40 year old patient with hepatic encephalopathy

 

1.Which clinical history and physical findings are characteristic of Tracheo oesophagal fistula?

A. Dysphagia is the common presentation of tracheo oesophagal fistula(TOF)

     This patient has clinical symptoms suggestive of Tuberculosis which could be one of the reason for   TOF .

     Laryngeal crepitus is positive in this patient which can be seen in TOF

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

A.IRIS can be prevented by initiating the ART before the development of advanced Immunosuppression i.e;starting the therapy before CD4 cell count decreases more

This patient has  CD4 count of 420 when ART is initiated .So this patient has very less chances of developin IRIS.

Risk factors for IRIS : Low baseline CD4 count

                                     High viral load

                                     Short time interval between starting ATT & HRTT

1.What is the evolution of 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 patient’s problem?

A.3 years ago:Diagnosed with hypertension 3 years ago

   21 days ago: Received vaccination at PHC which was  followed by high grade fever with chills and rigor which relieved on medication

  18 days ago:  With similar complaints , patient went to a local hospital and took antipyretics but fever didn’t subside

11 days ago:C/O generalized weakness ,facial puffiness and generalized edema.Patient was in a drowsy state.

4 days ago:

              - Presented to casuality in altered state with facial puffiness and periorbital edema and weakness of right upper limb and lower limb.

              -By evening patient developed peri orbital edema.

              -Blood tinged serous discharge from left eye.

This patient has uncontrolled blood sugar levels. He has DKA of which he is unaware off.

He is diagnosed with Acute oro rhino cerebral mucormycosis which can be commonly seen in patients with incontrolled sugar levels.

This fungus,enters sinuses and then go to brain.

This patient also has acute ifarct in left frontal and temporal lobe.

 

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?

A.Inj – amphotericin B – It is a antifungal drug.

    Itraconazole 200 mg – Adjusted to his creatinine clearance.

    Patient has to be given Deoxycholate but not given as it is not avaliable

   Treatment of DKA:

              -Fluid replacement through 1st peripheral line

              -Regular insulin through 2nd peripheral line

              - Bicarbonate replacement

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

A.In this COVID pandemic , steroids are used in treatment of COVID patients.

Steroids reduce the inflammatory response and reduces the damage of the lungs by cytokine storm driven by overactive immune system.

Excess use of steroids can  decrease immunity and also increase blood sugar levels in both diabetics and non diabetics which makes the patient more prone to fungal infections like mucormycosis. 

Infectious disease and hepatology:

1.Cause of liver abscess in this patient?

A. Most likely cause is Amoebic liver abscess because of the following findings:

            Age of the patient

            Single abscess

            Right lobe involvement

2.How do you approach this patient?

A.Invesigations:

         -CBP : Leucocytosis

         -LFT : Elevated Alkaline phosphatase

         -RFT

          -Urine analysis

          -USG : Single hyperechoic  oval shaped mass in right lobe

                                          Response to treatment

                     Hypoechoic due to liquefaction of mass

Treatment:

           -Inj.Zostum 1.5gmIV BD – It is a combination of Cephalosporin , Sulbactum.It is a antibiotic to treat if there is any bacterial cause for liver abscess and to prevent secondary infections of liver abscess.

          - Inj Metrogyl 500mg IV TID – It is Metronidazole to treat amoebic cause

         -Inj Optineurin 1amp in 100 ml NS – It is a multivitamin drug.

         -Inj Ultracet ½ QID – It is a combination of tramadaol(Opiod analgesic) and  acitominophen(analgesic and anti pyretic)

         -Tab Dolo 650 mg SOS.

3.Why do we treat both amoebic and pyogenic liver abscess here?

A.Secondary bacterial infections are common in amoebic liver abscess.

    So the patient is being treated for both amoebic liver abscess and pyogenic liver abscess.

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

A.Serology can confirm the diagnosis

Increase in IgG antibody titer can confirm the diagnosis.

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

A.Locally made alcohol is not prepared under aseptic conditions ,it could be bacterially contaminated.

This could have lead to liver abscess in this patient.

2.What is the etiopathogenesis of liver abscess in a chronic alcoholic patient?

A.Alcoholism,mainly locally prepared alcohol is a predisposing factor for formation of both amoebic and pyogenic liver abscoess because of the adverse effects of alcohol over the liver.

But it is also proven that alcoholism is never an etiological factor for formation of liver abscess.

3.Is liver abscess more common in right lobe?

A.Liver abscess is more common in right lobe because right lobe receives blood from superior mesenteric and portal veins.

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

A.  –Abscess not responding to medical theray.

      - Impending rupture

     -Secondary infections

     - Left lobe liver abscess as it can rupture into pericardium

   - Large cavity >5cm

 

  Pulmonology: 

 1.What is the evolution of 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 patient’s problem?

A.1st episode of SOB – 20 years ago

    2nd episode of SOB – 12 years back

  Since then she has been having SOB episodes for past 12 years.

  Diagnosed with diabetes – 8 years ago

  Anaemia and took iron injections – 5 years ago

  Generalized weakness  1 month back

  Diagnosed with hypertension – 20 days back

  Pedal edema – 15 days back

  Facial puffiness – 15 days back

Anatomocal localization of problem : Lungs, heart

Primary etiology of problem : chronic use of chulha since 20 years.

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

A.Head end elevation

          - Decreases incidence of Ventilator associated pneumonia.

         - Decreases incidence of aspiration.

         - improves Oxygenation

        - Increases end expiratory lung volume

Oxygen inhalation – to maintain SPO2 above 92%

Intermittent BiPAP – Supplies positive pressure ventilation

Inj Augumentin 1.2 gm IV BD – It is a combination of Amoxicillin , Clavulinate used to treat bacterial infectons.

Tab azithromycin 500 mg OD – It  belongs to macrolide class of drugs.

Inj Lasix IV BD – It is used as diuretic.

          Given if SBP > 110mm hg

Tab Pantop 40 mg PO OD – It is a PPI

Inj Hydrocortisone 100 mg IV – It is a steroid

Neb with Ipravent ,Budecort 6 hrly

Tab Pulmoclear100 mg PO OD

 

3.Cause of her current exacerbation?

A.Infection could have exacerbated COPD.

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

A.Yes . ATT could have affected her symptoms ,as ATT are nephrotoxic which would be the cause of raised RFT.

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

A.Hyponatremia in this patient is due to decrease in water excretion which may be related to enhanced release of both angiotensin and vasopressin.

This can be exaggerated by diuretic therapy.

Cardiology:  

 

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

A.Alcoholic since 40 years.It is one of the risk factor for heart failure.

    Diabetic since 30 years.

   Hypertension since 19 years.

  Patient have stage 4 CKD which is a risk factor for HF.

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

A.Patient is diagnosed with CKD stage 4 .

                         CKD leads to decrease in EPO which inturn leads to decrease in production of RBC.

A.Alcohol can impact the RBC production by decreasing the number of precursor cells in bone marrow.

   Alcohol also impacts RBC maturation.

 Alcohol induced malnutrition leads to defective absorption of iron and folic acid which are needed for formation of Hb.

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

A.Uncontolled diabetes in this patient is the cause of non healing ulcer and blebs

   Due to poor blood circulation ulcers take long time to heal.

  CKD can also lead to delayed wound healing.

   Anaemia leads to decrease in oxygen carrying capacity.Due to low oxygen levels there is delayed wound healing

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

A. Impaired glucose tolerance

     Diabetes mellitus

    Micro vascular complications – Diabetic triopathy(Neuropathy,retinopathy,nephropathy)

    Macrovascular complications-CAD,Peripheral vascular diseases.

 

1.Whai is the difference between heart failure with preserved ejection fraction(HRpEF) and heart failure with reduced ejection fraction (HRrEF)?

A.Ejecton fraction : Amount of blood pumped out of the heart with each beat

                                     Normal EF – 55-70%

In HRrEF , EF is <40% –Known a Systolic heart failure

                         In systolic failure left ventricle is more affected.

In HRpEF , EF is >50% – known as Diastolic heart failure

                         Very Commonly associated with obesity,elderly females,OSAS,CKD.

                         RVEDP and LVEDP increases commonly in HRpEF.

Risk of CAD in HRrEF and HRpEF are same.

2.Why haven’t we done pericardiocentesis in this patient?

A.Pericardiocentesis is usually done in patients in whom effusion is not resolving spontaneously .

In this pericardial effusion is resolving on it’s own.

So pericardiocentesis is not done in this patient.

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

A. Age

Hypertension

Diabetes Type 2

Kidney disease.

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

A.

 Gastroenterology and pulmonology:

 

  1.What is the evolution of 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 patient’s problem?

 

 5 years ago – Pain abdomen and vomitings which were treated conservatively

 Patient stopped  alcohol consumption on advice of physician and was symptom free for 3 years.

But again started  consuming alcohol following which he developed recurrent episodes of pain abdomen and vomitings.

He had 5-6 episodes of pain abdomen nad vomitings last year which was treated by local RMP.

In last 20 days he consumed  5 bottles of toddy per day.

He consumed alcohol 1 week back following which he developed painabdomen and vomitings since 1 week and fever since 4 days.

Present complaints – Pain in  umbilical region,left hypochondriac,left lumbar and left hypogastric region

Pain is of throbbing type and radiating to the back .

1 episode of vomiting which is non bilious , non projectile,containing food particles and water.

High grade continuous fever associated eith chills and rigor.

Constipation since 4 days and passing flatus.

Burning micturition since 4 days associated with supra pubic pain ,increased frequency and urgency of urine.

Anatomical localization: Pancreas

Primary etiology: Alcohol consumption.

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

Inj Meropenam TID for 7 days :

         It is a Beta lactam antibiotic (Carbapenam)acting against variety of bacteria.

Inj Metrogyl 500 mg IV TID for 5 days

Inj Amikacin 500 mg IV BD for 5 days

       It is a aminoglycoside.

TPN (Total parenteral nutrition)

IV NS/RL at rate of 121 ml/hour

      To treat dehydration

Inj Octreotide 100 mg SC BD

     It is a somatostatin analogue.It decreases exocrine secretion of pancreas and has anti inflammatory and cyto protective effects.

Inj Pantop 40 mg IV OD

Inj Thiamine 100 mg in 100 ml NS IV TID

Inj Tramadol in 100 ml NSIV OD

      Opiod analogue to relieve pain.

 

1.What is causing the patient’s dyspnea?How is it related to pancreatitis?

 

Pancreatitis may be associated with pulmonary complications.

Pancreatic eznzymes through hematogenous route reaches lung and destroys lung tissue leading to pulmonary complications like dyspnea

2.Name the possible reasons why patient has developed a state of hyperglycaemia?

Due to autodigestion of pancreas ,there is damage to pancreatic tissue including damage to beta cells of pancreas.

This leads to decrease in insulin realease from beta cells of pancreas.

Leads to hyperglycaemia.

Hypergylcaemia is used as one of the prognostic marker in Pancreatitis.

3.Whai is the reason for his elevated LFT’s?Is there a specific marker for alcoholic fatty liver disease?

A.Elevated Lft is due to Alcohol consumption leading to liver damage in turn leading to raised LFT

 Gamma Glutamyl Transferase (GGT) is specific marker for alcoholic liver disease.

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

IV fluids -125ml/hour

                  To treat dehydration

Inj Pan 40 mg OD

Inj Zofer 4 mg IV SOS

Inj Tramadol 1 amp in 100 ml NS IV SOS

Tab Dolo 650 mg SOS

GRBS 6^th hourly

Bp charting 8^th hourly

 

Neurology:

 

1.What is Myelopathy hand?

A.Myelopathy hand is due to involvement of pyramidal tract.

There is loss of power of adduction and extension of ulnar two or three fingers and an inability to grip and release rapidly with these fingers.

2.What is finger escape?

A.Involuntary abduction of fifth finger caused by unopposed action of extensor digiti minimi.

This is known as Waretenberg sign.

This finding of weak finger adduction in cervical myelopathy is known as Finger escape sign.

3.What is Hoffmann sign?

A.This is elicited by flicking the nail of middle finger,if there is any flexion of ipsilateral thumb or index finger,it is considered as positive.

Positive Hoffmann sign is seen in corticospinal tract dysfunction localized to cervical segment of the spinal cord.It can also be seen in multiple sclerosis. 

1.What is the evolution of 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 patient’s problem?

A.7 days ago – Patient had giddiness in morning with 1 episode of vomiting which subsided on taking rest.

4 days ago – Patient consumed alcohol followed by which he developed giddiness that increased on standing and walking

There is history of postural instability ,associated with 2-3 episodes of vomiting that is non bilious,non projectile without food particles.

On day of admission – Slurring of speech,deviation of mouth that resolved.

Anatomical localization : Infarct in cerebellar hemisphere

Etiology : This patient has HTN for which he is not taking medication

HTN is a risk factor for infarct which could result in stroke leading to deprivation of nutrients and oxygen  

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

A.Tab Vertin – 8 mg : This belongs to betahistine group used to treat vertigo.

                                        It is a weak agonist at H1 receptors

  Tab Zofer 4mg : This is ondansetron which is a antiemetic.

  Tab Ecospirin 75 mg: this is an NSAID that is used as antiplatelet drug that prevents the formation of blood clots.

  Tab Atorvastatin 40mg: This belongs to Statin group of drugs used to treat dyslipidaemias.

  Tab Clopidogrel 75 mg : It is a antiplatelet drug that can be used prophylactically to prevent morbidity and motality due to CVD etc

  Thiamine : In alcoholics , thiamine is usually depleted .As this patient is chronic alcoholic thiamine is given to prevent Wernicke’s encephalopathy.

 Tab MVT : It is methycobalamin to treat Vit B12 deficiency.

3.Did the patient history of denovo HTN contribute to his current condition?

A.HTN itself is a risk factor for infarcts.

  High blood pressure causes the arteries either to block or burst in the brain leading to death of brain cells due to deprivation of oxygen and nutrients.

This leads to disabilities in speech,movement etc.

4.Does the patient history of alcoholism made him more susceptible to ishaemic or haemorrhagic stroke?

A.Ischaemic stroke is due to blockade of blood vessel by a clot.

   Haemorrhagic stroke is due to rupture of blood vessles.

A study revealed that light and moderate alcohol consumption seems to lower the risk of ischaemic stroke but had no impact on haemorrhagic stroke.

The adverse effects of alcohol consumption on blood pressure is a major risk factor for stroke may increase the risk of haemorrhagic stroke and outweighs the benefits of moderate alcohol consumption.

1.What is the evolution of 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 patient’s problem?

A.8 months ago – Bilateral gradually progressing pedal edema present in both sitting and standing position which relieved on medication.

Since 6 days – Dragging type of Pain  radiating along the leftupper limb

Since 5 days – Palpitations in night times along with dyspnea at the time of palpitations.

Chest pain associated with chest heaviness.

2.what is the reason for recurrence of hypokalemia in her?important risk factors for her hypokalemia?

A.risk factors for hypokalemia:

            Inadequate intake.

           Patient on diuretics , steroids

           Renal tubular acidosis

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

A.ECG changes in hypokalemia:

         Flattening of T wave.

         ST segment depression

       Prominent U wave.

      Prolonged QT interval.

Symptoms of hypokalemia:

       Muscle weakness ,

       Paralysis

       Polyuria due to nephrogenic diabetes insipidus

       Constipation, Ileus

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

AIf a patient had a stroke then there is increased risk for the patient getting a stroke.

Brain cells are injured in stroke due to deprivation of oxygen and nutrients leading to formation of scar tissue affecting electrical activity in brain.

Disrupting the electrical activity can lead to seizure.

Patient who had haemorrhagic stroke is more susceptible for seizures than to a person who had ischaemic stroke.

2.In the previous episodes of seizures patient didn’t loss his consciousness but in recent episode he lost his consciousness ,what might be the reason?

A.In previous episodes,patient didn’t loss his consciousness because he might have had simple partial seizures which are not associated with loss of consciousness.

Now the patient had generalized tonic clonic seizures (GTCS) .GTCS is usuallt accompanied by loss of consciousness.

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

A.The patient had several falls when he was inebriated and this would have caused intra cranial bleeds which were left untreated and in due course of time this led to ataxia.

2.What was the reason for his IC bleed ?Does alcoholism contribute to bleeding diathesis?

A..Risk of haemorrhagic stroke is directly proportional to amount of alcohol intake.

   Patient is a chronic alcoholic . This would have led to liver dysfunction inturn leading to impaired coagulation mechanism as coagulation factors are produced from liver.

This would have led to intra cranial bleeding.

1.Does the patient history of RTA have any role in patient’s present condition?

A.If the patient have sustained head injuries in RTA and left untreated ,in due course of time ,this could have led to her present condition.

2.What are the warning signs of CVA?

A.Weakness ,numbness in part of the body.

    Headache associated with vomiting.

   Confusion

   Altered state of consciousness.

   Impaired coordination of movements

  Dystonia.

3.What is the drug rationale in CVA ?

A.Inj Mannitol 100ml/IV/TD.

   Tab Ecospirin 75mg/PO/OD : this is an NSAID that is used as antiplatelet drug that prevents the formation of blood clots.

Tab atorvas 40 mg PO/HS This belongs to Statin group of drugs used to treat dyslipidaemias

4.Does alcohol have any role in attack?

A.Patient is a chronic alcoholic .Alcohol increases the risk of haemorrhagic stroke.

Risk of haemorrhagic stroke is directly related to amount of alcohol consumed.

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

A.His lipid profile is almost normal except for decrease in HDL cholesterol.

So,dyslipidaemias contributing the cause for his attack has very less chance.

1.What is the evolution of 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 patient’s problem?

A.Patient was asymptomatic 9 days ago

Suddenly started talking to himself , laughing.

He was unable to get up from the bed and move around .He needed assistance.

Decrease in food intake since 9 days

Taken to RMP ,he was given IV fluids and referred to higher hospital

He stopped drinking same day citing body pains the day before

Short term memory loss 9 days ago where he couldn’t recognize his family members.

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

A.Thiamine :

       In alcoholics thiamine is depleted ,to replace losses ,thiamine is given.

Lorazepam :

  It increases the inhibitory effect of GABA

Lactulose :

   In decreases the production and absorption of ammonia.It is used to treat symptoms of encephalopathy

Potchlor liquid :

  To treat low potassium

3. Why have neurological symptoms appeared this time that where absent during withdrawl earlier?What could be the possible cause?

A.Due to excess alcohol consumption ,kidneys are damaged leading to increased accumulation of toxins 

And due to excess thiamine deficiency

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

A.Patient is a chronic alcoholic .In chronic alcoholics,Thiamine deficiency is quite common.

Thiamine deficiency can lead to Korsakoff psychosis,wernicke’s encephalopathy

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

A.Patient is a chronic alcoholic.

Alcohol reduces the functioning capacity of kidney leading ti decrease in GFR.

Alcohol consumption also leads to high blood pressure that is a risk factor for kidney damage.

6.What is the probable cause for normocytic normochromic anaemia?

A.Normocytic normochromic anaemia is common in patients with CKD.

7.Could chronic alcoholism have aggrevated the foot ulcer formation?If yeshow and why?

A.Alcohol delays wound healing and also predisposes the patient to infections further delaying the wound healing

 

1.Why is the child excessively hyperactive without much of social etiquitties?

A.Child seems to be suffering from ADHD (Attention deficit hyperactivity disorder)

Child suffering from this disorder appear to be absent minded , unable to carry out instructions , constantly fidgeting , acting without thinking,Having difficulty in organizing tasks.

2.Why doesn’t the child have excessive urge of urination at night time?

A.If the cause is psychological , at night the child would be relaxed and sleeping but at day times he must be stressed out .So the child could have excess urge to urination at day time not at night.

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

A. Reassurance of patient.

1.What can be the cause of her condition?

A.Cortical vein thrombosis detected on MRI could be the cause of her condition..

2.What are the risk factors for cortical vein thrombosis?

A.Prothrombotic sates : Anti thrombin deficiency,Protein C and Protein S deficiency,HRT.

   Mechanical : Trauma, lumbar puncture.

   Infections : Meningitis , mastoiditis , otitis meadia.

   Inflammatory : SLE,Sarcoidosis, IBD

   Drugs : OCP , steroids , cyclosporine

  Vasculitis : Bechet’s disease , Wegeners granulomatosis.

  

3.There was seizure free period in between but again sudden episode of GTCS why?Resolved spontaneously why?

A.Seizures are resolved after medical intervention

  Sudden episode of GTCS could be due to persistence of excitable foci leading to abnormal firing of neurons.

4.What drug was used in suspicion of cortical vein thrombosis in this patient?

A.Tab Ecospirin

           It is a antiplatelet drug.It prevents aggregation of platelets.

1.What was the most probable diagnosis in this patient?

A.On USG guided aspiration , Blood was aspirated .

Most probable diagnosis could be abdominal haemorrhage(bleeding into abdomen) due to perforation of abdominal organs.

2.What was the cause of her death?

A.Patient could have died due to complications following laparotomy surgery like bleeding , sepsis etc…

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

A.Long time use of NSAID could lead to potential Gastro intestinal complications .

NSAID’s are known to cause injury to GI mucosa ranging from minor lesions such as erosions to major lesions like ulcers that leads to complications like bleeding , perforation,obstruction.

1.What is 1.What could be the cause for his SOB ?

A.There is high creatinine (10gm/dl)in this patient indicating renal failure (AKI)

Due to renal failure , there would be build up of fluid in the body i.e; fluid overload leading to dyspnea.

Patient also has anaemia that leads to decreased oxygen carrying capacity leading to dyspnea.

2.Reason for intermittent episodes of drowsiness?

A.Hyponatremia could have been the cause for his drowsiness.

3.Why did he complain of fleshy mass like passage in urine?

A.Due to kidney disease his urine would be frothy due to proteins in urine and pus cells due to urosepsis.This would have appeared as fleshy mass

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

A.Haemorrhage is the most common complication

  Incontinence due to damage to external spinchter mechanism.

  Urethral stricture.

 Bladder neck contracture.

 Retrograde ejaculation.

the evolution of 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 patient’s problem?

A.Since 2-3 years ,facial puffiness on and off

   SOB grade 2 since 1 year and diagnosed with hypertension.

   He was apparently asymptomatic 2 days ago

   He developed SOB grade 2 that progressed to grade 4

  Oliguria since 2 days.

  Anuria since morning

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

A.Inj Dobutamine 3.6ml/hour :

      Causes strong ionotropic effect and weak ionotropic effect

Tab Digoxin 0.25 mg :  :

      It increases the force of contraction by inhibiting Na – K ATPase pump

 Inj Unfractionated heparin infusion 5ml/hr :

It is used as anticoagulant.

Tab Acitrom 2mg OD : 

         It is a anticoagulant to prevent formation of blood clots

Tab Cardivas 3.125 mg  :

        It is a beta blocker

Tab Dytor 10mg/PO/OD :

      It is a loop diuretic to treat fluid overload

Tab Pan D 40mg PO/OD :

     It is a PPI

Inj Thiamine 100mg in 50 ml NS IV/TID

Inj HAI sc

  

3.What is the pathogenesis of renal failure due to heart failure(cardiorenal syndrome)?Which type of cardiorenal syndrome in this patient?

A.Failing heart fails to generate forward flow resulting in renal hypoperfusion . Inadequate renal afferent flow activates RAAS ,the sympathetic nervous system and asrginine vasopressin secretionleading to fluid retention increased preload and inturn worsening pump failure. 

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

A.Obesity

   Hypertension

  Sedentary lifestyle

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

A.Patient is kept on anticoagulants .

So aPTT and INR are monitored to know if patinent has chance of bleeding , HIT(Heparin induced thrombocytopenia)

  

1.What is the evolution of 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 patient’s problem?

A.Patient was diagnosed with HTN and type 2 DM

   Asymptomatic 3 days back , then he developed mild chest pain in right side of chest

Dragging type of pain radiating to the back. 

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

A.Tab Aspirin 325 mg PO/STAT : At this dose aspirin acts as antiaggregatnt.

   Tab Atorvas 80 mg PO/STAT : It is a cholesterol lowering agent , belongs to statin group of drugs

  Tab Clopibb 300mg PO/STAT : It is used to reduce formation of clots in blood vessles.

  Inj HAI 6u/IV STAT : To treat patient’s hyperglycaemia.

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

A.PTCA was done 3 days after appearance of symptoms.

    Ideally it should be performed in 12 hours of onset of symptoms.

   It would have been better if PTCA was avoided.uch as erosions to major lesions like ulcers that leads to complications like bleeding , perforation,obstruction.