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
a). What is the problem representation of this patient and what is the anatomical localization for his current problem based on the clinical findings?
ANS)Problem Representation:-
He had a sudden onset of generalised tonic clinic seizure-10yr
he is a diabetic - 2yr
drooping of his eyelids and sudden change in his behaviour.-1.5yr
walking into things and he would often fall-1.5yr
started avoiding people and started being on his own. -1.5yr
Non productive cough-8mon
continued to feel fatigued-6mon
Anatomical localization :-
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
B/l ptosis
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)
As pt is having frequent fall h/o,vertical gaze palsy,emotional liability, mild dementia,resting tremors could be either:
PROGRESSIVE SUPRANUCLEAR PALSY
PARKINSONISM DISORDER
both could be differentiated as downwardgaze palsy ABSENT in parkinsonism and it responds well to levodopa.
DEMENTIA can be ruled out by assessing the higher mental status, cortical lobe functions assessment
As pt mmse score 30 dementia (mc type alzhimers disease) could be less likely.
C)What is the efficacy of each of the drugs listed in his current treatment plan
fficacy 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)
QUESTION-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
a). What is the problem representation of this patient and what is the anatomical localization for his current problem based on the clinical findings?
ANS)
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
pt could be having HEARTFAILURE SEC TO CORONARY HEART DISEASE. and mc cause is lt heart failure leading to rt heart failure.
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:-
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/
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 hyperkalemic
4)furosemide 80mg
5)telmisartan 40mg
QUESTION-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
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:
ANS)
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
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
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?
Efficacy of vaptans over placebo:-
Objective
Tolvaptan, an oral antagonist of the vasopressin V2 receptor, has been found to improve hyponatremia in patients with mixed etiologies. This study analyzed a subgroup of patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) to evaluate the efficacy and safety of tolvaptan in this group.
Design and patients
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).
Results
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.
Conclusions
Results for the SIADH subgroup were analogous to those of the combined SALT population regarding efficacy and safety but demonstrated a greater improvement in the physical component of the SF-12 Health Survey than in the full mixed etiology SALT patient group.
Can 3%nacl be given in SIADH?
Osmolality of 3% nacl is greater than urine osmolalityin severe siadh. so when 1000ml of 3%nacl is given,all the nacl will be excreted but in larger vol of 1700ml of urine. so net end result is loss of 700 ml of the abnormally retained water leading to correction of dilutional hyponatremia. 3%nacl is infused slowly ,preferably with inj loop diuretic to avoid vol overload and LVF.
Simultaneous water restriction corrects hyponatremia.
QUESTION-4
4) Please mention your individual learning experiences from this month.
ANS)
Learned about managing a Type-1 DM case in young female, how to fix the dose
Reviwed Literature and searched case reports about causes of sudden hypotension and cardiac arrest in chronic liver disease with tense abdomen(one of our case collapsed in front of us while we are trying to check his weight, made him to get up from supine to standing position)
Saw a case of acute infarct in right pons and superior cerebellar peduncle,Reviwed literature that there in poor prognosis associated with infarct/hemorrhage occurring In pons
Examined 27/m with acute pancreatitis with possible VSD,Reviewed literature on systolic murmurs
Reviewd literature on HIV in anaemia.
Discussed with faculty about mortality meet presentation.
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