MEDICINE BLENDEDMONTHLY ASSESSMENT
Procedure.
The Hoffmann's reflex test itself involves loosely holding the middle finger and flicking the fingernail downward, allowing the middle finger to flick upward reflexively. A positive response is seen when there is flexion and adduction of the thumb on the same hand.
Interpretation.
A positive Hoffmann’s reflex and finger jerks suggest hypertonia, but can occur in healthy individuals, and are not useful signs in isolation. In cerebellar diseases, the reflexes may be pendular, and muscle contraction and relaxation tend to be slow, but these are not sensitive or specific to cerebellar signs.
.Case 8
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
Questions.
1.1) 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
Case1.
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html
Questions.
1.What is the difference between heart failure with preserved ejection fraction and with reduced ejection fraction?
Ans. Preserved ejection fraction is also known as diastolicheart failure. In this the heart muscle contracts normally but the ventricles do not relax during ventricular filling.
It is preceded by chronic comorbidities with such as hypertension. Type 2 diabetes mellitus, obesity and renal insufficiency.
Reduced ejection fraction is also known as systolic heart failure.
It is preceded by acute or chronic loss of cardiomyocytes due to genetic mutation ,myocarditis or valvular disease.
2. Why haven't we done pericardiocentesis in this patient?
Ans. It is not done because the effusion was self healing.
3. What are the risk factors for development of heart failure in this patient?
Ans. Alcohol abuse increases the risk of atrial fibrillation heart attack and congestive heart failure
High blood pressure
Smoking
AV block can be associated with severe bradycardia and hemodynamic instability. It has a greater risk of progress into third degree heart block or asystole.
Worsening of pericardial effusion leading to cardiac tamponade.
4. What could be the cause for hypertension in this patient?
Ans. Visceral pericardium may have thickened and which is restricting the heart to expand causing hypotension.
Case 2
https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html
Questions.
1. What are the possible causes for heart failure in this patient?
Ans. The patient was diagnosed with type 2 diabetes mellitus 30 years ago and was also diagnosed with diabetic triopathy indicating uncontrolled diabetes which is a major risk factor for heart failure.
He was also diagnosed with hypertension and 19 years back which is a potential risk factor for heart failure.
He is a chronic alcoholic since 40 years which is also a risk factor for heart failure.
The patient has elevated creatinine and AST/ALT ratio>2 and was diagnosed with chronic kidney disease stage lV.
2. What is the reason for anaemia in this patient?
Ans. 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.
3. What are the reason for blebs and non healing ulcer in the legsof the patient?
Ans. Diabetes mellitus is responsible for non healing ulcer and blebs formation in this patient .CKD please also known to cause delay in healing of wounds. Anaemia can also slow down the process of healing due to low oxygen levels.
4. What sequence of stages of diabetes has been noted in this patient?
Ans.There are 4 stages in Diabetes mellitus.1. insulin resistance 2.prediabetes3.type 2 diabetes and vascular complications including retinopathy neuropathy nephropathy etc.
This patient is diagnosed with diabetic triopathyexhibiting sequence of neuropathy retinopathy and nephropathy.
The patient has been diagnosed with diabetic retinopathy CKD stage IVand shows signs of diabetic neuropathy such as numbeness.
Case 3:
https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html
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 anatomical site is blood vessels
Etiology.
The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly coronary and cerebral vessels. Moreover hypertension appears to increase the susceptibility of small and large arteries to atherosclerosis.
The most likely cause of arterial thrombosis is artery damage due to atherosclerosis. Atherosclerosis occurs when a person build up plaque on the walls of their arteries. The arteries then begin to narrow and Harden, which increases a person's risk of developing arterial thrombosis.
2. What are mechanism of action indication and efficacy over placebo of of each of the pharmacological and non pharmacological interventions used for this patient?
Pharmacological interventions
1.TAB.Dytor
To its action in antagonizing the effect of aldosterone, spironolactone in the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
2.TAB.Acitrom
Acenocoumarol inhibits the action of an enzyme vitamin k epoxide reductase which is required for regeneration and maintaining levels of vitamin k required for blood clotting.
3.TAB Cardivas.
Mechanism. Regulate Glucose metabolism.
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake especially by skeletal muscle and fat and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhance proteins synthesis; targets include skeletal muscle, liver and adipose tissue.
5.TAB DIGOXIN.
6. Hypoglycemia symptoms explained.
7. Watch for any bleeding manifestations like petechiae,bleeding gums.
APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drugs warfarin to make sure that drugis producing the desired effect.
3. What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardiorenal syndrome is seen in this patient?
4. What are the risk factors for atherosclerosis in this patient?
Ans effect of hypertension.
They can also impair blood vessels ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery clogging process known as Atherosclerosis.
5. Why was the patient asked to to get those APPT INR tests for review?
Ans.APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drugs warfarin to make sure that drugis producing the desired effect.
Here an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed although local protocols may vary in their starting doses and titration schedule.
Case 4
https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1
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.TIMELINE OF EVENTS-
• Diabetes since 12 years - on medication
• Heart burn like episodes since an year- relieved without medication
• Diagnosed with pulmonary TB 7 months ago- completed full course of treatment, presently sputum negative.
• Hypertension since 6 months - on medication
• Shortness of breath since half an hour-SOB even at rest
Anatomical localisation - Cardiovascular system
Etiology: The patient is both Hypertensive and diabetic , both these conditions can cause
- Atherosclerosis: there is build up of fatty and fibrous material inside the wall of arteries.(PLAQUE)
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.Pharmacological interventions:
TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient
MOA: METOPROLOL is a cardiselective beta blocker
Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause your heart to beat more slowly( negative chronotropic effect)
and with less force( negative inotropic effect). Beta blockers also help open up your veins and arteries to improve blood flow.
Indications: it is used to treat Angina, High blood pressure and to lower the risk of hear attacks .
Non pharmacological intervention advised to this patient is: PERCUTANEOUS CORONARY INTERVENTION.
Percutaneous Coronary Intervention is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup ( atherosclerosis).
3) What are the indications and contraindications for PCI?
Ans. INDICATIONS:
Acute ST-elevation myocardial infarction (STEMI)
Non–ST-elevation acute coronary syndrome (NSTE-ACS)
Unstable angina.
Stable angina.
Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
High risk stress test findings.
CONTRAINDICATIONS:
Intolerance for oral antiplatelets long-term.
Absence of cardiac surgery backup.
Hypercoagulable state.
High-grade chronic kidney disease.
SWChronic total occlusion of SVG.
An artery with a diameter of <1.5 mm.
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?
ANS.
Although PCI is generally a safe procedure , it might cause serious certain complications like
A)Bleeding
B) Blood vessel damage
C) Allergic reaction to the contrast dye used
D) Arrhythmias
E) Need for emergency coronary artery bypass grafting .
Because of all these complications it is better to avoid PCI in patients who do not require it.
⁃ OVER TESTING AND OVER TRAETMENT HAVE BECOME COMMMIN IN TODAY’S MEDICAL PRACTICE.
⁃ Research on overtesting and overtreatment is important as they are more harmful than useful.
Harms to patients
. Performing screening tests in patients with who at low risk for the disease which is being screened.
For example:Breast Cancer Screenings Can Cause More Harm Than Good in Women Who Are at Low Risk. A harmless lump or bump could incorrectly come up as cancer during routine breast screenings. This means that some women undergo surgery, chemotherapy or radiation for cancer that was never there in the first place.
.Overuse of imaging techniques such as X- RAYS AND CT SCANS as a part of routine investigations.
Overuse of imaging can lead to a diagnosis of a condition that would have otherwise remained irrelevant - OVERDIAGNOSIS.
Also the adverse effects due to this are more when compared to the benefits.
.Overdiagnosis through overtesting can psychologically harm the patient.
Hospitalizations[41] for those with chronic conditions who could be treated as outpatients[ can lead to economic burden and a feeling of isolation.
Harms to health care systems
The use of expensive technologies and machineries are causing burden on health care systems.
Case 5.
https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1
Questions.
1. What is the evolution of the symptomatology in this patient in terms of even timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient's problem?
Ans . The anatomical localisation of etiology is blood vessels.
Myocardial infarction is usually due to turbotech occlusion of the coronary vessel caused by rupture of a vulnerable plaque.
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.Pharmacological interventions.
TAB ASPIRIN.
Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase activity. Until recently has been has been mainly used for primary and secondary prevention of arterial antithrombotic events.
Tab.Atrovas.
The active metabolite of clopidogrel selectively inhibits the binding of adenosine triphosphate to its platelet P2Y12 receptor and the subsequent ADP mediated activation of the glycoprotein GPllb/lllA complex thereby inhibiting platelet aggregation. This action is irreversible.
Inj .HAI S/C.
Mechanism. Regulate Glucose metabolism.
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake especially by skeletal muscle and fat and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhance proteins synthesis; targets include skeletal muscle, liver and adipose tissue.
5.ANGIOPLASTY.
Angioplasty also known as ballo
on angioplasty and percutaneous transluminal angioplasty is a minimally invasive endovascular procedure used to widen narrow or obstructed arteries or veinstypically to treat arterial atherosclerosis.
3. Did the secondary PCTA do any good to the patient or it was unnecessary?
Ans. The secondary PCI was not necessary in this patient.
PCI performed from 3 to 28 days after MI I does not decrease the incidence of death reinfarction or New York heart association (NYHA)classIV heart failure but it is associated with higher rates of both procedure related And true STelevation reinfarction.LatePCI leads to the increased risk of periprocedural complications long term bleeding and stent thrombosis.
Case6:
https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h
Questions.
1. How did the patient get relieved from the shortness of breath after IV fluids administration by rural medical practitioner?
Ans. Because of the fluid loss occur to the patient there is decrease preload so SOB occurred due to decreased cardiac output.
IV fluids administered- there is increase preload-SOBrecreased due to better of cardiac output
2 what is the rationale of using torsemide in this patient?
Aans. It is used to relieve abdominal distention .
3. What what's the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Ans. It is for the treatment of UTI.
Rationale-used for any bacterial infection.
GASTROENTEROLOGY (PULMONOLOGY)
Case1.
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html
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?
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?
A) * Non pharmacological interventions : drains ( malecot & icd )
* Even i as a treating physician will follow the same approach
Case 2.
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
Questions.
1.What is causing the patient's dyspnea? How is it related to pancreatitis?
Ans. The cause of dyspnea is pleural effusion.
2) Name possible reasons why the patient has developed a state of hyperglycemia.
Ans. These hyperglycemia could be the result of a hyperglucagonemia secondary to stress.
The result of decreased synthesis and release of insulin secondary to the damage of pancreatic beta cells.
Elevated levels of catecholamines and cortisol .
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
LFT are increased due to hepatocyte injury. If the liver is damaged or not functioning properly ALTcan be raised in the blood. Higher than normal limits on this test can be sign of liver disease.
Elevated alanine transaminase and aspartate transaminase usually one to four times the upper limits off normal alcoholic fatty liver.
The reasons for a classical 2:1 excess of serum ALT activity compared to serum ALT activity in alcoholic hepatitis have been attributed to
1. Decreased ALT activity most likely due to b6 depletion in the livers of alcoholics.
2 . Mitochondrial damage leading to the increased release of mAST in serum.
4) What is the line of treatment in this patient?
Ans. plan of action of treatment.
Investigations.
1. 24 hour urine protein
2. Fasting and postprandial blood glucose.
3. Hba1c
4.USG guided pleural tapping.
Treatment
1. IVF:125 ml/hr.
2.inj PAN 40 mg i.v OD.
3.Inj ZOFER 4 mg i.v sos.
4.inj Tramafol 1 amp in 100 ml NS i.v sos.
5.Tab Dilo 650 mg sos.
6.GRBS charting 6 th hourly.
7. BP charting 8 th hourly.
Case 3
https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
Questions.
1. What is the most probable diagnosis in this patient?
Ans. Differential diagnosis.
1.Ruptured liver abcess.
2. Organized collection secondary to Hollow viscous perforation.
3. Organised intraperitoneal hematoma
4. Grade 3 RPD of right kidney.
The most probable diagnosis is there is abdominal hemorrhage. This will give rise to the abdominal distension and the blood which is aspirated.
2. What was the cause of death?
Ans. After leaving the hospital the patient underwent laparotomy another hospital. The next day the patient died. This may be due to complications of laparotomy such as hemorrhage infection or damage to the internal organs.
3. Does her NSAIDS abuse have something to do with her condition? How?
Ans.NSAID induced renal dysfunction has a wide spectrum of negative effects including decrease glomerular perfusion, decreased glomerular filtration rate and acute renal failure. They also cal hepatotoxicity.
NEPHROLOGY
Case 1
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
Questions.
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.
Case 2
https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html.
Questions
1.Why is the child excessively hyperactive without much of social etiquettes ?
Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, or excessive activity and impulsivity, which are otherwise not appropriate for a person's age
For a diagnosis, the symptoms have to be present for more than six months, and cause problems in at least two settings (such as school, home, work, or recreational activities).
2. Why doesn't the child have the excessive urge of urination at night time ?
Since the child doesn’t have excessive urge of urination at night but at day there might be a psychiatry related condition
1. Psychosomatic disorder
2. Undiagnosed anxiety disorder
3. How would you want to manage the patient to relieve him of his symptoms?
bacterial kidney infection, the typical course of treatment is antibiotic and painkiller therapy.
If the cause is an overactive bladder, a medication known as an anticholinergic may be used. These prevent abnormal involuntary detrusor muscle contractions from occurring in the wall of the bladder
To treat attention deficit hyperactivity disorder:
For children 6 years of age and older, the recommendations include medication and behavior therapy together — parent training in behavior management for children up to age 12 and other types of behavior therapy and training for adolescents. Schools can be part of the treatment as well.
Methylphenidate A stimulant and a medication used to treat Attention Deficit Hyperactivity Disorder. It can make you feel very ‘up’, awake, excited, alert and energised, but they can also make you feel agitated and aggressive. They may also stop you from feeling hungry.
Amphetamine belongs to a class of drugs known as stimulants. It can help increase your ability to pay attention, stay focused on an activity, and control behavior problems. It may also help you to organize your tasks and improve listening skills.
Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)
Case 1
https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html
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.
INFECTIOUS DISEASE AND HEPATOLOGY
Case 1
https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html
Liver abscess
1.Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors
present in it ?
1ans- yes, it could be due to intake of contaminated toddy
What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per 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.
3ans-yes right lobe is involved due to its moreblood supply.
4.What are the indications for ultrasound guided aspiration of liver abscess?
4ans- Indications for USG guided aspiration of liver abscess
1. Large abscess more than 6cms
2. Left lobe abscess
3.Caudate lobe abscess
4. Abscess which is not responding to drugs.
Case 2
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
QUESTIONS:
1) Cause of liver abcess in this patient ?
ANS. Amoebic liver abscess (ALA ) seen commonly in the tropics is predominantly confined to adult males, especially those who consume locally brewed alcohol, although intestinal amoebiasis occurs in all age groups and in both genders.
It has been argued that socioeconomic factors and poor sanitary conditions are the primary culprits that casually link alcohol to ALA.
However , there has emerged an abundance of data that implicates alcohol in a more causal role in facilitating the extra intestinal invasion of the infective protozoan and the subsequent development of ALA.
2) How do you approach this patient ?
ANS. When patient presents with chief complaints of abdominal pain, fever -
1. Detailed history regarding each of the symptom should be taken.
2. General examination to know the overall health status should be carried out.
3. Following general examination, systemic examination should be done.
Patient’s symptoms point out to the involvement of Gastrointestinal system, therefore special emphasis should be on per abdominal examination.
4. Through history and examination , we arrive at provisional diagnosis.
5. To confirm the diagnosis, investigations, imaging tests should be taken.
6. For this patient based oh his symptomatology , the following investigations should be done.
CBP, LFT, RFT, Urine analysis
7. Imaging tests- CXR, USG abdomen.
Based on the results of these the diagnosis can be confirmed, treatment can be initiated.
This patient is diagnosed with Liver Abscess (by the above approach).
The following treatment can be given.
In practice an empirical treatment is given to treat both amoebic and pyogenic liver abscess
This includes use of Broad spectrum antibiotics( for pyogenic liver abscess) , Metronidazole ( for amoebic liver abscess)
Analgesics and anti inflammatory drugs -to relieve pain and fever.
Multivitamin supplements
Saline infusion- to maintain fluid levels.
All the above medicines should be given for 7- 10 days.
Following this review the patient and see if there is any improvement.
USG abdomen should be done se if the abscess is resolving.
Investigations ( CBP, LFT , RFT ) should be done to check for the improvement.
If the abscess did not resolve Ultrasound guided aspiration should be done.
3) Why do we treat here ; both amoebic and pyogenic liver abcess?
ANS. The presentation for both amoebic , pyogenic liver abscess is the same (ie) pain abdomen, fever, constitutional symptoms like nausea and vomiting , loss of appetite, in some cases there may be pulmonary symptoms.
Investigations-
There is leucocytosis, elevated alkaline phosphatase, ALT, AST
USG-a hypo echoic mass for both type of abscess.
Amoebic and pyogenic liver abscess can be differentiated only by culture and sensitivity of the aspirate obtained by USG guided aspiration of abscess.
USG guided aspiration has the following risk factors associated with it:
1) If abscess is thin walled there is a risk of rupture.
2) If abscess is on the posterior aspect of the liver, it will not be accessible.
3) There is also a risk of bleeding.
Blood culture taken prior to the administration of antibiotics is helpful for identifying the causative organism but as this patient had already taken antimicrobials before he came to the hospital, there is severe abdominal pain treatment is started immediately without a blood culture report.
Considering that it is difficult to distinguish amoebic liver abscess from pyogenic liver abscess,
We treat both forms of Liver abscess empirically using-
• Broad spectrum antibiotics- a combination of penicillin , cephalosporin, aminoglycosides
• Metronidazole- has both antibacterial and antiprotozoal activity.
4) Is there a way to confirmthe definitive diagnosis in this patient?
ANS. Liver abscess can be confirmed by USG Abdomen.
It presents as single/ multiple, round/ oval, hypoechoic- hyper echoic mass more commonly is the right lobe of the liver.
However USG cannot differentiate an amoebic liver abscess from pyogenic liver abscess.
For this
• Blood culture
• USG guided aspiration of the abscess should be done.
This aspirate should be subjected to antigen testing for :
Subjected to microbiological culture and sensitivity to identify pyogenic organisms.
INFECTIOUS DISEASE ( Mucormicosis, Opthalmology, Otorhinolaryngology, Neurology).
Case 1
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html
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.3 years ago- diagnosed with hypertension
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
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-
patient presented to casualty in altered state with facial puffiness and periorbital oedema and weakness of right upper limb and lower limb
towards the evening patient periorbital oedema progressed
serous discharge from the left eye that was blood tinged
was diagnosed with diabetes mellitus
patient was referred to a government general hospital
patient died 2 days ago
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?
Ans.The proposed management of the patient was –
inj. Liposomal amphotericin B according to creatinine clearance
200mg Iitraconazole was given as it was the only available drug which was adjusted to his creatinine clearance
Deoxycholate was the required drug which was unavailable.
Management of diabetic ketoacidosis –
Fluid replacement- The fluids will replace those lost through excessive urination, as well as help dilute the excess sugar in blood.
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.
Insulin therapy- Insulin reverses the processes that cause diabetic ketoacidosis. In addition to fluids and electrolytes, patient will receive insulin therapy.
3) 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 increasing.
QUESTION 9
http://medicinedepartment.blogspot.com/2021/05/covid-case-report-logs-from-may-2021.html?m=1
Sort out these detailed patient case report logs into a single web page as a master chart
2) In the master chart classify the patient case report logs into mild, moderate severe
3) Indicate for each patient, the day of Covid when their severity changed from moderate to severe or vice versa recognized primarily through increasing or decreasing oxygen requirements
4) Indicate the sequence of specific terminal events for those who died with severe Covid (for example, altered sensorium, hypotension etc).
I have compiled all the data collected in the form of an excel spreadsheet, so as to be able to draw a comparative analysis about the progression of disease and the outcome in various patients.
https://dandushivani.blogspot.com/2021/06/covid-e-lgs.html
MASTER CHART.
https://drive.google.com/file/d/157FUqNM3w8J7FUbk-jjkZPDW0EqrDZl3/view?usp=drivesdk
