Adult Exam 2

NPH insulin

Humulin/Novolog; intermediate acting

onset: 2-4hr peak: 4-10hr duration: 10-16hr

can be used as a basal insulin (long acting, for type 1)

only basal insulin that can be mixed with short or rapid acting insulins

NPH and Aspart

compatible

Novolog should be drawn into the syringe first

the injection should be made immediately after mixing

NPH and Lispro

compatible

humalog should be drawn into the syringe first

injection should be made immediately after mixing

NPH and regular insulin

always draw the regular (clear) insulin into the syringe first

lispro

humalog; rapid acting insulin

want food tray within 30 minutes

MoA: rapidly increases peripheral glucose uptake and inhibit liver from changing glycogen to glucose

onset:15 min , peak: 60-90 min duration:3-4hr

can be used with intermediate or long-acting insulin (clear to cloudy)

regular insulin

short acting

onset: 30min to 1 hr; peak:60-90min; duration: 3-4hr

regular insulin exerts peak action in 2-3hrs

can be used with intermediate or long acting (clear to cloudy)

NPH/Reg mix 70/30

intermediate acting; insulin stimulates glucose uptake, inhibits hepatic glucose production

onset: 30-60min; peak: 2-12hrs; duration:24 hours

monitor BG q6hr, dosing should be done at same time every day

glargine (lantus)

long acting insulin

onset: 1-2hr; peak: none; duration: 24hrs

no peak means no high risk for hypoglycemia

determir

levemir; long acting insulin

onset: .8-4hrs; peak; no pronounced peak; duration: 16-24hrs

can be given twice daily

must not be diluted or mixed with other insulin/solution in the same syringe

glyburide

diabeta; sulfonylureas

take with meals

stimulates release from the pancreas and enhances cellular sensitivity to insulin

type 2 diabetes

ADR: weight gain, hypoglycemia

amitriptyline (elavil)

TCA antidepressant

used for diabetic neuropathy pain

helps closing nerve pathways

works by inhibiting reuptake of NE and serotonin (these NT play a role in transmission of pain throughout the spinal cord); SSRIs do the same purpose

metoclopramide (relgan)

antiemetic, dopamine antagonist

suppresses postop nausea

administered IVP over 2 minutes

can give undiluted

can have EPS and parkinsonian and dystonic side effects

insulin education

storage: do not heat/freeze

in-use vials may be let at room temperature up to 4 weeks

extra insulin should be refrigerated

avoid exposure to direct sunlight, extreme heat or cold

store prefilled syringes upright for 1 week if two insulin types (30 days for one)

insulin adminstration

inject at 90 degree angle, rotate injection

rapid/short acting insulin before meals

intermediate/long acting background insulin once or twice a day

monitor glucose every 4 hours and notify clinic if it continues to rise

signs of hyperglycemia

skin hot and dry, dehydration present, altered LOC, lethargic, stupor, coma with HHS, nausea, vomiting, abdominal cramps

signs of hypoglycemia

dizziness, cool and clammy skin, numbness, nervousness, tremors, mental confusion, faintness, vision changes, tachycardia, pallor

illness and diabetes

continue drug therapy and food intake

keep taking fluids (minimum 4oz/hr)

assess BG levels q1-2 hours

if on insulin, more may be needed

teaching: lantus/humalog and cold symptoms

develops a sore throat, cough and fever:

pt needs to monitor BG q4hr and notify doctor if it continues to rise

infection and other stressors increase BG and the pt will need to test BG frequently, treat elevations appropriately with insulin and call the HCP if glucose levels continue to be elevated

discontinuing glargine will contribute to hyperglycemia and may lead to DKA decreasing carbohydrate or caloric intake is not appropriate as the pt will need more calories when ill

diabetic ketoacidosis

acute complication associated with glucose in the blood and insufficient insulin

usually with type 1 DM

serious and rapid

DKA manifestations

kussmaul respirations

poor skin turgor

tachycardia

dry mucous membranes

thirst

soft and sunken eyes

sweet breathe

ketone in urine

DKA pathophysiology

cells are hungry and thirst due to lack of glucose in cells→ the body burns fat tissue for energy source, fatty acids are burned contributing to metabolic acidosis→ muscles try to help and burn proteins in muscles→ liver tries to make ketones to help, makes new glucose to help (goes directly to blood stream instead)→ kidneys increase urine output to try to get rid of glucose in blood, which gets rid of fluids and electrolytes→ respiratory system does kussmaul respirations, which are super deep and fast to get rid of Co2 to help reverse acidosis

hyperosmolar hyperglycemia syndrome

happens in patients that produce enough insulin to prevent DKA, but not enough to prevent hyperglycemia, osmotic diuresis (polyuria) and extracellular fluid depletion

\-lose mass amounts of electrolytes and fluids

\-usually start off as dehydrated

\-usually in patients >60yo with T2

\-glucose >600

\-marked increase in serum osmolarity

\-ketone bodies are both absent in blood and urine (different than DKA)

HHS manifestations

presents fewer earlier symptoms due to some pancreas unction

\-then all of a sudden very severe hyperglycemia

\-more severe neuro symptoms (somnolence, coma, seizures)

\-the hyperosmolarity calls for major fluid replacement

HHS treatments

immediate IV fluids of NS or 1/2NS first, then insulin, then switch to D5W when glucose levels around 250mg (to avoid hypoglycemia)

monitor airway!!

cardiac monitoring with DKA/HHS

vital signs: BP, P, R q15 min until stable, BP needs to come up

record F&E levels

Na, Cl, P, K after insulin given and urine output established

hypokalemia is a significant cause of mortality in the treatment of DKA (normally occurs when insulin is given too soon)

I/O be very careful

ECG reflects K levels and cardiac response

hypovolemic shock (check skin), tachycardia

priority for HHS/DKA

\-airway and breathing first

\-priority therapy: immediate IV fluids of NS→ insulin→ switch IV to D5W when glucose levels around 250mg (to avoid hypoglycemia)

\-insulin is carefully administered with fluid resuscitation or water and glucose will enter cell and can lead to depletion of vascular volume (hypovolemia)

\-regular insulin given IV to decrease glucose in blood and send it to the starving cell and thus ketones are decreased

DKA labs

glucose >250

ph

ketones

byproduct from fat breakdown

alters pH balance, causing metabolic acidosis

HHS labs

glucose >600

high BG levels increase serum osmolality and causes neuro symptoms (somnolence, coma, seizure, hemiparesis, aphasia, stroke)

type 1 diabetes

autoimmune

manifestations develop when pancreas can no longer produce insulin- then rapid onset with ketoacidosis

T1D symptoms

weight loss (rapid, unexplained), polydipsia, polyuria, polyphagia, weakness and fatigue

type 2 diabetes

nonspecific symptoms

fatigue, recurrent infection, recurrent vaginal yeast/candida infection, prolonged wound healing, visual changes, onset is gradual

prediabetes

blood glucose levels elevated but not high enough for diagnostic criteria for diabetes

increased risk for development of T2 diabetes defined as: impaired glucose intolerance (2hr oral glucose tolerance test 140-199) OR impaired fasting glucose (100-125)

asymptomatic but long term damage already occurring

foot and toe care

wash feat daily with mild soap and warm water, test water temp with elbow, pat feet dry (between toes), examine daily, no lotion between toes, apply foot powder on sweaty feet, no rubbing alcohol, iodine, or strong adhesives on cuts 

do not go to salons!! nurses are not allowed to cut nails

exercise and diabetes (education)

Minimum 150 minutes/week mod-intensity aerobic physical activity 

Resistance training three times/week if not contraindicated 

Monitor blood glucose before, during, & after exercise 

Exercise best one hour after meal. Glucose-lowering effect up to 48 hours after exercise 

Before exercise, if blood glucose is

fasting/nonfasting norms

prediabetes:

\-2 hr oral glucose test (140-199)

\-impaired fasting glucose (fasting glucose 100-125)

\
diabetes:

\-fasting glucose >126

\-two hour plasma glucose level >200

\-random plasma glucose level >200 with hyper/hypoglycemia symptoms

HgA1C

6\.5% or higher

neuropathy

distal symmetric, most common form affects hand and/or feel bilaterally

common cause of hospitalization with daibetes

difficult to heal, infection risk high

s/s: pain at rest, cold feet, loss of hair, delayed cap refill, dependent rubor (redness)

angiopathy

chronic hyperglycemia

damage to blood vessels

neuropathy

nerve damage, visual inspection, sensory examination, palpation

retinopathy

eye damage, dilated eye examination and fundus photography

get checked every 6 months because risk for detached retina

hypertensive retinopathy creates blockages in retinal blood vessels

can lead to optic disc edema and nerve edema (papilledema)

can cause sudden visual loss

nephropathy

kidney damage, urine for albuminuria, serum creatinine

peripheral neuropathies patho

persistent hyperglycemia leads to an accumulation of sorbitol and fructose in the nerves that causes damage, result is reduced nerve conduction and demyelination, ischemic damage by chronic hyperglycemia in blood vessels that supply the peripheral nerves

basal cell membrane thickens

autonomic retinopathy

can affect nearly all body systems

can cause hypoglycemic unawareness

\-ex: gastroparesis

thyroid function labs

TSH stimulation test: increase in TSH after TRH injection suggests hypothalamic dysfunction

no change after TRH injection suggests anterior pituitary dysfunction

levothyroxine (synthroid)

for hypothyroidism and myxedema (non-pitting)

monitor angina and cardiac dysrhythmias, thyroid hormone levels

given once a day, on an empty stomach

too much causes thyrotoxicosis

treatment is usually lifelong

thyrotoxicosis

tachycardia, angina, tremor, nervousness, insomnia, hyperthermia, heat intolerance, sweating, GI, diarrhea

propylthiouracil (PTU)

fastest

inhibits T4 synthesis

hyperthyroidism

prevents iodine binding

methimazole (tapazole)

watch for jaundice

used for hyperthyroidism

take same time every day, monitor T3, CBC (lowers PLT, WBC)

prevents iodine binding

radioactive iodine (RAI)

used to distinguish Grave’s disease from other forms of thyroiditis

pt with Grave’s shows a diffuse, homogenous uptake of 35-95% whereas pt with thyroiditis shows an uptake less than 2

takes 3 months, given in larger doses for thyroid cancer

need radiation precautions during 1st week, avoid children and pregnant women

SSKI solution

Lugol’s solution

decrease thyroid vascularity-short term, usually pre-op 1-2 weeks

grave’s disease

hyperthyroidism and thyrotoxicosis, autoimmune disease, marked by thyroid enlargement

more females, 30-50 years old

causes: toxic nodular goiter, thyroiditis, iodine excess, pituitary tumor, thyroid cancer

grave’s assessment

RAIU used to differentiate Grave’s from other forms of thyroiditis

do not palpate in hyperthyroid state (large thyroid can cut off airway)

grave’s interventions

antithyroid medications, radioactive iodine therapy, surgical intervention

\-watch for arrhythmias

\-IV fluids to replace fluid and electrolyte loss

\-encourage exercise to relieve nervous tension

\-support the head

\-good grooming to address self-esteem issues

\-STRIDOR is a STAT situation

\
manage respiratory distress, reducing fever, replacing fluid, and eliminating or managing initiating stressors

grave’s goals

goals of care: block adverse effects of excess thyroid hormone, suppress over secretion of thyroid hormone, prevent complications

grave’s eye care

exophthalmos (bulging eyes), acropachy (clubbing of the digits)

\-if exophthalmos is present-prevent dry eyes, keep head of bed elevated to reduce pressure, dark glasses and eye exercises

\-sometimes eyes taped shut with doctors order, avoid eye patches because may cause abrasions

meds and hypothyroidism

avoid amiodarone, lithium, and pain meds

can increase hypothyroidism risk

teaching and hypothyroidism

\-medication management

\-thyroid hormone therapy (need for lifelong therapy, taking thyroid hormone in the morning before food, need for regular follow-up care and monitoring of thyroid hormone levels)

\-caution pt not to switch brands of the hormone since the bioavailability of thyroid hormones may differ

\-emphasize the need for a comfortable, warm environment because of cold intolerance

\-teach ways to prevent skin breakdown, use soap sparingly and apply lotion to skin

\-caution the pt, especially if older, to avoid sedatives; if used, lowest dose, monitor mental status, LOC, respirations

\-discuss ways to minimize constipation

ways to minimize constipation

gradual increase in activity and exercise

increased fiber in diet

use of stool softeners

regular bowel elimination time

tell pt to avoid using enemas, cause vagal stimulation, can be hazardous if heart disease is present

myxedema coma

maintain a patent airway

\-determine intitial cause, usually from UTIs/infections

replace fluids with IV normal or hypertonic saline

give levothyroxine sodium IV as prescribed, give glucose IV as prescribed, give corticosteroids as prescribed

Check temperatures hourly, Monitor blood pressure hourly, cover with warm blankets (do not use heaters because of decreased sense or burning and vasodilation), monitor for changes in mental status, turn every 2 hours, institute aspiration precautions

post-thyroidectomy complications

Hypothyroidism 

Damage or inadvertent removal of parathyroid glands (tetany, low calcium) 

Hemorrhage 

Injury to laryngeal nerve (long term hoarseness) 

Thyrotoxic crisis 

Infection 

post-thyroidectomy care

Humidified O2, suction, and trach tray at bedside 

HOB elevated to semi-fowler's position 

Support head with pillows, avoid flexion of neck and any tension on suture lines 

Assess s/s hemorrhage or tracheal compression 

Irregular breathing, neck swelling, frequent swallowing, sensation of fullness at incision site, choking, and blood on anterior or posterior dressing 

Laryngeal stridor may occur d/t swelling or tetany (note early, respond STAT) 

MD might order IV calcium gluconate to avoid emergency. Long-term takes calcium p.o. 

Monitor vital signs. Check tetany (paresthesias) for 72h 

Control post-op pain 

carpal spasm

Trousseau’s sign

hypocalcemia

occurs with hypoparathyroidism, decreased PTH

encourage mobility to avoid bone calcification

hypoparathyroidism education

High-calcium diet: vitamin D, green leafy vegetables, soybeans, tofu 

postop care (inadvertent parathyroidectomy)

If day surgery: ambulate soon, go home same day, soft food next 

Teach: 

* Hoarseness, voice changes may persist, should not have difficulty breathing 
* Diet to avoid weight gain, balanced with exercise at home 
* Life long medication needs (contraindicated meds, timing of meds with meals) 
* Calcium p.o. 

AKA post-op goal

preserve greatest extremity length and function while removing all infection, pathologic or ischemic tissue, reach maximum rehab potential

AKA preop amputation

Teach patient about periop care, help pt and family understand that rehab can result in active, useful life, discuss reason for surg, impact of lifestyle

Teach upper body exercises to promote arm strength with BKA, prosthesis fitting may be immediate or delayed 

AKA teaching

avoid flexion contractures-patients should avoid sitting in a chair for more than 1 hour with hips flexed and having pillows under surgical extremity 

check circulation under dressing several times per day 

when lying in bed, make sure limbs are always straight!! 

Always lie on abdomen for 30 minutes 2-4 times a day to prevent hip contractures  

AKA hemorrhage

be alert, may see with immediate postop prosthesis application

Note drop in BP or urine output, increased HR< mental status change, skin cool and pale 

* Assess dressing and vital signs 


* Keep surgical tourniquet available 
* Notify surgeon immediately! Begin efforts to control hemorrhage 

phantom pain

may feel as if removed limb is still present after surgery (90% occurrence) Pain is real! Need management! Pain meds!! 

Teach about phantom pain/ sensation- may feel as if removed limb is still present after surgery (90% occurrence), may become chronic or subside Pain management, mirror therapy (reduces phantom pain by looking in mirror at moving arm, giving illusion that limb is moving) 

stump positioning/care

Need to protect skin!! 

Teach stump position, elevate first 24-48 hours after surgery, position to prevent hip or knee flexion contracture 

Avoid flexion contractures (hip flexion) 

Pt should avoid sitting in a chair for more than 1 hour with hips flexed or having pillows under surgical extremity 

Position hip in extension while prone Should lie on abdomen for 30 minutes 3-4x per day 

DO- keep limb flat, lie prone ( on stomach), equal weight on both hips while sitting 

DON'T- rest stump on crutch handles or arm of wheelchair, sit for long periods, now pillows under knees, no knee bending for prolonged periods 

Check circulation under dressing several times per day, begin active ROM of all joints ASAP post surgery 

atenolol (tenormin)

Cardioselective blocker 

Blocks beta-1 adrenergic receptors, reduces BP by doing so, decreases CO and reduce sympathetic vasoconstrictor tone, decreases renin secretion by kidneys 

Monitor pulse and BP regularly, use with caution in patients with diabetes because may depress the tachycardia associated with hypoglycemia and adversely affect glucose metabolism 

propranolol (inderal)

Blocks b1 and b2 adrenergic receptors, reduce BP by blocking b1 and b2 adrenergic effects 

Same as cardioselective, expect may cause bronchospasm, especially in patients with a history of asthma 

beta blocker and respiratory

Non-cardioselective blockers may cause bronchospasms 

Especially cautious with asthma 

HTN discontinued

sudden discontinuation may cause withdrawal syndrome, including rebound HTN, tachycardia, headache, tremors, apprehension, sweating

risk factors of HTN

blacks, hispanics (less likely to receive treatment), men (more common before middle age), women (increased with oral contraceptives; more common after menopause)

Age, alcohol use, tobacco use, diabetes, elevated serum lipids, excess dietary sodium, gender, family history, obesity, ethnicity, sedentary lifestyle, socioeconomic status, stress 

primary HTN risks

Altered endothelial function, increased SNS activity, increased Na intake, overproduction of Na retaining hormones, overweight, diabetes, tobacco, excess alcohol 

compliance with blood pressure meds

Cost of medications and unwanted side effects 

Measures to enhance compliance 

* Individualize plan 
* Active patient participation 
* Select affordable drugs 
* Involve caregivers 
* Combination drugs 
* Patient teaching 

hypertensive encephalopathy

A syndrome in which a sudden rise in BP is associated with a severe headache, nausea, vomiting, seizures, confusion, and coma 

Manifestations: result of increased cerebral capillary permeability, which can lead to cerebral edema and disruption in cerebral function 

secondary HTN

discover primary diagnosis 

Often present in patients with obstructive sleep apnea; cirrhosis, aortic problems, drug-related, endocrine, neurologic, or renal problems, pregnancy-induced, or sleep apnea 

hypertensive crisis

Rapid and severe elevation in BP in the absence of organ injury 

History of HTN, not adherent or undermedicated 

Causes: acute aortic dissection, exacerbation of chronic hypertension, head injury, monoamine oxidase inhibitors are taken with tyramine-containing foods, pheochromocytoma, preeclampsia, eclampsia, rebound hypertension, recreational drug use, renovascular hypertension 

* Cocaine, amphetamines, PCP, LCD, leads to seizures, stroke, MI, or encephalopathy 

hypertensive emergency

Organ injury!! 

SBP >180mmHg and/or DBP >120mmHg 

Target organ damage 

Requires hospitalization 

Very severe problems can result if prompt recognition and treatment is not obtained 

* Encephalopathy, intracranial or subarachnoid hemorrhage, HF, MI, renal failure dissecting aortic aneurysm or retinopathy 

BUN and HTN

Hypertension is one of the leading causes of chronic kidney disease 

Some degree of renal disease is usually present even with mild hypertension 

Used to screen for renal involvement and provide baseline information about kidney function 

6-24

serum creatinine

Used to screen for renal involvement and provide baseline information about kidney function 

Clearance reflects the GFR; decreases in creatinine clearance indicate renal insufficiency 

male: 0.74-1.35; female: 0.59-1.04

target organ damage

Impairment of major body organs due to elevated blood pressure 

Increased creatinine, increased BUN 

 Target organ diseases occur most frequently in 

Heart 

* CAD, atherosclerosis 
* Left ventricular hypertrophy 
* Heart failure 

Brain: CVD 

* TIA/stroke, atherosclerosis 
* Hypertensive encephalopathy, changes in autoregulation 

PAD

thickening of artery wall, involves progressive narrowing and degeneration of arteries of upper and lower extremities, related to other cardiovascular disease, higher risk of mortality, CVD mortality, major coronary events and stroke 

* Risk factors: age, obesity, smoking, DM, hypertension, hyperlipidemia, family history 
* Atherosclerosis is leading cause in majority of cases 


* Assessment: past health history (diabetes, smoking, hypertension, hyperlipidemia, obesity, loss of hair on legs, decreased peripheral pulses, intermittent claudication, HISTORY AND PHYSICAL 
* Acute arterial ischemia: sudden interruption of arterial blood flow caused by embolism, thrombus-requires immediate intervention 

venous diseases

primarily effect lower extremities and are categorized as thrombus or chronic venous insufficiency 

* Lot of exudate (turns skin a bronzy color, RBCs stain the skin) 
* Treatment for venous ulcers is compression! 


* Never want to compress an arterial ulceration (bc it would cut off circulation and end up with amputation) 

arterial disease manifestations

rubor/pallor

skin is thin/dry, cool

no edema

ulcers drain minimally

nails are thick and brittle

weak pulse

paresthesia

venous disease manifestations

skin bronze-brown, thick, hard, warm

edema: engorged with sluggish blood flow, drainage moderate to large amount

painful (elevation relieves pain)

pulse: normal

PAD nursing care

* Diet (low fat, lots of fruits and veggies, grains) 
* Medications (blood pressure, cholesterol, statins) 
* Reduce CVD risk factors, smoking cessation, control diabetes and hypertension 
* Exercise!! Walking is most commonly prescribed 

ankle-brachial index

\#1 way to determine PVD: ankle-brachial index 

PAD screening tool that is done by using hand-held doppler 

ABI is calculated by dividing the ankle systolic BP by the higher of the left and right brachial SBPs 

post femoral-popliteal bypass graft surgery

Acute Intervention:   

* Frequent monitoring __after surgery__ 
* Administer IV fluids to keep the BP WNL, \[adequate\], to balance risk for occlusion with risk for stress on graft 
* Assess 6 P’s, distal to operative site __– initially hourly__ 

__NOTE:__ Make take several hours to see significant improvement. Time is needed for improvement after surgery. Assess patient’s baseline (pre-surgery) 6 P’s to determine improvement. May look discolored, cool. Check baseline!!!!! 

Position to avoid knee-flexion except with exercise 

Turn and position frequently 

six P’s

*Paresthesia*: numbness and tingling 

*Pain*: severe, unrelieved by pain relief measures  

*Poikilothermic* (adaptation of the limb to environmental temp – most often cool) 

*Pallor*: coolness and loss of normal color of extremity 

*Paralysis*: loss of function 

*Pulselessness*: diminished/absent peripheral pulses (capillary refill norm = < 2 seconds) 

post-op risks for abdominal aneurysm repair

EVAR is less invasive 

Most common complication is endoleak, seepage of blood back into old aneurysm 

Aneurysm growth above rupture, aortic dissection, bleeding, renal artery occlusion from stent migration, incisional infection 

Intraabdominal hypertension 

abdominal aortic aneurysm (triple A)

most common

They don’t know they have it, can palpate it during assessment 

Back pain, stomach pain 

If ruptured and bleeds into peritoneal, will bleed to death 

aneurysm assessment

Deep diffuse chest pain 

Signs of rupture: Diaphoresis, paleness, weakness, tachycardia, hypotension, abdominal/back/groin pain, flank ecchymosis (Grey Turner’s sign) or periumbilical pain; changes in level of consciousness, or a pulsatile abdominal mass (abdominal tenderness) 

History and physical exam 

Watch for signs of cardiac, pulmonary, cerebral, and lower extremity vascular problems 

Establish baseline data to compare postoperatively 

Provide emotional support and preop teaching 

Schedule preop visit to ICU if possible 

Post op routine: monitor graft, aseptic technique to change dressing 

Perform neurovascular checks every hour!! Check baseline data 

Infarct bowel; lack of bowel sounds, fever, abdominal distention, diarrhea, bloody stools 

Mark pulse locations with felt-tip pen; May need Doppler 

Note skin temperature & color, capillary refill time, sensation, & movement 

aneurysm guidelines

Goal: Prevent aneurysm rupture  

Correct any obstructions 

Small aneurysm (4 -5.4 cm) – conservative therapy (decrease lipids & b/p, stop smoking, surveillance every 6-12 mos). Use of statins, ACE inhibitors. Less than 4 cm-surveillance every 3 years.  

5\.5 cm or greater– surgical repair recommended (plus other considerations such as genetic disorder, expands rapidly, symptomatic, or risk for rupture high) 

aneurysm and BP

systolic: less than 120mmHg

diastolic: less than 80mmHg

TNM

T: tumor size and invasiveness

N: presence or absence of regional spread to the lymph nodes

M: metastasis to distant organ sites