Question

1. Brooke has been feeling ill lately and she goes to the emergency room. She has been vomiting excessively for 4 days and unable to hold down any food or water. Tests are run, and her arterial blood gas comes back as follows:

pH: 7.6

pCO₂: 55mmHg

HCO₃^-:  28mEq

Diagnose the acid base disturbance. How do you know (i.e. is pH alkaline or acidic, is pCO2 alkaline or acidic, is bicarb alkaline or acidic) (3 POINTS)? What is likely the cause of this imbalance, why? How would the respiratory system compensate for this imbalance (2 POINTS)? How would the urinary system compensate for this imbalance.

2. What is the glomerular filtration rate (GFR)? How does the GFR relate to net filtration pressure? What are 2 physiological mechanisms that can change the GFR, briefly explain how they affect the GFR? Identify a hormone that will increase the GFR. Identify a hormone that will decrease the GFR .

Answer 1

1. Acid base disturbance

Test	Patient value	Normal value	Remark
pH	7.6	7.35 - 7.45	Alkaline
pCO2	55mmHg	35 - 45 mmHg	High
HCO3-	28 mEq/L	22 - 26 mE/L	slightly high

Here the pH level show that the blood is alkaline. The partial pressure of CO2 is high. The bicarbonate level is slightly high.

The patient's condition is due to Vomiting for 4 days.

Vomiting generates metabolic alkalosis by the loss of gastric secretions. The gastric secretions contains hydrochloric acid in large amount. Loss of fluid and Nacl in vomitus results in contraction of ECF and increased secretion of renin and aldosterone. Severe vomiting also causes loss of potassium and sodium. The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions by the action of aldosterone, leading to metabolic alkalosis.

Respiratory compensation for metabolic alkalosis occurs. In the lungs, carbondioxide is retained through slower breathing or hypoventilation. CO2 is then consumed toward the formation of the carbonic acid intermediate, thus decreasing pH.

2. The rate at which the plasma is filtered by the glomeruli in the kidney is called glomerular filtration rate.

Sodium concentration in the filtrate increases when GFR increases, and it will decrease when GFR decreases.

Net filtration pressure (NFP) = glomerular blood hydrostatic pressure - [ capsular hydrostatic pressure + blood colloid osmotic pressure]

1. Intrinsic mechanism - Myogenic mechanism and tubuloglomerular feedback
2. Extrinsic mechanism - Neural mechansim and hormonal mechanism

• Myogenic mechanism - increased blood pressure causes stretching of blood vessels resulting in opening of cationic channels resulting in depolarization. Opening of the voltage dependent calcium channels takesplace resulting in calcium flux. Intracellular calcium level increases with resultant vasoconstriction.
• Tubuloglomerular feedback mechanism - Decreased arterial pressure causes decreased glomerular hydrostatic pressure reduced GFR that eventually cause a decrease in afferent arteriolar resistance. At the same time the decreased GFR causes increased renin and the mechanism increases efferent arteriolar resistance with resultant decreased glomerular hydrostatic pressure and the mechanipepsm continues. The mechanism causes increased proximal sodium chloride reabsorption.
• Neural mechanism - the sympathetic nerve activity increases with decreased blood pressure and increased exercise. It causes

- vasoconstriction in skin and GI tract.

- Vasoconstriction of afferent arterioles in kidneys leading decreased GFR, decreased urine production and increasing blood volume.

- increasing cardiac output.

• Hormonal mechanism - Angiotensin II and Atrial natriuretic peptide

Regulation	Major stimulus	Mechanism	Effect on GFR
Angiotensin	Decreased blood volume or decreased blood pressure	Constriction of both afferent and efferent arterioles	Decreases GFR
Atrial natriuretic peptide	Stretching of arterial walls due to increased blood volume	Relaxation of mesangial cells increasing filtration surface	Increases GFR