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 clinical data analysis 'to develop my competency in reading and comprehending clinical data including history ,clinical findings, investigation and diagnosis and come up with the treatment plan.This is the link of questions asked regarding the cases http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1

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

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

1)what is the evolution of the symptomatology in this patient interms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient problem ?

Ans)Evolution of symptomatology
1st episode of sob - 20 yr back
2nd episode of sob - 12 yr back
From then she has been having yearly episodes for the past 12 yrs 
Diagnosed with diabetis - 8yrs back
Anemia and took iron injections - 5yr ago
Generalised weakness - 1 month back 
Diagnosed with hypertension - 20 days back
Pedal edema - 15 days back
Facial puffiness- 15 yrs back
Anatomical location of problem - lungs
Primary etiology of patient- usage of chulha since 20 yrs might be due to chronic usage 

2)what are the mechanism of actions indications and efficacy over placebo of each of the phramacological and nonphramacological interventions used for this patient?

Ans) 1) Head end elevation :# MOA;
.improves oxygenation 
.decreases incidence VAP
.increases hemodynamic performance 
.increases end expiratory lung volume
.decreases incidence of aspiration 
#Indication: .head injury
.meningitis 
.pneumonia 
2) oxygen inhalation to maintain spo2
3) Bipap:non invasive method
#MOA :assist ventilation by delivering positive expiratory and inspiratory pressure with out need for ET incubation9

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


4. Could the ATT affected her symptoms if so how?
Ans)Yes ATT affected her symptoms
Isoniazid and rifampcin -nephrotoxic - raised RFT was seen

                                                              

2) NEUROLOGY

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

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

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

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

Primary etiology :- alcohol

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

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

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

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


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

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

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

Ans) DEHYDRATION


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

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


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

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

                                                      


2Q)
B) https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1


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?


giddiness :-7 days back
 giddiness after alc consumption :- 3days back
Bilateral Hearing loss :- 3days back
aural fullness :- 3days back
presence of tinnitus:- 3days back
Vomiting- 2-3 episodes per day
H/o postural instability
Slurring of speech and deviation of mouth :- 1day back (resllved on same day)

Anatomical localisation :-cerebellum
Primary etiology :- alcohol and HTN


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) Veratin:- moa:- 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:- to prevent diseases of inner ear like menieres disease

Zofer:- moa:- binds to a receptor known as 5-HT₃, thus inhibits the binding of serotonin to it and prevents vomiting and nausea

Ecosprin:- moa :- It irreversibly inhibits prostaglandin H synthase (cyclooxygenase-1) in platelets and megakaryocytes, and thereby blocks the formation of thromboxane A2 .

Atorvostatin :- moa :- 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.

Clopidogrel :- moa :- 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.


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

Ans) Blood vessels damaged by HIGH B.P can narrow,rupture or leak.
High B.P also causes blood clots to form in the arteries leading to the brain,blocking blood flows and potentially causing a stroke.


4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Ans) Alcohol causes atrial fibrillation leading to stroke.


                                                  


2Q)
C) http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html


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

Ans) episode of paralysis of both upper and lowerlimbs(rt and left) -10yrs back
right and left paresis due to hypokalemia -1year back
pedal edema(bilateral)-8 months
blood infection -7 months back
Pain along her left upper limb associated with tingling and numbness-6 days
Palpitations - since 5 days and it is more rapid since yesterday night
Chestpain -since5 days
Difficulty in breathing-5 days


2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
Ans) Reason for recurrence hypokalemia might be due to increased urine output.
Risk factors: - female , low BMI



3) What are the changes seen in ECG in case of hypokalemia and associated symptoms
Ans) T-wave :- inversion and flattening (mild)
Q-T interval :- prolonged
Visible U wave

                                              

2Q)
D) 
https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html


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)

                                               

2Q)
E) https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

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

                                                 

2Q)
F) http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html

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


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.

                                                  

2Q)
G) https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html


1)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. 


2)What is finger escape ?

Ans) 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"


3)What is Hoffman’s reflex?

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.

                                               

2Q)
H) https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=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 intervention⁷ 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.

3.CARDIOLOGY





A) Link to patient details:



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



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





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?        



On USG , only a small pocket of 1cm effusion which was obliterating with inspiration was found . As there is risk for lung injury pleural tap has been avoided





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



Smoking ,alcohol consumption, high crp levels,dm,htn.



4.What could be the cause for hypotension in this patient?



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



B) Link to patient details:



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)

• Old Age

• Smoking

• High blood pressure

• Alcohol consumption

• Obesity



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



As the pt complaints of decrrased urinary ourput which is due to poor blood flow to the kidneys which results in the less functioning of the kidney.

Erythropoeitin is a hormone produced primarily by the kidney and it plays an important role i RBC production.





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



 Blebs are usually the result of a chronic illness such as heart failure in this patient as he has the cardinak sign i.e. pedal edema



Non healing ulcer is due to venous insufficiency.





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



STAGE 1: insulin resistance

STAGE 2: prediabetes

STAGE 3:diabetes type 2

STAGE4: microvascular complications





C) Link to patient details:

 



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?



1st episode of sob -1YR ago (grade 2)



      Diagnosed With HTN-1YR ago



      2nd episode of sob-2days ago (grade 2to grade 4)



      Facial puffiness on and off since 2 to 3yrs



      Decreased urine output-since 2 days



      Anuria-since morning



ANATOMICAL LOCALIZATION OF PROBLEM-



Left atrium  embolisationn



Loss of atrial systolic function (atrial contribution to Ventricular filling is lost)



And Left atrial dilatation causes statis of blood in LEFT ATRIUM and may lead to thrombus formation in left atrial appendage



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



    TAB DYTOR 10mg for treating Hypertension



        Tab CARDIVAS- Beta blocker



Beta-blockers are used as first line therapy since they reduce the ectopic firing that initiates the arrhythmia. They are particularly useful in patients associated with Coronary artery disease, Hypertension and Cardiac failure.



Rhythm control - IV Flecainide can be used for pharmacological cardioversion and will restore sinus rhythm. (IV Amiodarone if any heart disease present)



TAB DIGOXIN -slows the rate at which electrical currents are conducted from.atria to ventricle



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



Age >45yrs



    Hypertension





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



 APTT -to look out for bleeding disorders like bleeding gums Etc



      INR - to see the effects of anticoagulants on clotting system





D) Link to patient details:



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?



• Diabetes melites type 2 - 12yrs

• Heart burn like episode - 1yr

• Pulmonary TB - 7months

• HTN - 6months

• Sweating on exertion& SOB - day before admission

Anatomical localisation :- B.V

Primary etiology :- HTN, AGE



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



 Tab MET XL 25MG/STAT:- MOA :- long acting BETA-BLOCKER.

It works by relaxing the B.V , showing the heart rate by dping this, it reduces the workload on heart by pumping the blood effectively.

INDICATIONS :- High blood pressurr with angina.



3) What are the indications and contraindications for PCI?



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.

Chronic 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?



People suffer complications including bleeding, blood clots, infection, heart rhythm disturbances and even death from heart attack if PCI is performed in a patient who doesnot need it.





E) Link to patient details:



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 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:

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?



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?



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:



https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h



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

 

Patient has been administered I.V fluids which acted as placebo effect



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



Diuretics are used to decrease plasma volume and oedema.

this decreasres cardiac output reuslting in reduction of BP,amd thus reducing peripheral vascular resitance.



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



 Ceftriaxone works by inhibiting the mucopeptide synthesis in the bacterial cell wall.

The beta-lactam moiety of ceftriaxone binds to carboxypeptidases, endopeptidases, and transpeptidases in the bacterial cytoplasmic membrane. These enzymes are involved in cell-wall synthesis and cell division.

It is used as a prophylactic treatment.







4) Gastroenterology (& Pulmonology) 



A) Link to patient details:



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?



 Pain abdomen and vomiting -5yrs back



          Alcohol free period-3yrs



Started alc consumption again-recurrrent episodes of pain abdomen and vomiting(5-6epi)



  Increased alcohol consumption (past 20days)toddy



Last Alcohol consumption was 1 week back-he again had pain abdomen and vomiting from 1week



Fever-from 4 days



(High grade)



 Constipation, burning micturation -since 4days



Anatomical localization :pancreas



Cause of pancreatitis-may be due to alcohol





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?



INj MEROPENAM -Broad spectrum antibiotic



          Inj.METROGYL -Nitroimidazole drug



          Inj.AMIKACIN -Aminoglycoside antibiotic



All the above mentioned 3 antibiotics are used to control infection and to prevent septic complications of acute pancreatitis



Total pancreatic nutrition(TPN)--fluids are given to vein,it provides most of the nutrients body needs



TPN has proteins,carbohydrates, fats,minerals,vitamins



 IV NS/RL at the rate 12ml/hr-treat dehydration



  Inj OCTREOTIDE -Used here to decrease exocrine secretion of pancreas and it also has anti inflammatory  effects



INJ.PANTOP -PPI used for its anti pancreatic secretory effect



INJ.THIAMINE -B1 supplement



It is given here because; due to long fasting & TPN  usage , body may develop B1 deficiency



ING. TRAMADOL



It is an opioid analgesic, given to releive pain.







B) Link to patient details:



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?



Acute pancreatitis in its severe form is complicated by multiple organ system dysfunction, most importantly by pulmonary complications which include hypoxia, acute respiratory distress syndrome, atelectasis, and pleural effusion. The pathogenesis of some of the above complications is attributed to the production of noxious cytokines







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





Hyperglycemia develops rather often in the early phase of acute pancreatitis, mainly in patients with severe disease [1–3]. This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress or the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells [4–7].







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



Elevated liver enzymes in the setting of acute pancreatitis point toward choledocholithiasis as the cause, with an alanine aminotransferase greater than three times the upper limit of normal having a positive predictive value of 95% for gallstone pancreatitis 



In heavy drinkers, serum GGT, AST, ALT, ferritin and albumin were all significantly higher than in moderate drinkers or abstainers 



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



Clinicians employ goal-directed fluid therapy with either normal saline or lactated Ringers, give timely analgesics and antiemetics, and replete electrolytes as needed. The current recommendations are also to initiate feeding trials within 24 hours of disease onset instead of keeping the patient nill per mouth (NPO). There are no clear indications for the type of diet, but typically small low-fat, soft or solid meals correlate with shorter hospital stays than starting a clear liquid diet with slow advancement to solid meals. Enteral feeds via a feeding tube are preferred to total parenteral nutrition in patients unable to tolerate PO.









C) Link to patient details:



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



 

Questions:





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



Ruptured liver abscess 



2) What was the cause of her death?



Spontaneous gas-forming pyogenic liver abscess (GFPLA) is a rare complication with a high fatality rate in spite of aggressive management. Clinical spectrum of GFPLA can mimic hollow viscus perforation as it usually accompanied by pneumoperitoneum and peritonitis. 



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



NSAIDs rarely affect the liver

NSAIDs are absorbed completely and undergo negligible liver metabolism.

5) NEPHROLOGY

CASE-1:
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html

1Q)what could be the cause for his SOB

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

2Q) Reason for Intermittent Episodes of drowsiness

Ans) Hyponatremia was the cause for his drowsiness

3Q)why did he complaint of fleshy mass like passage inurine

Ans) plenty of pus cells in his urine passage appeared as
fleshy mass like passage to him

4Q) What are the complications of TURP that he may have had

Ans) Difficulty micturition
Electrolyte imbalances
Infection

        CASE-2:
https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html

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

Ans) Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, or excessive activity and impulsivity, which are otherwise not appropriate for a person's age
For a diagnosis, the symptoms have to be present for more than six months, and cause problems in at least two settings (such as school, home, work, or recreational activities).

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

Ans) Since the child doesn’t have excessive urge of urination at night but at day there might be a psychiatry related condition
1. Psychosomatic disorder
2. Undiagnosed anxiety disorder

3Q) How would you want to manage the patient to relieve him of his symptoms?

Ans) bacterial kidney infection, the typical course of treatment is antibiotic and painkiller therapy.
If the cause is an overactive bladder, a medication known as an anticholinergic may be used. These prevent abnormal involuntary detrusor muscle contractions from occurring in the wall of the bladder

To treat attention deficit hyperactivity disorder:
For children 6 years of age and older, the recommendations include medication and behavior therapy together — parent training in behavior management for children up to age 12 and other types of behavior therapy and training for adolescents. Schools can be part of the treatment as well.

Methylphenidate A stimulant and a medication used to treat Attention Deficit Hyperactivity Disorder. It can make you feel very ‘up’, awake, excited, alert and energised, but they can also make you feel agitated and aggressive. They may also stop you from feeling hungry.

Amphetamine belongs to a class of drugs known as stimulants. It can help increase your ability to pay attention, stay focused on an activity, and control behavior problems. It may also help you to organize your tasks and improve listening skills
                                       
6) Infectious disease and Hepatology:

       CASE-1:
https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html

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

 Ans)Yes it can cause as he is drinking toddy since 30years. Amoebic liver abscess (ALA) is the most common manifestation of invasive amoebiasis caused by Entamoeba histolytica (EH). Several studies from India have reported a strong link between consumption of toddy and the occurrences of ALA. Toddy is a local alcoholic beverage consisting of fermented palm juice.

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

ANS)according to some studies, alcoholism mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver. It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess.

3Q) Is liver abscess more common in right lobe ?
  
Ans)yes right lobe is involved due to its moreblood supply

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

Ans) Indications for USG guided aspiration of liver abscess

      CASE-2:
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html

1Q) Cause of liver abcess in this patient ?

Ans):cause of liver abcess in this patient is ENTAMOEBA HISTOLYTICA

2Q) How do you approach this patient ?
   
Ans)APPROACH IN THE PATIENT OF AMOEBIC LIVER ABCESS

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

Ans)  Amoebic liver abscess: The first line treatment in uncomplicated amebic abscess should be amebicidial drugs. Metronidazole is the drug of choice and has replaced the use of emetine and chloroquine. Metronidazole is effective against both the intestinal and hepatic phase. 750 mg three times a day for 7–10 days is recommended.
           Payogenic liver abscess: Treatment usually consists of placing a tube through the skin into the liver to drain the abscess. Less often, surgery is needed. You will also receive antibiotics for about 4 to 6 weeks. Sometimes, antibiotics alone can cure the infection.

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

Ans)1. Large abscess more than 6cms
         2. Left lobe abscess
         3.Caudate lobe abscess
         4. Abscess which is not responding to drugs\

7)INFECTIOUS DISEASES (MUCORMYCOSIS, OPHTHAMALOGY, ENT, NEUROLOGY)

    CASE-1:
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html

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

Ans) Timespan of symptomology:
       3 years ago- diagnosed with hypertension
       21 days ago- received vaccination at local PHC which was followed by fever, chills, and rigors.
        18 days ago- complained of similar events and went to the the local hospital, it was not subsided upon taking medication(antipyretics).
    11 days ago - c/o Generalized weakness and facial puffiness and periorbital oedema. Patient was in a drowsy state.
        4 days ago- (a). patient presented to casualty in altered state with facial puffiness and periorbital oedema and weakness of right upper limb and lower limb (b). towards the evening patient periorbital oedema progressed (c). serous discharge from the left eye that was blood tinged (d). was diagnosed with diabetes mellitus.
2 days ago- died.
the fungus enters the sinuses from the environment and then the brain.

The patient was also diagnosed with acute infarct in the left frontal and temporal lobe. Mucormycosis is associated with the occurrence of CVA.

2Q) What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?

Ans) Inj. Amphotericin- B: Amphotericin B is an example of a “polyene” type of antifungal. Polyenes bind to fungal ergosterol (the primary sterol in fungal cell membranes). This alters cell membrane permeability, and intracellular components leak from the cell. 
       Deoxycholate Amphotericine B: Amphotericin B deoxycholate belongs to the polyene class of antifungals. It is also known by the name conventional amphotericin B and has been used for the treatment of invasive fungal infections for more than 50 years.

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

Ans) High steroid usage during COVID 19 treatment causes high blood sugars and suppress the immune system. Due to high population in the state there are easy chances of containmant by the fungus Mucormycosis. 


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