medicine bimonthly assessment

 

Name                           :           Sakilam Lasya

Roll num                      :           117

Batch                           :           2017

MEDICINE  BIMONTHLY ASSESSMENT

I have been given the following cases to solve in an attempt understand the topic of ‘ patient clinical data analysis to develop my competency in reading and comprehending clinical data including history , clinical findings , investigations , and diagnosis to come up with treatment plan

This is link of questions asked regarding the case :

  medicinedepartment.blogspot.com/2020/09/medicine-paper-for-october-2020-first.html?m=1

1.PULMONOLOGY

A.Acute exacerbation of COPD

 Link to patient details:

 

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

 

Question – 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 :

 

Ø  In 2001                        :           SOB [ 1 week in the month of January ]

Intestinal perforation surgery

 

Ø  In 2013                        :           diagnosed with diabetes

 

Ø  In 2016                        :           anemia

 

Ø  april 2021                    :           latest episode of SOB

generalized weakness

 

Ø  28 th april 2021           :           bronchiectasis

Diagnosed with HTN

 

Ø  3 rd may 2021             :           pedal edema

Facial puffiness

 

Ø  15 th may 2021           :           drowsiness

Decreased urine output

 

Anatomical localization :

 

Ø  Bronchioles and alveoli

 

Primary etiology :

 

Ø  Allergens : to paddy [ since the episodes coincide with paddy crop]

       Chula usage [ from 20 yrs ]

 

Question -2 :

 

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

 

Treatment	Mode of action	Indications	Efficacy
Inj Augmentin	Inhibits bacteriak cell wall synthesis Penicillin antibiotic	Bronchiectasis
Tab Azithromycin	Interferes with bacterial protein synthesis Macrolide antibiotic	Bronchiectasis
Inj Lasix	Increase urine output Loop diuretic	Pedal edema Facial puffiness Decrease urine output
Tab Pantop	Proton pump inhibitor	Prescribed with antibiotics
Inj hydrocortisone	Reduces inflammation	COPD
Neb ipravert , budecort	Bronchodilators	COPD
Tab Pulmoclear	Bronchodilator and mucolytic	COPD
Inj HAI	Peripheral utilization of glucose Fast acting insulin	Raised blood glucose
Inj Thiamine	Supplements vit B 1	Vitamin B1 deficiency
Head end elevation	Increases expiratory lung volume and oxygenation	SOB
O2 inhalation	Supplements o2	Hypoxia
Intermittent BiPAP	Creates positive pressure to push air into lungs	COPD
Chest physiotherapy	Strenghthens muscles and increase lung capacity	Chronic lung disease
Vitals monitoring	Measures important body functions
GRBS 6 hrly	To check glucose levels	DM

 

 

Question – 3 :

 

 What could be the causes for her current acute exacerbation?

 

Ø  Bronchiectasis : HRCT shows evidence of bronchiectasis  20 days ago

Ø  Bronchiectasis is one of the risk factor for the acute exacerbation of COPD

 

Question – 4 :

 

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

 

Ø  The possible reason for her weakness could be ATT

Ø  Some of the 1 st line drugs eg . Isoniazid and Rifampicin cause damage to kidney which might have caused pedal edema , facial puffiness and decreased urine output

 

Question -5 :

 

What could be the causes for her electrolyte imbalance?

 

Ø  Hyponatremia :   Right heart failure

    Respiratory acidosis

    Hypoxia

Ø  Hypochloremia  :  compensated respiratory acidosis

 

 

2.NEUROLOGY :

A.Altered sensorium :

 Link to patient details:

 

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

 

Question-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:

Ø  1 year back                 :     an episode of SEIZURES for first time

Ø  4 months back           :     last episode of SEIZURES

Ø  On 9^th may 2021        :     Laughing and talking to self

                                            Oriented to time ,place ,person only from time to time

                                            Unable to get up from bed

                                            Decreased food intake

                                            Short term memory loss

Ø  On 15^th may 2021     :      admitted to tertiary care hospital

Anatomical localization :

Ø  Thalamus and hypothalamus

Ø  Wernickes Encephalopathy due to excess alchohol

Primary etiology :

Ø  Vitamin B 1 deficiency due to excess alcohol consumption

Ø  Increased serum urea ,creatinine due to kidney failure

Question -2 :

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

DRUG	MODE OF ACTION	INDICATION	EFFICACY
NS and RS	Fluid and electrolyte replenishment	Fluid and electrolyte imbalance
Thiamine	Thiamine stores are replenished	Thiamine deficiency due to alcohol consumption
Lorazepam	Increases levels of GABA	Reduce stress and anxiety
Pregabalin	Mimics GABA , Binds to alpha 2 delta receptors	For seizures
HI injection	Reduces blood sugar by peripheral glucose uptake	Increased blood sugar on RBS
Lactulose	Improves mental status	Improves cognitive function in hepatic encephalopathy
KCl injection	Potassium supplement	Decreased serum k+
Potchlor	Potassium supplement	Decreased serum k+
GRBS 6 th hourly	To monitor blood glucose levels	k/c/o diabetes with increased blood sugars

 

Question -3 :

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

 

Ø  Chronic alcohol intake has worsened condition of patient over time

 

Question -4 :

 What is the reason for giving thiamine in this patient?

Ø  The effects are seen in this patient as memory loss , confusion , etc

Ø  Thiamine deficiency occurs in chronic alcoholism

Ø  So we are giving thiamine to supplement the deficiency

Question – 5 :

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

 

Ø  2D Echo shows left ventricular hypertrophy , which is one of the cause of pre renal acute kidney injury

Ø  Alchoholic cirrhosis can also lead to acute kidney injury [since the patient is alchohol addicted

Question -6 :

What is the probable cause for the normocytic anemia?

 

Ø  Alchohol decreases number of precursors of rbc s in bone marrow

Ø  Further alchohol induced malnutrition leads to iron and folic acid deficiency anemias

Question -7 :

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

 

Ø  Alcohol leads to malnutrition which decreases the ability of wound healing and causes neuropathy  

Ø  The combined effect of diabetes and alchoholism has lead to foot ulcer in this patient

B.Cerebellar ataxia :

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

 

Question -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 :

Ø  on 13 th May 2021   :   Gidddiness  and vomiting

Ø  on 16 th May 2021   :   Giddiness – sudden onset, continuous , gradual progression

                                      bilateral hearing loss , aural fullness , tinnitus

                                      vomitings – 2 episodes / day , non projectile  , non bilious

Ø  on 18 th  May 2021  :   slurring of speech

                                      deviation of mouth

Anatomical localisatiion :

Ø  Right inferior cerebellar hemisphere 

Primary etiology :

Ø  Increased serum cholesterol leads to formation of embolus which causes infarct and stroke

 

Question – 2 :

 

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

 

Treatment	Mode of action	Indication	Efficacy
Tab . Vertin	Histamine analogue	Dizziness
Inj . Zofer	Inhibits serotonin by binding to 5HT3 receptor	Nausea , vomiting
Tab . Ecosporin	Antiplatelet action by inhibiting formation of thromboxane A2	Infarct in brain
Tab :. Atorvostatin	HMG CoA reductase inhibitor , decrease cholesterol	High serum cholesterol
Tab . Clopidogrel	Inhibits platelet aggregation	Infarct in brain
Inj . Thiamine	Supplements vitamin B1	Vitamin B1 deficiency
Tab . MVT	Supplements vitamin B12	Vitamin B 12 deficiency

Question – 3:

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

 

 

Ø  Yes , hypertension can cause stroke

Ø  Hypertension > damage to blood vessels >blood clot >infarct >stroke

Ø  But in this patient since the hypertension is recent , it might not be the cause of stroke

Question – 4 :

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

Ø  Alcohol > liver damage >decrease clotting factors > Hemorrhagic stroke

C. Recurrent hypokalemic paralysis :

C) Link to patient details:

 

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

 

 

Question -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 :

Ø  October 2020     :   pedal edema

Ø  April 2021         :    neck pain     

Ø  6 days back        :   pain radiating to left arm

Ø  5 days back        :   palpitations

                               Dyspnoea

                               Chest pain with heaviness 

 Anatomical localization :

Ø  Cervical spondylosis :  at the level of C 2,3,4 veretebrae

Ø  Hypokalemic paralysis :  serum

Primary etiology :

Ø  Cervical spondylosis :   aging

Ø  Recurrent hypokalemic paralysis : genetic mutation

Question – 2 :

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

 

Ø  Reason for recurrent hypokalemia : genetic mutation in CACNA1S or SCN4A gene

Question- 3 :

 

 What are the changes seen in ECG in case of hypokalemia and associated symptom

 

Ø  ECG  changes in hypokalemia :

1)      Increased P wave amplitude

2)       Prolonged PR interval

3)      Widespread ST segment depression and T wave flattening

4)      Prominent U waves [ most common seen in V2-V3 leads ]

D . Seizures :

 Link to patient details:

 

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

 

 

Question -1 :

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

 

Ø  Yes , there is association between seizure and brain stroke

Ø  Injury to brain

 

              Scar tissue

 

            Disrupts electrical activity of brain

 

                Seizures

 

 

Question – 2:

 In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he did . Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?

 

Ø  The 1 st episode of seizure was 5 yrs back , immediately following head trauma

Ø  Over the time the infarct must have grown in size

Ø  This may be the reason for the unconsciousness in the latest episode

E. Ataxia :

 Link to patient details:

 

 

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

 

Question -1 :

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

Ø  The multiple unattended head injuries are maybe the reason for ataxia in the past year

Question -2 :

What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?

 

Ø  Yes , alcohol contributed to bleeding diathesis

Ø  Alcohol         liver damage              decreases clotting factors            bleeding

Ø  Since the patient gave the H / O binge of alcohol 3 hrs prior to attack , it must have triggered the sudden bleeding

F. CVA :

 Link to patient details:

 

 

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

 

Question – 1 :

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

 

Ø  Yes, head trauma has lead to cerebrovascular accident in this case

Question – 2 :

What are warning signs of CVA?

 

Ø  Warning signs of CVA :

1.      BALANCE : sudden dizziness , loss of balance or coordination

2.      EYES : sudden trouble seeing in one / both eyes

3.      FACE : facial weakness

4.      ARM : weakness , unable to raise both arms equally

5.      SPEECH : impaired , slurred

Question – 3 :

What are warning signs of CVA?

 

Ø  Drug rationale in CVA :

1.      MANNITOL : lowers intracranial pressure

2.      ECOSPORIN : Antiplatelet action

3.      ATORVASTATIN : Decreases cholesterol levels

Question – 4 :

Does alcohol has any role in his attack?

 

Ø  Yes , alcohol damages liver function

Ø  This reduces production of clotting factors leading to bleeding

Ø  This can cause stroke

Question – 5 :

Does his lipid profile has any role for his attack??

 

Ø  Yes , lipid profile has a role in development of stroke

Ø  This patient shows decrease in HDL cholesterol levels

Ø  An increase LDL and decreased HDL can cause large artery atherosclerosis leading to stroke

Ø   However , small artery occlusion due to dyslipidemia is rare

G . Cervical myelopathy :

 Link to patient details:

 

 

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

 

 

sQuestion – 1 :

What is myelopathy hand ?

 

Ø  MYELOPATHY HAND : Loss of power of abduction and extension of the ulnar two to three fingers and inability to grip and release rapidly with these fingers

Ø  This occus due to pyramidal tract involvement

Question – 2 :

What is finger escape ?

                                 

Ø  FINGER ESCAPE : also known as Wartenberg sign

Ø  This is involuntary abduction of little finger caused by unopposed action of extensor digiti minimi 

Question – 3:

What is Hoffman’s reflex?

 

Ø  HOFFMAN’S REFLEX : also known as finger flexor reflex

Ø  Verifies presence / absence of issues arising from corticospinal tract

Ø  Positive reflex – flexion and abduction of thumb

Ø  Positive reflex suggests hypertonia , but also seen in healthy individuals

H . Seizures :

Link to patient details:

 

https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1                

 

Question – 1 :

 

What can be  the cause of her condition ?                             

 

Acute cotical venous sinus thrombosis [ CVST ] with hemorrhagic venous infarction involving right posterior temporal lobe

Question – 2 :

What are the risk factors for cortical vein thrombosis?

 

Ø  RISK FACTORS FOR CVST :

a)      Hepatitis C infection

b)      Problem with blood clotting eg . antiphospholipid syndrome , protein c or s deficiency

c)      Sickle cell anemia , chronic hemolytic anemia

d)      Collagen vascular diseases

e)      Cancer , obesity

Question – 3:

What drug was used in suspicion of cortical venous sinus thrombosis?

 

Ø  CLEXANE : contains enoxaparin

Ø  It is anticoagulant which is used here to treat CVST

3 . CARDIOLOGY:

A. Pericardial Effusion :

 Link to patient details:

 

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

 

 

Question – 1:

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

 

Ø  Left Heart failure :

With reduced ejection fraction	With preserved ejection fraction
Also known as systolic heart failure	Also known as diastolic heart failure
Inability of heart to contract enough to provide blood flow forward	Inability of left ventricle to relax normally resulting in fluid backup in lungs
Enlarged left ventricle , cardiomegaly seen	Normal / slightly enlarged ventricle , pulmonary congestion seen

 

Question -2 :

Why haven't we done pericardiocenetis in this pateint?        

 

Ø  Patient has pericardial effusion , which was mild at beginning and progressed to moderate level later

Ø  The patient is responding well with conservative treatment [ effusion size decreased from 2.07 cm to 1.4 mm ]

Ø  Because of the above reason and complications associated with pericardiocentesis , we have not done pericardioccentesis in this patient

Question – 3:

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

 

Ø  Risk factors :

1. smoking

2. alcohol

3.diabetes mellitus

4. Hypertension

Question -4 :

What could be the cause for hypotension in this patient?

 

Ø  Cause of hypotension :

 

Pericardial fluid accumulation in pericardial sac

 

            Decreases maximum size of ventricles

           

                       Lowers end diastolic volume 

 

              Decrease stroke volume [ determinant of SBP ]

 

                                     HYPOTENSION

B . Diastolic heart failure :

 Link to patient details:

 

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

 

Question -1 :

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

Ø  Cause of heart failure :

a)      AGEING :  causes stiffening of heart muscle

b)      CHRONIC HYPERTENSION :   leads to left ventricular hypertrophy and increase connective tissue content

Question -2 :

what is the reason for anaemia in this case?

 

Ø  Cause of anemia :

a)      Elderly patient

b)      Chronic Alcohol consumption leads to malnutrition and anemia

c)      CHRONIC KIDNEY DIEASE :  leads to erythropoietin deficiency and then anemia

d)     Associated comorbidities : diabetes

Question- 3 :

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

Ø   

Ø  The reason for ulcers in this patient is poor wound healing due to diabetes

Question -4:

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

 

   Diabetes mellitus [ 30 yrs ago ]

 

   Diabetic retinopathy [ 4 yrs ]

  

   Diabetic nephropathy i. e . CKD [ at present ]

   Diabetic neuropathy i. e reduced sensation leading to foot ulcer [ at present ]

C. CCF with atrial fibrillation :

 Link to patient details:

 

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

 

Question – 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 :  

Ø  10 yrs back  :    inguinal hernia surgery

Ø  3 yrs back    :    on and off pain at surgical site

                          On and off facial puffiness

Ø  1 yr back      :    SOB

                          Developed hypertension

Ø  2 days ago    :    decreased urine output

                          SOB

Anatomical localization :

Ø  Atria

Primary etiology :

Ø  Hypertension

Question – 2 :

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

 

 

Treatment	Mode of action	Indication	Efficacy
Inj Dobutamine	Ionotropic action  Weak chronotropic action	Atrial fibrillation Congestive cardiac failure
Tab Digoxin	Ionotropic action	Atrial fibrillation Congestive cardiac failure
Inj unfractionated heparin	Inactivates thrombin and activated factor 10 A	Atrial thrombus
Tab Carvediol	Beta blocker	Atrial fibrillation
Tab Acetyl cysteine	Mucolytic
Tab Acitrom	Anticoagulant	Atrial thrombus
Tab Dytor	Loop diuretic	Cardiorenal syndrome
Tab pan D	Proton pump inhibitor	Gastric irritation
Tab Taxim	Antibiotic	Infection
Inj thiamine	Vit b1 supplement	Vit B 1 deficiency
Inj HAI	Peripheral utilization of glucose	Increased blood sugar

 

Question – 3 :

What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient? 

 

Ø  Cardio renal syndrome :

               Heart failure

   

                   Decreased cardiac output

 

          Renal hypoperfusion

 

        

            Renal dysfunction

 

 

         Cardiorenal syndrome

 

Ø  type 4 cardiorenal syndrome : chronic nephrocardiac

Question – 4 :

 What are the risk factors for atherosclerosis in this patient?

 

Ø  Risk factors for atherosclerosis :

1.      Diabetes mellitus

2.      Hypertension

3.      Age ; 52 yr

Question – 5 :

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

Ø  APTT and INR were asked for review because – patient is prescribed anticoagulant medicine whose most common side effect is BLEEDING

D. Acute coronary syndrome :

Link to patient details:

 

https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1

 

Question – 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 :

Ø  12 yrs back            :    type 2 DM            

Ø  1 yr back                :    heartburn

Ø  7 months back        :    diagnosed with TB

Ø  6 months back        :    hypertension

Ø  Half an hour ago    :     SOB

Anatomical localization :

Ø  Coronary arteries

Primary etiology :

Ø  age : 67 yrs

Ø  H/O DM 2 since 12 yrs

Ø  H/O hypertension

Question – 2 :

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

 

Treatment	Mode of action	Indications	Efficacy
Tab . Metaprolol	Beta blocker	NSTEMI
PCI	Surgery for coronary artery blockage	NSTEMI

 

Question – 3 :

What are the indications and contraindications for PCI?

 

Ø  Indications of PCI :

1.      STEMI

2.      NSTEMI

3.      Unstable angina

4.      Stable angina

5.      Angina equivalent [ dyspnoea , arrhythmia ]

Ø  Contraindications of PCI :

1.      Hypercoagulable state

2.      Intolerance to oral antiplatelets

3.      Abvsence of cardiac surgery backup

4.      High grade CKD

Question -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?

 

Ø  If unnecessary PCI is performed it leads to certain complications such as

1.      Injury to heart arteries

2.      Infection at the catheter site

3.      Bleeding

4.      Allergic reactions and kidney damage due to dye used

5.      Blood clots leading to heart attack

E. Acute MI :

LINK TO PATIENT DETAILS  :

https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1

 

Question – 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 :

Ø  On 12 may 2021 :   chest pain

Ø  On 14 may 2021 :   giddiness and profuse sweating

Anatomical localization :

Ø  Right coronary artery [ inferior wall MI ]

Primary etiology :

Ø  Atherosclerosis due to DM ,HTN

Question -  2 :

What are mechanism of action, indication and efficacy over placebo of each of the

pharmacological and non pharmacological interventions used for this patient

Treatment	mode of action	Indications	Efficacy
Tab aspirin	Antiplatelet action by inhibiting PG synthesis	Right coronary artery blockage
Tab Atorvastatin	Inhibits HMG CoA reductase and decrease cholesterol production	Coronary blockage
Tab Clopidogrel	Aqntiplatelet action	Coronary blockage
Inj HAI	Fast acting insulin	Increased blood glucose

 

 

 

 

Question – 3 :

 

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

 

Ø  The PTCA procedure was necessary here to restore blood flow because patient was starting to develop symptoms of cardiogenic shock

 

 

F. Cardiogenic shock :

 

LINK TO PATIENT DETAILS :

 

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

 

Question – 1 :

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

 

Ø  The patient has cardiogenic shock

Ø  In this case fluid resuscitation corrected the hypovolemia and thus provided temperory relief to patient

 

Question – 2 :

 

 What is the rationale of using torsemide in this patient?

 

Ø  Patient has high serum urea and creatinine levels and electrolyte imbalance due to cardiorenal syndrome

Ø  Torsemide is a loop diuretic

Ø  It help in clearance of accumulated metabolites and restores electrolyte balance

 

Question – 3 :

 

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

 

Ø  There is no evidence suggestive of UTI

Ø  So it might be prophylactic for UTI

 

 

4. GIT :

 

A. Pancreatitis

 

 Link to patient details:

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html

Question -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

Ø  5 yrs back                    :           fever and vomiting

Ø  6 th May 2021             :           pain abdomen and vomitings from this day

Ø  9 th May 2021             :           constipation

Burning micturition

                                                Fever

Anatomical localization :

Ø  Abdomen

Primary etiology :

Ø  Alcohol consumption

Question -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?

Treatment	Mode of action	Indication	Efficacy
Inj meropenem	Inhibits synthesis of bviral cell wall components Broad spectrum antibiotic	Prophylaxis  [complications of acute pancreatitis ]
Inj Metrogyl	Inhibits protein synthesis antibiotic	Prophylaxis
Inj Amikacin	Inhibits bacterial protein synthesis Aminoglycoside antibiotic	Prophylaxis
IV NS/RL	Fluid and electrolyte replacement	Dehydration
Inj Octreotide	Somatostatin analogue	Excess pancreatic secetion
Inj Pantop	Proton pump inhibitors	Reduces pancreatic secretions
Inj Thiamine	Supplements vit B1	Vitamin B1 deficiency
Inj Tramadol	Opioid analgesic	Pain

 

B. epigastric pain

 

Link to patient details:

 

https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html

 

question -1 :

 

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

 

Ø  The dyspnoea is most probably due to pancreatitis

Ø  Pancreatitis leads to multiorgan failure

Ø  The most common organ involved is lung leading to pulmonary complications

Ø  These are divided into 3 stages

Ø  STAGE 1 : no radiological changes , but pulmonary complications seen

Ø  STAGE 2 : Radiologial changes seen

Ø  STAGE 3 : ARDS

Ø  According to reports the patient is in stage 2 , xray showing pleural effusion which is the cause of dyspnoea

Question – 2 :

 

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

 

Ø  RISK FACTORS :

1.      Age

2.      Insulin resistence

3.      Chronic alcohol consumption

4.      Pancreas damaged : source of insulin gone

Question – 3 :

 

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

 

Ø  Inflammation of gall bladder due to gall stones ;lead to increased LFT s

Ø  Both AST and ALT are non specific indicators for liver disease

Ø  But in case of alcoholic fatty liver AST > ALT

 

Question -4 :

 

What is the line of treatment in this patient?

 

Ø  IVF : maintains fluid level

Ø  Inj Pan D : reduces gastric irritation

Ø  Inj Zofer : reduces nausea ,vomiting

Ø  Inj tramadol : opioid analgesic

Ø  GRBS : to monitor blood glucode

Ø  Tab Dolo : analgesic and antipyretic

Ø  Bp monitoring

 

C. Abdominal pain;

 

 Link to patient details:

 

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

 

Question – 1 :

 

 what is the most probable diagnosis in this patient?

 

Ø  The rise in AST and ALT suggests liver abscess

Ø  It is the most possible diagnosis

Ø  Other differentials :

1.      Organized hematoma : no trauma history

2.      Subdiaphragmatic fluid collection : radiological evidence absent

 

 What was the cause of her death?

 

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

 

Ø  NSAIDS caused afferent arteriole constriction leading to increased bp

 

 

5.Nephrology :

 

A.Post TURP with ATN :

Link to patient details:

 

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

        

Question-1 :

.What could be the reason for his SOB

Ø  Acute tubular necrosis leads to retention of fluid in lungs

Ø  Edema in lungs lead to shortness of breath

Question-2:

Why does he have intermittent episodes of  drowsiness ?

 

Ø  Patient shows elevated levels of urea and creatinine in RFT due to kidney injury

Ø  This increased creatinine is the cause of drowsiness and altered mental state

Question-3 :

 Why did he complaint of fleshy mass like passage in his urine?

 

Ø  During Transurethral resection of the prostate ( TURP ) surgery ,we do electrocautery to minimise bleeding

Ø  This blood may clot and form scab

Ø  Clot retention is one of the common complications of TURP

Ø  This scab is passed from urethra following surgery , which is perceived by patient as passage of mass

Question -4 :

What are the complications of TURP that he may have had?

 

Complications of TURP :

Ø  Major:

 

1.      Clot retention

2.      Failure to void

3.      Uncontrolled acute hematuria

4.      UTI

5.      Chronic hematuria

 

Ø  Minor:

 

1.      Bladder perforation

2.      Sepsis

3.      DIC

B.Frequent urination :

Link to patient details:

 

 

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

 

 

Question-1 :

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

 

Ø  The patient is a child with hyperactive nature, no social etiquettes, doesn’t pay attention at school

Ø  The reason for his hyperactivity could be ADHD (Attention deficit hyperactivity disorder)

Question-2 :

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

 

Ø  The child doesn’t show symptoms of nocturnal enuresis

Ø  This points towards psychosomatic origin of disease i. e .  anxiety ,stress etc.

Ø  Since there is no probable organic cause , excessive urge of urination is absent at night

Question -3 :

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

 

1)      Further investigations to rule out any organic cause . This includes :

Ø  Proper USG

Ø  Complete blood count

Ø  Blood and urine sugars

2)      Diagnosis of any anxiety disorder if present

3)      In the absence of organic cause , treatment would be BEHAVIOURAL THERAPY

4)      Ditropan – to decrease urgency and frequency of urination

5)      Assurance to mother and child

6 . Infectious disease

A. Dysphagia ,fever,cough :

 Link to patient details:

 

 

https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html

 

Question -1 :

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

 

v  Positive findings of tracheoesophageal fistula :

History:

1.      C/O difficulty in swallowing i. e . Dysphagia

2.      C/O cough on food intake

3.      H/O retroviral disease

Physical findings:

1.      Laryngeal crepitus

2.      Endoscopy showing large opening with proliferative growth in mid esophagus

3.      CECT :  Fistulous communication between left main bronchus and mid thoracic esophagus

4.      Barium swallow showing abnormal contrast due to communication between esophagus and bronchial tree

Question – 2 :

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

 

Ø  The chances of development of immune reconstitution inflammatory syndrome in this patient is high .

Ø  The following are the risk factors present in this patient :

1)      Fever since 2 months

2)      Diagnosis of TB after initiation of ART

3)      Lymph node enlargement in mediastenum

4)      CRP + ve

 

7. Infectious disease and hepatology

A.Liver abscess:

Link to patient details:

 

 

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

 

Question – 1 : .

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

Ø  Cause of liver abscess in this patient is consumption of locally brewed toddy

Ø  Yes , locally made alchohol acted as factor for liver abscess in this patient

Question -2 :

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

           

Ø  Liver abscess can be pyogenic ,amoebic or hydatid

Ø  Infections are acquired from blood stream ( portal and systemic circulation)

Ø  The most common pathophysiology is bowel content leakage and peritonitis . Bacteria travel via portal blood vessels into liver .

Ø  In this case , Alcohol consumption specially locally prepared alchohol plays major role in liver abscess ( pyogenic and amoebic )

Ø  Alchohol acts as predisposing factor

Ø  Factors responsible for association between alcohol and liver abcess are as follows:

a)      Poor nutritional status due to alchohol consumption

b)      Presence of infective organisms in the locally prepared alchohol

c)      Immunity of the patient

d)     Damage to liver done by alchohol

Question -3 :

 Is liver abscess more common in right lobe

 

Ø  Yes ,liver abscess is more common in right lobe compared to left lobe

Ø  Single lesions are more common in right lobe

Ø  This is attributed to comparatively more blood supply via superior mesenteric vein on right side

Question -4 :

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

 

Ø  1) If the abcess is large ( 5cm or more) because it has more chances to rupture.

Ø  2) If the abcess is present in left lobe as it may increase the chance of peritoneal leak and pericardial leak.

Ø  3) If the abcess is not responding to the drugs for 7 or more days

B.Liver abscess

Link to patient details:

 

 

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

 

Question -1 :

Cause of liver abcess in this patient ?

 

Etiology of liver abscess :

Ø  Pyogenic liver abscess – polymicrobial

·         Staphylococcus

·         E .coli

·         Klebsiella

·         Streptococcus

Ø  Amoebic liver abscess– most commonly caused by Entamoebahisolytica

Ø  In this patient, occasional toddy consumption acted as source of pathogens

Question- 2 :

How do you approach this patient ?

 

Treatment of liver abscess :

Ø  Empirical antibiotics : cover both bacterial and amoebic causes

·         For bacterial cause : penicillin +cephalosporin is given ( zostum1.5 gm i.v. BD injection)

·         For amoebic cause : metronidazole ( Metrogyl 500mg i.v. TID injection )

Ø  Percutaneous drainage of abscess is not done in this patient because of the response to antibiotic therapy and associated complications of drainage

Ø  Ultracet to relieve pain

Ø  Dolo 650 mg for fever

Question-3 :

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

 

Ø  Based on the following :

Ø  Age of patient – 21 yr ( young age ) , male gender

Ø  Single abscess

Ø  Right lobe involvement

Ø  Chest x ray showing no involvement

The abscess is more likely to be amoebic liver abscess

Since we cannot take risk we treated patient for both bacterial and amoebic cause

Question- 4 :

Is there a way to confirmthe definitive diagnosis in this patient

Ø  Yes we can confirm the diagnosis in this patient by :

·         Detection of serum antibodies against Entamoeba

·         Culture and sensitivity report of the aspirate

8 . Infectious disease :

A.Mucormycosis:

Link to patient details:

 

 

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

 

Question -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 :

a)      Fever with chills and rigors    :     18 -04-2021

b)      Facial puffiness :28-04-2021

c)      Periorbital oedema :    28-04-2021

d)     Generalised weakness.               :   28-04-2021

( Right upper & lower limb )

e)      Altered sensorium  :     4-05-2021

f)       Serous discharge from left eye  :     4-05-2021

g)      Oral and nasal cavity involvement :     4-05-2021

Anatomical localisation:

a)      Eye

b)      Nasal & sinus mucosa

c)      Oral cavity

d)     Brain

Primary etiology :

Ø  Rhizopus : fungus

Question – 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?

 

Ø  Drugs that can be used to treat mucormycosis are :

1)      Amphotericin – B

·         Liposomal

·         Deoxycholate

2)      Posaconazole

 

Ø  Efficacy of drugs :

v  Liposomal AmpB>DeoxycholateAmpB>Posaconazole

 

Ø  DeoxycholateAmpB is cheaper compared to Liposomal AmpB

 

Ø  Approach to patient :

 

1.      Stabilise the patient

2.      Treat the diabetic ketoacidosis

3.      Treatment with antifungal preferably Liposomal AmpB

Question – 3 :

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

 

Ø  The reason for recent increase in the cases of mucormycosisis immunocompromised state following recovery from COVID -19 infection

 

9.INFECTIOUS DISEASE : 

 

Sl No	Patient’s E Log	Age (Yrs)	Sex	Severity of Disease	Day of severity	Complications	Final outcome
1.	https://nikhilasampathkumar.blogspot.com/2021/05/covid-pneumonia-in-pre-existing-case-of.html	58	F	Moderate		Viral Pneumonia with pre existing interstitial lung disease.	Resolution
2.	https://nehapradeep99.blogspot.com/2021/05/a-50-year-old-female-with-viral.html	50	F	Moderate	Recovered on the 11th day	Viral Pneumonia secondary to Covid 19	Resolution
3.	https://143vibhahegde.blogspot.com/2021/05/covid-in-26-yo-female.html	26	F	Severe	4/5/21, became severe	Viral pneumonia secondary to Covid infection with renal complications	Death
4.	https://gsuhithagnaneswar.blogspot.com/2021/05/29-year-old-male-patient-with-viral.html?m=1	29	M	Mild		Viral pneumonia secondary to Covid	Resolution
5.	https://anuragreddy72.blogspot.com/2021/05/case-discussion-on-hypokalemic-periodic.html	45	M	Severe		Altered Sensorium, Azotemia and Hypokalemia	Resolution
6.	https://vijaykumarkasturi.blogspot.com/2021/05/65-years-old-male-with-viral-pneumonia.html	65	M	Severe	on 17/5, became moderate	Viral pneumonia secondary to Covid	Death
7.	https://drsaranyaroshni.blogspot.com/2021/05/a-67-year-old-lady-in-icu-with-covid.html	67	F	Moderate		Viral pneumonia secondary to Covid	Resolution
8.	https://bhavaniv.blogspot.com/2021/05/35yrm-with-viral-pneumonia-secondary-to.html?m=1	35	M	Mild	on 17/5, became mild	Viral pneumonia secondary to Covid	Resolution
9.	https://vidya36.blogspot.com/2021/05/a-45-year-old-female-with-viral.html	45	F	Mild		Viral pneumonia secondary to Covid	Resolution
10.	https://rishithareddy30.blogspot.com/2021/05/covid-case-report.html	50	F	Moderate		Viral pneumonia secondary to Covid and de novo Diabetes Mellitus	Resolution
11.	https://93deepanandikonda.blogspot.com/2021/05/42-years-female-patient-with-viral.html	42	F	Moderate		Viral pneumonia secondary to Covid	Resolution
12.	https://vignatha45.blogspot.com/2021/05/58-years-female-patient-with-viral.html	58	F	Moderate		Viral pneumonia secondary to Covid	Death
13.	https://jahnavichatla.blogspot.com/2021/05/covid-case-discussion.html	55	M	Severe		Covid with ICU psychosis	Resolution
14.	https://vaishnavimaguluri138.blogspot.com/2021/05/viral-pneumonia-secondary-to-covid-19.html	35	M	Mild	Severe on 19/5	Viral pneumonia secondary to Covid	Resolution

 

15.	https://prathyushamulukala666.blogspot.com/2021/05/a-62-year-old-male-patient-with-fever.html	62	M	Moderate		Viral pneumonia secondary to Covid with hypertension	Resolution
16.	https://meesumabbas82.blogspot.com/2021/05/a-38-yo-male-with-viral-pneumonia.html	38	M	Moderate		Viral pneumonia secondary to Covid	Resolution
17.	https://sudhamshireddy.blogspot.com/2021/05/a-65-year-old-female-with-fever.html	65	F	Severe		Viral pneumonia secondary to Covid	Death
18.	https://nehae-logs.blogspot.com/2021/05/case-discussion-on-viral-pneumonia.html	63	M	Moderate	on 17/5, became severe	Viral pneumonia secondary to Covid	Resolution
19	https://srilekha77.blogspot.com/2021/05/a-48-year-male-with-viral-pneumonia-due.html	48	M			Viral pneumonia secondary to Covid	Resolution