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Pharmacology #3 > Lipid lowering and anti-diabeetus drugs > Flashcards

Lipid lowering and anti-diabeetus drugs Flashcards

1
Q

Why do you want to lower the lipid content?

A

Because you get clogged arteries

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2
Q

How does plaque form?

A

Artery walls are damaged (probably due to age and wear and tear), cholesterol particles infiltrate the artery wall at the site of damage, plaque forms, as more cholesterol and other materials are incorporated into the plaque the plaque grows, the plaque grows some more and blood flow is blocked or a clot can form and occlude other vessels

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3
Q

Which cholesterols are the bad ones?/

A

LDLs

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4
Q

Is there an inflammatory component to to all this business?

A

Indeed there is

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5
Q

What are the jobs of good and bad cholesterol?

A

Good (HDL) regulates the storage of LDL and promotes excretion

Bad (LDL) stores the cholesterol in the blood stream

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6
Q

What do fibric acid derivatives do to treat this lipid problem?

A

They increase peripheral lipolysis and decrease hepatic triglyceride production

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7
Q

Fibrotic acid derivatives are mostly used for lowering triglycerides. What are some side effects?

A 
great.
abdominal discomfort- diarrhea
nausea
blurred vision
increased risk of gallstones
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8
Q

Which drug is the only one that is suitable to treat dyslipidemia?

A

niacin- nicotinic acid

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9
Q

Another drug used to treat dyslipidemia is a bile acid sequestrant. What do they do?

A

These basically sequester cholesterol. So instead of the lipid being stored in the blood, the lipid is turned more into bile acid. This occurs because the bile acid resorption is blocked. There isn’t enough bile acid around when this happens so your body wants to make some more of it. Cholesterol is necessary to make bile acid, so the cholesterol is sequestered to make bile acid instead of having it stored in the blood

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10
Q

What do statins do?

A

They lower cholesterol by inhibiting its biosynthetic pathway. Consequently they have tons of side effects

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11
Q

Cholesterol absorption inhibitors. How do they work?

A

They inhibit the absorptions of dietary cholesterol and inhibits the reabsorption of biliary cholesterol
Basically this inhibits the formation of LDL

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12
Q

Why do cholesterol absorption inhibitors inhibit formation of the LDL?

A

Well if you don’t let the body absorb the cholesterol then how can you make LDL?

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13
Q

What is glycogenesis?

A

The process of glycogen synthesis in which glucose molecules are added to chains of glycogen for storage

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14
Q

What is glycogenolysis?

A

The reverse of glycogenesis

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15
Q

Gluconeogenesis is what?

A

It is a metabolic pathway that results nth generation of new glucose from non carbohydrate carbon substrates.

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16
Q

Hyperglycemia is what? Hypoglycemia?

A

It’s high blood sugar

Low blood sugar

17
Q

Glucagon and insulin are the principle hormones that regulate what?

A

Blood sugar levels

18
Q

Which cells of the pancreas secrete glucagon and insulin?

A

Alpha cells secrete glucagon

Beta cells secrete insulin

19
Q

What is normal fasting blood sugar levels and normal post meal blood sugar levels?

A

70-100 for fasting

70-140 for post meal

20
Q

What is your A1C test/levels?

A

Its a test that measures the glycation of hemoglobin. It provides a window into the average blood sugar of an individual over period of months

21
Q

What is a good HbA1c score?

A

Below 6

22
Q

What does insulin ultimately do?

A

It binds to a cell and the cell takes up the glucose from the blood

23
Q

What is type I diabeetus?

How do you treat it?

A

It’s an autoimmune disorder where your body attacks your beta cells. Your body doesn’t make insulin.
You give yourself insulin injections

24
Q

What is type II diabeetus?

How do you treat it?

A

The cells don’t respond to insulin, so cells don’t absorb glucose.
Change your diet and take insulin

25
Q

What do you use to treat type I diabetes?

A

Insulin. That’s all you need

26
Q

What is the overall treatment scheme for the drugs treating type II diabetes?

A

They all stimulate the beta cells of the body to secrete more insulin

27
Q

What regulates insulin release from pancreatic beta cells?

A

A K+ channel regulates insulin release from pancreatic beta cells by sensing ATP/ADP

28
Q

Can you elaborate on the K+ channel and insulin interaction?

A

If you’re fasting, so ATP/ADP is low then the potassium channel will be open. This hyper polarizes the cell and the voltage gated calcium channel isn’t opened.
If you’ve just eaten and ATP/ADP levels are high, you potassium channel stays closed and the cell depolarizes, and the voltage gated calcium channel opens, which allows the release of insulin vesicles to occur.
Think of it kind of like a presynaptic terminal- calcium needs to come in for the neurotransmitter to be released

29
Q

How do Sulfonylureas work? (this is the standard of care)

A

The binding of this drug to the working beta cell reduces the efflux of potassium. This ends up closing the channel and the membrane depolarizes, opening the voltage gated calcium channels which leads to an influx of calcium. Insulin is released

30
Q

Some drugs are used before meals. One of these is meglitinides. What is a side effect if you take this and don’t eat?

A

Hypoglycemia

31
Q

Sulfonylureas and meglitinides achieve the same result.

A

Excellent

32
Q

On beta cells of the pancreas there is a receptor called GLP-1 (glucagon like peptide 1). What happens if this receptor is stimulated?
What do drugs do that act on this receptor?

A

Insulin is released.

Some drugs stimulate insulin release and some drugs inhibit degradation of the receptor

33
Q

Why is metformin such a good drug?

A

It doesn’t stimulate insulin secretion, but it does increase glucose uptake and utilization in skeletal muscle. This bypasses the insulin resistance mechanism.

34
Q

T/F metformin decreases hepatic glucose production?

A

Fact.

35
Q

There are drugs that decrease insulin resistance. That’s great, but what is insulin resistance?

A

Insulin resistance is a pathological condition in which cells fail to respond to the normal actions of insulin. The body produces insulin, but the cells are resistant to it and are unable to use it effectively. This leads to high blood sugar.

36
Q

How do drugs that regulate insulin resistance (PPAR-gama drugs) work?

A

They regulate fatty acid storage and glucose metabolism. The PPARgama drugs stimulate lipid uptake and adipogenesis by fat cells.

37
Q

What do alpha-glucosidase inhibitors do?

A

They act by inhibiting the digestion of glucose

38
Q

What does alpha-glucosidase do?

A

It breaks down starch and disaccharides to glucose.

39
Q

T/F alpha glucosidase inhibitors speed up the digestion and absorptions of carbohydrates in the GI tract.

A

False, they delay digestion

Pharmacology #3 (7 decks)

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