Bi weekly exam 7th sept

Ans 1- Anatomical diagnosis- Glomerulus of the kidney

    Histological? Loss of effacement of foot process of podocytes of basement membrane

? Membranous glomerulonephropathy 


  Etiological diagnosis- Diabetes,hypertension

      Diabetic nephropathy


Ans2-  Azotemia -it is defined as increase in Blood urea nitrogen with BUN to creatinine ratio less than 20:1 suggestive of either renal or post renal azotemia

https://www.ncbi.nlm.nih.gov/books/NBK538145/

The causes for post renal ruled out by radiological imaging.



b.   ANAEMIA-erythropoeitin deficiency in CKD,uraemia induced inhibitors of erythropoeisis, shortened erythrocyte survival


CKD patients have increased iron losses, estimated at 1–3 g per year in hemodialysis patients, due to chronic bleeding from uremia-associated platelet dysfunction, frequent phlebotomy, and blood trapping in the dialysis apparatus. CKD patients, particularly hemodialysis patients, also have impaired dietary iron absorption.


https://jasn.asnjournals.org/content/23/10/1631



  c.  HYPOALBUMINEMIA

1.Reduced protein consumption and inflammation. ,due to downregulation production of albumin mrna by the liver leading to decreased synthesis ,increased catabolism and vascular permeability.


https://jasn.asnjournals.org/content/21/2/223


2. Chronic proteinuria


d.  ACIDOSIS

Renal failure (as there is decreased synthesis of bicarbonate resulting in high anion gap metabolic acidosis)



3.According to KDIGO guidelines,oral replacement therapy is initiated when plasma hco3- is <22mEq/l

Iv replacement formula:HCO3=0.5×wt (Kg)×(24-SERUM HCO3)

                                                        Or (Desired increase in dr. Hco3)

Link: https://www.uptodate.com/contents/sodium-bicarbonate-drug-information?topicRef=127552&source=see_link#F221615


The bicarbonate deficit for this patient wt.being 55kg is 300meq/lit

Therefore a bolus dose of 150meq/l was given 

Followed by replacement orally till the decision for haemodialysis was made.


In patients of CKD bones release bicarbonate and phosphate by process of demineralisation to compensate for the additional acid being accumulated, thus causing osteopenia,therefore oral bicarbonate therapy is initiated to counter this effect.



4.  On the day of admission the patient had egfr of 7.5ml/min/1.73m2 with urine output less than 100ml in 24hrs with high anion gap metabolic acidosis


According to IDEAL study INITIATING DIALYSIS EARLY AND LATE

Guideline 1.3, patients with egfr between 9 to 6ml/min/1.73m2 can be monitored under close supervision and taken up for dialysis when they become symptomatic.


The patient did not show symptoms of metabolic acidosis like acidosis breathing until 3rd day of admission  and was hence taken up for haemodialysis. 


https://documentcloud.adobe.com/link/track?uri=urn:aaid:scds:US:9eea1006-ab8f-4db7-a7dc-41e6e832420d.



5.factors other than hypertension and diabetes that lead to her condition.

 

Infection-causing Acute kidney injury,


?IgA glomerulonephritis


Lupus nephritis


Renal artery stenosis


https://www.niddk.nih.gov/health-information/kidney-disease/chronic-kidney-disease-ckd/causes



7.pathophysiology of cardiorenal syndrome  in hfpef patients as described in the link below


Main mechanism

1.INCREASE in intra abdominal and central venous pressure

2.activation of renin angiotensin system

Other

1.Sympathetic overactivity

2.oxidative injury and endothelial dysfunction

Precipitating factors

Infections

Drugs such as NSAIDS


https://documentcloud.adobe.com/link/track?uri=urn:aaid:scds:US:9eea1006-ab8f-4db7-a7dc-41e6e832420d


Evaluation is by 

History- suggestive of cardiac involvement with symptoms of orthopaedic PND, palpitations ,chest pain,fatigue, hypotension,diminished peripheral pulses,abnormal heart sounds


Examination.-elevated JVP,generalised edema with pleural effusion, crackles or rakes on auscultation

 

Investigations

BNP,urinalysis,electrocardiogram


https://www.ncbi.nlm.nih.gov/books/NBK542305/



10.The other similar patient

Diagnosis  .PRE RENAL AKI  ( BUN >20:1) on CKD secon day to decreased consumption of fluids due to episode od diarrhoea 10 days back

The patient can be managed conservatively with adequate fluids and glycemic control.


USG-the disparity in kidney size of more than 3cms between them can be due to 

1.increase in size 

2.renal artery stenosis with over compensation of the normal kidney



Comments

  1. [9/14, 9:40 AM]

    Chandana, Manasa, answer to the question asked on Saturday 2-4 given by Zain here

    "CKD patients have increased iron losses, estimated at 1–3 g per year in hemodialysis patients, due to chronic bleeding from uremia-associated platelet dysfunction, frequent phlebotomy, and blood trapping in the dialysis apparatus. CKD patients, particularly hemodialysis patients, also have impaired dietary iron absorption."

    https://zainalammohammed59.blogspot.com/2020/09/bi-weekly-exam-7th-sept.html?m=1


    [9/14, 9:41 AM] So for all practical purposes if the above quote is true, every dialysis patient may need iron to increase their hb by 1-3 g per year?

    How much iron tablets in Dose would that work out to be?


    [9/14, 9:44 AM] Zain what kind of signals lead to "downregulation production of albumin mrna by the liver leading to decreased synthesis" as mentioned in your answer here

    https://zainalammohammed59.blogspot.com/2020/09/bi-weekly-exam-7th-sept.html?m=1



    [9/14, 9:46 AM] Zain you need to cite the reference for this statement in your answer

    "ACIDOSIS

    Renal failure (as there is decreased synthesis of bicarbonate resulting in high anion gap metabolic acidosis)"
    [9/14, 9:48 AM] Rakesh Biswas: Zain have the kdigo guidelines cited any evidence based reference for their guideline that you cited in your answer and I quote below:

    "According to KDIGO guidelines,oral replacement therapy is initiated when plasma hco3- is <22mEq/l"

    ReplyDelete

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