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Exam Part II
Exam Part II
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 breakdown produce 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)
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
Meglitinides
Work quickly
Repaglinide
of insulin
(Prandin)
Nateglinide (Starlix)
Sulfonylureas
Glipizide (Glucotrol)
Glimepiride
(Amaryl)
Work quickly
Glyburide (DiaBeta,
Glynase)
Dipeptidy peptidase-4
(DPP-4) inhibitors
Saxagliptin
release of glucose
headache; inflammation of
(Onglyza)
Sitagliptin (Januvia)
Linagliptin
(Tradjenta)
Biguanides
Metformin
(Fortamet,
liver; improve
decline in low-density
Glucophage, others)
sensitivity to insulin
lipoprotein (LDL), or
"bad," cholesterol
Thiazolidinediones
Improve sensitivity to
Rosiglitazone
high-density lipoprotein
(Avandia)
release of glucose
(HDL), or "good,"
Pioglitazone (Actos)
cholesterol
Alpha-glucosidase
inhibitors
Acarbose (Precose)
Miglitol (Glyset)
sugars
Injectable medications
Medications
Action
Advantages
Amylin mimetics
Hypoglycemia; nausea or
Pramlintide
(Symlin)
insulin injections
weight loss
site
Incretin mimetics
Nausea or vomiting;
Exenatide (Byetta)
Liraglutide (Victoza)
metformin and
weight loss
damage or failure
sulfonylurea
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,
resistance
losing
weight
decreases
insulin
Blood sugar control = 70-140 mg/dl. The ADA recommends keeping blood sugar
as close to 110 as possible.
Hemoglobin A1C expressed as a %, reflects the average blood glucose over the
past 3 months.
ADA now recommends that A1C be used to diagnose type 2 and screen for
prediabetes. Normal Hemoglobin A1C =5%.5.7-6.4 pre-diabetic. < 7.0 is the
target for a diabetic..
A1c (%)
6
7
8
9
10
Blood glucose
(mg/dL)
126
154
183
212
240
Thiazolidinediones TZDs glitazonesmechanism of action-decreases insulin resistance at the cell level. May cause
fluid retention, use caution with history of CHF.
*rosiglitazone(avandia)-liver function tests required!
pioglitazone(Actos)
BLACK BOX WARNING for Avandia increased risk of heart disease and
stroke. May cause fluid retention/edema, therefore contraindicated in pts. with
CHF.
September, 2010 FDA advised people to stop taking unless they were not able
to lower blood sugar with any other treatment.
In Europe, the FDA equivalent has stopped the use of this drug. (European
Medicines Agency)
Evidence- based Recommendation: TZDs ( avandia and actos) are NOT firstline options. Metformin is first line recommendation.
Combination Drugs
*Glucovance-Glyburide/metformin-sulfonylurea + biguanide
*Avandamet-rosiglitazone/metformin TZD + biguanide
Types of Insulin
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
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 DECREASE
hypoglycemia
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
pH
Blood gases
I.
Physiological controls
A. Chemical buffer systems in ICF and ECF
1.
Bicarbonate-carbonic acid
a.
Ratio of bicarb to carbonic acid is 20:1
b.
Responsible for 45% of all H+ buffering
2.
Inorganic phosphates
3.
Plasma proteins
4.
Intracellular buffers - proteins, organic & inorganic phosphates
5.
RBC buffers - hemoglobin
B.
Respiratory - removal of CO2
1.
PaCO2 is an acid, serum CO2 is a base
2.
Rise in PaCO2 is powerful stimulus for increased respirations tidal volume & rate
3.
Consistent PaCO2 > 50 mm Hg desensitizes the respiratory center
4.
Compensation
a.
metabolic acidosis - increased respirations
b.
metabolic alkalosis - decreased respirations
c.
respiratory compensation has limits
C.
II.
III.
Renal regulation
1.
Bicarbonate is reabsorbed from kidney tubules. Kidney
manufactures bicarbonate
2.
Hydrogen ion - excreted during acidosis and retained during
alkalosis
3.
Kidneys can compensate for respiratory imbalances over a period
of days
Tests to measure acid-base
A. Anion gap Na+ - (CL- + HCO2) = 12 -15 mEq/L
1.
Determines if metabolic acidosis is from excessive acid or loss of
bicarbonate
B.
pH - reflects H+ concentration
C.
Total serum CO2 - indirect measure of bicarbonate
1.
Increased in metabolic acidosis
2.
Decreased in metabolic alkalosis
3.
Total CO2 is 95% HCO3 and 5% CO2 gas and H2CO3
D. Blood gases
1.
Normal values
a.
pH 7.35-7.45 (usually fatal if < 6.8 or > 7.6)
b.
PaCO2 35-45 mm Hg
c.
PaO2 80-100 mm Hg
d.
HCO3 22-26 mEq/L
e.
O2 saturation (SaO2) 95-100% - Oxyhemoglobin
dissociation curve
f.
Base excess/deficit -2 to +2 mEq/L
g.
O2 content - 15-23 vol% - measurement of total O2 in
blood, including that bound to Hgb and free dissolved in
plasma)
2.
Pediatric procedures
a.
Transcutaneous pO2 monitoring - 50-100 mm Hg
i.
special heated electrode placed on head, chest or
thigh
ii. warmth causes O2 to diffuse out of capillaries
iii. electrode measures O2 at skin surface
iv.
proportional to capillary O2
b.
Fetal scalp vein pH 7.25-7.40
i.
Helps determine if cesarean section is needed
How to analyze ABGs
A. Determine if acidosis or alkalosis by looking at pH
B.
Determine the primary disturbance
1.
Look at the HCO3 and CO2 - which one goes in the same direction
as the pH? If the CO2 is in the same direction, it is respiratory; if
the HCO3 is in the same direction, it is metabolic.
a.
CO2 > 40 = acidosis
b.
CO2 < 40 = alkalosis
c.
HCO3 > 24 = alkalosis
C.
d.
HCO3 < 24 = acidosis
e.
May have a combined cause
Compensation
1.
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. Compensation
may be partial or complete. Renal can completely compensate for
respiratory.