Aldosterone promotes Na+ retention and K+ loss because when aldosterone levels increase, there is a low Na+ or high K+ concentration in the blood. Review the Clinical Investigation: Primary Aldosteronism, Conn’s Syndrome and complete the interactivities.

Read the overview and complete the interactivities that follow.

Karen is a 43-year-old lawyer with mild hypertension treated with an angiotensin receptor blocker. She visited her physician complaining of muscle weakness, headaches, frequent urination, and unusually great thirst. Her blood pressure—particularly her diastolic pressure—was significantly elevated. The physician noted the absence of edema, and the presence of more PVCs (premature ventricular contractions) in her ECG than she had previously shown. Her urine sample displayed proteinuria and was slightly alkaline, and her blood test revealed that she had hypokalemia (low plasma K+ concentration). More specialized blood tests measuring plasma renin activity and aldosterone concentration were ordered. After these results were obtained, the physician ordered a test in which plasma aldosterone concentration was measured before and after Karen drank a saline solution to determine the effects of sodium loading. The physician subsequently requested that Karen obtain an abdominal CT scan. Karen had significant diastolic hypertension without edema, hypokalemia, polyuria, and polydipsia (great thirst and drinking). Her urine sample was slightly alkaline, and her specialized blood tests indicated an abnormally high ratio of plasma aldosterone to renin activity. When a sodium-loading test was performed, in which Karen drank a saline solution, her plasma aldosterone concentration remained elevated. The physician requested an abdominal CT scan, which showed a mass in her right adrenal gland.

QUESTIONS

1. How do the kidneys handle potassium, and how is this regulated?

2. What is polyuria, and why might Karen have polyuria and polydipsia?

3. Why would Karen’s urine be slightly alkaline?

4. What is the normal relationship between plasma renin and aldosterone?

5. How would plasma renin and aldosterone levels normally respond to sodium loading?

6. What is the likely explanation for Karen’s symptoms?

List the route of "Sally" sugar molecule from the pasta on a fork to its providing nutrition to the cardiac muscle. This is JUST a list of structures [from the mouth to where the food is absorbed into the blood to the muscle]. Be complete.

1. Patients with a specific shared brain lesion have a specific set of behavioral deficits. Does this show that this brain area is necessary for that behavior, sufficient, neither, or both? What do we mean by a visual object agnosia?

2. What are some tests you would give to a patient to try to diagnose or rule out this condition?

3. Describe an experiment that would illustrate the function of the amygdala in emotional processing.

1. What is the major excitatory neurotransmitter in the brain?
2. Which group of neurotransmitters is more likely to act on ionotropic receptors, and which is more likely to act on metabotropic receptors?
3. Name one similarity and one difference between nicotinic and muscarinic receptors, and one similarity and one difference between AMPA and NMDA receptors.
4. Name a disease that is due in part to too little dopamine, and a disease that is due in part to too much dopamine in the brain. What does these tell us about one of dopamine’s function in the brain?

Explain in detail the mechanisms of fluid exchange between capillaries and the interstitium. Then, define edema, and use cause-and-effect arguments, explain how each of the following conditions cause edema. Be sure to explain the underlying mechanism causing the edema.

The prostate is a reproductive gland found in the male. Explain why prostate abnormalities often present with urinary symptoms.

1. Explain the following.

a. Compare the right and left ventricular pressures and right and left ventricular volumes.

b. What will happen to cardiac output during exercise? Explain what physiological changes occur that cause this change in cardiac output?

1) What is meant by the term ''resting membrane potential''?

2) What is the usual resting membrane potential of an excitable cell (e.g.neuron) at rest? Why? How is it established?

3) How do the concentration of K+ and Na+ differ in the ECF and the ICF?

Discuss how each step of an action potential compares between a sensory neuron, interneuron, and motor neuron.

Carbohydrates aid fat metabolism by:

A. Donating acetyl-CoA during beta-oxidation

B. Generating pyruvate needed to form oxaloacetate which keeps the citric acid cycle turning as fats form acetyl-CoA

C. Preventing the formation of ketones by generating acetyl-CoA

D.Generating glucose which provides energy needed for beta-oxid ation which forms acetyl-CoA for the citric acid cycle

At what age is a baby ready to receive foods other than milk (1 pt) and why? Provide 2 reasons why this age is recommended or what are the cues that the baby is ready? (2 pts; 1 pt each).

Write about your review of available literature on the different approaches in the classification of nerve fiber?