BIMONTHLY EXAM FOR THE MONTH OF FEBRUARY

February 20, 2021

BIMONTHLY EXAM FOR THE MONTH OF FEBRUARY

"This is my submission for the Bimonthly internal assessment for the month of February."

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/2021/02/medicine-paper-for-february-2021.html?m=1

Mentioned the links to the referrals, log links and youtube videos

Thank you :)

1Q. 50 year man, he presented with the complaints of

Frequently walking into objects along with frequent falls since 1.5 years

Drooping of eyelids since 1.5 years

Involuntary movements of hands since 1.5 years

Talking to self since 1.5 years

https://archanareddy07.blogspot.com/2021/02/50m-with-parkinsonism.html?m=1

https://youtu.be/kMrD662wRIQ

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

This was our unit case, and the first time I've seen a case with Progressive Supranuclear Palsy

50 year old man, detected to be a diabetic 9 months back, presented with the complaints of:

Frequently walking into objects along with frequent falls since 1.5 years

Drooping of eyelids since 1.5 years

Involuntary movements of hands since 1.5 years

Talking to self since 1.5 years

Bed wetting since 1 year

The patient also has had 3 suicidal attempts in the past.

He had reduced arm swing and facial apathy.

All of this fitting into a neurodegenerative disorder known as Progressive supranuclear palsy.

ANATOMICAL LOCALIZATION TO HIS PROBLEMS:

The anatomical localization to his problems appears to be in the brain

The anatomical location is in the Basal ganglia and substantia nigra

Goes in favour of a neurodegenrative disorder

The basal ganglia and the midbrain. In the midbrain, vertical and torsional saccades are controlled by the rostral interstitial medial longitudinal fasciculus (RIMLF).

'Isolated dysfunction of vertical eye movements is due to a midbrain lesion affecting the rostral interstitial nucleus of the medial longitudinal fascicle, with impaired vertical saccades only, the interstitial nucleus of Cajal or the posterior commissure; common causes with an acute onset are an infarction or bleeding in the upper midbrain or in patients with chronic progressive supranuclear palsy (PSP) and Niemann-Pick type C '

https://www.researchgate.net/publication/264988625_Central_ocular_motor_disorders_including_gaze_palsy_and_nystagmus

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 his problems and current outcomes.

We came to a diagnosis that the patient probably has Progressive supranuclear palsy.

The other differential we had in mind was Myasthenia gravis as the patient complained of ptosis which progressed by the night. We performed an Ice Pack test to rule out Myasthenia Gravis. After an Ice pack test, in Myasthenia Gravis, the eyelid droop improves by atleast 2-3 mm, which wasn't seen in this patient & also the drooping of his eyelids were intermitted.

Upon examination, he found that he was unable to move his eyeballs upwards and he would frequently walk into objects and have frequent falls.

Postmortem autoradiographic studies indicate that pharmacologically defined D2 dopamine receptors are decreased in the striatum, but striatal D1 dopamine receptors are preserved. This situation contrasts with that found in Parkinson's disease, in which striatal dopamine loss is associated with normal or elevated numbers of striatal D2 receptors."

https://www.sciencedirect.com/topics/neuroscience/progressive-supranuclear-palsy

"In 1955, Richardson was visited by a good friend and 52 year old business executive because of clumsiness, trouble in seeing, and mild forgetfulness. During the next 4 years, Richardson was puzzled as his friend progressively developed an unusual constellation of signs that included supranuclear ophthalmoplegia affecting chiefly vertical gaze, pseudobulbar palsy, dysarthria, dystonic rigidity of the neck, and mild dementia."

In their 1963 reports, Richardson and Olszewski had called the condition heterogeneous system degeneration, a term first used by W. J. C. Verhaart for a similar case he described in 1958. However, as they were not certain that the disease was a primary degeneration or that it was related to other system degenerations, it was agreed that they shouldchoose another term. They briefly considered ‘Can't look down disease’,"

https://www.sciencedirect.com/topics/neuroscience/progressive-supranuclear-palsy

TIMELINE OF EVENTS

c) What is the efficacy of each of the drugs listed in his current treatment plan

The patient was put on Syndopa

Quetiapine

A randomized, double-blind, placebo-controlled trial, we evaluated 361 patients with early Parkinson's disease who were assigned to receive carbidopa–levodopa at a daily dose of 37.5 and 150 mg, 75 and 300 mg, or 150 and 600 mg, respectively, or a matching placebo for a period of 40 weeks, and then to undergo withdrawal of treatment for 2 weeks

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699657

P - A total of 361 subjects

I - 317 took the medication

C - 90 received Placebo

O -

Levodopa, in a dose–response pattern, significantly (P<0.001) reduced the worsening of symptoms of Parkinson's disease as reflected in the change between the total score on the UPDRS at baseline and that at week 42 (i.e., two weeks after washout of the study medication), as compared with the change in the placebo group.

Strong dose–response benefit was detected during the period in which the medication was administered beginning at week 9, when the full dose of 600 mg daily was reached in the group receiving the highest dose of levodopa, and it persisted through week 40. The scores on the UPDRS in the three levodopa groups worsened during the two-week washout period, but these groups did not deteriorate to the level observed in the placebo group, and the group receiving the highest dose of levodopa had the best result. The adverse events that were significantly more common among those receiving levodopa at 600 mg daily than in the placebo group were dyskinesias, nausea, infection, hypertonia, and headache.

An analysis of the results of SPECT after the exclusion of the 19 subjects without a dopaminergic deficit who returned for the neuroimaging study at week 40 showed a significantly greater decrease in β-CIT uptake among those receiving levodopa than among those receiving placebo (P=0.036).

Quetiapine

12 week double blind randomized placebo-controlled trial of quetiapine for psychosis in Parkinson’s disease

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699657/

P - Twenty-four eligible subjects were included in the study with met UK Brain Bank criteria for idiopathic PD. They were screened over a 16-month period for a target of 60

I - Eleven patients were randomized to quetiapine

C - 13 to placebo

O - In this study they were not able to show that quetiapine at doses of up to 150 mg/day was able to significantly improve psychosis compared to placebo. Unlike some other atypical antipsychotics, quetiapine did not appear to worsen PD motor functioning. Its use was limited by a faster drop out compared with placebo, although this was not statistically significant.

2Q. Patient was apparently asymptomatic 2 years back then he developed weakness in the right upper and lower limb, loss of speech.

More here: https://ashfaqtaj098.blogspot.com/2021/02/60-year-old-male-patient-with-hrref.html?m=1

Case presentation links:

https://youtu.be/7rnTdy9ktQw

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

Problem representation:

A 60 year old man with a history of CVA 6 months back presented with

Dyspnea since 2 months

Bilateral pedal edema since 2 months

Reduced urine output since 2 months

Generalised weakness since 2 months

His examination findings were Visible apical impulse, Pericardial bulge, visible pulsations, dilated veinsshift of apex beat to 6th ICS, Thrill at the apex, Loud S1 present, loud P2 present, S3 Accentuating on inspiration- RVS3, Expiration - LVS3

His Ecg shows poor R wave progression

Chest Xray PA shows Cardiomegaly

His 2Echo is suggestive of Heart failure DCMP with Hypokinesia at RCA, LCX

Anatomical diagnosis:

The location to his problems is at the Heart, secondary to atherosclerosis of the vessels

Risk factors:

Alcohol

Age of 60 years

Male gender

'In vivo imaging techniques applied in humans and the success of antithrombotic and fibrinolytic therapy in ACS established in practice the role of thrombosis in their pathogenesis. A number of microanatomic mechanisms underlie acute coronary thrombosis. According to autopsy studies—clearly biased toward fatal outcomes—a through-and-through rupture of the plaque’s protective fibrous cap most commonly causes lethal coronary thrombosis. Other mechanisms that account for a minority of fatal coronary thromboses include superficial erosion, intraplaque hemorrhage, and the erosion of a calcified nodule. Thus, physical disruption of the atherosclerotic plaque accounts for almost all acute coronary thromboses.'

'Disrupted plaques provoke thrombosis in several ways. First, contact with collagen in the plaque’s extracellular matrix can trigger platelet activation. Second, TF produced by macrophages and SMCs activates the coagulation cascade. The disrupted plaque thereby represents a “solid-state” stimulus to both thrombosis and coagulation; these pathways reinforce each other, as thrombin generation amplifies the activation of platelets and other cells in the lesion. Conversion of fibrinogen to fibrin and release of von Willebrand factor from activated platelets can provide the cross-linking molecular bridges between platelets that yield the dense, 3-dimensional network of platelets entrapped in fibrin characteristic of the “white” arterial thrombus.'

https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.105.537878

Etiology to his current problems :

CAD leading to DCMP

Diagnosis:

DCMP with an EF of 34% secondary to CAD

CVA 6 months back (? Left ischaemic stroke

Please chart out the sequence of events timeline between the manifestations of each of his problems and current outcomes.

TIMELINE OF EVENTS

What is the efficacy of each of the drugs listed in his current treatment plan

1) Fluid <1 L/ day and salt restriction <2g/day

Impact of Dietary Sodium Restriction on Heart Failure Outcomes

https://www.sciencedirect.com/science/article/pii/S2213177915006551

This is a randomized controlled trial

P - Sodium intake data was available for 833 patients

I- 145 were salt restricted

C- 688 salt unrestricted

O-

Sodium intake data were available for 833 of 902 (92%) subjects enrolled in HART.

The median sodium intake was 3,336 mg/d (Range: 2,701 to 4,237 mg/d; range 1,250 to 15,678 mg/d).

Based on the mean sodium intake before primary outcome events (death or HF hospitalization), patients were classified into restricted (n = 145 [17.4%]) and unrestricted (n = 688 [82.6%]) sodium intake groups.

Sodium restriction was associated with significantly higher risk of death or HF hospitalization (42.3% vs. 26.2%, p = 0.004), derived from an increase in the rate of HF hospitalization (32.3% vs. 20.0%, p = 0.015) and a nonsignificant increase in the rate of cardiac death and all-cause mortality.

In these analyses of data from HART, there was no demonstrable evidence that dietary sodium restriction is associated with lower rate of death or HF hospitalization. In fact, dietary sodium restriction was associated with increased risk of adverse outcomes, particularly HF hospitalization.

2) SPIRINOLACTONE

Randomized Aldactone Evaluation

https://pubmed.ncbi.nlm.nih.gov/10471456/

P - In a doubleblind study, we enrolled 1663 patients who had severe heart failure and a left ventricular ejection fraction of no more than 35 percent and who were being treated with an angiotensin-converting-enzyme inhibitor, a loop diuretic, and in most cases digoxin.

I - total of 822 patients were randomly assigned to receive 25 mg of spironolactone daily

C - 841 to receive placebo

O -

The trial was discontinued early, after a mean follow-up period of 24 months, because an interim analysis determined that spironolactone was efficacious. There were 386 deaths in the placebo group (46 percent) and 284 in the spironolactone group (35 percent).

This 30 percent reduction in the risk of death among patients in the spironolactone group was attributed to a lower risk of both death from progressive heart failure and sudden death from cardiac causes. The frequency of hospitalization for worsening heart failure was 35 percent lower in the spironolactone group than in the placebo group.

In addition, patients who received spironolactone had a significant improvement in the symptoms of heart failure, as assessed on the basis of the New York Heart Association functional class.

Gynecomastia or breast pain was reported in 10 percent of men who were treated with spironolactone, as compared with 1 percent of men in the placebo group (P<0.001).

3) TELMISARTAN AND METOPROLOL:

https://www.ahajournals.org/doi/10.1161/CIRCHEARTFAILURE.116.003529

'A systematic literature review identified 57 randomized controlled trials published between 1987 and 2015, The random-effects network meta-analysis suggested that the combination of ACEI+BB+MRA was associated with a 56% reduction in mortality versus placebo.

ARNI+BB+MRA was associated with the greatest reduction in all-cause mortality versus placebo.'

3Q. 52 year old male , shopkeeper by profession complains of SOB, cough ,decrease sleep and appetite since 10 days and developed severe hyponatremia soon after admission.

More here https://soumya9814.blogspot.com/2021/01/this-is-online-e-log-book-to-discuss.html?m=1

Case presentation video:

https://youtu.be/40OoVEQBgS4

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

Problem representation:

A 52 year old man, who is a known to be a Diabetic and hypertensive presented with:

Dyspnea since 10 days

Productive cough since 2 days

Disturbed sleep since 10 days

Anatomical localization:

The anatomical location of the problem is in the lungs

Lower respiratory tract infection

No respiratory examination has been mentioned in the elog.

However his problems list are:

- Hyponatremia

-Lower respiratory tract infection

-Uncontrolled blood sugars

-Dimorphic Anemia

Unclear on the details of his ?UTI. CUE shows 5-6 pus cells, with no patients complaints with a negative urine culture & sensitivity report.

SIADH:

https://geekymedics.com/syndrome-of-inappropriate-antidiuretic-hormone-secretion-siadh/

TIMELINE OF EVENTS

c) What is the efficacy of each of the drugs listed in his current treatment plan especially for his hyponatremia? What is the efficacy of Vaptans over placebo? Can one give both 3% sodium as well as vaptan to the same patient?

Randomized, double-blind, placebo-controlled trial to evaluate the efficacy and safety of tolvaptan in Chinese patients with hyponatremia caused by SIADH

https://pubmed.ncbi.nlm.nih.gov/24906029/

P - 37 patients have been included in this study

I - Hyponatremic SIADH patients received tolvaptan (N = 19) at an initial dose of 15 mg/day with further titration to 30 mg/day and 60 mg/day based on serum sodium concentrations.

C - 18 patients received placebo

O -

Primary endpoint was the change of the serum sodium from baseline to days 4 and 7.

At day 4, average daily changes in serum sodium levels from baseline was 1.9 ± 2.9 mmol/L in the placebo group and 8.1 ± 3.6 mmol/L in the tolvaptan group; at day 7, the values were 2.5 ± 3.9 mmol/L and 8.6 ± 3.9 mmol/L for the placebo and tolvaptan groups

. At days 4 and 7, daily urine output and proportions of patients with normalized serum sodium were significantly superior in the tolvaptan group.

The most common adverse events occurring in the tolvaptan group were dry mouth and thirst. Tolvaptan demonstrated superiority to placebo in the treatment of Chinese SIADH patients.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4078649/

In this prospective observational study, data of 60 hospitalized patients having hyponatremia from February 2013 to July 2013 were collected and analyzed. Patients either received oral Tolvaptan or intravenous infusion of 3% hypertonic saline solution. The serum sodium concentration before administration of treatment and 24 h and 48 h after the administration of the drugs were recorded and analyzed.

Observation:

'Tolvaptan and 3% hypertonic saline solution had significant effects in raising serum sodium level in hyponatremic patients at both 24 h and 48 h (P < 0.0001). This increase was about 8.030 ± 0.6507 mEq/L and 12.33 ± 0.6489 mEq/L for 3% hypertonic saline and about 5.111 ± 0.6616 mEq/L and 10.11 ± 0.6230 mEq/L for Tolvaptan, after 24 h and 48 h, respectively

Both drugs had significant effects in raising serum sodium level in hyponatremic patients; however administration of 3% hypertonic saline solution had a slightly superior efficacy in raising the serum sodium concentration at both 24 h and 48 h periods in Hyponatremic patients compared with oral Tolvaptan.'

I don't think both Nacl and Tolvaptan could be given at the same time as there is a risk of overcorrection leading to hypernatremia.

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

1st of February - Monday
Attended rounds
And 2-4 pm discussion

2nd February - Tuesday
Leave because of I'll health

3rd February - Wednesday
I was on leave

4th February - Thursday
Attended rounds and examined my patients
1. A 50 year man with Progressive supranuclear palsy
2. A 41 year man with Pancreatic pseudocyst
3. 73 year man with CAD showing a bifascicular block on the ECG posted for left inguinal hernia surgery
4. 50 year old man with HFrEF
5. 45 year man with Fever and Rashes

Discussed about our cases in the 2-4pm session

5th February - Friday

After attending rounds, examined our PSP case
Performed an Ice pack test to rule out Myasthenia Gravis which came out to be negative

Learning points on rounds :
Causes of Copd exacerbation:
LV failure
Pneumothorax
Pulmonary embolism

Discussed regarding PSP in our 2-4pm session

Started our PSP patient on SYNDOPA

6th February - Saturday

Attended rounds
2-4 pm session

7th February - Sunday

8th February - Monday
Went for rural area service postings

9th February - Tuesday

Few learning points on rounds :
Gravelurea
Pleural fluid level to be detected on chest xray and usg chest
Trihexyphenydryl
Night blindness
Lambart Eaton syndrome and Myasthenia gravis differences
Cheliditi syndrome
Oxygen masks
Cardioversion
P on t phenomenon
Spleen accumulation of iron
Gamna-Gandy bodies (GGBs)

10th February - Wednesday

Admitted a case of 30 year woman viral fever with thrombocytopenia with a platelet count of 2000cells/cumm

11th February - Thursday

Attended post duty rounds
Learning points on rounds:
Why stk is working more for heart and more for brain
Ketosis
Bp variability
Sulfasazaline
Ventilator - lung pressures
Mri in ankylosing spondylitis
Discussed about cases in 2-4 pm session

12th February - Friday

Attended rounds
Attended 2-4pm session

13th February - Saturday

Did duty
Admitted interesting cases
Total 6 admissions yesterday
Will be updating on all the cases soon.
1. 60 year old woman with Hypertensive emergency
2. 42 year old man with Left lower limb cellulitis with AKI
3. 50 year old man with CKD with heart failure, Anemia under evaluation
4. 60 year woman with AKI secondary to sepsis (? UTI )
5. 40 year old man who presented with alcoholic liver disease currently in withdrawal
6. 55 year old man with Acute Gastroenteritis

14th February - Sunday
Attended post duty rounds

15th February - Monday

Attended rounds
Discussed about Vaptan indications on rounds
Attended 2-4 pm session

16th February - Tuesday
Attended rounds
Followed by Mortality and morbidity meeting