BIMONTHLY EXAM FEB 17 2021

BIMONTHLY EXAMFebruary 17, 2021FEBRUARY BIMONTHLY EXAM  the patient data in the links below and answer the following questions:

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 

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

Case presentation links: 

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?

problem presentation:

drooping of eyelids since 8 to 9 months refractory to treatment

involuntary movements of bilateral upper limbs

frequent episodes of fatigue since one year

thin stream of urine with bed wetting since one year

according to attenders 

change in behavior (talking to self) since 1.5 years

anatomical localisation of lesion

b/l ptosis-weakness of levator palbebral superioris

(without loss of frowning)

self talk-frontal lobe

vertical gaze palsy:

the centres and pathway for vertical gaze:

vertical gaze palsy is 

supranuclear

nuclear

infranuclear (eg.nmj disorders)

the doll's eye manaever is used to differentiate between supra and below

suggesting the activation of vestibulo -occular system which directly activates the thalamo-mesencephalic centre, 

therefore intact doll's eye, suggests a supranuclear lesion

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. 

 etiology

b/l ptosis-

https://www.medicaleducationleeds.com/paces/ptosis/#:~:text=Differential%20Diagnosis%20of%20ptosis%3A,Horner's%20syndrome

1)mysasthenia gravis

2)3rd nerve pasy

3)horner's syndrome

4)myotonic dystrophy

5)kearnes syres(mitochondrial )

6)occuplopharyngeal muscular dystrophy

7)cerebral ptosis(other conditions to be correlated)

The size of pupis being normal:rules out horner's or 3rd cn palsy(as a single nucleus supllies both levator palpebral superioris ,its lesion causing b/l ptosis

mysasthenia-no history of fluctuation/fatigueable ptosis

myotinic dystrophy-no other signs of the disease, especially on sustained contraction of the muscles

the KS syndrome has age of onset before 20

occulo pharngeal-intact bulbar cranial nerves rules this out.

self talking and altered behavior-frontal lobe of the brain.

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

efficacy of drugs

syndopa was initiated to differentiate psp from Parkinson's disease 

https://www.nejm.org/doi/full/10.1056/nejmoa033447

In this 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. The primary outcome was a change in scores on the Unified Parkinson's Disease Rating Scale (UPDRS) between baseline and 42 weeks

The severity of parkinsonism increased more in the placebo group than in all the groups receiving levodopa: the mean difference between the total score on the UPDRS at baseline and at 42 weeks was 7.8 units in the placebo group, 1.9 units in the group receiving levodopa at a dose of 150 mg daily, 1.9 in those receiving 300 mg daily, and –1.4 in those receiving 600 mg daily (P<0.001

Question2

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:

progressive sob from grade 2 to 4 since 2 months

orthopnea,pnd

b/l pedal edema upto knee since 2 months

Generalised weakness since 2 months

H/o cva (rt hemiparesis recovered) with persistent loss of speech since 2 years.

anatomical localisation

based on history:pnd ,sob with orthopnea suggest left heart failure

based on examination:

shift of apex to 6th ics,presence of thrill palpable at apex(?s1), nature of the apex not mentioned

presence of loud p2 ,dilated veins ,pedal edema,s3 in both apical and left parasternal areas.

(?biventricular failure)

Theory based points from Hurst manual of Cardiology

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. 

etiology:

CAD

Ecg showing 

1)normal axis

2)pathological Q waves from v1 to v6

3)poor R wave progression

suggest a CAD probably involving LAD and LCX territory 

confirmed with finding on the echo

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2350191/#:~:text=CAD%20can%20lead%20to%20heart,and%20impaired%20contraction%20in%20systole.

1)heart failure in the setting of CAD occurs due to 

 myocardial infarction (MI) frequently leads to permanent death of cardiac muscle. The infarcted segment is akinetic/dyskinetic, thus leading to inadequate relaxation in diastole and impaired contraction in systole

2)subsequent remodeling of the ventricle can occur in myocardial segments that are remote from the site of infarction. Such regional remodeling frequently results in a distortion of ventricular structure and geometry, and can contribute to a further decline in ventricular function . Ventricular dilatation can promote annular dilation, with consequent mitral regurgitation, which can predispose to heart failure.

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

1)salt and fluid restriction

https://pubmed.ncbi.nlm.nih.gov/23787719/#:~:text=Conclusion%3A%20Individualized%20salt%20and%20fluid,Quality%20of%20life%3B%20Salt%20restriction.

Ninety-seven stable patients in NYHA class II-IV, on optimal medication, with previous signs of fluid retention, treated with either >40 mg (NYHA III-IV) or >80 mg (NYHA II-IV) of furosemide daily were randomized to either individualized salt and fluid restriction or information given by the nurse-led heart failure clinics, e.g. be aware not to drink too much and use salt with caution, and followed for 12 weeks. Fluid was restricted to 1.5 L and salt to 5 g daily, and individualized dietary advice and support was given.

Results After 12 weeks, significantly more patients in the intervention than in the control group improved on the composite endpoint (51% vs. 16%; P < 0.001), mostly owing to improved NYHA class and leg oedema. No negative effects were seen on thirst, appetite, or QoL

2)benfomet as thiamine replacement in alcoholic pts

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4550087/

33)aldactone(spironolactone)

https://www.aafp.org/afp/2001/1015/p1393.html

Based on earlier work suggesting a benefit of therapy,2 the Randomized Aldactone Evaluation Study (RALES) was undertaken to evaluate the role of spironolactone when used in addition to standard therapy for CHF. Standard therapy in this study did not include beta blockers

 S-The investigators prospectively enrolled 1,663 patients with severe (New York Heart Association [NYHA] class IV) CHF (Table 1).4 Most of the enrolled patients were white men averaging 65 years of age. These patients had a left ventricular ejection fraction of 35 percent or less and marked physical limitations related to CHF. Patients were excluded if they had unstable angina or moderate renal failure, and if they were hyperkalemic.

All patients who could tolerate the drug were given an ACE inhibitor and a loop diuretic, and 70 percent were taking digoxin. Only 10 percent were taking beta blockers. Patients were randomly assigned to receive placebo or 25 mg of spironolactone daily in addition to their current regimen. After eight weeks, if the patient showed worsening CHF and had a stable potassium level, the dosage was increased to 50 mg daily. The dosage was decreased to 25 mg every other day if at any time the patient became hyperkalemia4)furosemide 80mg5)telmisartan 40mg

Q.3.52 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 presentation:

sob grade 2 or 3?non progressive since 10 days

cough with sputum since 10 days

decreased sleep since 10 days

decreased appetite since 10 days

after admission:

drowsiness and giddiness

anatomical localisation:

sob without pedal edema, pnd, orthopnea can be localised to the lung

(sob on evxertion grade 2 can also be localised the heart but no history or examination finding of pedal edema or jvp rise rules it out)

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

. 

Answer..

Patient has SOB grade 2 and evaluation he has severe Anemia which lead to heart failure. The treating team have given him iv fluids 100ml/hour which was not mentioned in the blog, giving iv fluids to him is contraindicated and further  deteriorated the patient symptoms worsened the condition of the patient. And giving him Fluids which might be the cause of his hyponatremia is purely because of dilutional.

And the treating team has failed to control his blood sugars which can be controlled in him. 

If I would be the member of the treating team

First I would have given him fluid restriction and preload reducing agents like lasix because he has heart failure and dilated ivc.

Giving him the lasix would be my main concern in him. Second thing is controlling blood sugars.

I would rather not have done HRCT CHEST in this patient which is not at all indicated in him.

Sequence of the events which deteriorated the patient.

He presented with sob grade 2 and decreased sleep and generalised weakness.

On evaluation patient had Anemia which lead to heart failure and type 2 Diabetes mellitus which is poor control. 

Poor control of sugars is shown in fig.

BIMONTHLY EXAM

February 17, 2021

FEBRUARY BIMONTHLY EXAM

Questions:

Q.1) Please go through the patient data in the links below and answer the following questions:

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 

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

Case presentation links: 

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?

problem presentation:

drooping of eyelids since 8 to 9 months refractory to treatment

involuntary movements of bilateral upper limbs

frequent episodes of fatigue since one year

thin stream of urine with bed wetting since one year

according to attenders 

change in behavior (talking to self) since 1.5 years

anatomical localisation of lesion

b/l ptosis-weakness of levator palbebral superioris

(without loss of frowning)

self talk-frontal lobe

vertical gaze palsy:

the centres and pathway for vertical gaze:

vertical gaze palsy is 

supranuclear

nuclear

infranuclear (eg.nmj disorders)

the doll's eye manaever is used to differentiate between supra and below

suggesting the activation of vestibulo -occular system which directly activates the thalamo-mesencephalic centre, 

therefore intact doll's eye, suggests a supranuclear lesion

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. 

 etiology

b/l ptosis-

https://www.medicaleducationleeds.com/paces/ptosis/#:~:text=Differential%20Diagnosis%20of%20ptosis%3A,Horner's%20syndrome

1)mysasthenia gravis

2)3rd nerve pasy

3)horner's syndrome

4)myotonic dystrophy

5)kearnes syres(mitochondrial )

6)occuplopharyngeal muscular dystrophy

7)cerebral ptosis(other conditions to be correlated)

The size of pupis being normal:rules out horner's or 3rd cn palsy(as a single nucleus supllies both levator palpebral superioris ,its lesion causing b/l ptosis

mysasthenia-no history of fluctuation/fatigueable ptosis

myotinic dystrophy-no other signs of the disease, especially on sustained contraction of the muscles

the KS syndrome has age of onset before 20

occulo pharngeal-intact bulbar cranial nerves rules this out.

self talking and altered behavior-frontal lobe of the brain.

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

efficacy of drugs

syndopa was initiated to differentiate psp from Parkinson's disease 

https://www.nejm.org/doi/full/10.1056/nejmoa033447

In this 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. The primary outcome was a change in scores on the Unified Parkinson's Disease Rating Scale (UPDRS) between baseline and 42 weeks

The severity of parkinsonism increased more in the placebo group than in all the groups receiving levodopa: the mean difference between the total score on the UPDRS at baseline and at 42 weeks was 7.8 units in the placebo group, 1.9 units in the group receiving levodopa at a dose of 150 mg daily, 1.9 in those receiving 300 mg daily, and –1.4 in those receiving 600 mg daily (P<0.001

Question2

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:

progressive sob from grade 2 to 4 since 2 months

orthopnea,pnd

b/l pedal edema upto knee since 2 months

Generalised weakness since 2 months

H/o cva (rt hemiparesis recovered) with persistent loss of speech since 2 years.

anatomical localisation

based on history:pnd ,sob with orthopnea suggest left heart failure

based on examination:

shift of apex to 6th ics,presence of thrill palpable at apex(?s1), nature of the apex not mentioned

presence of loud p2 ,dilated veins ,pedal edema,s3 in both apical and left parasternal areas.

(?biventricular failure)

Theory based points from Hurst manual of Cardiology

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. 

etiology:

CAD

Ecg showing 

1)normal axis

2)pathological Q waves from v1 to v6

3)poor R wave progression

suggest a CAD probably involving LAD and LCX territory 

confirmed with finding on the echo

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2350191/#:~:text=CAD%20can%20lead%20to%20heart,and%20impaired%20contraction%20in%20systole.

1)heart failure in the setting of CAD occurs due to 

 myocardial infarction (MI) frequently leads to permanent death of cardiac muscle. The infarcted segment is akinetic/dyskinetic, thus leading to inadequate relaxation in diastole and impaired contraction in systole

2)subsequent remodeling of the ventricle can occur in myocardial segments that are remote from the site of infarction. Such regional remodeling frequently results in a distortion of ventricular structure and geometry, and can contribute to a further decline in ventricular function . Ventricular dilatation can promote annular dilation, with consequent mitral regurgitation, which can predispose to heart failure.

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

1)salt and fluid restriction

https://pubmed.ncbi.nlm.nih.gov/23787719/#:~:text=Conclusion%3A%20Individualized%20salt%20and%20fluid,Quality%20of%20life%3B%20Salt%20restriction.

Ninety-seven stable patients in NYHA class II-IV, on optimal medication, with previous signs of fluid retention, treated with either >40 mg (NYHA III-IV) or >80 mg (NYHA II-IV) of furosemide daily were randomized to either individualized salt and fluid restriction or information given by the nurse-led heart failure clinics, e.g. be aware not to drink too much and use salt with caution, and followed for 12 weeks. Fluid was restricted to 1.5 L and salt to 5 g daily, and individualized dietary advice and support was given.

Results After 12 weeks, significantly more patients in the intervention than in the control group improved on the composite endpoint (51% vs. 16%; P < 0.001), mostly owing to improved NYHA class and leg oedema. No negative effects were seen on thirst, appetite, or QoL

2)benfomet as thiamine replacement in alcoholic pts

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4550087/

33)aldactone(spironolactone)

https://www.aafp.org/afp/2001/1015/p1393.html

Based on earlier work suggesting a benefit of therapy,2 the Randomized Aldactone Evaluation Study (RALES) was undertaken to evaluate the role of spironolactone when used in addition to standard therapy for CHF. Standard therapy in this study did not include beta blockers

 S-The investigators prospectively enrolled 1,663 patients with severe (New York Heart Association [NYHA] class IV) CHF (Table 1).4 Most of the enrolled patients were white men averaging 65 years of age. These patients had a left ventricular ejection fraction of 35 percent or less and marked physical limitations related to CHF. Patients were excluded if they had unstable angina or moderate renal failure, and if they were hyperkalemic.

All patients who could tolerate the drug were given an ACE inhibitor and a loop diuretic, and 70 percent were taking digoxin. Only 10 percent were taking beta blockers. Patients were randomly assigned to receive placebo or 25 mg of spironolactone daily in addition to their current regimen. After eight weeks, if the patient showed worsening CHF and had a stable potassium level, the dosage was increased to 50 mg daily. The dosage was decreased to 25 mg every other day if at any time the patient became hyperkalemia4)furosemide 80mg5)telmisartan 40mg

Q.3.52 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 presentation:

sob grade 2 or 3?non progressive since 10 days

cough with sputum since 10 days

decreased sleep since 10 days

decreased appetite since 10 days

after admission:

drowsiness and giddiness

anatomical localisation:

sob without pedal edema, pnd, orthopnea can be localised to the lung

(sob on evxertion grade 2 can also be localised the heart but no history or examination finding of pedal edema or jvp rise rules it out)

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

. 

Answer..

Patient has SOB grade 2 and evaluation he has severe Anemia which lead to heart failure. The treating team have given him iv fluids 100ml/hour which was not mentioned in the blog, giving iv fluids to him is contraindicated and further  deteriorated the patient symptoms worsened the condition of the patient. And giving him Fluids which might be the cause of his hyponatremia is purely because of dilutional.

And the treating team has failed to control his blood sugars which can be controlled in him. 

If I would be the member of the treating team

First I would have given him fluid restriction and preload reducing agents like lasix because he has heart failure and dilated ivc.

Giving him the lasix would be my main concern in him. Second thing is controlling blood sugars.

I would rather not have done HRCT CHEST in this patient which is not at all indicated in him.

Sequence of the events which deteriorated the patient.

He presented with sob grade 2 and decreased sleep and generalised weakness.

On evaluation patient had Anemia which lead to heart failure and type 2 Diabetes mellitus which is poor control. 

Poor control of sugars is shown in fig.

Anemia with heart'failure 

⬇️

Fluids and poor control of sugars

⬇️

His symptoms worsened, sob increased and landed in hyponatremia

⬇️

Poor control of sugars continued and didn't restricted fluids.

⬇️

Hyponatremia in this case was due to two reasons, iv fluids and poor sugar Control.

⬇️

Patient developed symptoms of hyponatremia like disturbed sleep pattern, drowsy and mild altered sensorium.

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?  

Answer.

There is no role in giving him monocef and metrogyl to him. Their diagnosis is not explaining the treatment.

Efficacy of vaptans over placebo

https://acsjournals.onlinelibrary.wiley.com/doi/full/10.1002/cncr.28468

Can one give both 3% sodium as well as vaptan to the same patient?  

We shouldn't give both at the same time.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5752787/

Question 4.

1. LEARNT HOW TO DO ASCITIC TAP UNDER GUIDANCE OF OUR PGS.

2. LEARNT HOW TO DO PLEURAL TAP UNDER GUIDANCE OF OUR PGS.

3. ASSISTED IN CENTRAL LINE.

4. LEARNT MANAGEMENT AND  FLUID RESUSCITATION IN DKA PATIENT.