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  • Previous studies reveal three systems closely involved in AMD pathogenesis: lipid metabolism, oxidation and inflammation. These systems are also involved in Alzheimer’s disease, atherosclerosis and glomerulonephritis.
  • Along with other molecules, oxidized lipids and lipid-related molecules accumulate in the Bruch’s membrane (BrM) of retina, brain parenchyma, arterial intima, and glomerular basement membrane (GBM).
  • These lesions cause an increased inflammatory response by activating the complement system as well as recruiting macrophages. As excessive inflammatory damage builds up, pathologic events occur in the eye, brain, blood vessels and kidneys.
  • Alzheimer’s disease (AD), atherosclerosis (AS) and glomerulonephritis (GN).
  • Under oxidative stress, lipid deposits called drusen form in the retina and trigger chronic inflammation by activating the complement system. Then, immune cells such as macrophages facilitate more severe pathogenesis.
  • Although endogenous Coenzyme Q10 is the most active antioxidant in human, statin treatment have been found to decrease this natural defense mechanism [129, 130].
  • There are several types of drusen with different morphology and contents [33]. Soft drusen have homogenous content and exist in the macula region, while hard drusen have substructures and appear in both macular and peripheral regions [33, 34].
  • Drugs that resemble our endogenous antioxidant Coenzyme Q10 might be able to address the oxidized versions of cholesterol such as 7kCh or 24S–OHC discussed in this review.
  • . Since anti-Aβ antibodies demonstrated limited efficacy, one potential direction is to turn our research attention to pharmacological agents that target ApoE.
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  • Targeted sequencing was performed by others on 3,340 AMD samples from the Michigan, Mayo, AREDS, Pennsylvania (MMAP) sample set
  • Since fundus photographs were taken starting at year 2 (20), we also eliminated any progression events reported within the first 2 y, as these were unlikely to be the result of treatment assignment.
  • 3 or 4 AMD at baseline who had been treated with placebo or the AREDS formulation were evaluated for differences in the risk of progression to NV
  • , we selected rs3766405 and rs412852 to tag the two major CFH haplotypes as has been done previously (12, 13).
  • Klein et al. (10) first observed that the benefit of the AREDS formulation was eliminated for subjects with high-risk CFH alleles. The authors postulated that this effect was due to the high-dose zinc component of the AREDS formulation. Awh et al. (12) analyzed the response to AREDS nutritional supplements as influenced by CFH and ARMS2 genetic risk in 989 AREDS subjects and confirmed the observation of Klein et al. with regard to CFH, while identifying an opposite interaction with ARMS2 polymorphisms.
  • Analysis of CFH and ARMS2 genotype groups from a validation dataset reinforces this conclusion
  • In particular, Awh et al. (12) have stated that genotype groups, defined by combinations of variants in the CFH and ARMS2 genetic regions, can identify individuals who benefit greatly from treatment with the AREDS formulation, as well as those who derive no benefit, or are maybe even harmed.
  • Age-related macular degeneration (AMD) is the leading cause of severe vision loss in the elderly and has major economic and quality-of-life impact
  • . We show that individual variation at complement factor H and age-related maculopathy susceptibility 2, genes which predispose to AMD, also determines the effectiveness of nutritional prophylaxis
  • We identified strong interaction of genetics with AREDS formulation treatment on the development of NV. Individuals with high CFH and no ARMS2 risk alleles and taking the AREDS formulation had increased progression to NV compared with placebo.
  • . By aggregate analysis of multiple (thousands) random discovery and validation sets generated through resampling of the main dataset, predictors of NV progression can be accurately identified by observing their incremental contribution to model accuracy.
  • We restricted this analysis to subjects with category 3 or 4 AMD at baseline, which are the subgroup of subjects for whom the AREDS formulation was reported beneficial in the original AREDS analysis (9).
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  • Besides proteins, miRNAs are interesting biomarker candidates for AMD, since AMD-specific miRNA profiles have been identified in plasma and serum.
  • Supplements Abstract “Omics” refers to high-throughput analyses of genes, proteins, or metabolites in a biological system, and is increasingly used for ophthalmic research. These system-based approaches can unravel disease-related processes and are valuable for biomarker discovery. Furthermore, potential therapeutic targets can be identified based on omics results, and targeted follow-up experiments can be designed to gain molecular understanding of the disease and to test new therapies. Here, we review the application of omics techniques in eye diseases, focusing on age-related macular degeneration (AMD), diabetic retinopathy (DR), retinal detachment (RD), myopia, glaucoma, Fuchs' corneal dystrophy (FCD), cataract, keratoconus, and dry eyes. We observe that genomic analyses were mainly successful in AMD research (almost half of the genomic heritability has been explained), whereas large parts of disease variability or risk remain unsolved in most of the other diseases. Other omics studies like transcriptomics, proteomics, and metabolomics provided additional candidate proteins and pathways for several eye diseases, although sample sizes in these studies were often very small and replication is lacking. In order to translate omics results into clinical biomarkers, larger sample sizes and validation across different cohorts would be essential. In conclusion, omics-based studies are increasing in ophthalmology, and further application to the clinic might develop in the years to come. Integration of genomics with other type of omics data has the potential to improve the accuracy of predictive tests. Moreover, in the future, omics may lead to stratification of patients into subgroups based on molecular profiles, enabling the development of personalized treatments. Common eye diseases are often complex, multifactorial diseases without classic Mendelian inheritance. Several genetic and environmental risk factors have been associated with these diseases, but their combinatorial effects and implication in pathogenic mechanisms remain poorly understood.1 Low-throughput genetic and subsequent functional testing of candidate genes and proteins provide only limited information for these type of diseases. Therefore, there is a need for high-throughput analyses, so that a whole system can be evaluated in a hypothesis-free way.2 Omics is the large-scale characterization and quantification of biological molecules, which went through rapid advancements over the last years due to technological improvements in sequencing techniques, mass spectrometry, and bioinformatic analyses. However, due to the very large scope of the datasets and disease heterogeneity, it might be challenging to extract biologically meaningful information from omics studies. Here, we discuss the use of omics techniques in ophthalmic research, focusing on age-related macular degeneration (AMD), diabetic retinopathy (DR), retinal detachment (RD), myopia, glaucoma, Fuchs' corneal dystrophy (FCD), cataract, keratoconus, and dry eyes. We describe the omics technologies used in ophthalmology, provide an overview of the achievements in each of these diseases so far, and discuss the potential for the future.  Omics Techniques Omics experiments can be performed on different layers within a biological system (Fig. 1). On the genomic level, the majority of discoveries have been made by genome-wide association studies (GWAS), in which DNA samples of large case–control cohorts are genotyped using microarrays, targeting a large number of single nucleotide polymorphisms (SNPs) distributed over the genome. Subsequent statistical analysis determines for each variant whether the frequency is significantly different in cases compared to controls.3 This approach is designed to detect associations of genetic variants that are mostly common in the population, which in general have small or modest effect sizes. In order to identify rare variants with relatively larger effect sizes, microarrays targeting rare variants (exome chips), whole exome sequencing (WES), or even whole genome sequencing (WGS) is more effective.4,5 Although WES and WGS have not been used very extensively yet in common eye diseases because of the still relatively high costs, an increase in their use is expected in the upcoming years. Furthermore, relevant information can be extracted by developing and applying algorithms to detect gene–gene and gene–environment interactions. These higher-order interaction effects may explain additional genetic variability in common eye diseases.
  • The largest GWAS so far, which analyzed DNA samples of 16,144 patients and 17,832 controls using exome chips, identified 52 AMD-associated genetic variants at 34 genomic loci.22 Additionally, two relatively small case–control WES studies have been reported for AMD.23,
  • AMD research would benefit from lipidomics studies, of which one has been reported so far
  • This might change in the future, if, for example, a genetic test could predict the efficiency of complement-inhibiting treatment for AMD patients. 
  • On the genomic level, the majority of discoveries have been made by genome-wide association studies (GWAS), in which DNA samples of large case–control cohorts are genotyped using microarrays, targeting a large number of single nucleotide polymorphisms (SNPs) distributed over the genome.
  • complement cascade, lipid metabolism, and extracellular matrix (ECM) remodeling to be the major pathways implicated in AMD pathogenesis (Supplementary Table S1).
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  • ar edema will develop in the interval before the next examination). The algorithm extends the screening interval for patients with a low risk of proliferative retinopathy or clinically significant macular edema to 3 or 4 years, which would reduce the frequency of eye examinations in the population of patients with type 1 diabetes by more than 50% over a 20-year period.
  • Diabetes Control and Complications Trial (DCCT) and the Epidemiology of Diabetes Interventions and Complications (EDIC) Research Group
  • ady been studied, notably by Aspelund et al.5 Their algorithm used both epidemiologic and clinical data, including the type and duration of diabetes, glycated hemoglobin or mean blood glucose levels, blood pressure, and the presence and grade of retinopathy
  • patients receiving hydroxychloroquine and its analogues state that screening should begin 5 years after the initiation of these agents in most patients, barring any macular abnormalities detected on baseline testing
  • ecting disease at a stage at which treatment will make a difference. However, even when a screening test is considered to be effective, questions remain. At what age should screening begin or end? How frequently should screening be performed?
  • mellitus. In the current cost-conscious era of health care, there is a movement to reduce unnecessary screening for several retinal diseases; this movement is heading toward what the authors call an “evidence-based retinal screening schedule.”
  • However, emerging data indicate that anti-VEGF injections can reverse diabetic retinopathy and perhaps even increase perfusion of the retina.10 Thus, screening algorithms and intervals may be entirely different in the future with broader use of advanced retinal imaging to detect retinal nonperfusion that is amenable to treatment.
  • beyond 1 year in low-risk patients was reasonable, since the data showed little difference between the 1-year and 2-year screening frequency with respect to clinical outcomes.4
  • Similarly, a tiered approach based on weight gain in newborns and baseline fundus photographs has been proposed to reduce unnecessary screening for retinopathy of prematurity.3
  • s. They found that an accurate assessment of the risk of proliferative diabetic retinopathy or clinically significant macular edema was possible with the use of only the patient’s current retinopathy status and glycated hemoglobin levels.
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1 annotations
  • hyper-permeable choroidal capillaries, which, in association with retinal pigment dysfunction, cause a serous detachment of the neurosensory retina
  • Other associations to CSCR have been described. Cotticelli determined that the odds ratio of Helicobacter pylori in CSCR patients is 4.6 (95% CI 1.28–16.9) and other prospective studies revealed that H. pylori infection was present in 53% and 69% of patients with CSCR.[16][17][18] Rahbani-Nobar demonstrated that treating the H. pylori infection is associated with more rapid sub-retinal fluid resorption.[19] Methylenedioxymethamphetamine (MDMA), also known as ecstasy, and sildenafil have also been associated with development of CSCR.[20][21]
  • exact mechanisms behind CSCR have not been elucidated, many associations have been found
  • Central serous chorioretinopathy is associated with increased sympathetic activity, and obstructive sleep apnea is known to cause such increases
  • Foveal or peri-foveal leakage can be present in 50% of eyes. Prunte and Flammer demonstrated the presence of delayed arterial filling and ischemia followed by capillary and venous congestion in areas of the choroid affected by CSCR, either or both of which could be the mechanism for increased permeability.[11]
  • A study showed that patients with CSCR have increased sympathetic activity and decreased parasympathetic activity based on tests of autonomic activity and reactivity.[9] Other theoretical causes of choriocapillary hyper-permeability and RPE damage include epinephrine,[32][44] ischemia,[32][11] inflammatory including H. pylori infection, and hormonal causes.[45] Epinephrine and norepinephrine has also been shown to be elevated in patients with active CSCR.[36][46]
  • Central serous chorioretinopathy (CSCR) is the fourth most common retinopathy after age-related macular degeneration, diabetic retinopathy and branch retinal vein occlusion
  • Most patients who present with CSCR are between the ages of 28 to 68 years with an average age of 43 years.
  • Typically, patients complain of central vision loss or distortion with a possible central scotoma
  • who are over 50 years of age are more likely to have bilateral disease (50%) with RPE loss and choroidal neovascularization compared to those less than 50 years of age (28.4%).
  • Typically, patients complain of central vision loss or distortion with a possible central scotom
  • Typical fluorescein angiography include the ink blot appearance (31%), smokestack pattern (12%), and minimally enlarging spot (7%).[50] Fluorescein angiography is also used to rule out sub-retinal neovascularization.[1]
  • A RPE detachment may be seen on OCT in up to 63% of eyes[49] and if it encircles the detachment, a “halo” may be seen around the detachment.[48]
  • Moreover, near infrared fundus autofluorescence (NIA) imaging (787nm) is able to study the RPE, the choriocapillaris, and choroid, by determining melanin fluorescence .
  • Acute CSCR is a self-limited condition with resolution of neurosensory retinal detachment and generally good recovery of visual acuity within three months.[2] Of note, recurrences of CSCR have been documented in up to 50% of patients within one year.[51]
  • presenting
  • Spironolacton
  • Furthermore, OCT can be helpful in following chronic CSCR patients to track resolution. Enhanced depth imaging OCT technology has been able to identify choroidal thickening bilaterally, even in patients with unilateral CSCR.[35]
  • Limited studies investigating prognostic markers found that outer nuclear layer thickness at the fovea correlates with BCVA in patients with resolved CSCR[53] and that total foveal thickness correlates with BCVA in patients with chronic CSCR with symptoms for 21.8 (7-36) months.[54]
  • Melotonin is an endogenous neuromodulator that has been linked to circadian cycles and sleep regulation, aging, and neuroprotection via an antioxidant mechanism.61 Melotonin also has an inhibitory effect on corticosteroids and has a minimal side effect profile, making it a target for CSCR treatment.
  • As CSCR usually resolves spontaneously within 2 to 3 months, observation is currently standard of care for newly presenting cases.[8]
  • . Patients with Type A personality should be addressed by lifestyle modification and stress management, however there is no high quality data to support this.
  • . Initiation of medication should be postponed or avoided if serum potassium concentration is >5.5 mEq/L, creatinine clearance is <50 mL/min, or serum creatinine is >2 mg/dL in men and >1.8 mg/dL in women
  • Unlike conventional laser, SML can be safely applied to the fovea. Fluorescein angiography and indocyanine green (ICG) angiography can be supplemented to determine areas of treatment.
  • Low-dose aspirin has been explored in treating CSCR. Elevated levels of plasminogen activator inhibitor 1 (PAI 1), a marker of platelet aggregation, have been linked to steroid use and have been measured in patients with CSCR.[63]A prospective study of 113 eyes with CSCR showed faster improvement in BCVA compared to control.[63]
  • Photodynamic therapy (PDT) with verteporfin, a photosensitizer that accumulates in vessels and helps target therapy, causes endothelial damage and vascular hypoperfusion to inhibit the choroidal hyperpermeability seen in CSCR. Several reports and studies have demonstrated that PDT can be used in chronic CSCR patients to decrease SRF and improve BCVA.[77]
26 annotations
  • SF3B1 drive age-related clonal hematopoiesis, myelodysplastic syndromes (MDS) and other neoplasms
  • . To understand the molecular basis of these observations, we analyzed global RNA splicing in Sf3b1K700E/+ hematopoietic cells
  • . However, we found a little overlap between aberrantly spliced mRNAs in mouse versus human, suggesting that anemia may be a consequence of globally disrupted splicing.
  • The mutations are missense, heterozygous and cluster strongly within HEAT domains 4–8 of the protein, suggesting that they may be neomorphic gain-of-function variants.2
  • . However, the molecular effects of SF3B1 mutations and the mechanisms through which they drive clonal expansion and dyserythropoiesis remain obscure.
  • Furthermore, it was recently demonstrated in primary human cancers and cell lines that SF3B1 mutations are associated with aberrant splicing through recognition of alternative 3′ ss located around 10–25 nt upstream of the canonical 3′ ss.13
  • All animal studies were performed according to the Animals Scientific Procedures Act 1986 (ASPA), as recently revised to transpose European Directive 2010/63/EU on the protection of animals used for scientific purposes.
  • Next, as SF3B1-K700E behaves like an initiating mutation in MDS7 and can also drive clonal hematopoiesis in elderly individuals,8
  • In human SF3B1-mutant MDS, ring sideroblasts are thought to arise as a result of aberrant splicing of key genes involved in heme biosynthesis, such as ABCB7, TMEM14C, ALAS2 and SLC25A37.11, 25, 30, 35 In keeping with the mouse–human differences in target transcripts, we did not find the splicing or expression levels of any of these genes to be noticeably disrupted by Sf3b1-K700E, and, consistent with this, did not identify ring sideroblasts in the bone marrow of mutant mice.
  • corroborated by their recent identification in hematopoietic cell clones found in at least 2% of otherwise healthy individuals aged 70 years or older.8
  • . Despite these marked differences, Sf3b1K700E/+ mice did go on to develop progressive anemia, a central feature of SF3B1-mutant MDS.
  • Briefly, a pool of two BACs containing the region of interest of the Sf3b1 locus, RP24-64H9 and RP24-439B17, were used to generate the gateway-adapted intermediate plasmid by inserting the ‘U’ and ‘G’ cassettes.14
12 annotations
4 annotations
  • Other benefits of teledermatology and teledermoscopy reported by patients included shorter waiting times, more frequent monitoring, and improved privacy and comfort. One study measuring patient satisfaction using a 5-point satisfaction scale reported higher satisfaction with waiting times (2.9 FTF vs 4.0 teledermatology) and overall satisfaction compared with FTF (3.8 FTF vs 4.5 teledermatology).3
  • A systematic review7 published in 2011 found that the accuracy of FTF dermatology was better than SAF teledermatology for diagnosing skin conditions (weighted mean difference, 11% for primary, 19% for aggregated diagnostic accuracy). However, the authors concluded the levels of diagnostic accuracy and concordance of both SAF and LI teledermatology were still acceptable compared with FTF dermatology.
  • In 2 of 11 studies a total of 55 (100%) consumers submitted their own images (with and without dermoscopy) and reported they were satisfied with the ease of use14 and willing to pay out-of-pocket costs for teledermatology services.32 Economic modeling was used to estimate willingness to pay,32 suggesting consumers would pay an average of A$110 to have teledermoscopy review as a health service option, in addition to the currently available options of skin self-examination, skin cancer clinic, or general practitioner clinic.
  • Future researchers in this field should aim to overcome the methodological limitations including lack of histopathology as reference standard, sample and diagnostic bias.
  • The most methodologically sound way to test the diagnostic accuracy of teledermatology would be assigning different clinicians for the teleconsultations and FTF consultations, to prevent bias resulting from recall of the lesions and associated diagnosis the second time they see them.
  • Very few studies (4 of 21) assessed health services outcomes measures.10,31,36,38 Those that did found the use of teledermatology could reduce waiting times and result in earlier assessment and treatment, patients reported high satisfaction and were willing to pay out of pocket for access to such services. On the other hand, clinicians reported higher diagnostic difficulty for teledermatology cases compared with FTF consultations and levels of diagnostic agreement were found to be related to clinician-reported diagnostic confidence.
  • The evidence from this review also supports the implementation of teledermatology as a referral and/or triage tool.
7 annotations
  • While histopathology is still the most accurate diagnostic method for skin cancers and remains the gold standard, it is important to take this margin of diagnostic discordance into account when setting thresholds for acceptable levels of diagnostic accuracy for new diagnostic tests.
  • For the diagnosis of skin lesions, this is not straightforward. When a biopsy is taken the reference standard is the histopathologic result but when the lesion is considered benign, the clinical diagnosis by the dermatologist is accepted as the reference standard.
  • When separating malignant and benign lesions, telediagnoses of malignant lesions were histopathologically confirmed in 62% to 100% of cases, depending on the study. Of note, the study reporting 100% agreement between telediagnosis and histopathological diagnosis for malignant lesions only included 8 malignant lesions.26
  • One study reported very high sensitivity and specificity of teledermatology for both malignant melanocytic lesions (sensitivity, 100%; specificity, 97%-98%; n = 6) and malignant nonmelanocytic lesions (sensitivity, 97%; specificity, 92%-94%, n = 58), for both clinical and dermoscopic images (no significant differences between these methods).11
  • One study35 reported higher diagnostic difficulty for teledermatology consultations vs FTF consultations. Clinicians using teledermatology reported 61% to 87% cases as high difficulty compared with the clinician seeing patients FTF, who reported 54% as high-difficulty diagnose
  • . Addressing the limitations of previous research will help to determine whether teledermoscopy is a safe and appropriate alternative to in-person assessment, which is particularly important for countries with high rates of skin cancers and geographically dispersed populations, including Australia and the United States.
  • An Australian study of 49 participants examining the introduction of mobile dermoscopy into current skin self-examination recommendations reported barriers to effective self-monitoring.13
  • Four other studies reported diagnostic accuracy of teledermatology, without any comparison with FTF diagnoses. These studies reported agreement between telediagnosis and the reference standard of 51% to 100%.
  • 40 lesions, 24 did not meet the asymmetry and color rule communicated to consumers as a method for identifying concerning lesions. However, none of these lesions were subsequently diagnosed as melanoma.
  • Four studies examined the effect of teledermatology consultations on waiting times to FTF appointments, waiting time to diagnosis, and/or waiting time to surgery. Reductions in waiting times in teledermatology groups were reported in all studies.
  • The most methodologically sound way to test the diagnostic accuracy of teledermatology would be assigning different clinicians for the teleconsultations and FTF consultations, to prevent bias resulting from recall of the lesions and associated diagnosis the second time they see them
11 annotations
  • The intervention group was more likely than the control group to submit images from the legs, but this did not improve their ability to find all the lesions that were concerning on CSE.
  • Specific to skin cancer early detection, dermoscopes have been developed that can be attached to smartphones (forming a mobile teledermoscope). This device allows magnified images of skin lesions to be taken under polarized light for electronic transmission to a specialist.
  • We also sought to estimate the sensitivity, specificity and concordance of mobile teledermoscopy when compared with clinical skin examination (CSE).
  • Both groups overlooked a similar number of lesions, and we combined them for clinical accuracy analyses
  • > 30% of lesions from the back, which is important as the back is a common location of melanoma in both men and women.[23
  • Our null results could either indicate that the 10-step guide is insufficient to improve the thoroughness of SSE, or that the mobile teledermoscopy instructions sufficiently guided people towards a thorough SSE in both groups
  • Lesions found during systematic examinations are generally thinner than melanomas found otherwise
  • However, it was apparent in our study findings, corroborating our previous findings,[27] that consumers tend to photograph many unconcerning lesions such as actinic or seborrhoeic keratoses, indicating that better training or instructions are needed to improve lesion selection.
  • mobile teledermoscopy.
  • On average, participants overlooked two suspicious skin lesions that the doctor considered would have been worthwhile photographing for further monitoring. However, the numbers were small and the study lacked anatomical images to determine the exact location of each lesion.
  • oups, range 0–21) were submitted. Of these, two were of poor quality and did not allow telediagnosis; three showed only the anatomical location but excluded the dermoscopic image.
  • The importance of a whole-body CSE is reinforced by several studies that indicate that up to one-third of melanomas may be missed if only the index lesion is examined.[30-32]
12 annotations
  • Almost all risk prediction models also contain the number and size of nevi, as well as the presence of nevi with atypical features that are independently associated with melanoma risk. In the absence of formal population-based screening programs for melanoma in most countries worldwide, people with high-risk phenotypes may need to consider regular monitoring or self-monitoring of their nevi,2 especially since most melanomas are self-detected or found by a friend or relativ
  • Recommendations for follow-up frequency vary between different sets of international guidelines, with some recommending a physician visit every 3 months.6
  • A New Zealand study examined a hybrid model, whereby patients went to a nurse-staffed virtual clinic for their clinical and dermoscopic pictures to be taken and sent to teledermatologist.15 Interestingly, only 36% of the virtual clinic patients were recommended treatment compared with patients in the face-to-face clinic (60%), potentially as a result of the absence of full-body examination at the virtual clinic.
  • Although there is limited support for the sensitivity of skin self-examination,8 a number of studies have reported that the majority of initial and subsequent second melanomas are found by the patients themselves or their partners,9 especially among young people.10
  • . For example, moving follow-up from specialized melanoma clinics to family physicians has been tested in trials in the United Kingdom,
  • he study by Wu and colleagues11 in this issue adds significantly to the discussion on whether regular follow-up visits with clinicians could be replaced by patient self-monitoring with remote feedback by a teledermatologist
  • Recent results of other small studies indicate that people are just as likely to send clinically evaluable pictures if they use mobile teledermoscopy at home in their privacy.13
  • In conclusion, the findings from Wu and colleagues11 provide further support for the feasibility of consumer-driven mobile teledermoscopy.
8 annotations
  • kin lesion assessment and initiating referrals to dermatologists. Indeed, examination has shown to increase appropriate skin cancer diagnosis
  • Summarized evidence suggests that the diagnostic accuracy of in-person dermatology is better than teledermatology, and that the diagnostic concordance of teledermatology with in-person dermatology is overall acceptable
  • It is pointed out that teledermatology may decrease the likelihood of in-person examination by a dermatologist, and this may lead to worse diagnostic outcomes by inability to conduct a total body skin examination.
  • evaluation, which can be a useful adjunct to primary care. Waiting time for in-person dermatology appointment is often noted as a factor in patient preference for teledermatology, and some patients can avoid in-person referrals completely.
  • In practice, teledermatology is particularly useful for evaluating conditions such as rashes, eczema, psoriasis or inflammatory conditions, although it is not an adequate substitute for total body skin examination when dealing with suspected malignancies like melanoma
  • profound impact that lesion-based examination and targeted examination of high-risk populations by nondermatologists can have on skin cancer diagnosis.2–5
  • Some studies report that teledermatology has inferior diagnostic accuracy compared with in-person evaluation.7
  • Telemedicine can become an important element to improving health care access and delivery, reducing wait times for physician visits,9 and reducing costs.
8 annotations
  • Skin cancer is the most common cancer in the US, accounting for almost half of all cancers.
  • The app also reminds users to monitor any skin changes over time, and it includes information on skin cancer prevention.
  • number of smartphone apps claim to be able to assess certain skin changes and inform individuals whether such changes warrant a visit to a dermatologist for further analysis.
  • SkinVision uses a mathematical theory called "fractal geometry" to analyze photos of skin lesions and moles taken by the user
  • Three of the apps used algorithms to assess the risk of cancer among 188 photos of skin lesions
  • The other three apps that used algorithms, however, were found to incorrectly categorize a large number of skin lesions.
  • "With an accuracy of 81% in detecting melanoma, the algorithm might have some potential in the future for the evaluation of melanocytic nevi, but is to date insufficient to detect melanoma accurately," noted the researchers.
  • Melanoma is a skin cancer that forms in the cells responsible for skin pigmentation, known as melanocytes
  • before it has spread to other parts of the body - it is almost always curable.
  • The app then calculates a person's risk of skin cancer dependent on the characteristics of their mole.
  • most accurate app missed almost 30% of melanomas, diagnosing them as low-risk lesions.
  • The published studies suggest that, at this point, there is large variability in the sensitivity and specificity of these applications for melanoma detection.
  • Accuracy of a smartphone application using fractal image analysis of pigmented moles compared to clinical diagnosis and histological result,
13 annotations
  • In the setting of a pleural collection, consolidation and infective symptoms, imaging alone is unable to exclude infection, and thoracocentesis with microbiological assessment is required. Presence of gas locules within the c
  • In the setting of a pleural collection, consolidation and infective symptoms, imaging alone is unable to exclude infection, and thoracocentesis with microbiological assessment is required. Presence of gas locules within the collection or thickened enhancing pleural margins are strongly indicative of infection (see below).
  • ssed. The pleura is thickened due to fibrin deposition and in-growth of vessels with enhancement. At the margins of the empyema, the pleura can be seen dividing into parietal and visceral layers, the so-called split pleura sign, which is the most sensitive and specific sign on CT, and is helpful in distinguishing an empyema from a peripheral lung abscess (see: empyema vs lung abscess) 2-3.  The inner walls of the empyema are smooth.
  • cause of a large unilateral pleural collection. It is a potentially life-threatening condition requiring prompt diagnosis and treatment.
  • In the setting of a pleural collection, consolidation and infective symptoms, imaging alone is unable to exclude infection, and thoracocentesis with microbiological assessment is required. Presence of gas locules within the collection or thickened enhancing pleural margins are strongly indicative of infection (see below
  • 3. Pleural fluid is typically unilateral or markedly asymmetric
  • larger in one projection (e.g. frontal) compared to the orthogonal projection (e.g. lateral) 3. The lenticular shape (biconvex) is also suggestive of the diagnosis, as transudative/sterile pleural effusions tend to be crescentic in shape (i.e. concave towards the lung, see empyema vs pleural effusion). 
7 annotations
  • e portal vein to the hepatic vein, this intervention allows portal blood an alternative avenue for draining into systemic circulation.
  • A rare but serious complication is persistent TIPS infection, also known as endotipsitis.[6]
  • transient post-operative hepatic encephalopathy
  • . Decreased portal venous pressure in turn lessens congestive pressures along veins in the intestine so that future bleeding is less likely to occur. The reduced pressure also makes less fluid develop, although this benefit may take weeks or months to occur.
  • A less common, but more serious complication, is hepatic ischemia causing acute liver failure
  • Portal venous congestion causes venous blood leaving the stomach and intestines to be diverted along auxiliary routes of lesser resistance in order to drain to systemic circulation.
  • a special mesh tube known as a stent or endograft to maintain the tract between the higher-pressure portal vein and the lower-pressure hepatic vein.
  • The channel for the shunt is next created by inflating an angioplasty balloon within the liver along the tract created by the needle.
  • TIPS has shown some promise for people with hepatorenal syndrome.[2] It may also help with ascites.[3]
  • 25% of patients who undergo TIPS will experience transient post-operative hepatic encephalopathy caused by increased porto-systemic passage of nitrogen from the gut.[4
  • g catastrophic bleeding or direct liver injury, are relatively uncommon.
  • with the jugular vein as the usual entry site.
  • Thus, in people with advanced liver disease the shunting of portal blood away from hepatocytes is usually well tolerated.
  • Acute hepatic dysfunction after TIPS may require emergent closure of the shunt.
  • Lastly, the TIPS may become blocked by a blood clot or in-growth of endothelial cells and no longer function. This has been significantly reduced with the use of polytetrafluoroethylene (PTFE)–covered stents.[7]
  • Access to the liver is gained, as the name 'transjugular' suggests, via the internal jugular vein in the neck.
  • is normalized and the coronary and umbi
17 annotations
  • Contents[show] Biography Emery Huang is born in 1984. He is an adorable little kid who goes to a school where he has become wildly popular with everyone, especially the girls, simply because he's Asian. Emery loves dating the other girls at his school and it has become a running gag in the show for him to be seen with a new girlfriend in every episode. Emery acts like a stereotypical "ladies man" which, for kids as young as the girls he's dating, is exactly the perfect and most ingenious way to make a girl fall in love with you. Girls serve him hand and foot and are even so committed to their love for him, that they will willingly allow him to date another girl at the same time and be with him at the same time she is. Of course, they're only little kids, so basically, Emery gets to do whatever he wants with whoever he wants. He takes advantage of them as he's with a completely different girl in every episode. However, a girl named Bianca that he was seen dating in "The Shunning" was mentioned to still be in a relationship with him in a future episode. She was also the latest girl that he was seen dating, so this may have been the girl that he was going out with for the longest time, having dated her for at least eight episodes. (Seven if you chronologize episodes by broadcast order as opposed to production order). Emery's most notable relationship in the show would be that of his with Evan. The two of them are two peas in a pod together and could even be easily mistaken as twins. Most of the time, they are best friends who live off of each other and work together as a team and they often times flaunt their friendship in other people's faces. However, there are many times where they have shown to be polar opposites, with Evan being the two-shoes-do-gooder and Emery being the casual minded rule bending rebel. For instance, in the episode "Blind Spot", Evan was infected with the chicken pox and he spent his time trying to give it to Emery as a cruel joke and it turned into a huge scene. Emery eventually got infected but not after multiple clever and well-thought-out close calls avoiding him. Evan then congratulated his germs for helping him get his brother sick. Overall, Emery and his brother are on and off "frenemies" sort of speak, which is basically the relationship that every pair of siblings has for each other anyway. Personality Emery's personality is at a higher maturity level than his actual age. He acts like a stereotypical adult in his 20's. The guy he acts like is a ladies man who can get whoever he wants as a girlfriend. In every episode, he has a different girlfriend and sometimes, he'll go through multiple relationships over the coarse of a single episode and sometimes, he'll have two girlfriends at once. He'll always be mediocrely happy with his relationships he'll go through them like it's nobody's business. He is also introverted by filtering his thoughts and keeping them to himself. When he loses to Eddie in a game in the pool, he throws a tantrum which shocks Eddie and Louis. Eddie convinces Emery to speak his mind and Emery voices his strong yet not so nice opinions to Louis which hurt him. Louis ends up proud of Emery for voicing his opinions. Emery then reveals to Louis that he keeps jars under his bed to yell in when he is stressed out, which is something they agree to keep a secret from Jessica. Relationships Family Evan Huang
  • Family Evan Huang: Emery and Evan are the best of friends and they always get along all the time. They have an unspoken bond with each other, mostly because they have the same opinions and lifestyle. They work together as a team most of the time and the two of them together are unbeatable and they definately like to show off their friendship and rub it in the faces of others. However, like most siblings, Emery and Evan will occasionaly get
2 annotations
  • ulcerative colitis is usually limited to the mucosa and submucosa 5
  • Inflammatory pseudopolyps may be seen if large enough, in well distended bowel. In areas of mucosal denudation, abnormal thinning of the bowel may also be evident 2
  • The entire colon may be involved, in which case oedema of the terminal ileum may also be present (so-called backwash ileitis)
  • Involvement of the rectum is almost always present (95%) 1
  • frequently sessile and may appear to be a simple stricture.
  • Mucosal ulcers are undermined (button-shaped ulcers). When most of the mucosa has been lost, islands of mucosa remain giving it a
  • Mucosal ulcers are undermined (button-shaped ulcers). When most of the mucosa has been lost, islands of mucosa remain giving it a pseudopolyp appearance.
  • It is however contraindicated if acute severe colitis is present due to the risk of perforation
  • Non-specific findings, but may show evidence of mural thickening (more common), with thumbprinting also seen in more severe cases
  • CT will reflect the same changes that are seen with a barium enema,
  • In chronic cases, the bowel becomes featureless with the loss of normal haustral markings, luminal narrowing and bowel shortening (lead pipe sign).
  • , fat submucosal deposition is seen particularly in the rectum (fat halo sign). Also in this region, extramural deposition of fat, leads to thickening of the perirectal fat, and widening of the presacral space 1,2.
  • Small islands of residual mucosa can grow into thin worm-like structures (so-called filiform polyps)
  • t is
  • CT will reflect the same changes that are seen with a barium enem
  • ross section of the inflamed and thickened bowel has a target appearance due concentric rings of varying attenuation, also known as mural stratification 1-2.
16 annotations
  • immune systems because of illness or drugs, including:
  • signs of potential infection, including increased redness, swelling or discharge at a surgical site, or breakdown of a wound.
  • heart rate of more than 130 beats per minut
  • suspected sepsis and any high risk criteria and lactate below 2 mmol/litre: consider giving intravenous fluid bolus (in line with recommendations in section 1.8).
  • systolic blood pressure of 90 mmHg or less, or systolic blood pressure more than 40 mmHg below normal
  • carry out a venous blood test for the following: blood gas including glucose and lactate measurement blood culture full blood count C-reactive protein urea and electrolytes creatinine a clotting screen
  • source of infection
  • Do not rely on fever or hypothermia to rule sepsis either in or out
  • such as new onset
  • heart rate of 91–130 beats per minute or new-onset arrhythmia, or if pregnant heart rate of 100–130 beats per minute
  • refer[4] to critical care[5]
  • they meet any high risk criteria (see tables 1, 2 and 3) or
  •  mmol/litre: consider giving intravenous fluid bolu
  • Take into account that women who are pregnant, have given birth or had a termination of pregnancy or miscarriage in the past 6 weeks are in a high risk group for sepsis
  • Assess people who might have sepsis with extra care if they cannot give a good histor
  • the very young (under 1 year) and older people (over 75 years) or people who are very frail
  • factors that increase risk of sepsi
  • such as new onset abnormalities of behaviour, circulation or respiration.
  • have gestational diabetes or diabetes or other comorbidities
  • Take into account that some groups of people with sepsis may not develop a raised temperature. These include: people who are older or very frail people having treatment for cancer people severely ill with sepsis young infants or children
  • 1.6 Managing and treating suspected sepsis in acute hospital settings
  • Do not use a person's temperature as the sole predictor of sepsis.
  • give intravenous fluid bolus without delay (within 1 hour of identifying that they meet any high risk criteria in an acute hospital setting) in line with recommendation
  • r central venous access and initiation of inotropes or vasopressors.
  • give intravenous fluid bolus without delay (within 1 hour of identifying that they meet any high risk criteria in an acute hospital setting) in line with recommendations in section 1.8.
  • Alert a consultant to attend in person if an adult, child or young person aged 12 years or over with suspected sepsis and any high risk criteria fails to respond within 1 hour of initial antibiotic and/or intravenous fluid resuscitation. Failure to respond is indicated by any of: systolic blood pressure persistently below 90 mmHg reduced level of consciousness despite resuscitation respiratory rate over 25 breaths per minute or a new need for mechanical ventilation lactate not reduced by more than 20% of initial value within 1 hour.
26 annotations
  • al cold hemoglobinuria - Wikipediahttps://en.wikipedia.org/wiki/Paroxysmal_cold_hemoglobinuriaCachedSimilarParoxysmal cold hemoglobinuria (PCH), also known as Donath-Landsteiner syndrome, is a disease of humans that is characterized by the sudden presence of hemoglobin in the urine (called hemoglobinuria), typically after exposure to cold temperatures. It carries the name of the Austrian internists Julius Donath ...Paroxysmal Cold Hemoglobinuria: Background, Pathophysiology ...emedicine.medscape.com/article/200947-overviewCachedSimilar1 Apr 2015 - Paroxysmal cold hemoglobinuria (PCH) has the distinction of being the first, albeit rarest, type of autoimmune hemolytic anemia (AIHA) to be identified. ... In the latter half of the 19th century, the most common cause of paroxysmal cold hemoglobinuria was congenital or adult tertiary ...(function(){var l3=14;var l4=18;var l5=24;var t=15;try {if (t > l3){let n = 3;if (t > l4)n = t <= l5 ?4 :5;document.getElementById('rhs_title').className+=' rhstl'+n;} }catch (e){};})();People also askWhat is PCH in medical terms?D006457. Paroxysmal cold hemoglobinuria (PCH), also known as Donath-Landsteiner syndrome, is a disease of humans that is characterized by the sudden presence of hemoglobin in the urine (called hemoglobinuria), typically after exposure to cold temperatures.Paroxysmal cold hemoglobinuria - Wikipediahttps://en.wikipedia.org/wiki/Paroxysmal_cold_hemoglobinuriaSearch for: What is PCH in medical terms?What causes a cold agglutinin?This eventually causes red blood cells to be prematurely destroyed (hemolysis) leading to anemia and other associated signs and symptoms. Cold agglutinin disease can be primary (unknown cause) or secondary, due to an underlying condition such as an infection, another autoimmune disease , or certain cancers .Cold agglutinin disease - Genetic and Rare Diseases Information Centerhttps://rarediseases.info.nih.gov/diseases/6130/cold-agglutinin-diseaseSearch for: What causes a cold agglutinin?What is the Donath Landsteiner antibody?Practice Essentials. Two forms of cold antibody autoimmune hemolytic anemias are generally recognized: Donath-Landsteiner hemolytic anemia (DLHA) and cold agglutinin disease. DLHA is an intravascular hemolytic anemia caused by a cold-reacting immunoglobulin (Ig).11 May 2017Donath-Landsteiner Hemolytic Anemia: Practice Essentials ...emedicine.medscape.com/article/955176-overviewSearch for: What is the Donath Landsteiner antibody?What is biphasic antibody?Autoanti-P (Donath-Landsteiner) is an autoantibody of P specificity and is seen in individuals with paroxysmal cold hemoglobinuria (PCH). In PCH, autoanti-P is of IgG isotype and is a biphasic hemolysin (it is capable of hemolysis only after incubation at two different temperatures in vitro).P antigen system - Wikipediahttps://en.wikipedia.org/wiki/P_antigen_systemSearch for: What is biphasic antibody?FeedbackParoxysmal cold hemoglobinuria (PCH): MedlinePlus Medical ...https://medlineplus.gov › Medical EncyclopediaCachedSimilar1 Feb 2016 - Read our article and learn more on MedlinePlus: Paroxysmal cold hemoglobinuria (PCH)Paroxysmal Cold Haemoglobinuria. PCH information | Patienthttps://patient.info › Professional ReferenceCachedSimilar17 Sep 2010 - Paroxysmal cold haemoglobinuria (PCH) is an autoimmune haemolytic anaemia , caused by cold-reacting immunoglobulins. Paroxysmal Cold Haemoglobinuria ... After the acute phase is over, patients should be followed up for a few months in the haematology clinic. They may require daily/weekly review ...Haematology: Autoimmune haemolytic anaemia | GPonlinehttps://www.gponline.com/haematology-autoimmune.../haematology/.../1118275Cached29 Feb 2012 - Two forms of cold AIHA are cold haemagglutinin disease (CHAD) and paroxysmal cold haemoglobinuria (PCH), which is caused by antibody binding to erythrocytes in the cold, but activating complement and causing haemolysis at 37°C. Mixed AIHA, which is caused by both warm IgG and cold IgM ...Haematology Test Information | Pathology Serviceshttps://www.pch-pathlab.com/cms/?q=node/49CachedUnless otherwise specified, sample type required is venous blood in EDTA anticoagulant. Routine hospital turnaround times listed in each test refer to the average time taken from receipt in the laboratory to authorisation, while routine GP turnaround times refer to the average time between when they are collected by the ...Autoimmune Hemolytic Anemia - Hematology and Oncology - MSD ...www.msdmanuals.com › ... › Anemias Caused by HemolysisCachedSimilarAutoimmune hemolytic anemia is caused by autoantibodies that react with RBCs at temperatures ≥ 37° C (warm antibody hemolytic anemia) or < 37° C (cold agglutinin disease). Hemolysis is usually extravascular. The direct antiglobulin (direct Coombs) test establishes the diagnosis and may suggest the cause. Treatment ...[PDF]Guidelines for the investigation and treatment of Primary immune ...nssg.oxford-haematology.org.uk/...haematology/.../H-100-autoimmune-haemolytic-a...Cachedapheresis haematology consultant on-call). •. General Measures for all types of AIHA: • Stop the offending drug if a drug-induced haemolytic anaemia. • Treat any underlying infection if there is an infective cause (PCH is often precipitated by an upper respiratory tract infection, possible offending organisms include varicella,.Haematology Made Easy - Page 186 - Google Books Resulthttps://books.google.co.uk/books?isbn=1477246517Erhabor, ‎Adias - 2013 - ‎Antiques & CollectiblesIn people with PCH, a polyclonal IgG usually with anti-P autoantibody binds to red blood cell surface antigens in the cold. This can occur in a susceptible individual as blood passes through cold extremities in cold weather. When the blood returns to the warmer central circulation, the red blood cells are lysed with ...Management of paroxysmal cold haemoglobinuria: not only avoiding ...onlinelibrary.wiley.com/doi/10.1111/j.1365-2141.2008.07129.x/fullby N Win - ‎2008 - ‎Cited by 2 - ‎Related articles28 Jun 2008 - Whilst agreeing with the major recommendations, we would like to highlight the management and transfusion support for cases with paroxysmal cold haemoglobinuria (PCH), from the perspective of the National Health Service Blood and Transplant (NHSBT) reference service. Although PCH is a ....mfr{margin-top:1em;margin-bottom:1em}#brs{}#brs{margin-bottom:28px}#brs .med{color:#222;height:auto;padding-bottom:8px}.brs_col{font-size:14px;margin-top:-1px;padding-bottom:1px;display:inline-block;line-height:20px;vertical-align:top;max-width:100%;box-sizing:border-box}#brs ._e4b{margin:0;clear:both}#brs a{padding:3px 32px 3px 0;display:inline-block;float:left}#brs a{text-decoration:none}g-section-with-header{display:block;margin:40px 0}._ojo{padding:0 0px 12px 0px}Searches related to PCH haematologyparoxysmal cold hemoglobinuria symptomscold agglutinin disease vs paroxysmal cold hemoglobinuriaparoxysmal cold hemoglobinuria vs paroxysmal nocturnal hemoglobinuriaparoxysmal cold hemoglobinuria datparoxysmal cold hemoglobinuria treatmentdonath landsteiner testparoxysmal cold hemoglobinuria testbiphasic hemolysinif (document.querySelector("#taw").clientHeight == 0 && document.querySelector("#topstuff").clientHeight == 0){var positiveClientHeight = function(element){return element.clientHeight>0;};var firstVisibleElement = Array.from(document.querySelector("#rso").children) .find(positiveClientHeight);var sectionWithHeaderElement = firstVisibleElement && firstVisibleElement .querySelector("div g-section-with-header");if(sectionWithHeaderElement){sectionWithHeaderElement.style.marginTop = "0";} } 12345678910Next#foot{visibility:inherit}
1 annotations
  • Place the hand around patient’s lower ribs and approach costal margin to pull spleen forward
  • underlies 9-11 ribs
  • Arterial supply: Splenic artery from celiac trunk
  • If history suggest splenomegaly but is not palpable: Roll the patient on to the right lateral position with flexion of left hip and knee and examine as before
  • . Move hand up diagonally from right iliac fossa, towards left upper quadrant on expiration
  • Castell’s sign: With the patient supine, percussion in the lowest intercostal space in the anterior axillary line (8th or 9th) produces a resonant note if the spleen is normal in size. This is true during expiration or full inspiration. A dull percussion note on full inspiration suggests splenomegaly
  • Reticuloendothelial system hyperplasia (Removal of defective erythrocytes)
  • Acellular deposition: Metabolic disorders
  • Cellular deposition: Neoplasia
  • Primary hypersplenism: Dacie’s syndrome (Splenomegaly of unknown cause + Pancytopenia)
  • Splenomegaly Pancytopenia Normal bone marrow (Primary) or Hypercellular bone marrow (secondary) Reversibility by splenectomy
  • Banti’s disease: Congestive splenomegaly with hypersplenism occuring in cirrhosis and portal hypertension
  • Pain and a heavy sensation in LUQ radiating to back
  • Radiation to left shoulder tip in splenic infarction
  • 1. Inspection: Fullness in LUQ that descends on inspiration (massive splenomegaly)
  • Early satiety in massive splenomegaly
  • Pruritus (Hodgkin lymphoma, Polycythemia)
  • Fingers insinuation: cannot get between spleen and ribs
  • Spleen is not normally palpable (palpable when 2-3 times enlarged). Enlargement takes place in a superior and posterior direction before it becomes palpable subcostally. A palpable spleen must be reported in following points:
  • Palpable splenic rub: Present or not
  • Low diaphragm
  • . Auscultation: Venous hum or a friction rub may be heard
  • bimanually palpable and not ballotable
  • Chronic Malaria, Chronic Kala-azar
  • Chronic Malaria, Chronic Kala-aza
  • Leucopenia: Malaria, Kala-azar, Enteric fever, Felty’s syndrome
  • Cell morphology: Leukemia, Hereditary spherocytosis, Thalassemia
  • Liver function tests Hyperbilirubinemia: Hemolytic anemias, Other hemolytic conditions, Hepatitis, Chronic liver disease
  • Flow cytometry for lymphoproliferative profile (CLL, Hairy cell leukemia, lymphomas)
  • Mosaic pattern in small bones of hand: Thalassemia
  • Paul-Bunnell test (Infectious Mononucleosis)
  • Rose-Waaler test (Felty’s syndrome)
  • Kveim skin test (Sarcoidosis)
  • Erlenmeyer flask sign in distal femur: Gaucher’s disease
34 annotations
8 annotations
  • Arterial supply: Splenic artery from celiac trunk
  • Place the hand around patient’s lower ribs and approach costal margin to pull spleen forward
  • underlies 9-11 ribs
  • Castell’s sign: With the patient supine, percussion in the lowest intercostal space in the anterior axillary line (8th or 9th) produces a resonant note if the spleen is normal in size. This is true during expiration or full inspiration. A dull percussion note on full inspiration suggests splenomegaly
  • . Move hand up diagonally from right iliac fossa, towards left upper quadrant on expiration
  • Acellular deposition: Metabolic disorders
  • Splenomegaly Pancytopenia Normal bone marrow (Primary) or Hypercellular bone marrow (secondary) Reversibility by splenectomy
  • Banti’s disease: Congestive splenomegaly with hypersplenism occuring in cirrhosis and portal hypertension
  • Pain and a heavy sensation in LUQ radiating to back
  • If history suggest splenomegaly but is not palpable: Roll the patient on to the right lateral position with flexion of left hip and knee and examine as before
  • 1. Inspection: Fullness in LUQ that descends on inspiration (massive splenomegaly)
  • Reticuloendothelial system hyperplasia (Removal of defective erythrocytes)
  • Radiation to left shoulder tip in splenic infarction
  • Cellular deposition: Neoplasia
  • Primary hypersplenism: Dacie’s syndrome (Splenomegaly of unknown cause + Pancytopenia)
  • Pruritus (Hodgkin lymphoma, Polycythemia)
  • . Auscultation: Venous hum or a friction rub may be heard
  • bimanually palpable and not ballotable
  • Leucopenia: Malaria, Kala-azar, Enteric fever, Felty’s syndrome
  • Liver function tests Hyperbilirubinemia: Hemolytic anemias, Other hemolytic conditions, Hepatitis, Chronic liver disease
  • Flow cytometry for lymphoproliferative profile (CLL, Hairy cell leukemia, lymphomas)
  • Early satiety in massive splenomegaly
  • Spleen is not normally palpable (palpable when 2-3 times enlarged). Enlargement takes place in a superior and posterior direction before it becomes palpable subcostally. A palpable spleen must be reported in following points:
  • Palpable splenic rub: Present or not
  • Fingers insinuation: cannot get between spleen and ribs
  • Low diaphragm
  • Chronic Malaria, Chronic Kala-aza
  • Chronic Malaria, Chronic Kala-azar
  • Cell morphology: Leukemia, Hereditary spherocytosis, Thalassemia
  • Paul-Bunnell test (Infectious Mononucleosis)
  • Rose-Waaler test (Felty’s syndrome)
  • Kveim skin test (Sarcoidosis)
  • Mosaic pattern in small bones of hand: Thalassemia
  • Hypersplenism or Immune-mediated destruction of one or more blood cell line (for correction of cytopenias)
  • Erlenmeyer flask sign in distal femur: Gaucher’s disease
  • Massive splenomegaly (for control of symptoms)
  • Medicine
37 annotations
  • Whilst they will certainly know which antibiotics are required and also be aware of local hospital policy, they should not be the first point of contact for routine non-emergency queries
  • However, it is more appropriate than involving Infection Control at this stage (A) as this risks damaging your professional relationship with your colleague and does not explore the cause of the problem.
  • keeping patients under your care safe and uncompromised when you leave. Having failed to obtain an answer from the ward by phone, going to the ward would be the best way of ensuring that outstanding tasks are completed. It also helps to verify whether the lack of an answer suggests that the ward is busy and may need support
  • Speaking to the relative and not the patient is least acceptable as you are not directly addressing the concerns of the patient (E).
  • FY1 doctors should never discharge patients without close supervision so Option (A) is inappropriate.
  • s slightly better than leaving without telling anyone in this scenario (B). A text message is a much less certain way of communicating (C).
  • next correct option is to consult with the nurse in charge on the ward (D). Whilst the nurse in charge may well be very knowledgeable and experienced, it is not appropriate to prescribe any medication purely on the advice of a nurse without consulting further with a senior medical colleague or confirming the dose etc in the BNF
  • Option (B) is a useful action in due course, but does not address the immediate issue
  • The next most appropriate action would be to ask a registrar/specialty trainee, who has more experience, to review the patient
  • . A more senior doctor will be in a position to 'chase up' the admitting unit to complete the relevant paperwork and drug chart, but they will also have to other duties that require attention from someone at their leve
  • AEDCB scoring 14 of a possible 20 marks.
  • Option (A) but doesn't allow an opportunity for amicable resolution (B)
  • iscuss their concerns A. Refer the family's request back to your consultant and ask him to speak to them again
  • D. Explain to both Mrs Hill and her husband why he is not being discharged today
  • C. Tell Suzanne politely, but clearly, that you cannot tell her the results because of patient confidentiality
  • s less appropriate than Option (C) because finding one can cause a delay.
  • Option A is however preferable to option B, because you would be passing the problem on to a colleague who has no formal clinical responsibility for this patient – this lies with the medical team
  • D. Arran
  • B. Suggest she discusses the issues with her specialty trainee*
  • Mrs Hill remains unhappy or you are needed urgently on another ward then it would be appropriate to involve a more senior doctor on your team (A)
  • Explain to Ben the potential safety risks to patients if he continues to ignore the issue
  • You answered DBAEC scoring 14 of a possible 20 marks.
  • ). Prescribing decisions are complex and certain drugs are only used routinely by specialists
  • You answered CDBAE scoring 12 of a possible 20 marks.
  • E. Ask an FY1 colleague to assist you with completing your tasks
  • B. Call security for assistance C. Tell the patient that his behaviour is inappropriate and will not be tolerated
  • A. Talk to her about the circumstances of her distress
  • E. Offer to go with her to talk to her consultant
  • A. Suggest to Simon that he tells his educational supervisor* about the advertisement
  • It is not appropriate to hand over non-emergency jobs to the on-call team, especially if colleagues could have helped during the day (H).
  • A. Arrange for a translator to ask the patient if he knows how he is supposed to take the medication
  • being
  • H. Ask the nurse who dispen
  • It is not your role to act as Simon's senior (H)
  • E. Try to answer any questions Mr Gordon has
  • e FY2 that they have made an error B. Cross out the prescription on Mrs Hobbs' drug chart, dating and initialling the amendment
  • B. Inform your specialty trainee in theatre that you are extremely busy and need some help
  • B. Prevent him from taking both tablets now
  • scussion and this is best done in a non-confrontational manner (A). It is important that the FY1 involved with the issue is provided with someone to discuss the incident with, to facilitate reflection (E) and you may need advice from a senior doctor in the team to help with this difficult situation (G). It is not appropriate for you to have a private conversation with the consultant (B), expect the FY1 to deal with the problem directly with the consultant without a third party (C), to discuss your consultant's behaviour with the nurses (D) or apologise on behalf of the consultant (F). Whilst you may wish to see if your FY1 colleague is managing his workload, it is not a priority in answering this question (H).   68. You are reviewing one of your patients, Mrs Hobbs, who is on your ward being treated for an infection in her toe. During a routine examination, you notic
  • of the tasks G. After the tasks have been completed, seek advice from your educational supervisor* about how to approach situations such as these
  • . Tell Mr Gordon the other doctor has now finished her shift so you are now taking over responsibility for Mrs Gordon
  • Re-examine Mrs Gordon's knee
  • ore the issue D. Discuss the situation with a senior colleague E. Recommend to Ben that he raises this with his educational supervisor*
  • n constitute an assault. Similarly, prescribing extra sedation might exa
  • D. Advise Amadi to seek time off work from his consultant
  • . It is customary for nursing staff to provide telephone updates to patients.
  • Advise your FY1 colleague to speak to his educational supervisor*
  • expect the FY1 to deal with the problem directly with the consultant without a third part
48 annotations
  • Otherwise, use a 28% Venturi mask at a flow rate of 4 L/min, and aim for an oxygen saturation of 88–92
  • easier to use one, and that it will help to deliver a maximum dose.If the person is likely to become fatigued, a nebulizer may be more appropriate if available in primary care, depending on local protocol
  • 88–92%.If the oxygen saturation remains below 88%, change to nasal cannulae at 2–6 L/min or a simple mask at 5 L/min with target saturation of 88–92%, and request an emergency ambulance.
  • mainly based on expert opinion in the British Thoracic Society Guideline for emergency oxygen use in adult patients
  • clarithromycin 500 mg twice daily for 5 days.
  • , frequent exacerbations, or antibiotic use in the past 3 months), prescribe co-amoxiclav 500/125 mg three times daily for 5 days
  • eumonia depending on local antibiotic prescribing guidelines.Prescribe amoxicillin 500 mg three times daily for 5 days, or if there is a true allergy to amoxicillin, dox
  • clarithromycin
  • Acute confusion.Marked reduction in activities of daily living.Marked breathlessness and tachypnoea.Pursed-lip breathing.Use of accessory muscles at rest.New-onset cyanosis or peripheral oedema.
  • A reduction in activities of daily living, is confined to bed, or is on long-term oxygen therapy (LTOT)
  • alternative way of caring for people who would otherwise need to be admitted or stay in hospita
  • Refer the person to a respiratory specialist for consideration of long-term non-invasive ventilation (NIV) if they have persistent hypercapnic ventilatory failure during exacerbations despite optimal medical therapy.
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  • . Statistically, the diseases to highly suspect for patients with massive UGIB are peptic ulcer diseases (PUD) and esophageal varices. Massive LGIB is typically due to diverticulosis or angiodysplasias
  • Gastrointestinal bleeding (GIB) is a common emergency department complaint with a wide spectrum of presentations.
  • nly on the evaluation and management of massive GIB which is defined for the purposes of this module as bleeding of the gastrointestinal tract associated with hemodynamic instability, acute anemia, and/or the need for blood transfusion.
  • However, it is important to be aware that approximately 10% of melena comes from a lower GI source and 10% of hematochezia comes from an upper GI source.
  • Known PUD, chronic epigastric pain, heavy alcohol use, gastrotoxic medications (e.g., NSAIDS, ASA, or steroids)
  • Severe liver disease, alcoholism, hemorrhoids on physical exam (external evidence of possible portal hypertension)
  • A type and screen should be obtained on all patients with significant GIB. Crossmatched blood should be immediately ordered if the need for blood transfusion is clearly indicated or highly anticipated
  • stable patients, orthostatic vital signs can be obtained to assess for significant blood loss as suggested by a systolic blood pressure drop of more than 10mmHg or a pulse increase of more than 20 beats/minut
  • or at determining the presence or absence of active bleeding when they rely on nasogastric aspiration. In patients with hematochezia or melena without hematemesis, nasogastric aspiration has been found to have poor diagnostic performance in excluding an upper GI source.
  • EGD is the diagnostic test of choice to evaluate the upper GI tract in patients who present with hematemesis or melena. While hematochezia or BRBPR typically represent bleeding from a lower source, in the setting of hemodynamic compromise a brisk UGIB should also be considered as bleeding from the upper GI tract is overall much more common
  • ctreotide is a vasoactive protein that causes selective vasoconstriction of the splanchnic vasculature. Blood flow to the upper GI tract is decreased thereby reducing blood loss. It is given as a bolus followed by a drip
  • The rectal exam plays an essential role in the evaluation of GIB in both characterizing the stool color (brown vs black vs maroon) and the presence of gross or occult blood.
  • . While definitive diagnosis of the underlying lesion typically occurs outside the ED by an endoscopic procedure, the main diseases to consider for patients presenting with massive UGIB are peptic ulcer disease or varices. Diverticulosis and angiodysplasias
  • it is important to remember that initial blood counts may be normal early in the disease course because bleeding involves the loss of whole blood and thus a proportionate loss of cells and plasma
  • Colonoscopy remains the diagnostic test of choice to evaluate LGIB. However, it may not be possible in the setting of massive bleeding. Under these circumstances, mesenteric angiography can be used to both localize and treat the source. However, it is an invasive procedure that can lead to complications including contrast allergy, contrast induced renal failure, and bleeding from arterial puncture. An alternative approach in a patient who continues to actively bleed but has been stabilized is to first proceed with nuclear imaging. A 99mTechnetium labeled red cell scan can detect bleeding at a slower rate than angiography: 0.1 ml/min versus 0.5 mL/min, respectively. It can help confirm that the bleeding is rapid enough to be detectable by angiography and thus merits the risks of an invasive procedure.
  • serial Hgb/HCT measurements are important in assessing the degree of acute blood loss.
  • , esophageal tamponade can be attempted as a stabilizing maneuver. In this procedure a specialized gastric tube – typically the Sengstaken-Blakemore – which has two expanding balloons is placed. One balloon is expanded in the stomach and the other in the esophagus to achieve tamponade.
  • cirrhosis who present with UGIB should receive prophylactic antibiotics– typically a floroquinolone such as ciprofloxacin- as it reduces the incidence of infection and decreases mortality.
  • Due to the pain and iatrogenic vomiting associated with nasogastric tube insertion and its questionable accuracy, the routine use of nasogastric aspiration has been called into question
  • If massive bleeding precludes the use of colonoscopy, mesenteric angiography may achieve hemostasis through injection of intra-arterial vasopression or embolization
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  • . Lower blood pressure in the legs (result in a ABPI < 1) is an indicator of peripheral arterial disease (PAD)
  • values less than 0.90 have been shown to have a sensitivity of 90% and a specificity of 98%* for PAD.
  • ABPI >= 0.8.
  • A 19-year-old lady presents with recurrent episodes of pain in her hands
  • e vertebral arteries may have diminished flow. This may result in diminished flow to the brain with neurological sequelae such as syncope.
  • Sources are left atrium with cardiac arrhythmia (mainly AF), mural thrombus
  • 50% of upper limb emboli will lodge in the brachial artery
  • claudication, ulceration and gangrene
  • Becks Triad:HypotensionMuffled heart soundsRaised JVP
  • some cases are reported to occur following trauma
  • Often laceration to lung parenchyma with flap
  • Associated with pulmonary contusion
  • Avoid over hydration and fluid overload
  • Haemothoraces large enough to appear on CXR are treated with large bore chest drain
  • Arterial blood gases and pulse oximetry importan
  • Deceleration injuriesContained haematoma
  • Entrance wound in one hemithorax and exit wound/foreign body in opposite hemithorax
  • common cause is mechanical ventilation in patient with pleural injury
  • aradoxus
  • Multiple rib fractures (at least two fractures per rib in at least two ribs)
  • Most common cause is lung laceration with air leakag
  • traumatic pneumothoraces should have a chest drai
  • traumatic pneumothorax should never be mechanically ventilated until a chest drain is inserted
  • Surgical exploration is warranted if >1500ml blood drained immediately
  • Pulsus paradox
  • Early intubation within an hour if significant hypoxia
  • myocardial infarctionSequelae: hypotension, arrhythmias, cardiac wall motion abnormalities
  • Widened mediastinum
  • More common on left side
  • Insert gastric tube, which will pass into the thoracic cavity
  • Mediastinal haematoma or pleural cap suggests great vessel injuryMortality is 20%
  • Adsons test.
  • mpact on the history and nature of disease presentation. In the region of the subclavian and axillary arteries the collateral vessels passing around the shoulder joint may provide pathways for flow if the main vessels are stenotic or occluded.
  • . When manual tasks are performed in which the hand works overhead the signs and symptoms will be maximal and this is the basis of Adsons test.
  • evaluating patients with suspected PAD, for example a male smoker who presents with intermittent claudication
  • Venous ulcers are often treated with compression bandaging
  • s. Because of the acute nature of the condition there is no time for the development of a collateral circulation so the limb is usually pale and painful
  • 30% of upper limb emboli will lodge in the axillary artery
  • symptoms are worst in cold weather.
  • theroma are the most common, trauma may result in vascular changes and long term occlusion but this is rare
  • Cardiac arrhythmias may cause result in impaired consciousness in addition to the embolus
  • is with calcium antagonists
  • acute ischaemia may
  • occur as a result of acute thrombosis
  • Condition may complicate pre-existing malignancy (especially breast cancer) or arise as a result of repetitive use of the limb in a task such as painting a ceiling
  • Usually affects hands > feet
  • duplex ultrasound and treatment is with anticoagulation
  • 70%
48 annotations