis: Chlamydia.Secondary: Benzathine Penicillin Q week x 3 weeks same dose . IM Ceftriaxone Single dose and PO doxycycline x7days or PO Azithromycin Single dose. 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.Chancroid: Heamophilus Ducreyi = Gram –ve B. Coli => 3rd Cephalosporins VI. Mycoplasma Hominis.Gonococcal: Gram –ve.

And S Aureus (Bullous impetigo).Non gonococcal: IV Semi-synthetic Penicillin + Genta or 3rd Ceph. Urinary Tract Infections: A. TMP/SMX • Inpatient: IV Quinolones. VIII.DOC = IV Peni 2 million Q4h . BONE BIOPSY AND CULTURE if BCx are sterile TREAT: IV Semisynthetic Penicillin + Genta or 3rd Ceph until culture results obtained. Staph Saprophyticus (Honeymoon cystitis). Klebsiella. Enterococci. Diagnose with Giemsa or Wright stain = Donovan bodies – Punch biopsy if necessary TREAT: DOXYCYCLINE OR TMP/SMX. IV VANCO. TREAT: If blood cultures +ve or facial erysipelas => IV ATBx . Coli. Impetigo/Erysipela: Group A BetaHemol. If mother has disease but no vesicles apparent (not active). Enterobacter. IV ATBx x 6-12 weeks. Clindamycin. If allergic.Cystitis: E. FIRST: U/A (nitrites = Gram –ve) TREAT: • Uncomplicated: 3 days of TMP/SMX or Quinolone • Diabetic: 7 days • Pregnant: Amoxicillin or Nitrofurantoin B. IV Ampicillin/Genta. .If allergic: Cephalexin. then Proteus.Donovania Granulomatis – painless red nodule. OR ERYTHROMYCIN G. Then alter according to . then elevated granulomatous mass in perineal area.Gonococcal: IV Ceftriaxone XII. Septic Joint: FIRST: TAP IT + CULTURE – XRAY TREAT: . vaginal delivery. Healing and scar formation. If Chronic Osteomyelitis: IV x 12weeks then PO x 8-12 weeks.Amoxicillin twice daily for 7 -10 days .Genital Herpes: Herpes Simples II – Tzanck test and culture TREAT: ACYCLOVIR – famcyclovir – valacyclovir. C-section if active disease in pregnant. XI.Pyelonephritis: FIRST: U/A and US to r/o obstruction TREAT: • Outpatient: 10-14 days fluoroquinolones. 3rd cephalosporins IX.If allergic = IV Cefazolin if minor or IV Vanco if major allergy If oral therapy only: . Infective endocarditis: FIRST: Blood Cultures + Transesophageal Echocardiogram TREAT: IV Semi synthetic Penicillin + IV Ampicillin + Genta. If non gonococcal. Osteomyelitis FIRST: X-Ray+++ Takes two to three weeks before we see signs NEXT: Technecium bone scan or MRI NEXT: Blood Culture. or macrolides (Clarithromycin or Azithromycin) are alternatives: X.

Headache. . GIVE PROPHYLAXIS IF: . Encephalitis are managed symptomatically. lymphadenopathy. Fungal etiology. .Fever. and occasionally. persistent bacteremia despite ATBx.DENTAL PROCEDURES: AMOXICILLIN OR CLINDA IF ALLERGIC (azithromycin. or Cephalexin) . Prosthetic valve obstruction. Lyme Disease: . circumcision. Actinobacillus Actinomycetemocomitans.95% recover without intervention. systemic emboli.Bite often not remembered may be missing in the question stem . Transesophageal Echocardiography. may cause maculopapular rash. 8 weeks if it’s prosthetic valve. Splenic rupture => .Symptoms 3-30days after bite. Needs 24h of attachment to transmit borrelia burgdorefri. Intubation. H/O Bacterial Endocarditis. . maculopapular rash.Weeks later: NEUROLOGIC SYMPTOMS – FACIAL PARALYSIS. OTHER: 1) Infectious Mononucleosis: . . LABOR WITH ONLY MVP. MITRAL VALVE PROLAPSE W/O REGURGITATION. MENINGOENCEPHALITIS.Ixodes scapularis (dammini) tick. Recurrence of infection despite ATBx. IF HACEK organisms (Hemophilus aphrophilus.Other: MYOCARDITIS. Congenital Malformation except in ASD only Primum.NO PROPHYLAXIS IN CARDIAC CATH+++. . PERICARDITIS . Flexible bronchoscopy. Self-limited. IV VANCO IF PENI RESISTANT.Bronchoscopy rigid only . Do nothing. TAKE TO OR IF: CHF. Mycoarditis. Kingella Kingae): DOC = CEFTRIAXONE x 4 weeks. SMG.CARDIAC CONDITIONS: Mitral Valve prolapse (WITH REGURGITATION).FIRST: Monospot (heterophil agglutination test) – Atypical lymphocytes on blood smear . XIII. TREAT CARDIAC AND FACIAL PALSY WITH PO DOXY TREAT JOINTS WITH A MONTH OF ORAL DOXY TREAT MYOCARDITIS. Clarithromycin.ERYTHEMA MIGRANS resolving in a few weeks.Months: JOINT INVOLVEMENT DIAGNOSE: Clinical (ERYTHEMA + ONE LATE MANIF) + LAB (ELISA +WB) TREAT MINOR SYMPTOMS WITH DOXYCYCLINE OR AMOXICILLIN. Eikenella Corrodens. and NEURO WITH IV CEFTRIAXONE XIV.Hepatitis. Hypertrophic cardiomyopathy. . Extravalvular infection. Cardiobacterium hominis. Hysterectomy. sore throat. Memory . malaise. If amp/amox given because of Cx+ve for Strep. C-section. Flu-like syndrome.URINARY OR GI PROCEDURES: AMP/GENTA OR VANCO/GENTA IF ALLERGIC .cultures x 4-6 weeks. ASD ostium secundum. Hemophilus parainfluenzae.

5) ANTHRAX: . and generates edema.Complicated cases: ARDS – DELIRIUM – HSMG/JAUNDICE – MYOCARDITIS .Inhalational Anthrax: 10 days after exposure.MUCOCUTANEOUS LYMPH NODE SYNDROME .Prevent with protective clothing.PROPHLAXY AFTER TICK BITE IS NOT CURRENTLY RECOMMENDED.Cutaneous Anthrax within 2 weeks of exposure provokes toxin which impairs neutrophils. High LFT’s . .Transmission: DIRECT INOCULATION OR INHALATION . FLUSHED FACE AND INJECTED CONJUNCTIVA .5mm 4) BOTULISM: Difference between adult and infant botulism: . Steroids in refractory disease.Differentiate from Meningococcemia . The capsule allows host defense evasion.FEVER AND 4 OF: ♣BILATERAL CONJUNCTIVITIS MUCOUS MEMBRANE CHANGES: STRAWBERRY♣ TONGUE desquamation.Adult: ingestion of pre-formed toxin from canned food . First. vomiting => self-limited or may spread with meningitis. . removal of ticks at frequent intervals.B. .IF PREGNANT: CHLORAMPHENICOL.Asian Chilren at higher risk . then painless black eschar. . 3) KAWASAKI Syndrome: .Bioterrorism .g.Naturally occurring: exposure to sheep. horses.TREAT with ASIPIRIN AND IV Ig in high doses.2-14days: Flu-like.TREAT WITH PO or IV DOXYCYCLINE++ .: honey-related = floppy-baby syndrome). Pneumonitis (usual cause of death). CERVICAL ♣LYMPHADENOPATHY . TREAT WITH BOTULINUS ANTITOXIN FROM AUTHORITIES AFTER REPORTING TREAT RESPIRATORY FAILURE WITH INTUBATION AND MECHANICAL VENTILATION.MAJOR COMPLICATION: CORONARY ARTERITIS = 1 OUT OF 4 => AMI .Infant: ingestion of organisms with elaboration or toxin in vivo (e. goats .DIAGNOSE WITH SKIN BIOPSY OR SEROLOGY (not until 2 weeks later) .COUMADIN FOR CORONARY ARTERY ANEURYSMS > 6. Regional lymphadenopathy ++. Anthracis = Gram+ve Bacillus aerobic spore-forming. .Exposure to the woodtick Dermacentor Andersoni EASTERN USA .Emergency Splenectomy 2) Rocky Mountain Spotted Fever: .day 2-6: RASH WRITS AND ANKLES SPREADS CENTRALLY – PALMS AND SOLES+++ . then mediastinitis. then ulcerates.Labs: Thrombocytopenia. . erythematous papule. nausea. erythema)♣EXTREMITY CHANGES (edema. tick-repellant. headache. then vesiculates. Flu-like symptoms.

TREAT: No specific treatment recommendations can be made at this time. GRAM STAIN CUTANEOUS LESION =>BOXCAR SHAPE CAPSULE ORGANISM – CULTURE – PCR . CSF. .CDC . ASSESS PUPIL SIZE.TREAT WITH: DOC = CIPROFLOXACIN X 7-10DAYS (IF NATURALLY OCCURING – 60 DAYS IF BIOTERRORISM).  NO: Respiratory distress? If yes => Suspect case of SARS.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. dysphagia. coffeeground emesis. even bowel perforation.Kaplan notes . Infectious disease consultation is recommended.ADMIT and ISOLATE (Universal Precautions for now) . DOXYCYCLINE = FIRST-LINE ALTERNATIVE. spores germinate in macrophages in lungs or multiply in lymphatics causing hemorrhagic lymphadenitis – overwhelming sepsis.WHO PUPIL SIZE. . including agents with activity against both typical and atypical respiratory pathogens. Catarrhal stage. DIAGNOSE BY ISOLATING ORGANISM FROM NASOPHARYNGEAL CULTURE (Bordet-gengou agar). MANAGEMENT: . recheck in 3 days. and convalescent stage.Within hours. 7) SARS = coronavirus DIAGNOSE: Fever 38deg. AND ACCOMMODATION.Throat Swab for SARS Test – CXR – CBC/Diff – GOT/GPT – LDH – CPK .PROPHYLAXIS AFTER EXPOSURE TO SPORES: SINGLE-DRUG THERAPY. Fever. Can be only oropharyngeal: regional lymphadenopathy. REACTIVITY. sore throat. . References: . rebound tenderness. or Platelet<150K  YES: Respiratory distress? If yes => Suspect case of SARS. Treatment choices may be influenced by severity of the illness. TREAT WITH ERYTHROMYCIN x 10 days. diarrhea. abdominal pain. 6) Whooping Cough: B. . SHAPE. If no => Quarantine but no need for reverse isolation. etc. cervical edema.Add rifampin if inhalational/systemic X 2 WEEKS .CMDT . Pertussis. Imminzation available.GI anthrax: 2-5 days after ingestion. CXR IS FIRST STEP (Mediastinal widening = hallmark). rhinitis. (The parasymp system controls constriction -dilatation is controlled by the symp system. REACTIVITY.DIAGNOSE WITH PLEURAL FLUID. paroxysmal stage (whoop cough). h/o travel or contact. and URI. Empiric therapy should include coverage for organisms associated with any community-acquired pneumonia of unclear etiology. If no => Home rest with quarantine.History of contact or travel .

preganglionic lesion is more serious. Mostly in young females & unilateral . (in Pharmacological mydriasis. bilateral. but fail to dilate a postganglionic lesion. CVA.interruption of sympathetic innervation of eye (interruption of sympathetic pathways in the medulla.heterochromia of the iris may occur (affected side being less pigmented).125%.significant possibility that there is an underlying malignancy Adie’s tonic pupil. 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. There may be transient dilation of conjunctival vessels and increased accommodation. poor responsiveness to light good response to accommodation. Retina is light sensitive Cause lesions in Edinger Westphal nucleus associated with neurosyphilis. A) Unequal Pupils . Horner’s syndrome – occulo-sympathetic paralysis-. Parasympathetic dysfunction at or distal to ciliary ganglion.. spinal cord. There is a segmental palsy of the iris sphincter muscle.-. migraine variants and apical lobe bronchogenic carcinoma. aneurysms of the carotid or subclavian arteries. Pupil must be small . MS and midbrain tumors. 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. ipsilateral anhidrosis may be secondary to lung cancer. but Atropine (antagonist) produces poor dilatation.) Two most common pupillary problems: anisocoria and decreased pupillary constriction to light.parasymp system is dominant because the iris sphincter is a stronger muscle. If associated with altered deep tendon reflexes (hypo. Syringomyelia if newly acquired in an adult --must be thoroughly investigated -. mediastinal tumors. relative mydriasis in bright illumination. Pupil contracts with Physostigmine (agonist). poor to absent light reaction. hydroxyampthetamine 1% will dilate a pre-ganglionic lesion. The brain perceives the same stimulus as having a decreased intensity and dilates both pupils. There has to be extensive retinal or . Causes are vertebral fractures.idiopathic benign internal ophthalmoplegia. slow constriction in prolonged light.or areflexia) is called Holmes-Adie syndrome.Anisocoria: 20% of the population have perceptible anisocoria. etc. no response). Lyme disease . This is due to poor transmission of the light to the brain via a damaged optic nerve. 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. If both eyes are functioning poorly. B) Equal Pupils: Argyl Robertson pupil –miosis. ptosis. a slow contraction to prolonged accommodation-. more pronounced in darkness. If longstanding--. there will not be an relative afferent pupillary defect. pupil is hypersensitive to weak pilocarpine 0. demyelinating disease.a slow redilatation after completion of accommodation (the near stimulus is removed). slow dilatation in prolonged darkness. or peripheral sympathetic trunk) causing miosis.

25%. Downward deviations occur in patients with hydrocephalus (setting sun). Vertical gaze paresis is classical for dorsal midbrain lesions.optic nerve damage for an RAPD to be demonstrable. Drugs. temporal Arteritis. must be used TID or QID to maintain mydriasis. Destructive lesions result in ocular deviation to the same side but inability to turn to the opposite side. coma. Pilocarpine in 0. histamine Pinpoint Pupils: Pontine hemorrhage or infarct. Apart from atropine. Cyclopentolate: maximal dilatation at 25 to 75 minutes. morphine.5%. Frontal lobe lesions prevent conjugate movements to the opposite side on demand but normal movements on pursuit. Brain stem pathology is associated with multiple cranial nerve palsies and contralateral hemiplegia. See section on acute glaucoma for exception. Thalamus. must be used TID to QID. May be caused by optic neuritis. proparacaine 0. These cause corneal toxicity with repeated use--NEVER prescribe for home use. Parkinson’s disease and Phenothiazine toxicity. etc. . Anesthesia. chiasmal tumors. scopolamine: dilatation at about 1 hour. unilateral mydriasis via Hippocampal herniation through the Tentorium with compression of CN III as it exits brainstem. gliomas. pilocarpine instillation. Oculogyric crises are spasms of upward gaze typical of post-encephalitic states. Generally needed only once per day. Media opacities like cataracts or vitreous hemorrrhages alone would not be sufficient. retinal detachment.total gaze palsy (ie inability to move both eyes together in a certain direction). Miosis. such as pinealomas (Parinaud’s). and 1.5%. MS and 3rd ventricle tumours. homatropine: maximal dilatation is rapid. OCULAR MOVEMENTS: If supranuclear control is lacking -. Patients with congenital achromatopsia and congenital stationary night blindness have been known to show a transient pupillary constriction to darkness. lesions in the Subthalamus. class of drugs which cause pupillary dilatation: Alpha adrenoceptor agonists (sympathomimetics) such as epinephrine Small Pupil: Cause: Meningitis. ischemic optic neuropathy. acute angle-closure glaucoma. lasting 6 to 24 hours. Tetracaine 1%. interruption of ascending Sympathetic pupillodilator fibers Large Pupil: Causes: Traumatic irridioplegia. CVA. deviation with coarse nystagmus or internuclear ophthalmoplegia can result. Mydriasis. AV malformations. limitation of gaze excursion. thalamic pathology and transiently in newborns. Irritative lesions cause the eyes to deviate to the opposite side acutely. Occipital lesions cause impairment of the pursuit movement to the same side and a homonymous field defect to the opposite side.0%. 0. retinal artery or vein occlusion.

the right forearm was kept in the supine position. Both ankle reflexes were absent and the right knee jerk was diminished. AV malformations or hydrocephalus. 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. Two days later. especially below the knees. although weak flexion of the metacarpophalangeal joints of these fingers was attempted by the interossei. All ocular muscle palsies and ptosis may be mimicked by myasthenia gravis. On physical examination the patient did not appear to be ill. Would you expect damage to be central (spinal cord. 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. No flexion was possible at the interphalangeal joints of the index and middle fingers. wrist flexion was weak and was accompanied by adduction. As a result of this. brain) or peripheral? Why? Would you request that an MRI be done? Would you hospitalize the patient? . Here a Tensilon test is diagnostic. He had no pyrexia. while shaving. 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. The latter two fingers were weakened by the loss of the flexor digitorum superficialis. 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. the middle fingers tended to remain straight. In younger patients up to 25% have a thymoma. while the ring and little fingers flexed. 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. Flexion of the terminal phalanx of the thumb was lost due to paralysis of the flexor pollicis longus. He also developed a numb sensation over the lower part of both legs and the feet. 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. There was also sensory loss of the skin of the distal parts of the dorsal surfaces of the lateral three and one-half fingers. The muscles of the thenar eminence were paralyzed and the right thumb was laterally rotated and adducted. and a mild form of facial nerve palsy involving the right side of the face. often indicative of MS. Examination of his leg muscles showed obvious signs of muscle weakness involving both legs. He had sensory deficits for touch and pain sensations in the distribution of the stocking area of both feet and lower legs. but can also be the result of head trauma. Motor loss consisted of paralysis of the pronator muscles of the forearm and the long flexor muscles of the wrist and fingers. brain stem neoplasms. with the exception of the flexor carpi ulnaris and the medial half of the flexor digitorum profundus. loss of the medial rectus adduction in the contralateral eye and a jerky nystagmus in the abducting eye. When the patient was asked to make a fist of his right hand. he noticed a weakness of the muscles on the right side of his face. the index and.

slumped in a chair apparently confused and paralyzed on the right side. the patient also complains that her left leg is numb and she has lost voluntary movements of her right leg. He was apparently well until 4 days after his birthday. She has a reflex response when her Achilles tendon is tapped (ankle reflex). including pin pricks and touch. the patient cannot tell in which direction it is moved. 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. he was unable to produce any intelligible speech and appeared to understand only very simple phrases. she cannot discriminate whether she is touched with two objects close together or just one object.#3: A successful 48-year old attorney was told he was hypertensive. fine discrimination and vibration? There was no loss of pain and temperature. But this time. She has normal sensation above her pelvic region on both sides. she has no reflex response when the tendon of the quadriceps is tapped (knee jerk) on the right side. 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. the patient cannot tell the difference whether she is touched with the dull . She has no sensation when stimulated. Where is the lesion? #5: Now it's the same case. "like a shade coming down. These attacks each lasted less than an hour. there was Babinsky response on the right. She has a knife wound low on her right side in the back. Motor problems on the left. he complained to his wife of a left-sided headache." involving his left eye. On the left leg. but within several days. She cannot feel when the tuning fork stops vibrating. She can tell the difference between the sharp point versus the dull point of the safety pin on the right leg. a middle-aged lady was brought to the emergency room. He was referred for neurologic evaluation but because of a busy schedule. became hyperactive. Neurologic examination in the hospital revealed total paralysis of the right arm and severe weakness of the right face. She complains of numbness on her right leg and especially on her thigh. canceled the appointment. Her left side is totally normal. Deep tendon reflexes were initially depressed on the right side. When her right toe is moved up or down. Why was the territory of the anterior cerebral artery not infarcted? #4: After a fight in a bar. Several weeks later. The leg was only mildly affected. Which sensory tract was spared? Explain the results of the Achilles and quatricepes reflex tests. The patient was globally aphasic. when he developed several episodes of blurred vision. along a strip on her thigh on the right side. She found him 1/2 hour later. Although she can feel that she is touched on the right leg (except where noted above). but did not take his blood pressure medications. What's the territory? Headache and Visual problems on the right. Her sensory findings for her right leg are the same as during the previous examination. Upon examination you find the following.

right hemiparesis. incomplete extraocular movements on the left side. The blood pressure. the right one has the plantar extension. she had noted dull pain in the left hand during the past year. There was marked atrophy of all muscle groups in the left arm. pulse rate and temperature were in the normal range. The right plantar extensor response was equivocal. and the erythrocyte sedimentation rate was 30 mm/h. the left side of her face appeared drier than on the right. There was . you can feel a rhythmic oscillation. foot and leg on the right side upon command. a right pupil that was smaller than the left. 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. In addition. following an episode of severe coughing. the Achilles tendon reflex is much more brisk on the right side than the left side. she seemed slightly more alert and made purposeful movements with her left hand--but not her right hand. decreased right corneal reflex. She was still unresponsive to spoken commands and had a rigid neck. 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. in addition. The headaches began approximately 2 years previously.200 µL. especially on the right side. She complained of headache and a painful neck.part or the sharp part of the needle --> they both feel dull to her. All reflexes appeared within normal range. with a right facial droop. there is also some resistance to movement of the foot and lower leg. When stroking the bottom of her feet. and right hyperreflexia. A few days later. but the left was normal. She is unable to move her toes. When quickly dorsoflexing her right foot. 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. 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. she can accurately identify when the tunning fork stops and whether you move her toe up or down. however. right 3 mm). Other findings included bilateral papilledema. During the past month she also has found that her walking is "stiffer than usual. the white blood count was 11. a left ptosis. Examination was remarkable for mild thoracic kyphoscoliosis. She was lethargic. However. You test reflexes: the knee jerk is still absent on the right side. There were right motor problems and problems with especially the left eye. A CT scan showed a high-density area in the cisterns. 1 mm." There have been no bowel or bladder abnormalities and her general health is otherwise well. on her left leg. Both pupils were round and reactive. There was. Dull occipital pain had persisted on and off since that time. Over the area of the right quadriceps. The patient's right arm was hypertonic and paretic. you note some twitching of the muscle fibers. but the other extremities were normal. and right nasolabial droop. Cranial nerve testing revealed a pupillary asymmetry (left.

Vibratory and position sense were now impaired in the left arm. who had traveled to many countries. When the right side of her face is touched with a sharp or a dull object. How would you explain the motor problems to her face? Would you expect that sounds appear louder on the right side? Why? How do you explain the lack of pain discrimination on the right side of her face versus . had paralyzed vocal cords and a diminished gag reflex. She can accurately detect. although no abnormalities could be detected on examination. Upon examination the following are noted. nausea and vomiting? Vibration and position sense impaired on left arm. there was impaired pain and temperature sensibility. vertigo. however. on both sides of the body. Why? #9: A 53-year old woman is referred to the neurologist. and the gag reflex was diminished. with moderate spacticity of both legs. 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. Why? What caused the vertigo. he developed difficulty swallowing and complained of intractable hiccups. Position and vibration perception were normal throughout. She was areflexic in the left arm and hyperreflexic in the right arm and in both legs. 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. ptosis. the right side shows little motility. and there was an intention tremor on the left.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. Touching various parts of her body with dull and sharp objects. When asked to smile. She can accurately localize where she is touched on her body and all limbs. but otherwise unremarkable. the patient can draw the lips back on the left side and she can wrinkle her forehead on that side. she cannot distinguish the sharp one from the dull one--both stimuli feel dull to her. was admitted to the hospital because of a sudden onset of facial numbness. There was subjective numbness of the right arm. The arm and leg on the left side were clumsy. On the right side of the body. Why was there a Horner's syndrome? The patient had difficulty in swallowing. Gait was mildly stiff legged. she makes accurate responses when touched on the right side. anhydrosis) was apparent. Examination revealed impaired sensation over the left half of the face. and vomiting. When the left or right corneas are lightly touched. Over the ensuing 12 hours. however. ataxia. on the left side both stimuli appear dull to her (on her body and upper and lower limbs). She is numb on the left side of her body. when the tuning fork stops vibrating and if the toes are moved up or down. She complains about numbness on the right half of her face and loss of motor control also on the right side of the face. only the left one responds with an eye blink. She has no motor problems involving her body and upper or lower limbs. Why? Pain and temperature were impaired on the right side of the body. A leftsided Horner's syndrome (miosis. nausea. the vocal cord was paralyzed.

the patient was alert. the left eye moved laterally but the right eye looked straight ahead. There was a left facial asymmetry. 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. Although he was apparently in good health. Sensory examination was normal. The neurological examination found the following. Testing for eye movements: when asked to look to the left. His family took him to the emergency room. although confused and unable to give a coherent history. when he developed early morning headaches which would awaken him from sleep. Review of systems revealed weight loss of 15 pounds over the past month. The plantar response was extensor on the left (Babinsky sign) and flexor on the right. The remainder of the cranial nerves were normal. Two days earlier he developed progressive weakness of his left hand and an unstable gait. Reflexes were increased on the left and plantar responses were extensor bilaterally. incontinent of urine and appearing bewildered. 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. there were exaggerated biceps. Testing the sensory system. the right eye tended to move laterally. 3 weeks previously he had fractured his wrist falling . he could not pull his lips back on command. the severity of the headaches was increasing with time. triceps.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. he could wrinkle his forehead. The landlady remembered that 2 months earlier he had been involved in a fight in a bar. All other sensory systems were intact. however. at rest. On the left side of his face. On examination. knee and ankle reflexes on the left limbs but normal on the right. Although the headaches typically disappeared shortly after arising from bed. although the patient had a tendency to fall when turning rapidly. 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. the only finding was that the right eye did not constrict in response to light. Testing the motor system. he had also bitten his lip. 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. 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. his landlady had entered the apartment on the day of admission because he did not respond to her calls. Fundoscopic examination revealed bilateral papilledema. Gait was stable.

The nerve can be repaired up to 12 months post-trauma. and a glucose level of 70mg/dL. Over the next 36 hours. disheveled. On what area would you have them focus the MRI? Would you hospitalize the patient? Yes. brain) or peripheral? Why? The damage would involve the peripheral nervous system. vasomotor control return at this time. and polymorphonuclear neutrophils. and urinalysis were within normal limits. Motor problems on the left because the motor fibers crossed therefore the symptoms were opposite to the lesion. touch and tactile sensation are the last to return. and there was a left sided plantar extensor response. The patient recovered only minimally. xanthochromia. #3: A CT scan revealed an infarct in the territory of the middle cerebral artery of the left side. Patient has polyneuropathy. a protein level of 80 mg/dL. Pain caused by deep pressure is the first sign of recovery. The reflexes were normal and symmetric. A CT scan of the head was obtained. the patient was unconcerned. Angiography revealed occlusion of the internal carotid artery. and dirty. On examination.5 mm per day is the average rate of regeneration. #2: Would you expect damage to be central (spinal cord. 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. lymphocytes. The patient appeared to fall asleep when left alone. and no abnormalities that would result from dysfunction of other cranial nerves. Cell counts in all tubes showed red blood cells. probably Gullain-Barré syndrome. normal extraocular movements. sensory and motor systems were equally affected on both legs-indicating most likely peripheral involvement Would you request that an MRI be done? No. 20/µL. The reflexes were either diminished or absent-central problems would cause hyperreflexia. 4/µL. Once the nerve has entered the distal segment.down stairs. Until recovery of function. Neurologic examination showed normal optic fundi. . Vital signs. Sensation returns before voluntary movement. The wound has to be cleaned and be free of infection. this segment becomes sensitive to mechanical stimulation (Tinel’s sign). 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. A lumbar puncture showed an opening pressure of 180 mm of water. complete blood count. 800/µL. The peripheral nerves dealing with breathing and/or swallowing could become involved. Bruises on his head and legs were consistent with recent trauma from a fall. the patient became deeply obtunded and seemed to develop a left-sided hemiparesis.

The lesion therefore is at the posterolateral quadrant of the spinal cord at level L2. The knee jerk is absent which means either the sensory or motor component is absent. However. What structure is included in the lesion to give the plantar extension (Babinsky sign)? The corticospinal tract on the right side. In this case. Explain the results of the reflex tests and the resistance felt when dorsoflexing the foot. the proximal portions of the dorsal root and zone of Lissauer was damaged. If done. The visual problems are called "amaurosis fugax" = transient monocular blindness due to interruption of blood flow from the ophthalmic artery to the retinal artery. the incoming sensory information (proprioception) is absent on the right side (L2-4). 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). Would you request a lumbar puncture? What might it show? The bilateral papilledema suggests increased intracranial pressure. #4: To have absence of all sensation. therefore there is no loss of discriminatory touch or vibration on that side. indicates that the lesion is at the L2 level. In this case.e. i. The anterolateral system was spared. together with the hyperreflexia. There were right motor problems and problems with especially the left eye. the problem with the eye is caused by involvement of the cranial nerve III. fine discrimination and vibration. The Achilles tendon reflex is hyperreflexic. it does not appear to be due to hypertension. blood supply from the right internal carotid system supplied the blood to the left anterior cerebral artery.e. This area as well as the level of anesthesia and other sensory losses. the damage must occur either to the incoming afferents (i.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. Why was the territory of the anterior cerebral artery not infarcted? There was collateral circulation via the anterior communicating artery. It could be an aneurysm. anesthesia. Damage to posterior column on the right side could explain the lack of proprioception. putting pressure on the medial . The Achilles reflex is normal therefore sensory and motor root segments of S1-2 are intact. the posterior columns are intact on the left side.The CT scan showed that the infarct included the territory of the middle cerebral artery but the occlusion involved the internal carotid artery. dorsal root) or the posterolateral area in the spinal cord where the fibers enter (i. indicate an upper motor problem = damage to the corticospinal tract. Where is the lesion and which areas are included? This is a lateral hemisection of the spinal cord (Brown-Sequard syndrome) at L2 level. the finding would be blood in the CSF. #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. # 6: The sudden onset suggests involvement of blood vessels. The spasticity and clonus. zone of Lissauer). a lumbar puncture is not advisable. however. What is the diagnosis? Subarachnoid hemorrhage on the left side of the midbrain.

Why would one side of her face be drier? Interruption of sympathetic ANS. . Therefore the vagal nerve complex and/or nucleus ambiguus were damaged. most likely one of the cerebellar peduncles was involved. Arteriography. loss of some eye movements). the tract is located in the lateral portion of the medulla and was damaged. this is called Horner's syndrome. 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. Why? The lower motor neurons innervating the pharynx and larynx were damaged. Why were the arm and leg on the left described as clumsy? There is also an intention tremor. this is also part of Horner's syndrome. Together with the intention tremor. The patient had difficulty in swallowing.portion of the left cerebral peduncle (especially motor pathways to the arm and face. usually in the cervical spinal cord. Why was there a Horner's syndrome? There is a descending tract dealing with sympathetic information going to the upper thoracic 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). had paralyzed vocal cords and a diminished gag reflex. 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. Serologic testing of the CSF and serum was positive for syphilis. in the lateral medulla on the left side. arms and hands). the intermediolateral cell column was affected giving the Horner's syndrome. carried out on an emergency basis. As the cavity expands. revealed occlusion of the posterior inferior cerebellar artery with "beading" (evidence of inflammation) of vertebral arteries and anterior inferior cerebellar arteries. Over the ensuing six months. In this case. Most likely. this is ataxia. In this case. presumably infarction. Brainstem = Crossed signs: Ipsilateral Nerve Palsy (Left). Lumbar puncture revealed 40 white blood cells (mostly lymphocytes) per cc of CSF. The patient was treated with intravenous penicillin. there was greater involvement of the left portion of the spinal cord. tract or nuclei must be involved. The initial symptoms are loss of pain and temperature bilaterally but only for arm and shoulder regions. ptosis and anhydrosis due to interruption of sympathetic innervation of the face including the eye. this indicates damage to tracts or areas associated with the cerebellum. #8: MRI demonstrated an abnormality. the sign for the latter are decreased corneal reflex and nasolabial droop) and the CN III (signs are small pupil. and contralateral motor sings (right). Why was sensation impaired over the face? The trigeminal nerve. many of his deficits resolved and he resumed his activities including his painting. #7: What could be the cause for the unequal size of pupils and ptosis? Left eye: miosis. the posterior columns might be involved (with loss of discriminatory touch) as well as the anterior horn (causing paralysis of muscles in shoulders.

#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. the spinal component dealing with pain and temperature. Note: The corticobulbar tract also involves other cranial nerves. Pain and temperature were impaired on the right side of the body. the information has not yet crossed. which has crossed. on the right was also damaged. It is therefore absent on the right. Note: CN V is responsible for the sensory component of this reflex. left face. The innervation of the cornea does consist primarily of pain fibers but there is sufficient touch innervation to get the corneal response. although it may be sluggish. Would you expect that sounds appear louder on the right side? Why? The sounds would be louder in the right ear. Vibration and position sense impaired on left arm. Where would you expect the lesion to be? At the level of the pons but the caudal portion. 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. cuneate nucleus is more rostral and was not damaged. 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. #10: Which structure was involved to give you the exaggerated reflexes on the left upper and lower limb? This is hyperreflexia. this is an upper-motor-neuron sign and the corticospinal tract (or motor cortex) is damaged. 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. Why? Only the gracilis nucleus/tract were damaged. What caused the problems with the facial muscles? The problem was only with movement of the lower. Why? ALS damage gives contralateral signs. The stapedius muscle. The plantar extension on the left is also indicative of this type of damage. CN V. however. This suggests damage to the contralateral (right) corticobulbar tract.What caused the vertigo. How do you explain the results when testing the corneal reflex? CN VII is responsible for the motor component of the corneal reflex. the loss of pain on the body is due to damage of the ALS. the damage is either to the nerve or nucleus of CN VII on the right. sparing the medial lemniscus and the corticospinal tract. is innervated by CN VII. which dampens incoming sounds. However. What would an MRI show? . only the lateral tegmental portion is involved. the medial rectus is required to move the eye medially and oppose the lateral rectus muscle. nausea and vomiting? Damage to the vestibular area.

Treatment is surgical removal of blood and closure of bleeding veins.AGE MEN>45 WOMEN>55 (If you give male gender as a risk factor don't add age and vice versa) . Patient has less than 2 risk factors or more than 2.DM . Now: after assessing your patient: . #11: What is the most likely cause of the patient's symptoms? Metastic tumor in the right frontal lobe. the drop in CSF pressure associated with lumbar puncture or both. The fight in the bar could have caused arachnoid tearing which was aggravated by his fall. TYPE A PERSONALITY IS NOT RISK FACTOR.] What is the most likely diagnosis? Right-sided subdural hemorrhage confirmed by CT. Cerebral metastes usually occur in the setting of widely disseminated cancer therefore one should investigate the extent of cancer spread.CURRENT SMOKING .low HDL<35 Note: TG are NOT A RISK FACTOR YET. Compromised were the CNIII and portions of the cerebral peduncle involving the corticospinal and corticobulbar tracts.html OLD REQUEST: Next step in of Cholesterol/LDL labs Basically.HTN>140/90 . [xanthochromia = old and fresh blood. References: http://www.edu/~m555/cases/cases. both findings suggesting cerebral involvement. increased protein and glucose. spread via blood supply. Prognosis is poor. FIRST OF ALL: RISK FACTORS: . His level of consciousness had deteriorated and he seemed to have had a seizure (incontinence and a bitten lip).indiana. What do the findings from the lumbar puncture indicate? The findings indicate subdural hemorrhage. HDL>60 IS PROTECTIVE AND NEGATES ONE RISK FACTOR.FAM/H FIRST DEGREE RELATIVES CAD<55 MEN <65WOMEN . in this patient chest X-ray revealed metastic lesions of lung and bone. The majority of patients with brain metastasis die of complications from systemic cancer rather than from direct effects of the brain tumor. think of it this way. 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. #12: Could the patient's problems be due to recent trauma? Yes. increased pressure.Less than 2RF: . triggered by the blood mass. The worsening of the patient's condition was caused by imminent herniation of the brain.An infarct to the right ventromedial quadrant of the mesencephalon. The medial portion of the cerebral peduncle contains corticopontine fibers which do not give a symptom.

body mass index 31. so primary prevention has a goal for LDL of < 100. CAD S/P Inf MI 8 years ago. His uncle had an MI at 58. ASpirin. IF non-conclusive THEN AORTOGRAM. She is on Glyburide. Lipid Panel: Total Chol=288 TG= 262 HDL 37 LDL=199 This guy also has more than 2 risk factors. and hypothyroidism. Introduce Diet and Medications HMG CoA Reductase. NIACIN AND GEMFIBROZIL ARE FIRST LINE UNLESS CHOLESTEROL IS REAL HIGH.Blueprints medicine Rupture Thoracic Aorta Suspect with Deceleration injury of Fx of hard to break bone (Scapula. BP 170/100.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. . Sternum). Reference: -CTB -Swanson . She denies any sympptoms. A 51 yo male comes to ur office for yearly visit. CXR is First step If Wide Mediastinum = NONINVASIVE TESTS: Spiral CT or Transesophageal Echo. Atenolol. but according to CTB. She is a lifelong NONsmoker. Playing with her blood sugar medications in hope to reduce the TG will not do much since she is already borederline. Chol >200 and LDL>160. . LDL >190 => START MEDICATION. and brother at 55yo.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. He never had an MI. and thyroxine. Niacin would increase her BS. Usually HMG CoA is first line in high cholesterol. 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.

If +ve => Family colonoscopy q1-2y starting from 25yo or 5 years younger than the earliest diagnosed in the family.FOBT + Flex Sig Q 5 y . 80 are positive AND sick (True Positives). And 90 are NEGATIVE AND SICK (False Negatives).HNPCC = suspect after colonic adenoma => Genetic screening.the pt's test result is 7. 2> at what age is FOBT recommended? AVERAGE RISK: . Means out of the 100 people sick.FOBT annually >50yo in average risk individuals . 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. 100 will have the disease and 900 wil be well. Means if we assume a number of 1000 people. when shud we start colonoscopy/sigmoidoscopy? START COLONOSCOPY 8-10 YEARS AFTER DIAGNOSIS. If not possible. 90% (810)are NEGATIVE AND WELL (True negatives). PPV = True positive/all positives = 80/80+90 x100 = 47%.PSA is ordered . 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 answer is 47%. can anyone plz explain how u arrive at this.5-1%/year Other: . . Frequency: every 1-2 years – multiple biopsies each time (@least 32).the prevelance of prostate ca in this age group is 10.Examination finds a 1cm nodule in his prostate.commonly PSA greater than 4 is considered abnormal.what is ur best estimate that this man is actually having ca prostate. Means out of the 900 well population .familial polyposis = genetic screen at 10yo.using this standard this test has a sensitivity of 80 and specificity of 90.The specificity is 90%.The sensitivity is 80%. yearly sigmoidoscopy at 12 yo. If diag +ve = surgery before 20yo. . Random Q & A from exam 1>in UC.THEN Surgical Repair Bistats Q A 55 yr old man visits his physician with a complaint of urinary infrequency. and 20 are negative AND sick (FAlse Positives) . The best estimate that the patient is ACTUALLY HAVING CA PROSTATE = Positive Predictive Value. Endometrial cancer screening (endom aspiration or transvaginal US) at 2535yo for women.Barium Enema Q5-10 years FAM/H OR 1ST DEGREE RELATIVE WITH COLORECTAL CA: .Colonoscopy Q 10years . The prevalence in this population is 10%.

strong association with alcoholism. OR DILTIAZEM. THEN Surgical Repair 6>what is the clinical association for ADHD genetically? TOURETTE SYNDROME. IF non-conclusive THEN AORTOGRAM. COLI.. If no history of travel. 13>drug of choice for eclampsia MAGNESIUM SULFATE 14>drug for narcolepsy FORCED NAPS AT REGULAR TIMES IS TREAMENT OF CHOICE. Salmonella. 8>drug of choice for VF and AF V-FIB IMMEDIATE DEFIBRILLATION A-FIB SYNCHRONIZED CARDIOVERSION IF UNSTABLE. most common = campylobacter. 7> IF A ASTHAMAA AND HTN IN A PT GIVE CA CHANEEL BLOCK SAME IS WITH ACHALSIA ND HYPERTENTION. CXR is First step If Wide Mediastinum = NONINVASIVE TESTS: Spiral CT or Transesophageal Echo. 10>drug of first choice in depression SSRI = FLUOXETINE 11>what the adult form of conduct disorder ANTISOCIAL PD = Long criminal record.most common cause: NO BLOOD/ WBC +VE => INVASIVE. CLINICAL ASSOCIATION. OCD. BETA-BLOCKER. Liars with no remorse. But remains awake if short episode) = TRICYCLIC ANTIDEPRESSANTS . 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. EXCEPT ANTISOCIAL WHICH BEFORE 18YO WOULD BE CONDUCT DISORDER. DRUG: PSYCHOSTIMULANTS IF CATAPLEXY PRESENT (sudden loss of muscle tone precipitated by loud noise or emotion = pathognomonic. tortured animals when kids. AVOID VERAPAMIL/DIG…USE PROCAINAMIDE/QUINIDINE 9>diarrhea in mexico with no blood and wbc in stool. Yersinia. GENETICALLY REALTED = STILL UNDER INVESTIGATION. TRAVELER = E.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). and set fires. 12>can we diagnose a pt of 15 yrs with personality disorder YES. drug abuse and somatization disorder. CAREFUL IF THAT’S WPW. (Montezuma’s revenge). DIGOXIN. IV VERAPAMIL. Sternum). Other invasive: Shigella.

AN= WEIGHT LOSS – SPORTS – AMENORRHEA – MAJOR DEPRESSIVE DISORDER with atypical features (leaden paralysis..... 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.. purging etc. fasting. poor impulse control). exercise.....BN = RELATIVE GOOD WEIGHT FOR AGE – BORDERLINE PERSONALITY DISORDER (body image. exercise. 18>black male.15>pt with wt loss. 21> IN A PATIENT WITH ACUTE LUNG INJURY BREATHING SPONTANEOUSLY. 20>effects of malignany on psychological state I CAN’T FIGURE OUT THIS QUESTION.HTN which drug to administer THIAZIDE DIURETIC 19>smoking cessation.…. RISK OF LUNG CANCER DECREASES BY 80-90% AFTER 15YEARS BUT NEVER REACHES LEVELS OF NON-SMOKERS. good academics. purging. Definitive treatment with radioactive iodine or surgery is delayed until euthyroid.female.effect on lung changes FEV1 IMPROVES FIRST YEAR.... . RATIO SHOULD NOT BE DECLINING SINCE FEV1 AND FVC ARE DECLINING “PHYSIOLOGICALLY” AT SAME RATE.15 yrs:diagnosis? MAIN QUESTION is it Anorexia or Bulimia? Both have fasting. OTHER: RISK OF HEART ATTACK IS DECREASED BY 50% WITHIN 24H OF QUITTING. THEN STARTS DECLINING SEMIPHYSIOLOGICALLY MORE THAN NON-SMOKERS.BUT B4 THAT U HAVE TO C WEATHER THERE IS ANY TENDERNESS AT TH E GRAFT SITE OR FEVER IS . overeating). 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 . NEEDS MORE EXPLICIT.. HE ALSO SAID NEVER D/C CYCLOSPORIN BUT JUST DEC TH EDOSE AND GIVE PT ACE INHIBITERS. 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...HTN AND NEPHROTOXICITY. USUALLY .WEATHER ITS BCZ KIDNEY IS BEING REJECTED BY THE PT OR ITS DUE TO CYCLOSPORIN U HAV ETO DO BIOPSY. Risk of having a stroke and brain aneurysm declines by 30-50%. BUT LESS THAN CURRENT SMOKERS.30s.. Joins level of non-smokers after 2 years. 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 .

. Reference: http://www....html My review of the exam I had one of those days..WHAT U WILL DO. and on the basis of current retrospective studies. and increases during the first three months post partum before returning to the prepregnancy rate. Some Dependent children live with birth parents or other relatives but are subject to government monitoring.. 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 .. SLOW DEEP TENDON REFLEXES WITHDRWAL.. Other Dependent babies are placed in foster care. the rate of relapse declines during pregnancy. if the minor chooses to give birth and not place the baby with adoptive parents.... If the minor and the baby's father and any other willing relatives cannot or will not support or care for the baby... And it's over. D/C LITHIUM AND START HER ON SYNTHYAROID .. This could result in the baby becoming Dependent... That's when the CD of Kaplan was useful... SO THANKS PHARMAA GOOOD Q. On the other hand.net/~tjc/pregnancy.. It had given me the opportunity to take a whole day .. although patients with severe MS may have difficulty fully caring for their newborns.albany.. 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.JUST CHECK TH E LEVEL AND DEC THE DOSE AND START PT ON THE MEDICATION THEN SLOWLY INC THE MEDCIATION IN A THERAPETIC RANGE. However. especially in the third trimester. the minor's parents are NOT legally obligated to support the baby. the government may step in. but generally: the parents of a pregnant minor cannot legally force their child to have an abortion. Postpartum IVIg treatment is beneficial in preventing acute childbirth-associated exacerbations in patients with Relapsing/Remitting Multiple Sclerosis... I took a break at the end of every block. Multiple Sclerosis and Pregnancy In women with Multiple Sclerosis..CHECK LITHIUMMM LEVEL .. the lifetime risk rate does not appear to change because of pregnancy. MS has little or no effect on the course of pregnancy or delivery. Unique Ethics case: Minor patient doesn’t want to abort but mother wants her to It's depending on the states..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. long-term disability is not higher in pregnant women or even women experiencing relapses during the pregnancy year..? START HER ON SYNTHYROID..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.

5 min after each block. Ten minutes between the 7th and 8th one. Beleive me.Mechanism of alcohol-induced hypoglycemia (Inhibition of gluconeogenesis). It started with "easy" questions. And reconstruc the scenario in your mind.OB-GYN usual OB complications: Arrest of Descent ..Multiple Sclerosis and Pregnancy. coz you're cutting yourself short on the questions at the end of the last block. When reading the questions. you miss the clues easily if you don't read it that way. I made observations when was my score coming down (After lunch. X-rays of Fractures.. It was pretty easy. I had time to read the Question stem twice. You'd know the answer right off the bat.doesn't read the same as 30YO PRESENTS TO THE CLINIC WITH BURNING SENSATION IN LEFT SHOULDER AND UPPER LEFT CHEST. You have to rearrange it in your mind. I made my "break plan". And when I did it.Derma: the mundane ones. PATIENT'S LABS ARE. .Hirsutism . I had definitely just about 1% of pathophysiology. 2 Q.. I helped myself with my finger following each and every word. Before I went this morning. . 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. AT THAT TIME. . The examples I had posted before SHOULD BE MORE THAN ENOUGH. HE REFUSED TO CHECK HIS BLOOD CHOLESTEROL. and the other hand hiding the choices. and 90% of management with about 40% treatment. .exam. you get a little impatient and you tend to want to do it without a break. PATIENTS UnDERWENT APPENDECTOMY. I had learned som much from doing questions.Blah blah blah.Gynecomastia in male with infertility . Because I would be feeling sleep y by then. I always finished ontime. Type on the search button ABG and it'll take you to them. READ THE QUESTION STEM LIKE IF YOUR LIFE DEPENDED IN IT. Because. USE YOUR HANDS ON THE SCREEN MONITOR.I had about 4 ABG Questions.HTN + Hypokalemia = Think Hyperaldosteronism even if positive family history of essential hypertension . then a piece of history which may be relevant but it distracts you. 10 min on the block after lunch.. but two hours answering questions is not good.EKG: VERY EASY ones: V Fib. Effect of the latter on the first. TWO YEARS AGO. And 2 graphs for Arrest of descent. last block). VERY EASY ONES. Obvious. A 30 TO WITH CHEST PAIN AND EKG CHANGES IN THE SETTING OF 2 RISK FACTORS AMONG WHICH FAMILY HISTORY . So I made a point to take longer breaks on those times. I used the scratch laminated paper to SUMMARIZE the questions stem. HE STATES HIS FATHER DIED OF HEART ATTACK AT 55YO. There is ALWAYS something to look for. MI . Now about the topics: The usual: . If your mind is not trained to filter the parasites. .Placenta Previa .Risk factors for Breast Cancer . their strategy is to put the Cheif complaint. Power of attorney = Treat like if it's patient talking to you. then something about family history. 10 min for "lunch" which was a turkey sandwich.I had the usual ATHMA treatment changes .LOTS OF ETHICS. then putting again something relevant to the present. THE CHEST PAIN EXACERBATES ON EXERTION.

Alzheimer and genetic testing for iff-spring possible? What is it? What does it predict? . and when to wean patient off).Down and Alzheimer.Transplantation: Very easy: Increase the steroids if acute rejection at 30 days for ex. I SHALL REMAIN HELPING FOR WHOMEVER NEEDS HELP. 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 don't know if I will get it.Prevention of Rheumatic Fever: What antibiotic and for how long. So let us know your experience. They don't name it Zenkel. USE ME PLEASE. but tricky. as they would appear on the Step2 outline.. GUIDANCE OR SPECIFIC MEDICAL QUESTIONS. I am available for questions or more details. Meningomyelocele. . For the colleague who asked about not sholwing up to the test today please follow with us and tell us what happened.Zenkel Diverticulum: 2 Q.Achilles Tendon rupture is also called Hell Cord rupture hehehe . . Know about permissive hypercapnia in ARDS. .Didn't have much of the nephropathies. MS.Neuro: again very easy ones. . ? . SINCERELY HASSAN . which will have to go to reprocessing and paying for the test again with ECFMG. Usual stroke. I specifically asked. 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. Finally: I will be available for any questions. . I KNOW AND HAVE BEEN THROUGH A LOT. Also Complications of MEch Ventilation: Barotrauma if pressurecontrolled ventilator.CSF findings in Antisocial PD. . IF I DON'T KNOW I WILL POINT YOU TO THE RIGHT RESOURCE. with a touch of care from me:) THANKS TO EVERYBODY WHO SUPPORTED ME ALL THROUGHOUT. But I feel releived I took the test.Fractures of children = Treatment: Cast. . I WISH AND HOPE IT'LL BE THE LAST WITH STEP2.2 Q on Mechanical Ventilation: Recognize indication for weaning (Type Mechanical Ventilation notes #2: don't read everything. Splint. The guy said at the end of each day they send the data to ECFMG including NO SHOWS. Only the modes of ventilation.