Tuesday, 14 August 2012

Case discussion


65 year male recently got bed restricted due to generalized weakness following anorexia and vomiting.
He has been using lithium carbonate for his manic-depressive illness for some 15 years.
On examination he is lethargic but able to communicate, Temp: 101f, pulse 124bpm and respiratory rate 16 /min. Blood pressure 100/60 lying and 70/40 on sitting.
Investigation: Lithium 1.5 mmole/lit;  Urea 20mg/dl and S. creatinine 1.3mg/dl. Na 169 ,  Ca 2.3mmole/l.
Glucose 4mmole; urine osmolality 240.
Give probable reason for patients hypernatremia, polyurea and polydipsia?

This patient has developed nephrogenic diabetes inspidus due to prolong use of lithium for his
Manic-depressive illness. Lithium block the action of ADH as well as adenylate cyclase in collecting duct
, thereby excessive water excretion or we can say decreased water absorption has led to increased serum osmolality and decreased urine osmolality. In this way thrist mechnism is stimulated to compensate increased serum osmolality.


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Common Drugs causing nephrogenic diabetes inspidus:
Lithirm
Amphotericin B
Demeclocycline

Sunday, 12 August 2012

Polyurea with headache

29 year woman with 1 month history of headache , increased thrist and urinary frequency.
Urinary out put over 24 hours was 8 liters.Fluid deprivation test was performed with following
results:

 Time                              Serum Osm                  Urine Osm                    Serum ADH             Urine output

Baseline                           144                              80                                 2                                  -

1 hour                               147                             80                                  2                              600

2 hour                               150                              80                                  2                               500


Q.        What is the diagnosis?
Q.         Treatment?


Answere:    This patient has central diabetic inspidus and his defect seems to be severe.The D/D should include both central and nephrogenic dI, as well psychogenic polydipsia and diuretic use.

Desmopressin( Vasopressin) is the prefered teatment.








Vasopressin



Wednesday, 8 August 2012

Urinary Anion Gap

In a patient with non-anion gap metabolic acidosis, calculating the urine anion gap can help differentiate between diarrhea and renal tubular acidosis (RTA) as the etiology.
 
A. What is the urine anion gap and how is it calculated?
 
B. In the following case, please determine if the patient has a non-anion gap metabolic acidosis due to diarrhea or RTA:
 
A 24 year old male dancer comes to attention due to a low serum bicarbonate on routine blood work. Additional results include:
Serum: Na 140 meq/L, K 3 meq/L, HCO3 14 meq/L, Cl 116 meq/L
Urine: Na 50 meq/L, K 30 meq/L, Cl 40 meq/L.


Answere:


Urine anion gap is calculated by subtracting the urine concentration of chloride(anions) from the concentrations of sodium plus potassium (cations):
= Na+ + K+ − Cl
where the concentrations are expressed in units of milliequivalents/liter (mEq/L).
In contrast to the serum anion gap equation, the bicarbonate is excluded. This is because urine is acidic, so the bicarbonate level would be negligible.
Urine anion gap is an 'artificial' and calculated measure that is representative of the unmeasured ions in urine. Usually the most important unmeasured ion in urine isNH4+.
  • A positive urine anion gap suggests a low urinary NH4+ (e.g. renal tubular acidosis).
  • A negative urine anion gap suggests a high urinary NH4+ (e.g. diarrhea).

Case Discussion


56 year male , ex smoker with significant history of Ischemic heart disease
Presented in emergency with the complaint of Generalized weakness, Short
Of breath and decreased urine output for last 2 weeks.
He was already investigated outside in cardiology services which he often
Visisted for his chronic heart ailment. His serum creatinine jumped from 0.7
Mg/dl to 4.1 mg/dl in 1 week period.
His past history entails stent placement 8 year back after angiography. Since  then
He was on heart medication including anti hypertensive agent s whose is prescription
Was not brought by him and he does not  know the names for all medications.
On examination he was conscious , well oriented and mobile with regular pulse
96 bpm and BP 80/6o with diminished perepheral pulses. He pale , not icteric
Not cyanosed with dry peripheries and flat neck veins.
Systemically he was ok except slight tenderness on right hypochondrial region.

Discussion:
Now this middle age guy has developed acute kidney injury. And the reason for
This is quit well infromed for his low blood pressure with significand heart disease
With medication whose names are not described. Well we can presume medication
In this scenario would be diuretic , ace inhibitors, anti platelets, Beta blockers etc.
This could cause volume depletion and AKI. ACE inhibitors can cause AKI.
He might have developed unstabel angina/MI which has cused AKI. He may have atherembolic disease.

Tuesday, 7 August 2012

Case Discussion


30 year male admited through emergency in a severe metabolic acidosis state and drowsy.
He had outside s.creatine of 15mg/dl, and xray showing homogenous opacity involving right
Apex of lung. There was recent history of taking ATT, which he soon gave up after using few
Days as he became more nauseated and had vomiting too. There was an aditional history of
Difficulty in passing urine since many years, and also required once catheterization suprapubically.
We got him inserted Double lumen cather and dialysed , later on Ultrasound kidneys and bladder
Showed markly dillated PC system leaving no cortex bilatteraly and thick wall , mild trabeculated
Bladder.
We concluded that he would be having stricture urethra by his tory which was substaciated with
The fact  when he was tried to pass cather but failed to proceed and subsequently suprabubic cathe
Erization done as he was in retention of urine.
Regarding his homogenous opacity in lung we would work him up for tuberculosis by Blood CP, ESR
Mauntox test, Sputum AFB or moring gastric lavage for AFB or BAL. Urine Dr and C/s.