Sunday, 30 May 2021

Medicine assessment

Below are my answers to the Medicine Assignment based on my comprehension of the cases


Name: K.S.SASIRA

Roll no. : 166

MBBS 8SEM


Question no.1 : Pulmonology 

 Link :



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?

 ■ Symptomatology :

    ■  shortness of breath on and off for the past 20 years , occurring around January (when she worked at the paddy fields) these episodes were all relieved upon taking medication.

 ■ Her latest episode of shortness of breath started 30 days ago, Initially the SOB occurred on exertion and was relieved upon rest. From 2 days ago she started having SOB even at rest (grade IV) and was not relieved with nebulizers. 

▪︎ 1 month back she was experiencing generalized weakness 

▪︎ 20 days ago due to the ongoing Covid 19 pandemic she had an HRCT which showed signs of bronchiectasis.

Pedal edema since 15 days upto the level ankle and pitting type.

Facial puffiness since 15 days.

▪︎She has drowsiness since 2 days

▪︎ She has decreased urine output for the past 2 days.

 
■  Anatomical localization :
   
                                                       Lungs , heart
 
■  Primary etiology :
  
                                      Exposure to paddy fields


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

          ■  The placebo effect is the positive effect on a person's health , It is triggered by the person's belief in the benefit from the treatment and their expectation of feeling better, rather than the characteristics of the placebo.




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

                One of the potential causes could be right heart failure


4) Could the ATT have affected her symptoms? If so how?
 
                                 No 

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

                     Subjects with heart failure may show hyponatremia, magnesium, and potassium deficiencies ; the latter two play a pivotal role in the development of cardiac arrhythmia


Question no. 2 : neurology

H) Link :



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.



Question no.3 : Cardiology 


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

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

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

HFpEF is preceded by chronic comorbidities, such as hypertension, type 2 diabetes mellitus (T2DM), obesity, and renal insufficiency, whereas HFrEF is often preceded by the acute or chronic loss of cardiomyocytes due to ischemia, a genetic mutation, myocarditis, or valvular disease  


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

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

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


■ risk factors for development of heart faliure in this patent

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

■ high blood pressure

Smoking

■ Diabetes

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


4.What could be the cause for hypotension in this
  
      ■  visceral pericardium may have  thickened which is restricting the heart to expand causing hypotension 

(May be secondary to TB)




C) Link :

 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?


■ *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 damage 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?


■ 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? 

 ■  *cardiorenal syndrome type 4 is seen in this patient.



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

    ■ 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?


■  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.



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 loss occurred to the patient
there is decreased preload- so, SOB occurred due to decreased CO
IV fluids administered- there is increased preload- SOB decreased due to better of cardiac output.

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

Torsemide used to relieve abdominal distension.

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

IT IS THE TREATMENT FOR UTI
Rationale- Used for any bacterial infection.



● Question no. 5 : Nephrology and urology 

Link :

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.


 ● Question no. 6 : Infectious diseases

 
Link - 



Questions:


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

         clinical history and physical findings in this patient are positive for -

 ▪︎Cough since 2 months on taking food and liquids and regurgitation of food seen.

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

 ▪︎H/O weight loss of 10 Kgs since 2 months, hoarseness of voice, inadequate sleep since 2 months

 ▪︎Laryngeal crepitus positive

All the above findings are very much indicative of tracheo esophageal fistula


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

       There is a very high chance of development of immune reconstitution inflammatory syndrome in this patient

 ■Immune reconstitution inflammatory syndrome (IRIS)

                                                                                                  This is the condition mostly seen in AIDS after initiating antiretroviral therapy (ART) therapy in HIV-infected / immuno compromised patients resulting from restored immunity to specific infectious or non-infectious antigens 

        

 Risk factors:    





 Pathogenesis:


As in this patient's case there was initiation of ART was done 2 months back which presented with complaints




Prevention :    In light of what is known of the risk factors and immunopathogenesis of IRD, it follows that a range of different interventions may reduce the risk and severity of unmasking and paradoxical forms of IRD. These include the initiation of ART much earlier in the course of HIV progression, preventive therapy for OIs prior to ART eligibility, pre-ART screening for OIs, use of optimized treatment for OIs, adjustment of the timing of starting ART during OI treatments, and immunosuppressive and immunomodulatory therapies.


 

● Question no.7 : Infectious disease and Hepatology



A) Link :



Questions:

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 , alcohol consumption has 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.

▪︎ The cause in this patient , most likely is biliary duct obstruction ,which can be figured out from his LFT investigations (Raised direct bilirubin and ALP)



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

▪︎ Since the liver receives its blood circulation from the systemic and portal circulations, it is more susceptible to getting infections and abscesses from the bloodstream.

▪︎ Proximity to gall bladder is another risk factor for the liver.

▪︎ The usual pathophysiology for pyogenic liver abscesses is bowel content leakage and peritonitis. Bacteria travel to the liver via the portal vein and resides there. Infection can also originate in the biliary system. Hematogenous spread is also a potential etiology.

▪︎ Septic emboli cause several microabscesses which combine to form one large abscess.








3. Is liver abscess more common in right lobe ?
       
▪︎ 50% of solitary liver abscesses occur in the right lobe of the liver (a more significant part with more blood supply), less commonly in the left liver lobe or caudate lobe.

▪︎ right lobe recieves blood supply from - superior mesenteric and portal veins




4.What are the indications for ultrasound guided aspiration of liver abscess ?

▪︎ Indications -

                           1. size 5.5cm and more

                           2. lesion appearing to be superinfected

                           3.  Large abscess impending for rupture




B) Link :



QUESTIONS:


1) Cause of liver abcess in this patient ?



■ Single abcess,

■ Right lobe involvement,

■ Route of ingestion is orofecal route 


2) How do you approach this patient ?

▪︎ 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 

▪︎ 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 

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



3) Why do we treat here ; both amoebic and pyogenic liver abcess? 
  
   ▪︎We treat both amoebic and pyogenic liver abscess emperically as there is no         distinguished clinical features 





  ▪︎ we cover both bacterial causes with broad spectrum antibiotics and also amoebic causes mostly with metronidazole.






▪︎ we administer patient with analgesic and antipyretic such as tab.dolo &tab.Ultracet.


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

      ■ (Anti amoebic antibodies )ELISA is the confirmatory investigation 



●  Question no.8 : Infectious diseases



 Link :



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?

Symptoms-

  ▪︎Fever since 10 days

  ▪︎facial puffiness and periorbital edema after 6 days associated with weakness in   right upper and lower limb 

 ▪︎ following which he developed altered sensorium 2days later

■ Anatomical position -
                                               Orbit and maxillary sinus

Primary etiology- 
                                     Infection in a immunocompromised patient 


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?

  ▪︎ I would like to start the patient on Amphotericin b 
     As of now , there is no proper study made showing proper efficacy of drugs like           Amphotericin b but till date this has shown promising results.


3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time? 
 
 ▪︎ Due to the rise of covid 19 infections in the country , an excessive surge in patients with comorbities like HTN and most importantly diabetes a very important predisposing factor for the development of mucormycosis (immunocompromised patients as well).


Sunday, 23 May 2021

viral pneumonia secondary to covid-19

 70 year old male with cough, fever and shortness of   breath                   


This is online E log book to discuss our patient’s de-identified health data shared after taking his/her/guardian’s signed informed consent. Here we discuss our individual patient’s problems through series of inputs from available global online community of experts with an aim to solve those patients clinical problems with collective current best evidence based inputs. This e-log book also reflects my patient centered online learning portfolio and your valuable inputs on comment box is welcome .

 

I’ve been given this case 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, investigations, and come up with diagnosis and treatment plan.



K.S.SASIRA


MBBS 8 SEM


ROLL NO. : 166


Following is my view of the case based on history as per date of admission :
 
Case :
             A 70 year old male came to the opd on 15th may with the chief complaints of -

            1)Dry cough since 10 days 
            2)fever since 10 days 
            3)shortness of breath since 4 days 

History of presenting illness :
                                                      Patient was apparently assymptomatic 10 days back when he developed
 - Dry cough which was insidious in onset , intermittent in nature with no diurnal or positional variations and no aggravating or relieving factors were noted.
- fever which was insidious in onset , intermittent in nature not assocoated with chills and rigors, was relieved on medication.
-  later he developed shortness of breath 4 days back ,insidious in onset and gradual in progression with no complaints of vomitings , chest pain , loss of taste and smell.
 He tested positive on RTPCR COVID with CT score of 10/25 following which he was admitted to COVID ICU


Past history: 

■Not a k/c/o HTN ,DM,CAD,asthma,Tb 
■Non alcholic, non smoker 

Personal history:  

Diet - vegetarian
Appetite - normal
Sleep - adequate
Bowel and bladder movements -regular
Addictions-none
Allergies-none

Family history :

■There is no significant family history

General examination:

Informed consent was taken before examining the patient and the examination was done in a well lit and ventilated room. Patient is moderately built and nourished .

pallor:absent
■Icterus:absent
■Cyanosis:absent
■Clubbing:absent
■Lymphadenopathy:absent
■Edema:absent
■Dehydration : mild

Vitals-

 ■On the day of admission(15/05/2021):

▪︎Pulse rate - 82bpm
▪︎Blood pressure- 110/60mm Hg 
▪︎Afebrile
▪︎Respiratory-22/min
▪︎Spo2-86% on room air
            93% with 10 lit of O2

16/05/2021

▪︎Pulse rate - 99bpm
▪︎Blood pressure- 120/90mm Hg 
▪︎Afebrile
▪︎Spo2- 92% with 10 lit of O2


17/05/2021:

▪︎Pulse rate - 98bpm
▪︎Blood pressure- 120/80mm Hg 
▪︎Afebrile
▪︎Spo2- 96% with 4 lit of O2

18/05/2021:

▪︎Pulse rate - 86bpm
▪︎Blood pressure- 110/70mm Hg 
▪︎Afebrile
▪︎Spo2-95% with 6 lit of O2

19/05/2021:

▪︎Pulse rate - 84bpm
▪︎Blood pressure- 110/70mm Hg 
▪︎Afebrile
▪︎Spo2- 95% with 4 lit of O2

20/05/2021:

▪︎Pulse rate - 70bpm
▪︎Blood pressure- 110/70mm Hg 
▪︎ Afebrile
▪︎Spo2-93% on room air
           96% with 2 lit of O2

Systemic examination:

Cvs:- S1,S2 heart sounds heard,no murmurs.

Respiratory system:- bilateral air entry present

CNS:- intact

Abdomen :-soft and non tender.Bowel sounds are heard .
                        No organomegaly

Investigations

1) GRBS -401mg/dl on 16/05/2021


2)chest X-ray: 
                                                            
                                                                 16/05/2021





3)ECG

17/05/2021

4)

17/05/2021



Provisional diagnosis: 
                                         Viral pneumonia secondary to Covid 19 and denovo Diabetes mellitus

Treatment

15/05/2021

prone positioning
•O2 inhalation
•Inj.Dexamethasone-6mg/IV/OD
•Nebulisation with Duolin, budecort and mucomist-8th hourly
•Syp.Grillinctus-10ml/PO/TID
•T.PANTOP 40mg/PO/OD
•T.LIMCEE-OD
•T.PCM -650mg/PO/SOS
•IVF-NS with optineuron @ 75ml/hr continous

16/05/2021

•O2 inhalation
•Inj.Dexamethasone-6mg/IV/OD
•Nebulisation with Duolin, budecort and mucomist-8th hourly
•Syp.Grillinctus-10ml/PO/TID
•T.PANTOP 40mg/PO/OD
•T.LIMCEE-OD
•T.PCM -650mg/PO/SOS
•IVF-NS with optineuron @ 75ml/hr continous
•GRBS charting 6hourly
•Inj.HAI/SI/AS per slides
•Incentive spirometry

17/05/2021:

•O2 inhalation
•Inj.Dexamethasone-6mg/IV/OD
•Nebulisation with Duolin, budecort and mucomist-8th hourly
•Inj.Clexane 60mg/SI/BD
•Syp.Grillinctus-10ml/PO/TID
•T.PANTOP 40mg/PO/OD
•T.LIMCEE-OD
•T.PCM -650mg/PO/SOS
•IVF-NS with optineuron @ 75ml/hr continous
•GRBS charting 6hourly
•Inj.HAI/SI/AS per sliding scale
•Incentive spirometry

18/05/2021:

•O2 inhalation
•Inj.Dexamethasone-6mg/IV/OD
•Nebulisation with Duolin, budecort and mucomist-8th hourly
•Inj.Clexane 60mg/SI/BD
•Syp.Grillinctus-10ml/PO/TID
•T.PANTOP 40mg/PO/OD
•T.LIMCEE-OD
•T.PCM -650mg/PO/SOS
•IVF-NS with optineuron @ 75ml/hr continous
•GRBS charting 6hourly
•Inj.HAI/SI/AS per sliding scale
•Incentive spirometry

19/05/2021:

•O2 inhalation
•Nebulisation with Duolin, budecort and mucomist-8th hourly
•Inj.Clexane 60mg/SI/BD
•Syp.Grillinctus-10ml/PO/TID
•T.PANTOP 40mg/PO/OD
•T.LIMCEE-OD
•T.PCM -650mg/PO/SOS
•IVF-NS with optineuron @ 75ml/hr continous
•GRBS charting 6hourly
•Inj.HAI/SI/AS per sliding scale
•Incentive spirometry

20/05/2021:

•O2 inhalation
•IVF-NS with optineuron @ 75ml/hr continous
•Inj.Clexane 60mg/SI/BD
•GRBS charting 6hourly
•Inj.HAI/SI/AS per sliding scale
•Inj.Dexamethasone-6mg/IV/OD
•Syp.Grillinctus-10ml/PO/TID
•T.PANTOP 40mg/PO/OD
•T.LIMCEE-OD
•T.PCM -650mg/PO/SOS
T.Mut/OD
•Incentive spirometry
 

Later that day the patient was discharged and was adviced to take medications as follows-
•O2 inhalation to maintain Spo2 >90%/SOS
•Tab.PAN 40mg/PO/1-0-0 × 1 week
•T.LIMCEE-PO/0-1-0 × 1 week 
•Tab MVT/PO/0-1-0×1week
•Tab. DOLO 650mg/PO/SOS
•Syp.Grillinctus LS/PO/10ml/1-1-1×1week
•Incentive spirometry

Questions:-

 1)what could be the long term complications of left lobe consolidation in this patient?

2)Did the covid 19 trigger new onset diabetes in this patient or was he an undiagnosed diabetic?

Under the guidance of Dr.charan sir