Pharm Test 2 - Study Guide (26-30)

Front 1

Diabetes

what is the normal range of glucose

-tell me about glucose control

Back 1

70-100

keeping a blood glucose in normal range around the clock along with keeping blood pressure and blood lipids in a normal range.

insulin is the most commonly used medication

Front 2

Diabetes

what is type 1 diabetes

Back 2

Destruction of pancreatic Beta cell you can’t produce insulin
--The beta cells are responsible for the manufacturing of insulin.

Front 3

Diabetes

what is type 2 diabetes

Back 3

Insulin resistance is present in the major target areas and we have an aging pancreases. It still produces insulin just not as much as it use to

Front 4

Diabetes

Type 2 diabetic: what are the 3 main areas in which glucose is taken up.

what's unique about your muscle cells?

Back 4

Liver, muscle, and fat cells

In your muscle you don’t need to insulin to get glucose into the cells.

Front 5

Diabetes

in order to be a diabetic, what does the fasting glucose have to be?

Hgb A1C?

Back 5

In order to be a diabetic:
Fasting glucose of 126 x 2 separate tests this is a snap shot
or
Hgb A1C >7 –stays attached for 3 months. Gives me a better indicator of what the persons glucose levels are over an extended period of time new standard

Front 6

Diabetes
-Humalog (insulin lispro)

given for type 1 or type 2 diabetes?
onset
peak
duration

Short or rapid acting?

Back 6

type 1

O= 15-30min (starts working in 15-30 minutes- when its in it’s working) –given subQ
P=.5-2.5hr
D=3-6.5hrs


Rapid acting -its immediate (as soon as it’s in, it’s working)

Front 7

Diabetes
-Regular

onset
peak
duration

Short or rapid acting?

Back 7

O=30-60min
P=1-5hrs
D=6-10hrs

Short acting: works soon.

Front 8

Diabetes -
what type of insulin is the only insulin used for type 1 diabetic in a hyperglycemic state crisis and ketoacidosis.

Back 8

regular

Front 9

Diabetes -
what type of insulin is the only one that can be given IV, none of the other ones can.

Why do we use it?

Back 9

regular

to bring down sugar and it works instantanously.

Front 10

Diabetes
-Neutral Protamine Hagedorn
(NPH)

onset
peak
duration

Short or rapid acting?
what is this given with?

Back 10

O=60-120min
P=6-14hrs
D=16-24hrs


it’s not going to start working right away, but it will work later.

--Seen given with regular insulin as a combination.

Front 11

ketoacidosis
-cannot happen in what type of diabetes?
-what is it caused by?

Back 11

Cannot happen in type II diabetes
Caused by increased lipolysis
increase in free fatty acids
Ketoacids

Type 1 diabetic has an increase glucose demand but their insulin can’t keep up with it and the body demands exceeds that and it starts breaking themselves down to help.

Front 12

Know the S/S of ketoacidosis

Back 12

-Increased glucose levels (greater than or equal to 300)
-N/V
-Polyuria
-Possible cardiac changes 2° to decreased K+
-Fruit smell to breath (acetone)
-Kussmel resp: blowing off CO2, long expiratory phase prolonged expiratory, short inspiration.

Front 13

ketoacidosis

because of polyuria, what happens to sodium and potassium

Back 13

-Because of polyuria, sodium shifts into the cells and potassium bumps out.
-Intracellular you are hypokalemic. We have to shift the potassium back into the cell and we do that by drugs. (Hyponatremia)
-Fluid shift secondary to severe Na+ decrease

-Na shifts in cells, causes swelling of cells including the brain

Front 14

what is the treatment for ketoacidosis

Back 14

1 Correct acidosis by restoring glucose and potassium levels to normal)
2 Replace fluid loss
3 Restore K+/glucose levels to normal

Front 15

Treatment for ketoacidosis

Back 15

1. IV regular insulin followed by an insulin infusion
2. IV fluids .9% NS
-Can be as much as 2-4 L in 30-60 min.
-5% dextrose will be added to IV fluid when glucose levels reach 250mg/dl to off set hypoglycemia (add when sugar levels fall to protect the brain from seizing.)
-An insulin drip and CaCl may also be administered to shift K+

3. Potassium is the most preventable cause of death in patients with DKA.
-usually 20mEq/hr IV infusion

Front 16

______ is the MOST preventable cause of death in patients with DKA

Back 16

K+: Hypokalemia

Usually 20mEq/hr IV infusion

Front 17

What electrolyte needs close monitoring in Ketoacidosis?

Back 17

potassium K+

Front 18

Sulfonylureas drugs

1st generation drug:
2nd generation drugs:

Back 18

-Glipizide (Glucotrol) 2nd gen

-Glyburide (Micronase) 2nd gen
(causes more hypoglycemia)
High potency

-Chlorpropamide (Diabinese) 1st gen
Low potency

Front 19

Look for the ____ to identify Sulfonylureas drugs

Back 19

-ide

Front 20

Sulfonylureas drugs
-Glyburide & Glipizide

what is their action?

Back 20

Promote insulin secretion by the pancreas they make my beta cells produce more insulin


also promote tissue response to insulin it changes the chemical barrier to allow the insulin to get into the cell and take the glucose into it (all cells but muscle) specifically the adipose tissue cell

Front 21

Sulfonylureas drugs
-Glyburide & Glipizide


Use:
Onset of action
how is this drug given

Back 21

type 2 only

within 2 hrs of ingesting effects start working on an hour but you wont see effects on the monitor for 2 hours


PO

Front 22

Sulfonylureas drugs
-Glyburide & Glipizide

Education:

Back 22

Typically taken with breakfast but you need to check their sugar level before you give it.

Importance of follow-up, with kidney & liver function test, HgA1C, fasting glucose may or may not be done.

Follow diet, exercise, weight management(10% difference, can make a huge different)

Take medicine at the same time every day if possible,

may take with food if GI upset

Educate patient on S/S of hypoglycemia

Educate patient on how to monitor glucose. Falls under realm of pharmacist. Include understanding what is normal, low and high we teach documenting of results


Patient should wear a med alert bracelet or necklace and it needs to be in full view. Bracelet is better than a necklace. Necklaces are covered under their shirts.

don't take with alochol

Front 23

Sulfonylureas drugs
-Glyburide & Glipizide

What can mask Hypoglycemia?

Back 23

Beta-adrenergic blocking agents:

Beta blockers blocks beta receptors. The beta receptors responds to the body signals to do something. When it comes to the diabetic patient, we’re talking about the heart rate increasing. On the beta blocker, that heart can’t respond to the brain saying pump faster because we don’t have enough sugar and I would like you to circulate the blood faster because we need more sugar. if they are taking a beta blocker, they heart can’t do it because the receptors that should respond to the signal coming from the brain are blocked from the drug. They can’t respond. Instead of the patient respond and getting the heart rate of 120, which is increasing the circulation which increases glucose that is being produced in the liver . When you tell a patient to watch for the S&S of hypoglycemia and they are on these drugs, they won’t have a fast HR.
They still will get sweaty and shaky.

Front 24

Sulfonylureas drugs
-Glyburide & Glipizide

Lab monitoring

Back 24

Importance of follow-up, with kidney & liver function test, HgA1C, fasting glucose

Front 25

Biguanides - Metformin (Glucophage) one of the main meds for type ______

Back 25

2 diabetics.

Front 26

Biguanides
Metformin (Glucophage)

what is the action of this drug:

-increases the:
-where is it absorbed:
-what does it have nothing to do with:

Back 26

-Reduces glucose by decreasing production of glucose in the liver
-Suppression of glucogenesis (liver)

-Increase uptake of glucose by muscle than normally, and shuts liver down so it doesn’t keep producing glucose
-Absorbed in the small intestine
-Doesn’t do anything to pancreases

Front 27

Biguanides
Metformin (Glucophage)

what labs need to be monitored?

Back 27

bun and creat

>1.2 mg/dl increases the risk of lactic acidosis

Front 28

What is combined with the drug "Glucovance":

Back 28

Glyburide & Metformin


-less pills and better compliance

-it changes the structure of the cell so glucose can be uptaken and metaformin tells the liver that we'ren ot taking glucose from there

Front 29

Avandia (Rosiglitazone)

Mechanism of Action: (3)
Insulin:
Improves:
Decreases:

Back 29

-Insulin resistance inhibitor
-Improves target cell responses
-Decreases cellular insulin resistance

Insulin resistance inhibitors- going after cells that are resistant , mostly adipose tissue cells.

Front 30

Avandia (Rosiglitazone)

Uses:

Back 30

As an adjunct to diet and exercise in the treatment of type 2 diabetes

Front 31

Avandia (Rosiglitazone)

What disease process must this drug be used cautiously in?

Back 31

-Significant caution with patients with heart disease

-Increases potential for CHF

-Liver disease
-Renal impaired patient taking metformin
-Class II hypertension

Front 32

Avandia (Rosiglitazone)

If a pt had an MI, they have killed off cardiac tissue and they release enzymes in the blood steam.

When you kill off heart cells your killing off pump action of the heart. These drugs potentiate (cause to happen)............

Back 32

fluid retention. With the fluid retention you increase circulating blood volume, you get hypertension, you increase the pressure that’s occurring against the left ventricle.


You have an injured heart. The heart can’t accommodate these changes and it has to work harder. Working harder doesn’t happen, the fluid accumulates backs up in the lungs and you get a separation of fluids and you get water = Congestive Heart Failure

Front 33

Avandia (Rosiglitazone)

Side affect:

Back 33

is fluid retention- it increases circulating volume which increases the work of the heart
= increase CHF

Front 34

Avandia (Rosiglitazone)

preganncy category?

Back 34

C

Front 35

Avandia (Rosiglitazone)

Interactions:
-Insulin, what does it increase their potential for?

Back 35

increase potential for edema which increases the potential for hypoglycemia

Front 36

Gestational Diabetes

In early pregnancy increased release of insulin may cause __________.

Back 36

hypoglycemia

Front 37

Gestational Diabetes

In late pregnancy, increased insulin resistance from estrogen, progesterone and hPL, do what?

Back 37

make more glucose available to the fetus.

Front 38

Gestational Diabetes

Women with the inability to increase their insulin production will become ___________

Back 38

hyperglycemic.

Front 39

Gestational Diabetes

Treatment:

Back 39

Monitored and controlled with diet and insulin.

If early in pregnancy, we want the women to exercise so it takes up the sugar/glucose

Front 40

Gestational Diabetes

Drug of choice:

Back 40

Regular insulin

Typically women at not placed on oral agents even though some are category B

Front 41

Hypoglycemia

S&S
-what starts first?

Back 41

Blood sugar 70 or less

head ache, confusion, irritability, weak, faint feeling, warm flushed feeling

shaking and tremors, diaphoresis, tachycardia and palpitation,

Front 42

Hyperthyroidism
-who does it affect?
-common cause?
-what is it and what causes it

Back 42

-Usually seen in women 20-40
-Graves disease is most common cause

-Excessive thyroid hormone excretion
-Caused by autoimmune response

Front 43

Hyperthyroidism

S&S

Back 43

Everything speeds up

Metabolic rate goes through the roof (hot (why? Because your body is producing so much heat from your increased metabolism-

tremors, tachycardia, diarrhea, head aches, dysrhythmia, angina, nervousness, insomnia, rapid speech, heat intolerance, weight loss

Tachycardia can get so bad that it can affect oxygenation of the brain and people can pass out

Front 44

Hyperthyroidism

tell me about their TSH levels

Back 44

decrease TSH

Front 45

Propylthiouracil PTU

does it treat Hypothyroidism or Hyperthyroidism

Back 45

hyperthyroidism

Front 46

What is the usually time frame for suppressive treatment using PTU Propylthiouracil ??

Back 46

May take 6-12 mths to reach euthyroid state once we have the person there, we have to hold them there for 3-6 months before we go in and do whatever it is we’re going to do because this body has just been through a shock and we have to let the body recover

Front 47

How is radioactive Iodine used in the treatment of Hyperthyroidism

Back 47

Uptake of iodine absorbs itself in the thyroid gland (it doesn’t go anywhere else) The iodine does an uptake.

We give a little bit to evaluate the thyroid grand. Once we know what is there and if I choose to kill my thyroid gland then we get huge doses of radioactive iodine doses to kill it. (pills you swallow and then the iodine will diffuse through the body) but the only place it uptakes is at the thyroid drug. It burns the thyroid gland from the inside out and then it stops producing.

Front 48

radioactive Iodine and Hyperthyroidism

contraindications:

Back 48

When this is given, you can’t be pregnant (category x)you will destroy infants thyroid gland

Can’t pick up children for 3 days. Can’t hug anybody.
This is one way to treat graves disease. The other way is to surgically move it.

Front 49

radioactive Iodine and Hyperthyroidism

effects can take how long?

Back 49

Effects can take 2-3 mths or longer to know effects

Front 50

radioactive Iodine and Hyperthyroidism

what should you monitor?


patient care education:

Back 50

Monitor T4 & TSH, TSH levels should rise. It tells me that the gland is not producing it anymore.


-Limit contact with others to 30 min/day
-Push fluids
-Encourage frequent voiding to decrease irradiation to the Gonads

Front 51

What constitutes Hypothyroidism(S/S)

Back 51

everything slows down

weight gain,
constipation,
slow HR,
constantly tired
slow reflexes,
mentation changes
skin is dry,
hair is brittle

(weight gain, constipation, fatigue = top 3)

Front 52

What constitutes Hypothyroidism and TSH value

Back 52

Defined as increased TSH >5

*****New guidelines state treatment TSH >3*******

Front 53

Hypothyroidism

will they have an increase or decrease in levels of TSH

Back 53

increase

Front 54

Names of drugs used for thyroid replacement

Back 54

Levothyroxine
(Synthroid, Levothroid, Levoxyl)

Front 55

Thyroid replacement drugs

Levothyroxine
(Synthroid, Levothroid, Levoxyl)

Hypothyroidism or Hyperthyroidism?
what do they control:
what does it increase:

Back 55

Hypothyroidism

Controls protein synthesis;

increases metabolic rate;
cardiac output;
renal blood flow;
blood volume

O2 consumption;
body temperature

Front 56

What is the time frame for treatment of hypothyroidism

Back 56

-Medication will be life long
-Takes time to reach therapeutic levels (3-6mths) to see changes and we do this by blood monitoring

If your hypothyroid, its there for the rest of your life. You need to have supplement for the rest of your life.

Front 57

Levothyroxine (Synthroid, Levothroid, Levoxyl)

For hypothyroidism...
-Tell me about T4 and T3

Back 57

T4 is replaced with T3.
T3 is the (active hormone)

Front 58

Hyperthyroidism
What does T4 do?

If you have too much T4 or T3 you need something to inhibit it, like _____ or _________

Back 58

T4 stimulates metabolism.

PTU (Propylthiouracil)
Or Methimazole (tapazole)