Nifedipine

Steve Yentis

• Consultant Anaesthetist, Chelsea and Westminster Hospital
• Honorary Reader, Imperial College, London, UK

In this situation pulse pressure points diagram generic 30mg nifedipine with mastercard, 48 Single gene disorders the recurrence risk is very low for unaffected parents who have Box 10 prehypertension meaning in hindi proven nifedipine 30 mg. Angiomyolipomas may cause abdominal pain arteria yugular externa purchase 30 mg nifedipine free shipping, with or b without haematuria pulse pressure septic shock order 30 mg nifedipine free shipping, and multiple cysts can lead to renal failure blood pressure medication kosar buy nifedipine 30mg on-line. The value of other investigations in subjects with no clinical features is not of proven benefit arrhythmia treatment guidelines cheap nifedipine 30 mg visa. Clinical diagnosis is based on the Gent criteria, which require the presence of major diagnostic criteria in two systems, with involvement of a third system. Minor features indicating involvement of other symptoms include striae, recurrent or incisional herniae, and spontaneous pneumothorax. Pregnancy in women with Marfan syndrome should be regarded as high risk and carefully monitored by obstetricians and cardiologists with expertise in management of the condition. Decreased fluid and salt secretion is responsible for the blockage of exocrine outflow from the Box 10. Direct mutation analysis now forms the pulmonary stenosis dominant basis of both carrier detection and prenatal tests (see cardiac conduction chapter 18). Within features, dominant affected families, mutation analysis enables carrier detection hamartomas and prenatal diagnosis. If both partners carry an identifiable mutation, prenatal diagnosis can be offered prior to the birth of the first affected child. Presentation is with hypertrophy of the left cardiomyopathy and/or right ventricle without dilatation. Dystrophinopathy, caused by mutations in the X-linked gene causing Duchenne and Becker muscular dystrophies can sometimes present as isolated cardiomyopathy in the absence of skeletal muscle involvement. Restrictive cardiomyopathy may be due to autosomal recessive inborn errors of metabolism that lead to accumulation of metabolites in the myocardium, to autosomal dominant familial amyloidosis or to autosomal dominant familial endocardial fibroelastosis. Up to 15% of treated individuals develop neutralising antibodies that reduce the Genetics efficiency of treatment. It is one of the most common genetic diseases in humans Polydactyly and the incidence may be as high as 1 in 1000. Cataracts Renal tubular acidosis All affected individuals have renal cysts detectable on ultrasound scan by the age of 30. Screening young adults at risk will identify those asymptomatic individuals who are affected and require annual screening for hypertension, urinary tract Table 10. At least half the cases of congenital deafness have a Myopia Cleft palate genetic aetiology. Of genetic cases, approximately 66% are Arthropathy autosomal recessive, 31% are autosomal dominant, 3% are X linked recessive. These channels play a role in potassium homeostasis in the cochlea which is important for inner ear function. Mutations in Pendred syndrome is an autosomal recessive form of deafness each of these domains have been identified in the pendrin protein gene due to cochlear abnormality that is associated with a thyroid in different people with Pendred syndrome goitre. Skin disorders such as epidermolysis bullosa provide potential candidates for gene therapy, since the affected tissue is easily accessible and amenable to a variety of potential in vivo and ex vivo gene therapy approaches. Chromosomal translocations have been recognised for many years as being markers for, or the cause of, certain neoplasms, and various oncogenes have been implicated. Up to 5% of cases of breast, ovary, and bowel cancers are inherited because of mutations in incompletely penetrant, autosomal dominant genes. There are also several cancer predisposing syndromes that are inherited in a mendelian fashion, and the genes responsible for many of these have been cloned. Affected females Mechanisms of tumorigenesis Females at up to 50% risk having undergone prophylatic oophorectomy the genetic basis of both sporadic and inherited cancers has been confirmed by molecular studies. Several approaches are being investigated, including virally directed enzyme prodrug therapy, the use of transduced tumour infiltrating lymphocytes, 50% 50% 50% 25% 25% which produce toxic gene products, modifying tumour Figure 11. They are also evident in solid tumours, for example, an interstitial deletion of chromosome 3 occurs in small cell carcinoma of the lung. More than 100 chromosomal translocations are associated with carcinogenesis, which in many cases is caused by ectopic expression of chimaeric fusion proteins in inappropriate cell types. Burkitt lymphoma Burkitt lymphoma is common in children in parts of tropical Africa. Altered activity of the oncogene when translocated into regions of immunoglobulin genes that are normally undergoing considerable recombination and mutation plays an important part in the development of the tumour. Inherited forms of common cancers Inherited forms of the common cancers, notably breast, ovary Box 11. Determining the probability that any particular malignancy is inherited requires an accurate analysis of a three-generation family tree. Factors of importance are the number of people with a malignancy on both maternal and paternal sides of the family, the types of cancer that have occurred, the relationship of affected people to each other, the age at which the cancer occurred, and whether or not a family member has developed two or more cancers. The presentation may be with adenomatous polyposis as the only feature or as the Gardener phenotype in which there are extracolonic manifestations including osteomas, epidermoid cysts, upper gastrointestinal polyps and adenocarcinomas (especially duodenal), and desmoid tumours that are often Figure 11. Family members at risk should be screened with regular colonoscopy from the age of 10 years. Affected family members develop multiple sarcoma primary tumours at an early age that include breast cancer rhabdomyosarcomas, soft tissue sarcomas, breast cancer, brain tumours, osteosarcomas, leukaemia, adrenocortical carcinoma, brain tumour lymphomas, lung adenocarcinoma, melanoma, gonadal germ cell tumours, prostate carcinoma and pancreatic carcinoma. First-degree relatives in affected carcinoid, adrenocortical mucosal neuromas families should be offered predictive genetic testing. Mutation analysis again provides confirmation of the diagnosis in the index case and presymptomatic tests for relatives. The syndrome follows autosomal dominant inheritance, and clinical, biochemical and radiological screening is recommended for affected family members and those at risk, to permit early treatment of problems as they arise. Naevoid basal cell carcinoma the cardinal features of the naevoid basal cell carcinoma syndrome, an autosomal dominant disorder delineated by Gorlin, are basal cell carcinomas, jaw cysts and various skeletal abnormalities, including bifid ribs. Other features are macrocephaly, tall stature, palmar pits, calcification of the falx cerebri, ovarian fibromas, medulloblastomas and other tumours. The skin tumours may be extremely numerous and are usually bilateral and symmetrical, appearing over the face, neck, trunk, and arms during childhood or adolescence. Malignant change is very common after the second decade, and removal of the tumours is therefore indicated. Tuberous sclerosis Tuberous sclerosis is an autosomal dominant disorder, very variable in its manifestation, that can cause epilepsy and severe retardation in affected children. Hamartomas of the brain, heart, kidney, retina and skin may also occur, and their presence indicates the carrier state in otherwise healthy family members. In bilateral tumours the first mutation is inherited and the second is a somatic event with a likelihood of occurrence of almost 100% in retinal cells. Inherited mutation First event In unilateral tumours both events probably represent new Chromosome rearrangement somatic mutations. The retinoblastoma gene is therefore acting with gene disruption recessively as a tumour suppressor gene. New gene deletion Tumours may occasionally regress spontaneously leaving or point mutation retinal scars, and parents of an affected child should be examined carefully. A deletion on chromosome 13 found in a group of affected Loss of normal chromosome Second event and duplication of abnormal children, some of whom had additional congenital chromosome abnormalities, enabled localisation of the retinoblastoma gene to chromosome 13q14. The esterase D locus is closely linked to Recombination between the retinoblastoma locus and was used initially as a marker to chromosomes in mitosis identify gene carriers in affected families. Identification of an interstitial deletion of chromosome 11 in such cases localised a susceptibility gene to chromosome 11p13. These genes are not implicated in familial Wilms tumour, which follows autosomal dominant inheritance with reduced penetrance, and there is evidence for localisation of a familial predisposition gene at chromosome 17q. The terms multifactorial or polygenic Infections Congenital Diabetes Schizophrenia inheritance have been used to describe the aetiology of these heart disease disorders. The liability of a population to a particular disease follows a normal distribution curve, most General population people showing only moderate susceptibility and remaining Affected: population incidence unaffected. Relatives of an affected person will show a shift in liability, with a greater proportion of them being beyond the threshold. Genetic susceptibility to common disorders is likely to be due to sequence variation in a number of genes, each of which has a small effect, unlike the pathogenic mutations seen in mendelian disorders. Relatives of affected people Unravelling the molecular genetics of the complex multifactorial diseases is much more difficult than for single Affected: familial incidence gene disorders. Nevertheless, this is an important task as these diseases account for the great majority of morbidity and mortality in developed countries. In the future, understanding genetic Threshold susceptibility may enable screening for, and prevention of, value common diseases as well as identifying people likely to respond Liability to particular drug regimes. In Hirschprung disease (aganglionic megacolon) family data on recurrence risks support the concept of sex-modified polygenic inheritance, although autosomal dominant inheritance with reduced penetrance has been suggested in some families with Table 12. Mutations in the ret proto-oncogene Hirschsprung disease, according to sex of person affected on chromosome 10q11. The recurrence risk for bilateral cleft lip and palate is higher than the recurrence risk for cleft lip alone, and the recurrence risk for neural tube defect is 4% after one affected child, but 12% after two. In these disorders the risk of recurrence is higher if the disorder has affected the less frequently affected sex. A rational approach to preventing Heritability (%) multifactorial disease is to modify known environmental Schizophrenia 85 triggers in genetically susceptible subjects. Folic acid Asthma 80 supplementation in pregnancies at increased risk of neural Cleft lip and palate 76 tube defects and modifying diet and smoking habits in Coronary heart disease 65 Hypertension 62 coronary heart disease are examples of effective intervention, Neural tube defect 60 but this approach is not currently possible for many disorders. Peptic ulcer 37 Heritability the heritability of a variable trait or disorder reflects the proportion of the variation that is due to genetic factors. The level of this genetic contribution to the aetiology of a disorder can be calculated from the disease incidence in the general population and that in relatives of an affected person. Congenital adrenal hyperplasia due to 21-hydroxylase deficiency shows both linkage and association with histocompatibility antigens. This Homozygous affected combination of linkage and association is known as linkage disequilibrium and results in certain alleles at neighbouring Heterozygous carrier loci occurring together more often than would be expected by Figure 12. The rate of concordance in monozygous twins is high for disorders in which genetic predisposition plays a major part in 50 15 0 Rare (<1%) the aetiology of the disease. Examination of the placenta and membranes may help to distinguish between monozygous and dizygous twins but is not completely reliable. Only rarely is diabetes caused by the secretion dependent dependent diabetes diabetes of an abnormal insulin molecule. There is a strong genetic predisposition although other factors such as obesity are important. High circulating Lp(a) lipoprotein concentration has been suggested to have a population attributable risk of 28% for myocardial infarction in men aged under 60. The risk of coronary heart disease increases with age in heterozygous subjects, who may also have xanthomas. Familial aggregations of early coronary heart disease also occur in people without any detectable abnormality in lipid metabolism. Risks to other relatives will be high, and known environmental triggers should be avoided. Future molecular genetic studies may lead to more precise identification of subjects at high risk as potential candidate genes are identified.

Practice Guideline for the Treatment of Patients With Major Depressive Disorder pulse pressure usmle buy nifedipine 30 mg, Third Edition 111 169 arteria carotida purchase discount nifedipine online. American Psychiatric Association: Practice Guide A double-blind heart attack jack black widow order nifedipine 30 mg online, randomized blood pressure 700 nifedipine 20mg online, placebo-controlled line for the Treatment of Patients With Eating evaluation heart attack manhattan clique edit remix buy nifedipine pills in toronto. Deshmukh R heart attack signs and symptoms buy cheap nifedipine 20mg on-line, Franco K: Managing weight gain as Should a moratorium be placed on sublingual a side effect of antidepressant therapy. Cleve Clin J nifedipine capsules given for hypertensive emer Med 2003; 70:614, 616, 618, passim [G] gencies and pseudoemergencies Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition 113 221. Greenhalgh J, Knight C, Hind D, Beverley C, blind, randomized trial of sertraline and imipra Walters S: Clinical and cost-effectiveness of elec mine. Bush G, Fink M, Petrides G, Dowling F, Francis A: complaints: a review of patient self-assessment of Catatonia. Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition 115 268. Cuijpers P, van Straten A, Andersson G, van Oppen netic stimulation and electroconvulsive therapy in P: Psychotherapy for depression in adults: a meta Copyright 2010, American Psychiatric Association. Bibring E: Psychoanalysis and the dynamic psycho therapy versus supportive therapy in geriatric major therapies. New York, Basic Books, 1988 Factors associated with 1-year outcome of major [G] depression in the community. New B, Asen E, Dayson D, Jones E, Chisholm D, Everitt York, Grune and Stratton, 1956 [G] B: the London Depression Intervention Trial. Brenner C: Psychoanalytic Technique and Psychic Randomised controlled trial of antidepressants v Conflict. New York, International Universities couple therapy in the treatment and maintenance of Press, 1976 [F] people with depression living with a partner: clinical Copyright 2010, American Psychiatric Association. San Francisco, Calif, Jossey skill acquisition in the outcome of group cognitive Bass, 1979 [G] therapy for depression. Ayen I, Hautzinger M: [Cognitive behavior therapy 1015 [E] for depression in menopausal women: a controlled, 360. New York, Basic Books, Gijsbers-van Wilk C, Hendriksen M, Kool S, Peen 1995 [G] J, Van R, de Jonghe F: Short psychodynamic sup 349. Fava M, Kaji J: Continuation and maintenance influencing the utilization of time-limited, short treatments of major depressive disorder. McRoberts C: Comparative efficacy of individual ogy of treatment-resistant depression. Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition 119 tive behavioral therapy: preliminary findings. Coppen A, Bailey J: Enhancement of the antide the antidepressant effect of partial sleep depriva pressant action of fluoxetine by folic acid: a ran tion. Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition 121 413. Guscott R, Grof P: the clinical meaning of re results of a double-blind, randomized, placebo con fractory depression: a review for the clinician. McIntyre A, Gendron A, McIntyre A: Quetiapine systematic review of randomized trials. Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition 123 tiapine augmentation of fluoxetine in major depres 466. Barbosa L, Berk M, Vorster M: A double-blind, methylphenidate in outpatients with treatment randomized, placebo-controlled trial of augmenta resistant depression. Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition 125 499.

Open the flap on the backside of the kit and apply 2 drops of developer to the paper directly over each smear pulse pressure journal buy nifedipine discount. The principle of this test is the general reaction: Hemoglobin reacts with pseudo peroxide blood pressure medication for pilots buy nifedipine 20 mg visa, yielding H2O2 blood pressure weight loss purchase nifedipine 20mg otc, which reacts with benzidine orthotoluidine guaiac in the presence of oxygen to yield the color blue pulse pressure ratio purchase nifedipine 20 mg fast delivery. Lab Procedure: Feces for Ova and Parasites 18D Skills and Training Manual When: To examine a stool sample for the presence of parasites and their eggs prehypertension and ecg buy nifedipine 30 mg cheap. Strain about 3 ml of the specimen suspension through either the disposable filtering device or 2 layers of wet gauze placed in the funnel into a 15 ml conical centrifuge tube arteria 90 entupida discount 30mg nifedipine. Fold the tape over the near end of the slide and smooth the adhesive down along the full length of the slide. Using the paper tab, pull the tape back from the slide leaving the fold over the underside attached. Use a limited area of the tape surface to decrease the area for microscopic examination. Lab Procedure: Concentration Techniques for Ova and Parasites (Con-Trate Method) 18D Skills and Training Manual When: To microscopically examine a fecal specimen for the presence of parasites and parasite ova. Strain about 3 ml of the specimen suspension through the disposable filtering device into a 15 ml conical centrifuge tube. Prepare the blood for counting using either the Unopette system or the pipet method. Filling will cease automatically when the blood reaches the end of the capillary bore in the neck of the pipet. If there is a variation of more than 25 cells between any of the five areas, repeat the test. It occurs in conditions characterized by increased amounts of fibrinogen and globulin. Puncture the Unopette reservoir with the protective shield over the capillary pipet. Touch the tip of the capillary pipet to the blood specimen and allow the pipet to fill by capillary action. Squeeze the reservoir slightly, cover the overflow chamber of the pipet with the index finger, and insert the capillary pipet into the reservoir. Simultaneously, remove the finger from the overflow chamber and release pressure from the reservoir to draw the blood into the diluent. Squeeze the reservoir several times to rinse the pipet and to thoroughly mix the blood with the diluent. Let the reservoir stand for at least 10 minutes to allow the red cells to hemolyze. Convert to a dropper assembly by withdrawing the pipet from the reservoir and reseating it securely with the capillary tube exposed. Clean the capillary bore by inverting the reservoir and gently squeezing the sides to discard 3 to 4 drops. Charge both sides of the hemacytometer by gently squeezing the sides of the reservoir to expel the contents until the chambers are properly filled. Place the hemacytometer in a moist chamber (Petri dish containing a damp gauze pad). Lab Procedure: Crossmatching 18D Skills and Training Manual When: To determine the compatibility or incompatibility of donor blood units with a recipient and evaluate the incompatibilities. Obtain the donor units that are the same blood group and type as that of the recipient. Select the order of preference of donor blood, if the group and type for the recipient are not available. The antiglobulin phase of testing rarely uncovers clinically significant antibodies in a recipient whose antibody screening test is negative. Add check cells to all negative tubes to confirm the reactivity of the antiglobulin reagent. What To Do: Use the following photos and descriptions to properly identify various cellular blood components. To determine a white blood cell differential, a total of 100 cells should be counted with the number of each of the above noted as a percentage of the total. Lymphocytes (Figure 2) are round cells with a thin rim of deep blue cytoplasm surrounding a dark, condensed nucleus which takes up the majority of the cell. Figure 3 Normal monocytes these are usually the largest white cells seen in normal blood. Lesser numbers of white cells with Eosinophils large, bright red granules are called eosinophils (Figure 4). A normal red cell is about the size of the nucleus of a normal lymphocyte (see above Figure 2. Poikilocytosis refers to significant differences in the shape (normally a bi-concave disc) of individual red cells. Cells in which the normally pale central area has a collection of hemoglobin surrounded by a pale rim are called Target Cells (Figure 6). Platelets (Figure 7), cellular fragments (often with distinct Figure 7 granules) much smaller than the red or Normal red white cells, should be noted. On high cells with power oil immersion (1000X) each normal platelets platelet in a field represents a peripheral (the small count of 20, 000/cubic microliter. The purple cells are platelets in several fields should be platelets-there counted and averaged to get an idea of are 5) the peripheral count. Streptoccocus, Group A, B, C, G, Penicillin G or V Cephalosporin (1st generation), S. Corynebacterium diphtheriae Erythromycin and Antitoxin Clindamycin, Penicillin G 3. Moraxella catarrhalis Sulfa-trimethoprim, Azithromycin, doxycycline Amoxicillin-clavulanate D. Escherichia coli Sulfa-trimethoprim Cephalosporin (3rd generation), (if sensitive) fluoroquinolone 2. Haemophilus influenzae Ceftriaxone or Azithromycin, doxycycline, fluoroquinolone Amoxacillin-clavulanic acid 9. Haemophilus ducreyi Ceftriaxone or Amoxicillin-clavulanic acid, Azithromycin, fluoroquinolone Erythromycin A-29 A-30 Infecting Organism Medication of Choice Alternatives 10. Clostridium tetani Penicillin and tetanus toxoid Imipenem, Clindamycin, Metronidazole and tetanus immune globulin 2. It also does not account for local resistance patterns, cost-effectiveness, or what drugs may be available. Those in the 9 to 12 range are considered moderate, but may require airway control. Specific Test Function Brain Area Tested Points What is the year/season/month/date/day of the week Orientation (Frontal) 5 (1 for each correct answer) What state/county/hospital/floor are you in Name an object you point to , such as a Naming (Dominant Temporoparietal) 2 wristwatch or pen. Use discretion in planning Outdoor classes in the sun will be intense physical activities. Standing in the shade on a sunny day is cooler, and being below the crest of a hill, protected from the breeze eliminates the cooling effects of the wind, so it is warmer. Shaded Dry Suspend by wire or Bulb string/Support thermometer by hook Plywood top or string Globe Thermometer 12-14" x 8", light wood suspended by wire frame and cover with or string thermal screen, coolshade or equivalent or use std weather enclosure. Rubber Wet Bulb stopper Wick Bottom to Thermometer be open 3/8-5/8 in brass tube 3/4" Flask soldered onto sphere 6" diameter metal sphere 2 ft. Non-combat situations: Clear the decision not to resuscitate with medical consultants if possible. If it is not possible, do not resuscitate the following casualties: 1) Victim is obviously dead, characterized by signs such as: i. In a combat situation, body recovery should be attempted unless the attempt exposes the rescue team to undue danger. In non-combat situations, attempt body recovery only if it can be accomplished with a minimum of risk to the rescue team. If there is any suspicion of death as a result of foul play or other forensic circumstances (suicide, homicide, neglect, accident, etc. In the event of a military aircraft crash, do not disturb the scene except to assess and resuscitate any casualties which are not dead (see above). If the casualties must be moved to perform medical treatment, every attempt should be made to record the exact location where the patient was found, and his/her exact position (photographs from multiple angles are helpful). Body recovery may be the responsibility of local law enforcement or military authority, depending on the circumstances and location of the mishap. In most circumstances, it is best to leave the body or bodies in position until investigating authorities arrive and survey the site.

Lung cavity Suggested by: localized bronchial breathing hypertension lifestyle changes generic nifedipine 30 mg free shipping, otherwise normal examination blood pressure chart with age buy 30 mg nifedipine overnight delivery. Pulmonary Suggested by: chronic dry cough blood pressure chart by who nifedipine 20mg for sale, occupational exposure fbrosis/interstitial or evidence of underlying connective tissue disease blood pressure medication and lemon juice generic nifedipine 30 mg on-line. Incidental due to Suggested by: late in inspiration prehypertension meaning in urdu generic 30 mg nifedipine visa, disappear on normal secretions coughing blood pressure normal high buy line nifedipine. Pulmonary oedema Suggested by: background fatigue and exertional due to acute left breathless, cardiac risk factors. Displaced apex beat, ventricular failure or 3rd heart sound, bilateral basal fne crackles. Confrmed by: acute onset, (2) bilateral infltrates, (3) pulmonary capillary wedge pressure < 9mmHg or no congestive cardiac failure, (4) PaO2:FiO2<200 in the presence of good left ventricular function. Clubbing, cyanosis, reduced chest of cases have no expansion, coarse late inspiratory bibasal crackles. Specialist opinion about detailed lung function, lung biopsy, immunosuppression, antifbrotics, palliation. Consolidation Suggested by: reduced breath sounds, bronchial due to bacterial breathing, increased tactile vocal fremitus, reduced infection, but possibly percussion note. Clubbing, typically bilateral consolidation, and bilateral coarse late inspiratory crackles. Pulmonary Suggested by: chronic dry cough, occupational exposure or fbrosis/ evidence of underlying connective tissue disease. Clubbing, interstitial cyanosis, reduced chest expansion, coarse late inspiratory lung disease bibasal crackles. Severe pleural Suggested by: chest pain, weight loss, history of asbestos thickening. Attempts to examine the upper airway outside of a specialist setting may make matters worse. Anaphylaxis Suggested by: onset over minutes, history of recent allergen causing exposure, feeling of dread, fushing, sweating, facial laryngeal oedema, urticaria, warm clammy extremities, dyspnoea and oedema tachypnoea, wheeze. A lesion just above the carina can be immediately life-threatening as neither lung can be ventilated, and tracheostomy will also not get below the obstruction. Acute bilateral Suggested by: change in voice, bilateral reduced breath vocal cord sounds, and wheeze. Sudden stridor, severe cough, low-pitched, monophonic wheeze, and reduced breath sounds, typically on the right. Tracheal Suggested by: stridor, over weeks to months, bilateral tumours or reduced breath sounds, and bilateral wheeze. Can large airways be focal (unilateral) or bilateral wheeze, depending on site by mediastinal of obstruction. Endobronchial Suggested by: smoker, weight loss, cough, chest pain, and carcinoma haemoptysis, clubbed. Unilateral wheeze (typically occur (benign lesions below the carina) and unilateral reduced breath sounds. Inhalation of Suggested by: history of putting an object in mouth, foreign body. Tracheal Suggested by: stridor over weeks to months, bilateral tumours reduced breath sounds, and bilateral wheeze. Can be by mediastinal focal (unilateral) or bilateral wheeze, depending on site of masses obstruction. Tracheal blunt Suggested by: history, pain and swelling, change in voice trauma over minutes or hours after trauma. Exacerbation Suggested by: widespread polyphonic wheeze with of asthma exacerbations over hours. Pulmonary Suggested by: background fatigue and exertional breathless, oedema due cardiac risk factors. Any advanced Suggested by: progressive onset over weeks or months malignancy of specifc symptoms. Psychiatric Suggested by: sleep disorder, poor concentration, social illness (mainly withdrawal, lack of interest in usual activities, etc. Excessive Suggested by: gradual and progressive weight increase over caloric intake months to years, no other associated symptoms. Congestive Suggested by: weight gain over days to months, dyspnoea, cardiac failure orthopnoea, paroxysmal nocturnal dyspnoea (PnD), liver enlargement and tenderness, gallop rhythm, leg oedema. Hypothyroidism Suggested by: weight gain over weeks to months, cold intolerance, constipation, lethargy, coarse and dry skin, pufy eyelids. Premenstrual Suggested by: premenstrual weight gain over days, breast fuid retention swelling and tenderness, fnger swelling. Polycystic Suggested by: weight gain over years, oligomenorrhoea ovary or amenorrhoea, central obesity, hirsutism, acanthosis syndrome nigricans, acne. Liver cirrhosis Suggested by: weight gain over weeks to months, bilateral with ascites bulging fanks, shifting dullness, fuid thrill, sudden and rapid weight gain. Nephrotic Suggested by: weight gain over weeks to months, generalized syndrome oedema, pufy eyelids, abdominal distension, weight gain may be sudden and rapid. Also Smoking cessation, alcohol excess, menopause, klinefelter syndrome, Other endocrine disorders: hypopituitarism, acromegaly, insulinoma, hypogonadism. Oesophageal Suggested by: undigested solid food and fuid in vomitus, stricture heartburn. Confrmed by: barium swallow, oesophagogastroscopy showing food residue and fxed narrowing. Oesophageal Suggested by: dysphagia to solid food frst, then semisolid, carcinoma and fnally fuid. Confrmed by: barium swallow showing flling defect, fbreoptic gastroscopy with biopsy of tumour. Achalasia Suggested by: vomiting after large meals, undigested solid food and fuid, nocturnal regurgitation. Achalasia Suggested by: vomiting after large meals, undigested solid food and fuid, dysphagia to fuid, nocturnal regurgitation. Confrmed by: barium swallow demonstrating the absence of peristaltic contractions, oesophagogastroscopy showing dilatation. Gastric outlet Suggested by: intermittent vomiting h after eating, obstruction abdominal fullness or bloating, distended upper abdomen. Small intestinal Suggested by: abdominal pain, anorexia, bilious vomitus, tumour. Gastroparesis Suggested by: intermittent vomiting, occurs h after eating, due to diabetes abdominal fullness or bloating, distended upper abdomen, mellitus succussion splash, history of diabetes. Confrmed by: oesophagogastroscopy, double contrast barium meal showing normal mucosa but dilatation. Acute Suggested by: nausea and vomiting after fatty food with cholecystitis colicky abdominal pain. Initial investigations (other tests in bold below): test urine, examine stools (and send for culture, etc). Confrmed by: cultures of blood, stool, vaginal swab, for staphylococcus and toxin. Malaria Suggested by: recent travel to malaria zone, periodic (Plasmodium paroxysms of rigors, fever, sweating, nausea. Confrmed by: iblood glucose, dpH, ketonaemia or ketonuria or dplasma bicarbonate < 5mmol/L. Hypercalcaemia Suggested by: lethargy, confusion, constipation, muscle weakness, polydipsia and polyuria. Lead poisoning Suggested by: anorexia, personality changes, headaches, metallic taste, loss of sensation. Vitamin Suggested by: iintracranial pressure, drowsiness, A intoxication headache, irritability, muscle pain and weakness. Raised intracranial Suggested by: being worse in morning, on coughing and pressure leaning forward, papilloedema, pupillary dilatation, bradycardia, increased pulse pressure. Epilepsy idiopathic Suggested by: aura, altered consciousness, abnormal or seceondary to movements. Sliding Suggested by: occasional chest pain precipitated by heavy hiatus hernia meals, lying fat. Acute otitis Suggested by: fever, earache, decreased hearing, otorrhoea media (in if eardrum is perforated, accompanying upper respiratory children) infection symptoms. Anaphylaxis Suggested by: bronchospasm, laryngeal oedema, fushing, urticaria, angioedema. Also Diabetic gastroparesis, iintracranial pressure, oesophageal or pyloric obstruction, any viral or bacterial infection, etc. Remember that haemolysis causes iurinary urobilinogen and decreased serum haptoglobin. Hepatic failure causes increased serum unconjugated bilirubin, but intrahepatic or extrahepatic biliary obstruction results in increased serum conjugated bilirubin. Confrmed by: no bilirubin, no urobilinogen in the urine, and normal serum bilirubin. Confrmed by: i(unconjugated and thus insoluble) serum bilirubin, but normal (conjugated and soluble) bilirubin, and thus no ibilirubin in urine. Confrmed by: iserum conjugated bilirubin and thus iurine bilirubin but no iurobilinogen in urine. Confrmed by: iserum bilirubin (unconjugated and thus insoluble), but normal conjugated and thus soluble bilirubin, and in turn no bilirubin in urine. Malaria Suggested by: recent travel to malaria zone, periodic paroxysms of rigors, fever, sweating, nausea. Confrmed by: iserum bilirubin (unconjugated), but no (conjugated) bilirubin in urine. Confrmed by: drug levels and improvement after stopping the paracetamol, ofending drug. Alcoholic Suggested by: history of drinking, presence of spider naevi and hepatitis other signs of chronic liver disease. Confrmed by: iconjugated bilirubin and thus urine bilirubin but no iurobilinogen in urine. Confrmed by: +ve anti-mitochondrial antibody, iserum IgM, infltrate around hepatic bile ducts, and cirrhosis on liver biopsy. Drug Suggested by: drug history of oral contraceptive pill, induced phenothiazines, anabolic steroids, erythromycin, etc.

Quality 30 mg nifedipine. unboxing: iHealth Feel Wireless Blood Pressure Monitor.

References

• Juvela S. Aspirin and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. J Neurosurg 1995;82:945-52.
• Castellani M, Vanoli M, Cali G, et al. Ventilation-perfusion lung scan for the detection of pulmonary involvement in Takayasu's arteritis. Eur J Nucl Med 2001;28(12):1801-5.
• Du MQ, Diss TC, Dogan A, et al. Clone-specific PCR reveals wide dissemination of gastric MALT lymphoma to the gastric mucosa. J Pathol 2000;192:488.
• Anderson CS, Heeley E, Huang Y, Wang J, Stapf C, Delcourt C, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013 Jun 20;368(25):2355-65.
• Toyoda M, Ebihara Y, Kato H, Kita S. Tracheobronchial amyloidosis: histologic, immunohistochemical, ultrastructural, and immunoelectron microscopic observations. Hum Pathol 1993;24:970-6.
• Hartmann JT, Einhorn L, Nichols CR, et al. Second-line chemotherapy in patients with relapsed extragonadal nonseminomatous germ cell tumors: results of an international multicenter analysis. J Clin Oncol 2001;19(6):1641-1648.
• Eichhorn J, Sima D, Lindschau C, et al: Antiendothelial cell antibodies in thromboangiitis obliterans, Am J Med Sci 315:17-23, 1998.