exam part ii

8/10/2019 Exam Part II

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Acute Complications of Diabetes Mellitus

Review insulin/Glucose Utilization

o Insulin moves glucose into cell

o If insulin not present cells deprived of glucose which is needed forenergy

o Without insulin, glucose levels in the blood begins to rise

o As cells are deprived of glucose, the liver produces glucagon

o Glucagon increases BG by breaking down stored glucose in the liver

(glycogenolysis)

o Eventually, non carbs (fats & proteins) are converted to glucose

(gluconeogenesis)

The Polys Polyuria: excessive urination (with glycosuria)

Polydipsia: excessive thirst (from dehydration and hyperglycemia)

Polyphagia: excessive hunger (from using non-CHO sources for energy)

Ketoacidosis

Without insulin, fat is used for energy (gluconeogenesis)

Ketones result from breakdown of fatty acids

3 specific ketone bodies are produced

o Acetone (fruity breath)

o B hydroxybutyrate

o Acetoacetate

Ketones & Acid Base Balance

As ketones breakdownproduce H+ ionsdrop in pH

Serum bicarbonate decreases in attempt to maintain pH

Result is severe metabolic acidosis

Ketoacidosis

As bicarbs decrease, breathing becomes deep and rapid (Kussmaul respirations) to

release acid in form of CO2

Acetone: doesnt cause acidosis (eliminated in lungs fruity breath) Ketones eliminated in urine:ketonuria

Ketones in blood: ketoneumia

Two major complications

DKA: Diabetic Ketoacidosis (Type 1 DM)

HHNS: Hyperglycemic hyperosmolar state (Type 2 DM)


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o Also called HHNKS: Hyperglycemic, hyperosmolar non-ketotic syndrome

Similarities:

o Both most often caused by infection/stress

o Both have elevated blood glucose

o Both present with dehydration, polyuria, polydipsia, and electrolyte loss

o Both have altered mental status Differences

DKA HHNS

BG >300 (300-800) BG >600 (600-2000)

Serum & urine ketones No ketones

Fruity acetone breath No fruity breath

Acidosis (pH


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Some protocols: Need K+ > 3.5 before giving initial insulin

bolus

Why? Usually pH corrects itself with adequate hydration

and insulin replacement

o Hyponatremia

Na loses from: Osmotic diuresis

Vomitting/diarrhea

Correct with infusion of 0.9 NaCl

- need to do all three of these simultanenously

Nursing Care

Monitor!

o Response to therapy

Fluid volume status: hourly urine output

Insulin levels: monitor BG hourly Electrolytes (Na & K)monitor hourly

Mental status & LOCsudden complaints of HA may signal

cerebral edema. Hyponatremia may cause mental status changes

Cardiac statuscontinous EKG monitoring because of K probs

Patient and Family Education

o Listen: to gain insight into possible cause of hyperglycemic episode

o Possible issues: cost/availability of meds, not able to recognize stress/

infection, drug holiday, knowledge deficit, apathy or memory probs

(older adults)

Diabetes oral meds all rely on the insulin the body makes (so they will not be useful in

patients with type 1 diabetes. Most of these meds can be used in combo with each

other and with insulin

Oral medications

Medications

Action

Advantages

Possible side effects

Meglitinides

Repaglinide

(Prandin)

Nateglinide (Starlix)

Stimulate the release

of insulin

Work quickly

Severely low blood sugar

(hypoglycemia); weight gain;

nausea; back pain; headache

Sulfonylureas

Glipizide (Glucotrol)

Glimepiride

(Amaryl)


of insulin

Work quickly

Hypoglycemia; weight gain;

nausea; skin rash


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Glyburide (DiaBeta,

Glynase)

Dipeptidy peptidase-4

(DPP-4) inhibitors

Saxagliptin

(Onglyza)

Sitagliptin (Januvia)

Linagliptin

(Tradjenta)


of insulin; inhibit the

release of glucose

from the liver

Don't cause weight gain

Upper respiratory tract

infection; sore throat;

headache; inflammation of

the pancreas (sitagliptin)

Biguanides

Metformin

(Fortamet,

Glucophage, others)

Inhibit the release of

glucose from the

liver; improve

sensitivity to insulin

May promote modest

weight loss and modest

decline in low-density

lipoprotein (LDL), or

"bad," cholesterol

Nausea; diarrhea; rarely, the

harmful buildup of lactic

acid (lactic acidosis)

Thiazolidinediones

Rosiglitazone

(Avandia)

Pioglitazone (Actos)

Improve sensitivity to

insulin; inhibit the

release of glucose

from the liver

May slightly increase

high-density lipoprotein

(HDL), or "good,"

cholesterol

Heart failure; heart attack;

stroke; liver disease

Alpha-glucosidase

inhibitors

Acarbose (Precose)

Miglitol (Glyset)

Slow the breakdown

of starches and some

sugars

Don't cause weight gain

Stomach pain; gas; diarrhea

Injectable medications

Medications

Action

Advantages

Possible side effects

Amylin mimetics

Pramlintide

(Symlin)


of insulin; used with

insulin injections

May suppress hunger;

may promote modest

weight loss

Hypoglycemia; nausea or

vomiting; headache; redness

and irritation at injection


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site

Incretin mimetics

Exenatide (Byetta)

Liraglutide (Victoza)


of insulin; used with

metformin and

sulfonylurea

May suppress hunger;

may promote modest

weight loss

Nausea or vomiting;

headache; dizziness; kidney

damage or failure

monitor lipid levels for avandiamust be cautious if pt has past history of

heart failure

alpha inhibitors- believed to help with weight loss, when person ingests a lot

of starches really helps in the breakdown

Drugs for Diabetes Mellitus

What is diabetes? Basically, a lack of insulin or ineffective use of insulin causingsugar to build up in the blood.


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Functions of Insulin:

Allows glucose into cells

Allows glucose to enter liver

Prevents fat breakdown

Stores excess calories as fat

Who gets diabetes?

Type I Diabetes

No insulin, must be given by injection, prefer use of SQ insulin pump

Ketone prone

Autoimmune disease

Type II Diabetes

Insulin resistance

Deficient insulin secretion Obesity contributes significantly, losing weight decreases insulin

resistance

Blood sugar control = 70-140 mg/dl. The ADA recommends keeping blood sugaras close to 110 as possible.Hemoglobin A1C expressed as a %, reflects the average blood glucose over thepast 3 months.

ADA now recommends that A1C be used to diagnose type 2 and screen forprediabetes. Normal Hemoglobin A1C =5%.5.7-6.4 pre-diabetic. < 7.0 is thetarget for a diabetic..

A1c (%) Blood glucose(mg/dL)

6 126

7 154

8 183

9 212

10 240

Complications of diabetes mellitus (DM):

Stroke

ESRD (end stage renal failure)

Heart disease

Diabetic Retinopathy, neuropathy

Foot/leg amputation


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Oral Agents for Diabetes

Sulfonylureas-increase insulin secretionmechanism of action-improves insulin production from functioning beta cellsnot a good agent to be used alone; hypoglycemia reaction

*Glyburide(micronase) should be taken with meals

*Glipizide (glucotrol) should be taken before meals end up gaining weight

Biguanides-decrease hepatic glucose production, will not cause hypoglycemiamechanism of action-while in a fasting state, will diminish overproduction ofglucose from the liver.

-only comes in certain dose ratios

*Metformin(glucophage, glucophage XR)-lactic acidosis serious side effectContraindicated with contrast dye - Must HOLD if IV contrast dye given. In orderto use dye must be greater than 1.5

Thiazolidinediones TZDs glitazones-mechanism of action-decreases insulin resistance at the cell level. May causefluid retention, use caution with history of CHF.*rosiglitazone(avandia)-liver function tests required!pioglitazone(Actos)

BLACK BOX WARNINGfor Avandiaincreased risk of heart disease andstroke. May cause fluid retention/edema, therefore contraindicated in pts. withCHF.September, 2010FDA advised people to stop taking unless they were not ableto lower blood sugar with any other treatment.In Europe, the FDA equivalent has stopped the use of this drug. (EuropeanMedicines Agency)

Evidence- based Recommendation: TZDs ( avandia and actos) are NOT first-line options. Metformin is first line recommendation.

Combination Drugs*Glucovance-Glyburide/metformin -sulfonylurea + biguanide

*Avandamet-rosiglitazone/metformin TZD + biguanide


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Types of Insulin

Short or Rapid ActingLispro (Humalog)- onset 15, peaks 30-1.5hrs.Aspart (Novolog)-onset 10, peaks 1-3 hrs.Regular (Humulin R, Novolin R, Regular Iletin II)-onset 30-1 hr, peaks 2-4hrs.

Intermediate- NPH, Lente

Long Acting-Glargine (Lantus)- peakless, duration 24 hrs.

Combo Mixtures-

Insulin Pumps -3X as many diabetics are now using insulin pumps. Type 1&2.Pumps use rapid acting insulinLispro (Humalog), Aspart (Novolog). 50%delivered at a continuous basal rate, the remaining ia given as a BOLUS atmeals or snacks. Pumps are not for everyone. They are ore expensive andrequire more training.Medicare and most insurers do cover pumps.

Euglycemic protocol- sliding scale insulin used for non-diabetic and diabeticpatients.

Protocol extended beyond the diabetic population If patients show very high blood sugars after surgery; due to stress

of surgery; used to help them recover quickly

Hypoglycemiarecognize signs/symptoms. Including: headache, confusion,blurred vision, fatigue, hunger, irritability, shakinessCauses- too much insulin, skipping meals, not eating food,Treat if blood glucose is < 60 mg/dl. 15 grams of a simple CHO (6 ounces of

juice or fruit juice; regular soda). If not able t o swallow safely1 mg. glucagonIM or 25 gms. 50% dextrose IV.-recheck in 15 minutes-If patient is not responding well and cannot swallowgive IM glucagon; thepatients families are given

Hyperglycemia-

As blood glucose increases, the blood (intravascular space)becomes more hyperosmolar


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Cellular dehydration occurs as the hyperosmolar intravascularspace draws fluid from the more dilute intracellular and interstitialspaces

Recognize signs and symptoms:o Polyuria, polydyspia, unexplained weight loss, sore that is

slow to heal (or doesnt heal) If doesnt get treated, very high blood sugars can cause disruption

in fluid and electrolyte; causing them to become comatpossiblyhave a seizure

Insulin Aspart

Adult, adolescents, child

Intermittent SQ or continuous SQ

Rapid Acting

Onset 10-20 mins

Duration 3-5 hours

2-4 inj daily just prior to meal

Intermittent SQ 50-70% of total daily insulin may be given Aspart; remainder should

be intermediate of long acting insulin

Continuous: external insulin pump via continuous SQ infusion insulin dose should be

based on previous regimen

Insulin Lispro

Adult, adolescence, child

SQ 15 min before meals

Continuous SQ infusion (external insulin pump)

With infusion total daily dose should be based on previous regimen

50% given at meal related boluses remainder in basal infusion

Rapid acting

Onset 15-30 mins

Peak 30 mins to 1.5 hours

Duration 3-5 hours

Insulin Glargine

Adult and child

SQ 10 international units/day

Range 2-10 international units/day Long acting

Onset 1.5 hours

No peak

Duration >24 hours

Regular Insulin


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Adult

IV 5-10 units/hr until desired response then switch to SQ

SQ 30 mins before meal

Short acting

Onset 30 mins

Peak 2.5-5 hours

Duration 7 hours

Whenregular insulin is administered IV monitor glucose, K+, often to prevent fatal

hypoglycemia, and hypokalemia

Side Effects: blurred vision, dry mouth, flushing, rash, swelling, redness, peripheral

edema, hypoglycemia, anaphylaxis

Interactions:

alcohol, beta blockers, anabolic steroids, MAOIs increase hypoglycemia

Thiazides, thyroid hormones, oral contraceptives, epinephrine DECREASEhypoglycemia

Decrease K+ and Ca+ lab values

Nursing Considerations

Assess urine ketones during illness; insulin requirement may increase during stress,

illness, and surgery

Assess hypoglycemic reaction that can occur during peak time (sweating, weakness,

dizziness, chills, confusion, headache, nausea, rapid weak pulse, fatigue, tachy

Assess hyperglycemia, acetone breath, polyuria, fatigue, polydipsia, flushed, dry

skin, lethargy

Arterial Blood Gases

pH 7.35-7.45

PaCO2 35-45 mmHg

HCO3 22-26 mEq/L

PaO2 80-100 mm/Hg

O2 sat >95-100%

If pH normal - fully compensated

If pH abnormal, but both systems moving in diff directions partial compensated

CO2 respiratory

HCO3

metabolic

ROMES (Respiratory opposite, metabolic equal)

pH


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o A measurement of the acidity or alkalinity in the blood

o Inversely proportional to the number of hydrogen ions (H+) in theblood

o The more H+ present, the lower the pH will be; the fewer the H+ thehigher the pH

Acidic state (below 7.35)o Changes in body function in this state

Decrease in force of cardiac contractions Decrease in vascular response to catecholamines

Diminished response to the effects and actions of certainmedications

Alkalotic state (above 7.45)

o Changes in body function in this state Interferes with tissue oxygenation and normal neurological

and muscular functioning

pH above 7.8 or below 6.8

o will interfere with cellular functioning and if uncorrected will lead todeath

Normal pH is maintained using delicate buffer mechanisms between therespiratory and renal systems

o Respiratory Buffer Responseo Renal Buffer Response

Blood pH decreases, the kidnets will compensate by retainingHCO3-

Rises, kidneys excrete HCO3- through the urine

Blood gases

I. Physiological controlsA. Chemical buffer systems in ICF and ECF

1. Bicarbonate-carbonic acida. Ratio of bicarb to carbonic acid is 20:1

b. Responsible for 45% of all H+ buffering2. Inorganic phosphates3. Plasma proteins4. Intracellular buffers - proteins, organic & inorganic phosphates5. RBC buffers - hemoglobin

B. Respiratory - removal of CO2

1. PaCO2is an acid, serum CO2is a base2. Rise in PaCO2is powerful stimulus for increased respirations -

tidal volume & rate3. Consistent PaCO2> 50 mm Hg desensitizes the respiratory center4. Compensation

a. metabolic acidosis - increased respirationsb. metabolic alkalosis - decreased respirationsc. respiratory compensation has limits


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C. Renal regulation1. Bicarbonate is reabsorbed from kidney tubules. Kidney

manufactures bicarbonate

2. Hydrogen ion - excreted during acidosis and retained duringalkalosis

3. Kidneys can compensate for respiratory imbalances over a periodof daysII. Tests to measure acid-base

A. Anion gap Na+- (CL-+ HCO2) = 12 -15 mEq/L1. Determines if metabolic acidosis is from excessive acid or loss of

bicarbonate

B. pH - reflects H+concentrationC. Total serum CO2- indirect measure of bicarbonate

1. Increased in metabolic acidosis2. Decreased in metabolic alkalosis3. Total CO2is 95% HCO3 and 5% CO2gas and H2CO3

D. Blood gases1. Normal valuesa. pH 7.35-7.45 (usually fatal if < 6.8 or > 7.6)

b. PaCO235-45 mm Hgc. PaO280-100 mm Hgd. HCO322-26 mEq/Le. O2saturation (SaO2) 95-100% - Oxyhemoglobin

dissociation curvef. Base excess/deficit -2 to +2 mEq/Lg. O2content - 15-23 vol% - measurement of total O2in

blood, including that bound to Hgb and free dissolved in

plasma)2. Pediatric procedures

a. Transcutaneous pO2monitoring - 50-100 mm Hgi. special heated electrode placed on head, chest or

thigh

ii. warmth causes O2to diffuse out of capillariesiii. electrode measures O2at skin surfaceiv. proportional to capillary O2

b. Fetal scalp vein pH 7.25-7.40i. Helps determine if cesarean section is needed

III. How to analyze ABGsA. Determine if acidosis or alkalosis by looking at pHB. Determine the primary disturbance

1. Look at the HCO3and CO2- which one goes in the same directionas the pH? If the CO2is in the same direction, it is respiratory; ifthe HCO3is in the same direction, it is metabolic.

a. CO2> 40 = acidosisb. CO2< 40 = alkalosisc. HCO3> 24 = alkalosis


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d. HCO3< 24 = acidosise. May have a combined cause

C. Compensation1. Look at the value that is not the same as primary cause. If it is

going in the opposite direction (alkalosis or acidosis) as the

primary problem, then compensation is occurring. Compensationmay be partial or complete. Renal can completely compensate forrespiratory.

exam part ii

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