Online blended bimonthly assignment toward summative assessment for the month of May 2021

I HAVE BEEN GIVEN THE FOLLOWING CASES TO SOLVE IN AN ATTEMPT TO UNDERSTAND THE TOPIC OF PATIENT CLINCAL DATA ANALYSIS TO DEVELOP MY COMPETENCY IN READING AND COMPREHENDING CLINICAL DATA INCLUDING HISTORY,CLINICAL FINDINGS,INVESTIGATIONS AND DIAGNOSIS AND COME UP WITH A TREATMENT PLAN

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;

AT the month of january that year during which time she was working in a paddy field. For the next 8 years the patient has suffered from similar episodes of SOB every year each lasting aproximately 1 week For the past 12 years she has been having an yearly episodes now lasting around a month again around january. Until her latest episode the SOB was of grade II Her latest episode of shortness of breath started 30 days ago, her SOB was insidious in onset and gradual in progression. Initially the SOB occurred on exertion and was relieved upon rest. From 2 days ago she started having SOB even at rest (grade IV) Pedal edema since 15 days upto the level ankle and pitting type OTHER SYMPTOMS Facial puffiness since 15 days. She has drowsiness since 2 days She has decreased urine output for the past 2 days. ANATOMICAL LOCATION; LUNG ALVEOLI PRIMARY ETIOLOGY

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

A] Head end elevation

B] O2 inhalation to maintain SPO2 above 92%

C] Intermittent BiPAP for 2hrs

D] Inj. AUGUMENTIN 1.2gm IV BO

MECHANISM OF ACTION;

THIS BLOCKS THE ACTION OF 𝜷 -LACTAMASE

POTASSIUM CLAVULANTA CAN BE INCORPORATED WITH AMOXICILLIN TO FORM AUGUMENTIN

INDICATIONS;

1)lower respiratory tract infection

2)acute bacterial otitis media

3)sinusitis

4)skin and skin structure infections

5)urinary track infections

E] TAB. AZITHROMYCIN 500mg OD

mechanism of action;

Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit

INDICATIONS;

Azithromycin is an antibiotic. It's widely used to treat chest infections such as pneumonia, infections of the nose and throat such as sinus infection (sinusitis), skin infections, Lyme disease, and some sexually transmitted infections.

F]INJ.LASIX IV BO if SBP GREATER THAN 110 mmHg

mechanism of action;

Furosemide works by blocking the absorption of sodium, chloride, and water from the filtered fluid in the kidney tubules, causing a profound increase in the output of urine (diuresis). The onset of action after oral administration is within one hour, and the diuresis lasts about 6-8 hours

INDICATIONS;Furosemide is a type of medicine called a diuretic. It's used to treat high blood pressure, heart failure and oedema (a build up of fluid in the body). It's also sometimes used to help you pee when your kidneys aren't working properly. Diuretics are sometimes called "water pills/tablets" because they make you pee more.

G] TAB PANTOP 40mg PO OD

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. The covalent binding prevents acid secretion for up to 24 hours and longer.

INDICATIONS;

It is commonly used for the diagnosis or treatment of Gastro-esophageal reflux disease, Heartburn, Euophagus inflammation, Stomach ulcers. It has some side effects such as Loss of balance, Increased bone fractures, Skin itching, Diarrhea.

H] INJ. HYDROCORTISONE 100 mg

MECHANISM OF ACTION;

Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes

INDICATIONS;

Hydrocortisone is approved by the U.S. Food and Drug Administration as a prescription steroid medication that is indicated to treat inflammation, status asthmaticus, acute and chronic adrenal insufficiency, and as physiologic replacement in pediatric use.

I] IV NEB. with IPRAVENT, BUDECORT 6 hrly

J]TAB PULMOCLEAR 100 mg PO OD

MECHANISM OF ACTION;

They belong to the class of bronchodilators and mucolytics, respectively. Pulmoclear works by relaxing the airways and loosening the cough, thus making the expulsion of cough easy.

INDICATION;

Pulmoclear Tablet is used for relieving the symptoms of coughing, wheezing, congestion and blockage in the airways in a condition called chronic obstructive pulmonary disease (COPD

K] chest physiotherapy

Chest PT, or CPT expands the lungs, strengthens breathing muscles, and loosens and improves drainage of thick lung secretions. Chest PT helps treat such diseases as cystic fibrosis and COPD (chronic obstructive pulmonary disease).

L] GRBS 6 hrly

M] INJ. HAI SC ( 8 am- 2pm- 8pm) Temp, BP, PR, SPO2 monitoring I/O charting

N] INJ. THIAMINE 1 amp in 100 ml of NS )

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.

INDICATIONS;

Thiamine is taken for conditions related to low levels of thiamine, including beriberi and inflammation of the nerves (neuritis) associated with pellagra or pregnancy. Thiamine is also used for digestive problems including poor appetite, ulcerative colitis, and ongoing diarrhea

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

ANS; The most common cause of an exacerbation is infection in the lungs or airways (breathing tubes). This infection is often from a virus, but it may also be caused by bacteria or less common types of organisms

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

ans; RIFAMPICIN [DAILY OR INTERMITTENT] CAN CAUSES EDEMA BY IMMUNOALLERGIC MECHANISM EDEMA OF LOWER LIMB ARE A POTENTIAL SIGNAL IN PHARMACOVIGILANCE REQUERING MORE INVESTIGATION TO ARGUE WITH THE RELATION OF CAUSE AND EFFECT AND TO FIND RISK FACTOR TO MANAGE AND AVOID THESE EFFECT

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

ANS; RISK FACTORS

🡻

ACTIVATION OF RAS [RENIN ANGIOTENSIN-ALDOSTERON SYSTEM]

🡻

ELEVATED PLASMA ARGININE VASOPRESSIN

🡻

AGGREVATES ELECTROLYTE IMBALANCE

COMMON FACTORS;

1.RENAL INSUFFICIENCY

2.HYPOXIA

3.HYPERCAPNIA

4.RESPIRATORY ACIDOSIS

5.RIGHT SIDED HEART FAILURE WITH DEVELOPMENT OF

LOWER LIMB EDEMA

6.MALNOURISHED ETC.....

MOST COMMON ELECTROLYTE IS SODIUM ION DECREASES IN COPD

HYPOKALEMIA IS DEU TO TO INDEPENDENTLY OR COMBINED WITH HYPONATREMIA

LOWER LEVEL OF ELECTROLYTE LEADS TO ;

1) DECREASE OF pH

2) DECREASE OF paO2

3) DECREASE OF O2 SATURATION

4) INCREASE OF paCO2

NEUROLOGY

ans;

evolution of the symptomatology in this patient in terms of an event timeline;

, he had 2-3 episodes of seizures, one being 1 year ago and the most recent being 4 months ago. The most recent time, (4 months ago), he had developed seizures (most probably GTCS) following cessation of alcohol for 24 hours, which was associated with restlessness, sweating, and tremors. Following this episode, he started drinking again.

He was unable to lift himself off the bed and move around, and had to be assisted. It was associated with a decrease in food intake since 9 days

He also had short term memory loss since 9 days

. the primary etiology of the patient's problem

ALOCHOL INTAKE

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

ans;

1. IVF NS and RL @150ml/hr

mechanism of action;

Sodium Chloride is source of water and electrolytes. It is capable of inducing diuresis depending on the clinical condition of the patient. It is a crystalloid given intravenously in case of shock, dehydration, and diarrhoea to increase the plasma volume.

indication;

The following are primary indications for the use of normal saline infusion that have been approved by the FDA: Extracellular fluid replacement (e.g., dehydration, hypovolemia, hemorrhage, sepsis) Treatment of metabolic alkalosis in the presence of fluid loss. Mild sodium depletion

2. Inj. 1amp THIAMINE in 100ml NS, TID

Thiamine MOA

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.

Indications and Usage

Thiamine hydrochloride injection should be used where rapid restoration of thiamine is necessary, as in Wernicke's encephalopathy, infantile beriberi with acute collapse, cardiovascular disease due to thiamine deficiency, or neuritis of pregnancy if vomiting is severe.tion;

3. Inj. Lorazepam

mechanism of action;

Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system (CNS). It enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell

indication;

ATIVAN Injection is indicated in adult patients for preanesthetic medication, producing sedation (sleepiness or drowsiness), relief of anxiety, and a decreased ability to recall events related to the day of surgery.

4. T. Pregabalin 75mg/PO/ BD

MECHANISM OF ACTION;

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

INDICATION;

Pregabalin is indicated for the management of neuropathic pain associated with diabetic peripheral neuropathy, postherpetic neuralgia, fibromyalgia, neuropathic pain associated with spinal cord injury, and as adjunctive therapy for the treatment of partial-onset seizures in patients 1 month of age and older

5. Inj. HAI S.C.- premeal

6. GRBS 6th hourly, premeal: 8am, 2pm, 8pm,2am

7. Lactulose 30ml/PO/BD

MECHANISM OF ACTION;

Lactulose is used in preventing and treating clinical portal-systemic encephalopathy. Its chief mechanism of action is by decreasing the intestinal production and absorption of ammonia. It has also gained popularity as a potential therapeutic agent for the management of subacute clinical encephalopathy

INDICATION;Lactulose is a prescription drug used by mouth or rectally to treat or prevent complications of liver disease (hepatic encephalopathy). It does not cure the problem, but may help to improve mental status. Lactulose is a colonic acidifier that works by decreasing the amount of ammonia in the blood.

8. Inj 2 ampoule KCl (40mEq) in 10 NS over 4 hours

MECHANISM OF ACTION;

Potassium ions participate in a number of essential physiological processes, including the maintenance of intracellular tonicity; the transmission of nerve impulses; the contraction of cardiac, skeletal, and smooth muscle; and the maintenance of normal renal function.

INDICATIONS;

Potassium chloride is used to prevent or to treat low blood levels of potassium (hypokalemia). Potassium levels can be low as a result of a disease or from taking certain medicines, or after a prolonged illness with diarrhea or vomiting.

9. Syp Potchlor 10ml in one glass water/PO/BD

Mode of Action ;It helps to maintain potassium balance in the body by restoring normal potassium levels in patients with a low level of potassium...

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

ANS;. Altered sensorium due to alcohol withdrawal syndrome,DECREASE LEVEL OF THIAMINE LEADS TO THE SYMPTOMS

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

ANS;

Thiamine is a key vitamin in the maintenance of membrane integrity and osmotic gradients across cell membranes and is stored in body tissues predominantly as thiamine diphosphate (TDP). TDP participates in energy production as an essential cofactor for several enzymes in the TCA cycle and pentose phosphate pathways

Thiamine deficiency causes depletion of intracellular TDP, leading to a decreased activity of the TCA cycle and pentose phosphate pathways. Consequently, cellular energy (ATP) depletion and reduction of DNA/RNA and NADPH synthesis ensues, which results in low resistance to oxidative stress. Moreover, there is an accumulation of toxic intermediate metabolic products such as lactate, alanine and glutamate, reduced cellular pH in cells, and disruption of the homeostasis of cellular electrolytes, which results in cytotoxic edema.

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

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

ANS;

b]neurology

ANS;

the evolution of the symptomatology in this patient in terms of an event timeline

- history of giddiness

This was associated with 1 episode of vomiting on the same day.

from the bed and while walking.

- This was associated with Bilateral Hearing loss, aural fullness and presence of tinnitus.

- He has associated vomiting- 2-3 episodes per day, non projectile, non bilious containing food particles.

- Patient has H/o postural instability- he is unable to walk without presence of supports, swaying is present and he has tendency to fall while walking

PRIMARY ETIOLOGY;

obstruction of the posterior inferior cerebellar artery (PICA, also the most frequent location for a cerebellar infarct) leads to a headache and less commonly vomiting, vertigo, horizontal ipsilateral nystagmus, and truncal ataxia. Anterior inferior cerebellar artery (AICA) territory infarction more often leads to dysmetria, Horner's syndrome, unilateral hearing loss and ipsilateral facial paralysis or anesthesia with contralateral hemibody sensory loss of pain and temperature. Finally, obstruction of the superior cerebellar artery (SCA, located most rostral) tends to produce more ataxia, dysarthria, and nystagmus, with less vertigo, headache, and vomiting. However, presentations can often be atypical or overlap, in particular for hemorrhagic infarcts.

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;

Tab Veratin 8 mg PO TID

MECHANISM OF ACTION;

Betahistine is one of the few drugs known which is said to improve the microcirculation of the inner ear. It works as a histamine analogue through 2 modes of action(1) agonist of H1 receptors and (2) antagonist of H3 receptors. It has a weak effect on H1 receptors but strong effect on H3 receptors.

INDICATIONS;

Vertin Tablet is used to prevent and treat a disorder of the inner ear known as Ménière's disease. The symptoms include dizziness (vertigo), ringing in the ears (tinnitus), and loss of hearing, probably caused by fluid in the ear.

Inj Zofer 4 mg IV/TID

Mode of Action of Zofer

Zofer Injection works by inhibiting the action of a chemical substance known as serotonin. Serotonin is responsible for inducing nausea and vomiting. Ondansetron binds to a receptor known as 5-HT₃, thus inhibits the binding of serotonin to it and prevents vomiting and nausea.

Tab Ecosprin 75 mg PO/OD

MECHANISM OF ACTION;

Ecosprin is an antiplatelet medicine. It works by inhibiting the action of an enzyme, which makes platelets aggregate together to form a blood clot

INDICATION;

This tablet is also used to prevent heart attacks, stroke and heart-related chest pain (angina)

Tab Atorvostatin 40 mg PO/HS

Mechanism of Action

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

INDICATIONS;

Reduce the risk of non-fatal myocardial infarction.
Reduce the risk of fatal and non-fatal stroke.
Reduce the risk for revascularization procedures.
Reduce the risk of hospitalization for CHF.
Reduce the risk of angina.

BP monitoring- 4rth hourly

Tab Clopidogrel 75 mg PO/OD

MECHANISM OF ACTION;

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.

INDICATIONS;

FDA-approved indications for clopidogrel include: Use during a percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) and stable ischemic heart disease. Primary prevention of thromboembolism atrial fibrillation

Inj Thiamine 1 AMP in 100 ml NSPO/BD

Tab MVT PO/OD

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

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

YES THE PATIENT HAS HISTORY OF CHRONIC ALOCHOLISM AND IS SUSCEPTIBLE TO ISCHEAMIC TYPE OF STROKE

2C]

QUESTIONS

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) *Evolution of symptoms :patient was normal 8 months back then developed b/l pedal edema which gradually progressed.

Aggerevated in sitting and standing position, relived on taking medication

*Palpitations :since 5days, sudden in onset which is more during night

Aggerevated by lifting heavy weights, speaking continuously

*Dyspnoea during palpitations (NYHA-3) since 5 days

*pain:since 6days, radiating along left upper limb, more during palpitations and relived on medication.

Chest pain associated with chest heaviness since 5 days

Etiological agent :

*By localization, electrolyte imbalance (hypokalemia) causing the her manifestations like palpitations, chest heaviness, generalised body weak ness

*radiating pain along her left upper limb due to cervical spondylosis

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

A) Reason: recurrent hypokalemic periodic paralysis

Current risk factor:due to use of diuretics

Other risk factors

A) Abnormal loses:

Medications-diuretics, laxatives, enema, corticosteriods

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

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

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

D) psuedohypokalemia:delayed sample analysis, significant leukocytosis

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

A) changes seen in ECG :

Earliest change :decreased T-wave amplitude, ST depression, Twave - and inversion or flat;prolonged PR interval;presence of Uwaves

In Severe cases :ventricular fibrillation, rarely AV block

Symptoms of hypokalemia :

Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium.

2D)

QUESTIONS:

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

ANS;

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

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

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

2. In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?

ANS;

Initially the patient might have had Simple partial seizures (no loss of consciousness) and might have progressed to Generalised Tonic Clonic seizures (loss of consciousness)

Questions: 1) 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

2) 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

Questions

1.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

2.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

3.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.

4. 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

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?

Initially the patient might have had Simple partial seizures (no loss of consciousness) and might have progressed to Generalised Tonic Clonic seizures (loss of consciousness)

E) Link to patient details:

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

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

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

F) Link to patient details:

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

Questions

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

2.What are warning signs of CVA?

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

3.What is the drug rationale in CVA?

Ecospirin

For the prevention of heart attack, stroke, heart conditions such as stable or unstable angina (chest pain) due to a blood clot.

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.

4. Does alcohol has any role in his attack?

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

5.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.

2G]

QUESTIONS

a)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.

b)what is finger escape?

ANS;

Finger escape

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 finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign".

c)what is Hoffman's sign?

ANS;

Hoffman's sign or reflex is a test used 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

2H]

questions

1) What can be the cause of her condition ?

ANS;

According to MRI cortical vein thrombosis might be the cause of her seizures.

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

ANS;

Infections:

Meningitis, otitis,mastoiditis

Prothrombotic states:

Pregnancy, puerperium,antithrombin deficiency proteinc and protein s deficiency,Hormone replacement therapy.

Mechanical:

Head trauma,lumbar puncture

Inflammatory:

SLE,sarcoidosis,Inflammatory bowel disease.

Malignancy.

Dehydration

Nephrotic syndrome

Drugs:

Oral contraceptives,steroids,Inhibitors of angiogenesis

Chemotherapy:Cyclosporine and l asparginase

Hematological:

Myeloproliferative Malignancies

Primary and secondary polycythemia

Intracranial :

Dural fistula,

venous anomalies

Vasculitis:

Behcets disease wegeners granulomatosis

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

ANS;

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

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

ANS;

Anticoagulants are used for the prevention of harmful blood clots.

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

CARDIOLOGY;

3A]

QUESTIONS;

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

Ans:Preserved ejection fraction (HFpEF) – also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax).

Reduced ejection fraction (HFrEF) – also referred to as systolic heart failure

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

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

Ans: Pericardiocentesis is not done here Because the effusion was self healing ,It reduced from 2.4cm to 1.9 cm.

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

Ans: risk factors for development of heart faliure in this patent

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

high blood pressure

Smoking

Diabetes

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

wosening of pericardial effusion leaing to cardiac tamponade.

4.What could be the cause for hypotension in this

Ans : visceral pericardium may have thickened which is restricting the heart to expand causing hypotension

(May be secondary to TB)

3B]

QUESTIONS;

1QUESTION: What are the possible causes for heart failure in this patient?
ANS;
the patient has various comorbidities which could have led to a heart failure
1. The patient was diagnosed with type 2 diabetes mellitus 30 years ago and has been taking human mixtrad insulin daily and was also diagnosed with diabetic triopathy indicating uncontrolled diabetes which is major risk factor for heart failure.
2. The patient was also diagnosed with hypertension 19 yrs. ago which is also a risk factor for heart failure.
3. He is a chronic alcoholic since 40 years which is a risk factor towards heart failure.
The findings in this article provide longitudinal evidence that moderate and heavy alcohol consumption are associated with decreased LVEF and trend towards a higher risk of incident LV systolic dysfunction, compared to light drinkers.
4. The patient has elevated creatinine and AST/ALT ratios is >2 and was diagnosed with chronic kidney disease stage IV. CKD is also one of the risk factors for heart failure.

2 QUESTION: what is the reason for anaemia in this case?
ANS;
The patient has normocytic normochromic anaemia. it could be anaemia of a chronic disease as the patient is diagnosed with CKD stage IV.
Chronic kidney disease results in decreased production of erythropoietin which in turn decreases the production of red blood cells from the bone marrow.
Patient’s with anaemia and CKD also tend to have deficiency in nutrients like iron, vitamin B12 and folic acid essential in making healthy red blood cells

3 QUESTION: What is the reason for blebs and non-healing ulcer in the legs of this patient?
ANS;
The most common cause for blebs and non-healing ulcer in this patient is diabetes mellitus. CKD is also known to cause delay in healing of wounds along with poorly controlled diabetes. Anaemia can also slow down the process of healing due to low oxygen levels.

4 QUESTION: What sequence of stages of diabetes has been noted in this patient?
ANS;
There are 4 stages in type 2 diabetes- insulin resistance, prediabetes, type 2 diabetes and type 2 diabetes and vascular complications, including retinopathy, nephropathy or neuropathy and, or, related microvascular events.
The patient is diagnosed with diabetic triopathy exhibiting sequence of neuropathy, retinopathy and nephropathy
The patient has been diagnosed with diabetic retinopathy, CKD stage IV and shows signs of diabetic neuropathy such as numbness.

3C]

QUESTIONS;

Ans: Facial puffiness ( since 2 to 3 yrs)

Sob grade 2( 1yr ago)

Sob grade 2( 2days back again)

Sob grade 4

Decreased urine output ( since 2 days)

Anuria (since morning)

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: Dobutamine MOA: acts on beta 1 receptor

Beta1 ionotropic effect → increases heart contractility → increases cardiac output

Indications are cardiogenic shock , Reversible heart failure

Digoxin MOA: Digoxin has two principal mechanisms of action which are selectively employed depending on the indication: Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump, an enzyme that controls the movement of ions into the heart.

Indications are Atrial fibrillation ,atrial flutter,

Heart failure,Abortion

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

Ans: Pathogenesis of cardiorenal syndrome is described below in the picture:

Stage 3 cardio renal syndrome is seen in this patient

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

Ans: Hypertension is the risk factor for atherosclerosis in this patient.

3D]

QUESTIONS

Answer

Etiology- female sex age-67 years diabetes since 12 years hypertension since 6 months.

pathophysiology- MI occurs due to decreased myocardial oxygen supply due to severe coronary artery narrowing or acute atherosclerotic plaque rupture/erosion and superimposed thrombus formation.

Due to decrease in myocardial oxygen supply there is heartburn Due to heart muscle damage there is decrease in the pump function of left ventricle causing decrease in pulmonary circulation which leads to shortness of breathe (dyspnea). It occurs due to partial occlusion of a major vessel or a complete occlusion of a minor vessel (subendocardial).

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

Answer

Analgesic- To relieve distress , to lower adrenergic driveand therby reduce vascular resistance,BP, infarct size and susceptibility to ventricular arrhythmias Antiplatelet therapy- aspirin+ticagrelor aspirin daily improves survival, reduces risk of mortality, MI, stroke ticagrelor reduces recurrent ischaemic events. Glycoprotein II b /III a receptor antagonists- tirofiban , abciximab block the final common pathway of platelet aggregation and are potent inhibitors of platelet-rich thrombus formation Anticoagulants- heparin reduces the risk of thromboembolic complications and prevents re-infarction.

Angioplasty and coronary artery bypass surgery are the non pharmacological interventions , its outcome is determined by the number of diseased vessels, severity of cardiac dysfunction and the number of concomitant diseases as much as age itself.

3) What are the indications and contraindications for PCI?

Answer

Indications- ST-elevation myocardial infraction ( STEMI ) atypical chest pain, stable angina,

unstable angina, positive stress test Non ST-elevation myocardial infarction

Contraindications- Lack of cardiac support Coagulopathy Hypercoagulable states Critical left main coronary stenosis without collateral flow from a native vessel or previous bypass graft to the left anterior descending artery

Diffusely diseased vessel without focal stenosis A single diseased vessel providing all perfusion to the myocardium Total occlusion of a coronary artery Stenosis <50%

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?

Answer

Complications- Acute; occlusion of target vessels or a side branch by thrombus or a loose flap of intima (coronary artery dissection), and consequent myocardial damage Long term complication; re-stenosis

3E]

QUESTIONS

Ans;Evolution of symptomatology:

Uncontrolled DM2 since 8 years

3 days back Mild chest pain dragging type and retrosternal pain(radiated)

Anatomical localisation: Inferior wall of heart

Primary etiology: Diabetes type 2 (uncontrolled)

high blood glucose from diabetes can damage your blood vessels and the nerves that control your heart and blood vessels

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;TAB. ASPIRIN 325 mg PO/STAT

Mechanism of action: The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins.

TAB ATORVAS 80mg PO/STAT

Mechanism of action: 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 300mg PO/STAT

Mechanism of action: The active metabolite of clopidogrelselectively 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 6U/IV STAT

VITAL MONITORING.

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

Ans; Repeat PTCA provides a valuable, safe and cost-effective way of management for recurrence of stenosis after initially successful angioplasty. It increased the percent of patients with documented long-term success of angioplasty

Over testing and over treatment can raise a person’s risk of cardiovascular death by as much as four times.

3F]

QUESTIONS

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

ANS;

Because of the fluid loss occurred to the patient

there is decreased preload- so, SOB occurred due to decreased CO

IV fluids administered- there is increased preload- SOB decreased due to better of cardiac output.

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

ANS;

Torsemide used to relieve abdominal distension.

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

ANS;

IT IS THE TREATMENT FOR UTI

Rationale- Used for any bacterial infection.

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

And: Because of Thrombosis and to check on development of thrombosis, this patient is asked to get APTT,INR tests for review.

GASTROENTROLOGY AND PULMONOLOGY;

4A]

QUESTIONS;

Evolution of symptomatology

H5 years back-1st episode of pain abdomen and vomitings

Stopped taking alcohol for 3 years

1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again

20 days back increased consumption of toddy intake

Since 1 week pain abdomen and vomiting

Since 4 days fever constipation and burning micturition

Anatomical localisation: Pancreas and left lung

Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis

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?

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

4B]

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

ANS]

the patient has various comorbidities which could have led to a heart failure

1. The patient was diagnosed with type 2 diabetes mellitus 30 years ago and has been taking human mixtrad insulin daily and was also diagnosed with diabetic triopathy indicating uncontrolled diabetes which is major risk factor for heart failure

2. The patient was also diagnosed with hypertension 19 yrs. ago which is also a risk factor for heart failure

3. He is a chronic alcoholic since 40 years which is a risk factor towards heart failure

The findings in this article provide longitudinal evidence that moderate and heavy alcohol consumption are associated with decreased LVEF and trend towards a higher risk of incident LV systolic dysfunction, compared to light drinkers.

4. The patient has elevated creatinine and AST/ALT ratios is >2 and was diagnosed with chronic kidney disease stage IV. CKD is also one of the risk factors for heart failure

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

ANS]

The patient has normocytic normochromic anaemia. it could be anaemia of a chronic disease as the patient is diagnosed with CKD stage IV.

Chronic kidney disease results in decreased production of erythropoietin which in turn decreases the production of red blood cells from the bone marrow.

Patient’s with anaemia and CKD also tend to have deficiency in nutrients like iron, vitamin B12 and folic acid essential in making healthy red blood cells

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

ANS]

The most common cause for blebs and non-healing ulcer in this patient is diabetes mellitus. CKD is also known to cause delay in healing of wounds along with poorly controlled diabetes. Anaemia can also slow down the process of healing due to low oxygen levels.

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

ANS]

There are 4 stages in type 2 diabetes- insulin resistance, prediabetes, type 2 diabetes and type 2 diabetes and vascular complications, including retinopathy, nephropathy or neuropathy and, or, related microvascular events.

The patient is diagnosed with diabetic triopathy exhibiting sequence of neuropathy, retinopathy and nephropathy

The patient has been diagnosed with diabetic retinopathy, CKD stage IV and shows signs of diabetic neuropathy such as numbness

4C]

QUESTION

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

1ans* The exact pathophysiology of Attention Deficit Hyperactivity Disorder (ADHD) is not clear. With this said, several mechanisms have been proposed as factors associated with the condition. These include abnormalities in the functioning of neurotransmitters, brain structure and cognitive function.

* Due to the efficacy of medications such as psychostimulants and noradrenergic tricyclics in the treatment of ADHD, neurotransmitters such as dopamine and noradrenaline have been suggested as key players in the pathophysiology of ADHD.

* Depressed dopamine activity has been associated with the condition

2) What is the most probable diagnosis in this patient?

àDifferential Diagnosis:

· Ruptured Liver Abscess.

· Organized collection secondary to Hollow viscous Perforation.

· Organized Intraperitoneal Hematoma.

· Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.

· Grade 3 RPD of right Kidney

àThe most probably diagnosis is there is abdominal hemorrhage. This will give reasoning to the abdominal distention, and the blood which is aspirated.

2) What was the cause of her death?

ANS]

àAfter leaving the hospital, the patient went to Hyderabad and underwent an emergency laparotomy surgery. The patient passed away the next day. Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding), infection, or damage to internal organs.

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

ans]

àNSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure. Chronic NSAIDs use has also been related to hepatotoxicity. While the major adverse effects of NSAIDs such as gastrointestinal mucosa injury are well known, NSAIDs have also been associated with hepatic side effects ranging from asymptomatic elevations in serum aminotransferase levels and hepatitis with jaundice to fulminant liver failure and death

NEPHROLOGY

5A]

QUESTION;

1.what could be the cause for his SOB

Ans- His sob was is due to Acidosis which was caused by Diuretics

2. Reason for Intermittent Episodes of drowsiness

Ans-Hyponatremia was the cause for his drowsiness

3.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

4. What are the complicat ions of TURP that he may have had

Ans-

Difficulty micturition

Electrolyte imbalances

Infection

5B]

QUESTIONS;

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

* Depressed dopamine activity has been associated with the condition,

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

2ans:the child doesn’t have the excessive urge of urination at night time because ADHD is a physcosomatic disorder

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

TREATMENT

INFECTIOUS DISEASE

QUESTIONS;

QUESTION 1:

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

ANSWER:

Cough since 2 months on taking food and liquids

•difficulty in swallowing since 2 month . It was initially difficult only with solids but then followed by liquids also.

•laryngeal crepitus- positive

These favour for tracheo esophageal.fistula

QUESTION 2:

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

ANSWER:

Immune reconstitution inflammatory syndrome (IRIS) represents the worsening of a recognized (paradoxical IRIS) or unrecognized (unmasking IRIS) pre-existing infection in the setting of improved immunologic function.

The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression. IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.

Aggressive efforts should be made to detect asymptomatic mycobacterial or cryptococcal disease prior to the initiation of ART, especially in areas endemic for these pathogens and with CD4 T-cell counts less than 100 cells/uL.

Two prospective randomized studies are evaluating prednisone and meloxicam for the prevention of paradoxical TB IRIS.

7]INFECTIOUS DISEASE AND HEPATOLOGY

QUESTION

Liver abscess

1Q)do u think drinking locally made alcohol cause liver abscess in this patient due to predisposing factors present in it ? What could be the cause in this patient?

1ans- yes, it could be due to intake of contaminated toddy

2Q)what is the etiopathogenesis of liver abscess in a chronic alcoholic patient?(since 30 yrs - 1 bottle/day)

2ans - 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 is more common in right lobe?

3ans-yes right lobe is involved due to its moreblood supply

4Q) what r the indications for usg guided aspiration of liver abscess

4ans- Indications for USG guided aspiration of liver abscess

1. Large abscess more than 6cms

7B]

QUESTIONS;

1) Cause of liver abcess in this patient ?

1ans:cause of liver abcess in this patient is ENTAMOEBA HISTOLYTICA

2) How do you approach this patient ?

2 ans:APPROACH IN THE PATIENT OF AMOEBIC LIVER ABCESS

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

3ans:we treat the paient for both amoebic and pyogenic abcess so that we dont rely only on anti-amebic therapy and insure comple treatment of the cause

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

4 ans: he confirmatory test for amoebic abcess is

*Serologic testing is the most widely used method of diagnosis for amebic liver abscess. In general, the test result should be positive, even in cases when the result of the stool test is negative (only extraintestinal disease).

*The diagnosis of amebic liver abscess was based on four or more of the following criteria:

(i) a space-occupying lesion in the liver diagnosed by ultrasonography and suggestive of abscess,

(ii) clinical symptoms (fever, pain in the right hypochondrium (often referred to the epigastrium), lower chest, back, or tip of the right shoulder),

(iii) enlarged and/or tender liver, usually without jaundice,

(iv) raised right dome of the diaphragm on chest radiograph, and

(v) improvement after treatment with antiamebic drugs (e.g., metronidazole).

2. Left lobe abscess

3.Caudate lobe abscess

4. Abscess which is not responding to drugs

8]INFECTIOUS DISEASE(MUCORMYVOSIS,ENT, OPHTHALMOLOGY)

QUESTION

1.QUESTION: 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 aetiology of the patient's problem?

1. 3 years ago- diagnosed with hypertension

2. 21 days ago- received vaccination at local PHC which was followed by fever associated with chills and rigors, high grade fever, no diurnal variation which was relieved on medication

3. 18 days ago- complained of similar events and went to the the local hospital, it was not subsided upon taking medication(antipyretics)

4. 11 days ago - c/o Generalized weakness and facial puffiness and periorbital oedema. Patient was in a drowsy state

5. 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

6. patient was referred to a government general hospital

7. patient died 2 days ago

patient was diagnosed with diabetic ketoacidosis and was unaware that he was diabetic until then. This resulted in poorly controlled blood sugar levels. The patient was diagnosed with acute oro rhino orbital mucormycosis . rhino cerebral mucormycosis is the most common form of this fungus that occurs in people with uncontrolled diabetes 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

2.QUESTION: 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;

The proposed management of the patient was –

1. inj. Liposomal amphotericin B according to creatinine clearance

2. 200mg Iitraconazole was given as it was the only available drug which was adjusted to his creatinine clearance

3. Deoxycholate was the required drug which was unavailable

https://pubmed.ncbi.nlm.nih.gov/23729001/ this article talks about the efficacy and toxicity of different formulations of amphotericin B

along with the above mentioned treatment for the patient managing others symptoms is also done by-

I. Management of diabetic ketoacidosis –

(a) Fluid replacement- The fluids will replace those lost through excessive urination, as well as help dilute the excess sugar in blood.

(b) Electrolyte replacement-The absence of insulin can lower the level of several electrolytes in blood. Patient will receive electrolytes through a vein to help keep the heart, muscles and nerve cells functioning normally.

(c) Insulin therapy- Insulin reverses the processes that cause diabetic ketoacidosis. In addition to fluids and electrolytes, patient will receive insulin therapy

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

ans;

Mucormycosis is may be being triggered by the use of steroids, a life-saving treatment for severe and critically ill Covid-19 patients. Steroids reduce inflammation in the lungs for Covid-19 and appear to help stop some of the damage that can happen when the body's immune system goes into overdrive to fight off coronavirus. But they also reduce immunity and push up blood sugar levels in both diabetics and non-diabetic Covid-19 patients.

With the COVID-19 cases rising in India the rate of occurrence of mucormycosis in these patients is increasing

9]INFECTIOUS DISEASE (COVID-19)

Question A:

What is the reason for hypoalbuminemia in the patient?

Answer:

It may be due to pulmonary capillary leakage in lungs , in response to epithelial endothelial damage due to covid infection.

Question 2:

What could be the reason for exanthem on arms? Could it be due to covid-19 infection ?

Answer:

Yes, what the patient is experiencing is known as viral exanthem which is one of the cutaneous manifestation of COVID-19.

Question 3:

What is the reason for Cardiomegaly?

Answer:

The most probable cause of that appearance is AP view of the chest. When an anteroposterior view is taken, most times the CXR shows false cardiomegaly. To confirm the cardiomegaly a PA view of chest must be taken.

Another possible cause can be Direct Myocardial Cell Injury. The interaction of SARS-CoV-2 with ACE2 can cause changes to the ACE2 pathways, leading to acute injury of the lung, heart, and endothelial cells. A small number of case reports have indicated that SARS-CoV2 might directly infect the myocardium, causing viral myocarditis. However, in most cases, myocardial damage appeared to be caused by increased cardiometabolic demand associated with the systemic infection and ongoing hypoxia caused by severe pneumonia or ARDS

Question 4:

What other differential diagnoses could be drawn if the patient tested negative for covid infection?

Answer:

Possible alternative diagnoses may include:

• Influenza

• Mycoplasma pneumonia

• Parainfluenza

• Respiratory syncytial virus

• Streptococcus pneumonia

• Other viral or bacterial pneumonia.

Question 5:

Why is there elevated D-Dimer in covid infection? What other conditions show D-dimer elevation?

Answer:

It is well known that D-dimer are produced during fibrin breakdown and serve as a marker of fibrinolytic activity. A relationship between proinflammatory cytokines and markers of activation of the coagulation cascade, including D-dimer, has been demonstrated in critical patients or patients with sepsis .There is also evidence that under inflammatory conditions, the alveolar haemostatic balance is shifted towards a predominance of prothrombotic activity .In addition, pro-inflammatory cytokines may be involved in endothelial injury, and may activate coagulation and inhibit fibrinolysis in patients with severe sepsis.

• D-dimer can be elevated such as in pregnancy, inflammation, malignancy, trauma, liver disease (decreased clearance), heart disease, sepsis or as a result of hemodialysis, CPR or recent surgery)

D;Questions:

1. Is the elevated esr due to covid related inflammation?

Ans;

Erythrocyte sedimentation rate (ESR) is a blood test. It measures how quickly erythrocytes, or red blood cells, separate from a blood sample that has been treated so the blood will not clot.

The sustained high level of ESR possibly brings a negative effect on COVID-19 patients' prognosis

However the elevation in esr cannot be explained based on the present knowledge on Covid

2. What was the reason for this patient's admission with mild covid? What are the challenges in home isolation and harms of hospitalization?

Ans;

after 14 days of isolation he got tested again for COVID-19 which was positive . He then developed fever since 4 days, cough which was productive since 4 days and shortness of breath grade 3 since 2 days. He also had fatigue.He lost the sense of taste and smell.

Since the patient has SOB of grade 3. This poses a challenge for home isolation.

Patients with COVID-19 had almost 19 times the risk for acute respiratory distress syndrome (ARDS) than did patients with influenza, (adjusted risk ratio [aRR] = 18.60; 95% confidence interval [CI] = 12.40–28.00), and more than twice the risk for myocarditis (2.56; 1.17–5.59), deep vein thrombosis (2.81; 2.04–3.87), pulmonary embolism (2.10; 1.53–2.89), intracranial hemorrhage (2.85; 1.35–6.03), acute hepatitis/liver failure (3.13; 1.92–5.10), bacteremia (2.46; 1.91–3.18), and pressure ulcers (2.65; 2.14–3.27). The risks for exacerbations of asthma (0.27; 0.16–0.44) and chronic obstructive pulmonary disease (COPD) (0.37; 0.32–0.42) were lower among patients with COVID-19 than among those with influenza. The percentage of COVID-19 patients who died while hospitalized (21.0%) was more than five times that of influenza patients (3.8%), and the duration of hospitalization was almost three times longer for COVID-19 patients.

E Questions:

1) What was the reason for coma in this patient?

Ans;

The patient has an spo2 of 20%. This might have lead to cerebral hypoxia thus leading to coma.

Also, low blood potassium can make you short of breath, as it can cause the heart to beat abnormally. This means less blood is pumped from your heart to the rest of your body

Thus low spo2 and thus coma

2) What were the competency gaps in hospital 1 Team to manage this intubated comatose patient that he had to be sent to hospital 2? Why and how did hospital 2 make a diagnosis of hypokalemic periodic paralysis? Was the coma related?

Ans;

Hospital 1 might not have correlated Severe weakness of 4 limbs with low values of potassium which hospital 2 has diagnosed.

Yes, coma is related to Hypokalemia periodic paralysis as it might have caused cerebral hypoxia.

3) How may covid 19 cause coma?

Ans;

After cessation of sedatives, the described cases all showed a prolonged comatose state.

unconsciousness after prolonged periods of mechanical ventilation in the ICU.

F Question

1. What was the cause of his altered sensorium?

Can be any of the following reasons

An altered state is any mental state(s), induced by various physiological( increased hospital stay) , psychological( mental depression due to isolation), or pharmacological maneuvers or agents( drugs of COVID)

2. What was the cause of death in this patient?

This patient is an elderly chronic alcoholic and smoker.

This might have delayed his healing process thus causing death

Also he had elevation LFT and RFT values

H Questions:

1. Can psoriasis be a risk factor for severe form of COVID?

Elderly psoriasis patients and/or patients using conventional immunosuppressive regimens and biologic agents are at higher risk for infectious diseases.

But the frequency of COVID-19 does not increase in patients using immunosuppressants, including those receiving biological therapy with a diagnosis of psoriasis

2. Can the increased use of immunomodulatory therapies cause further complications in the survivors?

According to the present knowledge on Covid,there is no indication that people taking immunomodulatory drugs for other diagnosed conditions should be concerned that their medication increases their risk for severe COVID-19,"

3. Is mechanical ventilation a risk factor for worsened fibroproliferative response in COVID survivors?

patients of Covid with greater fibrotic changes required more prolonged mechanical ventilation, and this in turn was associated with an increased severity of systemic organ failure.

Hence Mechanical ventilation is risk factor

L Questions :-

1) What are the potential bioclinical markers in this patient that may have predicted the prolonged course of her illness?

The potential biochemical markers in this patient are

Elevated levels of

LFT- Total bilirubin : 1.24 mg/dl

Direct bilirubin : 0.67 mg/dl

SGOT : 73 units/ lit

SGPT : 80 units/ lit

ALP : 342 units/ lit

RFT Blood urea : 34 mg/dl

Sodium : 150 meq/lit

Potassium : 5.2 meq/lit

SERUM LDH 571 units/lit

FBS 332 mg /dl

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JATOTH JAYA

Online blended bimonthly assignment toward summative assessment for the month of May 2021

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