BIMONTHLY December
QUESTION NO 1)
1) pt presented vth unable to move his rt upperlimb followed by recurrent episodes of rt sided focal seziures. risk factors in him are alcoholic, smoker, diabetic,on presentation BP was high(170/100mmhg).
According to h/o pt might be having cerebrovascular event follwed by focal seziures.
Anatomical location could be ?frontal lobe involvement ( imp for cognitive functions and control of voluntary movements), ? parietal lobe (it processes information about movement)
could be? anterior circulation stroke.
2) sub cortical infract -
occur in the supplying area of a single, deep perforating brain artery and are mostly felt to be a consequence of cerebral small-vessel disease (CSVD).
Cortical brain infarcts - infarcts involving cortical gray matter, but may differ considerably in size. ... Small cortical infarcts were mainly localized in external watershed areas, whereas large cortical infarcts were localized primarily in large arterial territories.
3) Cerebrovascular diseases, including stroke, are viewed as the most common cause of epilepsy in the elderly population, accounting for 30%-50% of the newly diagnosed cases of epilepsy cases in this age group.
PATHOPHYSIOLOGY:
Neurotransmitter amino acids play an important role in the pathogenesis and development of epilepsy [. Increased concentration of the excitatory neurotransmitter glutamate (Glu), the disturbance of electrolyte balance, the destruction of phospholipid membranes, and the secretion of free fatty acids have been documented in the penumbral areas in the acute post-ischemic stroke phas
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC577138
4) in some of the ecg shows sinus tachycardia vth vpc's vth leftaxis deviation.i think pt doesn't need anticoagulatio
5) In elderly pts complex partial seziures vthout sec generalization are more commo
Antiepileptic drugs (AEDs) with fewer adverse effects, including cognitive effects, and AEDs without significant pharmacokinetic drug interactions are need
as LEVIPILL has high efficacy,no drug interactions.no cognitive effects,broad spectrum it is useful.pt is having recurrent episodes of focal seziures levipill dose was inc. but dose adjustment has to be made according to renal clearence.pt is still having seziure episode tab carbamazepine was useful high efficacy
as pt gfr was reduced levipill dose has to be tappered and pt to be kept on tab carbamazepin
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6706648
QUESTION 2
1)55yrs old man presented vtha) hypoglycemic episodes ? sec to drug induced b)hypoalbunemia ?sec to renal failure (spot protein/creat ratio 3.19) 24hrs urine protein not available? ad diabetic nephropathy is leading cause for renal failure.
c)anemia(hb 9.7)
2) in this pt could be due to? drug induced.
Glimepiride is metabolized by the liver to two major metabolites each of which has hypoglycemic activity. In renal disease these metabolites summed. Although the half-life is 5-7 h, the drug can cause severe hypoglycemia that lasts more than 24hrs. along vth insulin clearence is reduced.
QUESTION NO4)
1) 60 yrs woman who is k/c/o htn and diabetic presented vth complaints of chestpain acute onset, location?, radiating, pricking type vth no h/o fever cough cold sob palpitations sweatings. could be due to? lung pathology,? cardiac prob.
as the xray shows rt upper lobe consolidationit could be due to pulmonary prob.(? rt upper lobe pneumonia)
pt is having uncontrolled sugars diabetis can cause gastroparesis which can affect the normal spontaneous movement of the stomach muscles could be the reason for her constipatio
pt having ?acute renal injur
2) causes of uncontolled sugars:
not using diabetic medications
not following diabetic eating plan
being inactive
using certain medications ( ex-steroids )
infections(pneumonia,uti,sepsis,gastroenteritis
in this patient could be due to infection (?pneumonia
3) chest xray findings : PA view vth slightly rotated film towards ryt vth rt upper lobe consolidation vth rt mild pleural effusio
5th question
QUESTION NO5)
1) according to history anatomical localisation was liver involvement as pt was diagnosed to have
HEP B since 2yrs. and he is k/c/o alcoholic due to which pt has chronic liver failure leading
to ascites,portal htn, jaundice, hypoalbunemia, gi bleeds,
pt has renal failure could be due to hepb virus infection.
These viral components will typically get attacked by your antibodies in an attempt to fight the infection. Once this happens, the antibodies will bind with the virus, and the resultant debris will get deposited in the kidney. It can then set off an inflammatory reaction, which could cause kidney damage.
it could cause either PAN/MPGN/HEPATORENAL SYNDROME
In this pt could be? hepatorenal syndrome( cue not vaialable? to rule out glomerular injury causing albuminuria,hematuria)
https://www.verywellhealth.com/can-hepatitis-b-cause-kidney-disease-4107525
4) Some people who are receiving dialysis treatment have virus infection such as hepatitis B, hepatitis C and/or HIV that is present in their blood. These infections can be transmitted to other patients if blood is contaminated by the blood of another with a viral infection. Haemodialysis is performed by passing blood from a patient through a dialysis machine, and multiple patients receive dialysis within a dialysis unit. Therefore, there is a risk that these viruses may be transmitted around the dialysis session.
5) There is evidence to support the use of octreotide in variceal and non-variceal upper GI bleeding (UGB). As a somatostatin analogue, octreotide binds with endothelial cell somatostatin receptors, inducing strong, rapid and prolonged vaso-constriction [1]. Octreotide reduces portal and variceal pressures as well as splanchnic and portal-systemic collateral blood flows [2]. It also prevents postprandial splanchnic hyperemia in patients with portal hypertension [3] and lowers gastric mucosal blood flow in normal and portal hypertensive stomachs [4]. Octreotide inhibits both acid and pepsin secretion. As a result, it prevents the dissolution of freshly formed clots at the site of bleeding [5].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1750992/
QUESTION NO6)
1) As pt having h/o unable to do his weaving work properly sin 1yr ,forgetfullness of things, unintentionally picking of objects,urinary incontinence, suggests of temporal and parietal lobe involvement.
pt having slurring of speech,difficulty in swallowing could be due to cranial nerve involvement
as dementia progress(sev type)
2) evaluation :
https://www.aafp.org/afp/2018/0315/p398.html#afp20180315p398-t3
3)Vascular dementia symptoms vary, depending on the part of your brain where blood flow is impaired. Symptoms often overlap with those of other types of dementia, especially Alzheimer's disease dementia.
4) In this pt cause could be ALZHEIMERS DISEASE pathogenesis is
The first defined histopathologic features of AD were extracellular amyloid plaques and intracellular neurofibrillary tangles. More recently recognized histopathologic features include synaptic degeneration, hippocampal neuronal loss, and aneuploidy.
5) treatment modalities:
Donepezil is used to treat confusion (dementia) related to Alzheimer's disease. It does not cure Alzheimer's disease, but it may improve memory, awareness, and the ability to function. This medication is an enzyme blocker that works by restoring the balance of natural substances (neurotransmitters) in the brain.
On average, most studies with AChEIs reported by the pharmaceutical industry showed a cognitive enhancement of 2–3 points (vs placebo) in the ADAS-Cog score in clinical trials of 12–30 weeks’ duration, with improvement in 12%–58% of patients, 5%–73% of drop-outs, and side-effects in 2%–58% of cases . As compared with other AChEIs, donepezil exhibits the best pharmacological profile in terms of cognitive improvement (2.8–4.6 vs 0.7–1 points of difference with placebo in the ADAS-Cog scale), responders rate (40%–58%), drop-out cases (5%–13%), and side-effects (6%–13%
)https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2654795/
QUESTION NO7)
1) 22yrs old male presented vth c/o intermittent tonic type of seziure since 2months , along vth h/o fever low grade on and off, weight loss,dec appetite.
On/e: pt having lft supraclavicular lymphadenopathy, vth lft axillary lymphadenopathy vth dec breathsounds on lt side
Mri shows- ring enhancing lesions in lt cerebellum region
Could be the possibility of ? TUBERCULOMA
Primaryfocus from lung has to be confirmed vth sputum studies report..
Hiv status of the pt??
It results from the hematogenous dissemination of Mycobacterium tuberculosis from disease elsewhere in the body and the formation of small subpial and subependymal foci in the brain and spinal cord. In some individuals, these foci rupture and release bacteria into the subarachnoid space, causing meningitis.
Magnetic resonance spectroscopy of normal brain shows predominant peaks of N-acetylaspartate (NAA), choline, creatinine and myo-inositol with the highest peak being NAA. NAA is a healthy neuronal marker, choline represents energy store and choline is a marker of cellular turnover
Magnetic resonance spectroscopy is of great value in the diagnosis of tuberculoma in cases of ring-enhancing lesions on CT scan or MRI imaging. It demonstrates a very high lipid peak, reduction in NAA and creatinine and a choline/creatinine ratio of >1 Lipid peak in MRS in the context of a ring-enhancing lesion is very much specific for tuberculoma and has not been seen in any cases of NCC, the other common differential diagnosis of a ring-enhancing lesion. NCC demonstrates a high lactate and proteins like alanine, succinate, glutamate, glycine levels with some reduction of NAA and creatinine A high choline peak is seen in MRS in case of tumors, primary or secondary, because of very high cellular turnover. MRS can also differentiate tuberculoma or tuberculous brain abscess from pyogenic brain abscess by the presence of elevated levels of amino acid peaks in pyogenic brain abscess.
QUESTION NO8)
Dec 1st - read about the bronchestiasis and ARDS topic.
Dec 2nd- read about aplastic anemia and primary myleofibrosis.
Dec 3rd- attended neurology posting and saw a case of chronic AIDP who is in recovery phase.
Dec4th- duty day. And admitted cases
Dec 5th- read about resistant HTN and its treatment vthdoses and efficacy of antihtn drugs.
Dec 6th- There is a 60yrs old male case of DCMPsec to CAD vth hfref(ef -20%) vth diabetic neuropathy, who is k/c/0 htn, diabetic,denovo hypothyroidism. Read about the lasik dosages in heart failure,tripletherapy in decompensated heart failure..
Dec 7th- read about the approach in treatment of GTCS type,focal type seizures and status epilepticus .
Dec 8th- read about the approach to hypoalbunemia and its causes. Read about the iron def anemia.
Dec 9th- 25yrs old male presented vth weakness of b/l lower limbs , difficulty In getting up from squatting position,difficulty in climbing upstairs ass vth tingling sensation of b/l lower limbs who is a daily labourer and occasional toddy drinker examined the cns system Pt is having peripheral neuropathy(motor and sensory involvement).
Dec 10th - attended neurology posting.. discussed about the 55yrs old male case of dementia sec to Alzheimer’s disease.
Saw a case 30yrs old male presented vth tingling and numbness of b/l hand extrrmities started at lt middle finger ass vth loss of pain sensation on examination pt is having thickened ulnar nerve and radial nerve,popliteal nerve vth hypopigmented patch over lt handregion.got nerve studies of upper limbs outside shows significant sensory poly neuropathy diagnosis of HANSONS DISEASE send for skin biposy of lesions. And pt also has ptyriasis versicolor over chest andback of chest region.
Dec11th - duty day. Saw a 55yrs old female presented vth c/o giddiness followed by weakness of lt ul and LL vth chestpain and sweatings and she is k/c/o htn sin 1mnth but not using medication outside got bp checkwhich was 190/100mmhg took tab dipine 10mg and aten 50mg outside before coming here. On presentation pt is conscious, coherent vth bp- 130/100mmhg pr-64bpm, on /e pt having rt side deviation of mouth vth slurred speech reflexes exaggerated on lf side and ecg shows st depressions vth t wave inversions in v2-v4 and 2d echo shows ivc hypokinesia vth ef52% and dilated ivc, vth diastolic dysfunction.
Diag - acute cva lt sided hemiparesis? sec to cardioembolic stroke..
Mri/ct didn’t get it done bec pt attenders have affordability issues and went on lama.
Dec 12th - read about the pathophysiology of heart failure and types of cardiorenal syndromes and its mechanisms.
Dec13th- saw a case of 67 yrs old female presented vth involuntary movements of rt forearm and lf index finger ( PARKINSONISM DISEASE) read about pathophysiology of parkinsonism and mri findings of Parkinsonism.
Dec 14th - took the history of ckd case 65 yrs old female k/c/o htn sin 3yrs and diagnosed to be having renal failure 1yr back and on dialysis and having dcmp heart failure? Reno cardiac type.
Attended 2-4 discussion and learned about aortic stenosis.
Dec 15th- read about type of dementia and how to differentiate from each type.
Dec16th - attended rounds and 2-4 discussion disscused difference btwndry and wet gangrene, tretmentof heart failure
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