February assignment

 Question 1)

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.

frequent falls-

following table is from bradley tb of neurology

following clinical examination

cereballar lesions can be ruled out

nmj disorders- no history of fluctuation,pain,tone and power normal on examination

the differential of basal ganglia disorders can be derived 

and loss of vertical gaze can lead us to suspect progressive supranuclear palsy

(confirmed with imaging)

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 hyperkalemic

4)furosemide 80mg

5)telmisartan 40mg

Question 3

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)

cough with sputum

talley's book of clinical examination pg 130

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-1)uti can be due to uncontrolled dm2

2)drowsiness and giddiness 3 days post admission

With hyponatremia as probable cause

.with uncontrolled diabetes, hyperglycemia can be a cause of pseudohyponatremia

.after hospitalisation, hospital acquired pneumonia is main cause for euvolumic hyponatremia mainly SIADH

To diagnose SIADH

The patient's serum osmolality and serum hyponatremia should be low

And urine sodium should be high

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183532/#!po=20.7317

Hyponatremia in SIADH is a result of excess water and is not primarily due to serum sodium deficiency. It is the combination of water retention together with secondary solute loss, which results in reduction in serum sodium

Causes for SIADH:

Going by the history: infections primarily pulmonary can be the cause.

Management

The mainstay of treatment would be fluid restriction

And diuretics

And replacement of excess sodium in urine via hypertonic saline.

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?  

tolvaptan vs placebo

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3573862/

Hyponatremic patients in the SALT-1 and SALT-2 studies with a diagnosis of SIADH were identified based on clinical diagnosis by individual study investigators. Subjects were randomized to receive oral placebo (n=52) or tolvaptan 15 mg daily, with further titration to 30 and 60 mg daily, if necessary, based on the response of serum [Na+] (n=58).

In patients with SIADH, improvement in serum [Na+] was significantly greater (P<0.0001) with tolvaptan than placebo over the first 4 days of therapy as well as the entire 30-day study, with minimal side effects of increased thirst, dry mouth, and urination. Only 5.9% of tolvaptan-treated patients had overly rapid correction of hyponatremia as defined by current guidelines. After discontinuation of tolvaptan, serum [Na+] declined to values similar to placebo. A significant positive treatment effect favoring tolvaptan on the physical component, and a near-significant trend on the mental component, was found using the SF-12 Health Survey. Tolvaptan was associated with a significantly reduced incidence of fluid restriction.

https://www.sciencedirect.com/science/article/pii/S0085253815557803

This review focuses on why hyponatremia should be treated and the role of these antagonists in the treatment. Upon analysis of the available literature, we conclude that there is presently no role for vaptans in acute symptomatic hyponatremia. Although numerous therapeutic approaches are available for chronic symptomatic hyponatremia, vasopressin antagonists provide a simpler treatment option. Vaptans are efficacious in raising serum sodium in long-standing ‘asymptomatic’

3%NACL and tolvaptan

https://link.springer.com/article/10.1007/s00228-020-02848-6

From a total of 77 patients included in the analysis, 24 (31.2%) showed sodium overcorrection (> 10 mmol/L/24 h); 2 (2.6%) in heart failure cohort, 17 (22.1%) in SIADH cohort, and 5 (6.5%) in unknown cause cohort. More than half of patients (51.9%) were administered hypertonic saline prior to tolvaptan. Hypertension, cancer, diuretics, baseline serum sodium, and SIADH were associated with the risk of overcorrection in the univariable analysis.

from the above data,vaptans shouldnt be used in acute hyponatremia and prior administration of 3%NACL leads to over correction with the use of vaptan.

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

Feb1st-Reoccurance of DKA , learnt that one of the probable cause could be

Dawn's phenomenon-insufficient long acting insulin in the night.

Feb2nd-duty day

Managed case with pinpoint pupils and hyperthermia, with acute infacrt in the pons

(Always thought only pontine haemorrhage causes it, reviews literature on that)

Feb 3rd- difficult intubation of our 55/m with acute exaerbation of copd

Learnt procedural pitfalls in intubation

Feb 4th- Reviewed literature on differentiating between reoccurance of acute pancreatitis and necrotizing pancreatitis,learnt from discussion with surgery colleagues about it's further management

Feb5th-examined 27/m with acute pancreatitis with possible VSD, discussed about it with seniors about the differentiating factors between ASD and VSD

Reviewed literature on systolic murmurs

Feb6th-reviewed literature on spontaneous bacterial peritonitis and cops regarding our case

Feb 7th- taught juniors about insulin management,

Feb 8th-

Feb9th-duty day, management of admitted cases and referrals

Feb 10th-reviewd literature on HIV in anaemia and taught ascitic tap to UG students

Feb 11th-management of hypothyroidism in elderly, reviewed literature on when to treat, discussed with faculty around the same

Feb 12th- collected data for mortality meet ,and hyponatremia presentation

Moderated afternoon session

Feb 13th-exam paper 

Feb 14th-exam paper

Feb 15th- discussed with faculty about mortality meet presentation,reviews literature around it