January 2021 bimonthly exam

 https://medicinedepartment.blogspot.com/2021/01/medicine-paper-for-january-2021.html?m=1


Internal assesment to the questions asked in the above blog spot.


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


Case presentation  links: 


https://youtu.be/fz9Jssoc-mA


https://youtu.be/d4lLX04oL8s


https://youtu.be/CSCxw2zp7Oc



a). What is the problem representation of this patient and what is the anatomical localization for her current problem based on the clinical findings?


Altered sensorium  fever  headache neck pain : secondary to CNS pathology( neck rigidity)  : Meningitis 

                  Cns lupus

                    Corticosteroid induced psychosis 


Altered sensorium Secondary to electrolyte disturbance :hyponatremia.


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. 


3 years back : SLE 

1 month back : headache - stopped steroids- fever along with headache and neck pain - vomitings - altered sensorium ( in contact with active pulmonary TB )

A history of SLE and the medication she is using gives us a clue that she is immunocompromised and prone for opportunistic infections.

Hyponatremia is commonly associated with CNS Tuberculosis(infectious etiology) : fever cough altered sensorium explained.

Or hyponatremia itself is responsible for altered sensorium.


Plan would be cranial imaging and CSF analysis to find out the CNS pathology.


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? 


For example: 


Why was she given bisphosphonates? 

What is the efficacy of using primary bisphosphonate prophylaxis for patients started on corticosteroids?


Corticosteroids cause osteoporosis and are responsible for vertebral fractures and bisphosphanates are usefull in preventing and treating osteopororsis in patients on corticosteroids.


The use of bisphosphonates to reduce the risk of vertebral fractures and the prevention and treatment of steroid‐induced bone loss.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6461188/


What is the efficacy of using primary PPI prophylaxis during initiation of any  corticosteroids to prevent Gi ulcers? 

 

Corticosteroids are ulcerogenic and are responsible for causing PUD and gi bleeding.

The mechanism by which corticosteroids might induce GI bleeding or perforation has not been fully established, but corticosteroids may impair tissue repair, thus leading to delayed wound healing.8 In addition, the anti-inflammatory and analgesic properties of corticosteroids may mask symptoms of gastroduodenal ulcers and ulcer complications and thus possibly delay diagnosis.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4025450/


d) Please share any  reports around similar patients with SLE and TB meningitis?

She was diagnosed as having tuberculous meningitis based on the detection of acid-fast bacillus in cerebrospinal fluid, and began treatment with antituberculous agents.

https://pubmed.ncbi.nlm.nih.gov/10067053/


e) What is the sensitivity and specificity of ANA in the diagnosis of SLE?

Antinuclear antibody testing. A study of clinical utility - PubMed

The estimated sensitivityand specificityof the ANAtest for SLEwere 100% and 86%, respectively.




2) 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? 

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


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.

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


https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-10/How-to-quantify-salt-intake-in-certain-patients


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


https://youtu.be/jXVS5J1-RNE


What was the research question in the above thesis presentation


To study the 24 hour urinary sodium secretion in newly diagnosed hypertensive patients


Objectives: to analyse the 24 hour urinary sodium with respect to stages of hypertension 

To study effects of sodium on BMI

analyse 24 hour urinary sodium excretion in complications of hypertension which include opthalmic,renal and cardiovascular changes.


What was the researcher's hypothesis?


Researcher wanted to find out whether salt restriction in hypertensive patients,as hgave some sort of benefit to them,but in reality there are two categories of patients salt sensitive 

and insensitive groups.It is estimated that 50-60% are salt sensitive and only the sensitive group reacts to changes in dietary salt intake with alterations in blood pressure. It is estimated that about 50-60 % of hypertensives are salt sensitive


To find out this 24 hour urinary sodium excretion was assessed in 


Tot


What is the current available evidence for the utility of monitoring salt excretion in the hypertensive population? 

High dietary intake of sodium is seen in most of the subjects who have very high blood pressures

By the means of a self monitoring device

Subjects were 34 hypertensive patients who underwent successful 24-h home urine collection five times and 25 volunteers. Four volunteers were diagnosed as having hypertension based on home blood pressure (BP) readings. All subjects were asked to measure daily urinary salt excretion for 30 days by using a self-monitoring device which estimates 24-h salt excretion by overnight urine. The mean urinary salt excretion during the 30 days was 8.36 +/- 1.52 g/day and the range (maximum-minimum value) was 5.47 +/- 20.05 g/day in all subjects. Mean urinary salt excretion decreased from 8.52 +/- 1.63 g/day for the first 10 days to 8.31 +/- 1.54 g/day for the last 10 days (p < 0.05). The mean urinary salt excretion determined by a self-monitoring device using overnight urine was positively associated with that determined by 24-h home urine for five times in the hypertensive subjects (r = 0.63, p < 0.01). Results indicate that a self-monitoring device seems to be useful to monitor daily salt intake and to guide salt restriction.

This might be useful in subjects who are sensitive to sodium restriction 


Source:

https://pubmed.ncbi.nlm.nih.gov/20001461/



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. 


Study desing and methodology is good as it is a randomised double blided placebo controlled 


It is usefull for us locally also as CVA patients do present to us in our hospital.


And the study shower PICO formate where P :the population has similar  base line characteristics as CT confirmed ishchaemic stroke and Focal neurological defect is also present 

I : intervention was giving Tab Aspirin

C: placebo vs aspirin group

O: outcome is stroke progression where there are no significant differences in both the groups 

And its a cost effective analysis



4) Please mention your individual learning experiences from this month.


Procedural skills : 

Had put a central line for 45 year old male with CRF

Intubated a patient who eventually got extubated.

Took an abg 

A 50 year old man who presented with PSVT adenosine and vagal maneouver were done

Did a pelural tap for a pleural effusion patient


Theory: studied about ecg differention between RV MI and posterior wall MI

Studied about liver abscess and reviewed same case reports in view of it.



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? 


https://vamsikrishna1996.blogspot.com/2021/01/36-year-male-presented-to-casualty-at.html?m=1


Patient was a chronic smoker and alcoholic which could be the risk factors for his HTN AND CAD.



b) Please describe the ECG changes and correlate them with the patient's current diagnosis. 



Rythm - Initial ecgs rate is Irregular with VPC ,later becoming regular

Axis - Normal

VPCs followed by a compensatory pause

QS complexes in v1 - v3

Poor R wave progression

T-wave inversions in v4 - v6

Mild ST segment elevation in v1 - v4


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.


P


214 patients with stable angina, normal ventricular function and a proximal stenosis of the left anterior descending coronary artery > 80% 


I


Balloon angioplasty

Medical therapy alone


C


Balloon angioplasty (n = 72)

Medical therapy alone (n = 72)


O


At an average follow-up period of 3 years

p = 0.28, angioplasty vs. medical treatment

There was no difference in mortality or infarction rates among the groups



https://pubmed.ncbi.nlm.nih.gov/7594092/

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