Bimonthly assignment for the month of May 2021.

 M Bhuvana phanindra, Roll no: 74 , 8th semester.

This is the blog made in response to the following question paper.

http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1

Following is my reflection of answers to the questions posed:

1) pulmonology:

Patient details: https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html

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 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?

Answers:

1st ans: 

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 ans: 

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 ans:

evident electrolyte imbalance possibly due to kidney injury caused byATT.

4th ans:

ATT drugs isoniazid and rifampicin are nephrotoxic, possible acute kidney injury leading to her symptoms.

5th ans:

electrolyte loss due Kidney injury.

2) Neurology:

A)Patient details: https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

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) 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?

Answers:

1stans: 

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 ans:

I) Thiamine helps the body cells change carbohydrates into energy. It has been used as a supplement to cope with thiamine deficiency

ii) 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

iii)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.

iv)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.

v)Potchlor liquid is used to treat low levels of potassium in the body.

3rd ans:

Due to excess thiamine deficiency and excess toxins accumulation due to renal disease caused by excess alcohol addiction.

4th ans:

chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine, Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine, and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death.

5th ans:

The kidneys have an important job as a filter for harmful substances .alcohol causes changes in the function of the kidneys and makes them less able to filter the blood.alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function people who drink too much are more likely to have high blood pressure. High blood pressure is a common cause of kidney disease.

6th ans:

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 from intestine.

7th ans:

yes, 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 details: https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1

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 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?

Answers:

1st ans:

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 ans:

A) Tab Vertin 8mg- This is betahistine,which is an anti- vertigo medication MOA- It is a weak agonist on H1 receptors located on blood vessels of the inner ear. This leads to local vasodilation and increased vessel permeability. This can reverse the underlying problem. Indications- Prescribed for balance disorders. In this case it is used due to patients history of giddiness and balance issues.

B) Tab Zofer 4mg- This is ondanseteron- It MOA- It is a 5H3 receptor antagonist on vagal afferents in the gut and they block is an anti emetic receptors even in the CTZ and solitary tract nucleus.

Indications- Used to control the episodes of vomiting and nausea in this patient.

C) Tab Ecosprin 75mg- This is aspirin. It is an NSAID

MOA- They inhibit COX-1 and COX-2 thus decreasing the prostaglandin level and thromboxane synthesis

Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.

D) Tab Atorvostatin 40mg- This is a statin MOA- It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis. It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.

Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.

E) Clopidogrel 75mg- It is an antiplatelet medication

MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.

Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting

F) Thiamine- It is vitamin B1 It is naturally found in many foods in the human diet. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins. Indications- Given to this patient mainly to prevent Wernickes encephalopathy that can lead to confusion, ataxia and opthalmoplegia.

G) Tab MVT- This is methylcobalamin Mainly given in this case for vitamin B12 deficiency.

3rd ans:

A cerebellar infarct is usually caused by a blood clot obstructing blood flow to the cerebellum. High blood pressure that is seen in hypertension (especially if left untreated) can be a major risk factor for the formation of cerebellar infarcts.

Increased shear stress is caused on the blood vessels. The usual adaptive responses are impaired in this case, thus leading to endothelial dysfunction in this case. High BP can also promote cerebral small vessel disease. All these factors contribute to eventually lead to stroke.

4th ans:

Meta analysis of the relation between alcohol consumption and increased risk of stroke has mainly weighed in to the formation of two types- ischaemic and haemorrhagic stroke.

Ischaemic stroke- this is more common. This Is caused by a blood clot blocking the flow of blood and preventing oxygen from reaching the brain

Haemorrhagic stroke- occurs when an aneurysm bursts or when a weakened blood vessel leaks, thus causing cerebral haemorrhage

heavy drinkers have 1.6 more chance of intracerebral haemorrhage and a 1.8 increased chance of subaracnoid haemorrhage. The adverse effect on BP that is seen due to increased drinking is a major stroke risk factor and increase the risk of heart stroke.

Many studies show that with mild and moderate drinking. the risk of ischaemic stroke decreases due to decreased level of fibrinogen which helps in the formation of blood clots. However, heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP and heart rate.

So In this case, his history of alcoholism, coupled with his hypertension definitely could be a causative factor of his current condition.

C) patient details:http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html

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 the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?

3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?

Answers:

1st ans:

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 ans: 

diuretics usage,  Other risk factors :-

A) Abnormal loses:

Medications-diuretics, laxatives, enema, corticosteriods

Real causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis, hypomagnesenemia 

B) trance cellular shift : alkalosis, thyrotoxicosis, delirium tremans, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis

C) Inadequate intake: anorexia, dementia, stareation, total parental nutrition

D) psuedohypokalemia:delayed sample analysis, significant leukocytosis

3rd ans:

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 details:https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html

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?

Answers:

1st ans:

seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury

Seizures after haemorrhagic strokes are thought to be attributable to irritation due to (hemosideri. Deposits)caused by products of blood metabolism

Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause.

2nd ans:

progression of simple partial seizures into generalized tonic clinic seizures night be the cause of unconsciousness.

E) patient details:https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

Questions:

1) What could have been the reason for this patient to develop ataxia in the past 1 year?

2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?

Answers:

1st ans: 

cerebral hemorrhage into the frontal lobe, due to unattended head injury one year ago could have caused it.

2nd ans: 

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 details:http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html

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??

Answers:

1st ans:

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 ans:

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 ans:

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.

Rt feed RT feed is a nursing procedure to provide nutrition to those people who are either unable to obtain nutrition by mouth or are not in a state to swallow the food safely.

4th ans:

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 ans:

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 details:https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html

Questions:

1)What is myelopathy hand ?

2)What is finger escape ?

3)What is Hoffman’s reflex?

Answers:

1st ans:

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 ans:

Presence of weak finger adduction in cervical myelopathy is called - FINGER ESCAPE SIGN

3rd ans:

reflectory reaction of muscles after electrical stimulation of type 1a sensory fibres in their innervation nerves 

H) patient details:https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1

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?

Answers:

1st ans: 

cortical vein thrombosis

2nd ans:

3rd ans:

Seizures are resolved and seizure free period got achieved after medical intervention but sudden episode of seizure was may be due to any persistence of excitable foci by abnormal firing of neurons.

4th ans:

Anticoagulants are used for the prevention of harmful blood clots..

Clexane (enoxaparin) low molecular weight heparin binds and potentiates antithrombin three a serine protease Inhibitor to form complex and irreversibly inactivates factor xa.

3) cardiology

A)patient details:https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html

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?

Answers:

1st ans:

Preserved ejection fraction (HFPEF) - 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 (HFrEF) - also referred to as systolic heart failure HFPEF is preceded by chronic comorbidities, such as hypertension, type 2 diabetes mellitus (T2DM), obesity, and renal insufficiency, whereas HFrEF is often preceded by the acute or chronic loss of cardiomyocytes due to ischemia, a genetic mutation, myocarditis, or valvular disease

2nd ans: 

No because the effusion was self healing.

3rd ans:

risk factors for development of heart faliure in this patent

Alcohol abuse increases the risk of atrial fibrillation, heart attack and congestive heart failure

high blood pressure

Smoking

Diabetes

AV block can be associated with severe bradycardia and hemodynamic instability. It has a greater risk of progressing to third-degree (complete) heart block or asystole.

worsening of pericardial effusion leading to cardiac tamponade.

4th ans:

 secondary to tuberculosis,or maybe due to thickened visceral peritoneum.

B)patient details:https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html

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?

Answers:

1st ans: 

metabolism syndrome would be the best possible diagnosis.

2nd ans: 

alcoholism, chronic kidney disease

3rd ans:

 diabetes and alcoholism 

4th ans:

 chronic alcoholism leading to diabetes has led patient into tripathy- neuropathy -retinopathy and nephropathy.

C)patient details:https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html

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?

Answers:

1st ans: 

Hypertension- arteriosclerosis- arterial thrombosis .

ANATOMICAL localisation: Blood vessels.

Primary Etiology: hypertension.

2nd ans:

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 ans:

 cardiorenal syndrome type 4

4th ans: 

Hypertension

5th ans:  

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 details:https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1

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?

Answers: 

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.(PLAQUE)

2nd ans:

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 ans:

INDICATIONS:

Acute ST-elevation myocardial infarction(STEMI)

Non-ST-elevation acute coronary syndrome (NSTE-ACS)

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 ans:

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 details:https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1

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?

Answers:

1st ans:

 rupture of vulnerable plaque-coronary vessel occlusion- thrombosis-infraction.

ANATOMICAL localisation: blood vessels.

Primary etiology: infraction leading to decrease is systolic function.

2nd ans:

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 Ans:

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 details:https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h

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 ans:

 better cardiac output, Possible correction of hypotensive crisis .

2nd ans: 

reduce retention of fluid in body tissues.abdominal distension

3rd ans: 

treatment of UTI, if it was  prophylatic then the treating physician is exploiting it.and even can cause resistance in near future.

4)Gastroenterology (& Pulmonology).

A)patient details:https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html

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 ans:

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 ans:

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 details:https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html

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 ans: 

pleural effusion, pancreatic insult leading to pleural effusion.

2nd ans:

*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 ans:

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 ans:

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 PAN 40mg i.v OD

• Inj ZOFER 4mg i.v sos

• Inj Tramadol 1 amp in 100 mL NS, i.v sos

• Tab Dolo 650mg sos

• GRBS charting 6th hourly

. BP charting 8th hourly

C)patient details:https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html

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? 

Answers:

1st ans:

 ruptured liver abscess with fluid accumulation and internal hemorrhage

2nd ans: 

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 ans:

 NSAID abuse could have posible liver and kindey injury causing wide spectrum of problems within the body.

5) Nephrology (and Urology)

A)patient details:https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html

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 ans:

use of diuretics leading to acidosis could cause sob.

2nd ans:

hypernatremia

3rd ans:

large amount of pus cells could have been interpreted as fleshy mass.

4th ans: 

difficulty in micturition,Infection and electrolyte imbalance.

B)patient details:https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html

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?

Answers:

1st ans:

 why not we blame the innocence of childhood and merry ways children being active which seems to be mischievous to us is hyper active!

2nd ans: 

seems to a psychological feeling patient has developed to urinate over and over then awake.

3rd ans:

proper councling and therapy without destroying the patients activeness has to be done.

6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology).

patient details:https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html

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 ans:

 difficulty in swallowing, barium swallow, endoscopic findings.

2nd ans:

 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.

7) Infectious disease and Hepatology:

A)patient details:https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html

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 ans: 

possible, can be due to contaminated toddy.

2nd ans:

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 ans:

yes right lobe involvment due to highblood flow.

4th ans:

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 details:https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html

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 ans:

poor personal hygiene, malnutrition, eating contaminated food and drinking contaminated water .

2nd ans: 

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 ans: 

Since there is no definitive way of knowing without risking patient's health  ,we cannot take risk , we should treat for both.

4th ans:

abscess aspiration can give a defenitive diagnosis.

8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology).

A)patient details:http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html

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 ans: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 ans: 

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 ans: unnecessary prophylatic steroid usage, unhygienic masks, sedentary life style leading to metabolic syndrome leading to easy suseptability to infections.

9) Infectious Disease (Covid 19)

As these patients are currently taking up more than 50% of our time we decided to make a separate log link here:

http://medicinedepartment.blogspot.com/2021/05/covid-case-report-logs-from-may-2021.html?m=1

for this question that contains details of many of our covid 19 patients documented over this month and we would like you to:

1) Sort out these detailed patient case report logs into a single web page as a master chart 

2) In the master chart classify the patient case report logs into mild, moderate severe and 

3) indicate for each patient, the day of covid when their severity changed from moderate to severe or vice versa recognized primarily through increasing or decreasing oxygen requirements 

4) Indicate the sequence of specific terminal events for those who died with severe covid (for example, altered sensorium, hypotension etc). 

Answers:

https://kimselogs.blogspot.com/2021/05/covid-19.html?m=1

10) Medical Education: 

Experiential learning is a very important method of Medical education and while the E logs of the students in the questions above represent partly their and their patient's experiences, reflective logging of one's own experiences is a vital tool toward competency development in medical education and research. A sample answer to this last assignment around sharing your experience log of the month can be seen in the link below but while this is by a student onsite in hospital and not locked down at home we would be very interested to learn about your telemedical learning experiences from our hospital as well as community patients over the last month even while locked down at home: https://onedrive.live.com/view.aspx?resid=4EF578BAE67BA469!4180&ithint=file%2cdocx&authkey=!AOy7BpRTn42DBMo.

Answers:

Journey of a thousand miles starts with a single step ,fear of covering the longway goes away with starting the journey, likewise initial hesitation anxiety and inferiority complex where all found out to be passing clouds when I made my first e-log talking to the patient attendents, show where annoyed by a lot many twisted turning questions I posed ,who later thanked me and blessed me after they hear the update of there loved ones being okay. Being home and listening to classes online now seems to be a childsplay after I started learning from a patient centered problem centers learning each leading from one question to other, where a few hours of lessons and days of learning are required, effortlessly made us learn things in matter of minutes to hours. This is the best thing to have happened in the field of learing, there have been dreams about solving cases and finding answers. All thanks to rakesh biswas sir and medicine department for making us learn in sucha fun, effective and healthy way. Though this assignment was lengthy and extensive wring this answer made it all go away.