BIMONTHLY EXAM FOR THE MONTH OF JANUARY 2021
"This is my submission for the Bimonthly internal assessment for the month of January
Most of the information here have been collected from different reference sites, the links to which have been mentioned. The points copy pasted have been put in quotes.
The questions to the cases being discussed can be viewed from the link below 👇
https://medicinedepartment.blogspot.com/2021/01/medicine-paper-for-january-2021.html?m=1
1.26 year old woman with complaints of altered sensorium since day,headache since 8 days,fever and vomitings since 4 days
a). What is the problem representation of this patient and what is the anatomical localization for her current problem based on the clinical findings?
A 28 year old woman with the complaints of
Headache since 8 days
Fever since 4 days
Vomitings since 4 days
Altered sensorium since 1 day
28 year old woman with
1. Hyponatremia secondary to SIADH
2. Tubercular meningitis
3. Acute infarct in the left thalamic region
4. SLE with multiple joint pains
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.
1. Hyponatremia
From Harrison's principles of Internal Medicine
- Here is an interesting article that i found on Hyponatremia in Tubercular Meningitis
A study of hyponatremia in tuberculous meningitis
A Prospective study on 76 patients with Tubercular Meningitis,
34 (44.7%) TBM patients had hyponatremia (mild 3, moderate 23 and severe 8). Hyponatremia was due to cerebral salt wasting in 17, syndrome of inappropriate secretion of antidiuretic hormone in 3 and miscellaneous causes in 14 patients.
Hyponatremia occurred in 44.7% of TBM patients. Cerebral salt wasting was the commonest cause of hyponatremia and was related to the severity of TBM.
However, our patient was Euvolemic and in cerebral salt wasting the patients usually are hypovolemic. The likely cause of Hyponatremia in our patient was because of SIADH.
SIADH occurs commonly in lupus nephritis due to the tubulointerstitial damage.
2. Tubercular meningitis:
Patient presenting in altered sensorium with Fever, vomitings, neck rigidity goes in favour of meningitis.
CSF analysis shows CBNAAT to be positive and lymphocytosis, decreased glucose and increased protein.
3. Acute infarct in the left thalamic region
Hypovolemia due to cerebral salt wasting may contribute to stroke in tuberculous meningitis
This prospective cohort study 81 patients with TBM
' Out of 81 patients with TBM, 32 (39.5%) had ischemic stroke. CSW was the commonest cause of hyponatremia and occurred in 34 (42%) patients. Stroke occurred in tubercular zone in 10, ischemic zone in 15 and both in 7 patients. The patients with ischemic zone infarction were older and had stroke risk factors such as diabetes mellitus, hypertension and hyperlipidemia. Out of 16 (47%) patients with CSW, 10 (62.5%) had stroke during the polyuric phase. The patients with CSW had more frequent deep white matter infarcts (P = 0.01) which were in internal border zone in 4 (40%).'
Increased risk of ischaemic stroke in patients with SLE
Patients with SLE -
From 2000 to 2007, 11,637 newly diagnosed SLE patients
C - A control cohort of 58,185 subjects without SLE
O - During a follow-up period of up to 7 years, ischemic stroke developed in 258 (2.22%) of the patients with SLE and in 873 (1.5%) of patients in the comparison cohort.
Patients with SLE have an increased risk of stroke.
TIMELINE OF EVENTS
The patient was already on Hydrochloroquine,Sulfasalazine,Methylprednisolone,Alandronic acid and Cholecalciferol,Aceclofenac,Flupirtine,Gabapentine,Methylcobalamin tablets
C) What is the efficacy of using primary bisphosphonate prophylaxis for patients started on corticosteroids?
What is the efficacy of using primary PPI prophylaxis during initiation of any corticosteroids to prevent Gi ulcers?
To assess the benefits and harms of bisphosphonates for the prevention and treatment of Glucocorticoid induced osteoporosis in adults.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6461188/?report=reader
It included
1. Prevention or treatment of Glucocorticoid induced osteoporosis
2. Adults taking a mean steroid dose of 5.0 mg/day or active treatment including bisphosphonates of any type alone or in combination with calcium or vitamin D
4) comparator treatment including a control of calcium or vitamin D, or both, alone or with placebo
Patients - A total of 27 RCTs with 3075 participants in the review
- Pooled analysis for incident vertebral fractures included 12 trials (1343 participants)
Outcome -
In this analysis 46/597 people experienced new vertebral fractures in the control group compared with 31/746 in the bisphosphonate group; relative improvement of 43% with bisphosphantes.
- Pooled analysis for incident nonvertebral fractures included nine trials with 1245 participants
In this analysis 30/546 people experienced new nonvertebral fracture in the control group compared with 29/699 in the bisphosphonate group; relative improvement of 21% with bisphosphantes. The bisphosphonate groups reported stabilisation or increase in BMD, while the control groups showed decreased BMD over the study period.
At the lumbar spine, there was an absolute increase in BMD of 3.5% with bisphosphonates with a relative improvement of 1.10% with bisphosphonate.
At the femoral neck, the absolute difference in BMD was 2.06% higher in the bisphosphonate group compared to the control group with a relative improvement of 1.29%.
Pooled analysis of withdrawals from therapy were - 63/866 people withdrew in the control group compared to 76/924 in the bisphosphonate group; an absolute increased harm of 1% more withdrawals with bisphosphonates.
Conclusion - Overall the use of bisphosphonates to reduce the risk of vertebral fractures and the prevention and treatment of steroid‐induced bone loss.
According to me, Bisphosphonate therapy could be given along with corticosteroids to prevent steroid induced osteoporosis and fractures.
What is the efficacy of using primary PPI prophylaxis during initiation of any corticosteroids to prevent Gi ulcers?
Here are some interesting articles which i've found on this topic.
Use of COX 2 inhibitors and a proton-pump inhibitor for prevention of recurrent ulcer bleeding in patients at very high risk: a double-blind, randomised trial
https://pubmed.ncbi.nlm.nih.gov/17499604/
P - 441 consecutively presenting patients who were taking non-selective NSAIDs for arthritis were recruited to our single-centre, prospective, randomised, double-blind trial after admission to hospital with upper-gastrointestinal bleeding.
. All patients were given 200 mg celecoxib twice daily.
I - 137 patients were randomly assigned to receive 20 mg esomeprazole twice daily
C - 136 to receive a placebo for 12 months.
O - Combination treatment was more effective than celecoxib alone for prevention of ulcer bleeding in patients at high risk.
Concomitant use of proton pump inhibitors and systemic corticosteroids
Meta-analyses and case-control studies with more than 1000 patients were included.
This includes 970 articles, of which 3 were classified as relevant meta-analyses and 3 as relevant case-control studies. All meta-analyses indicated that peptic ulcer is, at the most, a rare complication of systemic corticosteroid therapy occurring in less than 0.4-1.8% of patients. As the incidence is low, there is no indication for routine prophylaxis with proton pump inhibitors in combination with systemic corticosteroids. There is convincing evidence showing an increased risk of ulcers and a poorer recovery from these when NSAIDs and systemic corticosteroids are used concomitantly; this is a combination for which a proton pump inhibitor should be prescribed.
Effect of antisecretory drugs and nitrates on the risk of ulcer bleeding associated with nonsteroidal anti-inflammatory drugs, antiplatelet agents, and anticoagulants
P- A case-control study matched 2,777 consecutive patients with UGIB (confirmed by endoscopy) with 5,532 controls
O- Proton pump inhibitors, H2-receptor antagonists, and nitrates reduced UGIB risk. PPI use was associated with greater reductions among both traditional NSAID and low-dose aspirin users and among patients taking Clopidogrel.
Antisecretory agent or nitrate treatment is associated with reduced UGIB RR in patients taking NSAID or aspirin.
Only PPI therapy was associated with a marked, consistent risk reduction among patients receiving all types of agents
Randomized controlled clinical trials of prostaglandin analogues, H2-receptor antagonists or proton pump inhibitors for the prevention of chronic NSAID induced upper GI toxicity were included.
Misoprostol was the only prophylactic agent documented to reduce ulcer complications. Standard doses of H2RAs were effective at reducing the risk of endoscopic duodenal but not gastric ulcers. Both double dose H2RAs and PPIs were effective at reducing the risk of endoscopic duodenal and gastric ulcers, and were better tolerated than misoprostol.
Misoprostol, PPIs, and double dose H2RAs are effective at preventing chronic NSAID related endoscopic gastric and duodenal ulcers
From, all these studies on giving Proton pump inhibitors along with corticosteroids i infer that,probably giving them would be benefitial in preventing gastric and duodenal ulcers.
d) Please share any reports around similar patients with SLE and TB meningitis?
Here's a case report of a 31 year old woman diagnosed with SLE and subsequently developed SLE myocarditis and Lupus Nephritis who also developed TB meningitis
Another case report of a 51 year old woman with SLE who later developed TB meningitis
e) What is the sensitivity and specificity of ANA in the diagnosis of SLE?
To determine the sensitivity and specificity of ANA and anti-dsDNA in SLE patients, using sera from Healthy controls and Multiple Medical problem patients.
The prevalence of ANA at a titer of ≥1:80 and ≥ 1:160 was 8% and 4%, respectively, in HC; and it was 12% and 6% respectively, in MMP patients. The prevalence of anti-dsDNA was 0% in HC and 3% in MMP patients. When using HC sera for the diagnosis of SLE, the sensitivity of ANA at a titer of ≥ 1:80 and ≥ 1:160 was 98% and 90%, respectively, with specificity of 92% and 96%, respectively. The specificity decreased to 88% and 94%, respectively, when using sera from MMP patients. The specificity of anti-dsDNA was 100% and 97%, when using sera from HC and MMP patients, respectively.
ANA and anti-dsDNA gave high sensitivity and high specificity in patients with SLE, even when using MMP patient's sera as controls.
2) Please go through the two thesis presentations below and answer the questions below by also discussing them with the presenters:
a)What was the research question in the above thesis presentation?
Could hypomagnesemia in type 2 DM lead to further more complications
b) What was the researcher's hypothesis?
According to the presenter, hypomagnesemia in type 2 diabetes mellitus could lead to further more complications and poor prognosis.
c)What is the current available evidence for magnesium deficiency leading to poorer outcomes in patients with diabetes?
Association of serum magnesium with Type 2 Diabetes Mellitus
This study was a prospective study done over a period of one month from March 1st to march 31st 2015.
P - 132 patients with Type 2 DM who were treated in the month march 2015 were included in the study.
They were divided into groups based on the duration of diabetes.
Group I (less than 5 years), group II (5 to 9 years) and group III (10 & more than 10 years)
72 patients (54.54%) were in group I and 30 of these were newly diagnosed.
22(15.90%) were in group II.
39(29.54%) were in group III and out of this 9 had DM for more than 20 years.
From this table, there seems to be no significant correlation between serum Magnesium level and Diabetic complications.
The study states a significant decrease in the serum magnesium levels in patients with Type 2 DM, in poor glycemic status and with multiple micro-macro vascular complications, it is important to insist magnesium supplementation on uncontrolled Type 2 diabetes.
Oral Magnesium Supplementation Improves Insulin Sensitivity and Metabolic Control in Type 2 Diabetic Subjects
A randomized double-blind placebo-controlled trial
P- 63 subjects withType 2 Diabetes Mellitus and low serum magnesium
I- 32 (91.4%) subjects who received MgCl2 group
C- 31 (88.6%) subjects in the placebo group
O-
'In this study, subjects who received magnesium supplementation showed an important increase in serum magnesium concentration (15.5%) and reductions of fasting glucose (−37.5%), HbA1c (−30.4%), and HOMA-IR index (−9.5%) that were more significant than those observed in control subjects, despite the fact that time since diagnosis of diabetes, doses and type of hypoglycemic drugs used, and lifestyle intervention were similar.
In this regard, although serum glucose (−27.5%) and HbA1c (−14.4%) levels were reduced in control subjects, HOMA-IR index (6.4%) increased and there were no significant variations in serum magnesium levels (−1.3%). This could be explained by taking into account the fact that control subjects remained with impaired metabolic control (average serum glucose and HbA1c 10.3 mmol/l and 10.1%, respectively), one of the most important sources for magnesium reduction. These findings support the necessity of oral magnesium supplementation to achieve an increase in serum magnesium concentration and to improve insulin sensitivity in type 2 diabetic subjects with decreased serum magnesium levels.'
Association of serum magnesium with type 2 diabetes mellitus and diabetic retinopathy
Out of 250 patients, Patients were divided based on serum magnesium level ≤ 1.7 mg/dL (group 1) and > 1.7 mg/dL (group 2).
110 patients (44%) were found to have hypomagnesemia. Glycemia by fasting blood sugar (P = 0.02), post-Prandial blood sugar (P = 0.04), and HbA1C(P = 0.01) was poorly controlled in hypomagnesemia group.
In group 1, 62.7% had non proliferative diabetic retinopathy and 21.8% had proliferative diabetic retinopathy, whereas in group 2, 14.3% had nonproliferative diabetic retinopathy and 8.6% had proliferative diabetic retinopathy.
Aim of the present study is to study serum magnesium level in patients with type 2 DM and to find the correlation between serum magnesium levels, HbA1c and diabetic complications.
100 patients with Type 2 DM (50 males and 50 females) who were diagnosed on the basis of ADA criteria or taking treatment for Diabetes were included in the study.
There was significant difference in the prevalence of hypomagnesemia (34% vs 6%) and serum magnesium levels between diabetics and control group. FBS (172.17±30.55 versus 137.06±37.76, p<0.0001), PPBS (243±61.21 versus 195.84±59.1, p = 0.0003) and HbA1C (8.42±1.292 versus 7.04±0.956, p<0.0001) were significantly higher in hypomagnesemic diabetics as compared to normomagnesemic diabetics. Significant proportion of hypomagnesemic diabetics were suffering from retinopathy as compared to normomagnesemic diabetics (47.06% versus 19.70%, p = 0.0042). Diabetic nephropathy, neuropathy, hypertension and IHD were also higher in hypomagnesemic diabetics as compared to normomagnesemic diabetics, but insignificant.
Low Serum Magnesium Levels and Foot Ulcers in Subjects with Type 2 Diabetes
'Cases - Thirty-three out-patients with type 2 diabetes and foot ulcers (16 women and 17 men) were compared with a control group
Controls - 66 out-patients with type 2 diabetes without foot ulcers
Outcome - Hypomagnesemia was identified in 31 (93.9%) subjects with foot ulcers, and 49 (73.1%) control subjects, p = 0.02. Subjects with foot ulceration had lower serum magnesium levels (1.48 ± 0.33) than those in the control group (1.68 ± 0.32), p <0.001. Logistic regression analysis showed a significant relationship between low serum magnesium levels and foot ulcers'
a)What was the research question in the above thesis presentation?
b)What was the researcher's hypothesis?
24 hours urinary sodium in newly diagnosed hypertensive patients
The hypothesis is that, the amount of salt consumed is almost equal to the sodium excreted in the urine, which could lead to increase in the blood pressure
c)What is the current available evidence for the utility of monitoring salt excretion in the hypertensive population?
Estimation of 24 hours urinary sodium excretion and relation to cardiovascular events
Data were obtained from 398 628 prospective cohort study participants (40–69 years) recruited between 2006 and 2010, with no history of CVD, renal disease, diabetes mellitus or cancer, and cardiovascular events and mortality recorded during follow-up
there was little evidence for an association between estimated 24-hour sodium excretion and CVD.
Effect of dose and duration of reduction in dietary sodium on blood pressure levels: systematic review and meta-analysis of randomised trials
Meta Analysis
133 studies with 12 197 participants were included. The mean reductions of 24 hour urinary sodium, SBP, and DBP were 130 mmol, 4.26 mm Hg and 2.07 mm Hg respectively. Each 50 mmol reduction in 24 hour sodium excretion was associated with a 1.10 mm Hg reduction in SBP and a 0.33 mm Hg reduction in DBP. Reductions in blood pressure were observed including hypertensive and non-hypertensive individuals.
For the same reduction in 24 hour urinary sodium there was greater SBP reduction in older people, non-white populations, and those with higher baseline SBP levels.
In trials of less than 15 days’ duration, each 50 mmol reduction in 24 hour urinary sodium excretion was associated with a 1.05 mm Hg SBP fall, less than half the effect observed in studies of longer duration. Otherwise, there was no association between trial duration and SBP reduction.
Effect of "no added salt diet" on blood pressure control and 24 hour urinary sodium excretion in mild to moderate hypertension
In this single center randomized study 80 patients (60 cases and 20 controls) not on any drug therapy for hypertension with mild to moderate hypertension were enrolled. 24 hour holter monitoring of BP and 24 hour urinary sodium excretion were measured before and after 6 weeks of 'no added salt diet'.
Seventy eight percent of all patients had moderate to high salt intake. After 6 week of 'no added salt diet' systolic and diastolic BP significantly decreased during the day (mean decrease: 12.1/6.8 mmhg) and at night (mean decrease: 11.1/5.9 mmhg) which is statistically significant in comparison to control group (P 0.001 and 0.01).
Urinary sodium excretion of 24 hour urine decreased by 37.1 meq/d +/- 39,67 mg/dl in case group which is statistically significant in comparison to control group (p: 0.001).
Only 36% of the patients, after no added salt diet, reached the pretreatment goal of 24 hour urinary sodium excretion of below 100 meq/dl (P:0.001). Despite modest effect on dietary sodium restriction, no added salt diet significantly decreased systolic and diastolic BP and so it should be advised to every hypertensive patient.
Salt restriction would certainly reduce the blood pressure and 24 hours urinary excretion of sodium does sound like a good way in measuring the salt intake but also it is important for blood pressure monitoring over 24 hours.
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-
Aspirin in the prevention of progressing stroke: a randomized controlled study
P - 441 patients with ischaemic stroke but not complete paresis were included. No antiplatelet drugs were allowed within the last 72hrs before onset. Delay until first trial dosage was maximized to 48hrs.
I - 220 patients received Aspirin (325mg)
C - 221 patients received placebo
O - 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. In the aspirin group, the relative risk was 0.95 (95% CI 0.62–1.45).
4) Please mention your individual learning experiences from this month.
January 1st 2021:
was posted in Unit 3 from this monthAttended rounds
Attended 2-4 pm session
January 2nd:
Discussed regarding SLE patient with TB meningitis in 2-4 pm session.
Discussed about the drugs causing lupus
January 3rd:
Attended rounds
Reviewed literature on SLE and TB meningitis and the various drugs causing lupus
January 4th:
Attended rounds and discussed about the various side effects of Bisphosphonates - some of them being osteonecrosis of the jaw & esophageal stricture
January 5th:
Discussed about an elderly woman with AKI on CKD
Attended rounds
January 6th:
Was my Opd duty day
Saw Opd cases
Went for PGY2 counselling
Evaluated a case of a 50 year old man complaining of jaw pain and with a hemoglobin of 17g/dl - Polycythemia vera
Discussed regarding oral anti diabetic drugs which cause weight loss and which cause weight gain with my Senior Resident
Admitted 2 cases
January 7th:
Attended rounds
Evaluated both the cases
One case was that of a
65 year old man with CKD secondary to diabetes and NSAID use
Known case of type 2 DM and hypertension
? Anemia of Chronic disease
Second case: 15 year old boy with Paraparesis since 6 months and a history of fever 6 months back
Discussed about the Paraparesis case with the Neurologist and came with a provisional of -
1. Compressive Myelopathy
2.? Non compressive Myelopathy -? Post infectious myelitis
3. Subacute combined degeneration
Discussed regarding 15 year old boy with Paraparesis in 2-4pm session and on rounds.
January 8th:
Examined 15 year old boy with Paraparesis
Helped in making the elog for both the admissions
Link to the elog 👇
https://priyankadevarapalli.blogspot.com/2021/01/15-yr-male-with-paraplegia.html
Got MRI spine done for the patient in order to look for any compressive lesions causing myelopathy
January 9th:
Attended rounds
Discussed about various causes of paraparesis
Learnt that ACA infarct especially in cases with a single ACA
could present like this along with posterior spinal artery infarct which in which the patients would have dorsal column as in our case
January 10th
Did duty
Admitted a case of a 67 year old woman in Altered sensorium, sepsis induced hyperglycemia, AKI on CKD with Left Pyelonephritis
Saw a emergency referral of a 55 year man with below knee amputation and recurrent atrial fibrillation
January 11th:
Attended rounds
Discharged patient of 67 year woman with AKI on CKD on LAMA
Attended 2-4pm class
January 12th
Attended rounds
Discussed about a CLD case who is HCV positive and am alcoholic in 2-4pm session
Discussed on Anti HCV drugs
Epicardial fat on scan
January 13:
It was my duty day
Admitted a 55 year man with? Acute glomerulonephritis
January 14:
Discharged the patient on discharge at request
Attended rounds
Discussed with the nephrologist on about pathogenesis of NSAIDs leading to CKD
Most nephrotoxic aminoglycoside is Gentamycin
January 15:
Attended rounds
Discussed how to differentiate Right heart failure from left heart failure on cvs examination
Discussed about a below knee amputation case with Recurrent Atrial Fibrillation
January 16th
Attended rounds
Discussed about 15 year boy with Paraparesis in the class and the use of csf analysis in him
Reviewed literature on sepsis acting as a trigerring factor for Atrial fibrillation
5) a) What are the possible reasons for the 36 year old man's hypertension and CAD described in the link below since three years?
The 36 year old man with CAD, the etiological reasons to his CAD could be due to the long standing hypertension since 3 years along with being an alcoholic and smoker since 15 years adds up to the risk factors.
b) Please describe the ECG changes and correlate them with the patient's current diagnosis.
The initial ecgs shows irregular rhythm along with VPS
There are progressive ST segment changes in the anteroseptal leads - ? STEMI involving LAD territory/ LAD aneurysm
c) Share an RCT that provides evidence for the efficacy of primary PTCA in acute myocardial infarction over medical management. Describe the efficacy in a PICO format.
Thrombolytic Therapy vs Primary Percutaneous Coronary Intervention for Myocardial Infarction in Patients Presenting to Hospitals Without On-site Cardiac SurgeryA Randomized Controlled Trial
jamanetwork.com/journals/jama/fullarticle/194837
P - Four hundred fifty-one thrombolytic-eligible patients with acute MI of less than 12 hours' duration associated with ST-segment elevation on electrocardiogram.
I - 225 received primary PTCA
C - 226 participants received accelerated tissue plasminogen activator (bolus dose of 15 mg and an infusion of 0.75 mg/kg for 30 minutes followed by 0.5 mg/kg for 60 minutes
O - The incidence of the composite end point was reduced in the primary PCI group at 6 weeks (10.7% vs 17.7%) and 6 months (12.4% vs 19.9%) after index MI. Six-month rates for individual outcomes were 6.2% vs 7.1% for death, 5.3% vs 10.6% for recurrent MI, and 2.2% vs 4.0% for stroke for primary PCI vs thrombolytic therapy, respectively. Median length of stay was also reduced in the primary PCI group (4.5 vs 6.0 days).
Conclusions Compared with thrombolytic therapy, treatment of patients with primary PCI with better clinical outcomes for 6 months after index MI and a shorter hospital stay.
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