GENERAL MEDICINE ASSIGNMENT OF MAY 2021

Medicine assignment for the month of May 2021

Name:E.Siddhanth

I have been given the following cases to solve in an attempt to understand the topic of 'patient clinical data analysis 'to develop my competency in reading and comprehending clinical data including history ,clinical findings, investigation and diagnosis and come up with the treatment plan.This is the link of questions asked regarding the cases 
http://medicinedepartment.blogspot.com/021/05/online-blended-bimonthly-assignment.html

Below are my answers to the medicine assignment based on my comprehension of the cases.

                             1)PULMONOLOGY

        CASE-1:

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

Ans)Evolution of symptomatology
       1st episode of sob - 20 yr back
       2nd episode of sob - 12 yr back
       From then she has been having yearly episodes for the past 12 yrs 
       Diagnosed with diabetis - 8yrs back
       Anemia and  took iron injections  - 5yr ago
       Generalised weakness  - 1 month back 
       Diagnosed with hypertension  - 20 days back
       Pedal edema - 15 days back
       Facial puffiness- 15 yrs back
       Anatomical location of problem - lungs
       Primary etiology of patient- usage  of chulha since 20 yrs might be due to chronic usage 

2Q)What r the mechanism of action indication and efficacy over placebo of each of the phramacological and nonphramacological interventions  used for this patient?

Ans)1) Head end elevation :# MOA;
            improves oxygenation 
            decreases incidence VAP
            increases hemodynamic performance 
            increases end expiratory lung volume
            decreases incidence of aspiration 
            Indication: .head injury
            meningitis 
            pneumonia 
         2) oxygen inhalation to maintain spo2
         3) Bipap:non invasive method
          MOA :assist ventilation  by delivering positive expiratory and inspiratory pressure with                out need for ET incubation9

3Q) Cause for current acute excerbation ?

Ans) it could be due any infection


4Q) Could the ATT affected her symptoms if so how?

Ans)Yes ATT affected her symptoms
        Isoniazid and rifampcin -nephrotoxic - raised RFT was seen
 

                                2)NEUROLOGY

       CASE 1:

1Q) 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) Timespan of patients symptomology:
       2 years ago: DM type 2 and antibiotic treatment
       1 year ago: Seizures 
       4 months ago: seizures following cessation of alcohol
       10 days ago: General body pains
        9 days ago: Patient started talking to himself and laughing. Sudden onset. Decreased                food intake. Short term memory loss.
        15 May: Admittted.

       Primary etiology of the patient: GABA system and glutamate systems are affected in the brain by alcohol consumption.

        GABA system: GABA is an inhibitory neurotransmitter that helps to regulate brain function by rendering nerve cells less sensitive to further signaling. single doses of alcohol facilitate the inhibitory function of the GABA receptor, contributing to alcohol intoxicating effects. During withdrawal, brain GABA levels fall below normal and GABA activity declines. The combination of reduced brain GABA levels and GABAa receptor sensitivity may be contributed an adaptation to the presence of alcohol. In the absence of alcohol, the resulting decrease in inhibitory function may contribute to Symptoms of nervous system hyperactivity associated with both acute and protracted AW.

      Glutamate system: The major excitatory neurotransmitter in the brain is glutamate, which communicates with three major subtypes of glutamate receptors. Among these, the N-methyl-D-aspartate (NMDA) receptor plays a role in memory, learning, and the generation of seizures. Alcohol inhibits the excitatory function of the NMDA receptor in laboratory studies at concentrations associated with mild to moderate alcohol intoxication in humans. As with the increased inhibitory function of the GABAA receptor, the decreased excitatory function of the NMDA receptor is consistent with alcohol’s general sedative effect. Long-term alcohol administration produces an adaptive increase in the function of NMDA receptors. Acute AW activates glutamate systems. In turn, AW seizures are associated with increased NMDA receptor function. Persistent alterations in NMDA receptor function may potentiate the neurotoxic and seizure-inducing effects of increased glutamate release during withdrawal.
     
        Pathophysiology: 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. Neuronal death in the mammillary bodies and thalamus were implicated in multiple cases of Wernicke encephalopathy studied. Studies involving computed tomography (CT) and magnetic resonance imaging (MRI) of patients with Wernicke encephalopathy revealed lesions in the thalamus with dilated ventricles and volume loss in the mammillary bodies. The lesions are usually symmetrical in the midbrain, hypothalamus, and cerebellum.  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. The increase in levels of urea, creatinine, uric acid leads to uraemic encephalopathy. which causes asterixis .The deficiency of thiamine and increase in levels of toxins in the body due to renal disease is the primary etiology of the patient's problem.


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

Ans)i) Inj. Thiamine: Alcoholic are at high risk of B1 deficiency. Thiamine is used to form             thiamine pyrophosphate which is am essential co-factor used by several cellular enzymes.
        ii)Inj. Lorazepam: It enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cells.
        iii)Tab. Pregablin: Pregabalin has demonstrated anticonvulsant, analgesic, and anxiolytic properties in preclinical models. The drug's exact mechanism of action is unclear, but it may reduce excitatory neurotransmitter release by binding to the α2-δ protein subunit of voltage-gated calcium channels.
        iv)Inj. HAI S.C.: Hepatic Arterial Infusion (HAI) is a medical procedure that delivers chemotherapy directly to the liver. The procedure, mostly used in combination with systemic chemotherapy, plays a role in the treatment of liver metastases in patients with colorectal cancer.
    Syp Potchlor: Helps to maintain K+ balance in the body if the patient is hypokalemic.

3Q) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?

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

4Q) What is the reason for giving thiamine in this patient?

Ans) Due to excess alcohol consumption there will be deficiency of thiamine in the body which is compensated by giving thiamine in quantities.

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

Ans) Alcohol may cause changes in the functions of kidney and effects the ability to regulate the water electrolyte balance in the body. It also effects the hormones acing on kidney. This may be the reason for kidney damage in this patient.

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

Ans) Alcohol causes iron deficiency due to its effects on production of new blood cell organs. It also decreases the iron absorption from the intestine.

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

Ans) Yes, as the patient is diabetic, there is a chance of formation of ulcers. Due to low immune system the healin

        CASE 2:

1Q)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) 7 days back- Giddiness and 1 episode of vomiting 
           Asymptotic for 3 days
           4 days back-Giddiness (sudden continuous and gradually progressive)
           Bilateral hearing loss with aural fullness and tinnitus
           Vomitings 2-3 episodes per day(non projectile non bilious with food particles 
           Postural instability Unable to walk without support and is swaying with tendency to fall                  while walking 
           Anatomical localisation
           Cerebellum which is responsible for postural stability ,ocular movements and                                 vertigo(central)

usually results from damage to the part of your brain that controls muscle coordination (cerebellum). conditions can cause ataxia, including alcohol misuse, certain medication, stroke, tumor, cerebral palsy, brain degeneration and multiple sclerosis.

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

Ans) Vertin Tablet is employed to stop and treat a disorder of the internal ear referred to as disease. The symptoms include dizziness (vertigo), ringing within the ears (tinnitus), and loss of hearing, probably caused by fluid within the ear. This medicine helps relieve the symptoms by reducing the number of fluid.

Zofer anti-emetics' primarily utilized in the prevention of vomiting (being sick) and nausea (feeling sick) that typically occur after cancer chemotherapy, radiation treatment or surgery.
Ecosporin commonly used for the diagnosis or treatment of Headache, migraine, fever, pharyngitis, neuralgia
Atorvostatin
Statins are effective in reducing both first-ever and recurrent stroke, and this effect seems driven by the extent of LDL-C lowering

Clopidogrel could be a variety of medicine called an antiplatelet: it reduces the danger of blood clots forming within your vascular system or blood vessels.

Mvt Methylcobalamin is employed in cyanocobalamin deficiency.

Methylcobalamin could be a kind of vitamin B that restores its level within the body thereby helping in treating certain anemias and nerve problems.

3Q) Did the patients history of denovo HTN contribute to his current condition?                                    

Ans) Raised blood pressure (BP) is common after stroke but its causes, effects, and management still remain uncertain.It exists in more than three quarters of patients, of which about half have a history of hypertension [1], and it declines spontaneously in two-thirds of cases returning to prestroke levels over the first week. Its decrease usually occurs 4–10 days after stroke, but in a significant percentage of patients it falls by about 25–30% just within the first 24 hours; particularly when they are moved to a quiet room, they are allowed to rest and their bladder is  empty

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

Ans) Yes, Atrial fibrillation and alcohol Drinking excessive amounts of alcohol can trigger atrial fibrillation – a type of irregulaR  heartbeat. Atrial fibrillation increases your risk of stroke by five times, because it can cause blood clots to form in the heart. If these clots move up into the brain, it can lead to stroke.  

         CASE: 3

1Q) 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) Timespan of symptomology:
     10 years ago: She had a episode of paralysis of both upper and lower limb.
     8 months back: She developed pedal edema which is gradually progressing.
     7 months back: Blood infection.
     Since 6 days: Radiating pain along the upper limb which is dragging in nature.
     Since 5 days: palpitations which are sudden in onset and more during the night time.         Dyspnoea during palpitations.

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

Ans) Use if diuretics, laxatives, corticosteroids, mineralocorticosteroids excess acidosis, familial hypokalemia may be cause of recurrent hypokalemia in her.

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

Ans) Earliest change in ECG: Decreased T-wave amplitude, ST depression, T-wave inversion, prolonged PR interval.
       Severe cases: Ventricular fibrillation, rarely AV block.

       CASE-4:

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

Ans) 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 hypoperfusion, 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 haemorrhagic stroke. In childhood, post‐stroke seizures can occur as part of perinatal birth trauma.

2Q) 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) Scar formation due to previous episode of seizures will worsen the symptoms on subsequent attack of another episode of seizure.

       CASE-5:

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

Ans) The patient has minor unattended head injuries in the past 1 yr. Accoding to the CT scan, the patient has cerebral haemorrhage in the frontal lobe causing probably for the occurrence of Frontal love ataxia


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

Ans) The patient has minor unattended head injuries. During the course of time the minor hemorrhages if present should have been cured on their own. But the patient is a chronic alcholic. This might have hindered the process of healing or might have stopped the healing rendering it to grow further more into 13 mm sized hemorrhages occupying Frontal Parietal and Temporal lobes

      CASE-6:

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


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

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


2Q) What are warning signs of CVA?

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 or loss 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

3Q) What is the drug rationale in CVA?

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.

4Q) Does alcohol has any role in his attack?

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


5Q) Does his lipid profile has any role for his attack??

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.

      CASE-7:

1Q) What is myelopathy hand?

Ans) 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. 

2Q)  What is finger escape?

Ans) Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi. This commonly results from weakness of some of the ulnar nerve innervated intrinsic hand muscles -in particular the palmar interosseous muscle to the little finger- caused by damage to their nerve supply (denervation).

3Q) 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. The doctor carries out the test procedure by 
         1)holding the middle finger at the joint closest to the fingernail 
         2)“flicking” the nail of the person’s middle finger, using their other hand. If there is no movement in the index finger or thumb after this motion, the person has a negative Hoffman’s sign. If the index finger and thumb move, the person has a positive Hoffman’s sign.

         CASE-8:
   
1Q) What can be  the cause of her condition ?      

Ans) Recurrent seizures resolved secondary to cortical vein thrombosis with hemorrhagic venous infarction in right posterior temporal lobe with Iron Deficiency Anemia.

2Q) 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 or acquired
  •          Iron deficiency.
  •         Certain infections.
  •         Dehydration.
  •         Cancer.
  •         Obesity.
  •          Inflammatory bowel diseases.

  • 3Q) There was seizure free period in between but again sudden episode of GTCS why? Resolved spontaneously why?
  •  
  • Ans) It is due to administration of Antiepileptic drugs as the effect of drugs weans off the seizures appear again followed by administration of phenobarbitone leading to spontaneous resolution of the seizures.

  • 4Q) What drug was used in suspicion of cortical venous sinus thrombosis?

  • Ans) Anticoagulants are used for prevention of blood clots. Ex: Clexane which binds and potentiates anti thrombin to form complex and irreversibly inactivates factor XA.

                                3)CARDIOLOGY

         CASE-1:

1Q)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 heartmuscle 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
 

2Q)Why haven't we done pericardiocenetis in this pateint?  

Ans) It’s resolving : 2.07cms effusion at the time of admission -1.4mm at the time of discharge)
   DM type 2 (since 1month) 
   So, No need of pericardiocentis.


3Q)What are the risk factors for development of heart failure in the patient?

Ans): Risk factors:
                    High blood pressure.
                    Coronary artery disease
                    Diabetes.
                    Some diabetic and hypertensive medications. 
       

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

 Ans) Decreased venous return cause decreased cardiac output which results in hypotension.

  •            CASE-2:
  • 1Q) What are the possible causes for heart failure in this patient?

  • Ans) Patient was diagnosed with diabetes mellitus 30 years ago. Patient was diagnosed with hypertension 19 years ago. Patient is also a chronic alcoholic since 40 years. Above factors are the possible causes for heart failure in this patient.

  • 2Q) What is the reason for anaemia in this case?

  • Ans) He is deficit in iron, vitamin B12 and folic acid which may lead to anaemia in this case.

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

  • Ans) The formation of the bleb and non-healing ulcer may be due to DM, and also CKD is known to delay the healing of this ulcer.

  • 4Q) What is the reason for blebs and non healing ulcer in the legs of this patient?

  • Ans) Stage 1: Insulin resistance
  •        Stage 2: Prediabetes
  •        Stage 3: DM-2
  •        Stage 4 : Microvascular complications.

  •          CASE-3:
  • https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html

  • 1Q) 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) Timeline of symptomology: 
  •      10 years ago: Surgery for inguinal hernia
  •       Since 2-3 years: Facial puffiness on and off.
  •       1 year ago: Shortness of breath ( Grade-2), Hypertension.
  •       2 days ago: Grade-2 to Grade-4 progression of SOB, decreased urine and anuria.

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

  • Ans) Tab. Dytor: It antagonizes the effect of aldosterone, spirolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent K+ loss.
  •       Tab. Acitrom: Maintains the level of vitamin K required for blood clotting.
  •       Tab. Cardivas: Carvediol blocks the action of epinephrine on blood vessels and heart, thus lowering the heart rate, blood pressure.
  •       Tab. Digoxin: It inhibits the action of the myocardial Na-K ATPase pump, this increasing the force of contraction.
  •       Inj. HAI: Regulates the glucose metabolism.
  • 3Q) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient? 

  • Ans) Cardiorenal syndrome type-4.

  • 4Q) What are the risk factors for atherosclerosis in this patient.
  •  
  • Ans) Hypertension impairs the blood vessels ability to relax and may stimulate the growth of smooth muscle cells inside the arteries. All these changes can contribute to the artery clogging process known as atherosclerosis.

  • 5Q) Why was the patient asked to get those APTT, INR tests for review?
  • Ans) To ensure that the anticoagulant taken by the patient is producing the desired effect.

  •          CASE-4:
  • 1Q)  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) Timespan of symptomology:
  •        Since 12 years: DM and on medication
  •        Since 1 year: Heart burn like episodes which is relieved with medication.
  •        7 months ago: Diagnosed with pulmonary TB with full course of medication.
  •        Since 6 months: Hypertension and on medication.
  •        Since half and hour: Shortness of breath even at rest.
  •         Anatomical localization: Cardiovascular system
  •         Etiology: hypertension and diabetic etiology

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

  • Ans) Tab. MET XL: Contains Metoprolol. Metoprolol is a beta-1-adrenergic receptor inhibitor specific to cardiac cells with negligible effect on beta-2 receptors. This inhibition decreases cardiac output by producing negative chronotropic and inotropic effects without presenting activity towards membrane stabilization nor intrinsic sympathomimetics.

  • 3Q) 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: 
  • Lack of cardiac surgical support.
  • Critical left main coronary stenosis without collateral flow from a native vessel or previous bypass graft to the left anterior descending artery.
  • Coagulopathy.
  • Hypercoagulable states.
  • Diffusely diseased vessels without focal stenoses.

  • 4Q) 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?

  • Ans) If PCI is performed in a patient who doesn't need it may have complications like:
  •         Bleeding
  •         Blood vessel damage
  •         Arrhythmias
  •         Need for emergency coronary artery surgery.
  •      Research on overtesting and overtreatment may harm the patient by following ways:
  •         Overuse of X-rays and CT scan can lead to cancers

  •         CASE-5:
  • https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1

  • 1Q) 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) Timespan of symptomology:
  •        Hypertension and DM since long.
  •        3 days ago: Chest pain which is insidious in onset with gradual progression and dragging type.
  •        Morning: Giddiness and Profuse sweating.
  •        Anatomical localization: Blood vessels.
  • 2Q) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

  • Ans) Tab. Aspirin: Aspirin is non-selective and irreversibly inhibits both forms (but is weakly more selective for COX-1). It does so by acetylating the hydroxyl of a serine residue. Normally COX produces prostaglandins, most of which are pro-inflammatory, and thromboxanes, which promote clotting.
  •       Tab. Atorvast: 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.
  •       Tab. Clopibb: 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/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.
  •       Inj. HAI: Regulates glucose metabolism.
  •      Angioplasty: It is used to widen narrowed and obstructed arteries or veins, typically to treat arterial athersclerosis.

  • 3Q) Did the secondary PTCA do any good to the patient or was it unnecessary?

  • Ans) Reasons for a Percutaneous Transluminal Coronary Angioplasty (PTCA) PTCA is performed to restore coronary artery blood flow when the narrowed artery is in a location that can be reached in this manner. Not all coronary artery disease can be treated with PTCA. IN this patient PTCA is not necessary. Late PCTA leads to the increased risk of periprocedural complications, long-term bleeding, and stent thrombosis.

          4)GASTROENTEROLOGY(&PULMONOLOGY)

      CASE-1:


1Q) 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) Timespan of symptomology
          5 years ago: 1st episode of pain abdomen and vomiting
           1 year back: 5 to 6 episodes of pain abdomen and vomitings
          20 days back: Increased consumption of toddy intake
          Since 1 week: Pain abdomen and vomiting 
          Since 4 weeks: Fever, constipation and burning micturition
       Anatomical localization: Pancreas and left lung

    Etiology: The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes attributed to alcohol.

2Q) 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) i)Inj. Metrogyl: Metronidazole is of the nitroimidazole class. It inhibits nucleic acid synthesis by forming nitroso radicals, which disrupt the DNA of microbial cells
         ii)Inj. Meropenam: Meropenem is bactericidal except against Listeria monocytogenes, where it is bacteriostatic. It inhibits bacterial cell wall synthesis like other β-lactam antibiotics. In contrast to other beta-lactams, it is highly resistant to degradation by β-lactamases or cephalosporinases.
         iii)Inj. Amikacin: The primary mechanism of action of amikacin is the same as that for all aminoglycosides. It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and tRNA acceptor sites, interfering with bacterial growth'
    TOTAL PARENTAL NUTRITION
         iv)Inj. Octerotide: Octreotide suppresses secretion of growth hormone (GH), and in many cases suppresses insulin-like growth hormone-1 (IGF-1) (somatomedin C). Sandostatin works centrally at the site of the tumor and binds to somatostatin receptors to regulate GH secretion and cell growth.
        v)Inj. Pantop: The mechanism of action of pantoprazole is to inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion. 
        vi)Inj. Thiamine: Mechanism of Action: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiamine diphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
        vii)Inj. Tramadol: Tramadol is a centrally acting analgesic with a multimode of action. It acts on serotonergic and noradrenergic nociception, while its metabolite O-desmethyltramadol acts on the µ-opioid receptor. Its analgesic potency is claimed to be about one tenth that of morphine



      .CASE-2:

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

Ans) Pleural effusion might be the cause of patients dyspnea.
        Presence of pleural effusion is currently considered an indication of severe pancreatitis and not just a marker of the disease[24]. Pancreatic ascites and pleural effusion are rare complications of both chronic and acute pancreatitis, and are associated with a mortality rate of 20% to 30%.

2Q) Name possible reasons why the patient has developed a state of hyperglycemia.
 
Ans) Hyperglucagonemia secondary to stress could be the result of patient developing hyperglycemia.
       Elevated levels of catecholamines and cortisol.
 
3Q) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?

   Ans) Elevated liver enzymes are a sign that a person has an inflamed or a damaged liver. Many conditions may cause liver inflammation or damage. In this case the probable reason may be due to liver injury. Alanine aminotransferace (ALT) and Asparate aminotransferase (AST) are the specific markers for alcoholic fatty liver disease. Glutamyl transpeptidase (GGT) is another marker of liver injury, and this enzyme is elevated in people who consumes alcohol. Of all the enzyme markers GGT is the most sensitive biomarker of alcohol consumption.
 
4Q) What is the line of treatment in this patient?

Ans) IVF: 125 ml/hr
       Inj. PAN 40mg i.v.
       Inj Zofer 4mg i.v.
       Inj. Tramadol 1amp in 100ml i.v.
       Tab. Dolo 650mg
       GRBS charting 6th hourly
       BP charting 8th hourly.

  •        CASE-3:

  • 1Q) What is the most probable diagnosis in this patient?

  • Ans) Abdominal Hemorrhage may be the most probable diagnosis in this patient.

  • 2Q) What was the cause of her death?

  • Ans) Cause of her death may be due to complications of laparotomy surgery such as hemorrhage, infection, or damage to internl organs.

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

  • Ans) NSAIDS are known to cause drug induced hepatitis which may lead to cirrhosis.

                           5) NEPHROLOGY

CASE-1:
Ans) His sob was is due to Acidosis which was caused by Diuretics

2Q) Reason for Intermittent Episodes of drowsiness

Ans) Hyponatremia was the cause for his drowsiness

3Q)why did he complaint of fleshy mass like passage inurine

Ans) plenty of pus cells in his urine passage appeared as
fleshy mass like passage to him

4Q) What are the complications of TURP that he may have had

Ans) Difficulty micturition
Electrolyte imbalances
Infection

        CASE-2:
 https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html


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

Ans) Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, or excessive activity and impulsivity, which are otherwise not appropriate for a person's age
For a diagnosis, the symptoms have to be present for more than six months, and cause problems in at least two settings (such as school, home, work, or recreational activities).

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

Ans) Since the child doesn’t have excessive urge of urination at night but at day there might be a psychiatry related condition
1. Psychosomatic disorder
2. Undiagnosed anxiety disorder

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

Ans) bacterial kidney infection, the typical course of treatment is antibiotic and painkiller therapy.
If the cause is an overactive bladder, a medication known as an anticholinergic may be used. These prevent abnormal involuntary detrusor muscle contractions from occurring in the wall of the bladder

To treat attention deficit hyperactivity disorder:
For children 6 years of age and older, the recommendations include medication and behavior therapy together — parent training in behavior management for children up to age 12 and other types of behavior therapy and training for adolescents. Schools can be part of the treatment as well.

Methylphenidate A stimulant and a medication used to treat Attention Deficit Hyperactivity Disorder. It can make you feel very ‘up’, awake, excited, alert and energised, but they can also make you feel agitated and aggressive. They may also stop you from feeling hungry.

Amphetamine belongs to a class of drugs known as stimulants. It can help increase your ability to pay attention, stay focused on an activity, and control behavior problems. It may also help you to organize your tasks and improve listening skills.



                    7) Infectious disease and Hepatology:

       CASE-1:

1Q) 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 can cause as he is drinking toddy since 30years. Amoebic liver abscess (ALA) is the most common manifestation of invasive amoebiasis caused by Entamoeba histolytica (EH). Several studies from India have reported a strong link between consumption of toddy and the occurrences of ALA. Toddy is a local alcoholic beverage consisting of fermented palm juice.

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

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.

3Q) Is liver abscess more common in right lobe ?
  
Ans)yes right lobe is involved due to its moreblood supply

4Q)What are the indications for ultrasound guided aspiration of liver abscess 

Ans) Indications for USG guided aspiration of liver abscess

      CASE-2:

1Q) Cause of liver abcess in this patient ?

Ans):cause of liver abcess in this patient is ENTAMOEBA HISTOLYTICA

2Q) How do you approach this patient ?
   
Ans)APPROACH IN THE PATIENT OF AMOEBIC LIVER ABCESS

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

Ans)  Amoebic liver abscess: The first line treatment in uncomplicated amebic abscess should be amebicidial drugs. Metronidazole is the drug of choice and has replaced the use of emetine and chloroquine. Metronidazole is effective against both the intestinal and hepatic phase. 750 mg three times a day for 7–10 days is recommended.
           Payogenic liver abscess: Treatment usually consists of placing a tube through the skin into the liver to drain the abscess. Less often, surgery is needed. You will also receive antibiotics for about 4 to 6 weeks. Sometimes, antibiotics alone can cure the infection.

4Q) Is there a way to confirmthe definitive diagnosis in this patient?

Ans)1. Large abscess more than 6cms
         2. Left lobe abscess
         3.Caudate lobe abscess
         4. Abscess which is not responding to drugs\


8)INFECTIOUS DISEASES (MUCORMYCOSIS, OPHTHAMALOGY, ENT, NEUROLOGY)

    CASE-1:
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html

1Q) 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) Timespan of symptomology:
       3 years ago- diagnosed with hypertension
       21 days ago- received vaccination at local PHC which was followed by fever, chills, and rigors.
        18 days ago- complained of similar events and went to the the local hospital, it was not subsided upon taking medication(antipyretics).
    11 days ago - c/o Generalized weakness and facial puffiness and periorbital oedema. Patient was in a drowsy state.
        4 days ago- (a).    patient presented to casualty in altered state with facial puffiness and periorbital oedema and weakness of right upper limb and lower limb (b).    towards the evening patient periorbital oedema progressed (c).    serous discharge from the left eye that was blood tinged (d).    was diagnosed with diabetes mellitus.
2 days ago- died.

the fungus enters the sinuses from the environment and then the brain.

The patient was also diagnosed with acute infarct in the left frontal and temporal lobe. Mucormycosis is associated with the occurrence of CVA.

2Q) 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) Inj. Amphotericin- B: Amphotericin B is an example of a “polyene” type of antifungal. Polyenes bind to fungal ergosterol (the primary sterol in fungal cell membranes). This alters cell membrane permeability, and intracellular components leak from the cell. 
       Deoxycholate Amphotericine B: Amphotericin B deoxycholate belongs to the polyene class of antifungals. It is also known by the name conventional amphotericin B and has been used for the treatment of invasive fungal infections for more than 50 years.

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

Ans) High steroid usage during COVID 19 treatment causes high blood sugars and suppress the immune system. Due to high population in the state there are easy chances of containmant by the fungus Mucormycosis. 

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