1
AH1 exam 1
Diabetes:
o Group of metabolic diseases characterized by increased levels of glucose in the
blood = hyperglycemia
o Results from defects in: (could be both)*
▪ Insulin secretion
▪ Insulin action
o L
...
1
AH1 exam 1
Diabetes:
o Group of metabolic diseases characterized by increased levels of glucose in the
blood = hyperglycemia
o Results from defects in: (could be both)*
▪ Insulin secretion
▪ Insulin action
o Leading cause of death from disease
o High rate of cardiovascular disease (MI, stroke, peripheral vascular
disease)
Classifications
● major classifications of diabetes:
o type 1
o type 2
o gestational
o latent autoimmune diabetes of adults (LADA)
o diabetes associated with other conditions or syndromes
Prediabetes: impaired glucose tolerance or impaired fasting glucose
o refers to a condition where blood glucose levels fall between normal levels
and those considered diagnostic for diabetes
Diabetic Screening
● Determine risk factors: obesity, hypertension, sedentary lifestyle,
hyperlipidemia, smoking, genetic hx, ethnic group, woman who have ovary
syndrome or delivered infants weighing more than 9lbs
● Screen pts whose BMI greater than 25 and age greater than 45
● Child is overweight and has additional risk factors
● Screening is done with fasting serum glucose levels or glycosylated
hemoglobin (A1C)
Client education
● Exercise 3x weekly
o Pts w/ blood glucose levels of 250mg/dL and who have ketones DO NOT
EXERCISE****
● Good nutrition
o Pts who requires insulin should eat a 15g carb snack***
o Carbs: 45% of daily intake
o Protein: 15-20%
o Unsat/poluunsaturated fats: 30-35%
● Regular diet (eat at same times/same amounts) promotes control of glucose
levels2
● Diet low in saturated fats
● Include Omega-3 fatty acids and fiber
o Most important objective from nutrition and dietary management: maintain
reasonable weight, control blood glucose levels, and normalize lipids and BP to
prevent heart disease***
Risk Factors
● Metabolic syndrome
● Insulin resistance
o Pancreatitis and Cushing’s syndrome are secondary causes of diabetes
o Vision and hearing deficits
o Tissue deterioration (from aging) and affect ADL’s and ability to perform
glucose monitoring
o Fixed income (can’t afford insulin/meds)
● Age ^^^
Expected Findings
● Hyperglycemia: blood glucose greater than 250mg/dL
● Polyuria: excess urine production & frequency (osmotic diuresis)
● Polydipsia: excessive thirst bc dehydration
o Loss of skin turgor, skin is dry and warm
o Dry mucous membranes
o Weakness and malaise
o Rapid weak pulse and hypotension
● Polyphagia: excessive hunger&eating bc the cells do not receive glucose
o Weight loss
o Ketones accumulate in blood due to breakdown of fatty acids when insulin
is not available (causes metabolic acidosis)
o Kussmaul respirations: increased RR and depth, trying to excrete CO2
and acid
● Fruity breath
● Headache, nausea, vomiting, abdominal pain, fatigue, weakness, vision
changes, slow wound healing, etc
Lab Tests: two findings (on separate days) or atleast two of the following
● Manifestations of diabetes + casual blood glucose concentration greater
than 200mg/dL
● Fasting blood glucose greater than 126mg/dL
● 2hr glucose greater than 200mg/dL with oral glucose tolerance test
● Glycosylated hemoglobin (A1C) greater than 6.5%
● Urine ketones: high ketones in the urine with hyperglycemia (exceed
300mg/dL) is a medical emergency**
Diagnostic Procedures
● Self-monitoring blood glucose:3
o pt pricks their finger and applies a drop of blood to a test strip
Complications
o Diabetic Macrovascular complications result from changes in the medium to large
blood vessels
o Diabetic Microvascular disease is characterized by capillary basement
membrane thickening
Medications
Insulin: hormone secreted by beta cells, anabolic
● Actions:
o Transports and metabolizes glucose for energy
o Stimulates storage of glucose in the liver and muscle (form of glycogen)
o Signals liver to stop release of glucose
o Enhances storage of dietary fat in adipose tissue
o Accelerates transport of amino acids into cells
o Inhibits the breakdown of stored glucose, protein and fat
● Glucagon: released when blood glucose levels decrease, stimulates the liver to
release stored glucose
● After 8-12 hrs without food, liver forms glucose from the breakdown of
noncarbohydrate substances, including amino acids (gluconeogenesis)
Rapid acting insulin: Lispro, Aspart, Glulisine
o Administer before meals
o Onset: 10-30 min
o Peak: 1 hr
o Duration: 2-4 hrs
o Administer with intermediate or long acting
o Used for rapid reduction of glucose levels
Short acting insulin: regular- Humulin R, Novolin R
o Administer 30-60 min before meals
o 2 concentrations
o U-500 is reserved for pt with insulin resistant-not given IV
o U-100 is prescribed for most pts and may be given IV
o Onset: 30-60 min
o Peak: 2-3 hrs
o Duration: 4-6 hrs
Intermediate acting insulin: NPH4
o Adminster for glycemic control between meals and at night
o Not administered before meals
o Contains protamine (a protein), that puts a delay in insulin absorption or
onset and extends the duration
o Administer SQ only and can only mix with short-acting
o Onset: 2-4hrs
o Peak: 4-12 hrs
o Duration: 16-20 hrs
Very-Long acting insulin: Lantus, Glargine
o Administered once daily, at the same time each day
o Forms microprecipitates that dissolve slowly over 24hrs and maintains a
steady blood glucose with no peaks or troughs
o Admininster SQ, never IV
o Onset: 1-6 hrs
o Peak: none
o Duration: 24-36 hrs
Insulin Regimens
● Vary from 1-4 injections per day
● Usually, a combo of short-acting and longer-acting
● 2 approaches to insulin therapy:
o Conventional: simplify the insulin regimen to avoid acute complications of
diabetes
o Intensive: use a more complex insulin regimen to achieve as much control
over blood glucose levels as is safe and practical
● 4 main areas for injection: abdomen, upper arms, thighs and hips
Complications of Insulin Therapy
● Local Allergic Reactions
o Redness, swelling, tenderness, duration appears around injection site 1-2
hrs after administration
● Systemic Allergic Reaction
o Immediate local skin reaction that gradually spreads into generalized
urticaria (hives)
● Insulin Lipodystrophy
o Localized reaction in the form or either lipoatrophy or lipohypertrophy
o Lipoatrophy: loss of subcutaneous fat; appears as a slight dimpling or
more serious pitting of subcutaneous fat
o Lipohypertrophy: development of fibrofatty masses at injection site,
caused by the repeated use of an injection site
● Resistance to injected insulin
o Pts may develop insulin resistance and require large insulin doses to
control symptoms
● Hypoglycemia
o Low sugar in the blood, occurs when blood glucose falls less than
70mg/dL5
o Mild hypoglycemia s/s: sweating, tremors, tachycardia, palpitation,
nervousness, hunger
o Moderate hypoglycemia s/s:inability to concentrate, headache,
lightheadedness, confusion, memory lapses, numbness of the lips and
tongue, slurred speech, impaired coordination, emotional changes,
irrational behavior, double vision
o Severe hypoglycemia s/s: disoriented behavior, seizures, difficulty waking
up from sleep, or loss of consciousness
Methods of Insulin Delivery:
● Pens
● Jet Injection
● Pumps
*Pt may complain of headache and pain at injection site. Ensure patency of IV line used
for injection of 50% dextrose bc it is very irritating to veins*
Oral Hypoglycemics
Biguanides: Metformin
● Reduces production of glucose by the liver
● Increases tissue sensitivity to insulin
● Slows carb absorption in the intestines
Nursing considerations:
● Monitor GI effects
● Monitor for lactic acidosis
● Stop med for 48 hrs before any elective radiographic test and restart 48hrs after
Client education:
● Take with food
● Take Vitamin B12 and folic acid supplements
● Contact provider if manifestations of lactic acidosis (sluggishness,
hyperventilation)
● May be taken during pregnancy
● Never crush or chew
Sulfonylureas: Glipizide, glimepirirde, glyburide
● Stimulates insulin release from the pancreas causing decrease in blood sugar
levels
● Increases tissue sensitivity to insulin
Nursing considerations:
● Monitor for hypoglycemia
● Beta-blockers can mask tachycardia seen during hypoglycemia6
Client Education:
● Administer 30min before meal
● Monitor for hypoglycemia and report frequent episodes to the provider
● Avoid alcohol
Meglitinides: Repaglinide, nateglinide
● Stimulates insulin release from the pancreas
● Administered for post-meal hyperglycemia
Nursing Considerations:
● Monitor for hypoglycemia
● Monitor HbA1c every 3 months
Client Education
● Administer 15-30 min before meal
● Must eat 30min of administration
● Do not take if skipped a meal
Thiazolidinediones: Pioglitazone
● Reduces the production of glucose in the liver (gluconeogenesis)
● Increases tissue sensitivity to insulin
Nursing Considerations:
● Monitor for fluid retention, esp pts with hx of heart failure
● Monitor for elevation of ALT, LDH, and triglycerides levels
Client Education:
● Report rapid weight gain, shortness of breath, or decreased exercise tolerance
● Have liver function test at baseline and every 3-6 months after
Alpha-glucosidase inhibitors: Acarbose, miglitol
● Slow carb absorption
● Reduce post-meal hyperglycemia
Nursing Considerations:
● Alert the pt that GI discomfort (cramps, excessive gas, diarrhea) is common
● Monitor liver function every 3 months
● Treat hypoglycemia with dextrose
Client Education:
● Instruct pt to have liver function tests every 3 months
● Take med with the first bite of each meal
● Have dextrose paste available for hypoglycemia
Dipeptidyl peptidase-4 (DPP-4) inhibitors: Sitagliptin
● Augments naturally occurring intestinal incretin hormones, which promotes
release of insulin and decrease secretion of glucagon
● Lowers fasting and postprandial glucose levels
Nursing Considerations:
● Few adverse effects but upper respiratory manifestations: nasal and throat
inflammation and pancreatitis can occur7
● Alert the pt of GI discomforts
Client Education:
● Report persistent respiratory manifestations
● Report severe abdominal pain, with or without emesis
● Med only works if blood sugar is rising
Sodium-glucose cotransporter 2 inhibitors: Canagliflozin, dapagliflozin
● Blocks reabsorption of glucose from the kidneys
Nursing Considerations:
● Monitor for development of UTI and yeast infections in women
● Monitor postural hypotension in older adults
Client Education:
● Take med before first meal of the day
● Change positions slowly
● Monitor and report genital itching, burning, and increased drainage
Non-insulin injectable medications
Incretin mimetic: Exentadie, liraglutide
● Mimics the function of intestinal incretin hormone by decreasing glucagon
secretion and gastric emptying
● Decrease insulin demand by reducing fasting and postprandial hyperglycemia
Nursing Considerations:
● Adminster SQ 60min before morning and evening meal
● Monitor for gastrointestinal distress
Client Education:
● Do not administer after a meal
● Oral antibiotic, oral contraceptive, or acetaminophen should never be given
within 1 hr of oral exenatide or 2 hr after an injection of exenatide
● Can have decreased appetite and weight loss
● Wait for next scheduled dose if the scheduled med is missed
● Report severe abdominal pain
Amylin mimetic: Pramlintide
● A synthetic amylin hormone found in the beta cells of the pancreas, it suppresses
glucagon secretion and controls postpradial blood glucose levels
Nursing Considerations:
● Administer SQ immediately before each meal
● Do not administer if pt has hypoglycemia unawareness, or noncompliance/poor
adherence to treatment regimen and blood glucose monitoring
● Can be administered with insulin therapy and oral hypoglycemic agent
● Pre-meal doses of rapid- or short acting insulin should be reduced by 50% to
reduce risk of hypoglycemia
Client Education:
● Monitor and report frequent periods of hypoglycemia
● Monitor for injection site reactions8
Patient-Centered Care: Nursing Care
o Monitor the following:
▪ Blood glucose levels
▪ I&O and weight
▪ Skin integrity (wound healing)
▪ Sensory alterations: tingling numbness
▪ Visual alterations
▪ Dietary practices
▪ Exercise patterns
▪ SMBG skill
▪ Self-med administration profiency
o Teach pt to rotate injection site**
Retinopathy: damage to small blood vessels that nourish retina
Nephropathy: damage to kidney cells
Neuropathy: damage to nerve cells
Type 1: insulin-dependent diabetes or juvenile diabetes
o 5% of all diabetes ***
o destruction of beta cells of the islets of Langerhans in the pancreas
o absence of insulin production
Characteristics for type 1:
● onset any age, usually <30 years old
● thin at diagnosis; recent weight loss
● etiology:
o genetic
o immunologic
o environmental factors (virus)
● require insulin
● ketosis prone
● acute complications of hyperglycemia: keto acidosis
Osmotic diuresis: excess glucose in the urine and excessive loss of fluids and
electrolytes
Glycogenolysis: break down of stored glucose
Gluconeogenesis: production of new glucose from amino acids and other substrates
Diabetic Ketoacidosis: common in ppl with type 1**
● deficiency of insulin
● highly acidic ketones are formed
o ketone bodies: highly acidic substance formed when the liver
breaks down free fatty acids in the absence of insulin9
● results in metabolic acidosis
o No insulin is present to break down ketone bodies and ketoacidosis
3 main clinical features of Diabetic Ketoacidosis:
o Hyperglycemia
o Dehydration and electrolyte loss
o Acidosis
Treatment:
o Fluid replacement
o Correction of electrolyte imbalances
o Insulin administration
Type 2: non-insulin dependent or adult-onset diabetes
o affects 95% of ppl with the disease***
o inability of cells to respond to insulin
o decreased production of insulin
o linked to: obesity, sedentary lifestyle, and heredity
o metabolic syndrome often proceeds type 2
o a constellation of symptoms: hypertension, hypercholesterolemia,
abdominal obesity, other abnormalities
Characteristics of type 2:
● more common in people >30 years old
● obese
● can control blood glucose levels through weight loss if obese
● oral antidiabetics may improve blood glucose levels if dietary
changes do not work
● ketosis uncommon except in stress & infection
● acute complications: hyperglycemic hypersmolar syndrome (from
uncontrolled type 2; DEADLY)
o s/s: hypotension, profound dehyradtion, tachycardia, variable
neurological signs (alterations in consciousness, seizures,
hemiparesis)
o Treatment same as DKA
● intracellular reactions are diminished
● beta cells cannot keep up with increased demand for insulin = type
2
Symptoms:
● fatigue
● irritability
● polyuria
● polydipsia
● poor wound healing
● vaginal infections
● blurred vision (glucose levels are very high)10
*Consequence of Undetected diabetes is that long-term diabetes complications like eye
disease, peripheral neuropathy, peripheral vascular disease may develop before the
actual diagnosis of diabetes is made, which tells BGL have been high for a while.*
Gestational: onset is pregnancy
● high risk ethnic groups:
o Hispanic americans
o Native americans
o Asian americans
o African americans
o Pacific islanders
Latent Autoimmune Diabetes of Adults (LADA):
● Progression of autoimmune beta cells destruction in the pancreas is slower than
in types 1 and 2
● Not insulin dependent in the first 6 months of onset
● Clinical manifestations shares the same as type 1 and type 2
Foot Care
o Inspect feet daily
o Pat dry, esp between toes and avoid lotions
o Use mild foot powder
o Do not use at home remedies for foot care
o Best time to perform foot care is after bath/shower
o Avoid open toe, open-heel shoes
o Avoid prolonged sitting, standing and crossing legs
o If trimming toe nails: straight acrossed
Nutritional Guidelines:
o Meal planning to include food intake, weight management, and lipid/glucose
management
o Plan meals for appropriate timing, activity, onset, and peak of insulin
o Count grams of carbs
o Restrict calories and increase activity as appropriate for weight loss
o Use artificial sweeteners
o Read and interpret food labels
Illness
Teach pt guidelines to follow when sick:
● Monitor blood glucose every 3-4 hrs
● Continue taking insulin or oral hypoglycemic agents
● Consume 4 oz of sugar free, noncaffeinated liquid every 30min
● Meet carb needs thru soft foods (custard, gelatin, graham crackers)
● Test urine for ketones and report to provider if outside expected range
● Rest
● Call provider:
o Blood glucose greater than 240mg/dL11
o Fever greater than 101.5, does not respond to acetaminophen, and
lasts longer than 24hr
o Feeling disoriented or confused
o Rapid breathing
o Vomiting more than once
o Diarrhea more than 5x or longer than 24hr
o Inability to tolerate liquids
o Illness longer than 2 days
Complications:
● Cardiovascular and cerebrovascular disease
● Diabetic retinopathy
● Diabetic neuropathy
● Diabetic nephropathy12
Respiratory- Rhinitis, Sinusitis, Influenza, Pneumonia
Rhinitis:
● Inflammation and irritation of the mucous membranes of the nose
● Causes:
o Changes in temp or humidity
o Odors
o Infection
o Age
o Systemic disease
o Use of over the counter and prescribed nasal decongestants
o Presence of a foreign body
● Allergic rhinitis: seasonal rhinitis associated with exposure to airborne particles
such as: dust, dander, plant pollens
o May occur from allergies such as foods (nuts, shellfish, soy), medications
(penicillin, aspirin), and particles indoor/outdoor environment
o Most common cause of nonallergic rhinitis: common cold
Signs/Symptoms:
● Rhinorrhea: runny nose
● Congestion
● Nasal discharge (purulent with bacteria rhinitis)
● Sneezing
● Pruritis of the nose, roof of mouth, throat eyes, and ears
● Headache
Viral Rhinitis (Common Cold)
● Most frequent viral infection in the general population
● “common”: caused by a virus
● “cold”: refers to infectious, acute inflammation of the mucous membranes
of the nasal cavity
● Term is also used when the virus is influenza
Signs/symptoms:
● low-grade fever
● nasal congestion
● runny nose/nasal discharge
● halitosis
● sneezing
● teary watery eyes
● “scratchy” sore throat
● General malaise
● Chills
● Headache/muscle aches13
Medical Management
● warm saltwater gargles
● nonsteroidal anti-inflammatory drugs (NSAIDS)
o ex: aspirin, ibuprofen
o relieves headaches and pains
● Antihistamines used to relieve sneezing & runny nose
● Petroleum jelly to soothe dryness around the nose
Nursing Management
● Most viruses can be spread by:
o Direct contact with infected secretions
o Inhalation of large particles from others’ coughing or sneezing
o Inhalation of small particles (aerosol) that may be in the air for up to an
hour
Rhinosinusitis “sinusitits”
● Inflammation of the paranasal sinuses and nasal cavity
● Typical pathogens: Streptococcus pneumonia, Haemophilus influenzae, and less
commonly Staphylococcus aureus and Moraxella catarrhalis
Causes of Rhinosinusitis
Category Causes
Vasomotor Idiopathic
Abuse of nasal decongestants
Psychological stimulation (anger, Sexual assault)
Irritants
Mechanical Tumor
Deviated septum
Crusting
Hypertrophied turbinates
Foreign body
Cerebrospinal fluid leak
Chronic Inflammatory Polyps (in cystic fibrosis)
Sarcoidosis
Wegener granulomatosis
Midline granuloma
Infectious Acute viral infection14
Acute or chronic rhinosinusitis
Rare nasal infections (syphilis, TB)
Hormonal Pregnancy
Use of oral contraceptives
Hypothyroidism
Influenza
Seasonal influenza “flu”: occurs as an epidemic, usually in the fall and winter months
● Highly contagious acute viral infection, occurs in children & adults
● Caused by one of several virus families and can vary yearly
o Adults: contagious 24 hrs before manifestations develop & up to 5 days
after they start
Pandemic influenza: viral infection among animals or birds that has mutated and is
becoming highly infectious to humans
● Has potential to spread globally like H1N1 (swine flu)
Assessment
Expected Findings:
● Severe headaches
● Chills
● Fatigue, weakness
● Severe diarrhea & cough (avian flu)
● Fever
● Hypoxia (avian flu)
Medications
Antivirals
● Amantadine, rimantadine, and ribavirin
Influenza Vaccines
Client Education
● Encourage flu vaccines
● Reduce risk by washing hands & following cough etiquette
● Avoid close personal contact (handshaking, hugs, kissing)
● If flu manifestations occur: increase fluid intake, rest, and stay home
● Avoid travel to places with pandemic
● Be aware of public health announcements
Pneumonia
Expected Findings:
● Anxiety
● Fatigue
● Weakness
● Chest discomfort due to coughing
● Confusion from hypoxia (most common in older adults)15
Physical assessment findings:
● Fever
● Chills
● Flushed face
● Diaphoresis (sweating)
● Shortness of breath/difficulty breathing
● Tachypnea
● Sharp chest pain
● Sputum production (yellow-tinged)
● Crackles and wheezes
● Coughing
● Dull chest percussion over areas of consolidation
● Decreased O2 sats (range 95-100%)
● Purulent, blood-tinged or rust-colored sputum
Lab Tests
● Sputum Culture and sensitivity
o Obtain before starting antibiotic therapy
o Obtain by suctioning if pt unable to cough
o Difficult to obtain from older pts bc of weak cough reflex
● CBC: elevated WBC count
● ABG’s: hypoxemia (decreased PaO2 less than 80 mmHg)
● Blood culture: to rule out organisms in the blood
● Serum electrolytes: to identify causes of dehydration
Diagnostic Procedures
● Chest X-ray
● Pulse ox
Nursing Care
● Position pt high-Fowler’s
● Encourage coughing or suction to remove secretions
● Administer breathing treatments & meds
● Administer O2 therapy
● Monitor for skin breakdown around nose & mouth
● Deep breathing with incentive spirometer
● Promote adequate nutrition/fluid intake:
o Increase calories
o Aids in preventing secondary illnesses
o Fluid intake 2-3L/day
● Provide rest periods
● Reassure pt in respiratory distress
Medications
Antibiotics16
● Used to destroy infections
● Commonly used: Penicillin, Cephalosporins
● Given IV and then switched to oral form as condition improves
● Obtain sputum culture before giving first dose of antibiotic
Nursing Considerations:
● Observe pt taking cephalosporins for frequent stools
● Monitor kidney function
Bronchodilators
● Given to reduce bronchospasms and reduce irritation
● Short acting beta agonists like albuterol, rapid relief
● Cholinergic antagonists (anticholinergic meds) like ipratropium, block
sympathetic nervous system, allowing increased bronchodilation & decreased
pulmonary secretions
● Methylxanthines (theophylline) require close monitoring of serum medication
level due to narrow therapeutic range
Asthma
● Chronic inflammatory disorder of the airways that result in intermittent and
reversible airflow obstruction of the bronchioles
o Obstruction occurs either by inflammation or airway hyperresponsiveness
Risk Factors:
● Family hx of asthma
● Smoking & secondhand smoke exposure
● Environmental allergies
● Exposure to chemical irritants or dust
● Gastroesophageal reflex disease (GERD)
Medications
Bronchodilators (inhalers)
● Short acting beta2 agonists (rapid relief): albuterol
● Anticholergenic meds: ipratropium
● Methylxanthines: theophylline
● Long acting beta2 agonists: salmeterol
Nursing Considerations:
Albuterol: watch for tremors and tachycardia
Ipratropium: observe for dry mouth
Theophylline: Monitor serum levels for toxicity. Side effects: tachycardia, nausea and
diarrhea
COPD
● Combination of emphysema and chronic brochitits
● Inflammation of the bronchi and bronchioles due to chronic exposure to irritants
Risk Factors:17
● Advanced age
● Smoking
● Alpha1-antitrypsin (AAT) deficiency
● Exposure to environmental factors (air pollution)
Expected Findings:
● Chronic dyspnea
Physical Assessment Findings:
● Dyspnea upon exertion
● Productive cough (severe in the morning)
● Hypoxemia
● Crackles and wheezes
● Rapid and shallow respirations
● Use of accessory muscles
● Barrel chest or increased chest diameter
● Hyperresonance on percussion due to “trapped air” (w/ emphysema)
● Irregular breathing pattern
● Thin extremities and large neck muscles
● Dependent edema secondary to right sided heart failure
● Clubbing of fingers and toes
● Pallor and cyanosis of nail beds
● Decreased O2 sat
● Older adults w/ darker skin, lower O2 sats
Nursing Care:
● For pursed lip breathing:
o Form mouth like going to whistle
o Take a breath in thru the nose and out thru lips/mouth
o Don’t puff cheeks
o Take breaths deep and slow
Medications
Bronchodilators(inhalers)
Anti-inflammatory agents
● Corticosteroids: fluticasone
o Monitor for adverse effects: fluid retention, immunosuppression,
hyperglycemia, hypokalemia, poor wound healing)
● Leukotriene antagonists
● Mast cell stabilizers
● Monoclonal antibodies
Mucolytic agents
● thin secretions
● nebulizer treatment
● guaifenesin
● Combo of guaifenesin and dextromethorphan can be taken orally to loosen
secretions18
TB
● Infectious disease in the lungs caused by Myobacterium tuberculosis
o Can spread to any organ in the blood
Nursing Care
● Administer heated & humidified oxygen therapy
● Prevent infection transmission
o Wear a N95 HEPA filter or powdered air purifying respirator
o Place pt in a negative-ariflow room and imprement airborne precautions
o Use barrier protection
o Pt wears surgical mask if transporting out of the room
o Pt should sneeze/cough into disposable tissues
o Administer meds
o Promote adequate nutrition
▪ Encourage fluid-intake and well-balanced diet for adequate caloric
intake
▪ Ecourage foods rich in protein, iron & vitamins C and B
▪ Provide emotional support
Coronary Arteriosclerosis: most common cause of cardiovascular disease
● Abnormal accumulation of lipid or fatty substances and fibrous tissue in the lining
of arterial blood vessel walls
● The presence of inflammation attracts inflammatory cells, such as monocytes
(macrophages)
o Activated macrophages also release biochemical substances that can
further damage the endothelium by contributing to the oxidation of
low-density lipoprotein (LDL)
o Following the transport of lipids into the arterial wall, smooth muscles cells
proliferate and form a fibroud cap over a core filled with lipid and
inflammatory infiltrate:
▪ Atheromas: protrude into the lumen of the vessel, narrowing it and
obstructing blood flow
● A thrombus may then obstruct blow flow, leading to acute coronary syndrome
(ACS), which then can result in an myocardial infarction (MI), a portion of the
heart muscle no longer receives blood flow and becomes necrotic
Clinical Manifestations
● Produces signs/symptoms according to the location and degree of narrowing of
the arterial lumen, thrombus formation, and obstruction of blood flow to the
myocardium
● Lack of blood flow is usually progressive, causing an inadequate blood supply
that deprives the cardiac muscle cells of oxygen needed for their survival: known
as ischemia
● Decrease in blood supply or long enough duration, irreversible damage and
death to myocardial cells can occur19
● Significant myocardial damage may result in persistently low cardiac output &
heart failure where the heart cannot supply the body with enough blood
● Decrease in blood supply from CAD may cause the heart to abruptly stop
beating: sudden cardiac death
● Most common manifestation of myocardial ischemia is the onset of chest
pain
● Some complain of epigastric distress & pain that radiates to the jaw or left
arm*****
● Pts with hx of diabetes or heart failure may report shortness of breath
● Women show symptoms: indigestion, nausea, palpitations, and numbness
● Major cardiac event may be the first indication of coronary atherosclerosis**
Risk Factors
● Elevated low-density lipoprotein (LDL) cholesterol, known as bad cholesterol
● Pt at highest risk: those with known CAD, diabetes, peripheral arterial disease,
abdominal aortic aneurysm, or carotid artery disease
● Metabolic Syndrome
Nonmodifiable Risk Factors
● Family hx
● Increasing age (more than 45 yrs for men; more than 55 yrs for women)
● Gender (men develop CAD at an earlier age)
● Race (higher in African Americans than Caucasians)
Modifiable Risk Factors
● Hyperlipidemia
● Smoking
● Hypertension
● Diabetes
● Metabolic syndrome
● Obesity
● Physical inactivity
Diagnosis of this syndrome includes three of the following conditions:
● Insulin resistence
● Central obesity (waist circumference more than 35 inches in females, more than
40 inches in males)
● Dyslipidemia (triglycerides more than 150 mg/dL, HDL less than 50 mg/dL in
females, less than 40 mg/dL in males)
● BP persistently greater than 130-85 mmHg
● Proinflammatory state (high levels of C-reactive protein)
● Prothrombotic state (high fibrinogen level)
*many ppl with type 2 diabetes fit this*
Pathophysiology20
Controlling Cholesterol Abnormalities
● A fasting lipid profile should demonstrate the following values:
o LDL cholesterol less than 100mg/dL (less than 70mg/dL for very high-risk
patients)
o Total cholesterol less than 200mg/dL
o HDL cholesterol greater than 40 mg/dL for males & greater than 50mg/dL
o Triglyceride less than 150mg/dL
Dietary Measures
Total Calories: Balance intake & expenditure to maintain desirable weight
Total Fat: 25-35% of total calories
Saturated fat: <7% of total calories
Polyunsaturated fat: up to 10% of total calories
Monosaturated fat: up to 20% of total calories
Carbohydrates: 50-60% of total calories
Dietary fiber: 20-30 g/day
Protein: approximately 15% of total calories
Cholesterol: <200mg/day
*Eat a treat*
Physical Activity
● Atleast 150 minutes per week or vigorous intensity aerobic activity of atleast 75
minutes/week
Medications
● Lipid-lowering meds can reduce CAD mortality in pts with elevated lipid levels
and in at-risk pt with normal lipid levels
o Types lipid lowering agents:21
▪ 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) (or satins)
▪ Fibric acids (or fibrates)
▪ Bile acid sequestants (or resins)
▪ Cholesterol absorption inhibitors
▪ Omega-3 acid ethyl esters
▪ Proprotein convertase subtilisin-kexin type 9
Medication Therpeutic Effects Considerations
HMG-CoA Reductase
Inhibitors (Statins)
Atovastatin (Lipitor)
Simvastatin
(Zocor)
Total cholesterol
LDL
^ HDL
TGs
-Enhibit enzyme involed
in lipid synthesis
-Favorable effects pm
vascular endothelium,
including
anti-inflammatory &
antithrombotic effects
-Freq given as initial
therapy for significantly ^
cholesterol & LDL levels
-Myalgia & arthralgia:
adverse effects
-Myopathy &
rhabdomyolysis: potential
serious effects
-Monitor liver function tests
-contraindicted in liver
disease
-Check for drug
interactions
-Indication for use: ACS &
stroke
-Administer in evening
Fibric Acids (Fibrates)
Fenofibrate (TriCor)
Gemfibrozil (Lopid)
^ HDL
TGs
Synthesis of TGs &
other lipid
-Adverse effects: diarrhea,
flatulence, rash, myalgia
-Serious: pancreatitis,
heptoxicity, & rhabomyolsis
-Containdicted in severe
renal & liver disease
-**Use with caution in pts
who are taking satins***
Cholesterol Absorption
Inhibitors
Ezetimibe (Zeta)
LDL
Inhibits absorption of
cholesterol in small
intestine
-Better tolerated than bile
acid sequestrants
-Used in combo w: satins
-Side effects: abdominal
pain, arthralgia, myalgia
-Contraindicted in liver
disease
Omega-3-Acid Ethyl Easters
Fish oil capsules
TGs -May be used alone or in
combo with other agents22
Inhibit TG production in
liver
-side effects: GI distress,
taste perversion, rash, &
back pain
TG means: true glucose
Angina
● chest pain that is brought about by myocardial ischemia
● associated a significant with a significance obstruction of at least one
major coronary artery
● myocardium extracts a large amount of oxygen from the coronary
circulation to meet its continuous demands
● when demand ^^^ flow thru the coronary arteries needs to be increased
● when there is a blockage in a coronary artery, flow cannot be increased
and ischemia result
Several factors associated:
● physical excretion, which precipitates an attack by ^ myocardial oxygen demand
● Exposure to cold, which causes vasoconstriction & elevated BP, with increased
oxygen demand
● Eating a heavy meal, increases the blood flow to the mesenteric area for
digestion, thereby reducing the blood supply available to the heart muscle
o Severely compromised heart shunting of blood for digestion can be
sufficient to induce anginal pain
● Stress or any emotion-provoking situation causing the release of catecholamines
(increases BP, heart rate, myocardial workload)
Stages of Angina:
● Stable angina: predictable & consistent pain that occurs on exertion and relieved
by rest and/or nitroglycerin
● Unstable angina: (also called preinfarction angina or crescendo angina);
symptoms increase in frequency&severity; may not be relieved w/ rest or
nitroglycerin
● Intractable or refractory angina: severe incapitating chest pain
● Variant angina: (also called Prinzmetal’s angina): pain at rest w/ reversible
ST-segment elevation; thought to be caused by coronary artery vasospasm
● Silent ischemia: objective evidence of ischemia (such as electrocardiographic
changes w/ stress test), but pt reports no pain
Medical Management
● Objectives of meds are to decrease the oxygen demand of the myocardium & to
^ oxygen supply
Nitroglycerin23
● Potent vasodilator that improves blood flow to the heart muscle & relieves pain
● Dilates primarily the veins & to a lesser extent, the arteries
o Dilation of the veins causes venous pooling of blood throughout the body
o As a result less blood returns to the heart & filling pressure (preload) is
reduced
o Relax the systemic arteriolar bed, lowering BP & decreasing overload
▪ These effects decrease myocardial oxygen requirements
Beta-adrenergic Blocking Agents: metoprolol (Lopressor)
● Reduce myocardial oxygen consumption by blocking beta-adrenergic
sympathetic stimulation to the heart
● Result:
o Reduced HR
o Slowed conduction of impulses thru the conduction system
o Decreased BP
o Reduced myocardial contractility (force of contraction)
● Beta-blockers balance the myocardial oxygen needs (demands) and the amount
of oxygen available (supply)
o Helps control chest pain & delays the onset of ischemia during work or
exercise
● Reduce the incidence of recurrent angina, infarction, and cardiac mortality
o Dose can be titrated to achieve a resting heart rate of 50-60 bpm
Calcium Channel Blocking Agents:
● Decrease sinoatrial node automatically & atrioventricular node conduction
resulting in:
o Slower heart rate
o Decrease in the strength of myocardial contraction (negative inotropic
effect)
● ^ myocardial oxygen supply by dilating the smooth muscle wall of the coronary
arterioles
o They decrease oxygen demand by reducing systemic arterial pressure &
the workload of the left ventricle
● Most commonly used:
o Amlodipine (Norvasc)
o Diltiazem (Cardizem)
o They are commonly prescribed for hypertension
Antiplatelet and Anticoagulant Medications:
● given to prevent platelet aggregation & subsequent thrombosis, which impledes
blood flow thru the coronary arteries
Aspirin
● prevents platelet aggregation & reduces the incidence of MI and death in pts with
CAD24
● Pts should contine taking even if also take other analgesics like acetaminophen
(Tylenol)
Adenosine Diphosphate Receptor Antagonists (P2Y12)
● Clopidogrel(Plavix) most commonly prescribed in addition to aspirin for pts at
high rish for MI
● Prasugrel (Effient) may be prescribed during coronary events and interventions
Heparin***
● Prevents formation of new blood clots
● Dose of heparin is based on the results of the activated partial thromboplastin
time(aPTT)
● Heparin therapy is considered therpuetic when the aPTT is 2-2.5 times the
normal aPTT value *(TEST)*
● SQ injection of low-molecular-weight-heprin:enoxaparin (Lovenox) or dalteparin
(Fargmin) may be used to treat pts with unstable angina or Non-ST-segment
elevation myocardial infarction (NSTEMI)
● Heparin & warfarin can be used simultaneously
Labs to use for heparin: aPTT
Glycoprotein IIb/IIIa Agents
● Prevent platelet aggregation by blocking the GP IIb/IIIa receptors on the
platelets, preventing adhesion of fibrinogen & other factors that crosslink platelets
to each & form intracoronary vlots
● Examples: abciximab (ReoPro) or eptifibatide (Integrilin)
● IV administration indicated for hospitilazewd pts with unbstable agina & as
adjunct therpay for PCI
● Like heparin, bleeding is the major side effect (initiate bleeding
precations***
Nursing Interventions
Treating Angina
● Pt experiencing agina should stop all activities and sit or rest in bed in a
Semi-Fowler’s position
● Assess pt: vital signs & observe for signs of respiratory distress
o If pt is in the hospital, a 12-lead ECG is obtained & assessed for
ST-segment and T-wave changes
● Nitroglycerin is given sublingualy & pts response is assessed
o Relief of chest pain and effet on BP & HR
● Assess BP, HR, and ST segment (if pt is on a monitor with ST-segment
monitoring) each time
Acute Coronary Syndrome
● Emergency situation characterized by an acute onset of myocardial ischemia that
results in myocardial death25
Clinical Manifestations
● Chest pain that occur suddenly & continues despite rest & medications
● Combo of symptoms: chest pain, shortness of breath, indigestion, nausea,
anxiety
o Cool, pale, moist skin
o HR and Respirations faster than normal
Assessment and Diagnostic Findings (for Acute Coronary Syndrome & MI)
● Cardovascular
o Chest pain/discomfort not relieved by rest or nitroglycerin
▪ Heart sounds: S3 & S4; new onset of murmur
o Increased jugular venous distention if MI has caused heart failure
o BP elevated bc of sympathetic stimulation or decreased bc of decreased
contractibility, cardiogenic shock, or medications
o Irregular pulse could indicate atrial fibrillation
o ST-segment & T-wave changes, the electrocardiogram may also show
tachycardia, bradycardia, or other dysrhythmias
● Respiratory
o Shortness of breath, dyspnea, tachypnea, and crackles if MI has caused
pulmonary congestion
o Pulmonary edema may be present
● Gastrointestinal
o Nausea, indigestion, vomiting
● Genitourinary
o Decreased urinary output may indicate cardiogenic shock
● Skin
o Cool, clammy, diaphoretic, and pale appearance due to sympathetic
stimulkation may indicate cardiogenic shock
● Neurologic
o Anxiety, restlessness, and lightheadedness may indicate ^ sympathetic
stimulation
o Or decrease in contractility and cervral oxygenation
o Same symptoms could indicate cardiogenic shock
● Psychological
o Fear with feeling of impending doom or denial that anything is wrong
MI Classification
● Affected area of the heart: anterior, lateral, inferior, or posterior
● ECG changes produced: ST elevated myocardial infarction vs non-ST elevation
myocardial infarction
● Time frame within the progression of the infarction: acute, evolving, old
Heart Failure26
● Clinical syndrome resulting from structural or functional cardiac disorders that
impair the ability of the ventricles to fill or eject blood
● Referred to as Congestive Heart Failure bc many pts experience pulmonary or
peripheral congestion with edema
● “Heart Failure”: indicates myocardial disease with impaired contraction of the
heart (systolic dysfunction) or filling of the heart (diastolic dysfunction) may cause
pulmonary or systemic congestion
Chronic Heart Failure
● Approx.. 6 million ppl in the US have heart failure; 870,000 new cases each year
● Most common reason for hospitalization of ppl older than 65
● 2nd most common reason for visits to physician’s offices
● Approx.. 25% of pts discharged after treatment for HF return within 30 days
Clinical Manifestations Assessment (signs/symptoms)
● Congestion
o Dyspnea
o Orthopnea
o Paroxysmal nocturnal dyspnea (difficulty breathing @ night)
o Cough
o Pulmonary crackles that do not clear w/ cough
o Weight gain (rapid)
o Dependent edema
o Abdominal bloating or discomfort
o Ascites
o Jugular venous distention
o Sleep disturbance
o Fatigue
● Poor Profusion/Low Cardiac Output
o Decreased exercise tolerance
o Muscle wasting or weakness
o Anorexia or nausea
o Unexplained weight loss
o Lightheadedness or dizziness
o Unexplainable confusion or altered mental status
o Resting tachycardia
o Daytime oliguria w/ recumbent nocturia
o Cool or vasoconstricted extremities
o Pallor or cyanosis
Left-sided Heart Failure: LUNGS
● Pulmonary congestion occure when the left ventricle cant effectively pump blood
out to the aorta and the systemic circulation
● Increased left ventricular end-diastolic blood volume increase the left ventricular
end diastolic pressure27
o Decreases blood flow from the left atrium into the left ventricle during
diastole
● Blood volume & pressure build up in left atrium which decreases flow thru the
pulmonary veins into the left atrium
o Pulmonary blood volume and pressure increases in the lungs, forcing the
fluid from the pulmonary capillaries into the pulmonary tissues and alveoli
o Resulting in pulmonary intersistial edema & impaired gas exchange
● Clinical Manifestations:
o Dyspnea, cough, pulmonary crackles, and low O2 sats
o Extra heart sound; S3 or “ventricular gallop” could be heard bc of
abnormal ventricular filling
o orthopnea: difficulty breathing when lying flat
o paroxysmal nocturnal dyspnea (PND): sudden attacks of dyspnea at night
Right-Sided Heart Failure: SYSTEMS
● Right side cant eject blood effectively & cant accommodate all of the blood that
normally returns to it from venous circulation
o Causes congestion in the peripheral tissues & the viscera predominates
Medical Management
● Treatment options depend on the severity and could be oral & IV meds, lifestyle
changes, supplemental O2, and surgical interventions including: implantation of
cardiac devices and cardiac transplant
Medication Therapeutic Effects Considerations
Angiotensin-Convertin
Enzyme Inhibitors
Lisinopril (Prinivil)
Enalapril (Vasotec)
BP and afterload
Relieves s/s of HF
Prevents progression of
HF
-Observe for symptomatic
hypotension, increased
serum K+, cough &
worsening renal function
Angiotensin Receptor
Blockers
Valsartan (Diovan)
Losartan (Cozaar)
BP and afterload
Relieves s/s of Hf
Prevents progression of
HF
-Observe for symptomatic
hypotension, increased
serum K+, worsening renal
function
Hydralazine and Isosorbide
Dinitrate (Dilatrate)
Dilates blood vessels
BP and afterload
-Observe for symptomatic
hypotension
Beta-Adrenergic Blocking
Agents (Beta-Blockers)
Carvedilol (Coreg)
Bisoprolol (Zebeta)
Dilates blood vessles
s/s of HF and afterload
-Observe for decreased
heart rate, symptomatic
hypotension, dizziness,
fatigue28
Metoprolol (Lopresssor,
Toprol XL)
improves exercise
capacity
Diuretics
Loop diuretic
: Furosemide
(Lasix)
Thiazide diuretic
: metolazone
(Zaroxolyn)
Hydrocholorothiazide (HCTZ)
Aldosterone antagonist
:
Spironolactone (Aldactone)
Fluid volume
Overload
S/S of HF
Improves HF
sysmptoms in advanced
HF
-Observe for electrolyte
abnormalities, renal
dysfunction, diuretic
resistance, decreased BP
-monitor I&O and daily
weight
-Observe for hyperkalemia
& hyponatremia
Digitalis
Digoxin (Lanoxin)
Improves cardiac
contractility
S/S of HF
-observe for bradycardia
and digitalis toxicity
Pharmacologic Therapy
● Meds commonly prescribed: ACE inhibitors, beta-blockers, and diuretics
o Diuretics improve symptoms but may not affect survival
● Hydralazine & Isosorbide Dinitrate
o Combo is recommended for HF and may be more effective for African
Americans who do not respond to ACE inhibitors
● Beta-Blockers
o Produce side effects: dizziness, hypotension, bradycardia, fatigue,
depression
● Digitalis
o Key concern w/ digoxin: digitalis toxicity **
Physical Exam
● Assess: Rate and depth of respiration & effort required for breathing
● Auscultate: listen for S3 sounds, which is an early sign that increased blood
volume fills the ventricle with each beat
● Assess: peripheral pulses and rate their volume on a scale from 0 (not palpable)
to 3+ (bounding)
● Assess: feet and lower legs for edema; if pt is supine in bed assess sacrum and
back also
● Assess: abdomen for tenderness and hepatomegaly
● Meaure urinary I&O’s
o Oliguria: diminished urine out, less than 0.5 mL/kg/hr
o Anuria: urine output less than 50mL/24hr29
o Significant change in weight (2-3lbs increase in a day or 5lbs increase in a
week) tell provider and adjust meds
Pulmonary Edema
● Abnormal accumulation of fluid in the interstitial spaces & alveoli of the lungs
● Results from left ventricular failure
● Rapid increase in atrial pressure results in an acute increase in pulmonary
venous pressure
o This produces an increase in hydrostatic pressure that forces fluid out of
the pulmonary capillaries and into the interstitial spaces & alveoli
● Fluid within the alveoli mixes with air producing the classic sign of pulmonary
edema:
o Frothy pink (blood-tinged),sputum
● Large amounts of alveolar fulid creates a diffusion block that impairs gas
exchange
o Result: hypoxemia
Clinical Manifestations
● Restless and anxiety
● Sudden onset of breathlessness; sense of suffocation
● Tachypneic w/ noisy breathing and low O2 sats
● Crackles
● Reduced urine output
● Confusion; stupor
● S3 heart sound: gallop
Medical Managemant
Rapid-acting diuretics: Furosemide & bumetanide, promote fluid excretion
Morphine: decreases sympathetic nervous system response and anxiety and promotes
mild vasodilation
Vasodilators: (nitroglycerin) decrease preload and afterload
Inotropic agent: (digoxin) improve cardiac output
Antihypertensives: (ACE inhibitors & beta-blockers) decrease afterload
Nursing Care
● pt is positioned upright w/ legs dangling over side of bed
● Monitor vital signs every 15min until stable
● Monitor I&O’s
● Monitor pulmonary wedge pressures; cardiac output
● Check ABG’s, electrolytes (esp potassium if on diuretics), SaO2, chest x-ray
findings
● Maintain pt airway, suction if needed
● Administer high-flow oxygen
● Restrict fluid intake30
● Monitor hrly urine output: watch for intake greater than output or hrly urine less
than 30mL/hr
Thromboembolism
● Intracardiac thrombi can form in pts with Afib bc the atria do not contract
forcefully, resulting in slow turbulent flow
● Clots within the cardiac chambers can be detected by an echocardiogram
o Treated with anticoagulant agents: heparin & warfarin
● S/S:
o Leg pain and swelling, feels warm: DVT
● These clots can break off and travel thru the inferior vena cava & thru the right
side of the heart into the pulmonary artery (causes pulmonary embolus)
Pulmonary Embolism
● Blood clots in the lungs
● Indicators:
o Dyspnea
o Pleuritic chest pain
o Tachypnea
● Diagnostic Tests:
o Chest x ray
o Ventilation-perfusion lung scan
o High-resolution helical computed tomography
o Computed tomographic pulmonary angiogram
o Blood D-dimer assay is helpful screening test that identifies whether
clotting and fibrinolysis are taking place somewhere in the body
Peripheral Vascular Diseases
● Inadequate peripheral blood flow occurs when the heart’s pumping action
becomes inefficient
● Circulatory insufficiency of the Extremities:
o Most types of peripheral vascular disease result in ischemia
o Symptoms: pain, skin changes, diminished pulses, possible edems
● Characteristic. Arterial. Venous
ral Characteristics
s
mittent claudication to
sharp, unrelenting,
constant
shed or abset
ng, throbbing, cramping
nt, but may be difficult to
palpate thru edema
entation in area of medial
and lateral malleolus,31
characteristics ndent rubor—elevation
pallor of foot; dry, shiny
skin; cool to cold temp,
loss of hair over toes
and top of foot, nails
thick & rigid
skin thick and tough,
may be reddish blue,
frequently with
associated dermitits
Characteristics
on
of ulcer
e
base
dema
toes, toe webs, heel or
other pressure areas if
confined to bed
paiful
often involving joint
space
ar
o black/dry gangreaen
al unless extremity kept
in dependent position
constantly to relieve pain
al malleolus, lateral
malleolus, anterior tibial
area
al pain if superficial, could
be very painful
rficial
lar border
ulation tissue—beefy red
to yellow fibrinous in
chronic long term ulcer
rate to severe32
Physical Assessment
Palpation of pulses
● Determine presence/absence
o Absence may indicate that the site is stenosis: narrowing or
constricted
● Quality of peripheral pulses
Diagnostic Evaluation
Doppler Ultrasound Flow Studies
● When pulses cant be palpated, a handled continuous wave (CW) Doppler
ultrasound is used to detect blood flow in vessels
Venous thromboembolism
● Deep vein thrombosis (DVT) + pulmonary embolism (PE)= VTE
● Superficial veins, such as the greater saphenous, short saphenous (lesser
saphenous), cephalic, basilic, and expternal jugular veins, are thick-walled
muscular structures that lie under the skin
o Deep & superficial veins have valves that permit unidirectional flow back
to the heart
Clinical Manifestations:
● S/S are non specific
o Exception: phlegmasia cerulea dolens (massive iliofemoral venous
thrombosis)
▪ The entire extremity is massively swollen, tense, painful, and cool
to the touch
● Deep veins
o Edema
o Swelling
● Superficial veins
o Pain or tenderness
o Redness
o Warmth in involved area
Leg Ulcers
● Inadequate exchange of oxygen and other nutrients in the tissue
Assessment and Diagnostic Findings
● Hx of condition is important
● Examine pulses in lower extremities: femoral, popliteal, posterior tibial, dorsalis
pedis
● Cultures of the ulcer bed to determine whether an infecting agent is the primary
cause
Arteriosclerosis and Atherosclerosis
● Arteriosclerosis33
o Hardening of the arteries
o Muscle fibers and the endothelial of the walls of small arteries and
arterioles become thick
● Atherosclerosis
o Affecting the intima of large and medium-sized arteries
o Accumulation of lipids, calcium, blood compnents, carbs, and fibrous
tissue on the intimal layer of the artery
o Most common result: narrowing (stenosis) of the lumen, obstruction of
thrombosis, aneurysm, ulceration, and rupture
o Can develop at any point in the body
o 2 types of lesions:
▪ Fatty streaks: yellow and smooth, protrude slightly into the lumen of
the artery & composed of lipids and elongated smooth muscle cells
● Found in all age groups; even infants
● Do not cause clincal symptoms
▪ Fibroud plaques: smooth muscle cells, collagen fiber, plasma
components, and lipids.
● White to white-yellow
● Protrude into the arterial lumen, sometimes completely
obstructing it
● Found in the abdominal aorta and the coronary, popliteal,
and internal carotid arteries’
● Progressive lesions
Peripheral Arterial Occulsive Disease
● Main symptom: intermittent claudication described as aching, cramping, or
inducing fatigue or weakness that occurs w/ some degree of exercise or activity
o Relieved with rest
Pharmacologic Therapy:
Pentoxifylline (Trental) & cilostazol (Pletal)
o For treatment of symptomatic claudication
● Pentoxifylline
o Increases erythrocyte flexibility, lowers blood fibrinogen concentrations,
and inhibits neutrophil adhesion & activation
● Cilostazol
o Phosphodiesterase III inhibitor; a direct vasodilator that inhibits platelet
aggregation
Antiplatelet agents: aspirin & clopidogrel (Plavix)
● Prevent formation of thromboemboli, which can lead to myocardial infarction and
stroke
Statins
● Improve endothelial function in pt w/ PAD
● Improve symptoms of intermittent claudication
● Increase walking distance to the onset of claudication34
Hypertension
● Systolic BP of 140 mmHg or higher or diastolic blood pressure of 90 mmHg or
higher, based on the average of the two
BP Classification Systolic BP Diastolic BP
Normal <120 <80
Prehypertension 120-139 80-89
Stage 1 hypertension 140-159 90-99
Stage 2 hypertension Less than or equal 160 Less than equal 100
Medications
● Diuretics
● Calcium-channel blockers
● Angiotension-converting enzyme (ACE) inhibitors
o Lisinopril and enalapril
● Angitension II receptor antagonists
o Valsartan and losartan
▪ Good for pts taking ACE inhibitors who have a cough or
hyperkalemia
o Monitor for angioedema (swollen lips & face) and heart failure
o Pt should avoid foods high in potassium and monitor serum potassium
levels
● Aldosterone-receptor antagonists
o Eplerenone; blocks aldosterone action
▪ Promotes the retention of potassium and excretion of sodium and
water
o Monitor kidney function, triglycerides, sodium & potassium levels
o Pt education
▪ Hypertriclyceridemia, hyponatremia, kyperkalemia: risks increase
as dose increases
▪ Grapefruit juice & St. John’s wort can increase adverse side effects
▪ No salt substitutes
● Beta-Blockers
● Central-alpha2 agonists
o Clonidine
o Reduce peripheral vascular resistance & decrease BP by inhibiting the
reuptake of norepinephrine
o Monitor BP and pulse
● Alpha-adrenergic Antagonists
o Prazosin
o Reduce BP by causing vasodilation
o Start w/ low dose, usually given at night
o Monitor BP for 2hr after administration35
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