Diabetes Mellitus Drugs

Diabetes Mellitus Drugs

Insulin is usually given subcutaneously, either by injections or by an insulin pump. Research of other routes of administration is underway. In acute-care settings, insulin may also be given intravenously. In general, there are three types of insulin, characterized by the rate which they are metabolized by the body.

Humalog or lispro 15-30 min. 30-90 min 3-5 hours Rapid-acting insulin covers insulin needs for meals eaten at the same time as the injection. This type of insulin is often used with longer-acting insulin.
Novolog or aspart 10-20 min. 40-50 min. 3-5 hours
Apidra or glulisine 20-30 min. 30-90 min. 1-2½ hours
Regular (R) humulin or novolin 30 min. -1 hour 2-5 hours 5-8 hours Short-acting insulin covers insulin needs for meals eaten within 30-60 minutes
Velosulin (for use in the insulin pump) 30 min.-1 hour 2-3 hours 2-3 hours
NPH (N) 1-2 hours 4-12 hours 18-24 hours Intermediate-acting insulin covers insulin needs for about half the day or overnight. This type of insulin is often combined with rapid- or short-acting insulin.
Long-acting insulin covers insulin needs for about one full day. This type of insulin is often combined, when needed, with rapid- or short-acting insulin.
Lantus (insulin glargine) 1-1½ hour No peak time; insulin is delivered at a steady level 20-24 hours
Levemir (insulin detemir) 1-2 hours 6-8 hours Up to 24 hours
Humulin 70/30 30 min. 2-4 hours 14-24 hours These products are generally taken two or three times a day before mealtime.
Novolin 70/30 30 min. 2-12 hours Up to 24 hours
Novolog 70/30 10-20 min. 1-4 hours Up to 24 hours
Humulin 50/50 30 min. 2-5 hours 18-24 hours
Humalog mix 75/25 15 min. 30 min.-2½ hours 16-20 hours
*Premixed insulins are a combination of specific proportions of intermediate-acting and short-acting insulin in one bottle or insulin pen (the numbers following the brand name indicate the percentage of each type of insulin).

Lab Values

Arterial blood gases – review;    Anion gap (review);    ANC calculator.
Albumin 3.2 – 5 g/dl
Alkaline phosphatase
(Adults: 25-60)
33 – 131 IU/L
                Adults > 61 yo: 51 – 153 IU/L
Ammonia 20 – 70 mcg/dl
Bilirubin, direct 0 – 0.3 mg/dl
Bilirubin, total 0.1 – 1.2 mg/dl
Arterial Venous
pH 7.35 – 7.45 7.32 – 7.42
pCO2 35 – 45 38 – 52
pO2 70 – 100 28 – 48
HCO3 19 – 25 19 – 25
O2 Sat % 90 – 95 40 – 70
BUN 7 – 20 mg/dl
Male Female
Hemoglobin (g/dl) 13.5 – 16.5 12.0 – 15.0
Hematocrit (%) 41 – 50 36 – 44
RBC’s ( x 106 /ml) 4.5 – 5.5 4.0 – 4.9
RDW (RBC distribution width) < 14.5
MCV 80 – 100
MCH 26 – 34
MCHC % 31 – 37
Platelet count 100,000 to 450,000
CK-BB 0%
CK-MB (cardiac) 0 – 3.9%
CK-MM 96 – 100%
Creatine phosphokinase (CPK) 8 – 150 IU/L
Creatinine (mg/dl) 0.5 – 1.4
Calcium 8.8 – 10.3 mg/dL
Calcium, ionized 2.24 – 2.46 meq/L
Chloride 95 – 107 mEq/L
Magnesium 1.6 – 2.4 mEq/L
Phosphate 2.5 – 4.5 mg/dL
Potassium 3.5 – 5.2 mEq/L
Sodium 135 – 147 mEq/L
Ferritin  (ng/ml) 13 – 300
Folate  (ng/dl) 3.6 – 20
Glucose, fasting  (mg/dl) 60 – 110
Glucose (2 hours postprandial)  (mg/dl) Up to 140
Hemoglobin A1c <6% of total Hb
AACE Guidelines (2011)
Hemoglobin A1c, % (as a screening test)
5.4 – Normal
5.5-6.4 – High risk/prediabetes; requires screening by glucose criteria
6.5 -Diabetes, confirmed by repeating the test on a different day
In general, therapy should target a A1C level of 6.5% or less for most nonpregnant adults.
Iron  (mcg/dl) 65 – 150
Lactic acid  (meq/L) 0.7 – 2.1
LDH (lactic dehydrogenase) 56 – 194 IU/L
Cholesterol, total < 200 mg/dl
HDL cholesterol  35 mg/dL.  Negative risk factor:   60 mg/dL
LDL cholesterol 65 – 180 mg/dl
Triglycerides Normal: < 150 mg/dL.
Borderline-high: 150 to 199 mg/dL
High: 200 to 499 mg/dL
Very High: >499 mg/dL
Osmolality 289 – 308 mOsm/kg
SGOT (AST) < 35 IU/L  (20-48)
Testosterone – total(serum) Male: 300 to 1000 ng/dL
Female: < 62 ng/dLALT:
14-15 yr: 33-585 ng/dL
16-17 yr: 185-886 ng/dL
18-39 yr: 400-1080 ng/dL
40-59 yr: 350-890 ng/dL
> 60 yr: 350-720 ng/dLTanner Stage IV: 165-854 ng/dL
Tanner Stage V: 194-783 ng/dL
Thyroid Function Testing

Thyroid Function Test Measurement Normal Range
Total T4 (TT4) bound and free T4 4.5 -11.5 ug/dL
Free T4 (FT4) free T4 0.8 -2.8 ng/dL
Free T4 Index (FT4I) estimate of free T4
FT4I = TT4 x RT3U
1.0 -4.3 U
Total T3 (TT3) bound and free T3 75 -200 ng/dL
Resin T3 Uptake (RT3U) binding capacity of TBG 25 -35%
TRH TRH 5 -25 mIu/mL
TSH TSH 0.5 – 4.70 µIU/mLAmerican Association of Clinical Endocrinologists guidelines changed their normal range for TSH to
0.3 – 3.04 mIU/L.
Thyroglobulin Thyroglobulin 5-25 ng/mL
Radioactive Iodine Uptake (RAIU) Distribution of radiolabeled iodine in the thyroid 5 hr – 5 to 15%
24 hr – 15 to 35%

Free T4
 – much more useful then total T4 (e.g. interested in unbound or active form).  Total T4 not commonly measured. Greatly affected by TBG.  
Free T4 index
: indirect measure of free T4. Corrects for high/low values of TBG. 
Total T3
: not as useful as free T3, however, may be useful in locating problems with TBG, or if looking for problems with peripheral conversion of T4 to T3.  
Resin T3 Uptake
: if low, then TBG binding capacity is high. Opposite if high. 
: best measure to determine thyroid function.  
: nonspecific test that is elevated when the thyroid gland is inflamed or enlarged.

Free T3 2.3-4.2 pg/ml
Total iron binding capacity (TIBC) 250 – 420  mcg/dl
Transferrin > 200 mg/dl
Uric acid    (male) 2.0 – 8.0 mg/dl
                 (female) 2.0 – 7.5 mg/dl
WBC (cells/ml) 4,500 – 10,000
Segmented neutrophils 54 – 62%
Band forms 3 – 5%  (above 8% indicates left shift)
Basophils 0 – 1   (0 – 0.75%)
Eosinophils 0 – 3   (1 – 3%)
lymphocytes 24 – 44  (25 – 33%)
Monocytes 3 – 6   (3 – 7%)
(1) Segs and bands reported as a percentage:
WBC * ((segs / 100) + (bands / 100))(2) Segs and bands reported in total numbers:
WBC * (segs + bands)Neutrophils (aka polymorphonuclear cells, PMNs, granulocytes, segmented neutrophils,  or segs) fight against infection and represent a subset of the white blood count. Neutropenia by definition is an ANC below 1800/mm3 (some sources use a lower value).

Absolute neutrophil count (ANC) of 1000-1800:
Most patients will be given chemotherapy in this range.
Risk of infection is considered low.

Mild neutropenia – Absolute neutrophil count (ANC) of 500-1000:
Carries with it a moderate risk of infection.

Absolute neutrophil count (ANC) of less than 500
 neutropenia – high risk of infection. Remember that a reduced WBC is known as leukopenia.

The WBC consists of the following (differential):
Lymphocytes: 20-40%
Neutrophils: 50-60%
Basophils: 0.5-2%
Eosinophils: 1-4%
Monocytes: 2-9% (average: 4%).
ANC = Total WBC x (% “Segs” + % “Bands”)
Equivalent to: WBC x ((Segs/100) + (Bands/100))

The ANC refers to the total number of neutrophil granulocytes present in the blood.

Normal value:  1500 cells/mm3.
Mild neutropenia: 1000 – <1500/mm3.
Moderate neutropenia: 500 – <1000/mm3.
Severe neutropenia: < 500/mm3.

Laboratory Values


My Hurst Review Notes

Please explain how a HYPOTONIC solution is used for a client that has hypernatremia. Is it b/c the solution moves fluid out of the vascular space and thereby lowering the Na content?

Yes. Hypotonic solutions go into the vascular space and then shift out into the cells. They rehydrate, but do not cause hypertension. Also they are used for dilution when a client has hypernatremia, and for cellular rehydration.

why is hyperkalemia a sign and symptom of metabolic acidosis?

In metabolic acidosis the kidneys are sick and the lungs help correct the problem. The kidneys are not always the cause of metabolic acidosis. There is diabetic ketoacidosis, starvation, renal failure, and severe diarrhea which can also cause metabolic acidosis. Signs and symptoms depend on the cause of the metabolic acidosis. Additional signs and symptoms may include possible hyperkalemia. There can be a shifting of potassium from the intracellular spaces into the vascular spaces related to insulin deficiency or acute acidosis.

I just wanted to Clarify – when we say SEDATIVE regarding Mg & Ca, we are ONLY talking about the Muscles right? I was confused, because I assumed that this meant everything – therefore I thought that BP, RR, Pulse etc would drop w/ HYPO’s but it actually rises right?

We are talking about the patient’s entire body… so we are talking about LOC, RR, etc… Remember your patient is sedated when you have hypermagnesium and not sedated when you have hypomagnesium.

Why does hyperkalemia cause muscle twitching, then weakness, then paralysis? Why does hypokalemia cause muscle cramps and weakness?

Potassium is needed for skeletal and smooth muscle contraction, and nerve impulse conduction… so if you have too much or too little.. then your muscles will not work properly and the nerve impulses will not go to the muscle properly either.

I was refreshing my memory on cushings disease. I saw that cushings experience hyperglycemia, hypokalemia, and hypocalcemia. I understand the hyperglycemia, and hypokalemia but, why the hypocalcemia? thank you!

With Cushings you have too many of all steroids… steroids make you lose your calcium via the GI tract. 🙂

Please explain to me again how hyperventilation causes hypernatremia.

You are blowing off water vapor…so you would have too much Na left in the body and not enough water.

Can you go over how fluid volume affects the hemoglobin and hematocrit lab values?

Hemoglobin and hematocrit will go down if your patient is bleeding (loss of vascular volume) and up if your patient is dehydrated (blood is concentrated)

What is the treatment for mild fluid volume deficit?

PO fluids

Is chvostek and trousseau’s positive with calcium only or with magnesium as well? Thank you

Yes… anytime we have s/sx in the middle of the page etc.. then they go with both conditions.

In the patient with hyperkalemia, how exactly does calcium gluconate decrease arrythmias?

Calcium relaxes the muscles and the potassium will excite it and cause the arrhythmias… so that is why we would give Calcium gluconate.

Why does acidosis make you leak potassium out of your cells? And why does alkalosis make potassium go back into your cells?

Acidosis=hyperkalemia Acidosis makes K+ leak out of cell; to help maintain the neutral electrical charge because excessive H+ is moving into the cell, the K+ moves out Alkalosis=hypokalemia Alkalosis pushes K+ back into the cell; to help maintain the neutral electrical charge because excessive H+ is moving out of the cell, the K+ moves in.

In renal insufficiency, do you have metabolic acidosis because your kidneys are not working properly to excrete H+ ions? And to compensate, does your body make K+ go out of the cells and H+ to go in the cells in order to increase the pH?

If you have renal insufficiency.. you are retaining your potassium (b/c you excrete your potassium via your kidneys).. so your patient is hyperkalemia which equals acidosis.

Why does alkaseltzer/Antacids cause Metabolic Alkalosis?

Alkaseltzers and Antacids have a lot of base in them… that is why you take them for heart burn… you have an increase in the stomach acid with heart burn… so if you take too many then you will make the inside of your body more basic and there is nothing wrong with your lungs so it is metabolic.

Do the kidneys compensate slow or quickly?

Slowly.. it takes 3 days for the kidneys to compensate.

You said that you never start an antibiotic regime till the cultures are returned first, this is in any circumstance? But you sometimes will give a broad-spectrum antibiotic? Explain.

Ok… with this burn patient… they still need antibiotics in the time frame that it takes for the cultures to process etc… so we give them a broad spectrum antibiotic until we get the results of the cultures then we change the drug to one that is specific to the bacteria that is present in the patient’s body.

Why is vit c promoted in burn pt?

To help in the healing process.

When giving broad spectrum antibotics to the burn patient while waiting for the results of the culture (to give specific antibitics), wouldn’t the administation of broad spectrum antibitoics change the culture results?

No, you get the cultures first before giving the broad spectrum antibiotics.

With Burns I thought increased capillary permeability occurs. Why doesn’t potassium also leak out and cause hypokalemia instead of hyperkalemia? Thanks

Because the cells have lysed and the potassium has spilled out in the vascular space.

What is Tail of Spence?

Is part of the tissue of the breast which extends into the axilla (armpit).

What is the difference between respiratory depression and decreased respiratory rate?

Respiratory depression is less than 12 breaths per min. This patient will need to be intubated. Decreased RR is just less than their baseline but more than 12 breaths per min.

How should the pateint be positioned post thyroidectomy?

30 to 45 degrees

With an adrenal crisis will the pt be hypertensive or hypotensive?


Why is glucose not as readily absorbed by the intestines with a high fiber diet? So when the pt is hyperglycemic the sugar will not be absorbed as fast??

High fiber slows down glucose absorption in the intestines, therefore, eliminating the sharp rise/fall of the blood sugar

Does someone with Conn’s disease also lose potassium?

Conn’s syndrome= hyperaldosteronism so you retain too much sodium and water and will lose too much potassium.

Can you tell me, am I looking for hypoglycemia when the insulin peaks and why?

Yes, when the insulin peaks it has taken all the glucose back into the cell and the patient’s blood sugar is low and they need to eat.

Why does a patient present with a much higher blood sugar in HHNK then DKA since in type 2 the body makes at least some insulin?

It is a slower onset so as the blood sugar goes up and the client diureses they become hyperosmolar, this slow process, dehydration and delay in treatment can result in a blood sugar that can get really, really high.

A patient with DKA, the priority intervention would be to correct the acidosis by giving IV regular insulin. when giving IV regular insulin this will drive the BS down thus the cell will have energy instead of breaking down fats. is that correct?

By giving the insulin the glucose will be taken into the cell and will “feed” the cell so yes the cell will have the energy that it needs and will not need to break down the fat. If you don’t break down the fat then your patient will not become acidotic. The priority intervention is to fix the problem… get the blood sugar down… and that will fix the pH problem.

For DVT a treatment listed is use warm, moist heat to decrease inflammation…why would you not use ice/cool compress to decrease inflammation?

B/c that will promote vasoconstriction… and that will cause the blood to cause more irritation. It is the pooling of blood that is causing the irritation.

Why is coming out of REM sleep such a stressful time,so stressful that it causes MI in unstable angina pts?

It is not the fact that the patient is coming out of REM sleep… it is the dreams that the patient is having while in REM sleep that causes the stress on the body that can lead to an MI etc.

Is it correct that if you increase the afterload that the cardiac output would decrease?

yes… because the left side of the heart will have to work harder to push the blood forward… and it will decrease how much blood it can push out if the pressure/resistance is increased in the aorta (afterload)

What is the purpose of the Cardiac Catherization?

To visualize the coronary arteries and to see if there are any blockages

Could you explain how blood stasis and coagulation problem are the causes for DVT?

This means that the blood is staying in one place and pooling which will lead to thickened blood and it will cause clots to form.

What is the purpose of A-line? How can A-line help dx CHF?

An A-line gives you the patient’s BP continuously. You need to watch the patient’s BP since they will most likely be in a FVE and the increased BP will increase the workload on the heart.

A person who is in heart failure should be sat up in bed to decrease the workload of the heart, but what about reverse Trendelenburg to ensure the brain is perfused if the blood pressure has dropped? I am confused about when to sit them up in bed to decrease the workload of the heart and when to worry about perfusion to the brain.

When a person is in heart failure you put their HOB up to decreaes the amount of venous return therefore, it decreases the workload on the heart. Now, if you have someone who has a drop in BP due to a loss of volume then you put them in Trendelenburg to increase the venous return so the BP will increase.

When a person has DVT I do not understand when and when not to use SCD’s and TED hose, please explain.

You do not want to put the SCD hose or TED hose on the affected leg but you can put it on the unaffected leg.

If a patient has both arterial and venous insufficiency of an extremity, which would take priority treatment? I would assume arterial…

yes… since the arterial problem would effect the oxygenation of the patient.

Is the Troponin or CK-MB more helpful in determining a MI?

If you are only allowing me to pick one of those two, then I would pick troponin. Since it will only elevate if you have heart muscle damage.
What do we do if a patient becomes toxic on digoxin?

It depends on the cause. If an electrolyte is not within the normal range then it will be fixed. If the patient has an arrhythmia then it will be treated. Or the dose might be decreased. It depends on the patient.

How is BUN related to protein?

Protein breaks down to ammonia. If the liver is working properly, then the liver will convert the ammonia to urea. And if the kidneys are working properly, then the kidneys will excrete the urea. The by-product of turning the ammonia to urea is BUN.

In glomerulonephritis you said that the protein should decrease and in nephrotic patient protein should increase. How about in the patient with acute glomerulonephritis? What is the protein intake? Increase or decrease?


I thought that you would feel a bruit and hear a thrill?

You feel the thrill and hear the bruit.

Why do we restrict protein for patients with renal problems?

Remember, protein breaks down to ammonia then the liver converts it to urea. Then if the kidneys are working correctly, the kidneys will get rid of the urea. The by product of converting the ammonia to urea is BUN. So that is why we limit the protein in most kideny patients.

I would like to understand why dehydration causes a pulmonary embolism?

This can occur b/c the blood is concentrated when you are dehydrated and this could promote a clot forming. If the clot forms and then dislodges and goes to the lung… that is a PE.

If pulmonary embolism is suspected in a patient, is there a certain position you should turn the patient?

If your patient is having a hard time breathing, then you would want to sit them up. This is not to be confused when you get a air bubble in the heart… you would put this patient on their left side trendelenburg position.

Why does Hypoxia increase the workload on the right side of the heart?

Remember…that when you have hypoxia..you can also have pulmonary htn…which increases the workload on the right side of the heart since the right ventricle is not used to working hard to get blood to the lungs…so with the increase in the pressure in the lungs it increases the workload on the right side of the heart….which could lead to pure right sided heart failure.

Pneumothorax- what is Sub Q air and how do you know if you are feeling the Sub Q air?

The air is in the tissue under the skin. This can occur with a stabbing, gun shot wounds, other penetrations, or blunt trauma to your patient. Air can also be found in between skin layers on the arms and legs. Sub Q can often be seen as a smooth bulging of the skin. To know if your patient has Sub Q air, you wil need to palpate the area and it will feel like someone has put tiny tiny “packing bubbles” under the skin– (Packing bubbles: you know the packing bubbles that you would put around a plate or something if you have to ship it and it will protect it. The ones that everyone likes to play with and pop the bubbles). Also, your instructor most likely said it “feels like Rice Krispies sound”.

Clarify what trendelenburg and reverse trendelenburg positions are?

Trendelenburg position: A position in which the patient’s head is low and the body and legs are on an elevated and inclined plane. This may be accomplished by having the patient flat on a bed and elevating the foot of the bed. In this position, the abdominal organs are pushed up toward the chest by gravity. The foot of the bed may be elevated by resting it on blocks. This position is used in abdominal surgery. In treating shock, this position is usually used, but if there is an associated head injury, the head should not be kept lower than the trunk. Reverse Trendelenburg position: A position in which the patient’s feet are lower and the body and head are on an elevated and inclined plane. This may be accomplished by having the patient flat on a bed and elevating the head of the bed.

I understand the fact that a patient could be a diabetic for life because the pancreas is messed up, but I was just wondering, which type of diabetes would they have?

It depends on the extent of damage. If the pancreas is not working at all then it would be Type I. If it is making a little bit of insulin still it would be Type II.

Why would we give antacids for people with cirrhosis?

To decrease gastric distress and potential for GI bleeding.

I understand that liver people have ascites, but why does pancreatitis people have ascites, is it because the liver is involve?

This is because the digestive enzymes have gone into the blood and are eating holes in the vascular space. When you have holes in the vascular space then the volume will leak out resulting in ascites.

With cirrhosis we want to have a low protein diet, but their albumin is also very low. How does this imbalance get fixed?

You don’t want them to have a high diet in protein since it will break down into ammonia (protein breaks down to ammonia then the liver if it is working correctly will convert the ammonia to urea etc) and you don’t want them to have the regular daily allowance either since the ammonia will increase in their body but we don’t eliminate it from their diet since they do need it.

When irrigaing a patient with a colostomy do you place them on their right or left side or is there a certain position?

No, only when giving an enema because that is the natural flow of the GI tract and if you have a colostomy you don’t have the natural flow of the GI tract anymore.

Why does the patient with pancreatitis have bleeding problems? Is it because they may eventually have liver involvement?

Since the GI system is just one large system if the pancreas is sick then it could make the liver sick. So now I have to think about the job the liver conducts in the body and the number one thing is does is clot the blood. Since the pancreas is sick it has now affected the liver and the liver is sick.. so it is not able to do its job. Therefore the patient will not be able to clot their blood so the patient will be at risk for bleeding problems.

Why does the pulse pressure widen with an increased ICP?

Pulse pressure is the difference between systolic and diastolic blood pressures. Widening pulse pressure (the pulse pressure is greater than 50)also parallel rising ICP. Vital signs are a late sign of increased ICP. Cushing’s triad is the triad of hypertension, bradycardia and irregular respirations. It is sign of increased intracranial pressure. So you see you have an increase BP and a decrease in the HR.

Is there any other reason why it is important to check peripheral pulses before a cerebral angiography other than to determine if there is proper circulation to the extremities?

You always need to have a base line since this test is going through the femoral artery. I still want to make sure I am perfusing my leg.

Is the resulting headache from a lumbar puncture related to a drop in glucose from the loss of CSF?

It is from the loss of the CSF.

Why are chronic respiratory disorders (like COPD) not covered?

We prioritize information by looking at the practice statements released by the NCSBN (NCLEX Lady). These statement decide the content of the NCLEX. Remember, they are focused on safety, and safety issues are very prevalent in chest tubes and emergency treatment, not so much in the chronically ill patient. Also, there is so much information that could be covered we have to assume you have a knowledge base in common disorders like COPD, pneumonia, etc.

If you are walking with a patient would you walk beside, in front of, or behind the patient?


With a total hip replacement, are these patients suppose to remain flat in bed? Can we elevate the HOB at all since we are trying to avoid flexion at the hip?

First of all, you can’t leave your patient flat in the bed 24/7 because they could develop bed sores. You are able to elevate the HOB about 30 degrees but I would not put them up 90 degrees in the bed.

If a patient has injured their right leg and need to use a cane, would they hold the cane with their right or left hand?

You hold the cane in the strong hand.

Why does a patient with a stroke on the right side need to use a cane with the right hand?

Because that is the stronger side. With a right sided stroke the left side of the body will be affected.
What is prolapsed cord?

When the cord comes through the cervix first because the baby was not well engaged.

I do not understand why we place the patient in the supine position post-op after a VP insertion for hydrocephalus. Shouldn’t we raise the head of the bed to promote drainage of CSF?

The reason that we dont want to raise the head of the bed is because you don’t want to promote the drainage leaving the ventricle too fast (decreasing the ICP too fast)and because this could lead to the cerebral cortex pulling away from the dura causing the tiny vessles to rupture leading to a subdural hematoma.

What are the 3 C’s when studying tracheoesophageal fistula?

Coughing, choking and cyanosis especially with drinking.

Can an LVN start/insert an IV site on a patient’s peripheral vein? It this within the scope of practice for them, or do they need special certification from the hospital?

No, a LVN must have a special certification to be able to start IVs. So on the NCLEX you would not allow an LVN to start an IV.
I do not see any notes for Management and Delegation.

They are now included in the student manual for students attending the Live Review and are available for printing with the rest of the Online Review student notes.

Can a LPN discontinue an IV line?

Yes a LPN can discontinue an IV but a LPN just can’t start one.

Would you see a patient with a airway problem before a new admit patient? Because you said that a new admit is considered unstable and to stop whatever you are doing to go see the new admit. However, a person with a airway problem could be life threatening.

Yes, someone who is a new admit is unstable but with a priority question you go with the killer answer. And you also have to go by your ABCs.

Where are the PDF files located to print the notes on this section?

The notes are located under the 5th day bonus material listed as management and delegation.


  • Aspirin do not give together with other anticoagulants. Stop taking Aspirin some days before surgery. Do not give to children with viral infection(Reye syndrome)

NSAID’s e.g. Ibuprofen—Take with food; contraindicated for people with GI ulcers

  • Morphine: A respiratory depressant. It should be withheld if the respirations are below 10


  • Dilantin: Causes gum hyperplasia. Advice client to visit dentist frequently


  • Predisone: Causes Cushing like symptoms. Common side effects are immunosupression(monitor client for infection), hyperglycemia


  • Heparin: Monitor pt’s lab work-PTT. Antidote is protamine sulfate
  • Coumadin: Monitor pt’s lab work—PT. Antidote is Vitamin K


(8) Cogentin: Used to treat EPS

(9) Sinemet: Drug is effective when tremors are not observed


(10) Theophylline/Aminophylline: Side effects–Tachycardia


(11) Digoxin (Lanoxin): Signs of toxicity: Pt will complaint of visual change in colors. They would also complain of loss of appetite.


(12) Magnesium Sulfate: Monitor for deep tendon reflex and respiratory depression


(13) Hydrochlothiazide: Monitor potassium levels

(14) Lasix: Monitor potassium levels

(15) Aldactone: Potassium sparing


(16) Lithium Carbonate: Know therapeutic range (0.8 to 1.2mEq). Also know symptoms of toxicity. Adequate fluid and salt intake is important.

(17) MAOI inhibitors: Have dangerous food-drug interactions. Food with Tyramine should be avoided. For example: aged cheese, wine etc.

(18) Disulfiram (Antabuse): Used for alcohol aversion therapy. Clients started on Disulfiram must avoid any form of alcohol or they would develop a severe reaction. Teach pt to avoid some over-the-counter cough preparations, mouthwash etc.


(18) Oxytocin: Assess uterus frequently for tetanic contraction.


(19) Narcan: Reverses the effects of narcotics

(20) Calcium Gluconate: Antidote for magnesium sulfate

(21) Vitamin K: Antidote for Coumadin

Questions have been asked on NCLEX recently about the following drugs:

(22) Tegretol: side effects.

(23) Atropine: What checks do you do before giving this drug (BP.)

(24) Epogen: Used in treating anemia because it increases RBC production.

(25) Acyclovir: anti-viral medication used in treating shingles.


  • When a client is on antibiotics, teach the client to continue taking the medication even though they feel better
  • Monitor client taking antibiotics such as Vancomycin for ototoxicity. Pt will complain of tinnitus, room spinning (vertigo) and nausea.
  • Clients taking vasodilators e.g. Verapramil would complain of headache.


Hypertension on Diabetes Mellitus Patients


                        I decided to write on this topic because I am also curious of what is the pathophysiology of hypertension in the diabetic mellitus patients, however, before I can go any further, we need to define what hypertension is. According to authors,  Carie A. Braun and Cindy M. Anderson of the book this class is using entitled Pathophysiology, A Clinical Approach second edition  in page 373, “ hypertension is defined as a progressive cardiovascular syndrome detected by an elevation in blood pressure above 90 mm Hg or a diastolic pressure above 90 mm Hg or by the presence of organ damage due to persistent blood pressure elevations”. While Diabetes Mellitus is defined by the same authors in page 472 as, “a group of disorders, characterized by the inability to regulate the amount of glucose in the body, leading to inadequate metabolism of protein, fats and carbohydrates. The basic pathophysiology in various types of diabetes is further explained by the authors as:

1) A complete destruction of pancreatic beta cells leading to a lack of insulin secretion.

2) Reduced insulin secretion from impaired beta cell function in response to glucose stimulation.

3) A peripheral resistance to insulin.

 So what is the correlation of why patients who has Diabetes Mellitus almost all have hypertension and sometimes lead to their earlier death? My paper will try to delve on this topic.

Pathophysiology of Hypertension in Diabetes Mellitus Patients

As a nurse working in the field, I have had many patients who are Diabetics that also have uncontrollable hypertension. They are usually on medications such as Clonidine, Hydralazine, Norvasc, Lopressor to name a few. Why is this so? Well, the focus of the knowledge of my paper is our class book, Pathophysiology, A Clinical Approach second edition by authors Braun and Anderson. They said that there are chronic complications of Diabetes Mellitus, by having this disease it immediately increases your risk for developing irreversible clinical complications because of the degenerative changes throughout the body.  Chronic complications of diabetes develop primarily in tissues that are affected by the high levels of glucose circulating in the blood. In those tissues that require insulin for transport of glucose, hyperglycemia causes degenerative changes by thickening the basement membrane, promoting coagulation, obstructing perfusion inducing hypoxia and producing tissue necrosis. In those tissues that do not require insulin for glucose transport examples like red blood cells, lens, kidney and nerves, the excess glucose causes fluid to osmotically shift into these cells and causes the cells to rupture. Thus we have Microvascular (relating to small vessels), Macrovascular (relating to large vessels, Neuropathies. Even though, if an individual will keep its blood glucose levels in tight control around 70 to 120 mg/dl , they will less likely to develop these chronic complications.



Let us talk about the microvascular first, degenerative changes in small vessels most notably occur in the retinas, patients will develop retinopathy and in the kidneys, they are called nephropathy. With nephropathy, changes in the glomerular capillaries increase the intraglomerular pressure, causing hypertension within the kidney and it can be worsened in the presence of systemic hypertension. Chronic renal hypertension contributes to glomerular sclerosis, hypoxia and ultimately chronic renal failure. While macrovascular, it involves large vessels and include coronary artery disease, cerebrovascular disease (stroke) and peripheral vascular disease. Our book also mentioned than more than half of people with diabetes will die of heart disease or stroke: those with diabetes are two to four times more likely to have heart disease or suffer from a stroke than those without diabetes.

With all these complications of diabetes I talked about , the key prevention is a tight glycemic control. Also smoking cessation, management of hypertension, weight loss and lowering your lipids are some of the prevention strategies. Education on preventing complications can also be followed in alphabet.

A-    advice to follow diet, weight loss, exercise program and lifestyle modifications

B-    blood pressure reduction

C-    cholesterol reduction

D-    diabetes hyperglycemia control

E-     eye screening

F-     foot care




Braun, C.A., Anderson, C.M. Chronic Complications of Diabetes Mellitus. Page 481-482.

Pathophysiology: A Clinical Approach. 4th Edition.

Braun, C.A., Anderson, C.M. Hypertension. Pathophysiology. Page 373-374. Pathophysiology:

A Clinical Approach. 4th Edition.

Nursing Care Plan For Pain Medication

Scenario Case Study:

An 87-year-old man with history of Spinal Fusion, Benign prostatic hypertrophy, dementia, arthritis, Prostate cancer, Hypertension has recently been hospitalized. Patient said he always have pain in his back, Doctor ordered Morphine Sulfate 5 mg two times a day for recurrent pain in his back. He has allergies on Risperedal, Geodon, Phenothiazine. Patient has weakness in his lower extremities and has history of falls.


Nursing Diagnosis:


Desired Goal/Outcome:


Implementation/ Nursing Interventions/Teachings


Evaluation and Ongoing Assessment



Pt said he always have pain his back both upper and lower.

Alteration in comfort related to impaired mobility, arthritis and recurrent pain in his back.

Long term:

Client will identify specific pain level that will allow her to perform ADL’s, and pain will stay below the specific lever for remainder of cancer progression.


Prompt resident to notify staff upon onset of discomfort,


Vital signs  as needed,


Administer med as ordered by MD and monitor effectiveness,


Observe for nonverbal signs, diaphoresis, dilated pupils,


Provide alternative treatment e.i reposition, warm bath, elevation of limb, massage if not contraindicated, diversional activity of food/fluids, music, TV, wheel outside PRN.


 Note results and notify MD if no relief.

Cognitive-behavioral strategies can restore the client’s sense of self-control, personal efficacy, and active participation in his or her own care

Documentation of Pain mgt with Morphine should include the ff:


Pain scale used by the Pt.


The components, sensory and affective of pain


The amount of morphine, route and time each does is administered


The effectiveness of adjunct therapy and non-pharmalocologic interventions used


Any morphine –induced adverse effects


The pt should have adequate pain control with minimal adverse effects.



Temperature: 97.8, Respiration  :        20

BP               :    134/90


Patient always have frown in his face



Short Term:Client’s comfort level will increase within one day of hospital stay and client will be able to rest continuously for 7+ hours each night.


Teachings about Morphine Sulfate:

Adverse effect: Respiraty Depression, excessive sedation, hypotension, constipation, urinary retension and decreased urinary output, light headedness, dizziness and sedation, nausea and vomiting, prolonged used will produce physical dependence, teach patient after discharge on administration, adverse effects, avoidance of driving and other hazardous activities during drug therapy, avoidance of alcohol and concurrent CNS depressant therapy, unless a health care provider is managing the concurrent therapy, placement of drug securely away from children and anyone likely to abuse it.


Pain can reduce patient’s options to exercise control, diminish psychological well-being, and make them feel helpless and vulnerable. Therefore clinicians should encourage active client involvement in effective and practical methods to manage pain

Pt should remain from injury from orthostatic hypotension or sedation


Postoperative pain that morphine does not relieve may indicate post operative  complications, such as compartment syndrome


Increasing pain in a pt previously stabilized on a certain dose should not be automatically attributed to tolerance w/o investigating for evidence of disease progression or complications.


The pt and family should show an understanding of adverse effects if pt is discharged on morphine and should be able to describe how to manage those effects should they occur.


My LPN Valedictory Speech

Ladies and Gentlemen, Friends, family and educators welcome to this very memorable event.

To our most beloved teachers from whom our knowledge sprung and mould us to become future nurses. Thank you.

To my dear classmates, at last we have graduated! Our hard work has paid off!

It was the longest, the hardest and most enjoyable 15 months of togetherness, sacrifices and happiness.  I have never doubted our perseverance and our collective determination to forge into this “battle” starting from our Anatomy subject down to our last class of Maternity and Pediatrics. We have been built to move on dot com as our good professor Marc Pierre Loius puts it.

Lisa, Bren, Evelyn, Sharleen, Leo, Orianne, Margo, Gertrude, Rosenie, Jaqui, Yanic, Olga, Desmond, Cindy, Wilnive.. Finally, it is time to bid farewell to this chapter of our lives. And I am so excited to see you all soon in the nursing floor using our newly “acquired” Nursing Process and Critical thinking minds. Surely, this graduation is not the end my dear classmates, but this is a beginning of a beautiful journey towards the goals we have set to achieve in this path we called life. Plus, I have all your email addresses and I promise to those who will not reply to my digital correspondence to be immediately spam for all eternity. So please keep in touch and do not just poke me in facebook.

So what’s next for us? Exit exam? I can safely say that this is the first EXIT exam we shall be taking, for most of our professional student life; it has always been an ENTRANCE exam. Let us just hope that this Exit exam is much nicer than its sister, Entrance Exam. Then another relative of the exam family, NCLEX EXAM…I heard that this one is the Matriarch in the hierarchy of the EXAM Family. . What can I say? With all the nursing knowledge, our Professors pounded to our Hypothalamus. I am sure that our neurotransmitters will lead us to choose the right answers especially in the questions that are all select all that apply. J Therefore let us not forget to burn our midnight candles if we want NCLEX be inked in our resume.

From the sinoatrial node, atrioventricular node, to the bundle of his and purkinje fibers, my ever dearest classmates well done to all of us. to the facilitators of this glorious event,  the secretariat, the Master of ceremonies, our Director of Nursing Dr. Joemar Sales, Mr. Max Paul and Miss Ninnotte Paul, you made our QRS complex very stable indeed.

Again, Congratulations classmates for another milestone in our lives. May we continue to strive more for duty and excellence. I pray that the Lord almighty will continually bless the work of our hands, give us good health and strong mind to tackle the challenges ahead.

Gong xi ni men xie xie da jia! Maraming Salamat at Mabuhay! Merci Beaucoupe! Muchos Gracias! Spasiba! Thank you! And may God bless us all.