Apex Unit 10 Kidney Liver Endocrine Flashcards
All of the structures reside in the renal cortex EXCEPT the:
proximal tubule.
distal tubule.
collecting duct.
glomerulus
Collecting duct
The kidney is divided into the cortex and the medulla. The cortex is the outer region and the medulla is the inner region.
The nephron is the functional unit of the kidney. It consists of five major components: glomerulus, proximal tubule, loop of Henle, distal tubule, and collecting duct.
The renal cortex contains the glomeruli, proximal tubules, and distal tubules.
The renal medulla contains the loops of Henle and the collecting ducts.
The kidney produces: (Select 3.)
aldosterone.
renin.
antidiuretic hormone.
angiotensinogen.
1,25 {OH]2 Vitamin D3.
erythropoietin.
Renin
Erythropoietin
1,25 {OH]2 Vitamin D3
Explanation:
The kidney responds to, as well as produces, a wide variety of hormones and enzymes. In this question, we asked about the compounds that are produced in the kidney.
Renin is produced by the juxtaglomerular apparatus - specifically in the fenestrated epithelium in the afferent arteriole.
Erythropoietin is synthesized in the kidney and is secreted in response to hypoxia.
Under control of parathyroid hormone, the kidneys convert inactive vitamin D3 to active vitamin D3 (1,25 [OH]2 vitamin D3).
Why are the other answers wrong?
Angiotensinogen is manufactured in the liver.
Aldosterone is synthesized in the adrenal cortex.
Antidiuretic hormone is produced by the supraoptic nuclei and paraventricular nuclei in the hypothalamus. It is released into the circulation from the posterior pituitary gland.
Which statement BEST describes the pathway of blood through the kidney?
Glomerulus > proximal tubule > loop of Henle > distal tubule > collecting duct
Afferent arteriole > efferent arteriole > glomerular capillary bed > peritubular capillary bed
Glomerular capillary bed > afferent arteriole > peritubular capillary bed > efferent arteriole
Afferent arteriole > glomerular capillary bed > efferent arteriole > peritubular capillary bed
Afferent arteriole > glomerular capillary bed > efferent arteriole > peritubular capillary bed
Explanation:
At any given time, there are two types of fluid moving through the kidney: blood and tubular fluid. Knowing both pathways is essential to understanding the filtration, reabsorption, and secretion functions of the kidney.
The correct order for renal blood flow is: afferent arteriole > glomerular capillary bed > efferent arteriole > peritubular capillary bed.
Which factor increases renin release?
Positive end expiratory pressure
Hypervolemia
Angiotensinogen
Increased chloride delivery to the macula densa
Positive end expiratory pressure
Explanation:
Renin release is increased by three things: reduced renal perfusion, beta-1 activation, and decreased sodium and chloride delivery to the distal tubule.
PEEP reduces venous return and may reduce cardiac output. By extension, this reduces renal perfusion and stimulates renin release.
Antidiuretic hormone:
increases sodium reabsorption in the proximal tubule.
is produced in the posterior pituitary gland.
upregulates aquaporin-2 channels.
agonizes the V1 receptor to decrease cAMP.
Upregulates aquaporin-2 channels
Explanation:
ADH upregulates aquaporin-2 channels in the collecting ducts. This facilitates water reabsorption and restores blood volume and serum osmolarity.
Why are the other answers wrong?
ADH is produced in the supraoptic and paraventricular nuclei of the hypothalamus. It is released from the posterior pituitary gland.
ADH agonizes the V2 receptor (not V1) and increases (not decreases) cAMP.
It increases water reabsorption in the collecting ducts (not proximal tubule).
All of the following enhance renal perfusion EXCEPT:
thromboxane A2.
fenoldopam.
PGE2.
atrial natriuretic peptide.
Thromboxane A2
Explanation:
Thromboxane A2 is a renal vasoconstrictor. Its production is increased during renal ischemia.
Which condition increases glomerular filtration rate?
Afferent arteriolar constriction
Increased efferent arteriolar resistance
Cyclooxygenase inhibition
Increased plasma protein
Increased efferent arteriolar resistance
Explanation:
Glomerular filtration is dependent on renal blood flow and the hydrostatic pressure at Bowman’s capsule.
Constriction of the efferent arteriole increases hydrostatic pressure and GFR.
Constriction of the afferent arteriole reduces RBF and GFR.
Increased plasma protein raises plasma oncotic pressure and reduces GFR.
Cyclooxygenase inhibition by NSAIDs increases renal vascular resistance and reduces RBF and GFR.
Identify the BEST tests of tubular function. (Select 2.)
BUN
Urine osmolality
Fractional excretion of sodium
Creatinine clearance
Fractional excretion of sodium
Urine osmolality
Explanation:
Renal function tests assess glomerular filtration or tubular function.
Tests of GFR: BUN and creatinine clearance
Tests of tubular function: fractional excretion of sodium and urine osmolality
Anesthetic considerations for acute kidney injury include: (Select 2.)
diuretics should be used to convert oliguric to nonoliguric AKI.
hydroxyethyl starches are associated with an increased risk of renal morbidity.
renal dose dopamine prevents AKI.
prerenal azotemia can cause acute tubular necrosis.
Prerenal azotemia can cause acute tubular necrosis
Hydroxyethyl starches are associated with an increased risk of renal morbidity
Explanation:
Why are the other answers wrong?
Renal dose dopamine does not prevent nor treat acute kidney injury.
Attempting to convert oliguric to nonoliguric AKI with diuretics increases risk of additional renal injury as well as mortality.
Pathophysiologic considerations for end-stage renal disease include: (Select 3.)
megaloblastic anemia.
secondary hyperparathyroidism.
gap metabolic acidosis.
obstructive ventilatory defect.
increased bleeding time.
increased prothrombin time.
Increased bleeding time
Gap metabolic acidosis
Secondary hyperparathyroidism
Explanation:
Uremia increases bleeding time.
A gap metabolic acidosis is the result of accumulation of non-volatile acids.
Secondary hyperparathyroidism occurs as a result of impaired active vitamin D3 production and hyperphosphatemia.
Why are the other answers wrong?
PT, PTT, and platelet count are normal.
Erythropoietin production is reduced. This contributes to a normocytic normochromic anemia. Megaloblastic anemia is associated with nitrous oxide.
Fluid overload creates a restrictive ventilatory defect (not obstructive).
Drugs to avoid in the patient on dialysis include: (Select 2.)
meperidine.
succinylcholine.
dexmedetomidine.
vecuronium.
Meperidine
Vecuronium
Explanation:
This question asks about drugs that produce active metabolites that might increase morbidity in the patient with renal dysfunction.
Meperidine is metabolized to normeperidine. Accumulation of normeperidine can cause convulsions.
Vecuronium is metabolized to 3-OH vecuronium. Its duration is prolonged as a function of decreased clearance and an increased elimination half-life.
Succinylcholine and dexmedetomidine are ok to to use in the patient on dialysis, however there are some stipulations. When approaching a question like this, you’ll need to learn how to see through the shades of grey.
All of the following reduce the incidence of contrast induced nephropathy EXCEPT:
sodium bicarbonate.
low-osmolar contrast dye.
furosemide.
fluid bolus with 0.9% NaCl.
Furosemide
In most cases, acute kidney injury is preventable when radiocontrast media is used.
Preventative strategies include: intravenous hydration with 0.9% NaCl, low- or iso-osmolar contrast, and sodium bicarbonate.
Furosemide can reduce intravascular volume, concentrate radiocontrast media inside the kidney, and worsen kidney injury.
For the patient undergoing transurethral resection of the prostate, match each irrigation fluid with its unique anesthetic consideration.
Distilled water + Hemolysis
Glycine + Transient blindness
Sorbitol + Hyperglycemia
Normal saline + Risk of electrocution
TURP requires a continuous fluid source to facilitate visualization and irrigation of the bladder and prostate.
The ideal irrigation fluid provides good surgical visibility, is isotonic, and is absent of toxicity. Read on to review the key differences between each of the irrigation fluids (and a whole lot more).
Which finding represents an absolute contraindication to extracorporeal shock wave lithotripsy?
Diabetes
Pregnancy
Morbid obesity
Pacemaker
Pregnancy
You’ll need to understand the differences between absolute and relative contraindications to ESWL. Absolute contraindications include pregnancy and bleeding disorders/anticoagulation.
Morbid obesity and the presence of a pacemaker are relative contraindications.
Which structure is responsible for eliminating bacteria from the liver?
Sinusoid
Canaliculus
Kupffer cell
Acinus
Kupffer cell
The acinus (otherwise known as the liver lobule) is the functional unit of the liver.
The Kupffer cells are a type of reticuloendothelial cell that are responsible for removing bacteria and viruses that enter the liver from the intestine.
The sinusoids receive blood from the hepatic artery and portal vein. They contain large pores that permit easy passage of large molecules from the blood to the hepatocytes. The Kupffer cells are located in the sinusoids.
Bile canaliculi collect bile that’s produced by the hepatocytes.
Which statement MOST accurately describes hepatic perfusion?
The hepatic artery provides 75 percent of liver blood flow.
The portal vein provides 50 percent of liver blood flow.
The hepatic artery provides 75 percent of the liver’s oxygen content.
The portal vein provides 50 percent of the liver’s oxygen content.
The portal vein provides 50 percent of the liver’s oxygen content
The liver receives a dual blood supply. It receives blood from the hepatic artery and the portal vein.
The hepatic artery provides 25 percent of liver blood flow and 50 percent of the liver’s oxygen content. It provides comparably less blood than the portal vein, but it has a higher O2 content.
The portal vein provides 75 percent of liver blood flow and 50 percent of the liver’s oxygen content. It provides comparatively more blood than the hepatic artery, but because the portal vein contains blood that has passed through the splanchnic organs, it’s O2 content is less.
Hepatocytes produce: (Select 3)
thrombopoietin. alpha-1-acid glycoprotein. immunoglobulins. factor III. factor VII. factor VIII.
Thrombopoietin
Alpha-1-acid glycoprotein
Factor VII
Of all of the procoagulant proteins, factor VII has the shortest half-life. This explains why the PT is an early indicator of synthetic dysfunction.
Factor VIII is produced by the sinusoids and NOT by the hepatocytes. If the question asked about which factors are produced in the liver (not specific to the hepatocyte), then factor VIII would be a correct answer choice.
Factor III is produced by the vascular endothelium.
Match each laboratory test with its underlying pathology.
Bilirubin + Hepatic clearance
Transaminases + Hepatocellular injury
Prothrombin time + Synthetic function
5’-nucleotidase + Biliary obstruction
There’s too much to cover here, but you’ll find everything you need on the next page.
Select the statements that BEST describe hepatitis. (Select 2)
Alcohol abuse is the most common cause of chronic hepatitis.
Halothane hepatitis is an immune-mediated response.
Hepatitis A usually causes cirrhosis.
Hepatitis is usually transmitted via blood transfusion.
Halothane hepatitis is an autoimmune response
Alcohol abuse is the most common cause of chronic hepatitis
Hepatitis A is the most common form of viral hepatitis.
Hepatitis B and C (not A) can cause cirrhosis.
Hepatitis B and C can be transmitted in a blood transfusion, while hepatitis A and E are transmitted by the oral-fecal route. Hepatitis D is a co-infection that occurs with hepatitis B.
Halothane is metabolized to inorganic fluoride ions and trifluoroacetic acid (TFA). TFA can produce an immune mediated response leading to hepatitis.
Alcohol abuse is the most common cause of chronic hepatitis.
All the following drugs should be avoided in the patient with acute hepatitis EXCEPT:
propranolol.
acetaminophen.
tetracycline.
amiodarone.
Propranolol
Propranolol is a non-selective beta-blocker that reduces portal pressure by two processes:
Decreased cardiac output (beta-1)
Splanchnic vasoconstriction (beta-2)
This makes it a useful drug in the patient with hepatitis and elevated portal pressure. Propranolol is also useful in the patient with esophageal varices.
For the patient with acute hepatitis, you should avoid drugs that are hepatotoxic or inhibit CYP450 isoenzymes.
Acetaminophen, amiodarone, and tetracycline can cause hepatotoxicity.
Common physiologic changes in the patient with cirrhosis include all of the following EXCEPT:
decreased glomerular filtration rate.
increased cardiac output.
respiratory acidosis.
right-to-left shunt.
Respiratory acidosis
Patients with cirrhosis experience pulmonary vasodilation, right-to-left shunting, and hypoxemia. They hyperventilate in an effort to offset the reduction in PaO2. This creates a respiratory alkalosis (not acidosis).
A hyperdynamic circulation is common. Said another way, the SVR decreases with a reciprocal rise in CO. GFR is reduced.
Match each phase of liver transplantation with its MOST likely complication.
Pre-anhepatic phase + Pulmonary aspiration of gastric contents
Anhepatic phase + Profound reduction of cardiac output
Neohepatic phase + Hyperkalemia
You must understand the time course of the three phases of liver transplantation. We’ll cover these in detail on the next page.
All the following drugs improve biliary hypertension EXCEPT:
naloxone.
octreotide.
glucagon.
nitroglycerine.
Octreotide
Contraction of the sphincter of Oddi can increase biliary pressure. This may lead to two possible consequences:
Biliary colic
False-positive result of intraoperative cholangiogram
Drugs that relax the sphincter of Oddi and reduce biliary pressure include:
Glucagon Glycopyrrolate Atropine Naloxone Nitroglycerine Administering naloxone to an intraoperative patient is a poor choice, particularly when there are other alternatives available. Although there is some debate, octreotide (a somatostatin analogue) can increase biliary pressure.
Match each term with its definition.
Endocrine function + Hormone enters the blood and acts at distant site
Paracrine function + Hormone acts adjacent to its site of origin
Autocrine function + Hormone acts at its site of origin
Which hormones are released by the anterior pituitary gland? (Select 3.)
Corticotropin-releasing hormone
Antidiuretic hormone
Prolactin
Growth hormone
Oxytocin
Luteinizing hormone
Prolactin
Luteinizing hormone
Growth hormone
Many of you will encounter a question like this one. Know which hormones are released by each region of the pituitary gland!
The posterior pituitary releases two hormones:
Antidiuretic hormone
Oxytocin
The anterior pituitary releases six hormones. You can remember these with the mnemonic "FLAT PiG" Follicle stimulating hormone Luteinizing hormone Adrenocorticotropin Thyroid stimulating hormone Prolactin ignore Growth hormone
You should also be able to recognize the differences between the hypothalamic hormones and their corresponding pituitary hormones. All of these have either “releasing” or “inhibitory” in their name. We added corticotropin-releasing hormone to confuse you.
Anesthetic considerations for the patient with diabetes insipidus include:
three percent sodium chloride.
sodium restriction.
DDAVP.
demeclocycline.
DDAVP
Diabetes insipidus is caused by either inadequate ADH production or renal tubules that are not responsive to ADH. Either way, this causes a tremendous water loss from the body (up to 18+ L/day).
The most common cause of DI is pituitary surgery.
Treatment consists of DDAVP (a selective V2 agonist).
SC = 0.5 - 2 mcg bid.
Nasal = 5 - 40 mcg qd
The syndrome of inappropriate ADH is caused by too much ADH; the body retains too much water. Treatment includes: fluid restriction, hypertonic saline, and demeclocycline.
When compared to T4, which statements BEST describe T3? (Select 2.)
More protein bound
Shorter half-life
Higher concentration in the blood
Higher potency
Higher potency
Shorter half-life
You must be able to compare and contrast T4 to T3.
T4 is a prohormone
T3 has greater biologic activity
When compared to T4, the following are true of T3:
Higher potency
Shorter half-life
Less protein bound
Smaller concentration in the blood (bound + unbound fractions)
All of the following are consequences of excess thyroid hormone EXCEPT:
vasodilation.
hypoventilation.
tremors.
diarrhea.
Hypoventilation
Thyroid hormones increase the metabolic activity of nearly all the cells in the body. You must remember:
↑ Thyroid hormone → ↑ BMR → ↑ VO2 + ↑ CO2 Production
Vasodilation results from increased oxygen consumption. This helps improve tissue blood flow and oxygen delivery.
Increased carbon dioxide production requires that the patient increase (not decrease) minute ventilation.
Thyroid hormone excess increases the sensitivity of neuronal synapses in the spinal cord, leading to tremors.
Intestinal hypermotility results in diarrhea (risk of fluid and electrolyte imbalance).
A patient with untreated hyperthyroidism and atrial fibrillation presents for emergency surgery. What is the BEST intervention at this time?
Propylthiouracil
Esmolol
Amiodarone
Delay surgery until a euthyroid state is achieved
Esmolol
The hyperthyroid patient presenting for non-emergency surgery should be cancelled and managed medically until a euthyroid state is achieved. This patient requires an emergent operation, so you don’t have the luxury of canceling.
Esmolol is the best option. It reduces the SNS response, and it’s easily titratable. Having said this, propranolol is the only beta-blocker that inhibits the peripheral conversion of T4 to T3.
Propylthiouracil inhibits the conversion of T4 to T3, however this requires days to begin to take effect. You don’t have this much time.
We said that this patient has atrial fibrillation (a common consequence of hyperthyroidism). Amiodarone would treat this, however it contains a significant amount of iodine by weight. An important side effect of this drug is that it can cause hyper- or hypothyroidism. As such, it has the potential to worsen this patient’s condition.
All of the following are anesthetic considerations for myxedema EXCEPT:
hypernatremia.
low cardiac output.
restrictive lung disease.
impaired drug metabolism.
Hypernatremia
Hypothyroidism in its most severe form is called myxedema. This affects all the organ systems in the body.
Lack of thyroid hormone decreases heart rate, contractility, and cardiac output.
Pleural and pericardial effusions are common.
In the liver, decreased metabolism manifests as slowed biotransformation reactions.
Inappropriate secretion of ADH is common, so these patients retain free water. This contributes to a dilutional hyponatremia (not hypernatremia). Edema is a common finding.
Match each region of the adrenal gland with the class of hormones it produces.
Zona glomerulosa + Mineralocorticoids
Zona fasciculata + Glucocorticoids
Zona reticularis + Androgens
The adrenal gland is composed of the cortex (outer region) and medulla (inner region). You must know which hormones are produced in which regions.
Adrenal cortex:
Zona glomerulosa - mineralocorticoids (aldosterone)
Zona fasciculata - glucocorticoids (cortisol)
Zona reticularis - androgens (dehydroepiandrosterone)
Adrenal medulla:
Catecholamines (epinephrine and norepinephrine)
Order each drug in terms of its glucocorticoid potency.
(One is the most potent and four is the least potent)
Dexamethasone + 1
Methylprednisolone + 2
Cortisol + 3
Aldosterone + 4
Match each disease to its underlying pathophysiology.
Cushing’s syndrome + Excess cortisol
Addison’s disease + Inadequate cortisol
Conn’s syndrome + Excess aldosterone
*Inadequate aldosterone almost never occurs in isolation.
Signs of Cushing’s syndrome include: (Select 4.)
hypertension. hypotension. hyperkalemia. hypokalemia. metabolic alkalosis. metabolic acidosis. hyperglycemia. hypoglycemia.
Hypertension
Hypokalemia
Metabolic alkalosis
Hyperglycemia
Cushing’s syndrome results when the anterior pituitary gland releases an excessive amount of ACTH, which in turn increases cortisol release from the zona fasciculata of the adrenal cortex.
Remember that cortisol has glucocorticoid, mineralocorticoid, and androgenic effects.
A patient with adrenal insufficiency and sepsis requires an emergency intubation in the intensive care unit. Which drug should be avoided?
Etomidate
Propofol
Thiopental
Ketamine
Etomidate
Adrenal insufficiency is characterized by the destruction of all the cortical zones. This manifests as decreased production of mineralocorticoids, glucocorticoids, and androgens.
By inhibiting 11-beta-hydroxylase, a single induction dose of etomidate causes adrenocortical suppression for > 8 hours. This could potentially convert adrenal insufficiency to acute adrenal crisis.
Ketamine is often an attractive option in this context, but be aware that its negative inotropic properties can be unmasked in this patient population.
Match each pancreatic hormone with the cell type that produces it.
Glucagon + Alpha cells
Insulin + Beta cells
Somatostatin + Delta cells
Pancreatic polypeptide + PP cells
The pancreas produces two types of hormones:
Exocrine hormones are secreted into the duodenum for digestion (produced by the acini tissue).
Endocrine hormones are secreted into the systemic circulation for metabolism (produced by the islets of Langerhans).
Compared to type I diabetes mellitus, choose the statements that MOST accurately describe type II diabetes mellitus. (Select 2.)
It is usually caused by an autoimmune response.
Is usually associated with a thin body habitus.
It is more likely to cause hyperglycemic hyperosmolar syndrome.
Peripheral sensitivity to insulin is reduced.
Peripheral sensitivity to insulin is reduced
It is more likely to cause hyperglycemic hyperosmolar syndrome
You’ll need to be able to distinguish between the key features of T1DM and T2DM.
T1DM is:
Caused by beta cell destruction.
Most commonly caused by an autoimmune response.
Typically associated with a thin and wasting body habitus.
Is more likely to be associated with diabetic ketoacidosis.
T2DM is:
Usually caused by obesity.
Associated with a relative lack of insulin production and peripheral insulin resistance.
Is more likely to be associated with hyperglycemic hyperosmolar syndrome.
All of the following can mask the signs of intraoperative hypoglycemia EXCEPT:
propranolol.
general anesthesia.
diabetic autonomic neuropathy.
hydrochlorothiazide.
Hydrochlorothiazide
Intraoperative hypoglycemia can be difficult to diagnose. As serum glucose falls, the SNS is activated and circulating epinephrine stimulates gluconeogenesis and glycogenolysis in the liver to restore a normal serum glucose concentration.
Anything that blunts the SNS response can potentially mask the signs of intraoperative hypoglycemia. Examples include: general anesthesia, diabetic autonomic neuropathy, and beta-blockers (propranolol).
Thiazide diuretics have a unique side effect in that they increase serum glucose. Hyperglycemia is a side effect of these drugs (hydrochlorothiazide, metolazone, and indapamide).
Match each oral hypoglycemic agent with its unique risk.
Metformin + Lactic acidosis
Glyburide + Cross sensitivity with sulfa allergy
Rosiglitazone + Promotes edema
Metformin disrupts mitochondrial function, ultimately reducing the intracellular concentration of ATP. Recall that pyruvate is the final product of glycolysis, and in the setting of mitochondrial dysfunction, the cell will shift to anaerobic metabolism, and produces lactate.
Glyburide is a sulfonylurea. This class of agents can cause an immunologic response in patients with a sulfa allergy.
Rosiglitazone expands the ECF, which can lead to edema.
Which insulin preparation can be administered intravenously?
Very rapid-acting
Rapid-acting
Intermediate-acting
Long-acting
Rapid acting
Insulin preparations can be divided into the following groups:
Very rapid-acting Rapid-acting Intermediate-acting Long-acting Ultra long-acting Only regular insulin can be given IV (or IM), and regular insulin is the only short acting insulin in commercial use.
Which drugs should be avoided in the patient with carcinoid syndrome? (Select 3.)
Vasopressin Octreotide Ketamine Rocuronium Morphine Norepinephrine
Ketamine
Norepinephrine
Morphine
Carcinoid syndrome is associated with secretion of vasoactive substances from enterochromaffin cells. It is usually associated with tumors of the GI tract, but it can also arise from locations outside of the GI tract as well.
We tend to avoid drugs that can precipitate hormone release by the tumor, therefore avoid drugs that:
Release histamine (morphine)
Stimulate the SNS (ketamine)
Augment hormone release (norepinephrine)
Octreotide is a primary treatment for carcinoid syndrome, rocuronium doesn’t release histamine, and vasopressin is an acceptable treatment for hypotension.
Which of the following are increased in the serum of the patient with renal osteodystrophy? (Select 2.)
Parathyroid hormone
Calcitriol
Phosphate
Calcium
Phosphate
Parathyroid hormone
There are two “P’s” that are increased in the patient with renal osteodystroPhy: phosphate and parathyroid hormone. Here’s why…
The active form of vitamin D (calcitriol) is produced by the kidney. When the kidney fails to produce calcitriol, the body absorbs less calcium from the GI tract and serum calcium falls.
As a result, parathyroid hormone output is increased. This causes demineralization of calcium from bone, which aims to restore the serum calcium level. The tradeoff is that the bones become weaker and more susceptible to fractures.
As GFR declines (remember this patient has kidney disease), phosphate clearance is reduced, thereby increasing the serum phosphate concentration.
Identify the MOST potent stimulators of antidiuretic hormone secretion. (Select 2.)
Hypernatremia
Hyponatremia
Hypervolemia
Hypovolemia
Hypernatremia
Hypovolemia
ADH is produced in the supraoptic and paraventricular nuclei of the hypothalamus. It is released by the posterior pituitary gland.
There are two mechanisms that control ADH secretion:
1. Osmolarity of the ECF (think sodium concentration):
Increased ECF osmolarity → shrinkage of osmoreceptors in the hypothalamus → ↑ ADH secretion.
- Blood Volume:
↓ Blood volume → baroreceptor unloading in the carotid bodies, transverse aortic arch, great veins, and right atrium → ↑ ADH secretion.
Which substances are produced by the kidney? (Select 2.)
Antidiuretic hormone
Renin
Angiotensin II
Erythropoietin
Renin
Erythropoietin
Erythropoietin signals stem cells in the bone marrow to produce erythrocytes. Patients with renal failure make less erythropoietin, and this explains why they develop normochromic, normocytic anemia.
Renin is released by the juxtaglomerular apparatus in response to decreased renal perfusion. Renin release is the first step in the renin-angiotensin aldosterone system.
The kidneys do not produce antidiuretic hormone or angiotensin II.
Match each substance with its primary site of production.
Angiotensinogen + Liver
Angiotensin I + Systemic circulation
Angiotensin II + Lung
Aldosterone + Zona glomerulosa
The renin-angiotensin-aldosterone system is a hormone based system that moderates long term blood pressure control and fluid balance. There’s lots of information on this page, but you MUST know all of it!
Stimulus for RAAS Activation:
The juxtaglomerular apparatus of the afferent arteriole releases renin when there is decreased renal perfusion, hypovolemia, hyponatremia, or SNS activation.
Angiotensinogen → AT I → AT II → Aldosterone:
Renin converts angiotensinogen (produced in the liver) to angiotensin I (AT I). This occurs in the systemic circulation.
Angiotensin converting enzyme (produced in the lung) converts AT I to angiotensin II (AT II).
AT II stimulates aldosterone release from the zona glomerulosa in the adrenal cortex. It is also a potent vasoconstrictor.
Function of Aldosterone:
Aldosterone acts on the principal cells in the kidney. This restores plasma volume and blood pressure by promoting Na+ and water retention.
Aldosterone also causes potassium excretion.
