Bi monthly exam Feb 16
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
Case presentation links:
https://youtu.be/kMrD662wRIQa). 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
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.'
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
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/
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 hyperkalemia4)furosemide 80mg5)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:
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
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.
No respiratory examination has been mentioned in the elog.
However his problems list are:
- Hyponatremia
-Lower respiratory tract infection
-Uncontrolled blood sugars
-Dimorphic Anemia
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/
4) Please mention your individual learning experiences from this month.
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
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
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