Medicine online assignment

May 31, 2021

Medicine online assignment

PULMONOLOGY

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 ?

A)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?

2Ans)~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

~ oxygen inhalation to maintain spo2

~Bipap:non invasive method

#MOA :assist ventilation by delivering positive expiratory and inspiratory pressure with out need for ET incubation

3) what could be the cause for acute exacerbation of symptoms?

A) - It could be due any infection

4.could the ATT affected her symptoms if so how?

A) Yes ATT could have affected her symptoms

Isoniazid and rifampcin -nephrotoxic - raised RFT was seen.

NEUROLOGY

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

A) seizures - 1yr ago and recently 4 mon back

* irrelevant talking - since 9 days

* decreased food intake- since 9 days

* short term memory loss - since 9 days

# ANATOMICAL LOCALIZATION-

Lesion in the brain

# primary etiology - 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?

A) Thiamine-for balancing Thiamine deficiency

Lorazepam- acts by binding to BZD receptors at post synaptic end ,and enhance the inhibitory effects of GABA .

Pregabalin- By binding to alpha 2 subunits ,it decreases the synaptic release of neurotransmitters thus reducing neuronal excitability.

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

A) Due to excessive Thiamine deficiency

Toxins accumulation due to renal disease

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

A) Chronic Alcoholism causes thiamine deficiency by impairing the absorption through intestine .

Thiamine acts as cofactor enzyme for carbohydrate metabolism.

Deficiency causes accumulation of products like lactate and pyruvate

This causes wernicke's encephalopathy.

Thiamine is given to treat the deficiency of it.

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

A) Alcohol reduces the function of kidneys,make them less able to filter blood.

It also affects the ability to regulate fluid and electrolytes in the kidney.

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

A) Alcohol affects the production of new blood cells from bone marrow

Alcohol decreases Iron absorption from intestine

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

A) As patient is chronic alcoholic,it weakens his immunity ,which predisposes to poor healing.

NEUROLOGY

1) What is the evolution of the symptomology 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 patients problem?

ANS. Timeline of the patient is as follows-

7 days back- Patient gave a history of giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting

4 days back- Patient consumed alcohol; He developed giddiness that was sudden onset, continuous and gradually progressive. It increased on standing and while walking.

H/O postural instability- falls while walking

Associated with bilateral hearing loss, aural fullness, presence of tinnitus

Associated vomiting- 2-3 episodes per day, non projectile, non bilious without food particles

Present day of admission- Slurring of speech, deviation of mouth that got resolved the same day

Anatomical location- There is a presence of an infarct in the inferior cerebellar hemisphere of the brain.

Etiology- Ataxia is the lack of muscle control or co-ordination of voluntary movements, such as walking or picking up objects. This is usually a result of damage to the cerebellum (part of the brain that controls muscle co-ordination)

Many conditions cause cerebellar ataxia- Head trauma, Alcohol abuse, certain medications eg. Barbituates, stroke, tumours, cerebral palsy, brain degeneration etc.

In this case, the patient has hypertension for which he has been prescribed medication that he has not taken. Stroke due to an infarct can be caused by blockade or bleeding in the brain due to which blood supply to the brain is decreased, depriving it of essential oxygen and nutrients. This process could’ve caused the infarct formation in the cerebellar region of the brain, thus causing cerebellar ataxia.

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

ANS.

A) Tab Vertin 8mg- This is betahistine, which is an anti- vertigo medication

MOA- It is a weak agonist on H1 receptors located on blood vessels of the inner ear. This leads to local vasodilation and increased vessel permeability. This can reverse the underlying problem.

Indications- Prescribed for balance disorders. In this case it is used due to patients history of giddiness and balance issues.

B) Tab Zofer 4mg- This is ondanseteron- It is an anti emetic

MOA- It is a 5H3 receptor antagonist on vagal afferents in the gut and they block receptors even in the CTZ and solitary tract nucleus.

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

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

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

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

D) Tab Atorvostatin 40mg- This is a statin

MOA- It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis. It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.

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

E) Clopidogrel 75mg- It is an antiplatelet medication

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

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

F) Thiamine- It is vitamin B1

It is naturally found in many foods in the human diet. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins.

Indications- Given to this patient mainly to prevent Wernickes encephalopathy- that can lead to confusion, ataxia and opthalmoplegia.

G) Tab MVT- This is methylcobalamin

Mainly given in this case for vitamin B12 deficiency.

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

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

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

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

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

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

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

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

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

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

A) Bilateral pedal edema

Palpitations

Pain along left upper limb

Chest pain

Difficulty in breathing

Anatomical localisation - heart

Primary etiology- hypokalemia

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

*pedal edema is the reason for recurrence of hypokalemia

Risk factors- age, female gender

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

A) Inversion of T wave

Q-T interval prolongation

ST segment elevation

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

A) *Yes,seizures after ischemic stroke-increase in intracellular Na+ and ca+2 causing depolarization ,glutamate exictability,hypoxia,hyperperfusion injury

- seizures after hemorrhagic ,blood products may cause irritation .

Late onset of seizures cause gliotic scarring,due to persistent neuronal excitability.

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?

*previously,simple partial seizures( in which there will be no loss of consciousness) have occurred

Recently ,GTCS( in which LOSS of consciousnes will be present) have occured.

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

A) Multiple falls during the past 1 year ,would have lead to head injury affecting cerebellar functions and manifesting as gait.

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

A) Head injury might be the cause of IC bleed.

Alcohol contributes to bleeding diathesis, chronic alcoholics have decreased concentration of coagulation factors produced by liver ,which predisposes them to haemorrhagic stroke.

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

A) As facial bones are close to cranium ,there might be chances of cranial injuries.

As zygomatic arch and mandibular process are very close to cranium ,this might play a role in his condition.

2.what are warning signs of cvA?

A) Difficulty in walking

Dizziness

Difficulty in speaking

Loss of balance and coordination

Blurred vision

3.what is the drug rationale in cvA?

A) Inj.Mannitol 100 ml/IV / TD : Due it's osmotic effect , decrease cerebral edema

Tab.Ecosprin 75 mg /OD : prevents stroke

Tab.Atorvas 40 mg : lowers cholesterol ( statin)

4. does alcohol has any role in his attack?

A) As patient met with any accident,there might be unnoticed cranial injury ,which resulted in his condition.

As the patient is occasionally alcoholic,I don't think this might play a role.

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

A) Increased HDL-cholesterol decreases the stroke risk.

Increased LDL cholesterol increases the stroke risk.

1)What is myelopathy hand ?

A) Loss of power of adduction and extension of the ulnar 2,3 fingers and and an inability to grip and release rapidly with these fingers.

2)What is finger escape ?

A) Involuntary abduction of little finger caused by unopposed action of the extensor digiti minimi.

It is also known as wartenbergs sign

3)What is Hoffman’s reflex?

A) It is an neurological examination done to examine the reflexes of upper extremities.

1) What can be the cause of her condition ?

A) Cortical vein thrombosis with haemorrhagic venous infarction might be the cause of her condition.

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

A) Infections -meningitis, mastoiditis etc...

Mechanical - head injury,lumbar puncture

Inflammatory - sarcoidosis

Dehydration

Drugs like ocps,steroids

Malignacy conditions

Nephrotic syndrome

Vasculitis etc....

Pregnancy

Myeloproliferative disorders

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

A) seizure free period was due to medical interventions ,sudden episode of seizure may be due to persistence of excitable foci of neurons ,which excite by abnormal firing.

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

A) Inj.clexane 0.4 ml/sc was used.

CARDIOLOGY

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

A) In heart failure with preserved ejection fraction,heart muscle contracts ,but the ventricles do not relax during ventricular filling

In heart failure with reduced ejection fraction,heart muscles doesnt pump the enough blood to meet the body demands.

2.Why haven't we done pericardiocenetis in thiscase?.What are the possible causes for heart failure in this patient?

3) what are the risk factors for the development of heart failure in this patient?

A) Excessive alcohol consumption , smoking , Hypertension might be the reason for anemia.

4)what could be the reason for hypotension in this patient?

A) Hypotension may be due to diastolic dysfunction (Left ventricular collapse)

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

A) patient has been diagnosed as having CKD stage 4 ,which has pathogenesis of sodium and H2O Retention , resulting in its overload,which eventually causes increased preload.

Patient is also a known case of Hypertension since 19 yrs.

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

A) As patient is diagnosed of having CKD stage 4, which involves damage to kidneys,and eventually low erythropoietin production,which reduces RBC count, manifesting as anaemia.

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

A) As Diabetes results in poor healing ,and patient is type 2 diabetic,this could be the reason for non healing ulcer.

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

A) patient is type 2 diabetic since 30 years.

For 26 years,he is under regular tablets

From last 4 years ,he is on insulin

Later ,Stage 4 dysglycemic based chronic disease with vascular complications and retinopathy.

A) Facial puffines - since 2 years

Shortness of breath Grade 2 - since 1 year

Shortness of breath Grade 2 ( on exertion) - 2 days back ,which progressed to,

Shortness of breath Grade 4 ( at rest)

Decreased urine output - since 2 days

Anaemia since morning

* Anatomical localisation is Atrium

* Primary etiology is - 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?

A) DOBUTAMINE

MOA: By acting on beta 1 adrengic receptors , increases cardiac contractility ,thus increasing cardiac output.

Indications:

Cardiogenic shock

Heart failure ( reversible)

DIGOXIN

MOA: acts by inhibiting Na+ K+ ATPase

Indications;

Atrial fibrillation

Atrial flutter

CARDIVAS

MOA: acts by relaxing blood vessels.

Indications;

Myocardial infarction

Chronic heart failure

CARVEDILOL

MOA: by inhibiting beta 2 receptors,and preventing response to sympathetic stimuls results in decreased heart rate and decreased contractility.

Indications;

High blood pressure

Congestive cardiac failure

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

A)In heart failure, decreased cardiac output ,leads to decreased effective volume,which further results in decreased Renal blood flow.

This activates the RAAS cascade mechanism,and inflammatory pathways set in leading to renal involvement.

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

A) Hypertension

Age ( 52 yrs)

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

A) As to keep a check on thrombosis.

A) Heart burn - since 1 year

Tuberculosis- since 7 months

Shortness of breat - 30 mins before coming to hospital

* Anatomical localisation- coronary artery

* Primary etiology - Hypertension, atherosclerosis

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

A) MET XL

MOA: acts by relaxing blood vessels.

Indications ;

Arrhythmias

Angina pectoris

3) What are the indications and contraindications for PCI?

A) Indications:

* Unstable Angina

* Stable Angina

* Acute ST segment elevation MI

Contraindications:

* Intolerance for oral antiplatelets

* High grade CKD

* Hyper coagualbality states

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

A) *PCI cause several complications like :

-Severe bleeding

-blood vessel damage

- allergic reactions to the used contrast dye

-arrythmias

TO Avoid these complications we dont do the pci in the patient who doesnot need it.

* Research on overtesting and over treatment is important to current health system:

It increase the economic burden on the health care system due to excess use of machinaries for investigations .

A) Chest pain - since 3 days

Giddiness and profuse sweating ( morning after admission)

Anatomical localisation - inferior wall of heart ( ventricle)

Primary etiology - Atherosclerosis

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

A) ASPIRIN

MOA: Cox 2 inhibitor ,by reducing prostaglandin production , reduces inflammation ,sweeling ,pain.

Indications;

Fever

Mild tooth ache,muscle ache ,common cold

ATORVAS

MOA: HMGCO A Reducatse inhibitor

Indications;

High cholesterol

Reduces risk of stroke

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

A) Does good to patient ,by opening blocked arteries.

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

A) Fluid loss in patient ,leads to decreased preload,and so shortness of breath occured ( deceased cardiac output)

By giving IV fluids , preload increases and thus cardiac output ,thus patient relives from shortness of breath.

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

A) to prevent abdominal distension

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

A) ceftriaxone is the treatment for UTI ,used for any bacterial infection.

GASTROENTEROLOGY AND PULMONOLOGY

A) pain abdomen ,vomitings - 5 yrs back

Recurrent episodes of pain abdomen and vomitings since 3 yrs

Pain abdomen and vomitings since 4 days

Constipation , burning micturation ,fever since 4 days

Decreased air entry on left side

Increased abdominal distension

Left sided pneumothorax

Anatomical localisation - pancreas ,lungs

Primary etiology- chronic alcohol consumption

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?

A) .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 releive pain

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

A) plueral effusion is causing patients dyspnea

Blockage of pancreatic duct ,or acute pancreatitis may cause plueral effusion.

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

A) May be due to abnormalities in insulin secretion ,

Decrease in glucose utilisation

Increase in counterregulatory hormones.

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

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

A) IV colloids and fluids to maintain IV volume

Analgesic- to relive pain

Nasogastric suction

Monitor BP ,pulse , urine output

Antibiotics

Laparotomy and debridement

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

A) Ruptured liver abscess

Intraperitoneal haematoma

Abdominal haemorrhage

2) What was the cause of her death?

A)) May be due to complications of lapratomy surgery ( as she died nxt day of surgery), includes infections,organ damage, bleeding.

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

A) NSAID induced renal dysfunction

. decreased glomerular perfusion

. decreased GFR

.hepatoxicity

.Renal failure

NEPHROLOGY AND UROLOGY

1. What could be the reason for his SOB ?

A) May be due to acidosis ,by usage of diuretics

2. Why does he have intermittent episodes of drowsiness ?

A) May be due to hyponatremia

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

A) pus cells in the urine

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

A) difficulty in micturation

Infection

Electrolyte imbalance

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

*there could be some Psychological problem underlying in the child like ADHD

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

* The history and examination suggest that there is no underlying urinary tract pathology for frequent urination(in which frequent urination and bedwetting are commom) in this chiild,,so it could be psychological or idioathic..

3. How would you want to manage the patient to relieve him of his symptoms?A)Because all his urine reports and everything came fine..

And also he doesn't have the complaint at night time

So it was suspected to be a psychological cause

And would need therapy and counselling

INFECTIOUS DISEASES

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

A) Cough on taking foods and liquids which was initially non productive then associated with sputum which is white in colour and non foul smelling.

Difficult in swallowing since 2 months with solids and liquids. Patient is on RT feeding.

History of weight loss and SOB

One episode of vomiting

Fever episodes

Physical finding:

Thinly built and malnourished

Respiratory system examination: Wheeze present in bilateral mammary areas.

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

A) chances of IRIS are less ,but if present can be treated by prednisolone and meloxicam

INFECTIOUS DISEASES AND HEPATOLOGY

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 ?

A) Yes ,alcohol might have predisposed to liver absess in this patient.As history suggests that patient is chronic alcoholic since 30 years.

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

A) Excessive consumption of alcohol ,leads to inflammatory pathways , initiated by various chemical toxins that are released during breakdown of alcohol.

This inflammation leads to liver function damage manifesting as abscess.

3. Is liver abscess more common in right lobe ?

A) yes, because of involvement of portal vein circulation.

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

A) Caudate lobe abscess.

Left lobe abscess

Abscess >6 cms

Abscess not responding to medical treatment.

1) Cause of liver abcess in this patient ?

A) Here ; the cause of liver abcess is :

* Amoebic liver abcess (ALA ) seen commonly in the tropics is predominantly confined to adult males, especially those who consume locally brewed alcohol, although intestinal amoebiasis occurs in all age groups and in both genders.

* It has been argued that socioeconomic factors and poor sanitary conditions are the primary culprits that casually link alcohol to ALA.

* However , there has emerged an abundance of data that implicates alcohol in a more causal role in facilitating the extraintestinal invasion of the infective protozoan and the subsequent development of ALA.

## Hence the consumption of locally made alcohol ( toddy ) is the most likely cause of Liver abcess in this patient.

2) How do you approach this patient?

A) Broad spectrum Antibiotics

Analgesics

Anti pyretic( Dolo)

Metronidazole ( anti amboiec agent)

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

A) * Considering the following factors:

1) Age and gender of patient: 21 years ( young ) and male.

2) Single abcess.

3) Right lobe involvement.

## The abcess is most likely AMOEBIC LIVER ABSCESS …

** But most of the patients with amoebic liver abcess have no bowel symptoms, examination of stool for ova and parasite and antigen testing is insensitive and insensitive and not recommended.

# And considering the risk factors associated with aspiration for pus culture:

1) Sometimes ; abcess is not accessible for aspiration if it is in posterior aspect or so.

2) Sometimes ; it has thin thinwall which may rupture if u aspirate.

3) Sometimes ; it is unliquefied.

## There how can u confirm whether it is pyogenic/ amoebic , so we treat them both empirically in clinical practice.

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

A) Blood cultures

Entamoeba serology.

Liver abscess aspirate for culture

INFECTIOUS DISEASES(mucormycosis,ophthal mology,ent)

A) 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

* Primary etiology- orbital mucormycosis

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?

A) Inj.liposomal Amphotericin - B

MOA: acts by binding to ergosterol in fungal cell membrane ,whick makes it leaky and ultimately death

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

A) Increased usage of steroids in patients which disturb the symbiosis between bacteria and fungi.

Increased usage of antibiotics ,

Repeated usage of same mask , without washing, which helps in fungal growth.

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