GOO Flashcards

58 yrs. Female patient presented with persistent nonbilious vomiting Now is drowsy, hypokalemic, Hypochloremia and metabolic alkalosis .

1
Q

58 yrs. Female patient presented with persistent nonbilious vomiting Now is drowsy, hypokalemic, Hypochloremia and metabolic alkalosis .

Q. Why pt is hypoNa?

A

Na loss of vomiting

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2
Q

Q1. what is your Diagnosis?

A

GOO

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3
Q

Q2: Causes?

A

Begnin – > Pyloric stenosis
Malignant – Gastric / Pancreatic Ca.

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4
Q

Q3: Why K is low?

A

Loss in vomiting / ↑ Aldosterone secretion in response to hypovolemia and hyponatremia ( in exchanging with Na)

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5
Q

Q4: Why is Chloride low?

A

Loss in vomiting

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6
Q

Q5. Why alkalosis ?

A

Loss of Cl- in vomiting and H+ + hypovolemia
Acid loss lead to more production of NAHCO3 as it stimulate acid secreation leading to Alkoloritic state
Once ability of kidney and gut to excrete it saturated

 Another answer;
kidney try to compensate by preserving NaHCO3 to keep the electrochemical neutrality
Reduction in pancreatic juice secretion in response to loss of acid load in duodenum which will lead to NAHCO3 retention

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7
Q

Q6: Why hyponatremia ?

A

As this pt has Met Alkalosis so kidney will try to excrete mor NaHCO3 to compensate the condition and this will lead to hyponatremia.

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8
Q

Q7: Is NaHCO3 excreted as a whole ion?

A

Yes

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9
Q

Q8: Classification of Hyponatremia & give example to each ?

A

According to osmolarity could be
(Isotonic – Hypotonic (Hypo / Hyper/Euvolemic)- Hypertonic )
Depletion Loss of Na (Hypovolemic); Vomiting, Diarrhea, Diretics, Burns
Dilutional Excess of Water (Hypervolemic); HF , Over admin Glu 5%, SIADH, TURP
Loss of water and Na but Na is more – > Duritecs
Endocrine(Euvolemic) ; Addison dis / hypothyroidism
Pseudohypo; MM

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10
Q

Q9: complications of hyponatremia ?

A

Confusion – cerebral edema - agitation –
seizures – AKI –
Arrythmia

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11
Q

Q10: How to correct the condition of the patient ?

A

According to CCrisp protocol
ITU reg – NPO – Venous access – Labs – Fluid correction NACL
Endoscope Gastric dilatation

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12
Q

Q11: Who will you involve?

A

My Consultant / ITU reg. / Anesthesia in case of intubation / Cardio?

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13
Q

Q12:When will this patient be fit for surgery?

A

After improving of met acidosis / Correction of electrolyte and become hemodynamically stable.

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14
Q

Q13: What is Chloride shift?

A

Bicarbonate shifts out into the plasma and chloride shift into RBCs to make cellular balance

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15
Q

Q. Why are the Creatinine and urea are abnormal?

A

Due to decrease renal perfusion 2ry to dehydration.

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16
Q

Q. Why urine is acidic?

A

Presestant dehydration – increase aldosterone – act on distal tubule and CDs – > reabsorption of Na in exchange of K or H+ leading to loss of H in urine

17
Q

Q. what’s optimal fluid to give the pt? explain?

A

0.9% NaCl (better than Hartman as it has more Cl)+ KCL
this will replace Na K Cl loss and will help in correcting alkalosis

18
Q

Q. what bedside procedure used should pt have to help his condition?

A

Nasogastric Tube and urinary catheter (UOP)

19
Q

Q. As a surgical Reg whom you’re going to involve in the care?

A

Surgeon (My consultant) / HDU lvl 2 facility nurse staff for placement of lines and ecg monitoring and fluid and electrolyte therapy

20
Q

Q. when to consider this pt is fit for surgical intervention?

A

When acid base and electrolytes have been corrected