Case study Watch

pjp9494
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CASE STUDY 1:

A 72-year-old man is discovered, by his family, lying on the floor at home. He is found to have a left hemiparesis and a stroke is diagnosed. Clinical assessment of his volume status indicates dehydration: pulse 112 beats per minute, blood pressure 95/65 mmHg, lax skin and dry tongue. The following biochemical results were obtained on admission:

Na+
169 mmol/L
(135-145)
K+
3.9 mmol/L
(3.4-4.9)
Urea
23.5 mmol/L
(2.5-8.0)
Creatinine
160 μmol/L
(40-130)
Glucose
7.6 mmol/L
(4.0-5.5)

1. Describe and comment on the biochemical abnormalities?
2. How would you treat his fluid/electrolyte status?


CASE STUDY 2:

A 76-year-old male with a history of stroke is seen at a wellness clinic. Ambulatory blood pressure confirms refractory hypertension of 172/98 mmHg. Furosemide 20 mg daily is added and an appointment for MRI angiography is requested to exclude renal artery stenosis. The patient acknowledges that his roommate uses the same medication. Three days after furosemide, the nursing home on-call physician evaluates the patient. The physician notes a dehydrated and disoriented male with lax skin and dry mucosa. The medication is sitting adjacent to his bedside.


Serum urea and electrolytes are as follows:
Na+
127 mmol/L
(135-145)
K+
3.2 mmol/L
(3.5-5.1)
Urea
15 mmol/L
(2.5-8.0)
Creatinine
140 μmol/L
(40-130)

1. What do the patient’s sodium and water status indicate and how would you treat?



CASE STUDY 3.

A 57-year-old female is admitted following a shark bite with severe blood loss. On arrival, she is clinically shocked with a pulse rate of 116 beats per minute and 90/65 mmHg blood pressure. Blood testing produces the following:
Urea and Electrolytes
Na+
143 mmol/L
(135-145)
K+
3.6 mmol/L
(3.5-5.1)
Cl-
98 mmol/L
(98-107)
HCO3-
5 mmol/L
(22-29)
Urea
13.8 mmol/L
(2.5-8.0)
Creatinine
130 μmol/L
(40-130)
Arterial Blood Gases
H+
97 nmol/L
(35-45)
pCO2
2.7 kPa
(4.5-5.6)
pO2
16.1 kPa
(12-15)

1. Classify the acid-base disorder and explain the findings?

CASE STUDY 4.

A 22-year-old male motorcyclist is admitted following a severe head injury. The patient’s urine output exceeds 15 Liters over the next 24 hours. Serum sodium climbs from 148 mmol/L on admission (135-145 mmol/L) to 168 mmol/L on day 3 at which point urine osmolality is 80 mmol/kg.

1. What is the most likely diagnosis and how would you treat?

CASE STUDY 5.

A 46-year old male smoker presents with an unintentional weight loss of 50 lbs over three months. He admits to intermittent dry cough. On chest examination, he has signs of left lower lobe consolidation; water volume status is visually unremarkable (appears to be within normal limits). Chest x-ray confirms consolidation with hilar lymphadenopathy.

Lung cancer was provisionally diagnosed. Urea and electrolytes were measured.
Na+
124 mmol/L
(135-145)
K+
3.6 mmol/L
(3.5-5.1)
Urea
5.8 mmol/L
(2.5-8.0)
Creatinine
110 μmol/L
(40-130)

1. Describe and explain the biochemical abnormalities. (Give your assessment of the patient’s water and sodium status.) How would you treat his fluid and electrolyte abnormalities?
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mohammed karim
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is there answer for these Q ?
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Jpw1097
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Well what are your ideas first?
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pjp9494
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Hi Jpw1097, I don't get anything I am very confused in all this case study. If you can help out that would be great.
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Jpw1097
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Case 1 - the patient is dehydrated probably due to inadequate water intake. The dehydration has caused the patient to become hypernatraemic (i.e. high sodium levels) and hypovolaemic (low blood volume). The hypovolaemia causes the blood pressure to fall (hypotension) which impairs renal perfusion and can cause pre-renal acute kidney injury (AKI) which causes the urea and creatinine levels to rise as the kidney can no longer excrete them effectively due to reduce blood blow. The underlying issue here is the low blood volume, this can be corrected by giving IV fluids. This will reduce the sodium levels and also restore renal perfusion and so the urea and creatinine levels will fall.

Case 2 - furosemide is a loop diuretic, it inhibits the Na-K-2Cl cotransporter in the thick ascending limb. Furosemide normally causes hypernatraemia however it can also cause hyponatraemia if sodium losses are greater than water losses in the kidney. The patient has become dehydrated due to furosemide, again, the hypovolaemia/hypotension has reduced renal perfusion causing a pre-renal AKI which has caused urea and creatinine levels to rise. This would probably be managed by temporarily stopping the furosemide and giving fluids.

Case 3 - the patient has lost a lot of blood and has become hypovolaemic - in fact, the patient is suffering from hypovolaemic shock. This has reduced perfusion of tissues which is causing a lactic acidosis (as tissues respire anaerobically) - explaining the low HCO3-. As a result of this metabolic acidosis, the lungs try to compensate for this by excreting more CO2 by hyperventilating - this explains the low pCO2 and high O2. Again, as a result of the hypovolaemic shock, there is reduced renal perfusion causing a pre-renal AKI causing urea levels to rise. Depending on the level of blood loss, the patient will be given IV fluids or, if very severe, the patient will require a blood transfusion.

Case 4 - Following the head injury, the patient is passing large quantities of dilute urine. Head trauma can cause central diabetes insipidus - that is, the posterior pituitary does not release ADH/vasopressin. This reduces reabsorption of water in the collecting duct, causing large volumes of water to be lost in the urine. As a result of this, if the patient does not drink adequately to replaces these losses, they become hypernatraemic. This is usually treated by giving desmopressin, an analog of vasopressin/ADH.

Case 5 - The patient is hyponatraemic. This is a common paraneoplastic effect observed in small-cell lung cancer - a type of lung cancer. Small-cell lung cancers are derived from neuroendocrine tissue, and often secrete ADH/vasopressin. ADH increases reabsorption of water in the collecting duct, causing the patient to retain water - this is known as syndrome of inappropriate ADH secretion. This causes plasma sodium levels as well as plasma osmolality to fall (due to dilution). The fall in plasma osmolality (i.e. plasma concentration) causes water to move from the plasma/extracellular fluid to the intracellular fluid - therefore the volume of water in the extracellular fluid remains relatively unchanged while the total body water increases. Therefore, in SIADH you get a euvolaemic hyponatraemia. SIADH is treated by fluid restriction.

Hope that helps.
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pjp9494
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Thank you so much for your help.
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