Bimonthly assignment of Medicine for may2021
This is the blog made to answer the various questions raised from different cases in KAMINENI INSTITUTE OF MEDICAL SCIENCES
1)PULMONOLOGY
A)Patient
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
3) What could be the causes for her current acute exacerbation?
4. Could the ATT have affected her symptoms? If so how?
5.What could be the causes for her electrolyte imbalance?
1st ANSWER
With the evidence of exposure to dust from paddy field and other pollen material over the years besides winter season,SOB could have been triggered and progression of airway damage over the years evident with increasing severity over the years.
ANATOMICAL localisation: lower Airways ( ct findings)
PRIMARY ETIOLOGY: chronic exposure to lung irritants.(paddy dust).
2nd ANSWER
Efficacy of every other intervention is far better than placebo because placebo is something which is of zero efficiency.
Intervention-MOA-indication.
.head end elevation-positional elevation eases sob and mucous buildup-COPD
.chest physiotherapy-loosen mucus and clear airway- bronchiectasis
.BiPaP-augumented lung expansion- hypoventilation
.Augmentin.inj-reduce lung bacterial load-acute exacerbation in bronchiectasis
. Azithromycin- reduce lung bacterial load- acute exacerbation in bronchiectasis
.lasix- (furosemide)Na , cl absorption blockage in kidneys-fluid buildup and edema.
. hydrocortisone-anti inflammatory-any inflamation
.Nebulization with ipravent budecort- facilities breathing-COPD
.pulmoclear-reduces congestion in airways- COPD
. insulin- recudes blood glucose levels- diabetes mellitus.
3rd ANSWER
1)The possible causes of her acute exacerbation can be due to the following:
2)Exposure to allergens which could make it a possible occupational hazard
3)Infections by Moraxella, H. influenzae or Pneumococcus (Bacterial), Influenza, Rhinovirus, Coronavirus (Viral)
3)Dust or pesticides exposure
4th ANSWER
It could be bcz of kidney injury caused by ATT.
5th ANSWER
Due to loss of electrolyte.
NEUROLOGY
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
4) What is the reason for giving thiamine in this patient?
5) What is the probable reason for kidney injury in this patient?
6). What is the probable cause for the normocytic anemia?
7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
1st ANSWER
The patient is a chronic alcoholic, he drinks about 3-4quarters/day.he had developed seizures following the cessation of alcohol for 24hours it is due to the following reason:-alcohol affects the way in which nerve cells communicate. receptors are specialized proteins on the surface of nerve cells that receive chemical signals from one another. With long-term alcohol consumption, receptors affected by alcohol undergo adaptive changes in an attempt to maintain normal function.
Two important brain communication systems affected by alcohol involve the neurotransmitters:gamma-aminobutyric acid and glutamate.
ANATOMICAL localisation: Brain.
Primary etiology: thiamine deficiency.
2nd ANSWER
1)Thiamine helps the body cells change carbohydrates into energy. It has been used as a supplement to cope with thiamine deficiency
2)Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system.it enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell
3)pregabalin subtly reduces the synaptic release of several neurotransmitters, apparently by binding to alpha2-delta subunits, and possibly accounting for its actions invivo to reduce neuronal excitability and seizures.
4)Lactulose is used in preventing and treating clinical portal-systemic encephalopathy.its chief mechanism of action is by decreasing the intestinal production and absorption of ammonia.
5)Potchlor liquid is used to treat low levels of potassium in the body.
3rd ANSWER
It is possible that the patient developed higher dependence with time when compared his previous attempts to cease alcohol consumption.
4th ANSWER
As the patient is a chronic alcoholic, there is a possibility that he has developed Thiamine deficiency. If the thiamine deficiency is left untreated, these complications can result in irreversible damage to several parts of the CNS and develop Wernike’s Encephalopathy. Hence in order to prevent any irreversible damage, thiamine has been administered.
5th ANSWER
Elevated levels of urea and creatinine are suggestive of Prerenal Azotemia being the most likely cause of kidney injury in this patient. This can be a result of decreased blood flow to the kidneys possibly due to dehydration secondary to Alcoholism.
6th ANSWER
Alcohol causes iron deficiency or iron overload due its affect on production of new blood cells organs i.e,bonemarrow and the metabolism of iron.alocohol causes a affect on progenitor cells of blood causing decreased WBC .RBC.alochol decreases iron absorption
7th ANSWER
As the patient is diabetic the chance of ulcer formation increases .in a patient of chronic alcoholic theimmune system is weak due to the affect on blood cells formation and iron absorption.due to this healing of an ulcer dampens.
B) patient
Questions raised:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
3) Did the patients history of denovo HTN contribute to his current condition?
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
1st ANSWER
Timeline of the patient is as follows 7 days back- Patient gave a history of giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting 4 days back- Patient consumed alcohol; He developed giddiness that was sudden onset, continuous and gradually progressive. It increased on standing and while walking.
H/O postural instability-falls while walking Associated with bilateral hearing loss, aural fullness, presence of tinnitus
Associated vomiting-2-3 episodes per day, non projectile, non bilious without food particles
Present day of admission-Slurring of speech, deviation of mouth that got resolved the same day
Anatomical location- There is a presence of an infarct in the inferior cerebellar hemisphereof the brain.
Etiology- Ataxia is the lack of muscle control or co-ordination of voluntary movements, such as walking or picking up objects. This is usually a result of damage to the cerebellum.
2nd ANSWER
Ondansetron:
MOA: Blocks 5-HT action on Vagal afferents in GIT
Indication: Patient had non-projectile vomiting
Aspirin:
MOA: Aspirin exerts direct neuroprotective effects according to recent studies
Indication: Patient has Cerebellar infarction
Atorvastatin:
MOA: Reduces cholesterol synthesis by inhibiting HMG-CoA reductase
Indication: The cerebellar infarct could be a cause if ischemic stroke due to Atherosclerosis
Clopidogrel
MOA: Inhibits P2Y-12 receptors on platelets in-turn inhibiting their aggregation
Indication: Patient has a possible Ischemic Stroke
3rdANSWER
Yes, Hypertension is the most likely cause of this patient’s cerebellar infarct.
Uncontrolled Hypertension leads to endothelial dysfunction and injury. This in-turn could have caused a stroke leading to Infarction.
4th ANSWER
Hemorrhagic Stroke
Chronic Alcoholism leads to liver damage which is the source of blood clotting factors that include fibrinogen and factors II, V, VII, IX, X, XI, and XII. Scarcity of these factors makes the brain more susceptible to bleeding and can be a contributing factor to a Hemorrhagic Stroke.
C) patient
1st ANSWER
Electrolyte imbalance (hypokalemia) causing the her manifestations like palpitations, chest heaviness, generalised body weak ness
*radiating pain along her left upper limb due to cervical spondylosis
ANATOMICAL LOCALISATION: blood,kidney
Primary etiology: electrolyte imbalance.
2nd ANSWER
Diuretics usage, Other risk factors :-
1) Abnormal loses:
Medications-diuretics, laxatives, enema, corticosteriods
Real causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis, hypomagnesenemia
2) trance cellular shift : alkalosis, thyrotoxicosis, delirium tremans, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis
3) Inadequate intake: anorexia, dementia, stareation, total parental nutrition
4) psuedohypokalemia:delayed sample analysis, significant leukocytosis.
3rd ANSWER
Changes seen in ECG :
Earliest change :decreased T-wave amplitude, ST depression, Twave - and inversion or flat;prolonged PR interval;presence of Uwaves
In Severe cases :ventricular fibrillation, rarely AV block
Symptoms of hypokalemia :
Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium.
D) patient
Questions:
1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
2. In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?
1st ANSWER
If a patient has history of occurrences of stroke then he/she pose an increased risk of as there is injury to the brain which can lead to formation of scar tissue that might disrupt the electrical impulses, hence inducing a seizure.
A patient is more likely to develop a seizure after an episode of Hemorrhagic type of stroke and only 5% are likely to develop it within a few weeks of the stroke episode.
2nd ANSWER
Simple Partial Seizures with Secondary generalisation:
The patient's seizures were secondary to trauma
Initial episodes of seizures had unilateral clonal jerking and patient retained consciousness. This is evident of a Simple Partial Seizure
Recent episode had loss of consciousness. This indicates there the simple partial seizure had evolved into a Generalized Tonic-Clonic Seizure
E)patient
1st ANSWER
cerebral hemorrhage into the frontal lobe, due to unattended head injury one year ago could have caused it.
2nd ANSWER
alcohol abuse can make blood vessels non healable and also have narrowing effect which is the main reason for non healing haemorrhage which from frontal now extended into parietal and temporal lobes.
F) patient
Questions:
1.Does the patient's history of road traffic accident have any role in his present condition?
2.What are warning signs of CVA?
3.What is the drug rationale in CVA?
4. Does alcohol has any role in his attack?
5.Does his lipid profile has any role for his attack??
1st ANSWER
The closeness of facial bones to the cranium would suggest that there are chances of cranial injuries. Since the Zygomatic arch and Mandibular process is very close to the cranium, this might play a role in the patient's present condition
2nd ANSWER
Weakness or numbness of the face, arm or leg, usually on one side of the body
Trouble speaking or understanding Problems with vision, such as dimness orloss of vision in one or both eyes Dizziness or problems with balance or coordination
Problems with movement or walking Fainting or seizure
Severe headaches with no known cause, especially if they happen suddenly
3rd ANSWER
Mannitol- Because of its osmotic effect, mannitol is assumed to decrease cerebral edema. Mannitol might improve cerebral perfusion by decreasing viscosity, and as a free-radical scavenger, it might act as a neuroprotectant.
Ecospirin
For the prevention of heart attack, stroke, heart conditions such as stable or unstable angina (chest pain) due to a blood clot. Atrovas-Atorva 40 Tablet belongs to a group of medicines called statins. It is used to lower cholesterol and to reduce the risk of heart diseases. Cholesterol is a fatty substance that builds up in your blood vessels and causes narrowing, which may lead to a heart attack or stroke.
4th ANSWER
When the patient met with an accident there might be cranial damage which was unnoticed.
If so his occasional drinking may or may not have hindered the process of the minor hemorrhages getting healed and might have caused this condition
But since the patient is not a chronic alcoholic and so Alcohol might not have played any role.
Therefore it cannot be evaluated without further details
5th ANSWER
The inverse relationship between serum HDL-C and stroke risk. When taken together it seems clear that higher baseline levels of serum HDL-C lower the risk of subsequent ischemic stroke.
G) Patient
Questions:
1)What is myelopathy hand ?
2)What is finger escape ?
3)What is Hoffman’s reflex?
1st ANSWER
loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly,occuring due to pyramidal track involvment.
2nd ANSWER
Presence of weak finger adduction in cervical myelopathy is called - FINGER ESCAPE SIGN
3rd ANSWER
reflectory reaction of muscles after electrical stimulation of type 1a sensory fibres in their innervation nerves
H) patient
Questions:
1) What can be the cause of her condition ?
2) What are the risk factors for cortical vein thrombosis?
3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?
4) What drug was used in suspicion of cortical venous sinus thrombosis?
1st ANSWER
cortical vein thrombosis
2 nd ANSWER
The risk factors include the following:
Congenial or acquired heart diseases
Underlying Infection
Birth control pills use
Dehydration
Cancer
3rd ANSWER
Underlying unresolved edema is the probable cause for the recurrent precipitation of seizures. So when the edema resolved, the seizure resolved spontaneously
4 th ANSWER
Injection Clexane was used to resolve the thrombosis and Mannitol infusion was given to bring down cerebral edema.
3) CARDIOLOGY
A) patient
Questions:
1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
2.Why haven't we done pericardiocenetis in this pateint?
3.What are the risk factors for development of heart failure in the patient?
4.What could be the cause for hypotension in this patient?
1st ANSWER
Preserved ejection fraction - also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax).
Reduced ejection fraction is preceded by chronic comorbidities, such as hypertension, type 2 diabetes mellitus (T2DM), obesity, and renal insufficiency, whereas reduced ejection fraction is often preceded by the acute or chronic loss of cardiomyocytes due to ischemia, a genetic mutation, myocarditis, or valvular disease.
2nd ANSWER
As cardiac tamponade was ruled out, pericardiocentesis for pericardial effusion was not necessary because it was mild and the Diuretics are sufficient to help subside it.
3rd ANSWER
Possible Risk factors for development of heart failure in the patient include:
Diabetes
Hypertension
Older age
Male patient
4th ANSWER
The most likely cause of the hypotension can be Drug induced as the patient is on antihypertensive therapy that include furosamide and telmisartan.
The other possible causes could also include Viral myocarditis or Extensive Myocardial Infarction.
B) patient
Questions:
1.What are the possible causes for heart failure in this patient?
2.what is the reason for anaemia in this case?
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
4. What sequence of stages of diabetes has been noted in this patient?
1st ANSWER
metabolism syndrome would be the best possible diagnosis.
2nd ANSWER
alcoholism, chronic kidney disease
3rd ANSWER
diabetes and alcoholism
4th ANSWER
chronic alcoholism leading to diabetes has led patient into tripathy- neuropathy -retinopathy and nephropathy.
C) patient
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
4) What are the risk factors for atherosclerosis in this patient?
5) Why was the patient asked to get those APTT, INR tests for review?
1st ANSWER
Hypertension- arteriosclerosis- arterial thrombosis .
ANATOMICAL localisation: Blood vessels.
Primary Etiology: hypertension.
2nd ANSWER
1. TAB. Dytor
mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
2. TAB. Acitrom
mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting
3. TAB. Cardivas
mechanism:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.
4.) INJ. HAI S/C
MECHANISM:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5).TAB. Digoxin
mechanism:Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:
Positive lonotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump,an enzyme that controls the movement of ions into the heart.
6). Hypoglycemia symptoms explained
7). Watch for any bleeding manifestations like Petechiae, Bleeding gums.
8). APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
3rd ANSWER
cardiorenal syndrome type 4
4th ANSWER
Hypertension
5th ANSWER
APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
Here, an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed, although local protocols may vary in their starting doses and titration schedule.
D) patient
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
3) What are the indications and contraindications for PCI?
4) What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?
1st ANSWER
1st ans:
TIMELINE OF EVENTS
• Diabetes since 12 years on medication
• Heart burn like episodes since an year relieved without medication
• Diagnosed with pulmonary TB 7 months ago-completed full course of treatment, presently sputum negative.
Hypertension since 6 months - on medication
•Shortness of breath since half an hour-SOB even at rest
Anatomical localisation - Cardiovascular system Etiology: The patient is both Hypertensive and diabetic, both these conditions can cause
Primary Etiology- Atherosclerosis: there is build up of fatty and fibrous material inside the wall of arteries
2 nd ANSWER
MOA: METOPROLOL is a cardiselective betablocker
Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause your heart to beat more slowly( negative chronotropic effect)and with less force( negative inotropic effect). Beta blockers also help open up your veins and arteries to improve blood flow. Indications: it is used to treat Angina, High blood pressure and to lower the risk of heart attacks.
3rd ANSWER
INDICATIONS:
Acute ST-elevation myocardial infarction
Non-ST-elevation acute coronary syndrome
Unstable angina.
Stable angina.
Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope) High risk stress test findings.
CONTRAINDICATIONS:
Intolerance for oral antiplatelets long-term.
Absence of cardiac surgery backup.
Hypercoagulable state.
High-grade chronic kidney disease. Chronic total occlusion of SVG. An artery with a diameter of <1.5 mm.
4th ANSWER
Although PCI is generally a safe procedure, it might cause serious certain complications like
A)Bleeding
B) Blood vessel damage
C) Allergic reaction to the contrast dye used
D) Arrhythmias
E) Need for emergency coronary artery bypass grafting.
Because of all these complications it is better to avoid PCI in patients who do not require it.
E) patient
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
1st ANSWER
Rupture of vulnerable plaque-coronary vessel occlusion- thrombosis-infraction.
ANATOMICAL localisation: blood vessels.
Primary etiology: infraction leading to decrease is systolic function.
2nd ANSWER
1.TAB. ASPIRIN
mechanism:Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase (COX) activity. Until recently, aspirin has been mainly used for primary and secondary prevention of arterial antithrombotic events.
2. TAB ATORVAS
mechanism:Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
3. TAB CLOPIBB
mechanism: The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP mediated activation of the glycoprotein GPIIB/Illa complex, thereby inhibiting platelet aggregation. This action is irreversible.
4.INJ HAI
mechanism:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.ANGIOPLASTY
mechanism:Angioplasty, also known as balloon angioplasty and percutaneous transluminal angioplasty (PTA), is a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.
3rd ANSWER
The second PCI was NOT necessary in this patient.
PCI performed from 3 to 28 days after MI does not decrease the incidence of death, reinfarction or New York Heart Association (NYHA) class IV heart failure but it is associated with higher rates of both procedure-related and true ST elevation reinfarction.3 A retrospective analysis of the clinical data revealed The Thrombolysis in Myocardial Infarction (TIMI) Risk Score of 4 predicting a 30-day mortality of 7.3% in this patient. Late PCI leads to the increased risks of periprocedural complications, long-term bleeding, and stent thrombosis.
The high incidence of CAD and the increasing need for PCI provides an opportunity to evaluate its appropriate use and highlight potential overuse. PCI is frequently reported to be overused and inappropriately recommended. Behnke et al defined overuse as 'use of unnecessary care when alternatives may produce similar outcomes, resulting in a higher cost without increased value'.8Overuse causes a heavy financial burden on people living in countries, where fee-for-service and ill-regulated private healthcare provides much of the patient care. As a result, cost of healthcare increases and causes potential harm the patients.
F) patient
Questions:
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
2. What is the rationale of using torsemide in this patient?
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Answers:
1st ANSWER
Better cardiac output, Possible correction of hypotensive crisis .
2nd ANSWER
Reduce retention of fluid in body tissues.abdominal distension
3rd ANSWER
Treatment of UTI, if it was prophylatic then the treating physician is exploiting it.and even can cause resistance in near future.
Gastroenterology and pulmonology
A) patient.
QUESTIONS:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
2) What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?
Answers:
1st ANSWER
Evolution of symptomatology
5 years back-1st episode of pain abdomen and vomitings
Stopped taking alcohol for 3 years
1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again
20 days back increased consumption of toddy intake
Since 1 week pain abdomen and vomiting Since 4 days fever constipation and burning micturition
Anatomical localisation: Pancreas and left lung.
Primary etiology: Auto digestion of pancreas.
2nd ANSWER
compared to placebo(efficacy:0) efficacy of drugs used are good, I would use the same treatment approach if I where the treating physician.
B) patient
Questions:
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
2) Name possible reasons why the patient has developed a state of hyperglycemia.
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
4) What is the line of treatment in this patient?
Answers:
1st ANSWER
pleural effusion, pancreatic insult leading to pleural effusion.
2nd ANSWER
*This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress
* the result of decreased synthesis and release of insulin secondary to the damage of pancreatic B-cells
* elevated levels of catecholamines and cortisol
3rd Answer
LFT is increased due to hepatocyte injury
*If the liver is damaged or not functioning properly, ALT can be released into the blood. This causes ALT levels to increase. A higher than normal result on this test can be a sign of liver damage.
*elevated alanine transaminase (ALT) and aspartate transaminase (AST), usually one to four times the upper limits of normal in alcoholic fatty liver.
The reasons for a classical 2:1 excess of serum AST activity compared to serum ALT activity in alcoholic hepatitis have been attributed to
(i) decreased ALT activity most likely due to B6 depletion in the livers of alcoholics
(ii) mitochondrial damage leading to increased release of mAST in serum.
4th ANSWER
Plan of action and Treatment:
*Investigations:
*24 hour urinary protein
*Fasting and Post prandial Blood glucose
* HbA1c
* USG guided pleural tapping
Treatment:
.IVF: 125 mL/hr
. Inj Tramadol 1 amp in 100 mL NS, i.v sos
.GRBS charting 6th hourly
. BP charting 8th hourly
.Tab Dolo 650mg sos
.Inj PAN 40mg i.v OD
.Inj ZOFER 4mg i.v sos
C) patient
Questions :-
1) what is the most probable diagnosis in this patient?
2) What was the cause of her death?
3) Does her NSAID abuse have something to do with her condition? How?
1stANSWER
. Ruptured liver abscess with fluid accumulation and internal hemorrhage
2nd ANSWER
.Complications to surgery,hypotension, cardiopulmonary arrest, only if the discription and case taking was clear, there would have been a defenitive way to diagnose.
3rd ANSWER
. NSAID abuse could have posible liver and kindey injury causing wide spectrum of problems within the body.
5) Nephrology (and Urology)
A) patient
Questions:
1. What could be the reason for his SOB ?
2. Why does he have intermittent episodes of drowsiness ?
3. Why did he complaint of fleshy mass like passage in his urine?
4. What are the complications of TURP that he may have had?
Answers:
1st ANSWER
use of diuretics leading to acidosis could cause sob.
2nd Answer
hypernatremia
3rd ANSWER
large amount of pus cells could have been interpreted as fleshy mass.
4th ANSWER
difficulty in micturition,Infection and electrolyte imbalance.
B) patient
Questions
1.Why is the child excessively hyperactive without much of social etiquettes ?
2. Why doesn't the child have the excessive urge of urination at night time ?
3. How would you want to manage the patient to relieve him of his symptoms?
1st ANSWER
Why not we blame the innocence of childhood and merry ways children being active which seems to be mischievous to is and hyper active!
2nd ANSWER
Seems to a psychological feeling patient has developed to urinate over and over then awake.
3rd ANSWER
Proper councling and therapy without destroying the patients activeness has to be done.
6) INFECTIOUS DISEASES
A) patient
Questions:
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
Answers:
1st ANSWER
Difficulty in swallowing, barium swallow, endoscopic findings.
2nd ANSWER
In view of the patient condition patient is likely to develop immune reconstitution inflammatory syndrome. IRIS prevention can be effectively done by initiation of ART before development of advanced immunosuppression.
INFECTIOUS DISEASE and HEPATOLOGY
A) patient
Questions:
1. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ? What could be the cause in this patient ?
2. What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
3. Is liver abscess more common in right lobe ?
4.What are the indications for ultrasound guided aspiration of liver abscess ?
Answers:
1st ANSWER
Possible, can be due to contaminated toddy.
2nd ANSWER
According to some studies, alcoholism mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver. It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess.
3rd ANSWER
Yes, right lobe involvment is due to highblood flow.
4th ANSWER
Indications for USG guided aspiration of liver abscess
1. Large abscess more than 6cms
2.Left lobe abscess
3.Caudate lobe abscess
4. Abscess which is not responding to drugs
B) patient
QUESTIONS:
1) Cause of liver abcess in this patient ?
2) How do you approach this patient ?
3) Why do we treat here ; both amoebic and pyogenic liver abcess?
4) Is there a way to confirmthe definitive diagnosis of this patient?
Answers:
1st ANSWER
poor personal hygiene, malnutrition, eating contaminated food and drinking contaminated water .
2nd ANSWER
as the patient is responding with liquefaction of mass there seems to me no more narrowring so patient is treated for both bacterial and amoebic causes.
3rd ANSWER
Since there is no definitive way of knowing without risking patient's health ,we cannot take risk , we should treat for both.
4th ANSWER
Abscess aspiration can give a defenitive diagnosis.
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology).
A)patient
Questions :
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
2) What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
Answers:
1st ANSWER
*Fever since 10 days
*Facial puffiness and periorbital edema since 4 days
* Weakness of right upper limb and lower limb since 4 days
* Altered sensorium since 2 days
ANATOMICAL localisation: periorbital region.
Primary etiology: mucormycosis.
2nd ANSWER
Compared to placebo the efficacy of the drugs used is good. Amphotericin B is the drung of choice in the patient, I wasa physician would give the same .
3rd ANSWER
Unnecessary prophylatic steroid usage, unhygienic masks, sedentary life style leading to metabolic syndrome leading to easy suseptability to infections.
10)MEDICAL EDUCATION
I would not hesitate to say ..... "This was the most enjoyable way of learning we have ever went through".
I would like to thank Dr .RAKESH BISWAS SIR for giving us this opportunity to learn medicine in most enjoyable fashion.
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