General medicine assignment

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/2021/05/online-blended-bimonthly-assignment.html?m=1

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

1) PULMONOLOGY

1Q) https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html

1)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 

2)what are the mechanism of actions indications 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

3. Cause for current acute excerbation ?
Ans) it could be due any infection


4. 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

2Q)
A) https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

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) Type 2 DM - since 2 YRS
Seizures (2-3 eps) - 1month ago
Seizures -4months ago
Short term memory loss -9 days ago
Started talking - 9days ago
Started laughing -9 days ago
He was unable to lift himself off bed - since 9 days
Decreased food intake - since 9days
General body pains -1 day ago

Anatomical localisation :- brain (prefrontal cortex,hypothalamus & limbic system)

Primary etiology :- alcohol

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) 
RL & NS :- Electrolyte replenishment
Thiamine :- moa:- combines with ATP in liver , kidney & leucocytes produces thiamine diphosphate which axts as a coenzyme incarbohydrate metabolism in transketolation
Indication :- for low levels of thiamine. For digestive problems (alcoholics have thiamine deficiency)
Lorazepam:- moa :- lorazepam binds to benzodiazepine receptors on postsynaptic GABA-A lignd gated clorine channel neuron at several sites within the CNS. It Inhibits the effects of GABA which increases the conductance of chlorine ions into the xell
Indication :- anxiety disorfers with/ without depression symptoms
Pregabakin :- moa :- it may reduce excitatory neurotransmitter release by binding to the α2-δ protein subunit of voltage-gated calcium channels

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

Ans) Excessive drinking excites and irritates N.S
Body will be dependent on daily basis for alcohol
CNS cannot adapt with without alcohol
Cessation of alcohol leads to alcohol withdrawal symptoms.


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

Ans) Alcoholics have thiamine deficiency. As the patient decreased his food intake since 9days ge has been diagnosed as thiamine deficiency as thiamine is not produced in our body.
Thiamine is administered to the patient in order to keep the nervous system healthy

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

Ans) DEHYDRATION


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

Ans) kidney failure - as erythropoeitin is produced in kidney which plays a key role in the production of RBCs


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

Ans) yes, it has aggrevated thr foot ulcer formation due to anaemia caused by alcoholism

____________________

3)GASTROENTEROLOGY(&PULMONOLOGY)

      CASE-1:

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.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

          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:

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

 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:
• • https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
• 
  
• 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.

___________________

4) NEPHROLOGY

CASE-1:

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

1Q)what could be the cause for his SOB

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.

_____________

5)CARDIOLOGY

         CASE-1:

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

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:
• https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html. 
  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:
• https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.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:
•        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.

__________________

6) Infectious disease and Hepatology:

       CASE-1:

    https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html

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:

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

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\

___________________

7)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.