Quiz 5 Practice problems Flashcards
The antibiotics Penicillin G and Ampicillin are low molecular weight, acidic molecules. Like all small molecules, they will be removed from the blood into the initial filtrate in the renal corpuscle. However, they disappear from blood at a rate higher than can be accounted for by filtration due to the action of which cells?
Collecting tubule and collecting duct cells
Distal convoluted tubule cells
Mesangial cells
Podocytes
Proximal convoluted tubule cells
Thick ascending limb cells
PCTs can secrete organic acids and bases from the blood into the filtrate, which will result in rates of removal greater than that possible only by their filtration in the glomerulus
The blood filtration unit in the kidneys is formed by a collaboration between endothelial cells and what other cells?
Juxtaglomerular cells
Mesangial cells
Parietal cells
Podocytes
Proximal convoluted tubule cells
Podocytes also contribute to the filter unit of the glomerulus; specifically the filtration slits between the podocyte pedicles.
The majority of components present in the filtrate of kidney tubules arrive there from the blood primarily due to:
Active transport
Blood pressure
Diffusion
Osmotic pressure
Blood pressure provides the main driving force for production of initial filtrate from blood in the glomerular capillaries.
What situation favors the reabsorption of fluid from the filtrate in cortical kidney tubules back to the blood in peritubular capillaries?
Fenestrations of the endothelium of peritubular capillaries
High oncotic pressure of blood in peritubular capillaries
Leaks between tight junctions of peritubular capillaries
Robust transcytosis rates maintained by peritubular capillaries
The high oncotic pressure in the blood leaving via the efferent arterioles will automatically favor the flow of fluid from the filtrate back to the peritubular capillaries supplied by that arteriole.
D.
The PCT accomplishes about 65% of the recovery of fluid volume from the initial filtrate.
F
The thick ascending limb (TAL) is the site where Na,K-ATPase actively pumps Na+
from the filtrate into the medulla.
How does aldosterone stimulate sodium recovery from the terminal distal convoluted tubule and the collecting tubules and ducts?
It binds to and directly stimulates the Na,K-ATPase in tubule cells
It increases production of initial filtrate in the renal corpuscle
It opens apical sodium channels in tubule cells and stimulates production of Na,K-ATPase
It opens tight junctions between tubule cells
It promotes the fusion of cytoplasmic vesicles containing aquaporins with tubule cell membranes
Opens apical sodium channels…
Aldosterone has several actions that increase sodium recovery from the filtrate, including opening apical (luminal) sodium channels and increasing production of Na,K-ATPase.
The counter current exchange system operating in the kidney is most directly involved in what activity?
Adjusting the pH of the blood
Forming the initial filtrate
Maintaining the high salt concentration in the extracellular fluid of the medulla
Producing of high salt concentration in the extracellular fluid of the medulla
Regulating the rate of fluid flow through the nephron and collecting duct
Maintaining the high salt…
The countercurrent exchange system uses the geometry of parallel flows to supply blood to the medulla for nourishing cells without removing the high salt concentration of the interstitium. Some salt and water will exit with the blood, of course, but the bulk of the gradient is maintained.
If the [NaCl] of the fluid in a thick ascending limb entering the JGA (juxtaglomerular apparatus) is sensed by macula densa cells as being too high, a response is initiated that results in what change to a nearby structure?
The afferent arteriole constricts
The efferent arteriole constricts
The extraglomerular mesangial cells migrate into the capsule
The JG cells release renin
The podocytes contract
Afferent arteriole
What would be indicated by the absence of sharp-edged, fusiform vesicles in the cytoplasm of surface cells of the urothelium of the urinary bladder?
High levels of ADH in the blood
High levels of aldosterone in the blood
High levels of CCK in the blood
The bladder is empty
The bladder is full
bladder is full
The absence of sharp edged vesicles in the cytoplasm indicates that the bladder is full: the excess plasma membrane stored in these vesicles has been added to the surface, allowing it to expand.
The blood that supplies the counter current exchange system of the renal medulla comes most directly from what vessels?
Arcuate arteries
Cortical efferent arterioles
Juxtamedullary efferent arterioles
Interlobar arteries
Segmental arteries
Juxtamedullary efferent arterioles
The efferent arterioles of juxtamedullary renal corpuscles give rise to the vasa recta, which supply the medulla with blood via a countercurrent system.
H
D.
The proximal convoluted tubule (PCT) cells actively remove proteins that enter the initial by endocytosis. Numerous endocytic vesicles are formed at the base of the short microvilli that line the apical surfaces of the PCT cells.
An increase in the concentration of ADH in the blood will result in what rapid change in the kidney?
Afferent arterioles differentially constrict
Efferent arterioles differentially constrict
Collecting duct cells become less permeable to water
Collecting duct cells become more permeable to water
Renin release is decreased
Renin release is increased
Collecting Duct cells become more permeable to water
Antidiuretic hormone does what its name states: it acts “against” diuresis, which is an increased production of urine. When ADH binds to receptors on collecting tubules and ducts, vesicles containing aquaporins move from the cytoplasm to fuse with the plasma membrane and increase water flow across the cells. Especially in the medulla, the movement of water will be from the filtrate towards the interstitium due to the high salt concentration produced by the loop of Henle. This flow of water out of the filtrate decreases the volume of urine produced: anti-diuresis. More importantly, it increases the amount of water in the body.
What is the main driving force for glomerular filtration?
Hydrostatic pressure of the capillary.
Angiotensin II causes constriction of glomerular arterioles, if efferent is constricted more, what would be effect?
Increased glomerular capillary hydrostatic pressure; increased GFR.
blockage in teh urine leading to high creatinine…why?
increased capsular hydrostatic pressure…down GFR!
destruction of podocytes would lead to urine levels of what?
Albumin
what is the initial response to GFR when starting an ACE inhibitor
Decrease, action of angiotensin, mainly on efferent arteriale, will be inhibited. PGC will fall.
Infection, and serum creatine high…why low GFR?
sympathetic stimulation to the renal plexus due to the stress of the severe infection
Very high blood glucose patient. why would he have glucose in the urine?
saturation of luminal proximal convoluted tubular Na+-glucose symporters
Lasix or furosemide loop diuretics inhibit NKCC what would happen after high dose
Hypokalemia (low potassium in the blood) due to loss of the ion transporter!
defect in ADH receptor in kidney. what lab value would result?
urine specific gravity of less than 1.005. patient can’t concentrate urine so it is always dilute.
best explination for low potassium, low renin, and high aldosterone.
patient has aldosterone-secreting tumor. Renin is suppressed by the hypervolemia and hypertension resulting from the excess aldosterone.
You examine a tachycardic, tachypneic and diaphoretic man in the ER.
An ABG is obtained.
ABG VALUE
pH 7.53
PCO2 28
PO2 77
HCO3 23
NORMAL RANGES
7.35 – 7.45
35 –40 mmHg
61 –82 mmHg
19 –25 mmol/L
Metabolic acidosis (with respiratory compensation)
Metabolic acidosis and respiratory alkalosis
Metabolic alkalosis (with respiratory compensation)
Metabolic alkalosis and respiratory acidosis
Respiratory alkalosis (with metabolic compensation),
Respiratory alkalosis (with metabolic compensation),
pH 7.53 → alkalemia. PCO2 low, therefore respiratory. In an acute respiratory alkalemia expect HCO3 to fall 0.2 mmol/l for every mmHg fall in pCO2 = fall of 2.4. This small fall is within the variability of results so we don’t actually see a distinct fall here.
A 68-year-old man with chronic obstructive pulmonary disease (COPD) is seen in clinic follow-up. He is doing reasonably well on bronchodilators and chronic oxygen by nasal cannula at 3 LPM. An ABG is obtained. Describe the acid-base status of this patient.
ABG VALUE
pH 7.36
PCO2 58
PO2 62
HCO3 34
NORMAL RANGE
7.35 – 7.45
35 –40 mmHg
61 –82 mmHg
19 –25 mmol/L
Metabolic alkalosis (with respiratory compensation)
Metabolic alkalosis and respiratory acidosis
Respiratory acidosis (with metabolic compensation)
Respiratory acidosis and metabolic alkalosis
Respiratory alkalosis and metabolic alkalosis
Respiratory alkalosis and metabolic acidosis
Respiratory acidosis (with metabolic compensation) He is borderline acidemic with pH 7.36. The PCO2 is elevated, pegging this as a respiratory acidosis. In chronic respiratory acidosis HCO3 rises 0.4 mmol/l for every mm Hg rise in PCO2 18 x 0.4 = 7.2, which would give HCO3 of around 31, fairly close to the 34 observed. Chronic respiratory disorders can compensate back fairly close to a normal pH
Note: The patient could have arrived at the same set of values as a result of simultaneous respiratory acidosis and metabolic alkalosis. ABGs must always be interpreted in conjunction with the clinical information from the patient.In this case: is there a reason for a metabolic alkalosis? None is apparent. Thus Respiratory acidosis (with metabolic compensation) is a better answer than Respiratory acidosis and metabolic alkalosis. The former is the more economical diagnosis (Occam’s razor); there is also no clinical reason to suspect a metabolic alkalosis.
Case #3
A 15-year-old girl with known type 1 diabetes mellitus under poor control presents to the emergency room with polyuria, polydipsia, and diaphoresis. Vital signs show T 37.4°C, HR
113, RR 28, BP 100/68. ABG VALUE
pH 7.18 ( 7.35 – 7.45)
PCO2 23 (35 – 40 mmHg)
Sodium 130 (136-… )
Potassium 5.0 (3.3-…)
PO2 70 (61– 82mmHg)
Chloride 95 (95–…)
HCO3 8 (19 – 25 mmol/L )
Describe the acid-base abnormality.
Anion-gap metabolic acidosis (with respiratory compensation). Tha anion gap is elevated at 27; pH is depressed: HCO3 is low. These define an anion gap metabolic acidosis.
Note: The patient could have arrived at the same set of values as a result of simultaneous metabolic acidosis and respiratory alkalosis. As for the previous case, ABGs must always be interpreted in conjunction with the clinical information from the patient.In this case: is there a reason for a respiratory alkalosis? None is apparent. Thus acidosis (with respiratory compensation) is a better answer than Metabolic acidosis and respiratory alkalosis. The former is the more economical diagnosis (Occam’s razor); there is no clinical reason to suspect a respiratory alkalosis.
Case # 4
Acetazolamide is a diuretic that inhibits carbonic anhydrase at the brush border of proximal convoluted tubular epithelial cells. What primary acid-base abnormality might develop in a patient taking large doses of acetazolamide?
Metabolic acidosis. Inhibition of CA will impair bicarbonate reabsorption and proton secretion in the proximal tubule. Although the distal tubule will attempt to compensate, it may not be adequate.
Case # 6
Which substance’s blood concentration does the body guard most jealously? – i.e. which has the lowest coefficient of variation in health?
Note: Normal range is +/- 2 SD. CV = SD/Mean.
Sodium Normal range 135-145 mEq/l. CV 1.8 %
Potassium Normal range 3.5-5 mEq/l. CV 8.8%
Hydrogen ion Normal range 35-45 nmol/l. CV 6.25%
CO2 (pCO2) Normal range 35-45 mm Hg. CV 6.25%
Bicarbonate Normal range 19-25 mEq/l. CV 6.8%
A barely conscious 19 year old male enters the ER with shallow breathing and is know to have taken an overdose of morphine. Measurement of arterial blood gas shows pH 7.21, PaCO2 70 mm Hg, HCO3- 27 mM/L. What is the acid-base disturbance and is compensation occurring?
Normal: pH 7.4, PaCO2 40 mm Hg, HCO3- 24 mM/L
Answer
The low pH, high PCO2 and elevated HCO3- are indicative of respiratory acidosis. In this case it results from morphine-induced suppression of the respiratory center. To assess the degree of renal compensation, compare the measured and predicted values of HCO3-.
For acute respiratory acidosis:
- 1 mmHg increase in PCO2 è 0.1 mM increase in [HCO3-] due to mass action.
Thus, the predicted [HCO3-] is 24 + ((70 – 40) x 0.1) = 27 mM/L due to mass action The actual [HCO3-] also 27 mM/L
For chronic respiratory acidosis:
- 1 mmHg increase in PCO2 è 0.4 mM increase in [HCO3-] due to renal compensation - Chronic renal compensation would predict a [HCO3-] of approximately:
24 + ((70-40) x 0.4) = 36 mM/L whereas the actual is 27 mM/L.
Thus, the patient has a respiratory acidosis with no apparent renal compensation. However, mass action has increased HCO3- from 24 to 27 mM.
A 12 year old boy enters the emergency department after falling and hurting his arm. He is tachycardic and tachypneic (rapid breathing rate). While waiting to be seen by the doctor, he becomes increasingly agitated. Arterial blood gas show pH 7.52, PaO2 115 mm Hg, PaCO2 29 mm Hg, and HCO3- 23 mM/L. What does this mean and is renal compensation occurring?
Normal: pH 7.4, PaCO2 40 mm Hg, HCO3- 24 mM/L
Answer
The high pH and low PaCO2 are indicative of respiratory alkalosis due to the pain and anxiety causing him to hyperventilate. To assess the degree of renal compensation, compare the measured and predicted values of HCO3-
For acute respiratory alkalosis:
- 1 mmHg decrease in PCO2 è 0.2 mM decrease in [HCO3-] due to mass action.
Thus, the predicted [HCO3-] is: 24 - (40 – 29) x 0.2 = 22 mM/L) The actual [HCO3-] is 23 mM/L which is very close to predicted.
For chronic respiratory alkalosis:
- 1 mmHg decrease in PCO2 è 0.4 mM decrease in [HCO3-] due to renal
compensation.
- Thus renal compensation would predict a [HCO3-] of approximately: 24 - ((40-29)
x 0.4) = 19.6 mM/L or 20 mM/L.
- Thus there has not been sufficient time for renal compensation but mass action
has decreased HCO3- from 24 to 23mM.
A 19 year old insulin dependent diabetic patient was admitted with a history of polyuria (excessive production of urine) and thirst. She now feels ill and entered the hospital. She has a history of poor compliance with medical therapy. Ketones and glucose found in urine (normally not present). Blood glucose 19 mM/L (normal 11 mM/L). Measurement of arterial blood gas shows: pH 7.27, PaCO2 16 mm Hg, and HCO3- 7.1 mM/L, PaO2 128 mmHg. What is the diagnosis?
Normal: pH 7.4, PaCO2 40 mm Hg, HCO3- 24 mM/L
Answer
The low pH, low bicarbonate and low PCO2 are typical of a metabolic acidosis. The hyperglycemia, glycosuria and ketonuria indicate the presence of a diabetic ketoacidosis. The appropriate rule to assess compensation for a metabolic acidosis is: 1 mM decrease in [HCO3-] è1.3 mmHg decrease in PCO2 due to increased alveolar ventilation.
- Thus, the predicted PaCO2 is 40 – ((24 - 7.1) X 1.3) = 18 mmHg.
- Actual PaCO2 is 16 mmHg.
- Since the predicted (18 mmHg) and actual (16 mmHg) values of PaCO2 are very
close, the diagnosis is compensated metabolic acidosis.
A 40 yr. old male patient comes to the emergency room and is found to have been vomiting for several days (loss of gastric acid). Arterial blood gases revealed the following:
pH 7.5, PCO2 48 mmHg, HCO3- 37 mM/L. What acid-base disorder does he have and is there compensation?
Normal: pH 7.4, PaCO2 40 mm Hg, HCO3- 24 mM/L
Answer
The high pH, high bicarbonate, and high PCO2 are typical of a metabolic alkalosis. The appropriate rule to assess compensation for a metabolic alkalosis is: 1 mM decrease in [HCO3-] è0.7 mmHg increase in PCO2 due to decreased alveolar ventilation.
- Thus, the predicted PaCO2 is 40 + ((37 - 24) X 0.7) = 49 mmHg.
- Actual PaCO2 is 48 mmHg
- Since the predicted (49 mm Hg) and actual (48 mmHg) values of PaCO2 are
very close, the diagnosis is compensated metabolic alkalosis.
A hospital patient with AIDS has large amount of diarrhea over the past 4 hours. He becomes hypovolemic over a short period of time. Which of the following arterial lab results would best fit this clinical history?
a. pH: 7.15, pCO2: 55 mmHg, HCO3: 40 mEq/L
b. pH: 7.25, pCO2: 36 mmHg, HCO3: 15 mEq/L
c. pH: 7.40, pCO2: 40 mmHg, HCO3: 24 mEq/L
d. pH: 7.50, pCO2: 28 mmHg, HCO3: 24 mEq/L
The correct answer is: b Gut is alkaline so diarrhea promotes loss of bicarbonate, creating metabolic acidosis. Respiratory compensation (ie, increased alveolar ventilation to reduce PaCO2) is occurring but not yet complete. Could reduce PaCO2 lower to help restore pH.
The medical student next to you, realizing that there is an examination question on acid base balance, begins nervously hyperventilating and then faints. You make him breathe into a paper bag and he recovers. If you had drawn and analyzed his blood when he fainted you would have expected to see?
a. decreased pH, increased PCO2
b. decreased pH, decreased PCO2
c. elevated pH, decreased PCO2
d. elevated pH, elevated PCO2
C
