Bi monthly assessment
BI MONTHLY ASSESSMENT : (14/1/21)
Max Marks: 100 (10 marks for each first seven questions and 30 marks for the last question) .
Link to question paper :
https://medicinedepartment.blogspot.com/2021/01/medicine-paper-for-january-2021.html?m=1
1) 26 year old woman with complaints of altered sensorium somce 1 day,headache since 8 days,fever and vomitings since 4 days
More here: https://harikachindam7.blogspot.com/2020/12/26-year-old-female-with-complaints-of.html
a). What is the problem representation of this patient and what is the anatomical localization for her current problem based on the clinical findings?
Ans) PROBLEM REPRESENTATION :
26 yr old female who got evaluated for joint pains before and diagnosed as SLE with no other comorbities and is on immunosuppresants for SLE ,
Came with history of head ache since 8 days and fever plus vomitings , generalised weakness since 4 days and altered sensorium since one day.
So trigger point is Altered sensorium for which they came to hospital , which was intially thought to be due to
1) Hyponatremia.
2) Euvolemic Hyponatremia ( as there was no signs of fluid overload or hypotension) secondary to SIADH - (SIADH secondary to TUBERCULAR MENINGITIS) .
3) TUBERCULAR MENINGITIS. ( CSF cbnaat came positive and also cell count revealed lymphocytosis,
with low glucose and chloride and increased CSF protein. - evident of tb meningitis.
4) ACUTE INFARCT IN LEFT THALAMUS .( secondary to vasculitis ) .
Stroke in TBM patients may develop insidiously and present as asymptomatic or silent stroke. The most common vulnerable brain region was basal ganglia where has been described as ‘tubercular zone’. It is comprised of head of the caudate nucleus, anteriomedial thalami and anterior limb and genu of internal capsule.
In a study involving 122 TBM patients, 55 patients had stroke and 54% strokes were located in basal ganglia . Another study had similar results with 49% of infarctions in basal ganglia .
In our study, 50% of patients had stroke located in basal ganglia, which is consistent with previous studies. Strokes in ‘tubercular zone’ may be associated with basilar exudates.
Dense fibrinocellular exudates may wrap middle cerebral trunks and their penetrating branches, which may contribute to vasculitis and cause strokes in ‘tubercular zone’.
Age, CSF white blood cell and basal meningeal enhancement can predict the occurrence of acute ischemic stroke in young adults with TBM.
Stroke in TBM patients was mainly caused by vasculitis secondary to the meningeal inflammation, which can be classified into three patterns: 1) infiltrative, 2) proliferative and 3) necrotizing vascular lesions . Duration of TBM may determine the relative frequency of infiltrative, proliferative and necrotizing changes in the cerebral vessels.
b) What is the etiology of the current problem and how would you as a member of the treating team arrive at a diagnosis? Please chart out the sequence of events timeline between the manifestations of each of her problems and current outcomes.
A) As pt was on immunosuppresants for SLE , she had history of headache and fever and altered sensorium ,a diagnosis of TUBERCULAR MENINGITIS was made with help of CSF analysis.
Intially altered sensorium was thought secondary to hyponatremia. But it couldn't explain fever and headache.
Euvolemic Hyponatremia is secondary to SIADH ( due to TB).
TIMELINE OF EVENTS :
C) What is the efficacy of each of the drugs listed in her prior treatment plan that she was following since last two years before she stopped it two weeks back?
A) Pt was on medication for SLE (Hydrochloroquine-200mg/OD,Sulfasalazine,Methylprednisolone,Alandronic acid and Cholecalciferol,Aceclofenac,Flupirtine,Gabapentine,Methylcobalamin tablets), which she stopped 10 days back.
Methylprednisolone and Cyclophosphamide, Alone or in Combination, in Patients with Lupus Nephritis:
RANDOMISED CONTROL TRIAL :
-Therapy for patients with life-threatening sys- temic lupus erythematosus has included high doses of corticosteroids and cytotoxic or cytostatic drugs . Cyclophosphamide, given in intermit- tent intravenous boluses, has been widely used to treat renal , and central nervous system disease , but this therapy is sometimes withheld in the hope that disease might be controlled with corticosteroids or other immuno- suppressive drug.
P - 82 patients with lupus nephritis . To enter the study, patients had to have both glomerulonephritis and a diagnosis of systemic lupus erythematosus
I - High dose methyl prednisolone (1g/m2 BSA) - Once A month for 1 yr.
C - Comparision with standard therapy with cyclophosphamide (0.5-1g/m2 BSA) for 6 months then quarterly or
Combination of cyclophosphamide and methyl prednisolone.
O -The primary study outcome was the response to the study drugs as defined by 1) the percentage of patients who achieved renal remission, 2) the num- ber of nonresponders (nonresponse was defined as >10 erythrocytes per high-power field, cellular casts, proteinuria [>1 g of protein per day], and doubling of the serum creatinine level), and 3) the percent- age of adverse events.
Secondary outcome measures were renal failure that required dialysis (end-stage renal disease), sta- ble doubling of the serum creatinine level, and number of renal relapses (renal relapse was defined as a reactivation of renal disease after 6 or more months of remission).
Bisphosphonates for steroid induced osteoporosis :
P - We chose studies where participants were men and/or women over the age of 18, with underlying inflammatory disorders, initiating treatment or currently being treated with systemic corticosteroids (primary or secondary prevention), and who had not received bis- phosphonates in the six months prior to the start of the study.
Pri- mary prevention was defined by bisphosphonate treatment starting within three months of initiating corticosteroids. Due to con- troversy in the literature regarding low dose steroids and the risk of osteoporosis, only those trials where the mean corticosteroid dose was 7.5 mg/day or higher were used.
I -Controlled clinical trials that included any of the first or second generation bisphosphonates, alone or in combination with cal- cium and/or vitamin D, with the control group taking placebo, alone or in combination with calcium and/or vitamin D were in- cluded.
O -The primary outcome assessed and required for inclusion in the meta-analysis was percent change in BMD at one year at the lum- bar spine or femoral neck. Data regarding number of new verte- bral fractures was collected if present.
Corticosteroids are widely used to treat inflammation. Bone loss (osteoporosis) is a serious side effect of this therapy. We reviewed a total of 13 trials which included 842 patients. We found that the bone mineral density of the lumbar spine of patients taking bisphosphonate therapy improved 4.3% more than patients who had no treatment. At the femoral neck (top of the thigh bone), the bone mineral density improved 2.1% more in the treatment group. There was no difference in the number of spinal fractures between the the two groups. We found that bisphosphonates are effective at preventing and treating corticosteroid-induced bone loss at the lumbar spine and femoral neck. We do not have enough evidence to say whether or not bisphosphonates prevent fractures.
A total of 13 trials, including 842 patients are included in this meta-analysis. Results are reported as a weighted mean difference of the percent change in BMD between the treatment and placebo groups, with trials being weighted by the inverse of their variance.
The 95% confidence intervals (95% CI) are presented. At the lumbar spine, the weighted mean difference of BMD between the treatment and placebo groups was 4.3% (95% CI 2.7, 5.9). At the femoral neck, the weighted mean difference was 2.1% (95%CI 0.01, 3.8). Although there was a 24% reduction in odds of spinal fractures [OR 0.76 (95%CI 0.37, 1.53)], this result was not statistically significant.
- Efficacy analysis of hydroxychloroquine therapy in systemic lupus erythematosus:
Hydroxychloroquine (HCQ) is a widely prescribed medication to patients with systemic lupus erythematosus (SLE), with potential anti-inflammatory effects.
This study was performed to investigate the efficacy of HCQ therapy by serial assessment of disease activity and serum levels of proinflammatory cytokines in SLE patients.
Methods : In this prospective cohort study, 41 newly diagnosed SLE patients receiving 400mg HCQ per day were included.
Patients requiring statins and immunosuppressive drugs except prednisolone at doses lower than 10mg/day were excluded.
Outcome measures were assessed before commencement of HCQ therapy (baseline visit) as well as in two follow-up visits (1 and 2months after beginning the HCQ therapy). Serum samples of 41 age-matched healthy donors were used as controls.
Results : Median levels of IL-1β (p < 0.001), IL-6 (p = 0.001), and TNF-α (p < 0.001) were significantly higher, whereas, median CH50 level was significantly lower (p < 0.001) in SLE patients compared with controls.) Two-month treatment with HCQ resulted in significant decrease in SLEDAI-2K (p < 0.001), anti-dsDNA (p < 0.001), IL-1β (p = 0.003), IL-6 (p < 0.001) and TNF-α (p < 0.001) and a significant increase in CH50 levels (p = 0.012). The reductions in SLEDAI-2K and serum levels of IL-1β and TNF-α were significantly greater in the first month compared with the reductions in the second month.
Conclusion: HCQ therapy is effective on clinical improvement of SLE patients through interfering with inflammatory signaling pathways, reducing anti-DNA autoantibodies and normalizing the complement activity.
3)Please go through the two thesis presentations below and answer the questions below by also discussing them with the presenters:
https://youtu.be/sw8o8y5Yw_I
What was the research question in the above thesis presentation?
A) To study the association of serum magnesium levels of type 2 diabetes mellitus
C) What is the current available evidence for magnesium deficiency leading to poorer outcomes in patients with diabetes?
A) Clinically, hypomagnesemia may be defined as a serum Mg concentration ≤1.6 mg/dl.
Hypomagnesemia occurs at an incidence of 13.5 to 47.7% among patients with type 2 diabetes. Poor dietary intake, autonomic dysfunction, altered insulin metabolism, glomerular hyperfiltration, osmotic diuresis, recurrent metabolic acidosis, hypophosphatemia, and hypokalemia may be contributory. Hypomagnesemia has been linked to poor glycemic control, coronary artery diseases, hypertension, diabetic retinopathy, nephropathy, neuropathy, and foot ulcerations.
Hypomagnesemia been associated with type 2 diabetes, but also numerous studies have reported an inverse relationship between glycemic control and serum Mg levels.
Although many authors have suggested that diabetes per se may induce hypomagnesemia, others have reported that higher Mg intake may confer a lower risk for type 2 diabetes . It is interesting that the induction of Mg deficiency has been shown to reduce insulin sensitivity in individuals without diabetes, whereas Mg supplementation during a 4-wk period has been shown to improve glucose handling in elderly individuals without diabetes . In patients with type 2 diabetes, oral Mg supplementation during a 16-wk period was suggested to improve insulin sensitivity and metabolic control .
The mechanisms whereby hypomagnesemia may induce or worsen existing diabetes are not well understood. Nonetheless, it has been suggested that hypomagnesemia may induce altered cellular glucose transport, reduced pancreatic insulin secretion, defective postreceptor insulin signaling, and/or altered insulin–insulin receptor interactions
- Clinically, there are significant data linking hypomagnesemia to various diabetic micro- and macrovascular complications.
Cardiovascular :
In a study that involved 19 normotensive individuals without diabetes, 17 hypertensive individuals without diabetes, and 6 hypertensive individuals with diabetes, Resnick et al. documented the lowest mean intracellular Mg concentration among the last group. Similarly, based on data from the Atherosclerosis Risk in Communities (ARIC) Study, a multicenter, prospective cohort study that lasted 4 to 7 yr and involved 13,922 middle-aged adults who were free of coronary heart disease at baseline, an inverse association between serum Mg and the risk for coronary heart disease was observed among men with diabetes .
Diabetic Retinopathy.
The link between hypomagnesemia and diabetic retinopathy was reported in two cross-sectional studies that involved both “insulin-dependent” patients and patients with type 2 diabetes. Not only did patients with diabetes have lower serum Mg levels compared with their counterparts without diabetes, but also the serum Mg levels among the cohort with diabetes had an inverse correlation with the degree of retinopathy . A similar link, however, was not observed when Mg was measured within mononuclear cells. In a study that involved 128 patients with type 2 diabetes and poor glycemic control (glycosylated hemoglobin >8.0%), intramononuclear Mg concentrations were not observed to be lower among those with diabetic retinopathy but rather among those with neuropathy and coronary disease .
Foot Ulcerations.
Given the link between hypomagnesemia and risk factors for the development of diabetic foot ulcers (e.g., polyneuropathy, platelet dysfunction), Rodriguez-Moran and Guerrero-Romero suggested that hypomagnesemia may be associated with an increased risk of diabetic foot ulcers. Indeed, they observed a higher incidence of hypomagnesemia among their patients with diabetic foot ulcers compared with those without the condition (93.9% of the 33 patients with diabetic foot ulcers compared with 73.1% of the 66 patients without diabetic foot ulcers; P = 0.02).
Nephropathy.
In a comparative study that involved 30 patients who had type 2 diabetes without microalbuminuria, 30 with microalbuminuria, and 30 with overt proteinuria, Corsonello et al. observed a significant decrease in serum ionized Mg in both the microalbuminuria and overt proteinuria groups compared with the nonmicroalbuminuric group. Accordingly, in a recent retrospective study, an association between low serum Mg levels and a significantly faster rate of renal function deterioration in patients with type 2 diabetes was reported .
Others.
Finally, there also are data to suggest the association between hypomagnesemia and other diabetic complications, including dyslipidemia and neurologic abnormalities .
https://cjasn.asnjournals.org/content/2/2/366
B) What was the research question in the above thesis presentation?
https://youtu.be/jXVS5J1-RNE
A)The research question
1)will salt restricted diet decrease blood pressure?
2)can 24hr urinary sodium test reflect the amount of sodium consumed by an individual
B) What was the researcher's hypothesis?
Hypothesis is that, salt restriction doesn't effect blood pressure in all the individuals in the same way, and salt resistant individuals don't benefit from a restricted diet as much as a salt sensitive individual.
c) What is the current available evidence for the utility of monitoring salt excretion in the hypertensive population
The 24hr urinary sodium is a reflection of dietary sodium, and has better results than dietary recall method.
Daily salt intake based on 24-hour urinary sodium excretion (assuming that all sodium ingested was in the form of sodium chloride) with a formula: figure 2 shows a practical method to estimate salt or sodium intake.
Figure 2: Calculation for estimation of salt or sodium intake
Na (mg/day) = Na (mmol/day) x 23; NaCl = Na (g/day) x 100/ 39,3
1 gram salt (NaCl) = 393,4 mg Na = 17,1 mmol Na
B)
3) Please critically appraise the full text article linked below:
https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2796.2003.01233.x
What is the efficacy of aspirin in stroke in your assessment of the evidence provided in the article. Please go through the RCT CASP checklist here https://casp-uk.net/casp-tools-checklists/ and answer the questions mentioned in the checklist in relation to your article.
A) In acute stroke, progression has a severe impact on patient outcome and no effective treatment is known. The main objective was to evaluate the efficacy of aspirin for prevention of stroke progression thereby improving outcome.
P - Patients with ischaemic stroke but not complete paresis were included. No antiplatelet drugs were allowed within the last 72 h before onset. Delay until first trial dosage was maximized to 48 h.
Totally, 441 patients (220 aspirin, 221 placebo) completed the trial.
I - Interventions. Aspirin (325 mg) or placebo was given once daily for five consecutive days.
Neurological assessments were carried out three times daily during the treatment period to detect progression of at least two points in the Scandinavian Stroke Supervision Scale. Patient outcome was followed up at discharge and at 3 months.
Tablets of 325 mg aspirin or placebo, water solvable, were administered orally once a day for five consecutive days. The first dosage was given as soon as possible after inclusion. The trial treatment was discontinued if the main outcome event occurred, i.e. progression of stroke symptoms.
O - The main outcome event of the trial was a progression of stroke symptoms measurable as two points or more (not necessarily in the same item) worsening on the SSSS, compared with baseline, during 5 days of trial treatment.
The main results of the trial showed that aspirin treatment did not significantly reduce the rate of stroke progression. The progression rate was 15.9% amongst patients treated with aspirin and 16.7% for those on placebo.
Thus, the ability to live at home, to walk unaided, or need for further institutionalized care after discharge was not significantly improved in the aspirin group .
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