BIMONTHLY ASSESSMENT FOR FEBRUARY
BIMONTHLY ASSESSMENT FOR 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, links to which have been mentioned.The points copy pasted have been put in quotes.
The questions to the cases being discussed are from the link below:
https://medicinedepartment.blogspot.com/2021/02/medicine-paper-for-february-2021.html?m=0
1.) 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?
Change in behaviour and talking to self from 1.5 yrs.
Involuntary movements of bilateral upper limbs from 1 year.
Multiple episodes of fatigue from 1 year.
She has a thin stream of urine with bed wetting from 1 year.
Drooping of eyelids from 8-9 months, refractory to treatment.
-Anatomical location of lesion:
Sef talk- frontal lobe.
Vertical gaze palsy- centres and pathway- supranuclear, nuclear, infranuclear.
Doll’a eye manoeuver is used to differentiate between supra and below suggesting the activation of vestibulo occular system which directly activates the thalamo mesencephalic centre. Intact doll’s eye- supranuclear lesion.
Bilateral ptosis- weakness of levator palpebral superioris.
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.
Bilateral Ptosis:
Myasthenia gravis
Horner’s syndrome
3rd nerve palsy
Myotonic dystrophy
Cerebral ptosis
Occulopharyngeal muscular dystrophy
The size of the pupil is normal so we can rule out horner’s syndrome and 3 rd nerve palsy.
No history of fluctuations/ fatiguable ptosis- rule out myasthenia
No other signs of myotonic dystrophy.
Intact bulbar cranial nerves rules out occulopharyngeal muscular dystrophy.
Self talking and altered behaviour- frontal lobe of the brain.
c) What is the efficacy of each of the drugs listed in his current treatment plan
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)
2) 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:Progressive SOB grade 2-4 from 2 months.Orthopnea and PND from 2 monthsBilateral pedal edema upto knee from 2 months.Generalised weakness from 2 months.H/o cva (right hemiparesis recovered) with persistent loss of speech from 2 years.
Anatomical location:
PND ,SOB with orthopnea suggest left heart failure
Based on examination:
Shift of apex to 6th ICS,presence of thrill palpable at apex,
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 for thiamine replacement in alcoholic pts
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4550087/
3)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 hyperkalemia.
4)furosemide 80mg
5)telmisartan 40mg
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 REPRESENTATION:
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 exertion 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.
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 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
I would have given him fluid restriction and preload reducing agents like lasix because he has heart failure and dilated ivc.
Giving him 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.
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?
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/
4) Please mention your individual learning experiences from this month.
-Learnt how to log cases online.
-A case of ankylosing spondylitis with bilateral sensory motor axonal neuropathy of upper limbs
Did modified schobers test
Presented this case in 2-4 session
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?
Change in behaviour and talking to self from 1.5 yrs.
Involuntary movements of bilateral upper limbs from 1 year.
Multiple episodes of fatigue from 1 year.
She has a thin stream of urine with bed wetting from 1 year.
Drooping of eyelids from 8-9 months, refractory to treatment.
-Anatomical location of lesion:
Sef talk- frontal lobe.
Vertical gaze palsy- centres and pathway- supranuclear, nuclear, infranuclear.
Doll’a eye manoeuver is used to differentiate between supra and below suggesting the activation of vestibulo occular system which directly activates the thalamo mesencephalic centre. Intact doll’s eye- supranuclear lesion.
Bilateral ptosis- weakness of levator palpebral superioris.
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.
Bilateral Ptosis:
Myasthenia gravis
Horner’s syndrome
3rd nerve palsy
Myotonic dystrophy
Cerebral ptosis
Occulopharyngeal muscular dystrophy
The size of the pupil is normal so we can rule out horner’s syndrome and 3 rd nerve palsy.
No history of fluctuations/ fatiguable ptosis- rule out myasthenia
No other signs of myotonic dystrophy.
Intact bulbar cranial nerves rules out occulopharyngeal muscular dystrophy.
Self talking and altered behaviour- frontal lobe of the brain.
c) What is the efficacy of each of the drugs listed in his current treatment plan
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)
2) Patient was apparently asymptomatic 2 years back then he developed weakness in the right upper and lower limb, loss of speech.
a). What is the problem representation of this patient and what is the anatomical localization for his current problem based on the clinical findings?
Anatomical location:
PND ,SOB with orthopnea suggest left heart failure
Based on examination:
Shift of apex to 6th ICS,presence of thrill palpable at apex,
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.
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.
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 for thiamine replacement in alcoholic pts
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4550087/
3)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 hyperkalemia.
4)furosemide 80mg
5)telmisartan 40mg
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:
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 exertion grade 2 can also be localised the heart but no history or examination finding of pedal edema or JVP rise rules it out)
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 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
I would have given him fluid restriction and preload reducing agents like lasix because he has heart failure and dilated ivc.
Giving him 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.
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.
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/
4) Please mention your individual learning experiences from this month.
-Learnt how to log cases online.
-A case of ankylosing spondylitis with bilateral sensory motor axonal neuropathy of upper limbs
Did modified schobers test
Presented this case in 2-4 session
- A case of right lower lobe pneumonia.
-A case of dengue with thrombocytopenia.
Learnt about when to start platelet transfusion in thrombocytopenia.
-A case of liver cirrhosis with thrombocytopenia
Abdominal distension with everted umbilicus in cirrhotic patient
- A case of CVA with left hemiplegia with left LMN type facial palsy.
- Learnt how to different LMN from UMN lesions.
- Learnt how to differentiate types of haemorrhages in a brain CT. Read about the blood supply of brain.
-A case of dilated cardiomyopathy with HFrEF.
-learnt how to interpret ecg
-A case of iron deficiency anemia.
-learnt how to calculate the dose of iron to be given
-A case of right sided pleural effusion secondary to TB.
Asssisted in performing a pleural tap for this patient.
-A case of acute on chronic pancreatitis
Learnt RASON and BISAP scoring.
Learnt about when to start platelet transfusion in thrombocytopenia.
-A case of liver cirrhosis with thrombocytopenia
Abdominal distension with everted umbilicus in cirrhotic patient
- A case of CVA with left hemiplegia with left LMN type facial palsy.
- Learnt how to different LMN from UMN lesions.
- Learnt how to differentiate types of haemorrhages in a brain CT. Read about the blood supply of brain.
-A case of dilated cardiomyopathy with HFrEF.
-learnt how to interpret ecg
-A case of iron deficiency anemia.
-learnt how to calculate the dose of iron to be given
-A case of right sided pleural effusion secondary to TB.
Asssisted in performing a pleural tap for this patient.
-A case of acute on chronic pancreatitis
Learnt RASON and BISAP scoring.
