General medicine monthly assignment

 SECTION 1: (PULMONOLOGY)

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?

Ans:The patient's symptoms started 20 years ago during the winter season, and recurred very year during the same time. This indicates a gradual progression of shortness of breath. The seasonal incidence indicates the seasonal exacerbation of COPD. The anatomical localisation of the problem is in the lungs, specifically bronchial tubes. The ethology of this may be due to environmental exposure to pollutants.

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Ans: Head end elevation improves the breathing due to orthostatic dyspnoea as associated with the heart failure here. The O2 inhalation is shown to increase the O2 saturation and maintain optimum oxygen saturation. AUGUMENTIN and AZITHROMYCIN are given as antibiotics against infections. Steroids are given to prevent further damage to the lungs. Pulmoclear Tablet is used for relieving the symptoms of coughing, wheezing, congestion and blockage in the airways in a condition called chronic obstructive pulmonary disease (COPD). It contains a com. They belong to the class of bronchodilators and mucolytics.


3) What could be the causes for her current acute exacerbation?

Ans: Acute exacerbation of COPD associated with right heart failure and bronchiectasis.

4. Could the ATT have affected her symptoms? If so how?

Ans:Chronic obstructive pulmonary disease (COPD) and tuberculosis (TB) are two important causes of mortality and morbidity in our country and are among top 10 causes of death. The interrelationship between TB and COPD is very complex. A substantial number of TB patients develop post tubercular airway disease or TB-associated COPD.COPD patients are also at high risk of developing pulmonary TB.COPD also alters the clinical presentation of TB and is a risk factor for increased morbidity and mortality from TB.

5.What could be the causes for her electrolyte imbalance?

Ans:Patients with COPD tend to retain sodium. In addition, serum potassium should be monitored carefully, because diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels.

Beta-adrenergic agonists also increase renal excretion of serum calcium and magnesium, which may be important in the presence of hypokalemia.

Chronic respiratory acidosis leads to compensatory metabolic alkalosis. In the absence of blood gas measurements, bicarbonate levels are useful for following disease progression.


SECTION 2: (NEUROLOGY)

A)

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient's problem?

Ans:The patient was apparently asymptomatic 9 days ago, when he started talking, as well as laughing to himself, which was sudden in onset. He was conscious, but oriented to time, person and place only from time to time.He also had short term memory loss since 9 days, where he could not recognise family members from time to time. The primary etiology is probably due to alcohol intake.

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Ans:It is established that thiamine replacement is the primary treatment for WKS in order to reverse mental status changes and prevent further disease progression. Parenteral thiamine is used in the acute treatment of Wernicke's since intestinal absorption of thiamine may be impaired, as in the case of alcoholics.Seizures are managed with the standard antiepileptic drugs (AEDs) for tonic-clonic and partial seizures. Administration of lactulose, either orally, rectally, or via nasogastric tube, is the first-line therapeutic intervention used to reduce ammonia levels in the blood. Electrolytes are also correct accordingly.


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?

Ans:It is established that thiamine replacement is the primary treatment for WKS in order to reverse mental status changes and prevent further disease progression. Parenteral thiamine is used in the acute treatment of Wernicke's since intestinal absorption of thiamine may be impaired, as in the case of alcoholics.

5) What is the probable reason for kidney injury in this patient? 

Ans:The kidneys are hard at work on any given day in a healthy person, but the kidneys of a heavy drinker work overtime. A heavy drinker is defined as a woman who drinks more than seven times a week or a man who drinks more than 14 times a week. People who maintain this kind of drinking habit are at double the risk for developing kidney disease compared to the general population, including moderate drinkers.

One form of alcohol abuse that contributes to kidney disease is binge drinking, usually defined as consuming four or five drinks within two hours. Binge drinking causes a person’s blood alcohol content to rise to dangerous levels, which in turn causes the kidneys to lose their function so much, the term for this is acute kidney injury. Japan’s Internal Medicine journal noted that binge drinking can be a risk factor for such an emergency, including acute kidney injury (also known as acute kidney failure), a condition whereby the kidneys are unable to stop “dangerous levels of waste” from accumulating in the blood.


6). What is the probable cause for the normocytic anaemia?

Ans: It probably could be due to malnutrition associated with chronic alcoholism.

7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?

Ans:Alcohol consumption by diabetics can worsen blood sugar control in those patients. For example, long-term alcohol use in well-nourished diabetics can result in excessive blood sugar levels. Conversely, long-term alcohol ingestion in diabetics who are not adequately nourished can lead to dangerously low blood sugar levels. Heavy drinking, particularly in diabetics, also can cause the accumulation of certain acids in the blood that may result in severe health consequences. Finally, alcohol consumption can worsen diabetes-related medical complications, such as disturbances in fat metabolism, nerve damage, and eye disease.

B)

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient's problem?

Ans: The symptoms started a week ago when he experienced giddiness which reduced after that but then occurred again after 3 days following alcohol consumption. This was associated with Bilateral Hearing loss, aural fullness and presence of tinnitus. 2 days ago he came to the OPD due to slurring of speech and deviated mouth. The anatomical location is in right inferior cerebellar hemisphere. Primary etiology is due to hypertension.

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Ans:Ecosprin 75 mg Tablet is an anti-platelet medicine that contains acetylsalicylic acid (also known as Aspirin). It is used to prevent blood clot formation within the body. This tablet is also used to prevent heart attacks, stroke and heart-related chest pain (angina). Zofer is used for the associated vomiting. Statins are given to reduce the cholesterol. Clopidogrel prevents clot formation. Vertin Tablet is used to prevent and treat a disorder of the inner ear known as Ménière's disease. The symptoms include dizziness (vertigo), ringing in the ears (tinnitus), and loss of hearing, probably caused by fluid in the ear. This medicine helps relieve the symptoms by reducing the amount of fluid.
 
3) Did the patients history of de novo HTN contribute to his current condition?

Ans:Blood vessels damaged by high blood pressure can narrow, rupture or leak. High blood pressure can also cause blood clots to form in the arteries leading to your brain, blocking blood flow and potentially causing a stroke.

4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?


Ans: Drinking may, in fact, increase the risk of hemorrhagic stroke. This is more apparent when looking at the heavy drinking category.

C)

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?

Ans:10 yrs back had the episode of paralysis of both upper and lower limbsPatient was apparently normal 8months back then she developed bilateral pedal edema. Palpitations since 5days. Pain since 6days radiating along the left upper limb. Location of problem is in the neural system due to hypokalaemia. primary etiology of patient could be due to the electrolyte imbalances especially hypokalaemia. 

2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalaemia?

Ans:It could be due to refractory hypokalaemia. Risk factors associated with a low serum potassium levels (hypokalaemia) include female gender, intake of medication (diuretics), heart failure, hypertension, low body mass index (BMI), eating disorder, alcoholism, diarrhoea, Cushing's syndrome. 

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

Ans: ECG changes include flattening and inversion of T waves in mild hypokalaemia, followed by Q-T interval prolongation, visible U wave and mild ST depression4 in more severe hypokalaemia. Severe hypokalaemia can also result in arrhythmias such as Torsades de points and ventricular tachycardia.

D)

1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?

Ans:Stroke is the most common cause of seizures in the elderly population.There are several causes for early onset seizures after ischaemic strokes. An increase in intracellular Ca2+and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypo-perfusion  and hyperperfusion injury (particularly after carotid end arterectomy) have all been postulated as putative neurofunctional aetiologies. Seizures after haemorrhagic strokes are thought to be attributable to irritation caused by products of blood metabolism. The exact pathophysiology is unclear, but an associated ischaemic area secondary to haemorrhage is thought to play a part. Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause. Haemosiderin deposits are thought to cause irritability after a hemorrhagic stroke. In childhood, post‐stroke seizures can occur as part of perinatal birth trauma.


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?

Ans:In focal aware seizures (FAS), previously called simple partial seizures, the person is conscious (aware and alert) and will usually know that something is happening and will remember the seizure afterwards.Epileptic seizures can cause dynamic, reversible changes in brain function and are often associated with loss of consciousness.

E)

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

Ans: Ataxia could be due to the multiple falls he had that might have lead to trauma or it could also be due to a stroke.

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

Ans: His intracranial bleed could be either due to the trauma related to the falls or due to a stroke too. Chronic alcoholics have decreased concentrations of liver-produced coagulation factors and platelet abnormalities that predispose them to hemorrhagic stroke.


F)

1.Does the patient's  history of road traffic accident have any role in his present condition?

Ans: The road traffic accident could be implicated in CVA but not in this case scenario as the accident was 4 years ago.

2.What are warning signs of CVA?

Ans:The five warning signs of stroke are:
  • Sudden onset of weakness or numbness on one side of the body.
  • Sudden speech difficulty or confusion.
  • Sudden difficulty seeing in one or both eyes.
  • Sudden onset of dizziness, trouble walking or loss of balance.
  • Sudden, severe headache with no known cause.

3.What is the drug rationale in CVA?

Ans: Ecosprin 75 mg Tablet is an antiplatelet medicine that contains acetylsalicylic acid (also known as Aspirin). It is used to prevent blood clot formation within the body. This tablet is also used to prevent heart attacks, stroke and heart-related chest pain (angina). Atorvastatin is also given to reduce the cholesterol.

4. Does alcohol has any role in his attack?

Ans: Epidemiological evidence indicates that recent heavy alcohol consumption increases the risk for all major types of stroke, whereas light-to-moderate alcohol intake is associated with a decreased risk of ischemic stroke. Although heavy drinking elevates blood pressure, there is no firm evidence to indicate that alcohol consumption causes the formation of aneurysms, microaneurysms or other lesions in human arteries. Alcohol has been reported to precipitate vasoconstriction and rupture of small cerebral arteries in experimental animals. Alcohol-induced neck trauma has been shown to precipitate traumatic strokes, and alcohol-induced cardiac arrhythmias have been observed in patients with embolic brain infarction. The effects of alcohol on hemostasis, fibrinolysis and blood clotting are variable and could either prevent or promote the occurrence of strokes. The antiatherogenic effects of regular light-to-moderate alcohol consumption could be mediated by inhibition of low-density lipoprotein oxidation, and by elevated estrogen levels.

5.Does his lipid profile has any role for his attack?

Ans: The patients lipid profile seems to be normal except for low HDL.

G)

1)What is myelopathy hand?

Ans: A characteristic dysfunction of the hand has been observed in various cervical spinal disorders when there is involvement of the spinal cord. There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement.

2)What is finger escape?

Ans: Wartenberg's Sign refers to the slightly greater abduction of the fifth digit, due to paralysis of the abducting palmar interosseous muscle and unopposed action of the radial innervated extensor muscles (digiti minimi, digitorum communis ).

3)What is Hoffman’s reflex?

Ans: Hoffman's sign or reflex is a test that doctors use to examine the reflexes of the upper extremities. This test is a quick, equipment-free way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition.


H)

1) What can be  the cause of her condition ?

Ans: 
Here the patient has iron deficiency anaemia so it is possible that it caused her condition.
                             

2) What are the risk factors for cortical vein thrombosis?

Ans:

  • Problems with the way their blood forms clots.
  • Sickle cell anemia.
  • Chronic hemolytic anemia.
  • Beta-thalassemia major.
  • Heart disease — either congenital (you're born with it) or acquired (you develop it)
  • Iron deficiency.
  • Certain infections.
  • Dehydration.

  • 3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously  why?   

    Ans: The postictal state is a period that begins when a seizure subsides and ends when the patient returns to baseline. It typically lasts between 5 and 30 minutes and is characterised by disorienting symptoms such as confusion, drowsiness, hypertension, headache, nausea, etc                        
                 
    4) What drug was used in suspicion of cortical venous sinus thrombosis?


    Ans: Heparin should be considered seriously in the management of cerebral venous thrombosis (CVT), with subsequent conversion to warfarin as maintenance therapy suggested. Subcutaneous low ̶ molecular-weight heparin (Lovenox) also has been used in patients with venous sinus thrombosis. Thrombolytic therapy may be effective in CVT, but all studies so far describe its use only with local instillation by micro-catheter or direct instillation at the time of surgical thrombectomy.


    SECTION 3: (CARDIOLOGY)

    A)

    1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?

    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. The heart muscle does not contract effectively, and therefore less oxygen-rich blood is pumped out to the body.

  • 2.Why haven't we done pericardiocenetis in this patient?        

    Ans: Aortic dissection and post-infarction rupture of the free wall are contraindications to needle pericardiocentesis (surgical tamponade) due to the potential risk of aggravating the dissection or myocardial rupture via rapid pericardial decompression and restoration of systemic arterial pressure.
                 
    3.What are the risk factors for development of heart failure in the patient?

    Ans: The patient is old, and has a history of smoking and is also a known case of hypertension. These could've led to the development of heart failure in this patient.

    4.What could be the cause for hypotension in this patient?


    Ans: Among the heart conditions that can lead to low blood pressure are an abnormally low heart rate (bradycardia), problems with heart valves, heart attack and heart failure. Your heart may not be able to circulate enough blood to meet your body's needs.

    B)

    1.What are the possible causes for heart failure in this patient?

    Ans: Here the patient is old and has a history of chronic alcoholism and is a known case of hypertension and diabetes mellitus and chronic kidney disease. The patient is also obese and has central truncal obesity. These could be responsible for his heart failure.

    2.what is the reason for anaemia in this case?

    Ans: Chronic kidney disease, heart failure and also truncal obesity are all associated with normocytic normochromic anaemia as seen in this patient.

    3.What is the reason for blebs and non healing ulcer in the legs of this patient?

    Ans: These are caused due to his diabetes. Ulcers in people with diabetes are most commonly caused by:
    poor circulation
    high blood sugar (hyperglycaemia)
    nerve damage
    irritated or wounded feet

    4. What sequence of stages of diabetes has been noted in this patient?

    Ans: stage 1: defined as DCBD insulin resistance; stage 2: defined as DCBD pre diabetes; stage3: defined as DCBD type 2 diabetes; and. stage 4: defined as DCBD vascular complications, including retinopathy, nephropathy or neuropathy, and/or type 2 diabetes-related microvascular events. Here we see a stage 4 due to the diabetic nephropathy. 

    C)

    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?

    Ans: The patient had a episode of SOB a year ago which resolved until two days ago when he experienced SOB again. The anatomical localization of the problem is in the heart. The cause could be due to alcohol consumption and hypertension.

    2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

    Ans: Dytor is used to control hypertension.Acitrom tablet is an oral anticoagulant medicine that is used for the treatment and prevention of the formation of abnormal blood clots (thrombus) in blood vessels and disease associated with it. Acitrom works by inhibiting the action of an enzyme responsible for the formation of blood clots. Cardivas 3.125mg Tablet 10's belongs to a group of medicines called beta-blockers used alone or together with other medicines to treat high blood pressure (hypertension), chronic heart failure and myocardial infarction (heart attack). High blood pressure adds to the workload of the heart and arteries. It's used to control some heart problems, such as irregular heartbeats (arrhythmias) including atrial fibrillation. It can also help to manage the symptoms of heart failure, usually with other medicines.

    3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient? 

    Ans: The term cardio renal syndrome (CRS) refers to a condition in which either renal impairment occurs as a result of cardiac dysfunction, or heart structure and function are negatively affected by renal disorders. The damage/dysfunction can be produced in either the heart or the kidney by an acute or chronic disease of the other organ, or abnormal heart and kidney functions occur simultaneously as a result of a systemic disease. Here the patient is type 4.

    4) What are the risk factors for atherosclerosis in this patient?

    Ans: Risk factors for atherosclerosis, include:
    • High cholesterol and triglyceride levels.
    • High blood pressure.
    • Smoking.
    • Type 1 diabetes.
    • Obesity.
    • Physical inactivity.
    • High saturated fat diet.

    5) Why was the patient asked to get those APTT, INR tests for review?

    Ans: APTT measures heparin levels while INR is a measure of warfarin and they help to prevent and check out for toxicities or excess of these anticoagulants so that the patient won't bleed out.

    D)

    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?

    Ans: The patient had heart burn since a year and then developed SOB an hour ago. The problem is localised to the heart. It could be caused due to risk factors like her age and hypertension.

    2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

    Ans: Met XL 25 tablet is used to treat high blood pressure mainly, along with certain heart conditions such as angina (chest pain) and heart failure. belongs to a group of medicines called long-acting beta-blocker. Percutaneous coronary intervention (PCI), also known as coronary angioplasty, is a nonsurgical technique for treating obstructive coronary artery disease, including unstable angina, acute myocardial infarction (MI), and multi vessel coronary artery disease (CAD).

    3) What are the indications and contraindications for PCI?

    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.


  • 4) What happens if a PCI is performed in a patient who does not need it? What are the harms of over treatment and why is research on over testing and over treatment important to current healthcare systems?


    Ans: 

    • Medical therapy with high dose statins is preferred over balloon angioplasty in patients with mild anginal symptoms.
    • PCI is preferred over medical therapy if the patient has;
      • severe symptoms
      • failed medical therapy
      • high-risk coronary anatomy
      • worsening LV function
    If PCI is performed in a patient who does not need it, it is an unnecessary procedure done in the patient with many risks associated with the procedure with no benefit from it.
    • factors associated with increased rates of complications with PCI:
      • advanced age 
      • diabetes 
      • chronic kidney disease 
      • acute coronary syndrome 
      • heart failure 
      • multivessel coronary artery disease 
    • femoral vascular complications occur in about 2%-6% overall (mostly related to vascular access) and may include:
      • access site hematoma 
      • pseudoaneurysm 
      • arteriovenous fistula 
      • arterial dissection and/or occlusion 
      • retroperitoneal hematoma
    • complications from radial access may include:
      • loss of radial pulse reported in ≤ 5% of procedures 
      • radial artery spasm 
      • infrequent to rare adverse effects may include 
        • compartment syndrome 
        • pseudoaneurysm 
        • sterile abscess (with previous-generation hydrophilic sheaths)
    • Overtreatment: The main and worst consequence of overdiagnosis is overtreatment of an indolent lesion or disease which is unlikely to have any benefit for the patient. At the same time the likely interventions like surgery, radiation, and chemotherapy can have side effects resulting in significant morbidity and rarely even fatalities can occur.As over diagnosis in some non-neoplastic conditions leads to over-prescription and over medicalization, resulting in many undesirable and sometimes dangerous side effects; it can also contribute to the release of pharmaceuticals into the environment as, for example, in case of over- and misuse of antibiotics, thus contributing to the proliferation of antimicrobial resistance.

    • E)

    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?

    Ans: 
    Patient was apparently asymptomatic 3 days back and then he developed mild chest pain in the right side of the chest. The problem is in the heart of the patient. Elevations lead 2 and 3 and AVF indicate the problem is in inferior area, probably right coronary artery(90%).

    Causes:

    • Atherosclerosis – Also known as coronary artery disease, this condition is the most common cause of heart attacks and occurs when the buildup of fat, cholesterol, and other substances forms plaque on the walls of the coronary arteries
    • Coronary artery spasm – A rare cause of blockage, spasms of the coronary arteries can cause them to become temporarily constricted. 
    • Coronary artery tear – Also known as a spontaneous coronary artery dissection, a tear in a coronary artery can prevent blood from reaching the heart and cause a heart attack.

    2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

    Ans: Daily low-dose aspirin is a blood thinning medicine. Aspirin is also known as acetylsalicylic acid. Low-dose aspirin helps to prevent heart attacks and strokes in people at high risk of them. Atorvastatin belongs to a group of medicines called statins. It's used to lower cholesterol if you've been diagnosed with high blood cholesterol. It's also taken to prevent heart disease, including heart attacks and strokes. Clopidogrel is an anti platelet medicine. It prevents platelets (a type of blood cell) from sticking together and forming a dangerous blood clot. Taking clopidogrel helps prevent blood clots if you have an increased risk of having them. Inj HAI relaxes and dilates (expands) blood vessels resulting in lowered blood pressure. It is used to treat hypertension (high blood pressure). PTCA, or percutaneous trans luminal coronary angioplasty, is a minimally invasive procedure that opens blocked coronary arteries to improve blood flow to the heart muscle.


    3) Did the secondary PTCA do any good to the patient or was it unnecessary?
     Ans: In this patient the PTCA was unnecessary. Indications of PTCA depend on various factors. Patients with stable angina symptoms unresponsive to maximal medical therapy will benefit from PCI. It helps provide relief of persistent angina symptoms despite maximal medical therapy. Emergency PTCA is indicated for acute ST-elevation myocardial infarction (STEMI) suggesting 100% occlusion of the coronary artery. With acute STEMI, patients are taken directly to lab immediately upon presentation to help prevent further myocardial muscle damage. In non-ST-elevation myocardial infarction (NSTEMI), or unstable angina, (known as acute coronary syndromes), patients are taken to cardiac cath lab within 24 to 48 hours.

    F)

    1. How did the patient get  relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?

    Ans: The technique of fluid resuscitation to treat an episode of shock was first described by Dr. Thomas Latta nearly 200 years ago in a letter to the editor of The Lancet (Latta 1832). He injected repeated small boluses of a fluid solution equivalent to approximately ½ Ringers lactate and observed the clinical changes of his first patient (an elderly woman). The first bolus did not have any visible effect, but after multiple boluses (overall 2.8 litres) “soon the sharpened features, and sunken eye, and fallen jaw, pale and cold, bearing the manifest imprint of death's signet, began to glow with returning animation; the pulse returned to the wrist.” To give fluids during shock and observe the clinical improvement of the patient at bedside seemed reasonable in 1831 and still makes sense! In fact, optimal fluid management is a key component to improve the outcome of haemodynamically unstable ICU patients, since both hypovolaemia and hypervolaemia are harmful. This is the rationale behind using fluids in cariogenic shock.

    2. What is the rationale of using torsemide in this patient?

    Ans: Diuretics are used to decrease plasma volume and peripheral edema. The reduction in extracellular fluid and plasma volume associated with diuresis may initially decrease cardiac output and, consequently, blood pressure, with a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, the plasma volume and peripheral vascular resistance usually return to pretreatment values.

    3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?

    Ans: Here the ceftriaxone is administered for the treatment of UTI, though it also serves the purpose of prophylaxis. Here it is for the treatment.

    SECTION 4: (GASTROENTEROLOGY)

    A) 

    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?

    Ans: Patient was apparently asymptomatic 5 yrs back when he had pain abdomen & vomiting. He was symptom free for nearly 3 yrs. Last binge of  alcohol was 1 week back following which he again had pain abdomen & vomiting from 1 week and fever from 4 days. Then he developed constipation since 4 days and passing flatus. patient also had burning micturition since 4 days. The problem can be localised to pancreas. The cause of pancreatitis here may be attributed to alcohol.
     
    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?

    Ans: 1) ING. MEROPENAM ; TID for 7 days 

    * Meropenem ( broad spectrum Carbepenem ) an antibiotic.

    2) ING. METROGYL 500 mg IV TID for 5 days

    * inj. Metrogyl has METRONIDAZOLE

    Nitroimidazole drug ) an antibiotic

    3) ING. AMIKACIN 500 mg IV BD for 5days

    * It is an Aminoglycoside antibiotic 

    ## Here all three of these (Inj. Meropenem, Inj. Metrogyl, Inj. Amikacin ) are used as antibiotics to control infection and ; to prevent septic complications of acute pancreatitis.

    4) TPN ( Total Parenteral Nutrition )

    * Method of feeding that by passes gastrointestinal tract

    * Fluids are given to vein , it provides most of the nutrients body needs.

    * TPN has proteins, carbohydrates, fats, vitamins, minerals.

    5) IV NS / RL at the rate 12l ml per hour

    * Given for fluid replacement ie., treat dehydration 

    6) ING. OCTREOTIDE 100 mg SC , BD

    * It is a Somatostatin long acting analogue.

    * It is used here to decrease exocrine secretion of pancreas and it also has anti- inflammatory & cytoprotective effects.

    7) ING. PANTOP 40 mg IV , OD

    * Inj. Pantop has PANTOPRAZOLE ( Proton Pump Inhibitor) used for its anti pancreatic secretory effect.

    8) ING. THIAMINE 100 mg in 100 ml NS  IV , TID

    * It is B1 supplement. 

    * It is given here because; due to long fasting & TPN  usage , body may develop B1 deficiency 

    Wernicke encephalopathy secondary to B1 deficiency may be caused... so a prophylactic B1 supplemention is necessary.

    9) ING. TRAMADOL in 100 ml NS  IV , OD

    * It is an opioid analgesic, given to relieve pain.

    B)

    1) What is causing the patient's dyspnea? How is it related to pancreatitis?

    Ans: Acute pancreatitis in its severe form is complicated by multiple organ system dysfunction, most importantly by pulmonary complications which include hypoxia, acute respiratory distress syndrome, atelectasis, and pleural effusion. The pathogenesis of some of the above complications is attributed to the production of noxious cytokines. Clinically significant is the early onset of pleural effusion, which heralds a poor outcome of acute pancreatitis.

    2) Name possible reasons why the patient has developed a state of hyperglycaemia.

    Ans: Hyperglycaemia in the early phase of AP seems to be complicated and may arise from mechanisms such as uncontrolled pre-existing DM, damage to the endocrine pancreas due to severe attack of AP, and metabolic stress associated with critical illness

    3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?

    Ans: Patients with ALD may or may not have elevated serum aminotransferase levels. The absolute level of liver enzyme elevation does not correlate well with the severity of ALD, however, the pattern of elevation in transaminases is helpful in making a diagnosis of liver injury due to alcohol as AST is typically two to three times greater than ALT in alcoholic liver injury. They will also typically have an elevated serum gamma-glutamyltranspeptidase (GGT).

    4) What is the line of treatment in this patient?

    Ans: 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)

    1) what is the most probable diagnosis in this patient?

    Ans: Intra peritoneal haemorrhage.

    2) What was the cause of her death?

    Ans: Haemorrhage is the loss of blood components from the cardiovascular system. Hemorrhagic shock occurs when this blood loss leads to inadequate tissue oxygenation. This could've caused her death.

    3) Does her NSAID abuse have  something to do with her condition? How? 

    Ans: Non steroidal anti-inflammatory drugs (NSAIDs) are effective anti-inflammatory and analgesic agents and are among the most commonly used classes of medications worldwide. However, their use has been associated with potentially serious dose-dependent gastrointestinal (GI) complications such as upper GI bleeding. This could've caused haemorrhage in her.

    SECTION 5: (NEPHROLOGY)

    A)

    1. What could be the reason for his SOB ?

    Ans: Acute kidney failure may lead to a buildup of fluid in your lungs, which can cause shortness of breath.

    2. Why does he have intermittent episodes of drowsiness ?

    Ans: High levels of potassium in the blood – in severe cases, this can lead to muscle weakness, paralysis and heart rhythm problems. fluid in the lungs (pulmonary oedema) acidic blood (metabolic acidosis) – which can cause nausea, vomiting, drowsiness and breathlessness.

    3. Why did he complaint of fleshy mass like passage in his urine?

    Ans: It is probably due to the associated kidney infection.

    4. What are the complications of TURP that he may have had?

    Ans: 
    bleeding during the surgery, which requires a transfusion,
    improper fluid absorption,
    salt imbalances caused by fluid absorption issues,
    Impotence (erectile dysfunction),
    Incontinence,
    urethral stricture (narrowing) leading to a “split stream” of urine,
    post-TURP syndrome.

    B)

    1.Why is the child excessively hyperactive without much of social etiquettes ?

    Ans: Attention deficit hyperactivity disorder (ADHD) is a mental health disorder that can cause above-normal levels of hyperactive and impulsive behaviours. People with ADHD may also have trouble focusing their attention on a single task or sitting still for long periods of time. Both adults and children can have ADHD.

    2. Why doesn't the child have the excessive urge of urination at night time ?

    Ans: Overactive bladder (OAB) represents a syndrome characterised by a myriad of lower urinary tract symptoms (LUTS) including urinary urgency, with or without urgency incontinence, usually with frequency and nocturia, in the absence of infection or other identifiable causes. The true nature of OAB remains elusive – myogenic changes, neurologic changes, urothelial changes and afferent sensitization have been hypothesized to contribute to the symptomatology of OAB. Here it the urge of urination could be psychosomatic due to which at night time he doesn't have it.

    3. How would you want to manage the patient to relieve him of his symptoms?

    Ans: Principles of treatment are to reduce urinary incontinence by changing patient behaviour and teaching continence skills. As OBS is a symptom complex, 'no treatment' is an acceptable choice for some patients and caregivers.

    SECTION 6: (INFECTIOUS DISEASES)

    A)

    1) Which clinical history and physical findings are characteristic of tracheoesophageal fistula?

    Ans: Esophageal perforation is a rare disease, which can lead to significant morbidity and mortality. Its clinical presentation can mimic other disease processes and, therefore, it can be easily misdiagnosed. Candida infection of the oesophagus is an extremely rare cause of oesophageal perforation. Esophegeal perforation should be suspected on the basis of clinical presentation of sudden chest pain, fever, vomiting and subcutaneous emphysema. However, in children the presentation of oesophageal perforation can mimic many disease processes, such as pneumonia, lung abscess and sepsis, especially in patients with multiple medical problems. Therefore, a high index of suspicion is requiredIn this case report we present a patient with a spontaneous esophageal perforation that was associated with Candida infection and complicated by an esophagopleural fistula (EPF).

    2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it? 

    Ans: Immune reconstitution inflammatory syndrome (IRIS) is a condition seen in some cases of AIDS or immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse. Specific risk factors for the development of cryptococcal IRIS include shorter duration between cryptococcal diagnosis and ART initiation, low CD4 counts (<100 cells/μl), higher baseline plasma HIV RNA levels; and higher CSF cryptococcal antigen titres, opening pressures, WBC counts, and glucose levels. The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression. IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.

    SECTION 7: (INFECTIOUS DISEASE AND HEPATOLOGY)

    A)

    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 ?

    Ans:Yes it could be possible that drinking locally made alcohol may have caused liver abscesses in this patient as the locally made alcohol is sometimes contaminated with ethylene glycol or methylene or wood spirit which causes more damage to the liver than just alcohol. 

    2. What is the etiopathogenesis  of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)

    Ans: 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.

    3. Is liver abscess more common in right lobe ?

    Ans: The right hepatic lobe is affected more often than the left hepatic lobe by a factor of 2:1. Bilateral involvement is seen in 5% of cases. The predilection for the right hepatic lobe can be attributed to anatomic considerations. The right hepatic lobe receives blood from both the superior mesenteric and portal veins, whereas the left hepatic lobe receives inferior mesenteric and splenic drainage. It also contains a denser network of biliary canaliculi and, overall, accounts for more hepatic mass. 

    4.What are the indications for ultrasound guided aspiration of liver abscess ?

    Ans: 
    • complicated diverticular abscess
    • Crohn's disease related abscess
    • complicated appendicitis with appendicular abscess
    • tuboovarian abscess
    • post-surgical fluid collections
    • hepatic abscess (e.g. amoebic or post-operative)
    • renal abscess or retroperitoneal abscess
    • splenic abscess
    B)

    1) Cause of liver abscess in this patient ?

    Ans: liver abscess can develop from several different sources, including a blood infection, an abdominal infection, or an abdominal injury which has been become infected. The most common infecting bacteria include E coli, enterococcus, staphylococcus, and streptococcus. It could also be due to viral hepatitis.

    2) How do you approach this patient ?

    Ans: * INJECTION. ZOSTUM 1.5 gm IV BD (twice daily) 

     Zostum is a  combination of  drugs - SULBACTUM (pencillin) & CEFOPERAZONE(cephalosporin) [Antibiotic]: It is used here to treat if any bacterial cause ( since we can’t take the risk relying on only anti amoebic therapy) 

    * INJECTION. METROGYL 500mg IV TID ( thrice daily )

    Metrogyl has the drug called METRONIDAZOLE [Antibiotic]: For amoebic cause 

    * INJECTION. OPTINEURIN 1amp in 100 ml NS( Nor

    mal Saline) IV OD ( once daily)

    Optineurin is a multivitamin drug { A combination of B1,B2, B3, B5,B6, B12 } given here as a supplement 

    * TAB. ULTRACET 1/2 QID( four times a day)

    Ultracet is a combination of drugs - TRAMADOL(opiod analgesic) and ACETAMINOPHEN(analgesic and antipyretic) : Given for pain and fever 

    * TAB. DOLO 650 mg SOS (if needed) given for fever and pain. 

    3) Why do we treat here ; both amoebic and pyogenic liver abscess? 

    Ans: Considering the following factors: 
    1) Age of the patient (21) - young & gender- male ,
    2) Single abscess,
    3) Right lobe involvement, 
    The abscess is most likely to be AMOEBIC LIVER ABCESS. 
    Since we cannot take risk , we should however administer antibiotics also ( like in pyogenic liver abscess)

    4) Is there a way to confirm the definitive diagnosis in this patient?

    Ans: It can be done by aspiration of the abscess and culture of the fluid from it. this lets us know the causative organism.

    SECTION 8: (INFECTIOUS DISEASE)

    A)

    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?

    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
    The disease is localised to the frontal lobe of brain. Common causes of mucormycosis includes diabetes which the patient has.

    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?

    Ans: Mucormycosis is a serious infection and needs to be treated with prescription antifungal medicine, usually amphotericin B, posaconazole, or isavuconazole. These medicines are given through a vein (amphotericin B, posaconazole, isavuconazole) or by mouth (posaconazole, isavuconazole).

    3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time? 

    Ans: Mucormycosis, colloquially known as black fungus, is a serious fungal infection that was seen in far smaller numbers in India before Covid-19, too. But it is now affecting post-Covid patients in large numbers. As of May 22, the government has reported 8,848 cases of this fungal disease, which can lead to serious complications and has a high rate of mortality.Thus far, this surge has been attributed to the improper use of steroids to treat Covid-19 patients, coupled with poorly managed diabetes. But steroids in themselves are not the villains.

    SECTION 9:(Covid Infections)


    SECTION 10:

    May 23rd 2021

    At 12:00pm I got a case for the e log. It was a covid case. I read all the details of the patient and tried to understand what was going on.

    At 1:00pm I did research on COVID related e log case presentation.

    At 2:00 pm I called up the patient for a better and detailed history and to take the consent of the patient for the e-log.

    At 4:00pm I started with the proforma for the case and slowly filled the details accordingly.

    At 6:00pm I reviewed the blog and looked for any changes.

    At 7:00 pm I was done with the blog

    At 8:00 pm I read about covid and de novo diabetes.

    23rd may 2021

    At 12 pm I published the blog and shared it on the group.

    Personal experience:
    I was thrilled to be a part of this learning experience where in I could personally place myself in the shoes of a doctor and learn how to take a case properly. I keep learning new things through the blogs. This helps me a lot with integrating my knowledge practically. This real life experience shows us the hurdles in taking a case through phone. Nevertheless we always have a lot to learn. Thank you for this opportunity.









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