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Flashcards in Exam III Quan Study Guide Deck (57):
1

Importance of oxygen

Oxygen is the life-giving, life-sustaining element. Approximately 90% of the body's energy is created by oxygen. Nearly all of the body's activities, from brain function to elimination, are regulated by oxygen.

2

Oxygen is ------ at body temperature

inert

3

oxidation

Oxidation is gain of oxygen

4

Reduction

Reduction is loss of oxygen

5

What are the ROS

reactive oxygen species, oxidizes DNA, lipids, and proteins. They are molecules that are highly reactive, but small. They modulate activities of oxidized targets when they are controlled tightly. Reactive oxygen species is one of many cell-signaling processes.

6

What are the free radicals

Free radicals are atoms or groups of atoms with an odd (unpaired) number of electrons and can be formed when oxygen interacts with certain molecules. Once formed these highly reactive radicals can start a chain reaction, like dominoes

7

How are ROS formed

ROS are formed as a natural byproduct of the normal metabolism of oxygen and have important roles in cell signaling and homeostasis.

8

Oxidative stress

an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants

9

How do ROS damage cells?

In aerobic organisms the energy needed to fuel biological functions is produced in the mitochondria via the electron transport chain. In addition to energy, reactive oxygen species (ROS) with the potential to cause cellular damage are produced. ROS can damage DNA, RNA, and proteins, which, in theory, contributes to the physiology of aging.

10

Physiological functions of ROS

(-)). In the cardiovascular system, besides playing a critical role in the development and progression of vasculopathies and other important pathologies such as congestive heart failure, atherosclerosis and thrombosis, ROS also regulate physiological processes.

have important roles in cell signaling and homeostasis.[

11

Markers of liver disease

These tests include prothrombin time (PT/INR), aPTT, albumin, bilirubin (direct and indirect), and others. Liver transaminases (AST or SGOT and ALT or SGPT) are useful biomarkers of liver injury in a patient with some degree of intact liver function.

12

Liver and glucose metabolism

Energy is required for the normal functioning of the organs in the body. Many tissues can also use fat or protein as an energy source but others, such as the brain and red blood cells, can only use glucose. Glucose is stored in the body as glycogen. The liver is an important storage site for glycogen.

13

Liver plasma proteins

Other plasma proteins produced by the liver include albumin which binds many water-insoluble substances and contributes to osmotic pressure, fibrogen which is key to the clotting process, and certain globulins which transport substances such as cholesterol and iron.

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Acute phase protein

Acute-phase proteins are a class of proteins whose plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation. This response is called the acute-phase reaction (also called acute-phase response). Inflammatory cells and red blood cells.

15

What is heme?

an iron-containing compound of the porphyrin class that forms the nonprotein part of hemoglobin and some other biological molecules.

16

The rate limiting step in heme synthesis

ALA Synthase is the committed step of the heme synthesis pathway, & is usually rate-limiting for the overall pathway. Heme functions as a feedback inhibitor, repressing transcription of the ALA Synthase gene in most cells.

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Heme controls its own synthesis

At which step do you regulate heme synthesis?--
First step δ-ALA synthase and heme controls its own production

18

What is bilirubin

an orange-yellow pigment formed in the liver by the breakdown of hemoglobin and excreted in bile.

19

What is Jaundice?

a yellowish or greenish pigmentation of the skin and whites of the eyes due to high bilirubin levels

20

Three main causes of jaundice

Pre-hepatic jaundice

Pre-hepatic jaundice occurs when a condition or infection speeds up the breakdown of red blood cells. This causes bilirubin levels in the blood to increase, triggering jaundice.

Causes of pre-hepatic jaundice include:

malaria – a blood-borne infection spread by mosquitoes
sickle cell anaemia – an inherited blood disorder where the red blood cells develop abnormally; it's most common among black Caribbean, black African and black British people
thalassaemia – similar to sickle cell; it's most common in people of Mediterranean, Middle Eastern and, in particular, South Asian descent
Crigler-Najjar syndrome – a genetic syndrome where an enzyme needed to help move bilirubin out of the blood and into the liver is missing
hereditary spherocytosis – a genetic condition that causes red blood cells to have a much shorter life span than normal

Intra-hepatic jaundice

Intra-hepatic jaundice happens when a problem in the liver – for example, damage due to infection or alcohol, disrupts the liver’s ability to process bilirubin.

Causes of intra-hepatic jaundice include:

the viral hepatitis group of infections – hepatitis A, hepatitis B and hepatitis C
alcoholic liver disease – where the liver is damaged as a result of drinking too much alcohol
leptospirosis – a bacterial infection that's spread by animals, particularly rats
glandular fever – a viral infection caused by the Epstein-Barr virus
drug misuse – leading causes are ecstasy and overdoses of paracetamol
primary biliary cirrhosis – a rare condition that causes progressive liver damage
Gilbert's syndrome – a common genetic syndrome where the liver has problems breaking down bilirubin at a normal rate
liver cancer – a rare and usually incurable cancer that develops inside the liver
exposure to substances known to be harmful to the liver – such as phenol (used in the manufacture of plastic) or carbon tetrachloride (widely used in the past in processes such as refrigeration, although now its use is strictly controlled)
autoimmune hepatitis – a rare condition where the immune system starts to attack the liver
primary sclerosing cholangitis – a rare type of liver disease that causes long-lasting (chronic) inflammation of the liver
Dubin-Johnson syndrome – a rare genetic syndrome where the liver is unable to move bilirubin out of the liver

Post-hepatic jaundice

Post-hepatic jaundice is triggered when the bile duct system is damaged, inflamed or obstructed, which results in the gallbladder being unable to move bile into the digestive system.

Causes of post-hepatic jaundice include:

gallstones – obstructing the bile duct system
pancreatic cancer
gallbladder cancer or bile duct cancer
pancreatitis – inflammation of the pancreas, which can either be acute pancreatitis (lasting for a few days) or chronic pancreatitis (lasting for many years)

Some causes of jaundice are common, such as hepatitis and gallstones, whereas other causes, such as Crigler-Najjar syndrome and Dubin-Johnson syndrome, are much rarer.

21

Drug metabolism in the liver



The liver is the principal site of drug metabolism. Although metabolism typically inactivates drugs, some drug metabolites are pharmacologically active—sometimes even more so than the parent compound. An inactive or weakly active substance that has an active metabolite is called a prodrug, especially if designed to deliver the active moiety more effectively.

Drugs can be metabolized by oxidation, reduction, hydrolysis, hydration, conjugation, condensation, or isomerization; whatever the process, the goal is to make the drug easier to excrete. The enzymes involved in metabolism are present in many tissues but generally are more concentrated in the liver. Drug metabolism rates vary among patients. Some patients metabolize a drug so rapidly that therapeutically effective blood and tissue concentrations are not reached; in others, metabolism may be so slow that usual doses have toxic effects. Individual drug metabolism rates are influenced by genetic factors, coexisting disorders (particularly chronic liver disorders and advanced heart failure), and drug interactions (especially those involving induction or inhibition of metabolism).

For many drugs, metabolism occurs in 2 phases. Phase I reactions involve formation of a new or modified functional group or cleavage (oxidation, reduction, hydrolysis); these reactions are nonsynthetic. Phase II reactions involve conjugation with an endogenous substance (eg, glucuronic acid, sulfate, glycine); these reactions are synthetic. Metabolites formed in synthetic reactions are more polar and thus more readily excreted by the kidneys (in urine) and the liver (in bile) than those formed in nonsynthetic reactions. Some drugs undergo only phase I or phase II reactions; thus, phase numbers reflect functional rather than sequential classification.

22

Cytochrome P-450

are proteins of the superfamily containing heme as a cofactor and, therefore, are hemoproteins.

CYPs are the major enzymes involved in drug metabolism, accounting for about 75% of the total metabolism.[16] Most drugs undergo deactivation by CYPs, either directly or by facilitated excretion from the body. Also, many substances are bioactivated by CYPs to form their active compounds


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Acetaminophen toxicity

Acetaminophen is one of the most commonly used oral analgesics and antipyretics. It has an excellent safety profile when administered in proper therapeutic doses, but hepatotoxicity can occur after overdose or when misused in at-risk populations. In the United States, acetaminophen toxicity has replaced viral hepatitis as the most common cause of acute hepatic failure and is the second most common cause of liver failure requiring transplantation.

**look into what exactly they want for this**

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Alcohol toxicity

**look into what exactly they want for this**

25

Defense mechanisms against ROS

**look into this**

26

Important properties of liver

**look into this**

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Special features of liver anatomy

**look into this**

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Importance of Urea Cycle

Function. Organisms that cannot easily and quickly remove ammonia usually have to convert it to some other substance, like urea or uric acid, which are much less toxic. Insufficiency of the urea cycle occurs in some genetic disorders (inborn errors of metabolism), and in liver failure.

29

What are the major energy sources in the body?

There are 3 sources of calories (or energy), which are also known as macronutrients: carbohydrates, protein, and fat. Of these three, carbohydrates are the body's preferred source of energy. Carbohydrates break down into glucose, which is an immediate source of energy especially for the brain and muscles.

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Why is glucose so critical?

Inert, used in brain, plentiful. **look into this to see if there is anything else**

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What’s the long-term energy store?

Carbohydrates and lipids are both used for energy storage, but carbohydrates are used for short term storage whereas lipids are used for long term storage. Carbohydrates are able to more easily transport energy around the body because they are soluble in water.

32

Can you use amino acids as an energy source?

In contrast, ketogenic amino acids can produce ketones when energy sources are low. Some of these amino acids are degraded directly to ketone bodies such as acetoacetate (see ). They include leucine, lysine, phenylalanine, tryptophan, and tyrosine. The other ketogenic amino acids can be converted to acetyl CoA.

33

Plasma glucose concentration is the result of?

Glucose is transported from the intestines or liver to body cells via the bloodstream, and is made available for cell absorption via the hormone insulin, produced by the body primarily in the pancreas.

Glucagon increases blood glucose

34

Insulin and glucagon producing cells

Glucagon is secreted by the alpha cells of the pancreas when blood glucose is low.

Insulin: it's produced by the beta cells in the islets of Langerhans in the pancreas.

35

Source of glucose in fed and starving states

Fed: Normal glucose used from food - extra stored in glycogenesis
Starved: Glucose from gluconeogenesis and glycogenolysis

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Phases of insulin production after oral glucose

**look into this**

37

Insulin and glut-4

GLUT4 is the insulin-regulated glucose transporter found primarily in adipose tissues and striated muscle (skeletal and cardiac).

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effects of insulin

The actions of insulin (indirect and direct) on cells include: Increased glycogen synthesis – insulin forces storage of glucose in liver (and muscle) cells in the form of glycogen; lowered levels of insulin cause liver cells to convert glycogen to glucose and excrete it into the blood.

39

Causes of type 2 diabetes

Lack of exercise, unhealthy meals, Overweight/Obesity,

Insulin Resistance
That combination of factors—genetic susceptibility and lifestyle choices—leads to insulin resistance. If your body is insulin resistant, it doesn’t use insulin properly.

Your body may produce enough insulin to transport the glucose to the cells (you can read more about how insulin works in our article on insulin), but unfortunately, the body resists that insulin.

40

Function of glucagon

The pancreas releases glucagon when the concentration of glucose in the bloodstream falls too low. Glucagon causes the liver to convert stored glycogen into glucose, which is released into the bloodstream. High blood-glucose levels stimulate the release of insulin.

41

Function of epinephrine in energy metabolism

Epinephrine's binding to these receptors triggers a number of metabolic changes. Binding to α-adrenergic receptors inhibits insulin secretion by the pancreas, stimulates glycogenolysis (the breakdown of glycogen) in the liver and muscle, and stimulates glycolysis (the metabolic pathway that converts glucose into pyruvate) in muscle. β-Adrenergic receptor binding triggers glucagon secretion in the pancreas, increased adrenocorticotropic hormone (ACTH) secretion by the pituitary gland, and increased lipolysis by adipose tissue. Together, these effects lead to increased blood glucose and fatty acids, providing substrates for energy production within cells throughout the body.

Source: Boundless. “Epinephrine and Norepinephrine.” Boundless Biology. Boundless, 26 May. 2016. Retrieved 29 Nov. 2016 from https://www.boundless.com/biology/textbooks/boundless-biology-textbook/osmotic-regulation-and-the-excretory-system-41/hormonal-control-of-osmoregulatory-functions-232/epinephrine-and-norepinephrine-867-12114/

42

Phosphorylation in catabolism

The last process in aerobic respiration is oxidative phosphorylation, also known as the electron transport chain. **check this**

43

Causes of hypoglycemia

It often happens when a person with diabetes takes too much insulin. Also issues with irregular eating, alcohol abuse/hepatitis, Insulinoma, Not eating enough.

44

Causes of hypoglycemia

It often happens when a person with diabetes takes too much insulin. Also issues with irregular eating, alcohol abuse/hepatitis, Insulinoma, Not eating enough.

45

Ratios of insulin/glucagon

**look into this**

46

Substrates for gluconeogenesis

generation of glucose from non-carbohydrate carbon substrates such as lactate, glycerol, and glucogenic amino acids

47

Cori cycle

The Cori cycle (also known as the Lactic acid cycle), named after its discoverers, Carl Ferdinand Cori and Gerty Cori,[1] refers to the metabolic pathway in which lactate produced by anaerobic glycolysis in the muscles moves to the liver and is converted to glucose, which then returns to the muscles and is metabolized back to lactate.[2]

48

Major energy substrate during prolonged starvation

Fats are broken down into glycerol and free fatty acids, with the glycerol being utilized in the liver as a substrate for gluconeogenesis.

**glycerol

49

Metabolism during stress

Both epinephrine and cortisol are adrenal stress hormones that might be partly responsible for these reactions. Cortisol increases your metabolism, but it also makes you hungry. So while your body may be burning more calories when you're stressed, you may eat more to compensate.

50

Difference between type 1 and type 2 diabetes

Type 1: no insulin - the body's immune system destroys the cells that release insulin
Type 2: don't recognize insulin well.
In type 2 diabetes, the body isn't able to use insulin the right way. This is called insulin resistance. As

51

Ketoacidosis and type 1 diabetes

Diabetic ketoacidosis (DKA) is a life-threatening problem that affects people with diabetes. It occurs when the body cannot use sugar (glucose) as a fuel source because there is no insulin or not enough insulin. Fat is used for fuel instead.

52

Role of obesity in diabetes

People who are overweight or have obesity have added pressure on their body's ability to use insulin to properly control blood sugar levels, and are therefore more likely to develop diabetes.

53

Diabetes symptoms

The classic symptoms include feeling tired and sick, frequent urination, excessive thirst, excessive hunger, and weight loss.

Ketoacidosis, a condition due to starvation or uncontrolled diabetes, is common in Type I diabetes. Ketones are acid compounds that form in the blood when the body breaks down fats and proteins. Symptoms include abdominal pain, vomiting, rapid breathing, extreme lethargy, and drowsiness. Patients with ketoacidosis will also have a sweet breath odor. Left untreated, this condition can lead to coma and death.
With Type II diabetes, the condition may not become evident until the patient presents for medical treatment for some other condition. A patient may have heart disease, chronic infections of the gums and urinary tract, blurred vision, numbness in the feet and legs, or slow-healing wounds. Women may experience genital itching.

54

Diabetic vascular complications

Generally, the injurious effects of hyperglycemia are separated into macrovascular complications (coronary artery disease, peripheral arterial disease, and stroke) and microvascular complications (diabetic nephropathy, neuropathy, and retinopathy).

55

Glucose tolerance test


What is a glucose tolerance test?

A glucose tolerance test is used to help diagnose gestational diabetes and type 2 diabetes.
There are three versions of the oral glucose tolerance test: the 1-hour test, the 2-hour test, and the 3-hour test.
In the eight hours leading up to the test, you should not eat food or drink any beverages aside from water.

A glucose tolerance test measures how well your body’s cells are able to absorb glucose, or sugar, after you ingest a given amount of sugar. Doctors use fasting blood sugar levels and hemoglobin A1c values to diagnose type 1 and type 2 diabetes, and prediabetes. A glucose tolerance test can also be used. Doctors primarily use a glucose tolerance test to diagnose gestational diabetes.

Doctors often diagnose type 1 diabetes quickly because it usually develops quickly and involves high blood sugar levels. Type 2 diabetes, on the other hand, often develops over years. Type 2 diabetes is the most common form of diabetes, and it usually develops during adulthood.

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A1C test

The A1C test is a blood test that provides information about a person's average levels of blood glucose, also called blood sugar, over the past 3 months. The A1C test is sometimes called the hemoglobin A1c, HbA1c, or glycohemoglobin test.

57

Treatment for diabetes

Type 2 diabetes
Treatments include diet, exercise, medication, and insulin therapy.
Type 1 diabetes
Treatment aims at maintaining normal blood sugar levels through regular monitoring, insulin therapy, diet, and exercise.