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Advanced Pharmacology > Exam 4 - Diabetes/Dyslipidemia > Flashcards

Exam 4 - Diabetes/Dyslipidemia Flashcards

1
Q

What are the endocrine functions of the pancreas?

A
  • Contain the Islets of Langerhans; the controls centers for blood glucose
  • Insulin from beta cella
  • Glucagon from alpha cells
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2
Q

What are the exocrine functions of the pancreas?

A

Digestive enzymes

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3
Q

Describe the roles of insulin and glucagon on blood glucose levels?

A
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4
Q

What are the 4 main types of diabetes mellitus?

A
  • Type I: Insulin dependent, caused by beta cell destruction
  • Type II: Non-insulin dependent, caused by insulin deficiency and insulin resistance
  • Type III: Other causes like medications or pancreatitis, only temporary
  • Type IV: Gestational
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5
Q

What are the 3 cardinal symptoms of diabetes?

A
  • Polydipsia
  • Polyuria
  • Polyphagia
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6
Q

Describe the sorbitol pathway and it’s adverse effects?

A

When hyperglycemic, glucose is converted to fructose, then to sorbitol, a sugar alcohol. Sorbitol cannot leave the cell like glucose, this causes an increase in water within the cell, and the cells burst.
This causes diabetic retinopathy and peripheral neuropathy.

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7
Q

Describe the 2 different types of diabetes tests?

A
  • Fasting glucose test: the patient fasts overnight and has their glucose checked: normal is less than 100 mg/dL
  • Glucose tolerance test: The patient is given a large amount of glucose to drink and their glucose is checked at scheduled intervals to determine how the body is dealing with hyperglycemia.
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8
Q

Describe the structure of insulin?

A

A peptide containing the active form:
-alpha and beta chain held together by sulfide bonds
Proform:
-C peptide chain that is cleaved and has no known function. Not found in synthetic insulin

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9
Q

Describe the role of insulin secretagogues to cause insulin release?

A
  • Glucose - transported into beta cells via GLUT2, metabolized to create ATP. ATP closes K+ channels depolarizing the membrane. This causes Ca channels to open allowing Ca to destabilize insulin vesicles, causes exocytosis and insulin release.
  • This also caused by amino acids, hormones, fatty acids, incretins, and drugs (B agonists)

This happens constantly (constituitive activity) but increases with glucose levels

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10
Q

Describe the insulin receptor pathway?

A
  • Insulin lasts ~6 mins in the bloodstream
  • Binds to insulin RTK, causing dimerization
  • The beta subunits are phosphoylated causing activation of insulin response substrates (IRS)
  • Main effect is to move the GLUT transporter to the cell surface
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11
Q

Describe the various GLUT receptors location and function?

A
  • GLUT 1: in brain and RBC, uptake glucose regardless of concentration
  • GLUT 2: in beta cells of pancreas, regulating insulin release
  • GLUT 3: in brain, uptake glucose regardless of concentration
  • GLUT 4: most prevalent, found in muscle and fat, causes uptake of glucose, insulin dependent
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12
Q

What are the 4 different types of insulin preparations and examples?

A
  1. Rapid acting: lispro, aspart, glulisine
  2. Short acting (regular): novolin, humulin
  3. Intermediate acting: NPH
  4. Long acting: glargine, detemir
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13
Q

What are the types of insulin dosing regimens?

A
  • Tight control: implantable device
  • Basal: single injection of long acting
  • Bolus: coverage of carbohydrate intake
  • Correction: dose given to reduce hyperglycemia
  • Conventional: 70:30 mixture of NPH and short acting, not tight control but okay for those without other symptoms from the disease
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14
Q

How much insulin is required for carbohydrate and blood glucose coverage/correction?

A
  • Carbohydrate coverage bolus: 1 unit of rapid acting disposes of 12-15g of carbohydrates (4 units for 60g)
  • Hyperglycemia correction: 1 unit of rapid acting needed to drop 50mg/dL
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15
Q

What are the symptoms and treatments of hypoglycemia?

A
  • Anxiety, blurred vision, sweating, shakinesss, slurred speech, palpitations
  • Treatment: glucose (tablets, soda, juice), or glucagon injection
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16
Q

Describe the MOA, side effects, and examples of biguanides?

A

MOA: Reduces hepatic glucose production (gluconeogenesis)
Side effects: GI upset
Drugs: Metformin (Glucophage)

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17
Q

Describe the MOA, side effects, and examples of insulin secretagogues?

A

MOA: Bind to K+ channel causing depolarization and release of insulin
Side effects: reactions to sulfa drugs, black box warning for increased cardiovascular mortality.
Drugs: Sulfonylureas

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18
Q

Describe the MOA, side effects, and examples of Thiazolidinediones (Tzds)?

A

MOA: decrease insulin resistance by increasing insulin signal transduction via inducing PPAR-gamma.
Side effects: Risk of MI
Drugs: Avandia (rosiglitazone)

19
Q

Describe the MOA, side effects, and examples of alpha-glucosidase inhibitors?

A

MOA: blocks digestion of complex carbohydrates
Side effects: prominent GI effects: flatulence, diarrhea, abd pain
Drugs: Acarbose

20
Q

Describe the MOA and side effects of bile acid binding resins?

A

MOA: bind to bile acids to prevent reabsorption of glucose and cholesterol
Side effects: GI upset, must be taken with meals

21
Q

Describe the MOA and examples of amylin analogs?

A

MOA: mimics amylin release from beta cells which supresses glucagon release, decreasing circulating glucose
Drugs: Symlin

22
Q

Describe the MOA, side effects, and examples of incretin-based therapies?

A

GLP-1 agonists MOA: increase action of GLP-1 stimulating insulin release and inhibiting glucagon release.
DPP-4 antagonists MOA: DPP-4 normally inactivates GLP-1, antagonists prevent GLP-1 breakdown.
Side effects: Pancreatic cancer risk
Drugs: GLP-1: semaglutide. DPP-4: sitagliptin

23
Q

Describe the MOA, side effects, and examples of gliflozins?

A

MOA: Inhibts SGLT2 preventing glucose reabsorption in the PCT
Side effects: Glucosuria, osmotic diuretic, weight loss, dehydration
Drugs: -flozins

24
Q

What adjunctive therapies are useful in pre-diabetics?

A

Diet, exercise, weight loss, smoking cessation, statins if hyperlipidemic, low dose aspirin, managing blood pressure with ACEi and ARBs.

25
Q

Explain the treatment algorithm for patients with T2DM.

A
26
Q

Describe the process of atherogenesis?

A
  • LDL sequestered in intima of vessels when in excess
  • LDL is oxidized inside the cell triggering an immune response
  • WBC differentiate into macrophages that swallow the cholesterol
  • Cholesterol is not broken down in the body and crystalizes in the foam cell causing it to rupture and become necrotic, triggering more WBC
  • This becomes large enough that it becomes plaque and is bulging into the vessel, narrowing it.
    This is an immune process that creates endothelial inflammation
27
Q

Describe the difference between triglycerides and cholesterol?

A

Triglycerides
* Make up the majority of neutral fats
* Form adipose tissue and are the main storage form of fats
* When stored, can be catabolized into fatty acids for energy
Cholesterol
* Made of steroid base with an alcohol group
* Important precursor to hormones, membranes, vitamin D, and bile salts.
* Most is made in the liver, the rest is ingested

28
Q

What are the important steps in the mevalonate pathway?

A
29
Q

What are the 4 different lipoproteins?

A
  • Chylomicrons
  • VLDL
  • LDL
  • HDL
30
Q

Describe the function of chylomicrons and where they’re formed?

A
  • Formed in the intestines
  • Carry triglycerides and cholesterol
31
Q

Describe the function of VLDL and where it’s formed?

A
  • Secreted by the liver to the periphery
  • Becomes IDL and LDL
32
Q

Describe the function of LDL?

A
  • Transports cholesterol to cells
  • In excess becomes deposited in arteries
33
Q

Describe the function of HDL?

A
  • Scavenges cholesterol from cells
  • Low levels associated with atherosclerosis
34
Q

How can you determine CAD risk from LDL/HDL ratio?

A

Average risk is ~ 3.5 for males and females. The higher the ratio the greater the risk.

35
Q

What are the target levels for HDL, LDL, and triglycerides?

A
  • LDL: < 130
  • Triglycerides: < 120
  • HDL Men: > 40
  • HDL Women: > 50
36
Q

What are the primary and secondary causes of hypercholesterolemias?

A
  • Primary: Familial hypercholesterolemia
  • Secondary: see table, primarily diet induced
37
Q

Why is changing diet sometimes not enough to lower cholesterol?
What diet changes should be made?

A
  • Because cholesterol is not broken down by the body and is primarily endogenous, it can take years to lower cholesterol with diet alone.
  • Diet recommendations: Fat calories should be 20% of total calories, increase complex carbs and fiber, weight loss, increrase omega-3 fatty acids (reduce triglycerides)
38
Q

What is the MOA of statins?
Side effects?

A

MOA: Decrease cellular cholesterol synthesis by competitively inhibiting HMG-CoA reductase
Side effects: Avoid in pregnancy (blocks growth hormones), increased liver enzymes, CK elevation causing muscle pain

39
Q

Describe the MOA of Niacin (Vitamin B3)?
Side effects?

A

MOA: Reduces VLDL secretion from the liver
Side effects: Flushing, ithcing, dry skin, increased liver enzymes

40
Q

What is the MOA of fibrates?
Side effects?
Drugs?

A

MOA: Decreases VLDL and increase lipolysis in the liver via PPAR
Side effects: Rare
Drugs: Gemfibrozil

41
Q

Describe the MOA of ezetimibe and side effects?

A

MOA: Inhibits intesinal absorption of cholesterol by inhibition of NPC1L1
Side effects: possible hepatic, promotes arterial wall thickening

42
Q

What is the MOA of PCSK9 inhibitors?
Drugs?

A

Inhibits PCSK9 preventing binding to LDLR causing them to be recycled and the LDL-C to remain in the lysosome. Gicing with statins bc statins increase PCSK9.
Evolocumab

43
Q

What are the side effects of hypocholesterolemia?

A

Low LDL may cause:
* Cancer
* Hemorrhagic stroke
* Depression
* Anxiety
* Preterm birth/low birth weight

CHAD P.

44
Q

What is sitagliptan?

A

DPP 4 inhibitor - preventing breakdown of GLP-1, can be used in combination with a statin

Advanced Pharmacology (17 decks)

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