Med Surg Exam 1 Review - Clinical Nursing - Diabetes PDF

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Exam 1 Blueprint Remember to concentrate on nursing management – what does the nurse need to do? How does the nurse assess? What are the clinical manifestations? How does the nurse know the patient has responded to treatment? Diabetes (15-21%)  Normal blood sugar range o Target BS = 65-99 mg/dl o Pre-diabetic = 100-125 mg/dl o DM = BS > 126 mg/dl  Type 1 and type 2 o Type I  Body produces 0 insulin  Pt will always be on insulin  **ONLY treatment = insulin** o Goal: maximize glycemic control to minimize complications  Usually diagnosed by age 30  Can be triggered by autoimmune response  Can develop after bad viral illness  Strong family history puts you at risk  Usually thin at diagnosis; recent weight loss  Often have islet cell antibodies  Often have antibodies to insulin even before insulin treatment  Little or no endogenous insulin  Need exogenous insulin to preserve life  Ketosis prone when insulin absent  Acute complication of hyperglycemia: DKA o Type II  Onset any age, usually >30 years  Usually obese at diagnosis  No islet cell antibodies  Decrease in endogenous insulin, or increased with insulin resistance  Most Pts control blood glucose through weight loss if obese  Ketosis uncommon, except in stress or infection  Acute complication: HHKNS (hyperglycemic hyperosmolar syndrome)  May be on insulin but usually starts with a hypoglycemic  83% of the population that has diabetes has Type II  Risk factors  Genetics, lifestyle (BMI >26), sedentary lifestyle, low HDL, high triglycerides, avg. age 50 yo, obese  S/S  3 P’s: polyuria, polydipsia, polyphagia o Polyuria (increased urination) secondary to increased glucose in urine so body is pouring out the urine o Polydipsia (increased thirst) due to increased output and fluid shift from intracellular to vascular space o Polyphagia (increased hunger) b/c of lack of insulin  causes cells to breakdown proteins and fats as sources of energy  causes starvation  leads to patient eating more but even though eat more, still have unintentional weight loss  FBS >126  Recurrent infections , poor wound healing, fatigue, visual disturbances, renal insufficiency o Symptoms of Diabetes  Always tired  Frequent urination  Sudden weight loss  Wounds that won’t heal  Sexual problems (ED)  Always hungry  Blurred vision

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 Numb or tingling hands or feet (neuropathy)  Vaginal infections (yeast) 2 hormones that tightly regulate glucose: o Glucagon and insulin  Both secreted by the pancreas Process of diabetes o Carbs eaten  arrive in GI system  converted & absorbed through GI tract o Glucagon stored in muscles of liver released through gluconeogenesis  glucose then travels through blood stream to targeted cells  B5 levels increase so beta cells of pancreas respond & release insulin  insulin transports glucose into cell membrane to its interior to be metabolized  this is what gives our body fuel Hypoglycemia o BS < 65 mg/dl o S/S  Change in mental status for *elderly*  Sweating  Shaking  Dizziness  Fast heartbeat  Impaired vision  Weakness  Fatigue  Pallor  Irritability  Hunger  Lack of coordination  Sleepiness  **Can lead to seizures and coma** o How can it happen?  Too much insulin circulating  Overly high dose of oral hypoglycemic  Diabetics who take their insulin but then don’t eat  Increased metabolism due to exercise  Alcohol can decrease glucose levels by blunting release of glucose by the liver o How is it managed?  If conscious: 15g of carbs: juice, soda, bread, crackers  If unconscious: D50 if IV access; IM glucagon if no IV access  Check BS again in 15 min Hyperglycemia o S/S  Dry mouth  Increased thirst  Headache  Weakness  Blurred vision  Frequent urination o Diabetic Ketoacidosis (DKA)  S/S  BS > 250 mg/dl  Positive ketones in urine  Positive anion gap  Arterial pH < 7.3  Serum HCO3 < 15  3 P’s  Pt becomes dehydrated which leads to an electrolyte problem/imbalance which could increase or decrease K+ depending on what’s going on  Fluid shifts that occur from ICF to ECF  leads to delusions & hyponatremia  Causes  Pathologic process = a deficit of insulin causes fat store to be used as an energy source

Untreated the glucose deficit in the cells causes fat store to break down to provide energy  increased ketones  ketones are acids  metabolic acidosis o DKA = metabolic acidosis  Missed dose of insulin  Inadequate dose due to increased insulin needs secondary to stress or infection  Patient is newly diagnosed with onset diabetes  Pt at risk for?  Hypovolemia secondary to osmotic diuresis  Hypotension & tachycardia secondary to volume loss  Treatment  Fluid replacement normal saline  High fluid volume  18 gauge IV to handle such high amounts  Cardiac monitor b/c K+ affected  Correct electrolyte imbalances  Give insulin o Regular via IV drip then switch to sliding scale  If not treated  Develops Kussmaul breathing (rapid, deep respirations) as a compensatory mechanism due to acidosis  trying to blow off O2  Acetone breath  N/V  Lethargy  Coma Hyperosmolar hyperglycemic non-ketosis state (HHNK)  Causes  Occurs when there is sufficient insulin to break down fats & ketones released BUT not enough insulin to prevent severe hyperglycemia  Pt comes in w/ BS over 600 & severely dehydrated w/ electrolyte imbalances  May also present with neuro complications  High blood sugar WITHOUT ketones  Less common than DKA but much higher mortality rate  Infection = most common trigger  Diagnosed  BS > 600 mg/dl  Serum osmolality > 320  Profound dehydration  Serum pH > 7.3  Serum HCO3 > 15  Altered LOC  Treatment  IV fluids to decrease BS  Correcting dehydration sometimes prevents need to give insulin o

o

TABLE 51-7 Comparison of Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome Characteristics

DKA

HHS

Patients most

Can occur in type 1 or type 2

Can occur in type 1 or type 2 diabetes; more

commonly affected Precipitating event

diabetes; more common in

common in type 2 diabetes, especially older

type 1 diabetes

patients with type 2 diabetes

Omission of insulin; physiologic

Physiologic stress (infection, surgery, stroke, MI)

stress (infection, surgery, stroke, MI) Onset

Rapid (250 mg/dL (>13.9

Usually >600 mg/dL (>33.3 mmol/L)

mmol/L)

TABLE 51-7 Comparison of Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome Characteristics

DKA

HHS

Arterial pH level

350 mOsm/L

Plasma bicarbonate

9lb o History of HTN o Women w/ polycystic ovarian disease Complications of diabetes (effects every organ) o Diabetic macrovascular complications result from changes in the M to L blood vessels.  blood vessels thicken, sclerose, and become occluded by plaque that adheres to the vessel walls  eventually blood flow is blocked  3 most common vascular diseases in diabetics: CAD, CVD, PVD o Retinal issues  diabetic retinopathy o Skin infections; wounds that won’t heal o Neuropathy o Poor circulation related to vascular disease  can lead to foot amputations o Kidney disease  dialysis o Heart failure  MI twice as common in men w/ diabetes and 3x as common in women  Typical ischemic symptoms may be absent in diabetics secondary to autonomic neuropathy  “Silent MI”  only diagnosed on ECG o Liver disease o Periodontal disease

TABLE 51-8 Ocular Complications of Diabetes Eye Disorder

Characteristics

Retinopathy

Damage to the small blood vessels that nourish the retina.

Background

Early-stage, asymptomatic retinopathy. Blood vessels within the retina develop microaneurysms that leak fluid, causing swelling and forming deposits (exudates). In some cases, macular edema causes distorted vision.

Preproliferative

Represents increased destruction of retinal blood vessels.

Proliferative

Abnormal growth of new blood vessels on the retina. New vessels rupture, bleeding into the vitreous and blocking light. Ruptured blood vessels in the vitreous form scar tissue, which can pull on and detach the retina.

Cataracts

Opacity of the lens of the eye; cataracts occur at an earlier age in patients with diabetes.

Lens Changes

The lens of the eye can swell when blood glucose levels are elevated. For some patients, visual changes related to lens swelling may be the first symptoms of diabetes. It may take up to 2 months of improved blood glucose control before hyperglycemic swelling subsides and vision stabilizes. Therefore, patients are advised not to change eyeglass prescriptions during the 2 months after discovery of hyperglycemia.

Extraocular Muscle Palsy

This may occur as a result of diabetic neuropathy. The involvement of various cranial nerves responsible for ocular movements may lead to double vision. This usually resolves spontaneously.

Glaucoma

Results from occlusion of the outflow channels by new blood vessels. Glaucoma may occur with slightly higher frequency in the diabetic population.

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Medications o Insulins – know onset action, peak of each of the insulins.  Peak = greatest risk of hypoglycemia  Give snack at peak time  Rapid  Lispro (Humalog); aspart (NovoLog); glulisine (Apidra)  Onset: 15 min  Peak: 60 min  Duration: 2-4 hrs  Indications: used for rapid reduction of glucose level, to treat postprandial hyperglycemia, and/or to prevent nocturnal hypoglycemia  Short  Regular (Humulin R, Novolin R, Iletin II Regular)  Onset: 30-60 min  Peak: 2-3 hrs  Duration: 4-6 hrs  Indications: usually given 20-30 min before a meal; may be taken alone or in combination with longer-acting insulin  Intermediate  NPH (Humulin N, Iletin II Lente, Iletin II NPH, Novolin N (NPH))  Onset: 2-4 hrs  Peak: 4-12 hrs  Duration: 16-20 hrs  Indications: usually taken after food  Long  Gargine (Lantus); detemir (Levemir); glargine (Toujeo)  Onset: 1-6 hrs

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 Peak: continuous, no peak  Duration: 24-36 hrs  Indications: used for basal dose Oral hypoglycemic = decrease amount of circulating glucose

TABLE 51-6 Selected Oral Antidiabetic Agents Generic (Trade)

Action/Indications

Side Effects

Implications

Name Second-Generation Sulfonylureas glipizide

Hypoglycemia

Monitor patient for hypoglycemia.

(Glucotrol,

pancreas to secrete

Mild GI symptoms

Monitor blood glucose and urine

Glucotrol

insulin; may improve

Weight gain

ketone levels to assess

XL)

binding between insulin

Drug–drug interactions

effectiveness of therapy.

glyburide

Stimulate beta cells of the

and insulin receptors or

(NSAIDs, warfarin,

(Micronase,

increase the number of

sulfonamides)

Glynase,

insulin receptors

DiaBeta) glimepiride (Amaryl)

Patients at high risk for hypoglycemia: advanced age, renal insufficiency. When taken with beta-adrenergic

Used in type 2 diabetes to control blood glucose

blocking agents, may mask

levels

usual warning signs and symptoms of hypoglycemia.

Have more potent effects

Instruct patients to avoid the use of

than first-generation

alcohol.

sulfonylureas

Contraindicated with sulfa allergy.

May be used in combination with metformin or insulin to improve glucose control Biguanides metformin (Glucophag e, Glucophage XL, Fortamet) metformin with

Inhibit production of glucose by the liver Increase body tissue sensitivity to insulin Decrease hepatic synthesis of cholesterol Used in type 2 diabetes to

glyburide

control blood glucose

(Glucovance

levels

)

Lactic acidosis Hypoglycemia if metformin

Monitor for lactic acidosis and hypoglycemia.

is used in combination

Monitor kidney function.

with insulin or other

Patients taking metformin are at

antidiabetic agents

increased risk for acute kidney

Drug–drug interaction

injury and lactic acidosis with

GI disturbances

the use of iodinated contrast

Contraindicated in patients

material for diagnostic studies;

with impaired kidney or

metformin should be stopped

liver function,

48 hours prior to and for 48

respiratory

hours after the use of contrast

insufficiency, severe

agent or until kidney function is

infection, or alcohol abuse

evaluated and normal. Check for interactions with other medications.

Alpha-

TABLE 51-6 Selected Oral Antidiabetic Agents Generic (Trade)

Action/Indications

Side Effects

Implications

Delay absorption of

Hypoglycemia (risk

Must be taken with first bite of food

Name Glucosidase Inhibitors acarbose (Precose) miglitol (Glyset)

complex carbohydrates

increased if used with

in the intestine and

insulin or other

slow entry of glucose

antidiabetic agents)

into systemic circulation Do not increase insulin secretion Used in type 2 diabetes to

GI side effects (abdominal discomfort or distention, diarrhea, flatulence) Drug–drug interactions

to be effective Monitor for GI side effects (diarrhea, abdominal distention). Monitor for blood glucose levels to assess effectiveness of therapy. Monitor liver function studies every 3 months for 1 year, then

control blood glucose

periodically.

levels

Contraindicated in patients with GI

Can be used alone or in

or kidney dysfunction, or

combination with

cirrhosis

sulfonylureas,

Alert: Hypoglycemia must be

metformin, or insulin to improve glucose

treated with glucose, not

control

sucrose.

Non-Sulfonylurea Insulin Secretagogues repaglinide (Prandin) categorized

Stimulate pancreas to secrete insulin Used in type 2 diabetes to

as a

control blood glucose

meglitinide

levels

nateglinide

Can be used alone or in

Hypoglycemia/weight gain

Monitor blood glucose levels to

less likely than

assess effectiveness of

sulfonylureas

therapy.

Drug–drug interactions

Has rapid action and short half-life

(with ketoconazole

Should be taken only if able to eat

[Nizoral], fluconazole

(Starlix)

combination with

[Diflucan], erythromycin

categorized

metformin or

[E-Mycin], rifampin

as a d-

thiazolidinediones to

[Rifadin], isoniazid

phenylalanin

improve glucose

[INH])

e derivative

control

a meal immediately Educate patients about symptoms of hypoglycemia. Monitor patients with impaired liver function and renal impairment. Has no effect on plasma lipids Is taken before each meal Check for interactions with other medications.

Thiazolidinediones (or Glitazones) pioglitazone (Actos) rosiglitazone (Avandia)

Sensitize body tissue to

Hypoglycemia (risk

Monitor blood glucose levels to

insulin; stimulate

increased with the use

assess effectiveness of

insulin receptor sites to

of insulin or other

therapy.

lower blood glucose

antidiabetic agents)

Monitor liver function tests.

TABLE 51-6 Selected Oral Antidiabetic Agents Generic (Trade)

Action/Indications

Side Effects

Implications

and improve action of

Anemia

Arrange dietary education to

insulin

Weight gain, edema

Name

May be used alone or in

Decrease effectiveness of

combination with

oral contraceptives

establish weight control program. Instruct patient taking oral

sulfonylurea,

Possible liver dysfunction

contraceptives about increased

metformin, or insulin

Drug–drug interactions

risk of pregnancy.

Hyperlipidemia (has variable effect on lipids; pioglitazone may be preferred choice in patients with lipid abnormalities) Impaired platelet function Dipeptidyl Peptidase-4 (DPP-4) Inhibitors sitagliptin (Januvia) vildagliptin

Increase and prolong the action of incretin, a

Upper respiratory infection

Usually given once a day

Stuffy or runny nose and

Used alone or with other oral

sore throat

hormone that increases insulin

Headache

saxagliptin

release and decreases

Stomach discomfort and

(Onglyza)

glucagon levels, with

linaglipitin

the result of improved

(Tradjenta)

glucose control

(Galvus)

diarrhea Hypoglycemia, if used with sulfonylurea

antidiabetic agents Instruct patient about signs and symptoms of hypoglycemia and other adverse effects to report. Monitor kidney function.

alogliptin (Nesina) Glucagon-like peptide-1 agonist (GLP-1) liraglutide (Victoza) dulaglutide (Trulicity)

Enhances glucose-

Pancreatitis, weight loss,

Given once a day by

dependent insulin

diarrhea, nausea,

subcutaneous injection. For

secretion and exhibit

vomiting, reaction at

patients with type 2 diabetes

other

injection site, cough

(not indicated for type 1

antihyperglycemic

diabetes)

actions following their release into the circulation from the gastrointestinal tract. Sodium-glucose co-transporter 2 (SGL-2) Inhibitors dapagliflozin

For type 2 diabetes only.

(Forxiga)

Prevents the kidneys from

anagliflozin

reabsorbing glucose

Urinary tract infections Hypoglycemia May increase LDL and HDL

Improves glycemic control in patients with type 2 diabetes.

TABLE 51-6 Selected Oral Antidiabetic Agents Generic (Trade)

Action/Indications

Side Effects

Implications

Name (Invokana)

back into the blood,

empagliflozin

therefore lowering

(Jardiance)

glucose by releasing

cholesterol

glucose into the urine 

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Metformin is most common (most prescribed)  Must take every day  Still need to check BS regularly while on this  Needs to be help before surgery, especially if going to have some kind of diagnostic (check w dr first)