Pharm Exam 4 Part 4

Front 1

What does aspirin not affect?

Back 1

PT and aPTT

Front 2

Endocrine system

Back 2

odd organ system

None are usually connected

secrete hormones to excite target cells

Front 3

Pancreas

Back 3

made up of 2 types of secretory tissues, which reflect the dual function.

Exocrine(digestive enzymes) and endocrine

Front 4

Endocrine cell

-another name

-types of cells

-amount

Back 4

pancreatic islets (Islets of Langerhans)

Alpha cells produce glucagon (20%)

Beta cells produce insulin (75%)

Front 5

Discuss the pathway for insulin release

Back 5

90 BG > eat > increase BG > stimulate Beta cells > release insulin > insulin receptors in the liver where glucose is stored > BG decreases and insulin release does the same.

Front 6

Discuss the pathway for glucagon release

Back 6

90 bg > decrease in BG > Alpha cells stimulated to release glucagon > breaks down glycogen through glycogenolysis > increase in BG

Front 7

What lvls correlate directly with insulin lvls?

Back 7

Glucose lvls

Front 8

What are the four types of diabetes?

Back 8

Type 1 - insulin dependent

-generally autoimmune. 80-90% functioning beta cells are lost.-fatigue

-develop diabetic ketoacidosis -polydipsia, polyphagia, polyuria, wt loss

Type 2 - non-insulin dependent

-metabolic syndrome, less insulin, increased resistance to insulin

Type 3 - other causes of BG

Type 4 - Gestational

-7%, hormones block

Front 9

Type 2 Diabetes

Back 9

Treat via diet and exercise and medication

Clinical manifestations: recurrent infections, vision problems, neuropathy, dehydration(nonketotic hyperosmolar coma), nephropathy.

Front 10

Polyol pathway

Back 10

type 2 diabetes where it hold onto sorbitol and fructose, which will increase intracellular osmotic pressure.

Front 11

What is the microvascular disease caused by?

Back 11

Glycosilation

Front 12

What are the ways to DX diabetes?

Back 12

Fasting Blood glucose

-fasting, then given orange syrup(1 time)

Glucose tolerance test

-draw labs for a 3 hours period

Front 13

How will you be able to monitor how well diabteics are sticking to the regimen?

Back 13

Glucose POC, self monitoring

Hemogloblin A1C

-shows long term

Front 14

Diabetes Insipidus

Back 14

Nothing to do with Insulin

insufficiency with ADH(polyuria, polydipsia)

Neurogenic(not enough) and nephrogenic(not responding to)

Front 15

How do beta cells make insulin?

Back 15

1st preproinsulin

proinsulin

insulin(activated in granules)

Front 16

What is the C-peptide in insulin?

Back 16

No function connects alpha and beta (active forms of insulin)

Front 17

What insulin can we use, if we don't like recombinent?

Back 17

Porcine

only one amino acid off.

Front 18

GLUT2 transporters

Back 18

Important in that it has a low affinity, so the glucose will not go into beta cells so readily, if that were to occur, then the beta cells would constantly be releasing insulin.

Front 19

When GLUT2 allows glucose in the cell, what happens?

Back 19

Metabolism increases > ATP increases > K channel ATP sensitive close in excess amounts of ATP > current increases to depolarization > Ca++ opens up and exocytosis of insulin occurs.

Front 20

What is the insulin receptor?

Back 20

It is a tyrosine kinase receptor

dimer that sets off a phosphorylation cascade.

for membrane translocation of GLUT, increase glycogen formation, and activation of transcription factors

Front 21

GLUT 1, 3, 4, 5

Back 21

membrane translocation of GLUT

Front 22

GLUT1

Back 22

Brain and RBC

Front 23

GLUT 4

Back 23

only one with intermediate affinity of glucose

=5

Muscle and adipose

Front 24

GLUT 1 3 5 are

Back 24

high affinity transporters

Front 25

What are the 4 main effects of insulin?

Back 25

-Increase glucose absorption into all the cells of the body

-Promote glucose stores as glycogen

-Inhibits glycogenolysis

-Inhibits conversation of fatty acids and amino acids to ketones

Front 26

Rapid Acting Insulin

Back 26

lispro, aspart, glulisine

Front 27

Short Acting Insulin(Regular)

Back 27

Novolin, humulin

Front 28

Intermeadiate Acting Insulin

Back 28

Neutral Protamine Hagedorn, isophan

Front 29

Long Acting Insulin

Back 29

Glargine, detemir

Front 30

Insulin dosing

Back 30

some people want the low basal rate and give short acting for meals, others want less injections, so they take the 70/30.

Front 31

Insulin delivery

Back 31

SQ injections

Portable pens

Conintuous SQ insulin infusion

-sterile change Q 2-3 days

-Best for tight insulin control

Inject where fat is!

Front 32

Intensive Insulin regimen

Back 32

IIDM: tight control

Need basal and bolus

-sliding scale(illness increases the dose)`

Front 33

What is the complication of treatment for those with Diabetes?

Back 33

Hypoglycemia

anxiety, blurred vision, palpitations, shakiness, slurred speech, sweating

Treat: give sugar or glucagon

Front 34

Biguanines

Back 34

Metformin

1st line therapy(with meals)

Reduces hepatic production of glucose

Front 35

Insulin Secretagogues

Back 35

Stimulate the release of insulin by binding to K+ ATP sensitive channels.

Oldest class - sulfonylureas (Increased cardio mortality rate)

Meglitinides(shorter duration of action)

Front 36

Thiazolidinediones

Back 36

Decreases insulin resistance and increases insulin signal transduction.

Increase risk for MI

Had an access program, but you had to know it increases risk for MI

Front 37

Alpha-Glucosidase Inhibitors

Back 37

Block digestion of complex carbohydrates

good for pre-diabtics

GI effects: flatulence, diarhhea, and ABD pain

Front 38

Bile Acid Binding resins

Back 38

Large cation exchange resins-not absorbed that bind to cholesterol and surround it.

Bind bile acids-prevent reabsorption

GI upset

Front 39

Hyperglucagonemia

Back 39

Excess glucagon because of pts taking insulin or meds that increase insulin.

Front 40

Symlin (Amylin)

Back 40

Released by beta cells to suppress glucagon release.

Need to use with insulin

Decreases circulating glucose

Front 41

GLP-1

Back 41

Increases insulin, decreases glucagon

GI hormone

pancreatic cancer risk

Front 42

Januvia

Back 42

DDP-4 antagonist

found in gila monster saliva

Incretine therapy

Gi hormone

Front 43

Gliflozins

Back 43

SGLT2 inhibitor

SGLT2 (Proximal convoluted tubule: filter out 180 G, and 90% reabsorbed in distal segment) More glucose goes out into the urine. Osmotic diuretic.

Wt loss, dehydration, increase in urethral infections

Front 44

What the combination therapy steps?

Back 44

1. Biguanide

2. Biguanide + insulin OR Secretagogue

3. Biguanide + 2-3 other classes

4. Intensive Insulin Therapy

Front 45

What is the first measure of taking care of Diabetics?

Back 45

Eat right and exercise and check your feet and eyes

Front 46

Sterols

Back 46

Precursors to cholesterol

can be found in animals and plants

Need for many functions in the body.

Front 47

cholesterol

Back 47

we eat and make it through the mevalonate pathway.

Front 48

cholesterol synthesis

Back 48

acetyl-CoA > Mevalonate > squalene > cyclation of squalene > cholesterol

Front 49

Atherosclerosis

Back 49

leading cause of death in U.S.

Lipid deposits in CA

Front 50

HDL

Back 50

Good cholesterol. scavenger lipoprotein and takes lipids from different areas.

Want it to be Higher

Front 51

LDL

Back 51

Bad cholesterol, deposits lipids into the arteries. Higher lipid to protein. Transfer lipids to the cells. Excess amounts causes it to be deposited into the arteries.

Want it to be lower

Front 52

Reminant Lipid Particles

Back 52

breakdown of HDL and LDL

Front 53

Chylomicrons

Back 53

Formed in the intestine, then goes to helptic portal system and goes to the liver

Carry triglycerides and cholesterol

Front 54

VLDL

Back 54

Secreted by the liver, go to peripheral tissues and converted to IDL and LDL

Front 55

How does plaque formation occur?

Back 55

The LDL are swallowed up by macrophages > become foam cells > proinflammatory > Increased cytokines > increased cells and edema > release reactive oxygen species > oxidize the LDL > more inflammation > macrophages breakdown and become calcified

Front 56

If we take the total cholesterol and divide by the HDL, what should it look like?

Back 56

The number should be low.

Front 57

What the first thing we can do about dyslipidemia?

Back 57

Control diet and exercise.

<20% fat for total calorie intake

wt reduction

omega-3 fatty acids

Front 58

How much should fat be a part of your diet?

Back 58

<20%

Front 59

Where does the majority of the dyslipidemia medications work?

Back 59

In the hepatocyte.

Front 60

Statins

Back 60

LDL(-40%), prescribed in Coranary symptoms regardless of lipidemia. Look like HMG-CoA.

HDL(+10%). Modest decrease in triglycerides.

A: 40-70% oral bioavailablity

-extensive 1st pass, but that where it works

E: Heptic metabolism and kidney

Front 61

Niacin

Back 61

Decreases VLDL secretion from liver and LDL(-20%). HDL(+25%). Drop triglycerides.

2-6mg daily

cutaneous vasodilation, pruitis, dry skin, rash, ADB discomfort, elevation of liver enzymes

Front 62

Fibrates

Back 62

PPAR mediated lipolysis, decrease VLDL, LDL(-10%), HDL(+15%), drop triglycerides

Rare GI upset

Front 63

Bile acid binding resins

Back 63

LDL(-20%), HDL(+5%) & BG. May increase VLDL.

5-30 g/day mixed with liquid and must be with meals

Constipation, bloating, steatorrhea, oral drug absorption impairmentcompletely surround the fatty acids in gut. Not great for pts with malabsorption issues.

Front 64

Ezetmibe (Zetia)

Back 64

Blocks NPC1L1, inhibits cholesterol absorption

LDL(-20%), HDL(+5%)

A:Readily absorbed, increased with fibrates, decreased with resins.

D: Peak blood lvls 12-14 hrs T1/2: 22 hrs

E: 80% in feces