GENERAL MEDICINE ASSIGNMENT FOR MAY 2021
I have been given the following cases to solve in an attmept to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and coem up with a treatment plan.
This is the link of the questions asked regarding the case
Below are my answers to the Medicine Assignment based on my comprehension of the cases.
1) Pulmonology (10 Marks)
A) Link to patient details:
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;
Add 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 AND 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
2) Neurology
A) Link to patient details:
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;
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 patient?
6). What is the probable cause for the normocytic anemia?
ANS;
B) Link to patient details:
Questions;
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS;
the 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
C) Link to patient details:
Questions:
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) TIME LINE OF THE PAITIENT SYMPTOMATOLOGY:
8 MONTHS BACK--pt developed b/l pedal edema which is gradually progressed ,
aggrevated in sitting and standing position, relieved on taking medication
6 DAYS BACK -- PAIN radiating along left upper limb, more during palpitations and relived on medication.
Chest pain associated with chest heaviness since 5 days
5 DAYS BACK--- PALPITATIONS DEVELOPED, sudden in onset which is more during night, aggrevated by lifting heavy weights, speaking continuously
5 DAYS BACK--Dyspnoea during palpitations
ANATOMICAL LOCALIZATION :
PALPITATION
DYSPNOEA
CHEST PAIN
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
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
) Reason: recurrent hypokalemic periodic paralysis
Current risk factor:due to use of diuretics
Other risk factors
2) Abnormal loses:
Medications-diuretics, laxatives, enema, corticosteriods
Real causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis, hypomagnesenemia
3) trance cellular shift : alkalosis, thyrotoxicosis, delirium tremans, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis
4) Inadequate intake: anorexia, dementia, stareation, total parental nutrition
5) 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
D) Link to patient details:
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)
E) Link to patient details:
Questions: 1) What could have been the reason for this patient to develop ataxia in the past 1 year?
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 ?
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
F) Link to patient details:
Questions
1.Does the patient's history of road traffic accident have any role in his present condition?
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?
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?
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?
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??
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.
G) Link to patient details:
__*Questions*_
Q1)1)What is myelopathy hand ?
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.
Q2))what is finger escape?
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".
Q3)what is Hoffman's sign?
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
H) Link to patient details:
Q1) What can be the cause of her condition ?
According to MRI cortical vein thrombosis might be the cause of her seizures.
2) What are the risk factors for cortical vein thrombosis?
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?
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?
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 inactivate FACTOR Xa
3) Cardiology
A) Link to patient details:
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)
B) Link to patient details:
Q1)1.What are the possible causes for heart failure in this patient?
Ans;l Alcoholic cardiomyopathy is a form of heart disease caused by alcohol abuse. Long-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood
high blood glucose from diabetes can damage your blood vessels and the nerves that control your heart and blood vessels
High blood pressure can strain your heart, damage blood vessels, and increase your risk of heart attack
Diseases in the kidneys can affect the heart. It is common for people with chronic kidney disease or end-stage kidney disease to develop heart disease, including heart attack or heart failure.
2.what is the reason for anaemia in this case?
Ans; In the general elderly population, anemia is caused by nutritional deficiencies (primarily iron), chronic inflammation/CKD, or unexplained anemia of the elderly (a hypoproliferative anemia with blunted erythropoietin response)
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
Ans; When high blood sugar destroys nerves, they do not regenerate; thus many patients with diabetes are increasingly less sensitive to pain in their limbs. With this loss of sensation, patients don't feel developing blisters, infections, or existing wound changes. That means that wound healing is complicated not only by the fact that patients don't feel wounds as they occur, but they also have no pain to alert them that a wound is getting worse or infected.
4. What sequence of stages of diabetes has been noted in this patient?
Ans;stage 1: defined as DCBD (dysglycemia-based chronic disease )insulin resistance;
stage 2: defined as DCBD prediabetes;
stage 3: defined as DCBD type 2 diabetes; and
stage 4: defined as DCBD vascular complications, including retinopathy, nephropathy or neuropathy, and/or type 2 diabetes-related microvascular events.
All these stages have been noted in this CASE
C) Link to patient details:
Q1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans:Patient was apparently asymptomatic 2 days ago when he developed Shortness of breath Grade II (on exertion) which progressed to Grade IV (at rest) for which he visited local RMP and was referred to our hospital.Patient also complains of decreased urine output since 2 days and Anuria since morning.
Anatomical localization is heart
Primary etiology is atrial fibrillation
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) INJ. Dobutamine 3.6ml/hr was given to maintain the falling BP up to a MAP of 55 mmHg.
Mechanism of action: Dobutamine is a direct-acting inotropic agent whose primary activity results from stimulation of the ß receptors of the heart while producing comparatively mild chronotropic, hypertensive, arrhythmogenic, and vasodilative effects. It does not cause the release of endogenous norepinephrine, as does dopamine
.2) TAB. Digoxin 0.25mg OD 5/7 and INJ. Unfractionated Heparin 5000 IU TID.
Mechanism of action: 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
3[INJ. Unfractionated Heparin Infusion @5ml/hr
Mechanism of action: It produces its major anticoagulant effect by inactivating thrombin and activated factor X (factor Xa) through an antithrombin (AT)-dependent mechanism. ... By inactivating thrombin, heparin not only prevents fibrin formation but also inhibits thrombin-induced activation of platelets and of factors V and VIII.Other medications used during the course in hospital -
1. TAB. Cardivas3.125mg PO/BD
2. TAB. Dytor 10mg PO/OD
3. TAB Pan D 40mg PO/OD
4. TAB. Taxim 200mg PO/OD
5. INJ. Thiamine 100mg in 50ml NS IV/TID
6. INJ. HAI S.C 8U-8U-6U
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Ans; The pathophysiology of CRS can be attributed to two broad categories of "hemodynamic factors" such as low cardiac output, elevation of both intra-abdominal and central venous pressures, and non-hemodynamic factors or "cardiorenal connectors" such as neurohormonal and inflammatory activation.[5] It was previously believed that low cardiac output in heart failure patients result in decreased blood flow to the kidneys which can lead to progressive deterioration of kidney function. As a result, diuresis of these patients will result in hypovolemia and pre-renal azotemia.
In addition, CRS has been observed in patients with diastolic dysfunction who have normal left ventricular systolic function.[3]Therefore, there must be additional mechanisms involved in the progression of CRS. Elevated intra-abdominal pressures resulting from ascites and abdominal wall edema may be associated with worsening kidney functions in heart failure patients. Several studies have shown that as a result of this increased intra-abdominal pressure there is increased central venous pressure and congestion of the kidneys' veins, which can lead to worsening kidney function.[3]
In addition, many neurohormonal and inflammatory agents are implicated in the progression of CRS. These include increased formation of reactive oxygen species, endothelin, arginine vasopressin, and excessive sympathetic activity which can result in myocardial hypertrophy and necrosis.
Other cardiorenal connectors include renin-angiotensin-system activation, nitric oxide/reactive oxygen species imbalance, inflammatory factors and abnormal activation of the sympathetic nervous system, which can cause structural and functional abnormalities in both heart and/or the kidney. There is a close interaction within these cardiorenal connectors as well as between these factors and the hemodynamic factors which makes the study of CRS pathophysiology complicated.
4) What are the risk factors for atherosclerosis in this patien
Ans; High cholesterol and triglyceride levels.
High blood pressure.
Smoking.
Type 1 diabetes.
Obesity.
Physical inactivity.
High saturated fat diet
5) Why was the patient asked to get those APTT, INR tests for review?
Ans; Standard coagulation screening tests such as activated partial thromboplastin time (APTT), prothrombin time (PT), and the international normalized ratio (INR) are important constituents of basic examinations in clinical laboratories. APTT can be used as an indicator of intrinsic coagulation pathway activity, and a short APTT is linked to increased thrombin generation and increased risk for thrombosis.
D) Link to patient details:
Questions:
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?
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
Glimiprime M 2 Forte Tablet is a combination of two medicines: Glimepiride and Metformin. This medicine is used in the treatment of type 2 diabetes mellitus (DM). It improves blood glucose levels in adults when taken along with proper diet and regular exercise …
Telma 20 tablet is an antihypertensive medicine that is used to treat high blood pressure and can also help in reducing other heart problems It acts by relaxing the blood vessels and leads to lower blood pressure
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
E) Link to patient details:
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;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.
F) Link to patient details:
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: 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.
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.
4) Gastroenterology (& Pulmonology)
A) Link to patient details:
QUESTIONS:
- Q1) 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?
- A1) Timespan of symptomology:
- 5 years ago: 1st episode of pain abdomen and vomiting
- 1 year back: 5 to 6 episodes of pain abdomen and vomiting
- 20 days back: Increased consumption of toddy intake
- Since 1 week: Pain abdomen and vomiting
- Since 4 weeks: Fever, constipation and burning micturition
- Anatomical localization: Pancreas and left lung
- Etiology: The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes attributed to alcohol.
- Q2) 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?
- A2) Inj. Metrogyl: Metronidazole is of the nitroimidazole class. It inhibits nucleic acid synthesis by forming nitroso radicals, which disrupt the DNA of microbial cells.
- Inj. Meropenam: Meropenem is bactericidal except against Listeria monocytogenes, where it is bacteriostatic. It inhibits bacterial cell wall synthesis like other β-lactam antibiotics. In contrast to other beta-lactams, it is highly resistant to degradation by β-lactamases or cephalosporinases.
- Inj. Amikacin: The primary mechanism of action of amikacin is the same as that for all aminoglycosides. It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and tRNA acceptor sites, interfering with bacterial growth.
- TOTAL PARENTAL NUTRITION
- Inj. Octerotide: Octreotide suppresses secretion of growth hormone (GH), and in many cases suppresses insulin-like growth hormone-1 (IGF-1) (somatomedin C). Sandostatin works centrally at the site of the tumor and binds to somatostatin receptors to regulate GH secretion and cell growth.
- Inj. Pantop: The mechanism of action of pantoprazole is to inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion.
- Inj. Thiamine: Mechanism of Action: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiamine diphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
- Inj. Tramadol: Tramadol is a centrally acting analgesic with a multimode of action. It acts on serotonergic and noradrenergic nociception, while its metabolite O-desmethyltramadol acts on the µ-opioid receptor. Its analgesic potency is claimed to be about one tenth that of morphine.
- B) Link to patient details:
- https://nehae-logs.blogspot.
com/2021/05/case-discussion- on-25-year-old-male.html - Q1) What is causing the patient's dyspnea? How is it related to pancreatitis?
- A1) Pleural effusion might be the cause of patients dyspnea.
- Presence of pleural effusion is currently considered an indication of severe pancreatitis and not just a marker of the disease[24]. Pancreatic ascites and pleural effusion are rare complications of both chronic and acute pancreatitis, and are associated with a mortality rate of 20% to 30%.
- Q2) Name possible reasons why the patient has developed a state of hyperglycemia.
- A2) Hyperglucagonemia secondary to stress could be the result of patient developing hyperglycemia.
- Elevated levels of catecholamines and cortisol.
- Q3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
- A3) Elevated liver enzymes are a sign that a person has an inflamed or a damaged liver. Many conditions may cause liver inflammation or damage. In this case the probable reason may be due to liver injury. Alanine aminotransferace (ALT) and Asparate aminotransferase (AST) are the specific markers for alcoholic fatty liver disease. Glutamyl transpeptidase (GGT) is another marker of liver injury, and this enzyme is elevated in people who consumes alcohol. Of all the enzyme markers GGT is the most sensitive biomarker of alcohol consumption.
- Q4) What is the line of treatment in this patient?
- A4) IVF: 125 ml/hr
- Inj. PAN 40mg i.v.
- Inj Zofer 4mg i.v.
- Inj. Tramadol 1amp in 100ml i.v.
- Tab. Dolo 650mg
- GRBS charting 6th hourly
- BP charting 8th hourly.
C) Link to patient details:
Questions :-
- Q1) What is the most probable diagnosis in this patient?
- A1) Abdominal Hemorrhage may be the most probable diagnosis in this patient.
- Q2) What was the cause of her death?
- A2) Cause of her death may be due to complications of laparotomy surgery such as hemorrhage, infection, or damage to internl organs.
- Q3) Does her NSAID abuse have something to do with her condition? How?
- A3) NSAIDS are known to cause drug induced hepatitis which may lead to cirrhosis.5) Nephrology (and Urology)A) Link to patient details:1.what could be the cause for his SOBAns-His sob was is due to Acidosis which was caused by Diuretics2. Reason for Intermittent Episodes of drowsinessAns-Hyponatremia was the cause for his drowsiness3.why did he complaint of fleshy mass like passage inurineAns-plenty of pus cells in his urine passage appeared as fleshy mass like passage to him4. What are the complicat ions of TURP that he may have hadAns-Difficulty micturitionElectrolyte imbalancesInfectionB) Link to patient details:QuestionsQ1) Why is the child excessively hyperactive without much of social etiquettes ?A1) Inattention and hyperactivity/impulsivity are the key behaviors of ADHD. Some people with ADHD only have problems with one of the behaviors, while others have both inattention and hyperactivity-impulsivity. Most children have the combined type of ADHD.In preschool, the most common ADHD symptom is hyperactivity. Due to efficacy of the medications like dopamine and noradrenaline have been suggestive of pathology of ADHD.Q2) Why doesn't the child have the excessive urge of urination at night time ?A2)Q3) How would you want to manage the patient to relieve him of his symptoms?A3) Antideppresants like Bupropion, trazodoneAntipsychotics like Risperidone, aripiprazoleMood stabilizers like Carbamazepine are given to the patient to relieve the symptoms of ADHD.6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)A) Link to patient details:Questions:Q1) Which clinical history and physical findings are characteristic of tracheo esophageal fistula?A1) History findings - Any congenital heart diseases, history of mild respiratory distress, history of recurrent attacks of pneumonia.Physical findings- drooling, choking, respiratory distress, and feeding inability. Gastric distension is a common complication of a fistula between the trachea and distal esophagus. Reflux of gastric contents through the fistula tract results in aspiration pneumonia and increasing morbidity.Q2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?A2) The chances of this patient developing immune reconstitution inflammatory syndrome are high as she had a previous infection of TB.IRIS can be prevented by treating the patient with ATT with as early as possible. Prednisolone and meloxicam are used to prevent further TB IRIS.7) Infectious disease and Hepatology:A)Link to patient details:Q1) Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ?A1) Locally made alcohol like toddy may cause liver abscess if it is contaminated.Q2) What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day).A2) All patients of ALA had serum iron values within the normal range but higher than non-ALA cases. In the liver tissue, most patients with ALA had higher (grade II or III) iron deposition, than non-ALA cases (mostly grade I). Thus, patients with ALA, with or without alcohol indulgence, had higher iron levels when compared to the non-ALA cases. It appears that the higher incidence of ALA in alcoholic livers is possibly due to their higher iron content.Q3) Is liver abscess more common in right lobe ?A3) Due to more blood supply to the right lobe, liver abscess is more common in right lobe.Q4) What are the indications for ultrasound guided aspiration of liver abscess ?A4) Left lobe abscessCaudate lobe abscessLarge abscess more than 6cmsAbscess which is not responding to drugs.B) Link to patient details:QUESTIONS:Q1) Cause of liver abscess in this patient ?A1) Entamoeba Histolytica may be the cause of liver abscess in this patient.Q2) How do you approach this patient ?A2)
Q3) Why do we treat here ; both amoebic and pyogenic liver abscess?A3) Amoebic liver abscess-
Pyogenic liver abscess:Third generation cephalosporin with clindamycin or metronidazole.Broad spectrum penicillin with aminoglycosidesSecond generation cephalosporin with aminoglycosides.Q4) Is there a way to confirmthe definitive diagnosis in this patient?A4) Neutrophils leukocytosis, anemia of chronic disease,Blood cultures may reveal the diagnosis, imaging studies like Ultrasound , CT scans and hepatic scans are more sensitive and are the confirmatory test for the diagnosis of liver abscess.8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology) 10 MarksA) Link to patient details:Questions :Q1) 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?A1) Timespan of symptomology:3 years ago- diagnosed with hypertension21 days ago- received vaccination at local PHC which was followed by fever, chills, and rigors.18 days ago- complained of similar events and went to the the local hospital, it was not subsided upon taking medication(antipyretics).11 days ago - c/o Generalized weakness and facial puffiness and periorbital oedema. Patient was in a drowsy state.4 days ago- (a). patient presented to casualty in altered state with facial puffiness and periorbital oedema and weakness of right upper limb and lower limb (b). towards the evening patient periorbital oedema progressed (c). serous discharge from the left eye that was blood tinged (d). was diagnosed with diabetes mellitus.2 days ago- died.the fungus enters the sinuses from the environment and then the brain.
The patient was also diagnosed with acute infarct in the left frontal and temporal lobe. Mucormycosis is associated with the occurrence of CVA.Q2) 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?A2) Inj. Amphotericin- B: Amphotericin B is an example of a “polyene” type of antifungal. Polyenes bind to fungal ergosterol (the primary sterol in fungal cell membranes). This alters cell membrane permeability, and intracellular components leak from the cell.Deoxycholate Amphotericine B: Amphotericin B deoxycholate belongs to the polyene class of antifungals. It is also known by the name conventional amphotericin B and has been used for the treatment of invasive fungal infections for more than 50 years.Q3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?A3) High steroid usage during COVID 19 treatment causes high blood sugars and suppress the immune system. Due to high population in the state there are easy chances of containmant by the fungus Mucormycosis
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