144 Varshitha Kalidindi

 Welcome to my e-log!

I am Varshitha Kalidindi, a 2nd year MBBS student. Here is an assignment which was given to me and I will be answering it question wise below:-

Question 1: Competency tested for Peer to peer review and assessment : 

Please go through one particular answer of ten students in this link:

https://generalmedicinedepartment.blogspot.com/2021/06/bimonthly-formative-and-summative_19.html?m=1

and share your peer review of each answer with your quantitative marking input as well as qualitative insights into what was good or bad about the answer. 

Answer:-

R1.The answer that I will be reviewing is from the link given below:-

https://aitharaveena.blogspot.com/2021/05/online-blended-medicine-assignment-may.html

55 year old female with shortness of breath, pedal edema and facial puffiness

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

Questions

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

  ans) Evolution of symptoms

 • 1st episode of SOB :- 20 years ago (in month of January)

• Since then she had yearly episodes of SOB for 8 years lasting 1 week occurring around January

• 12 years ago another episode of SOB lasted for 20 days

•Then after yearly episodes for 12 years around january lasting for month SOB was (Grade- 2)

• Diagnosed with Diabetes 8 years ago 

• Anemia and took iron injection:- 5 years ago

• Generalized weakness :- 1 month ago

• Diagnosed with Hypertension:- 20 days back

• Pedal edema:- since 15 days

•Facial puffiness:- 15 years back

 LOCALISATION OF PROBLEM: Lungs

 Primary etiology : could be due to pollen allergy or due to usage of chulha since 20 years

My review: This is basically a pulmonology case, where the patient has been experiencing a shortness of breath on a yearly basis. She also has a history of diabetes and anemia. Some of her recent symptoms include hypertension, pedal edema, generalised weakness.

    This answer has very clearly shown the evolution of symptoms in the patient from the first episode till the present status. Also, the shortness of breath was even graded to explain in more detail what the patient was experiencing in particular. The anatomical localisation and primary ethology were mentioned as well. Overall, this answer was concise and to the point. It answers the question word to word. This answer could've maybe been improved by also mentioning how the anatomical localisation was done in the case. The primary etiology is meaningful and well described.

R2: The answer that I will be reviewing is from the link given below:-

https://amishajaiswal03eloggm.blogspot.com/2021/05/medicine-blended-assignment.html

  A 40 year old male with complains of irrelevant talking.

https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

• anatomical location and pathophysiology

         *  Ethanol is a central nervous system depressant that produces euphoria and behavioral excitation at low blood concentrations due to increased glutamate binding to N-methyl-D-aspartate (NMDA) receptors; at higher concentrations, it leads to acute intoxication by potentiation of the gamma-aminobutyric acid (GABA) effects, particularly in receptors with delta subunits. The local distribution of these subunits explains why the cerebellum, cortical areas, thalamic relay circuitry, and brainstem are the main networks that mediate the intoxicating effects of alcohol.

*Prolonged alcohol use leads to the development of tolerance and physical dependence, which may result from compensatory functional changes by downregulation of GABA receptors and increased expression of NMDA receptors with production of more glutamate to maintain central nervous system (CNS) transmitter homeostasis

*Abrupt cessation of chronic alcohol consumption unmasks these changes with a glutamate-mediated CNS excitation resulting in autonomic overactivity and neuropsychiatric complications such as delirium and seizures.The latter are usually of generalized tonic–clonic type and are mediated largely in the brainstem by abrogation of the tonic inhibitory effect of the GABAergic delta subunits

My review: The case being discussed here is basically of a patient who has a history of diabetes, seizures. He also has short term memory loss and speaks irrelevantly. The patient was diagnosed with Wernicke's encephalopathy.

This answer has been very creatively written with a nice flowchart explaining the evolution of the symptoms from when they first appeared. A diagram has been used judiciously to explain the effects of intoxication, chronic alcohol consumption and withdrawal on the homeostasis of GABA and glutamate. Also, all the points that the question has suggested have been answered as well. Overall, it is a very good answer.

R3:The answer that I will be reviewing is from the link given below:-https://caseopinionsbyrollno05.blogspot.com/2021/05/medicine-blended-assignment-may-2021.html

Link to patient details:

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?

Ans : The evolution of the symptomatology in this patient in terms of an event timeline

- history of giddiness

 This was associated with 1 episode of vomiting on the same day.

from the bed and while walking.

- This was associated with Bilateral Hearing loss, aural fullness and presence of tinnitus.

- He has associated vomiting- 2-3 episodes per day, non projectile, non bilious containing food particles.

- Patient has H/o postural instability- he is unable to walk without presence of supports, swaying is present and he has tendency to fall while walking 

PRIMARY ETIOLOGY;

Obstruction of the posterior inferior cerebellar artery (PICA, also the most frequent location for a cerebellar infarct) leads to a headache and less commonly vomiting, vertigo, horizontal ipsilateral nystagmus, and truncal ataxia. Anterior inferior cerebellar artery (AICA) territory infarction more often leads to dysmetria, Horner's syndrome, unilateral hearing loss and ipsilateral facial paralysis or anesthesia with contralateral hemibody sensory loss of pain and temperature. Finally, obstruction of the superior cerebellar artery (SCA, located most rostral) tends to produce more ataxia, dysarthria, and nystagmus, with less vertigo, headache, and vomiting. However, presentations can often be atypical or overlap, in particular for hemorrhagic infarcts.

My review: The patient has a history of giddiness. The patient has an episode of vomiting and also bilateral hearing loss, aural fullness and tinnitus is present. Also, 2-3 episodes per day of vomiting was seen. He struggles with walking without support.

    The answer has been described with the evolution of symptoms. The primary ethology and anatomical localisation have also been described and explained well. However, there could've been more effort in explaining the evolution of the symptoms in a more clear way.

R4: The answer that I will be reviewing is from the link given below:-https://blendedasessmentmadhukumar.blogspot.com/2021/05/medicine-blended-assesment-may.html

Patient details :

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?

Answer : 

8 months back: 

-Apparently normal

-Then she developed bilateral pedal edema which are gradually progressing and was present on both sitting and standing positions

-Relieved on taking medication 

6 days back: 

-Pain radiating along left upper limb which was dragging in nature

-Aggravated during palpitations and relieved on taking medication for palpitations 

-Chest pain associated with chest heaviness

5 days back: 

-Palpitations which were sudden in onset, more during night time 

-Aggravated on lifting weights, speak continuously 

-Relieved by drinking more water and taking medication 

-Dyspnoea during palpitations (NYHA-CLASS-3)

-No history of fever/vomiting/diarrhoea/muscle pain 

My review: The case is of a 45 year old female patient who has chief complaints of palpitations, chest heaviness, pedal edema, chest pain, radiating pain along the left upper limb, generalised weakness. She has been diagnosed with cervical spondylosis Recurrent hypokalemic paralysis.

  This answer has described the evolution of symptoms in the patient and has clearly described the symptoms as experienced by the patient, which is crucial when taking the patient's history. I would say that this is a well-composed answer.

R5: The answer that I will be reviewing is from the link given below:-

https://15abhishek.blogspot.com/2021/05/15-cabhishek-general-medicine-assignment.html?m=1

A 55-year-old female with shortness of breath ,pedal Edema ,and facial puffiness.

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

b)PHARMACOLOGICAL INTERVENTION

head end elevation

           MECHANISM:In an intervention study involving early mobilization of intubated abdominal surgery patients, it was  observed that high thoracic positions, such as sitting upright for 20 minutes, led to an improvement in transthoracic pressure, with consequent improvement in the Cst, rs. This gain enabled a reduction in the driving pressure required for the generation of a similar lung volume.

BiPAP

          MECHANISM: During systole, CPAP induced increase in intrathoracic pressure reduces the venous return, decreasing the right and left ventricular preload, thereby improving mechanics in an overloaded ventricle, whereas in diastole, CPAP increases pericardial pressure, reduces transmural pressure, and thus decreases afterload.

Agumentin(amoxicillin+calvulanic acid)

          MECHANISM: Amoxicillin binds to penicillin-binding proteins within the bacterial cell wall and inhibits bacterial cell wall synthesis. Clavulanic acid is a β-lactam, structurally related to penicillin, that may inactivate certain β-lactamase enzymes

Azithromycin

         MECHANISM: Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit 

inj.lasix

        MECHANISM: Furosemide, like other loop diuretics, acts by inhibiting the luminal Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle, by binding to the chloride transport channel, thus causing sodium, chloride, and potassium loss in urine.

tab.Pantop

         MECHANISM: The mechanism of action of pantoprazole is to inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion. The covalent binding prevents acid secretion for up to 24 hours and longer.

inj. hydrocortisone

        MECHANISM:Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes. Hydrocortisone has a wide therapeutic index  and a moderate duration of action.

Neb. with ipravent ,budecortisone

          MECHANISM: 

 *Ipravent belongs to a group of medicines known as anticholinergic bronchodilators. Anticholinergic bronchodilators work by relaxing the bronchial tubes (air passages) that carry air in and out of your lungs. This makes breathing less difficult.

*Budesonide is a potent topical anti-inflammatory agent. [19] It binds and activates glucocorticoid receptors (GR) in the effector cell (e.g., bronchial) cytoplasm that allows the translocation of this budesonide-GR complex in the bronchi nucleus, which binds to both HDCA2 and CBP

tab.pulmoclear

       MECHANISM: Pulmoclear Tablet is a combination of two mucolytic medicines: Acebrophylline and Acetylcysteine. It thins and loosens mucus (phlegm) making it easier to cough out.

chest physiotherapy

       MECHANISM:The aims of ACTs in patients with COPD are to assist sputum clearance in an attempt to reduce symptoms and paroxysmal coughing, slow the decline in lung function, reduce exacerbation frequency and hasten the recovery from exacerbations.

inj.thiamine

         MECHANISM:thiamine may augment aerobic metabolism in the critically ill, even in the absence of absolute deficiency. We hypothesized that the administration of intravenous thiamine to critically ill patients would cause an increase in oxygen extraction and V.o2. 

BP,PR,SPO2,Temp

          MECHANISM: All 3 vital signs acquired from a pulse oximeter (pulse rate, oxygen saturation, and respiratory rate) are predictive of COPD exacerbation events, with oxygen saturation being the most predictive, followed by respiratory rate and pulse rate.

I/O charting

      MECHANISM: Fluid overload or pulmonary/vascular congestion is a common clinical feature in patients with heart failure and is associated with adverse outcomes. Maintaining records of patients' fluid intake and output (I&O) has long been considered an important aspect of nursing care to assess hydration status.

c) The cause of acute Exaberation in this patient is probably due to generalised weakness due to the drugs or due to upper respiratory tract infection.

d)ATT could have effected the patient’s condition by causing generalised weakness.

e)*Hyponatraemia in COPD develops due to many reasons such as worsening of hypoxia, hypercapnia ,respiratory acidosis and right-sided heart failure with development of lower limb oedema ,it could also be due to renal insufficiency.

*respiratory acidosis with metabolic alkalosis( owing to renal compensation) in patients with COPD with hypercapnia is the usual cause of hypochloremia.

My review: The patient is a 55 year old female with shortness of breath, pedal oedema and facial puffiness. She has a history of Diabetes Mellitus and is currently receiving treatment for hypertension. Her drug history is as follows:-

Empirical ATT (Rifampicin:600mg, Isoniazid: 300 mg) started on 4/5/21 and terminated on 16/5/21. Currently being treated for DM with Tab. Zoryl M1 OD.                                                                       Currently being treated for HTN with Tab.Telma 40 OD.

This answer seems like a very flawless one as everything in the answer is very clearly written and the mechanisms of all the pharmacological interventions have been mentioned properly. I do consider this an answer well written.

R6: The answer that I will be reviewing is from the link given below:-https://preethicheera.blogspot.com/2021/05/general-medicine-case-presentation-may.html?

Link to patient's details:  m=1https://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?

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?

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)

My review: A 55 year old male patient came to OPD with c/o altered sensorium and involuntary movements. He had recurrent episodes of seizures since 5 years. These symptoms followed an injury to the head which was diagnosed as brain stroke.

    There are 2 questions here, both of which were answered in a clear way. The mechanism behind the brain stroke leading to seizures was explained in a detailed way. The second answer could've maybe been a bit more elaborate, like how the simple partial seizures progressed into generalised tonic clonic seizures.

R7: The answer that I will be reviewing is from the link given below:-

http://santhoshdarimedi.blogspot.com/2021/05/medicine-blended-assignment.html

Link to patient details: https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1

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

Ans : 7 days back : Giddiness associated with one episode of vomiting

Then asymptomatic for 3 days he consumed a small amount of alcohol 

Then he developed : giddiness associated with aural fullness ,bilateral hearing loss,tinnitus,2 to 3 episodes of vomiting's

DENOVO hypertension

LOCALISATION OF LESION: Presence of Infract in the Inferior Cerebellar hemisphere of the Brain

PRIMARY ETIOLOGY: Ataxia is the loss of muscle control or coordination of Voluntary movements such as, Walking or Picking up of objects.

In this case, Patient is a known case of denovo hypertension. For this he has not taken medication.

Stroke is due to infract can be caused by blockage or bleeding in the brain, due to which brain is deprevied of Nutrients and Oxygen. This may lead to infract formation.

My review: A 52 year old male came to the hospital 2 days back presenting with slurring of speech and deviation of mouth that lasted for one day and resolved on the same day. The patient also has history of postural instability and is unable to walk without supports. He also has history of giddiness and vomiting.

This answer has, in a very concise way, mentioned the evolution of the symptomatology of the patient. The anatomical localisation and the primary etiology have been mentioned and explained as well. I thin the localisation of the lesion can be explained more, like how was the lesion localised. Overall, the answer has done justice to the question.

R8: The answer that I will be reviewing is from the link given below:-http://pranaykumar32.blogspot.com/2021/06/general-medicine-assignment.html

Link to patient's details:https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.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?

Ans:-  EVOLUTION OF SYMTOMATOLOGY

》Diabetes for 12 years

》Heart burn like episodes for 1 year but it relieved 

》Pulmonary TB 7 months back - treatment took now she is sputum negative. 

》Hypertension for 6 months - on medications

》Day of admission to hospital:- SOB since half an hour  

•ANATOMICAL LOCATION OF PROBLEM: Cardiovascular system

•PRIMARY ETIOLOGY:- Atherosclerosis - Plague formation [hypertension + diabetes].

   My review: A 67 year old female patient came to the OPD with complaints of shortness of breath. She  has a history of diabetes. She also has a history of heartburn episodes and history of TB 7 months before, for which she completed the course of medication a month ago. She was diagnosed with Acute Coronary Syndrome.

;The evolution of the symptomatology mentioned here is clear. The anatomical localisation of the problem could've still been elaborated in a clear manner. The primary etiology of the patient's problem could've also been explained better and is probably too brief.

R9: The answer that I will be reviewing is from the link given below:-https://vidya36.blogspot.com/2021/05/medicine-blended-assignment.html

Link to patient's details:https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.htmli)

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

Answer:

• 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

• Heart failure with preserved ejection fraction:

 Heart failure with preserved ejection fraction (HFpEF), also referred to as diastolic heart failure, is characterized by signs and symptoms of heart failure and a left ventricular ejection fraction (LVEF) greater than 50%. Heart failure associated with intermediate reductions in LVEF (40% to 49%) is also commonly grouped into this category.

• Heart failure with reduced ejection fraction:

Heart failure with reduced ejection fraction happens when the muscle of the left ventricle is not pumping as well as normal. The ejection fraction is 40% or less. The amount of blood being pumped out of the heart is less than the body needs.

My review: A 78 year old patient came to the OPD with chief complaints of shortness of breath, chest pain, bilateral pedal oedema, facial puffiness. He is a chronic smoker and alcoholic. He also has history of hypertension and diabetes.

  The answer has done justice to the question asked. The difference between heart failure with preserved and reduced ejection fractions has been explained in a clear and concise way. It is clear answer.

R10:The answer that I will be reviewing is from the link given below:-https://gumudalavishal.blogspot.com/2021/06/medicine-blended-assignment.html

Link to patient's details:https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html

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

A:- The pt. had recurrent blebs and ulcer on lower limbs (foot). This is due to Type-2 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.

My review: A 73 year old male patient presented to the OPD with chief complaints of pedal edema, shortness of breath and decreased urine output. The patient is a chronic alcoholic and non-smoker. Blebs and ulcer were present on lower limbs.

   The reason for and mechanism behind the blebs and foot ulcers has been described clearly in this answer.

Q2) Share the link to your own case report of a patient that you connected with and engaged while capturing his/her sequential life events before and after the illness and clinical and investigational images along with your discussion of that case.

Answer:-

I haven't really connected with a patient yet, so here I am just mentioning another case that was mentioned in the discussion group. Here is the link to the blog that I made using that information:-

https://144varshithakalidindi.blogspot.com/2021/07/a-40-year-old-male-patient-with.html

Q3) (Testing peer review competency of the examinees) :

Please go through the cases in the links shared above and provide your critical appraisal of the captured data in terms of completeness, correctness and ability to provide useful leads to analyse the diagnostic and therapeutic uncertainties around the cases shared.

Answer:-

This is the link that I have chosen, it is CNS related.

https://pallavi191.blogspot.com/2021/06/gm-cases.html?m=1

I think that this case was very well-written and the various aspects crucial to the case have been mentioned, such as the histories of present illness, past history, personal history and family history. Also, all the examinations like the general and systemic examinations (CNS, CVS and respiratory systems) have been mentioned. Pictures have also been given.

   The provisional diagnosis has been mentioned as well along with various investigations that have been done on the patient like blood urea, serum creatinine, complete blood picture and serum electrolytes.

   The ECG graphs and chest x ray have been shown as well and the treatment and other observations were mentioned as well.

    Then the final diagnosis was also reached based on all of this information.

There was also a discharge summary at the end that summarises all of the information.

     The whole case is so complete and systematic. The information has been well segregated as well for easy understanding. It has been very able in providing useful leads to analyse the diagnostic and therapeutic uncertainties surrounding the case.

Q4: Testing scholarship competency of the examinees ( ability to read comprehend, analyze, reflect upon and discuss captured patient centered data as in their 'original' answers to the assignment for May 2021):

Please analyze the above linked patient data by first preparing a problem list for each patient (based on the shared data) and then discuss the diagnostic and therapeutic uncertainty around solving those problems. Also include the review of literature around sensitivity and specificity of the diagnostic interventions mentioned and same around efficacy of the therapeutic interventions mentioned for each patient.

Answer:-

The case is of a 23 year old male who came with chief complaints of sudden fall followed by weakness of both lower limbs (paraplegia) 10 day back, associated with bowel and bladder incontinence.

    The patient was apparently asymptomatic a month ago, following which he developed productive cough, low grade fever for which he underwent sputum studies and tested positive for AFB bacilli and started ATT - HRZE regimen, 2 tab according to weight/PO/OD.

 He developed generalised weakness and myalgia 15 days back. 10 days back, the patient suddenly fell down with neither loss of consciousness nor froathing. Patient has developed bowel and bladder incontinence ever since.

   He has a known case of TB since 1 month and used ATT for 2 years.

Nothing was unusual in general examination.

In systemic examination, it was noticed that there was increased tone in both the lower limbs and decreased power as well. There was nothing else abnormal in the systemic examinations.

 He was given vitamin supplementation for especially B vitamins and thiamine. He was also on ATT due to the TB. His BP, PR, Spo2 and temp are being charted.

Monocef injection was also added on fourth day, which is an antibiotic.

The diagnosis is quadreparesis secondary to infectious spondylitis and epidural abscess.

The patient was thus referred to higher centre for neurological decompression because the MRI showed the infectious spondylitis and epidural abscess. Also, some findings were suggestive of oedema and anterior ligamentous spread.

Q 5) Testing scholarship competency in  

logging reflective observations on your concrete experiences of this last month : (10 marks) 

Reflective logging  of one's own experiences is a vital tool toward competency development in medical education and research.

Please reflect on and share your telemedical learning experiences from the  hospital as well as community patients over the last month particularly while you were E logging their case report while even in the hospital or perhaps when locked down at home.

Answer:-

  I haven't yet E logged any case reports and do plan to do so soon. I am locked down at home at the moment and I have been attending the clinical postings online through google meet. I would like to describe the experience that I have had this last month.

   In the very first class that we had itself we had seen 9 different patients, about whom I'd like to mention here:-

Patient 1: Man with jaundice

Ascitic fluid retention. Possible portal hypertension, possible viral hepatitis

Has history of tobacco smoking, stopped it voluntarily on onset of fever. Irregular breathing. Diastolic heart failure

Patient 2: Female with pitting edema

Abnormal knees, possibly due to rickets. Shortness of breath. Generalized pruritus seen, maybe because didn't bathe for 15 days. Some chronic lung disease is possibly causing pedal edema. Renal failure is also present.

Patient 3: Female patient with diabetic ketoacidosis. pH is 6.9, her life was saved by the doctors when she was in this critical condition.

Nausea, vomiting also observed. Altered sensorium

Patient 4: Female patient infected with retrovirus. Very severe infection that looked like covid. Interstitial lung disease is usually idiopathic, but in her case the cause is due to an organism Pneumocystis carina.

She stopped using HART in April.

Patient 5: Female patient with fever for 12 days and abdominal rash. Depending on which day of fever the rash is seen, disease can be determined. It was chickenpox, but later it was followed by bleeding from nose and mouth, because of low platelet count. Platelets were administered and she is not bleeding now. Platelets decrease' is probably due to inflammation, which can be due to multiple reasons. If everything is ruled out, it is diagnosed as immune mediated and immunosuppressants shd be given. We should wait and watch for now.

.

Patient 6: Patient had diabetes and now has jaundice as well. Glucuronide transferase is probably impaired, mostly congenital. He is probably having type 1 diabetes.

Patient 7: Male patient speaking irrelevantly. Retrovirus +ve. He stopped medication from 6 months. Altered sensorium seen. He is unable to stand and walk due to paraplegia. Tone was checked to determine whether umn or lmn. Patient has hyptonia, there is a blister on a foot. Another leg is bandaged because of inflammation caused by a canula.

Patient 8: Male with pedal edema.

He has a canula. Scrotal swelling present. Renal failure has caused overload on heart, causing heart failure. Also, less haemoglobin and increased dilution.

Patient 9: Female patient has shotgun deformity (a fracture). Has shortness of breath and abdomen distension, similar to patient 1. BP is low. No finding in resp. findings. The ECG shows Atrial fibrillation, has no p wave. It could be the cause of shortness of breath as there is less time for gaseous exchange. The mitral valve is struggling to open. The pulmonary artery pressure is high. Left ventricle has poor contractility, systolic heart failure. Pulmonary oedema is also seen, but diuretic is not a good idea since she has low BP.

    These are all the patients that I have seen in the meeting and it was very interesting to see the various symptoms that these patients had and how this information was used to diagnose the conditions and decide what investigations to do and what treatment to give to the patient.