Medicine Discussion

-

 MEDICINE

 BIMONTHLY ONLINE

 ASSESSMENT -1


This is to discuss , understand and review clinical scenarios so as to improve my clinical competency via online e-logging clinical cases
The cases have been shared after patient / Guardian signed informed consent


S.Kavya , 8th sem
Roll no 121




1) Pulmonology  


complete details regarding the case are in the mentioned link above



(A)

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


Anatomical location - lungs

Primary etiology - usage of chulha since 20years, might be due to its chronic usage

And possible etiology - Any Exposure to the causative allergen in her paddy field since she has been having yearly episode  of SOB in the month January every year - it is same period of time (winter) paddy is grown


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

2Ans)Head end elevation  



MOA;

.improves oxygenation 

.decreases incidence VAP

.increases hemodynamic performance 

.increases end expiratory lung volume

.decreases incidence of aspiration 


Indication: 

.head injury

.meningitis 

.pneumonia 


oxygen inhalation to maintain spo2


Bipap:non invasive method



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



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

Could be due to any infection





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645331/


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

Yes, ATT affected her symptoms

  rifampicin - causes swelling  and streptomycin is a Nephrotoxic - Renal damge -lead to electrolyte imbalance


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

ATT could have caused renal damage which lead to her electrolyte imbalance


Neurology

(A)


Complete details regarding the case are in the mentioned link above


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?

Timeline of patient symptomatology:


2009 (12 years ago): Started drinking alcohol

                                     ||

2019 (2 years ago): Diagnosed with Diabetes Mellitus, prescribed oral hypoglycemics

                                      ||

2020 (1 year ago): Has an episode of seizures (most likely GTCS)

                                      ||

January 2021 (4months ago): Has another seizure episode (most likely GTCS)- following cessation of alcohol for 24 hours. Starts drinking again after seizure subsides

                                     ||             

Monday, May 10, 2021: Last alcohol intake, around 1 bottle. Starts having general body pains at night.

                                      ||

Tuesday, May 11, 2021: Decreased food intake. Starts talking and laughing to himself. Unable to lift himself off the bed, help required. 

 Conscious, but non coherent. Disoriented to time, person, place. 

                                     ||

Saturday, May 15, 2021: Is admitted to a tertiary care hospital for alcohol withdrawal symptoms, and is treated for the same.



Anatomical localisation of problem:   hippocampus and frontal lobe.


Primary etiology of patient's problem: Chronic Alcoholism


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


1) IVF - NS and RL 

MOA -maintains blood volume and electrolytes in the body and also provides Glucose to the body 

 indications: dehydration, hypovolemic shock, to restore fluids after burns. 

2) inj. Thiamine : MOA : vitamin B1, Provides energy in deficiency conditions

Indications: 

* deficient conditions, wernickes encephalopathy, Diarrhoea, ulcerative colitis. 

3) inj. Lorazepam _ Benzodiazepine 

MOA : enhances the inhibitory effects of GABA - INHIBITORY NEUROTRANSMITTER. 

indications; * anxiety disorders, panic disorders, seizures, pre operative sedation. 

4) tab. Pregabalin _anticonvulsant

MOA: binds to alpha 2 voltage gated calcium channels in cns and inhibits release of excitatory  neurotransmitters 

indications ;

*partial seizures 

*nerve pain

*fibromyalgia

5) inj. HAI - insulin 

#MOA : reduces blood glucose levels by increasing peripheral uptake of glucose by muscle.

 Indications: 

*Type 1 Dm

*uncontrollable type 2 DM 

* DKA 

6) Grbs; test to identify blood glucose levels 

7) lactulose : artificial Dischaaride

indications:

* chronic constipation

*hepatic encephalopathy

8) inj. Kcl _ electrolytes

MOA; prevents low blood levels of potassium

indications ;

* hypokalemia

To correct deficiency, vomiting, weakness

9) syrup potchlor- contains potassium chloride, and prevents low levels of potassium in the body 

indications;

*deficiency of potassium

* electrolyte imbalance

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





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




Thiamine is necessary to provide energy to the CNS, helps in conduction of nerve signals.



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


Creatinine and urea levels are very high, it denotes an acute onset- Acute Renal Failure.

It could be  due to dehydration  which lead to Acute tubular necrosis



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


 causes:

a. Increased oxidative stress and inflammation, leading to hemolysis of the RBCs


b. Decreased bone marrow production of RBCs, due to EPO deficiency owing to kidney failure

c. Loss of blood through chronic foot ulcer


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

Yes, as alcoholism itself can cause peripheral neuropathy ,which along with Diabetic neuropathy, can lead to a non-healing foot ulcer.




(B) 

https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1
Complete regarding the case are in the mentioned link above


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?


Anatomical location - right inferior cerebellar hemisphere

Primary etiology - Hypertension



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

1) Tab. Vertin-  Betahistine

 MOA: agonist of H1 receptor and antagonist of H3 receptor , improve the microcirculation of inner ear

indications:vertigo, tinnitus

2) inj.zofer- ondansetron - ANTIEMETIC 

MOA: binds to 5 HT3 receptor and thus inhibits the binding of serotonin to it . 

#indications: nausea and vomiting due to any cause

3) Tab. Ecosprin- antiplatelet drug

MOA : low dose Aspirin prevents blood clot formation by inhibiting the action of COX enzyme

# indications;

 *stroke 

* angina 

* heart attack

4) Tab. Atorvastatin- statins 

MOA :HMG CO-A reductase inhibitor, thus decrease cholesterol production in liver. 

indications; 

*MI 

*STROKE

*ANGINA

5) BP monitoring

6) Tab. Clopidogrel- antiplatelet drug

MOA: inhibits the binding of ADP to platelet P2Y12 receptor and subsequent ADP mediated activation of

 GP2b/3a complex, action which is irreversible. 

#Indications:

*during PCI 

*ACS 

*Prevention of Thrombiembolism

*carotid artery stenosis

7) inj. Thiamine- vitamin B1

MOA:combines with ATP to produce thiamine Diphosphate , coenzyme in carb metabolism, utilization of hexose in HMP pathway. 

#Indications; 

*to correct deficiency

*beri beri

*neuritis

8) Tab. Mvt. - vitamins and minerals 

Indication : to correct deficiency and anemia



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

Yes

Decreased blood supply to that area - infarction - cerebellar infarct

Hypertension - Atherosclerosis - Ruptures- Stroke- Cerebellar infarcts




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

Alcohol is a risk factor for atherosclerosis which causes - Ischemia - Ischemic stroke




(C) 

http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html
Complete details regarding the case are in the mentioned link above


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?


Primary etiology - Hypokalemia lead to manifestation like palpitation and dyspnea

For radiating pain along left upper limb is due to cervical spondylitis



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

Could be due to inadequate intake 

Could be inherited also




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


Earliest change sen in ECG is decreased T wave amplitude

ST depression, T wave inversion, flat

Prolonged PR

Uwaves







D) Link to patient details:

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


QUESTIONS

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


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?

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)



Loc - loss of consciousness


E) Link to patient details:

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


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

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 lobe 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

 

 Liver damage due to too much alcohol can stop the liver from synthesis of coagulants  this may be the reason for his IC bleed

     https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1341444/#:~:text=The%20impaired%20platelet%20function%2C%20together,associated%20with%20excessive%20alcohol%20intake.




F) Link to patient details:

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


Questions


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

Yes

Yes
One cause of stroke after trauma is a tear in the head or neck blood vessels that lead to the brain, which can be a source of blood clots that cause a stroke. If a tear in these arteries can be diagnosed at the time of the trauma, a patient could be treated with an anti-clotting medicine to help prevent stroke.


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.

New insights into the mechanisms of action of aspirin and its use in the prevention and treatment of arterial and venous thromboembolism

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. 


Insulin:

Hypoglycemia can cause focal neurologic signs that mimic stroke and can itself lead to brain injury..

Therefore, prompt measurement and normalization of serum glucose concentration is important. Subcutaneous insulin is administered to keep glucose less than 180 mg/dL. 

Antipyretics

Increased body temperature in the setting of acute ischemic stroke has been associated with poor neurologic outcome, possibly due to increased metabolic demands, enhanced release of neurotransmitters, and increased free radical production. 

Maintaining normothermia might improve the prognosis of patients with severe events using antipyretic medications and cooling devices. Antipyretic therapy is indicated for temperatures above 37.5 °C.


Thrombolysis

Intravenous administration of alteplase is the only US Food and Drug Administration (FDA)-approved medical therapy for treatment of patients with acute ischemic stroke


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


Research shows that drinking large amounts of alcohol can    greatly increase your risk of having stroke.




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)

Complete details regarding the case are in the mentioned link above
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.ht


1)What is myelopathy hand ?

a)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

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 sign

Hoffman's sign 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)


Complete details regarding the case are in the mentioned link above
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1                  
  
Possible questions: 
              
1) 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 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 ?









-

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

ANS;

Pericardiocentesis is done when the pericardial effusion is not resolving on its own . Here the pericardial fluid which has accumulated was resolving on itw own , at the time of admission it was 2.4mm and when discharged it was 1.9 mm . Therefore we did not do pericardiocentesis in this pt.      

       

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

ANS:   IN THIS PATIENT:

NON MODIFICABLE:

age

gender

MODIFIABLE:

hypertension

smoking

type 2 diabetes .

kidney disease.


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

The pt. was anemic with Hb of 8gm/dl . One of the severe complication of anemia is tissue hypoxia which further lead to hypotension.






(B)

 Link to patient details:
https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html. 

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

ANS:

obesity 

alcohol

diabetes

hypertension


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

Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia. 





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

The pt. had recurrent blebs and ulcer on lower limbs (foot). This is due to Type to diabetes mellitus.

Diabetic foot ulcers generally arise as a result of poor circulation in the foot region. While high blood sugar levels and nerve damage or even wounds in the feet may result in foot ulcers in many cases. 


In cases of poor circulation of blood, the foot ulcers take quite a bit of time to heal as the blood efficiency in the foot region is at a low level. Furthermore, many develop a bit of reduced sensation on the feet as a result of nerve damage or more.


There are many risk factors that may lead to foot ulcers at the end.

Poor quality or fitting of the footwear.

Unhygienic appearance of foot.

Improper care of the nails of the toe.

Heavy intake of alcohols and tobacco.

Obesity and Weight-related

Complication arising from Diabetes like eye problems, kidney problems and more.

Although aging or old age can also be counted among them.


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

  alcohol consumption lead to obesity which caused impaired glucose tolerance  - Diabetes mellitus -microvascular complications like triopathy and diabetic foot ulcer

macrovascular complications like coronary artery disease , coronary vascular disease and peripheral vascular disease.



C)

Link to patient details:

https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.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:. 


 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 of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.
The most likely cause of arterial thrombosis is artery  due to atherosclerosis. Atherosclerosis occurs when a person has a buildup of 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 each of the pharmacological and non pharmacological interventions used for this patient?

Ans: PHARMACOLOGICAL INTERVENTIONS
1. TAB. Dytor

mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.

2. TAB. Acitrom 

mechanism: 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:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.



4. INJ. HAI S/C

MECHANISM:Regulates 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 enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.TAB. Digoxin 

mechanism:

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

6. Hypoglycemia symptoms explained

7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.

8. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.



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: 




Cardiorenal syndrome type 4 is seen in this patient.




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

Ans: effect of hypertention
 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 get those APTT, INR tests for review?


Ans: APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is 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.

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?

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

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

Pharmacological interventions:

TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient
 MOA: 
METOPROLOL is a cardioselective 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 







3) What are the indications and contraindications for PCI?




     
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?

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 treatment have become common



E)

 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?

~symptamatology; 
*chest pain since 3 days
*profuse sweating and Giddiness since 1 day 
~anatomical localization: BV'S of heart 
~primary etiology; presence of risk factors like HTN AND DM which leads to ATHEROSCLEROSIS



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

   pharmacological ; 

Tab. Aspirin-ANTICOAGULANT
(low dose) 
MOA: COX inhibitor, resulting in inhibition of platelet aggregation
Indications;  angina, Stroke, MI



~ Tab. Atorvas - STATIN 
MOA: HMG _CO-A Reductase inhibitor and thus decreases cholesterol productiom in liver. 
Indications: 
*MI, Stroke, Angina


~Tab.clopibb _ antiplatelet drug
MOA:inhibits binding of ADP to platelet P2Y12 receptor and subsequent ADP mediated activation of GP 2b/3a  complex , thus inhibits platelet aggregation. 
Indications: *PCI , ACS, prevention of Thrombiembolism, carotid artery stenosis. 


Inj, HAI - INSULIN
MOA: reduces blood glucose by increasing  peripheral uptake of glucose by muscle. 
Indications: Type 1 DM
Type 2 DM, DKA 
vital monitoring. 



Non pharmacological; 
PTCA _procedure to restore the blood flow through  the artery. 
Types; *balloon angioplasty
*coronary stent
*atherectomy
*laser angioplasty




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

Not necessary
Because patient crossed the window period of 12 hours



F)

 Link to patient details:




1. How did the patient get  relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
Because of the fluid lossoccured to the patient 
There is 
Decreased preload → SOB occured due to decreased cardiac output
IV fluids administered → there is increase in preload → SOB  decreased due to better cardiac output 

2. What is the rationale of using torsemide in this patient?
Torsemide is used due to abdominal distension

3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Treatment for UTI 
Rationale - used for any bacterial infection .







4) Gastroenterology (& Pulmonology) 


A) 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?


Evolution of symptomatology 
5 years back-1st episode of pain abdomen and vomitings 
                                     ||

Stopped taking alcohol for 3 years

                                      ||

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

                                        ||

20 days back increased consumption of toddy intake

                                         ||

Since 1 week pain abdomen and vomiting

                                          ||

Since 4 days fever constipation and burning micturition


Anatomical localisation: Pancreas and left lung

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




2) What is the efficacy of drugs used along with other non pharmacological  treatment modalities and how would  you approach this patient as a treating physician?
1) ING. MEROPENAM ; TID for 7 days 

* Meropenem ( broad spectrum Carbepenem ) an antibiotic.

2) ING. METROGYL 500 mg IV TID for 5 days

* inj. Metrogyl has METRONIDAZOLE

( Nitroimidazole drug ) an antibiotic

3) ING. AMIKACIN 500 mg IV BD for 5days

* It is an Aminoglycoside antibiotic 

## Here all three of these (Inj. Meropenem, Inj. Metrogyl, Inj. Amikacin ) are used as antibiotics to control infection and ; to prevent septic complications of acute pancreatitis.

4) TPN ( Total Parenteral Nutrition )

* Method of feeding that by passes gastrointestinal tract

* Fluids are given to vein , it provides most of the nutrients body needs.

* TPN has proteins, carbohydrates, fats, vitamins, minerals.

5) IV NS / RL at the rate 12l ml per hour

* Given for fluid replacement ie., treat dehydration 

6) ING. OCTREOTIDE 100 mg SC , BD

* It is a Somatostatin long acting analogue.

* It is used here to decrease exocrine secretion of pancreas and it also has anti- inflammatory & cytoprotective effects.

7) ING. PANTOP 40 mg IV , OD

* Inj. Pantop has PANTOPRAZOLE ( Proton Pump Inhibitor) used for its anti pancreatic secretory effect.

8) ING. THIAMINE 100 mg in 100 ml NS  IV , TID

* It is B1 supplement. 





B) Link to patient details:



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

the cause of dyspnea might be PLEURAL EFFUSION



2.Name the possible reasons why patient had developed state of hyperglycemia

*This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress
* the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-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, ALT can be released into the blood. This causes ALT levels to increase. A higher than normal result on this test can be a sign of liver damage.

*elevated alanine transaminase (ALT) and aspartate transaminase (AST), usually one to four times the upper limits of normal in alcoholic fatty liver.

The reasons for a classical 2:1 excess of serum AST activity compared to serum ALT activity in alcoholic hepatitis have been attributed to

 (i) decreased ALT activity most likely due to B6 depletion in the livers of alcoholics

 (ii) mitochondrial damage leading to increased release of mAST in serum.



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

Plan of action and Treatment:

Investigations:

24 hour urinary protein 

Fasting and Post prandial Blood glucose 

HbA1c 

USG guided pleural tapping 

Treatment:

• IVF: 125 mL/hr 

• Inj PAN 40mg i.v OD 

• Inj ZOFER 4mg i.v sos 

• Inj Tramadol 1 amp in 100 mL NS, i.v sos

• Tab Dolo 650mg sos 

• GRBS charting 6th hourly 

• BP charting 8th hourly



C) Link to patient details:



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

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


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


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

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







5) Nephrology (and Urology) 


A) Link to patient details:


1. What could be the reason for his SOB ?

*possible reason in this patient : acute renal failure causing  Acidosis - SOB



2. Why does he have intermittent episodes of  drowsiness ?
 *The most probable cause for drowsiness in thi patient is Hyponatremia which was caused by diuretics




3. Why did he complaint of fleshy mass like passage in his urine?
It was due to pyuria ,for which he complaint of fleshy mass like passage



4. What are the complications of TURP that he may have had?
 
Infection
Electrolyte imbalance
Difficulty in micturation
Any bladder injury
Turp syndrome


B) Link to patient details:




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.





6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)


A) Link to patient details:




Questions:

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


The patient is a known case of Retroviral Disease but she was on her ART since 2 months. There might be a possible chance that her negligence to treat RVD is the cause of her Tracheo esophageal and also TB.
Physical finding 
According to CECT there is a fistulous communication between left main bronchi and mid thoracic oesophagus few centimetres below carina




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

Immune reconstitution inflammatory syndrome (IRIS) is a condition seen in some cases of AIDS or immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse. The suppression of CD4 T cells by HIV (or by immunosuppressive drugs) causes a decrease in the body's normal response to certain infections. Not only does this make it more difficult to fight the infection, it may mean that a level of infection that would normally produce symptoms is instead undetected (subclinical infection). If the CD4 count rapidly increases (due to effective treatment of HIV, or removal of other causes of immunosuppression), a sudden increase in the inflammatory response produces nonspecific symptomssuch as fever, and in some cases a worsening of damage to the infected tissue
reported to occur in 13%–45% of HIV-infected persons who start ART 








7) Infectious disease and Hepatology:


Link to patient details:





1. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors
 present in it ? 

What could be the cause in this patient ?

Yes, It could be due to intake of contaminated toddy

Like any other alcoholic drink, excessive toddy (8.1%)drinking can damage the liver.Even the alcohol content is less than that of wine, the patient has been drinking it since 30 years . Therefore it is the major predisposing factor




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



There can be various mechanisms by which toddy could influence EH virulence. The resident microbial flora in human colon is an important determinant of survival and virulence in EH. Alcohol consumption is known to induce intestinal bacterial dysbiosis, which may in turn alter the activity of EH. Undistilled local alcoholic beverages contain a large number of microorganisms that might have more propensity to cause intestinal dysbiosis. EH lacks mitochondria and obtains its energy from the fermentation of glucose. EH alcohol dehydrogenase 2 (EHADH2) is a key enzyme in this pathway7. Thus, expression of EHADH2 is required for the growth and survival of EH trophozoites in human. 

alcohol suppresses the function of Kupffer cells in the liver, which has the important role of clearing the amoeba. This leads to pathogenic invasion leading abscess formation



3. Is liver abscess more common in right lobe ?

Right lobe is more significant part with more blood supply. Therefore liver abscess is more common








4.What are the indications for ultrasound guided aspiration of liver abscess ?
 Large abscess more than 6cms
 Left lobe abscess
 Abscess failure to respond to drugs
 Any large abscess which is impending to rupture








B) Link to patient details:



QUESTIONS:


1) Cause of liver abcess in this patient ?

The patient is occasional toddy drinker which has high amount of Entamoeba histolytica. This causes liver abscess by suppressing the function of Kuffper cells.Therefore Toddy is most probable cause of Liver abscess in this patient




2) How do you approach this patient ?







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


As liver abscess is difficult to aspirate  due to

Risk of rupture
Unliquefied abscess
Thin walled abscess


Cannot be differentiated between them

So, we start giving treatment to both pyogenic and ameobic

INJECTION. ZOSTUM 1.5 gm IV BD (twice daily) 

 Zostum is a  combination of  drugs - SULBACTUM (pencillin) & CEFOPERAZONE(cephalosporin) [Antibiotic]: It is used here to treat if any bacterial cause ( since we can’t take the risk relying on only anti amoebic therapy) 

* INJECTION. METROGYL 500mg IV TID ( thrice daily )

Metrogyl has the drug called METRONIDAZOLE[Antibiotic]: For amoebic cause 

* INJECTION. OPTINEURIN 1amp in 100 ml NS( Nor

mal Saline) IV OD ( once daily)

Optineurin is a multivitamin drug { A combination of B1,B2, B3, B5,B6, B12 } given here as a supplement 

* TAB. ULTRACET 1/2 QID( four times a day)

Ultracet is a combination of drugs - TRAMADOL(opiod analgesic) and ACETAMINOPHEN (analgesic and antipyretic) : Given for pain and fever 

* TAB. DOLO 650 mg SOS (if needed) given for fever and pain 

* Here ; due to medical therapy his symptoms subsided and clearly we can see it in usg reports ( liquefaction) meaning abcess responded to our medical therapy. 

*And the patient was discharged on 10/5/21.

* We donot aspirate the pus since it is self resolving and aspiration is associated with several other complications.



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

Apart from serological examination which is positive in 94% of the cases..Further confirmation can be done by using Ultrasonography but these are not commonly used



8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology 


A) 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?


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


patient was diagnosed with diabetic ketoacidosis and was unaware that he was diabetic until then. This resulted in poorly controlled blood sugar levels. The patient was diagnosed with acute oro rhino orbital mucormycosis . rhino cerebral mucormycosis is the most common form of this fungus that occurs in people with uncontrolled diabetes ( https://www.cdc.gov/fungal/diseases/mucormycosis/definition.html ) the fungus enters the sinuses from the environment and then the brain.



Anatomical localisation : Medial canthus of left , Oral cavity and hardpalate, left nasal cavity and left frontal & temporal lobes 
Primary etiology 

Mucormycetes, the group of fungi that cause mucormycosis, are present throughout the environment, particularly in soil and in association with decaying organic matter, such as leaves, compost piles, and animal dung. 1  They are more common in soil than in air, and in summer and fall than in winter or spring. 2-4 Most people come in contact with microscopic fungal spores every day, so it’s probably impossible to completely avoid coming in contact with mucormycetes. These fungi aren’t harmful to most people. However, for people who have weakened immune systems, breathing in mucormycete spores can cause an infection in the lungs or sinuses which can spread to other parts of the body.



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?


Itraconazole acts by inhibiting the fungal cytochrome P-450 dependent enzyme lanosterol 14-α-demethylase. When this enzyme is inhibited it blocks the conversion of lanosterol to ergosterol, which disrupts fungal cell membrane synthesis. Itraconazole exhibits fungistatic (slows the growth) activity against yeast-like fungi and fungicidal (kills the fungus) activity against Aspergillus species
Amphotericin B binds with ergosterol, a component of fungal cell membranes, forming pores that cause rapid leakage of monovalent ions (K+, Na+, H+ and Cl−) and subsequent fungal cell death




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



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


Low oxygen, diabetes, high iron levels, immunosuppression, as well as several other factors including prolonged hospitalisation with mechanical ventilators, creates an ideal milieu for contracting mucormycosis,
Contamination in pipes of the oxygen cylinders
unhygienic masks" and poorly ventilated rooms could be a contributing factor
history of exhibiting poor hygienic practices, including wearing unwashed masks for a long time.
irrational use of steroids
Mucormycosis is more common among people whose immunity has lowered due to COVID, diabetes, kidney disease, liver or cardiac disorders, age-related issues, or those on immunosuppressive medication for auto-immune diseases.


9) Covid Master sheet


10) Experimental medical learning




Even during this pandemic, i could learn medicine through the online telecommunication and trying to reach the patient and help them through the various inputs i get from everyone

*I have taken pneumonia secondary to covid 19 with hypothyroidism case for the first time through telecommunication on 15 May 2021 and learnt how her hypothyroidism and ct severity affected her outcome

After this i took another case through telecommunication  POST TURP with acute pyelonephritis , went through the literatures and learnt many new things from this case

And other  patient with acute epigastric and rt hypochondric pain - Liver Abscess
Where i have learnt how serious is liver abscess in chronic alcoholic and outcome and treatment

All these cases actually taught me many new things and went through new literatures 


Really thankful to the Medicine Department for giving chance to improve our learning skills
And connecting us to the patients to help them
















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