Many people think that their inability to do endurance work is related to an inability of their lungs to supply O2 to the blood. Provide a detailed explanation that you would give to an undergraduate exercise physiology class to help educate them why this idea is incorrect.

The cone shaped sensor at the base of the semicircular canals involved with balance?

Saccule

Otoliths

Utricle

scala

media

Cupola

Coarctation of the aorta is a congenital birth defect that is usually fatal. When an aorta has a coarctation, one or more areas of the aorta are “pinched” so that the aortic diameter at that spot is severely reduced. This coarctation leads to a fatal combination of low arterial blood oxygen content and reduced cardiac tissue blood flow. Explain in detail why aortic coarctation leads to both low arterial blood oxygen content and reduced cardiac tissue blood flow.

Can the compensatory parasympathetic response stop vasoconstriction? why or why not?

Also, treatment fir autonomic disreflexia is removal of the painful stimulus that started the disreflexia in the first place. if that doesnt work, drugs that alter the autonomic nervous system (agonists and antagonists) must be used. suggest a drug mechanism that might work to stop the disreflexia (you dont need a name, just describe its action)

THANK YOU for helping a tired, brain dead student :')

Provide an example that illustrates Helman’s (2007) assertion that modern medicine also constitutes “a system of morality”?

What is the purpose of heat fixing a slide?

List the 4 major steps of the gram stain and explain what is happening to both Gram positive and Gram negative cells in each step.

Why don’t we heat fix in the capsule stain?

What are the major things that are done in the acid fast stain procedure that allow acid fast cells to be stained?

Hypothetically, let's say you perform an endospore stain and observe that the endospores formed in your specimen exhibit a spherical and subterminal morphology. Why is it useful know this?

It’s Friday morning and Sal Volpe is sitting in Dr. Lorraine’s exam room, dozing after another night of disrupted sleep. When the doctor knocks and walks in, she finds the 66-year-old man looking exhausted and uncomfortable. Sal gets to the reason for his visit immediately: He’s been suffering from “stomach aches” (dyspepsia) that wake him at night and nag him in between meals during the day. He describes his pain as gnawing, burning (maybe a 4 out of 10 on a pain scale) and points to the epigastric region of his abdomen. When he eats, he tells Dr. Lorraine, the pain goes away, but then he feels bloated and a little nauseated. The pain usually returns 2–4 hours later, depending on what he eats. Sal explains that he has had some pain relief from the over-the-counter drug Pepcid^® (famotadine).

Dr. Lorraine proceeds with the history and physical exam. She discovers that Sal has a family history for gastrointestinal cancer and has unintentionally lost 10 pounds since his checkup a year ago. His epigastric area is modestly tender to palpation. She suspects a peptic ulcer (gastric or duodenal), but the weight loss and family history make it prudent to eliminate the diagnosis of stomach (gastric) cancer. “Mr. Volpe, I think you may have a stomach or intestinal ulcer,” Dr. Lorraine says. “I suggest we perform an endoscopy to have a look. This involves passing a small tube with a small camera through your mouth and into your stomach. We can look at the wall of your stomach and small intestine, check for an ulcer, and remove a very small piece of tissue to test for infection. We call this a biopsy. We’ll also test the biopsy for cancer because of your family history. But, I really think we’re dealing with an ulcer here and not cancer.”

Later that month, the endoscopy is performed and it confirms Dr. Lorraine’s suspicions. Sal has a duodenal ulcer and infection with the bacterium Helicobacter pylori (H. pylori). This is not surprising since H. pylori is the cause of most peptic ulcer disease, particularly in the duodenum. Treatment involves complete eradication of the H. pylori with two different antibiotics, and a drug that decreases gastric acid secretion, a so-called proton pump inhibitor (PPI). Dr. Lorraine explains to Sal, “Mr. Volpe, you do not have stomach cancer, but you do have a duodenal ulcer caused by the H. pylori bacteria I was telling you about. Too much acid and inflammation from this infection is causing your pain. The good news is we can probably cure your ulcer by killing the bacteria, but you will have to take three different medications twice a day for 14 days. I’ll see you again in 3 weeks; we can do a simple breath test to determine if the H. pylori has been successfully eliminated.”

Short Answer Questions:

1. The structures in the epigastric region share a common nerve supply. Can you name the specific cranial nerve that serves this region and the part of the nervous system to which it belongs?
2. In order to understand the disease in Mr. Volpe’s alimentary canal, one must know the layers that make up its walls. Design a chart that identifies the four basic layers of the alimentary canal, the tissues that make up each layer, and the general function of each layer.
3. Dr. Lorraine suspects a peptic ulcer. This is an inflammatory lesion in the stomach or duodenal mucosa, which may extend through all layers of the alimentary canal wall. Describe the basic histological (tissue) structure of the mucosa layer in the alimentary canal. Identify the unique features of the mucosa in the stomach and in the duodenum, and explain how this uniqueness determines the function of the stomach and the duodenum.
4. Mr. Volpe asks, “What do the bacteria have to do with the ulcer?” Dr. Lorraine tells him that the H. pylori increases stomach acid secretion and, at the same time, breaks down the lining of your stomach and duodenum. What is the source and normal function of acid in the stomach and what regulates its production
5. Why is Mr. Volpe’s dyspepsia relieved by food, and aggravated 2–4 hours after a meal?

functional,hypothalamic amenorrhea

12. What is the activity of phosphatases, how do acid and alkaline phosphatase differ, and what are some possible causes of abnormal levels?

13. What is the activity of lactate dehydrogenase, and what might cause plasma levels to be abnormally elevated?

14. Given the abnormally elevated levels of both alkaline phosphatase and lactate dehydrogenase, is there one particular organ that is likely affected? Explain.

In the epinephrine GPCR pathway, what would happen if Adenylyl Cyclase was non-functional?

An individual is admitted to a hospital rehab center for opioid dependence. They began therapy using Suboxone (partial agonist) at 50 mg/day. Each week, their dosage was reduced by 10 mg until they weaned off the medication. They were then released and sent home. Explain what happened physiologically during their treatment

Do you think a ligand can be both a paracrine and autocrine signal? Explain your reasoning