Exam 2 Flashcards
What is BPH?
BPH = Benign Prostatic Hyperplasia
It’s non-malignant enlargement of the prostate, which is common in aging men.
BPH Risk Factors
AGE:
Rare before age 40
>50% of men in 60s have symptoms
90% of men in 70s/80s have symptoms
RACE:
Black, hispanic develop symptoms earlier than whites
Asians develop later than whites
Clinical Manifestations of BPH
urinary retention
bladder distention
frequency
urgency
incontinence
nocturia
dysuria
bladder pain
increased time to void, straining to void
Reductase Inhibitors
(Finasteride, Dutasteride)
used to reduce the size of the prostate in BPH.
Inhibits the conversion of testosterone to drotesterone, shrinking the prostate.
Side effects: impotence, decreased libido, decreased ejaculate volume.
Adrenergic Receptor Blockers
(Tamsulosin, Alfuzosin, Silodosin, Prazosin)
Used for BPH
Relax the smooth muscles in the neck of the bladder, relieving the obstruction and improving ability to urinate.
Side effects: may cause orthostatic hypotension. Antihypertensives may worsen BPH symptoms.
BPH Surgeries
Balloon urethroplasty
Intraurethral stent = looks like a little cage, and it keeps the urethra open.
TURP = snips away some of the excess tissue to relieve pressure on the urethra. High risk of bleeding, hypovolemia. Report large blood clots / dark red urine, signs of hypovolemia to the doctor.
TUNA = trans-urethral needle ablation
burn away the excess prostate tissue by needles. This one doesn’t have as much post-op needs as TURP.
TUIP = Trans urethral Incision of the Prostate
similar to TURP but not as problematic post-op.
Laser surgery = most frequently conducted by the younger surgeries.
BPH Nursing Priorities
After surgical interventions,
* Pre/post op antibiotics
* Insert urinary catheter: Only try X2 at the most. Call Urologist or the PCP. If we can’t get it X2, don’t try X3 due to excessive trauma.
* Monitor vital signs, particularly post op for TURP. That one is a ‘nasty surgery’ with lots of bleeding.
* Monitor for if the patient is still having difficulty urinating post-op.
BPH Patient Education
Avoid irritants like caffeine, spicy food, artificial sweeteners
Avoid alcohol
2000-3000mL per day of fluid, but restrict before bed
Don’t suppress urge to urinate
Take meds as prescribed
Monitor symptoms & report if they worsen.
Urinary Tract Infection (UTI) upper vs. lower
Infection in the urinary tract
Upper: Kidneys (Pyelonephritis)
Upper: Ureters
Lower: Urinary bladder (Cystitis)
Lower: Urethra
UTI Patho
Inflammation of the bladder from bacteria, obstruction of the urethra, orother factors.
Commonly caused by bacteria, but may be caused by parasitic/ fungal infections (this is only seen in immunosuppressed patients)
More common in women.
UTI Risk Factors for Females
Females have a short urethra
Increases with increase in sex
spermicidal compounds
lack of normally protective mucosal enzyme
Personal hygiene
Voluntary urinary retention
Increased risk in 2nd trimester of pregnancy & PP
anal intercourse
UTI risk factors for males
Prostatic hypertrophy
circumcision
Personal hygiene
voluntary urinary retention
Anal intercourse
UTI Clinical Manifestations
not feeling well
high temp
elevated WBC
mental status changes in older adults
Foul odor
burning when urinating
Pyuria = puss in the urine
UTI Short course
3 day course
Reduces cost & increases compliance
lower rate of side effects
Oral antibiotics such as TMP-SMZ, Ciprofloxacin, or enoxacin (Penetrex)
UTI Long Course
for Pyelonephritis, abnormalities, stones, recurrent frequent UTIs
7-10 day course
May use the same antibiotics as 3 day course
May require IV antibiotics if severe: ciprofloxacin, gentamicin, ceftriazone (Rocephin), ampicillin
Severe illness may require hospitalization
UTI Patient education for Women
urinate after sex
wipe front to back
Wear cotton underwear and loose-fitting clothing
UTI general patient education
keep genital area clean
take the full course of antibiotics
Empty bladder at least every 3-4 hours
Adequate fluids (up to 3L/day)
Avoid coffee/cola
Eat foods that can maintain acidic urine (pH<5.5) like blueberries, prunes, cranberries.
Drinking cranberry juice daily decreases the risk of UTI.
CAUTI (Catheter Associated Urinary Tract Infection)
UTI diagnosis related to catheter if the catheter has been there at least 48 hours
Prevented by not using a catheter unless indicated! only use for strict I/O, neurological diagnosis preventing control of urine outflow, skin breakdown - skin injury/ select surgical proceudres.
Meticulous care of the catheter is paramount to prevent infections.
Treat with antibiotics post dx
Meticulous Catheter Care
Sterile insertion
Keep foley bag below the bladder
Peri care at least once/shift and as needed
Clean from insertion site down the catheter
Do not open the system.
Use stat lock to prevent movement of the tube while inserted.
Hang bag on lower bed frame, not side rail.
Keep bag empty.
Discontinue catheter as soon as possible.
Perfusion
Perfusion refers to the flow of blood through arteries and capillaries delivering nutrients and oxygen to cells.
Perfusion is managed by cardiac output, which is the amount of blood pumped by the heart each minute.
What happens to organs if perfusion is altered?
Interference with tissue perfusion reduces blood flow through capillaries - which reduces O2, fluid, and nutrients to cells.
Occlusion, vasoconstriction, even dilation of arteries, atherosclerosis, thrombi
Ischemia is a reversible cellular injury that occurs when there isn’t enough O2 due to reduced perfusion.
Clinical Manifestations of poor perfusion
Muscles that hurt or feel weak when you walk.
A “pins and needles” sensation on your skin.
Pale or blue skin color.
Cold fingers or toes.
Numbness.
Chest pain.
Swelling.
Veins that bulge.
Nursing Assessment findings related to poor perfusion
Arrhythmias
Capillary refill >3 seconds
altered RR
Use of accessory muscles to breathe
Abnormal ABG
Chest pain, dyspnea, sense of impending doom
Change in BP (could be high or low)
Decreased urine output
Elevated BUN & Creatinine
Altered mental state, restlessness
Weak/absent peripheral pulse
Edema
Loss of hair to legs
Delayed wound healing
Normal blood path thru the heart
1) body
2) inferior/superior vena cava
3) right atrium
4) tricuspid valve
5) right ventricle
6) pulmonary arteries
7) lungs
8) pulmonary veins
9) left atrium
10) mitral or bicuspid valve
11) left ventricle
12) aortic valve
13) aorta
14) body.
Pre-hypertension
SBP: 120-129
AND
DBP: <80
treatment = lifestyle changes
Stage 1 HTN
SBP: 130-139
OR
DBP: 80-89
treatment = lifestyle changes and meds
Stage 2 HTN
SBP: 140-179
OR
DBP: 90-119
treatment = lifestyle changes and 2+ meds
Stage 3 HTN
SBP >=180
and/or
DBP> 120
treatment = IV meds
Thiazide Diuretic
Hydrochlorothiazide
Diuretic; used for HTN
Prevents tubular reabsorption of sodium, promoting sodium and water excretion and reducing blood volume.
Spironolactone may be used to treat ascites
Monitor for hypokalemia, vital signs for hypotension, dizziness, headache.
monitor fluid status for dehydration (daily weight)
Monitor electrolyte status
Beta Blockers
“LOLs”
Metoprolol/Lopressor
Atenolol/Tenormin
Labetalol / Trandate
Used for HTN and for post MI.
Used when HR/BP is too fast, like in hyperthyroidism/ Grave’s disease
Used to treat esophageal varices or gastric varices.
Contraindicated for COPD patients and patients with Printzmetal Angina.
Reduces BP by preventing beta receptor stimulation in the heart, resulting in decreased HR and CO
Monitor for hypotension. HR less than 60, BP less than 90/60 unless otherwise indicated in the orders.
Monitor for orthostatic hypotension, bronchospasm, fatigue, heart block, worsening HF.
ACE Inhibitors
Lisinopril/Zestril
Captopril/Capoten
Enalapril/Vasotec
Used for HTN
Blocks Angiotensin 1 from converting to Angiotensin 2. Prevents vasoconstriction and sodium/water retention.
Monitor for syncope, persistent cough
Monitor for angioedema.
Less effective for African Americans, who are also more likely to develop angioedema.
Calcium Channel Blockers
Nifedipine/Procardia
Verapamil/Calan
Used for HTN
Potentiates other meds, so there will be bigger side effects.
Don’t drink grapefruit juice.
Inhibits calcium transport into myocardial and vascular smooth muscle cells, resulting in
inhibition of excitation - contraction. Blocks calcium channels causing vasodilation.
Assess for headache, edema, hypotension.
ARBs “Sartans”
(Angiotensin 2 Receptor Blocker)
Losartan
Candesartan
Eprosartan
Used for HTN
Blocking vasoconstriction and aldosterone-secretion effects, lowering BP
Monitor closely if the client is on a diuretic. May cause additive hypotension.
Assess renal function and potassium level.
Monitor apical pulse and BP regularly.
Atherosclerosis
Hardening of arteries
Arteriosclerosis
Calcification of arterial walls
Peripheral Vascular Disease
Peripheral blood supply is impaired in the lower extremities due to atherosclerosis or arteriosclerosis
PVD Risk Factors
Age: 60-70 years old
African American men
Smoking
HTN
High cholesterol
Family history of PVD
Overweight
Physical Inactivity
PVD Priority Nursing Interventions
CHECK PULSES –> if you can’t find it, use the doppler, then call the provider.
Assess and evaluate cardiovascular risk status, family history, lifestyle
Encourage and teach healthy lifestyle changes
Encourage patient to take prescribed meds
Assess pulses for strength
Assess for pain, discoloration
Assess to detect changes and report changes to the provider
Position to avoid constriction - don’t bend knees
Change position hourly
HTN Emergency Clinical Manifestations
Severe headaches, especially to the back of the head
Confusion
Motor or sensory deficits
PVD Education
Stop smoking
Lose weight, low fat diet
Do not cross legs while sitting
Elevate feet at rest
Avoid sitting or standing for long periods of time
Avoid walking barefoot
Notify provider of any changes in color, sensation, temperature, or pulses
Aspirin (ASA)
Used for PVD
Antiplatelet
Prevents clot formation
Monitor for bleeding
Clopidogrel / Plavix
Used for PVD
Antiplatelet
Prevents clot formation
Monitor for bleeding
May take with ASA following revascularization
Cilostazol/Pletal
Pentoxifyline/Trental
Used for PVD
Antiplatelet and Vasodilator
Inhibit platelet aggregation, but mostly thins out the blood. Increases blood flow to the extremity, improving claudication
Decreases blood viscosity and increases RBC flexibility
PVD Surgical & Nonsurgical Treatment
Revascularization
Angioplasty – a stent in the vein to increase perfusion to the lower extremity.
Chronic Venous Insufficiency (CVI)
Insufficient venous return - O2 and nutrients don’t really get to the extremity so the cells begin to die
Vein blockage or valve leakage
Blood pools in the vein, causing stasis - discoloration, ulcers around the ankle
DVT linked to a higher risk for CVI
Little to no oxygen and nutrients
Risk factors for CVI
Obesity
Occupations with no movement or lots of standing in place
Thrombophlebitis
Priority Nursing Interventions for CVI
Assess discomfort
Assess long periods of sitting/standing
Assess edema of lower legs
Assess skin for ulcers, especially around the ankle area.
Bedrest with legs elevated above the heart level
Elastic support or compression hose
Do not wear tight, restrictive pants/socks/boots. Avoid girdles and garters that restrict circulation in upper leg.
Arterial Ulcer Signs
Intermittent claudication causes throbbing pain, usually in the calf area - then travels to the thighs and the buttocks. Predictable pain linked to activity.
Resting pain can occur, feels like burning
Legs might be cool to touch due to lack of blood flow
Sensation loss
Peripheral pulses absent/decreased –> LET PROVIDER KNOW!!
Bruit
Skin is thin, shiny, hairless, discolored
Toenails/nails are really thick
Venous Ulcer Signs
Aching pain
Mild compared to arterial ulcer; it increases with standing due to insufficient venous return.
Normal temp to the touch
Edema
Brown discoloration
Legs may be thin/shiny – it’s a bit like atrophied skin. Hard to move or spread for an IM shot.
Lower extremity skin becomes thicker, harder.
May experience recurrent ulcerations, especially in the medial or anterior ankle.
CVI diagnostic tests
Doppler ultrasound studies to look for vesicles
Angiography = a balloon is inserted to push the constricting plaque or thickened inner tissue back. Can place a stent in the lower extremity.
CVI treatment
garlic supplements
encourage regular exercise, which improves circulation and perfusion to the lower extremies
Blood thinning meds like clopidogrel/Plavix, Cilastozal/Pletal (both inhibits platelet aggregation and improves claudication), Pentoxifyline/Trental (decreases blood viscosity and RBC flexibility)
CVI Surgical/non-surgical treatment
Revascularization - put in a good vein bridge
Endarterectomy - go in and clean the vessel out
Bypass graft - reroutes blood flow around occlusion
Angioplasty is a non-surgical procedure to place a stent in a lower extremity
Clinical Manifestations of an AMI
Classic for males is crushing, constant pain - like an elephant sitting on their chest
Atypical pain
Reduced sensation of pain
SOB, pulmonary edema
Cold, clammy skin, pallor, diaphoresis
Indigestion/fullness
Nausea/vomiting
Dizziness, anxiety
Rapid, irregular HR
Palpiations
BP, cardiac output –> if the patient gets worse, they will develop left ventricular failure which results in hypotension
Stable Angina
predictable chest pain, usually with activity.
The patient can generally say what causes the pain, and the pain goes away when they stop doing that activity.
most common type of chest pain.
Usually relieved by rest and nitrates
Unstable Angina
unpredictable, more severe chest pain. Usually has to be treated in the hospital with an IV nitrate drip.
Still occurs at rest and continues even after the patient takes their nitroglycerine.
Generally will develop into an MI
Printzmetal Angina
Mostly related to smoking
The chest pain is cyclic at a time of day, like maybe just before going to bed.
Usually due to vasospasms
Assessment for AMI
Heart Sounds (S4 is an indication that the patient has had some kind of cardiac event)
Murmurs
report all abnormal blood sounds to provider
HR = initially high, then drops as the body tires out
BP
Pulse assessment
Chest pain
Dependent edema
Neurologic/psychological disturbances
Labs for an MI
CK = Creatine Kinase
CK-MB (also called MB Bands)
Cardiac Troponins, also called cardiac specific troponin
HDL
LDL
Triglycerides
Creatine Kinase (CK)
One of the labs for MI; can’t be used to diagnose on it’s own
Indicates brain, skeletal, or cardiac injury. The greater the damage to the cardiac muscle, the higher this number will be.
55-170 for men
30-135 for women
CK-MB
System indicator of an IM. Rises in response to an MI.
If >6% for both males and females, the patient has had an MI
Cardiac Troponins
Usually look at troponin I.
This is the best indicator of an MI
A higher level is released during an MI due to necrosis of the cardiac muscle. Happens within 3 hours of muscle injury.
>0.5ng/mL is an MI
HDL
High Density Lipoproteins
highly desirable!
Want them to be >40, but >60 actually provides the most protective effect.
HDLs clean up the vessel and transport cholesterol to the liver for excretion.
LDL
Low Density Lipoproteins
Not desirable!
They deposit cholesterol on the vessel wall.
100-129 is fine; prefer <100
Diagnostic tests for AMI
cardiac catheterization
Angiography
Echocardiogram
Transesophageal echocardiogram (TEE)
Electrocardiogram (ECG)
Statins
Priority med for hyperlipidemia
(The meds end in “statin”)
Lipitor (atorvastatin)
Zocor (Simvastatin) etc.
Statins lower cholesterol and inhibit enzymes to reduce LDL synthesis.
Monitor the patient’s liver enzymes, as it may cause elevated liver enzymes
Frequently cause muscle pain, tenderness, weakness so it’s usually given at night to reduce the experience of this pain.
Bile Acid Sequestrants
Priority Hyperlipidemia Med
Cholestyramin/Questran
Colestipol/Colestid
Colesevalem/Welchol
(have a “col” or “chol”)
Lowers LDL levels
Reduces reabsorption and cholesterol production in the liver
Biggest side effect is GI upset and constipation, so recommend to take with additional fluids
Can also cause GI tract obstruction, vitamin deficiences due to poor absorption.
AMI Modifable Risk Factors
HTN
cholesterol levels (LDL/HDL)
obesity (BMI>30)
sedentary lifestyle
smoking (promotes platelet aggregation),
diabetes
chronic stress
high fat/high sodium diet
AMI Non-Modifiable Risk Factors
age
genetics (HTN, hyperlipidemia, obesity can be genetic)
males have a higher risk
females after menopause b/c estrogen has a protective effect
African Americans
Non-STEMI AMI
less detrimental than a STEMI AMI.
Associated with a partial blockage of the coronary artery.
ST Depression due to partial thickness injury to the heart muscle.
STEMI AMI
indicates a complete blockage of the coronary artery.
ST segment elevation MI
Full thickness injury
Nursing Interventions for AMI
heart monitor
bed rest
Beta blockers to preserve the heart’s energy, although might also use ACE inhibitors or digoxin
Antiarrhythmic meds to prevent ventricular tachycardia
Prepare for cath lab procedure, such as angioplasty
Possible preparation for coronary artery bypass graft
TPA (Tissue plasminogen activator) or other fibrolytic. TPA is a clot-buster.
MONA cocktail
MONA / ANOM cocktail
Aspirin first! Chew the 325 mg
Nitroglycerin sublingual. 1 tablet every 5 minutes; max of 3 tablets. It’s a vasodilator.
headaches are a common side effect. Assess vitals between each dose. If the patient is male, cialis / viagra are contraindicated.
Oxygen 2-4L to keep a good O2 saturation
Morphine for pain; 2-4mg IV push. Assess RR, BP, HR before giving morphine!
Thrombolytics
Breaks up clots
Examples are reteplace, TPA, Alteplace, Streptokinase, Urokinase
Used during an MI, usually if the patient isn’t going to the cath lab and no contraindications such as a recent blood/already taking blood thinners, BP> 180/120.
Monitor for neurologic problems, as the clot could go to the brain. Consider strongly if the patient has to go to surgery or has a high BP (b/c this could cause the patient to bleed out faster)
AMI Patient Education
Lifestyle modification is the most important!!
Risk of reinfarction
Pharmacological prescribed meds
Weight reduction
Diet
Grave’s disease Pathophysiology (causes)
Graves’ disease is an immune system disorder that results in the overproduction of thyroid hormones (hyperthyroidism).
Too much iodine = too much thyroid hormone
Too many meds like levothyroxine (which increases thyroid hormone)
Increase release of T3 and T4
Thyroid cancer
Excess TSH
Pituitary tumor
Thyroiditis
Side effects of certain drugs (especially those that are used to treat hypothyroidism)
Fatigue due to extended hyper-activity
Affects cardiovascular, GI, neuromuscular systems
Pituitary Glands
Anterior = plays a major role in producing and secreting hormones
Posterior = ADH (stimulates kidneys to reabsorb water), plays a role in childbirth and the release of oxytocin, regulates fluid balance
Thyroid
Determines the rate of cellular metabolism
Parathyroid
secretes PTH to regulate calcium levels
Pancreas
regulates blood glucose levels
alpha cells = break down stored fat, carbs raise blood glucose level
beta cells = responsible for insulin, which transfers glucose across cell membranes and lowers blood glucose levels
Adrenal glands
adrenal cortex plays a vital role for survival and affects metabolism
Glucocorticoids stimulate most cells to increase the rate of glucose synthesis
Mineralocorticoids stimulate kidneys to reabsorb sodium and water
adrenal medula responds to physical and psychological stress; increases metabolism and blood glucose levels
gonads
responsible for sexual characteristics and reproduction
Thyroid hormone pathway
1a. hypothalamus releases TRH (Thrytotropin releasing hormone)
1b. Anterior pituitary releases TSH (Thyroid Stimulating Hormone). TSH is always the opposite of T3 & T4. TSH tries to slow the hyper and amp up the hypo.
Hypo = low T3/T4
Hyperthyroidism = high T3/T4
Calcitonin = puts Ca2+ “in” to the bones, which means in takes it out of the blood.
Hyperthyroidism Clinical Manifestation
Grape eyes (exopthalamos)
Golf balls in the throat
High BP (HTN crisis = 180/100)
High HR (Tachycardia = 100+)
Heart palpitations
High temp
hot & sweaty skin
High GI
Weight is low
Hyperthyroidism Causes
Grave’s Disease is the most common
Thyroiditis (viral / postpartum)
Excess iodine intake
Thyroid cancer
Toxic nodular goiter
Secondary to pituitary tumor
Hyperthyroidism Clinical Manifestation
Grape eyes (exopthalamos)
Golf balls in the throat
High BP (HTN crisis = 180/100)
High HR (Tachycardia = 100+)
Heart palpitations
High temp
hot & sweaty skin
High GI
Weight is low
Thyroid Crisis / Storm
All symptoms are exacerbated and the patient might go into severe cardiac distress/arrest
Extremely elevated T3/T4
Tachycardia, lethal cardiac rhythms
Elevated temps >102
HTN
Agitation, tremors, confusion, possible seizures
GI distress
older adults increased risk for HF / cardiac arrest
Hyperthyroidism Clinical Manifestations
Vital signs – tachycardic, hypertensive, elevated temp
Cardiac Rhythms – ventricular tachycardia, angina
Appetite
Weight loss
Heat intolerance
Thinning hair / hair loss
Goiter due to hyperactivity of the thyroid gland
Bulging eyes
Increased bowel elimination (diarrhea)
Problems/changes with their menstrual period, although women age 60+ have a higher change of developing hyper-thyroidism
Neurological effects
Possible fluid volume deficit
Hyperthyroidism lab tests / diagnostic procedures
Priority lab is T4
Lab Tests: Blood TSH, Free T 4 Total T 3, Thyroid stimulating immunoglobulins, Thyrotropin receptor antibodies.
Hyperthyroidism Diagnostic Procedures
Ultrasound
Electrocardiogram
Thyroid scan clarifies the size and function of the thyroid gland
New screening programs implemented by many healthcare facilities include screening for T4 and thyroid-stimulating hormone (TSH) in the newborn.
Most newborns with congenital hyperthyroidism have few, if any, clinical manifestations of thyroid hormone deficiency.
Collaborative Management of Hyperthyroidism
Radioactive Therapy
Antithyroid medications as prescribed, such as propylthiouracil (PTU) and Tapazole.
PTU blocks the synthesis of T3 and T4 and blocks synthesis of iodine
Thyroidectomy - usually in cases of thyroid cancer
If no cancer, might do a sub-total so that the patient still has some ability to create T3/T4 and doesn’t develop hypothyroidism
Ablation therapy – burn away sections of the thyroid gland to reduce the effect
Hyperthyroidism Nursing Interventions
Assess for VS, symptoms, thyroid storm
Medications such as PTU
Encourage rest, calm, cool environment.
Monitor daily weights, pulse rates, BP
Monitor nutrition status. Increased carbohydrate diet. Calories 4000-5000/ day.
Thyroidectomy post-op care
Semi-fowlers, support head & neck with pillows, monitor/record hemorrhage, assess back of the neck, dressing, pulse, cardiac rhythm, respiratory distress (rate, rhythm, depth), have suction equipment set up at the bedside to suction their mouth and keep the airway clear
O2 as needed
Have a tracheostomy set at the bedside for immediate placement as needed
Have suction equipment set up
Laryngeal nerve damage – monitor the patient’s ability to speak (monitor for hoarseness)
Could accidentally remove the parathyroid gland b mistake, so monitor for hypocalcemia (tingling of the toes, tetany, tingling of the fingertips, positive for Chvostek and Trousseau)
*If positive, administer IV Ca2+ to replace the calcium
Assess for symptoms of thyroid storm, such as extreme tachycardia and HTN and fever, extreme GI upset
Total Thyroidectomy is not the main intervention; usually only in cancer cases
Methimazole
Hyperthyroid med
NOT baby safe
Stops the thyroid from making T3 & T4
PTU (Propylthiouracil)
hyperthyroid med
“Puts thyroid underground”
Baby safe
Report fever/sort throat
Stops the thyroid from making T3 & T4
RAIU (Radioactive Iodine Uptake)
Destroys the thyroid in one dose. Very toxic and makes the patient radioactive.
Takes 6-8 weeks to be effective.
Before giving, always assure a pregnancy test is negative
Remove neck jewelry and dentures
5-7 days before, hold anti-thyroid meds
Awake – no anesthesia or conscious sedation
NPO 2-4 hrs before and 1-2 hrs after (NOT 12 hrs)
AVOID everyone!! For up to 7 days!!
* No pregnant people
* No crowds
* Not the same restroom (flush 3 times)
* Separate laundry baskets
Hypothyroidism
“Low and Slow”
Intolerant to cold, extreme fatigue, weight gain (although can develop anorexia), dull blank expression, thick tongue – slow speech
insufficient secretion of TH by the thyroid gland, caused by a decreased metabolic rate
Hypothyroidism Priority Lab
TSH
Hypothyroidism Pathophysiology
Autoimmune disorder - Hashimoto Thyroiditis destroys thyroid tissue.
Deficiency of thyroid hormone causes slowing of the metabolic rate.
Myxedema is a complication of longstanding hypothyroidism:
> unconsciousness
> mental sluggishness
> collapse of the cardiac system
> metabolic acidosis, lactic acidosis
Primary Hypothyroidism
= accounts for 99% of all cases: the tissue is destroyed/ atrophy of the thyroid gland
Could be iodine deficiency
Idiopathic (cause is unknown)
Secondary Hypothyroidism
caused by insufficient excretion of thyroid stimulating hormone, which results from a disease
o Patients may develop a goiter = thyroid gland is over-stimulated, which causes the goiter to form
If the goiter is present, it causes respiratory or neck difficulties and they may elect to do a thyroidectomy
Hypothyroidism -
Goiter assessment
Goiter = Hashimoto’s
Super depressed, fat, and lethargic
Myxedema coma:
*Low RR – respiratory failure
*Priority: place tracheostomy kit by the beside
*Key word: endotracheal intubation set up
*Low BP & HR “hypotension” ‘bradycardia”
*Low temp – cold intolerance
oNO ELECTRIC BLANKETS
Risk factors
o Post thyroidectomy
o Abrupt stop of levothyroxine
Hypothyroidism Clinical Manifestations
Low energy – fatigue, weakness, muscle pains, aches
Low metabolism = weight and water gain, edema in the legs and eyes
Low digestion (constipation)
hair loss = alopecia
Low mental status (forgetfulness, altered LOC)
Low modd-depression – apathy/confusion
Low libido – low sex drive
Slow dry skin turgor
Low and slow menstruation
*Amenorrhea = no period
*Slow heavy period = hypermenorrhea
Diet = low calories, low cholesterol
Hypothyroidism nursing interventions
Encourage exercise
Administer medications as prescribed (such as Synthroid)
Administer thyroid hormone
Monitor body temperature
Provide cardiac monitoring
Soybeans in large quantities are goitrogenic
Levothyroxine (Synthroid)
Increases blood levels of TH, raising the metabolic rate.
Give 1 hour before meals or 2 hours after meals
Report a pulse >100
May potentiate the effects of digoxin and anticoagulants
Also monitor blood glucose levels
Be cautious for older adults, as these adults have higher risk of cardiac arrest and other cardiac effects.
Report elevated HR and BP promptly
L = lifelong drive, long/slow onset (3-4 weeks until relief)
E = early morning & empty stomach: once per day, in the morning 60 minutes before breakfast
V = very hyper: report agitation / confusion!! These are the early signs of a thyroid storm
O = Oh, the baby’s fine. Pregnancy safe
No food, not a cure, no double doses, never abruptly stop meds (leads to myxedema coma)
Avoid narcotics / opioids
Avoid benzos like sedatives
cirrhosis
functioning liver tissue is destroyed and gradually replaced by fibrous scar tissue.
Irreversible
Treat symptoms: keep patient comfortable and oxygenated.
Cirrhosis Pathophysiology
Chronic end-stage liver disease
Irreversible destruction and degeneration of liver cells
Functional liver tissue is replaced with fibrous scar tissue
Complications:
Portal HTN, jaundice, bleeding esophageal varices, defects in coagulation, encephalopathy
Cirrhosis Risk Factors
Infection with Hep B, C, D
Injection drug use
Excessive alcohol use
Cirrhosis Clinical Manifestations
SOB
Itching skin due to more bile salts
Anorexia
Nausea/vomiting
Diarrhea to get rid of ammonia thru stool
Jaundice
Brown/dark urine secondary to bile obstruction
Tan/gray stool when there’s jaundice
Peritoneal ascites
Dilated vessels
Lungs can’t expand as they should, so respiratory difficulties
Encephalopathy / confusion b/c the liver can’t detoxify or get rid of waste (neurological effects)
High risk of bleeding / bleeding varices
Vomiting blood
Skin effects
Cirrhosis Nursing Assessment
Monitor for clinical manifestations
Measure abdominal girth
Assess nutritional status, muscle wasting
Assess color of urine
Assess respiratory status
Assess for bleeding varices
Weigh daily
Monitor I/O
High Calorie Diet
IV Fluids
Cirrhosis Treatment
Success = increased/improved coagulation studies; stable liver function tests.
Transjugular intrahepatic portosystemic Shunt (TIPS) relieves portal HTN and reduces the onset of esophageal varices and ascietes.
Sengstaken-Blakemore and Minnesota Tubes (also called balloon tamponades) are used for bleeding varices. can also use a beta blocker.
Paracentesis is done to relieve severe ascites that doesn’t respond to diuretic therapy.
Liver transplantation
Anticholelithic is given to promote bile flow
Diuretic (spironolactone) to treat ascites
Cirrhosis Education
Stop drinking alcohol!!!!!
Low sodium diet (<2g/day)
Fluids restricted to 1500 mL/Day
Veggie proteins provided with restricted red meat consumption
Parenteral nutrition as needed
Vitamin supplements that include Vitamin B complex, A, D, and E.
Carefully consider meds: NSAIDs may induce bleeding and talk with provider/pharmacist before taking OTC meds.
Albumin
Cirrhosis medication
Intravascular volume replacer
Lactulose
Cirrhosis medication
Used to treat hepatic encephalopathy
Cirrhosis Priority Labs
CBC
LFT: enzymes may be elevated due to release from inflamed cells
Liver biopsy
Esophagogastroduodenoscopy (EGD scope)
Diabetes Type 1
Autoimmune disorder in which antibodies are developed against the pancreas B cells or insulin.
2Ps: Polyuria, Polydipsia, Polyphagia
Exogenous insulin required for life
Formerly known as Juvenile Diabetes or Insulin Dependent Diabetes.
Type 2 Diabetes
Deficiency in insulin: cells become fatigued
Insulin resistance: body tissues don’t respond to insulin’s action due to unresponsive or insufficient numbers of insulin receptors
Gradual onset
Risk factors: runs in families, obesity, fat cells are resistant to insulin, 40+ years old, certain ethnicities, cardiac history, elevated cardiac lab values
Type 1 Diabetes Clinical Manifestations
Weight loss
fatigue
Recurrent infections
3Ps: Polyuria, Polydipsia, Polyphagia
T1D and T2D Nursing Assessment/Priorities
Monitor blood glucose
Ask about clinical manifestations
Neurological assessment
Nursing Priority is Patient Education
T1D & T2D Priority Labs
A1C –> 5.7-6.4% is prediabetes; 6.5%+ is diabetes
Fasting glucose >126mg/dL
2 hr Plasma >200 mg/dL with classic symptoms of hyperglycemia
T1D Medical Management / Meds
Medication: insulin
Consult RD and CDCES
Biguanide
T2D oral med
Metformin
Decreases the production of glucose in the liver and enhances transport of glucose into the cells.
Sulfonylureas
T2D oral med
glipizide
Increases the production of insulin by the pancreas.
T1D Education
Monitor blood glucose
Adhere to exercise and meal plan
Insulin: proper storage, administration, and injection sites
Insulin pump, pump care
Signs and symptoms of hypoglycemia
Follow up with provider
T2D Education
Monitor blood glucose
Adhere to exercise and meal plan
S/S of Hyper and Hypoglycemia
Proper administration of insulin, injections sites if applicable
Proper foot care
Importance of eye exams
Follow up with provider
DKA
Associated with Type 1 DM
Very little to no insulin production leads to increased glucose levels, which then leads to fat breakdown,
Positive ketones
Nursing Priorities - Treatment for DKA
Adequate ventilation
IV regular insulin administration
Isotonic solution (0.9% NS) –> this should change to 0.45 NS later, may add dextrose to prevent hypoglycemia
NGT if comatose
Electrolyte replacements if needed
Sodium Bicarbonate
Monitor cardiac rhythm
HHS
Hyperosmolar Hyperglycemic State (HHS)
ASsociated with Type 2 Diabetes
Insufficient amount of insulin
Major fluid loss
Precipitated by infection, acute illnesses, chronic illnesses
Elevated plasma osmolarity
Normal urine ketones
HHS Nursing Priorities - Treatment
Adequate ventilation
Maintain fluid volume; isotonic IV fluid solution
Correct shock
IV regular insulin administration
NGT if comatose
Electrolyte replacements if needed
Monitor cardiac rhythm
Basal dose of insulin
maintenance dose
Given around the clock–> ordered every so many hours and ordered for the same amount
Prandial dose of insulin
Pre-prandial dose: given before the patient eats.
Post-prandial dose: given after the patient easts
Most often, it will be a set dose or a sliding scale dose.
Corrective dose
usually given on a sliding scale.Take the glucose level every so many hours and insulin is given based on the glucose level. Might be given along with the basal dose.
Insulin injection sites
arms, but, thigh, stomach.
Make sure to punch and insert at a 45-90 degree angle. Want to hit the subQ fatty tissue, not muscle
