January exam

 QUESTION NO1)

A) 
 26 yrs old woman who is k/c/o SLE presented vth c/o headche, fever, vomitings,altered sensorium and stopped taking sle medication ( steriods, hcq) the possible DD in this case:

 1) ? SLE INDUCED ENCEPALITIS

 2) ? ACUTE MENINGITIS

 3) ?  SIADH 

 4) ? ACUTE CVA 

B)   Neuropsychiatric syndromes vth sle

NPSLE ASSOCIATED WITH CENTRAL NERVOUS SYSTEM

·         Aseptic Meningitis
·         Cerebrovascular disease

o    Stroke

o    Transient Ischemic Attack

o    Cerebral Venous Sinus Thrombosis

·         Cognitive Disorders

o    Delirium (Acute confusional state)

o    Dementia

o    Mild Cognitive Imapirment

·         Demyelinating syndromes

·         Headaches

o    Tension Headaches

o    Migraine Headaches

·         Movement disorders (Chorea)

·         Psychiatric Disorders

o    Psychosis

o    Mood Disorders

o    Anxiety Disorder

·         Seizure Disorders

·         Transverse Myelopathy

NPSLE ASSOCIATED WITH PERIPHERAL NERVOUS SYSTEM

·         Autonomic Neuropathy

·         Myasthenia Gravis

·         Peripheral neuropathy

·         Sensorineural Hearing Loss

o    Sudden Onset

o    Progressive

cranial neuropathy

The pathogenic etiologies of NPSLE manifestations are likely to be multifactorial and may involve autoantibody production, microangiopathy, intrathecal production of proinflammatory cytokines and premature atherosclerosis .


 Cellular and parenchymal changes in lupus murine models include neuronal cytotoxicity and atrophy of dendritic spines . Cerebral spinal fluid from lupus-prone mice and adult patients with NPSLE reduce the viability of proliferating neural cells lines .


 Postmortem histopathologic studies reveal a wide range of brain abnormalities caused by multifocal microinfarcts, cortical atrophy, gross infarcts, hemorrhage, ischemic demyelination and patchy multiple-sclerosis-like demyelination in people with SLE .

 A microvasculopathy which was formerly attributed to deposition of immune complexes but now is suspected to arise from activation of complement, appears to be the most common microscopic brain findings in SLE . Consistent with these small vessel changes, SPECT and MR spectroscopy studies suggest that both cerebral atrophy and cognitive dysfunction in SLE patients may be related to chronic diffuse cerebral ischemia.

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2981505/

 

As pt is having euvolemic hyponatremia could be due to siadh which is due to infection(? meningitis)

 

pt having neck rigidity,fever,headche,vomitings MRI brain and LUMBAR PUNCTURE SHOULD BE PLANNED TO RULE OUT MENINGITIS.

 

O/e pt is having dec power of upperlimbs vth exggerated reflexes CVA should be ruled out.

 

sle and hyponatremia:

 Hyponatremia can occur in patients with SLE by various causes such as renal disease, acute kidney injury, and medication use, but only very few case reports were found in literatures onhyponatremia in SLE

We found that hyponatremia was associated with increased ESR, CRP, and SLEDAI and decreased serum albumin and C3 levels by various statistical methods (univariate, multivariate and correlation analyses) in our cohorts of SLE, suggesting that hyponatremia in SLE is closely related to more severe inflammation.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4872139/

 Hyponatremia as an Inflammatory Marker of Lupus Activity Is a Fact or Fad: A Cross-Sectional Study

 Purpose: Systemic lupus erythematosus (SLE) is an autoimmune disease with multi-organ involvement. Hyponatremia is common in inflammatory diseases such as meningitis. Also, it has been found to be strongly associated with the degree of inflammation. However, it has not been fully evaluated in lupus. This study aimed to assess the inflammatory impact of hyponatremia in SLE patients and investigate its relationship with SLE disease activity.

Patients and Methods: A total of  101 patients with SLE were enrolled in this study and divided into two groups according to Na level; a normo-natremic group and a hyponatremic group. Demographic and clinical data were collected. SLE activity was assessed by the systemic lupus erythematosus disease activity index (SLEDAI). The estimated sedimentation rate (ESR) as well as levels of C-reactive protein (CRP) and complements (C3 and C4) were measured.
Results:
 The majority of patients were females (98 subjects) (97%) with a mean age of 33± 8 years. Out of 101 participants, 40 patients (39.6%) were hyponatremic with a mean Na level of 131.58± 3.11 mmol/L. There was a statistically negative correlation between both ESR and SLEADI score and Na level (r=− 0.436 and − 0.436, respectively) with p=0.002, whereas Na level was positively correlated with complements, Cl, and albumin levels (r=0.653, 0.314, and 0.460, respectively) (p=0.000, 0.027, and > 0.001, respectively). CRP was not correlated with Na level. ESR was independently correlated with hyponatremia at the 95% CI for Exp B (0.997– 0.058) with a p-value of 0.048.

Conclusion: Hyponatremia could be used as an indicator of SLE activity. Also, it might be an easily and rapidly detected as well as a prognostically useful marker of inflammation.

Time line events:



C) Steriods in sle:

Steroid medications work quickly to decrease the swelling, warmth, tenderness and pain that are related to inflammation. They do this by lessening the immune system's response. Prednisone is the most commonly prescribed steroid for lupus.

hcq in sle:-https://pubmed.ncbi.nlm.nih.gov/29987550/#:~:text=Conclusio

Background: 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 400 mg HCQ per day were included. Patients requiring statins and immunosuppressive drugs except prednisolone at doses lower than 10 mg/day were excluded. Outcome measures were assessed before commencement of HCQ therapy (baseline visit) as well as in two follow-up visits (1 and 2 months 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.

sulfasalazine is usually not prescribed in sle as it cause drug induced sle.

E) ANA sensitivity time diagnose sle :- ANA titer of 1:40 or higher is considered positive. An ANA titer of less than 1:40 is useful for ruling out SLE in children (sensitivity of 98%). A repeated negative result makes a diagnosis of SLE unlikely but not impossible. The ANA titer does not correlate with the severity of the disease.

 Objective: To determine the sensitivity and specificity of ANA and anti-dsDNA in SLE patients, using sera from HC and MMP patients.

Methods: Serum samples from HC, MMP and SLE patients, 100 in each group, were analyzed for the presence of ANA and anti-dsDNA, by indirect immunofluorescent assay, using a HEp-2 cell and Crithidia luciliae as substrates, respectively.

Results: 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.
Conclusion: ANA and anti-dsDNA gave high sensitivity and high specificity in patients with SLE, even when using MMP patient's sera as controls. Physicians should take care in interpreting ANA and anti-dsDNA results in MMP patients who do not have signs or symptoms of SLE or connective tissue diseases.
QUESTION NO 2)
To study the association of serum magnesium levels of type2 diabetesmellitus.
What is the current available evidence for magnesium deficiency leading to poorer outcomes in patients with diabetes? 
Hypomagnesemia has been linked to poor glycemic control, coronary artery diseases, hypertension, diabetic retinopathy, nephropathy, neuropathy, and foot ulcerations. The increased incidence of hypomagnesemia among patients with type 2 diabetes presumably is multifactorial.
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.
Clinically, hypomagnesemia may be defined as a serum Mg concentration ≤1.6 mg/dl 

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 

What was the research question in the above thesis presentation? 
1)Will salt restricted diet decrease blood pressure?
2)can 24hr urinary sodium test reflect the amount of sodium consumed by an individual.
what was the researchers hypothesis?
Hypothesis is that,salt restriction doesnt effect blood pressure in all the individuals in the same way, and salt resistant individuals dont benefit from a restricted diet as much as a salt sensitive individual.
What is the current available evidence for the utility of monitoring salt excretion in the hypertensive population?

In a large prospective cohort study, we demonstrate a consistent relationship between estimated urinary sodium excretion as a marker of sodium intake and elevation in blood pressure. These relationships were present both in the whole cohort and when restricted to subjects free of baseline comorbidity, specified by restricting analysis to those without baseline CVD, DM, or treated hypertension and with Charlson comorbidity score of zero. These findings are consistent with other cohort studies, interventional clinical trials, and meta-analyses.

The mechanisms by which dietary sodium contributes to raised blood pressure have been reviewed extensively elsewhere. Sodium excess has been associated with excess activation of the sympathetic nervous system, increased vascular tone, and endothelial dysfunction, as well as end organ damage with left ventricular hypertrophy, glomerulosclerosis, and arteriolosclerosis. In industrialized countries, diets rich in sodium and low in potassium are the norm. Processed meals are rich in sodium. Societies following a nonindustrialized diet low in sodium have low prevalence (<1%) of hypertension. Meta-analyses demonstrate that reduction in dietary sodium intake is associated with average reduction in systolic blood pressure of 3 to 5.4 mm Hg in hypertensive subjects. Our data add weight to the hypothesis that reduction of dietary sodium intake may lead to lower blood pressure. Unfortunately, we do not have long-term blood pressure changes to assess the influence of sodium intake on development of hypertension

https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.119.12726

QUESTION NO3) 

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 48HR.
Totally, 441 patients (220 aspirin, 221 placebo) completed the trial.

I- Aspirin (325 mg) or placebo was given once daily for five consecutive days.

C-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 3months.

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 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 abilty to live at home,to walk unaided,or need for further institutionalized care after discharge was not significantly improved in the aspirin group.

QUESTION NO4 )

Jan1- read about isolated urea elevation causes, cardirenal syndromes and its types.
Jan 2-attended icu rounds and read about article on HFREF and its managment 
Jan3-attended rounds. Read about sle and its neurological complications.
Jan4- attended 2-4 rounds discussed about sle and tb meningitis case vth acute cva and hyponatremia 
Jan5- 2nd unit opdduty day. Attended casuality after 4pm 
Jan6- attended pg counselling in the mng session. Followed up the admitted case aki on ckd sec to urosepsis vth cholelithiasis vthuncontrolled sugars.
Jan7- aki on ckd case pt has oliguria vth refractory hyperkalemia so placed central line in the early mng and took her for hemodialysis. In the aftn pt was given ironsucrose inj had febrile reaction and managed the case
Jan 8  and 9 on official leave for emergency purpose
Jan 10- followed up the admitted case pt had sudden fall in saturation’s from evng and tachycardia tachypnoea present.kept on o2 inhalation and intermittentcpap.
Jan 11- Pt had been shifted to 3rd session of hemodialysis  and on xray pt had b/l consolidatory changes which was suspected sec to blood tansfusion ?TRALI/? HAP
Jan12- attended 2nd unit ops duty day.Pt feeling dyspnea on xray b/l pulmonary infiltrates present (ARDS non cardiogenic pulmonary edema) and pt bilirubin raised suspected acute hemolytic reaction pt was kept on O2 inhalation and intermittentcpap . Admitted a case of diabetes vth uncontrolled sugars vth ketone bodies positive and kept on insulin infusion.
Jan 13-  followed up the admitted case continued same treatment and taken for 4th session of hemodialysis.
Jan 14- followed up admitted case. Attended 2-4 rounds discussion was done on liverabscess case
Jan15- Pt was subjectively feeling better. Requirment of o2 reducing.attended 2-4rounds read about heartfailure mid range reduced ejection fraction. Discussion was done on psvt and its mamanagment, causes.
Jan16- followed up the case. Taken for one more session of hemodialysis . Attended 2-4rounds, discussion was done chronic pancreatitis pain management. About transfusion ass reactions
Jan 17- on casuality duty day. Saw a case of k/c/o cops vth allergic bronchitis. Saw a case of intermittent palpitations lasting for 10mins. Managed case of chronic pancreatitis pain in the night.
QUESTION NO5 )
A) causes of young onset CAD are 1) atheromatous cad 2) non atheromatous cad 3)hyper coaguable states4) susbstance misuse
In this patient could be due to his risk factors alcohol and smoking since the age of 15yrs..

Ethnic wise south Asians especially Indians are more vulnerable to have CAD in young age group with a prevalence of 5% to 10%. Conventional risk factors such as smoking, diabetes, hypertension, obesity and family history seems to be as important as in older CAD subjects.

By far the most commonly associated risk factor is smoking in young CAD

Several genes associated with lipoprotein metabolism are now found to be associated with young CAD. Gamma glutamyl transferase, vitamin D2 and osteocalcin seem to be associated with premature CAD in some studies. Angiographic studies shows predominance of single vessel disease in young CAD patients.

Conventional CAD accounts for about 80% of CAD in young adults. About 4% of heart attacks in young adults are due to congenital abnormalities of the coronary artery anatomy, about 5% due to blood clots that originate elsewhere and are carried to otherwise normal coronary arteries, and block the artery, in another 5%, various disorders of the blood clotting system increase the risk of clot formation. The remaining 6% of CAD in young adults is due to spasm or inflammation of the coronary arteries, radiation therapy for chest tumors, chest trauma, and abuse of cocaine, amphetamines, and other drugs

In recent study from Nepal of young CAD less than 45 years angiography revealed 7.6% had normal or non critical disease, 6.1% had triple vessel disease, 36.9% had double vessel disease and 53.8% had single vessel disease[69].

Single vessel disease involving left anterior descendinartery is much more common in young women when compared with young men with CAD


 B) Ecg findings:-

ECG shows evolving myocardial infarction changes with progressive ST T changes and VPCs
Vpc is followed by a compensatory pause.
Rate - 75 
Rythm - Intial ecgs rate is Irregular with Vpc ,later becoming regular
Axis - Normal
St - elevations in v1-v4 ,about 2mm and increasing( (Anter septal MI ).
QS complexes in v1-v.  Indicating previous AWMI.
No LVH. 

 and echo showing hypokinetic segment in LAD territory (? LV aneurysm) that may also reflect his past LAD infarct. 

C) Efficacy of primary Ptca over medical management in MI patients:-

As compared with thrombolytic therapy, primary coronary angioplasty results in a higher rate of patency of the infarct-related coronary artery, lower rates of stroke and reinfarction, and higher in-hospital or 30-day survival rates. However, the comparative long-term efficacy of these two approaches has not been carefully studied

P- Total 394 pt ( 194- primary angioplasty, 201- iv streptokinase)

I- Primary angioplasty, and iv streptokinase.

c- Mortality was 13 percent in the angioplasty group, as compared with 24 percent in the streptokinase group (relative risk, 0.54; 95 percent confidence interval, 0.36 to 0.87). Nonfatal reinfarction occurred in 6 percent and 22 percent of the two groups, respectively (relative risk, 0.27; 95 percent confidence interval, 0.15 to 0.52). The combined incidence of death and nonfatal reinfarction was also lower among patients assigned to angioplasty than among those assigned to streptokinase, with a relative risk of 0.13 (95 percent confidence interval, 0.05 to 0.37) for early events (within the first 30 days) and a relative risk of 0.62 (95 percent confidence interval, 0.43 to 0.91) for late events (after 30 days). The rates of readmission for heart failure and ischemia were also lower among patients in the angioplasty group than among patients in the streptokinase group. Total medical charges per patient were lower in the angioplasty group ($16,090) than in the streptokinase group ($16,813, P=0.05).

o-As compared with thrombolytic therapy with streptokinase, primary coronary angioplasty is associated with better clinical outcomes over five years.

 

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