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235 Cards in this Set

  • Front
  • Back
UTERINE FIBROIDS
benign tumors in the
uterine corpus that may appear on the
broad ligament or cervix. They may be
related to levels of estrogen & HGH.
UTERINE FIBROIDS/Signs
& symptoms -
hypermenorrhea,
(dysmenorrhea or leukorrhea may occur)
pain, backache, constipation, urinary
frequency or urgency or intestinal
obstruction
UTERINE FIBROIDS Diagnosis-
blood tests,
palpation of the tumor, laparoscopy or D &
C. Treatment- observation, blood
transfusion or hysterectomy.
GESTATIONAL TROPHOBLASTIC DISEASE
(hydatiform mole)-developmental anomaly
of the placenta. The chorionic villi convert
into a mass of clear vesicles. (chorionic
tumor)
GESTATIONAL TROPHOBLASTIC DISEASE
Signs & symptoms
- rapid growth of
the uterus, vaginal bleeding & cramping.
Diagnosis- HCG levels are extremely high
for early pregnancy. Ultrasound fails to
reveal a fetal skeleton.
GESTATIONAL TROPHOBLASTIC DISEASE
Treatment
includes
D & C, weekly monitoring of HCG until they
remain normal for 3 consecutive weeks.
Periodic follow-up for 1 to 2 years because
of increased risk of neoplasm. Emphasize
contraception for a patient following
removal of a gestational trophoblastic
neoplasm until HCG is normal (may take as
long as 2 years).
GESTATIONAL TROPHOBLASTIC DISEASE Drug used
Methotrexate prophylactically is the drug
of choice for choriocarcinoma.
FIBROCYSTIC DISEASE OF THE BREAST
overgrowths
of fibrous tissue in the area of
the ducts forming small cysts that develop
& disappear quickly. Common between
ages of 30-50. Cysts have no malignant
potential however breasts that have cysts
are more prone to develop cancer.
Treatment-FIBROCYSTIC DISEASE OF THE BREAST
aspiration of fluid, medication
(Danocrine), analgesics for pain.
PYLORIC STENOSIS-
hyperplasia &
hypertrophy of the circular muscle at the
pylorus narrows the pyloric canal. Defect is
common in male infants between ages 1-6
months.
PYLORIC STENOSIS-Signs & symptoms
projectile
vomiting, visible reverse peristaltic waves,
weight loss, constipation & a hypertrophied
sphincter, the size of an olive can be felt in
the abdomen. Dehydration is common &
metabolic alkalosis will occur without rapid
intervention.
PYLORIC STENOSIS- Treatment
Treatment- surgical
intervention (pyloromyotomy performed by
laparoscopy).
PROSTATIC HYPERPLASIA
PROSTATIC HYPERPLASIA-considered normal
result of aging.
PROSTATIC HYPERPLASIA Signs & symptoms -
reduced stream force & caliber of urine, a
feeling of not emptying the bladder,
urinary retention.
PROSTATIC HYPERPLASIA Diagnosis-
rectal digital
exam of the prostate, intravenous
pyelography, elevated BUN & Creatinine
levels, UA & urine culture. Treatmentprostate
massage, fluid restriction, sitz
baths, regular sexual intercourse to relieve
prostatic congestion. TURP (transurethral
resection of the prostate).
PROSTATIC HYPERPLASIA . Nursing
interventions
Nursing
interventions include continuous irrigation
to prevent clotting & maintain patency
Chest Tumors
- benign or malignant –
malignant tumor can be primary, arising
within the lung, chest wall, or mediastinum
or a metastasis form a primary tumor
elsewhere in the body.
Bronchogenic Carcinoma –
arise from a single transformed epithelial
cell in the tracheobronchial airway. Tumors
of the mediastinum – neurogenic, thymus,
lymphomas, germ cell, cysts &
mesenchymal tumors. More common in
men, has a poor prognosis & is largely
preventable. Types include squamous,
oat-cell, adeno & large-cell (anaplastic)
carcinoma.
Lung Cancers –
Bronchogenic Carcinoma –
arise from a single transformed epithelial
cell in the tracheobronchial airway. Tumors
of the mediastinum – neurogenic, thymus,
lymphomas, germ cell, cysts &
mesenchymal tumors. More common in
men, has a poor prognosis & is largely
preventable. Types include squamous,
oat-cell, adeno & large-cell (anaplastic)
carcinoma.______
Lung Cancers – Chest Tumors s/s
Signs & symptoms - smoker’s
cough, wheezing, hemoptysis, dyspnea, &
chest pain.
Diagnosis- chest x-ray, sputum
for cytology, bronchoscopy, needle biopsy
of the lungs, tissue biopsy & thoracentesis.
Treatment includes pneumonectomy,
lobectomy, or wedge resection, radiation
& chemotherapy.
___________________________________________________
Cancer of the lip-
occurs most often in men. Risk
factors include smoking, sun & wind exposure.
Prognosis is good if the lesion is localized &
totally excised.
Cancer of the tongue- and treatment
common in men
related to persistent irritation caused by
tobacco use, food, chronic alcoholism,
or poorly aligned teeth. Treatment radiation
& surgical removal of the lesion
(may include removal of part or all of
the tongue)
Cancer of the mouth-
usually occurs in
middle-aged adults. Excision is
treatment of choice. It affects speech,
nutrition, facial features, & swallowing
Parenteral Nutrition -Total parenteral nutrition (IV
hyperalimentation) is
the IV
administration of carbs (high
concentration of dextrose), protein
(amino acids), electrolytes, vitamins,
minerals, & fat emulsions.
 Usually admin through subclavian vein
through a central venous catheter
(triple-lumen to also permit meds,
intralipid, or blood)
Parenteral Nutrition - Solutions
Solution: 500mL 50% dextrose, 500mL of
8.5% amino acid, electrolytes, minerals,
vitamins
 Always use infusion pump – discontinue
gradually allowing pt to adjust to ↓ levels
of glucose
Parenteral Nutrition - Solutions Complications
Pneumothorax, air
embolism, clotted or displaced cath,
sepsis, hyperglycemia, rebound
hypoglycemia, fluid volume excess
/overload; long-term use can lead to
gallstone formation & liver disease
Parenteral Nutrition - Nursing Diagnoses include:
Altered
nutrition, less than body requirements;
Risk for infection related to
contamination of central cath site; Risk
for fluid volume excess (FVE) or deficit
(FVD
STOMACH CANCER-
caused by
degenerative changes in gastric ulcers.
Men 2 times more frequently than women.
Middle-aged adults in the low
socioeconomic group are common
because of a diet high in starch, with few
fresh vegetables & fruits.
STOMACH CANCER-Diagnosis-
Diagnosis- x-ray
exam, gastric analysis & biopsy via
gastroscopy. Poor prognosis. Increased
incidence of stomach cancer in Japanese.
 Cancer of the esophagus- epidermoid
carcinoma is rare & affects people over
the age of 60
STOMACH CANCER/ caused by
STOMACH CANCER-caused by
degenerative changes in gastric ulcers.
Men 2 times more frequently than women.
Middle-aged adults in the low
socioeconomic group are common
because of a diet high in starch, with few
fresh vegetables & fruits.
STOMACH CANCER Diagnosis
Diagnosis- x-ray
exam, gastric analysis & biopsy via
gastroscopy. Poor prognosis. Increased
incidence of stomach cancer in Japanese.
 Cancer of the esophagus- epidermoid
carcinoma is rare & affects people over
the age of 60.
INTESTINAL OBSTRUCTION
85% of obstructions occur in small
intestine, adhesions are most common
cause, 15% in large bowel – most often
in sigmoid colon due to carcinoma,
diverticulitis, IBS, benign tumors.
o Mechanical – intraluminal or mural
obstruction from pressure on the
intestinal walls – polypoid tumors,
neoplasms, stenosis, strictures,
adhesions, hernias, abscesses.
o Functional – intestinal musculature
cannot propel contents – amyloidosis,
muscular dystrophy, diabetes,
Parkinson’s – can be temporary due to
surgery
COLORECTAL CANCER- Age, diet Hx of
COLORECTAL CANCER- Occurs in middleaged
adults, with low-residue diets of
refined carbohydrates & fats, incidence
increases with age – highest in ↑ age 85.
History of ulcerative colitis; diverticulitis &
polyps have been implicated in malignant
changes. Diagnosis- guaiac stool tests,
digital rectal exam & sigmoidoscopy. CEA
antigen (unreliable, can be elevated in
inflammation & other diseases). A CEA titer
less than 5 ng is considered normal. A CEA
greater than 10 ng must be investigated.
Treatment- surgery, radiation &
chemotherapy. 3 out of 4 people could be
saved by early diagnosis
COLORECTAL CANCE DX & treatment
Diagnosis- guaiac stool tests,
digital rectal exam & sigmoidoscopy. CEA
antigen (unreliable, can be elevated in
inflammation & other diseases). A CEA titer
less than 5 ng is considered normal. A CEA
greater than 10 ng must be investigated.
Treatment- surgery, radiation &
chemotherapy. 3 out of 4 people could be
saved by early diagnosis
RENAL TUMORS-highest in what sex, most common kind, early sign
Cancer of the kidney
accounts for approx. 2% of all cancers in
adults in the USA & affects 2x more men
then women. – Most common is renaladenocarcinoma – may metastasize early
to the lungs, bone, liver, brain &
contralateral kidney. – Usual sign that 1st
calls attention to the tumor is painless
Hematuria.
BLADDER CANCER-more common in , age group, risk linked to ,
more common in men,
than in women. Occurs after age 50.
Increased risk linked to occupations like
cable workers, petroleum workers,
hairdressers, weavers, aniline dye workers,
rubber workers, spray painters, & leather
finishers.
BLADDER CANCER- s/s DX, treatment
Signs & symptoms - intermittent
hematuria, clots in the urine, pain after
voiding, bladder irritability, nocturia,
dribbling & urinary frequency. Diagnosis
cystoscopy
& biopsy.
treatment- includes
cystoscope resection if the tumor is well
localized, radical cystectomy &urethrectomy with permanent ileal conduit
(male impotence & permanent sterility)
URINARY DIVERSION
procedures
performed to divert urine form the bladder
to a new3 exit site – usually through a
stoma
URINARY DIVERSION types 4 ,
Cutaneous Urinary Diversion – Ileal
Conduit ((Ileal Loop) – oldest
procedure – low # of complications.
o Cutaneous Ureterostomy – ureters
directed thru abdominal wall &
attached to stoma – used for pts with
advanced pelvic cancer, poor risk pts.
o Continent Ileal Urinary Reservoir
(Indiana Pouch) – for pts whose
bladder has been removed or no
longer functions
o Ureterosigmoidostomy – implantation of
the ureters into the sigmoid colon
CERVICAL CANCER age group, Risk factors, s.s DX
Squamous cell cancer
(10% are adenocarcinomas) – occurs most
commonly in women aged 30-45, but can
occur as young as 18. Risk factors –
multiple sex partners, smoking, chronic
cervical infection – usual asymptomatic
until well advanced. Diagnosis with Pap
smear, flowed by biopsy – HPV infections
are usually implicated.
HYDATIFORM MOLE S/s and treatment
HYDATIFORM MOLE - Placenta
abnormality, S/sx Uterine growth, bleeding,
cramping. Can’t see the baby on a normal
ultrasound, treatment C&D, monitor until
HCG levels stable for 3 weeks, emphasize
the importance of contraception.
UTERINE CANCER-most common in age, s/s and treatment
common in
postmenopausal women aged 50-60. Signs
& symptoms - abnormal uterine bleeding,
anovulation obesity, hypertension, &
familial tendency. Increased risk in a history
of uterine polyps or endometriosis. Can
NOT be Diagnosis from Pap smear. Biopsy
of endometrial endocervical or cervical
tissue. Schiller’s test: (staining of the vagina
with iodine, health tissue turns brown, malignant tissue cannot absorb the stain.
This is a definitive test for uterine cancer.
Treatment- surgical intervention ranging
from hysterectomy to pelvic exenteration,
chemotherapy, radiation & hormonal
therapy.
CANCER OF THE VULVA, age, risk
3-5% of all GYN
malignancies; seen mostly in
postmenopausal women, although
incidence in younger women is increasing.
Median age is 44 for cancer limited to the
vulva, 61 for invasive vulvar cancer.
Increased Incidence with HTN, obesity,
diabetes, more whites than nonwhites
VAGINAL CANCER result from
VAGINAL CANCER – usually results from
metastasized choriocarcinoma or cancer
of the cervix or adjacent organs.
rare & least
common genital cancer.
CANCER OF FALLOPIAN TUBES
OVARIAN CANCER most common cancer, lowest in what country, s.s risk
Ovary is common site
of primary & metastatic lesion from other
cancers – asymptomatic until well
advanced, incidence is highest in
industrialized countries, except Japan; 4
times increased risk of breast cancer.
Radiations thearapy TBI
Total body
irradiation (TBI) is a radiotherapy technique
used to prepare the body to receive a bone
marrow transplant.
Radiotherapy has a few
applications in non-malignant conditions,
such as the treatment of
trigeminal
neuralgia, severe thyroid eye disease,
pterygium, prevention of keloid scar growth,
& prevention of heterotopic bone
formation. The use of radiotherapy in nonmalignant
conditions is limited partly by worries about the risk of radiation-induced
cancers The
precise treatment intent (curative, adjuvant,
neoadjuvant, therapeutic, or palliative) will
depend on the tumor type, location, &
stage, as well as the general health of the
patient.
most common
malignancy of women,
BREAST CANCER- most common
malignancy of women, usually occurs after
age 35. Risk factors include family history,
long menstrual cycles, early menses, late
menopause, constant stress, first
pregnancy after age 35
Breast cancer
Commonly
metastases to lung, liver, bone, kidneys,
brain & adrenal glands. Signs & symptoms -
lump or mass, change in breast size or
symmetry, thickening, dimpling of skin,
unusual nipple discharge. Treatmentbased
on stage of disease. Lumpectomy,
modified radical mastectomy, radical
mastectomy, chemotherapy & radiation.
TNM staging system: Tumor size, Nodal
involvement, Metastatic Progress
PROSTATE CANCER-, TX<DX,S/s
bone metastasis is
common. Signs & symptoms - usually
asymptomatic, urinary retention, dribbling,
difficulty starting the stream & cystitis are
late symptoms. Diagnosis- biopsy.
Treatment- surgical intervention,
chemotherapy, & radiation
TESTICULAR CANCER
most common among males aged 15-
40; most common among Caucasians &
rare among African Americans
Testis cancer TX, risk
A major risk
factor for the development of testis cancer
is cryptorchidism. The three basic types of
treatment are surgery, radiation therapy, &
chemotherapy; one of the highest cure
rates of all cancers: (stage I can have a
success rate of >95%) when detected
early, recommend regular monthly
Testicle examine s/s of cancer
lump in one testis or a hardening of
one of the testicles
 pain & tenderness in the testicles
 loss of sexual activity Copyright 2007
MyStudyGroup101
 build-up of fluid in the scrotum
Copyright 2007 MyStudyGroup101
 a dull ache in the lower abdomen or
groin Copyright 2007 MyStudyGroup101
 an increase, or significant decrease, in
the size of one testis
 blood in semen
Testicular test to DX
DX by scrotal ultrasound & CT scans. Blood tests
are used to identify & measure tumor markers.
The diagnosis is made by performing an
orchiectomy, surgical excision of the entire
testis along with attached structures epididymis
& spermatic cord; A biopsy should not be
performed, as it raises the risk of migrating
cancer cells into the scrotum
Basal cell epithelioma, common in , risk factors and type of
most commonly
occurs in adults after age 40 in blond, fairskinned,
Caucasian males. Prolonged sun
exposure is the largest risk factor. Lesions
usually occur on the face. They are small,
smooth, pink, translucent papules that
progress to firm raised bordered lesions with
depressed centers.
Superficial basal cell epithelioma Risk and TX
epitheliomacommonly
found on the chest & back. It is
an oval or irregular shaped lesion, slightly
elevated & lightly pigmented. The lesion
appears scaly & may resemble eczema or
psoriasis. Risk factors for this lesion include
arsenic ingestion. Treatmentchemotherapy
(5-fluororacil), surgical
excision, radiation or chemosurgery.
Interventions include high protein diet;
avoid sun exposure & tender skin care to
prevent bleeding
Squamous cell carcinoma- DX, TX and risk factors area of body
occurs in
Caucasian males over age 60 from sun, exposure. Other risk factors include x-ray
therapy, arsenic ingestion (think gardener
using herbicides), carcinogen exposure
(tar, oil), & chronic skin inflammation &
irritation. Lesions of the lower lip & ears
have a poor prognosis but others have a
good prognosis. Diagnosis- by biopsy.
Treatment- chemosurgery, radiation,
electrodessication & curettage & excision
Malignant melanoma-TX, RISK FACTORS, LOCATION
more common in
women than men, ages 50-70. Very rare in
children. Risk factors include sun exposure,
fair skin type, pregnancy (hormones
increase both growth & incidence), family
history. Common locations are the head,
neck, legs, & back. All moles (nevi) that
change in color, size, texture, have
drainage or bleed should be investigated.
Diagnosis- biopsy. Treatment- surgical
tumor removal with wide resection,
lymphadenectomy, chemotherapy &
radiation.
Ocular Cancer
 Conjunctival nevus
a congenital benign
neoplasm is a flat slightly elevated brown
spot that becomes pigmented during late
childhood. Cop
Rhabdomyosarcoma
is the most common
malignant primary orbital tumor in
childhood, but can also develop in the
elderly. Copyright 2007 MyStudyGroup101
1. bASAL CELL IS
2. CONJUNCTIVAL CARCINOMA
3. OCULAR MELANOMA
4.ENUCLEATION
Basal cell is the most common malignant
tumor of the eyelid.
 Conjunctival carcinoma - grows in exposed
areas of conjunctiva
 Ocular Melanoma – very rare – usually
discovered on retinal exam.
 Enucleation – removal of the entire eye &
part of the optic nerve
BRAIN TUMORS
localized intracranial lesion
that occupies space in the skull. Secondary
brain tumors develop from metastasized
structures outside the brain & occur in 20-
40% of all cancer pts; incidence is higher
with age 50s, 60s & 70s slightly higher in
men then women.
-GLIOMAS
-PITUITARY ADENOMAS-
-ANGIOMAS
-ACOUSTIC NEUROMAS
-MENINGIOMAS
Gliomas – most common neoplasm –
45% of all brain tumors.
o Pituitary adenomas – 8-12% of all brain
tumors – symptoms caused as a result
of pressure on adjacent structures.
Copyright 2007 MyStudyGroup101
o Angiomas – mass of abnormal blood
vessels Copyright 2007
MyStudyGroup101
o Acoustic Neuromas-tumor of the eighth
cranial nerve.
o Meningiomas – common benign
encapsulated tumor on the meninges –
15-20% of all brain tumors; slow
growing, occurring most often in middle
age more often in women
BONE TUMORS
osteogenic,
chondrogenic, fibrogenic, muscle &
marrow cell tumors as well as nerve,
vascular & fatty cell tumors. Metastatic
tumors are more common then primary
bONE TUMORS BENIGN
OSTEOCHONDROMA
ECCHONDROMA
ANEURYSMAL
UNICAMERAL
Osteochondroma is the most
common – usually occurring as large
projection of bone at the end of long
bonds. Ecchondroma is common
tumor of the hyaline cartilage
Aneurysmal bone cysts seen in young
adults – painful palpable mass of the
long bones, vertebrae or flat bond.
Unicameral bone cysts occur in
children & cause mild discomfort
Malignant - Osteogenic sarcoma, AGE GROUP, RISK FACTOR
is the
most common & most often fatal
primary bone tumor; occurs more
frequently. In males aged 10-25 & in
older people with Paget’s due to
radiation exposure. Chondrosarcomas
– malignant tumors of the hyaline
cartilage
CHILDREN MOST FREQUENT CANCER 2 TYPES
2 types that account for 85%
of all primary malignant tumors are
osteogenic sarcoma & Ewing Sarcoma.
Osteogenic Sarcoma
most frequent
bone cancer in children – between 10-
25 years. – Primary sites are the
metaphysic of long bones of lower
extremitie
Ewing Sarcoma
arises in the marrow
spaces of bone – principal sites of
origin are shafts of long bones, trunk
bones, & skull – almost exclusively in
individuals under age 30, most
occurrences age 4-25.
Rhabdomyosarcoma –
soft tissue
sarcomas in muscles, tendons, bursae
& fascia or from such cells in fibrous,
connective, lymphatic or vascular
tissue. – The 4th most common type of
solid tumor in children
Wilms Tumor s/S AND TREATMENT DX
5th most common
childhood tumor, tumor of the kidney
with good prognosis if treated. Familial
link. Signs & symptoms - palpable, firm,
smooth mass in the abdomen,
hypertension, vomiting. Diagnosisurine
collection of catecholamines,
presence rules out (r/o) tumor.
Treatment includes radical
nephrectomy, radiation, &
chemotherapy. Palpation is
contraindicated because it could
cause rupture & seeding,
dissemination of the tumor
LIVER CANCER-RISK, S/S, TX
risk factors include cirrhosis.
Commonly found in middle-aged to older
males. Diagnosis- liver function studies,
biopsy & scan of liver. Treatment- surgical
removal of the liver. (Up to 90% of the liver
can be removed with no loss of function,
the liver can regenerate.)
PANCREATIC CANCER-TX, DX, S/S, WHIPPLE PROCEDURE?
positive correlation
between alcoholism & cancer of the
pancreas. Most common in older males.
Signs/symptoms- weight loss, anorexia,
weakness, nausea, jaundice & a palpable
abdominal mass. Recent onset of
diabetes mellitus. Diagnosis- liver function
studies, x-rays, scans, biopsy & elevated
fasting blood sugar. Treatment- “Whipple
procedure”- surgical removal of the head
of the pancreas, the common bile duct,
the distal part of the stomach, &
duodenum. Long, extensive surgery with
risks associated with long anesthesia time
& long exposure of the internal viscera
LEUKEMIA-ALL, CML, AML, S/S.DX,TX
malignant proliferation of blast
cells (pre-WBC). ALL (acute lymphoblastic
leukemia), common in young children,
reasonably good prognosis. AML (acute
myeloblastic leukemia) common in all
ages. CML ( chronic myelogenous
leukemia) uncommon before age 20.
Signs/symptoms- high fever, abnormal
bleeding, chills, pallor, recurrent infection,
& prolonged weakness. Diagnosis- bone
marrow aspirate with a large component
of immature WBCs. Treatmentchemotherapy,
bone marrow transplant
SARCOMAS-DX, TX, RISK FACTORS
malignant tumor of bone
more common in males, most frequently
children & adolescents. Signs/symptomsrapid
growth (tall for age). Diagnosisbiopsy,
bone scans & x-rays. Treatmentamputation
& radiation. Chemotherapy,
immunotherapy & bone transplants may
also be combined.
SARCOMAS, NURSING INTERVENTIONS
Nursing interventions
include teaching about phantom pain,
psychological support for alteration in
body image, proper body alignment &
positioning Adriamycin, Cytoxan, vincristine
(Oncovin), & prednisone. It has been
effective in producing a prolonged
remission
Alkylating agents:
react with DNA to inhibit
cell division/growth. Busulfan, carboplatin,
cisplatin, cyclophosphamide, ifosfamide,
melphalan, nitrogen mustard & thiotepa.
S/E- renal toxicity.
Nitrosoureas:
cross blood-brain barrier to
react with DNA to inhibit cell
division/growth. BCNU (carmustine), CCNU
(lomustine), methyl CCNU (semustine), &
streptozocin. S/E- myelosuppression,
especially thrombocytopenia.
Ribonucleotide Reductase Inhibitors
Hydroxyurea (Hydrea), trimetrexate
glucoronate (Neutrexin), 2-
deoxycoformycin (Pentostatin, Nipent,
DCF)
Enzyme Inhibitors
pentostatin (Nipent
Mitotic Inhibitors
vinca alkaloids,
vinblastine sulfate (Velban, Oncovin,
Vincasar), vincristine (Liposomal, Marqibo),
vinorelbine (Navelbine
Antimicrotubule or Taxanes
docetaxel
(Taxotere), paclitaxel (Taxol)
Antitumor antibiotics:
interfere with DNAdependent
RNA synthesis & bind with DNA
to block cell growth. Adriamycin,
bleomycin, dactinomycin, daunorubicin,
mithramycin, mitomycin, mitoxantrone.
S/E- cardiac toxicity. Targeted Therapies –
Topoisomerase I Inhibitors, Topoisomerase II
Inhibitors, Tyrosine Kinase Inhibitors,
Proteasome Inhibitors, Monoclonal Antibodies, Angiogenesis Inhibitors,
Tetanoids
Alkyl Sulfonates
busulfan (Myleran
Antimetabolites:
folic acid antagonist -
compete with metabolites during nucleic
acid production which prevents cell
growth. Methotrexate (MTX, amethopterin,
Folex, Mexate)
Pyrimidine Analogues
capecitabine
(Xeloda, cytarabine HCl (Cytosar-U, ARAC)
floxuridine (FUDR), 5-fluorouracil (5-FU,
Adrucil), gemcitabine HCl (Gemzar),
procarbazine HCL (Matulane)
Purine Analogues
cladribine (Leustatin),
fludarabine (Fludara), 6-mercaptopurine
(6-MP, Purinethol, thioguanine (Lanvis
Hormones, Hormonal Antagonists &
Enzymes:
change the chemical
environment by binding to hormone
receptor sites which prohibits the growth of
tumors susceptible to hormones.
Tamoxifen, androgens, anti-estrogens,
estrogens, progesterone & steroids
Targeted Therapies
Topoisomerase I Inhibitors, Topoisomerase II
Inhibitors, Tyrosine Kinase Inhibitors,
Proteasome Inhibitors, Monoclonal
Antibodies, Angiogenesis Inhibitors,
Tetanoids
Biologic Response Modifiers
class of agents used to enhance the body’s immune system. Interferon,
colony-stimulating factors, interleukins, tumor necrosis factor, monoclonal antibodies. Herbal
preps are generally not recommended for clients receiving BRMs
Incidence of breast, bladder, prostate, & colon cancer increase with age. Prevention includes
eating a high-residue diet, increased intake of cruciferous vegetables, vitamins A, D, & E,
carotene
Alternative/complementary treatments
include hypnosis, acupressure, acupuncture, Reiki
therapy, guided imager, therapeutic touch, homeopathy, vitamins A, E, & B complex
Seven Warning Signs of Cancer (American Cancer Society)
1. Changes in bladder or bowel habits
2. A sore that does not heal Copyright 2007 MyStudyGroup101
3. Unusual discharge or bleeding Copyright 2007 MyStudyGroup101
4. Thickening or lump in the breast or elsewhere Copyright 2007 MyStudyGroup101
5. Indigestion or difficulty swallowing Copyright 2007 MyStudyGroup101
6. Obvious change in a mole or wart Copyright 2007 MyStudyGroup101
7. Nagging cough or hoarseness
Terms to know:
Hypertrophy-
Atrophy-
Hyperplasia-
Neoplasia-
Metaplasia-
Dysplasia-
Terms to know:
Hypertrophy- enlargement of an organ or part due to ↑ in the size or number of cells.
Atrophy- normal in aging. Decrease in size or number of cells.
Hyperplasia- ↑ in new cells that results from a stimulus, reversible once the stimulus is removed.
Neoplasia- Malignant growth of new cells that doesn’t remove when the stimulus is removed.
Metaplasia- conversion of a cell from highly specialized to less specialized.
Dysplasia- bizarre cell growth that causes cells to be different in shape, size or arrangement than
cells from the same type of tissue. May be reversible.
Primary hypertension
Secondary hypertension
Primary hypertension, or essential
hypertension, develops without
apparent cause;
• Secondary hypertension develops as a
result of another illness or condition.
Blood pressure s/s
Often the
client with hypertension will have no symptoms
at all or might complain of an early morning
headache and fatigueMedications such as oral
contraceptives and bronchodilators can also
cause elevations in blood pressure
Malignant hypertension is managed with
administration of
Hypertensive crises is Hypertensive crises
exist when the diastolic blood pressure reaches
140
IV Nitropress, Nitroglycerine,
Nipride, Lasix, and other potent vasodilators
such as Procardia.
The atrioventricular
(AV) node is located in the interventricular
septum and receives the impulse
septum and receives the impulse and transmits
it on to the Bundle of His, which extends down
through the ventricular septum and merges
with the Purkinje fibers in the lower portion of
the ventricles.
SA node
The normal conduction system of the heart is
comprised of the sinoatrial (SA) node located
Life Span 1
© 2008 – 2013 MyStudyGroup101 LLC – All rights reserved. 5
at the junction of the right atrium and the
superior vena cava. This node is considered to
be the main pacer of the heart rate. This area
contains the pacing cells that initiate the
contraction of the heart.
Heart block can occur as a result of
structural
changes in the conduction system, such as
tumors, myocardial infarctions, coronary artery
disease, infections of the heart, or toxic effects
of drugs such as Digitalis. Heart block occurs
when there is a problem with the conduction
system of the heart
First-degree AV block
occurs when
the SA node continues to
function normally but transmission of the
impulse fails. Because of the conduction
dysfunction and ventricular depolarization, the
heart beats irregularly. These clients are usually
asymptomatic and all impulses eventually
reach the ventricles
Second-degree heartblock is a block in which impulses
reach the
ventricles but others do not.
third-degree
heart block or complete heart,
none of the
sinus impulses reach the ventricle. This results in
erratic heart rates where the sinus node and
the atrioventricular nodes are beating
independently. The result of this type of heart
block can be hypotension, seizures, cerebral
ischemia, or cardiac arrest. Detection of a
heart block is made by assessing the
electrocardiogram
Toxicity to Medications
Toxicity to medications, such as ----------------causes heart blocks
Digitalis, can
be associated with heart block. Clients taking
Digitalis should be taught to check their pulse
rate and to return to the physician for regular
evaluation of their Digitalis level. The
therapeutic level for Digitalis is 0.9–1.2 ng/ml. Digitalis exceeds 2.0
ng/mL, the client is considered to be toxic.
Clients with Digitalis toxicity often complain of
nausea, vomiting, and seeing halos around
lights.
Digitalis toxicity includes
Digitalis toxicity includes
checking the potassium level because
hypokalemia can contribute to Digitalis
toxicity. The physician often will order
potassium be given IV or orally and that the
Digitalis be held until serum levels return to
normal. Other medications, such as Isuprel or
Atropine, and Digibind are frequently ordered
to increase the heart rate. A high fiber diet will
also be ordered because constipation
contributes to Digitalis toxicity.
pacemakers concerns
avoid direct contact with electrical equipment.ä Wear a medic alert
• Take pulse for 1 full minute
• Avoid applying pressure over the
pacemaker. .
• Inform the dentis
• Avoid having a magnetic resonance
imaging (MRI).
detectors, and welding equipment
because they can interfere with
conduction.
• Be careful when using microwaves.
stand
approximately 5 feet away from the device
while cooking.
• Report fever, redness, swelling, or soreness
at the implantation site.
• If beeping tones are heard coming from
the internal defibrillator, immediately move
away from any electromagnetic source.
Stand clear from other people because
shock can affect anyone touching the
client during defibrillation.
• Report dizziness, fainting, weakness,
blackouts, or a rapid pulse rate.
• The client will most likely be told not to drive
a car for approximately 6 months blackouts, or a rapid pulse rate.
• The client will most likely be told not to drive
a car for approximately 6 months after the
internal defibrillator is inserted to evaluate
any dysrhythmias.
• Report persistent hiccupping because this
can indicate misfiring
Myocardial Infarction
When there is a disruption in blood supply to
the myocardium, the client is considered to
have had a myocardial infarction. Factors
contributing to diminished blood flow to the
heart include arteriosclerosis, emboli, thrombus,
shock, and hemorrhage. If circulation is not
quickly restored to the heart, the muscle
becomes necrotic. Hypoxia from ischemia can
lead to vasodilation of blood vessels. Acidosis
associated with electrolyte imbalances often
occurs, and the client can slip into cardiogenic
shock. The most common site for a myocardial
infarction is the left ventricle.
Myocardial Infarction The most commonly reported signs and
symptoms associated with myocardial
infarction include
Only 10% of
clients report the classic symptoms of a
myocardial infarction. Women often fail to
report chest pain and, if they do, they might
tell the nurse that the pain is beneath the
shoulder or in the back. Clients with diabetes
have fewer pain receptors and might report
little or no pain. Substernal pain or pain over the
precordium of a duration greater than
15 minutes
• Pain that is described as heavy, viselike,
and radiating down the left arm
• Pain that begins spontaneously and is
not relieved by nitroglycerin or rest
• Pain that radiates to the jaw and neck
• Pain that is accompanied by shortness
of breath, pallor, diaphoresis, dizziness,
nausea, and vomiting
• Increased heart rate, decreased blood
pressure, increased temperature, and
increased respiratory rate
Myocardial Infarction DX
diagnostic tools for determining the type and
severity of the attack:
• Electrocardiogram (ECG), which
frequently shows dysrhythmias
• Serum enzymes and isoenzyme tests that are useful in providing a
complete picture of the client’s condition are
white blood cell count (WBC), sedimentations
rate, and blood urea nitrogen (BUN
Angina pectoris
Nitro
ASA
occurs when there are
vasospasms. This pain is relieved by
nitroglycerine take one every 5 mins, no more than 3 at a time The client should be
taught to replenish his supply every 6 months
and protect the pills from light by leaving them
in the brown bottle. The cotton should be
removed from the bottle because it will
decrease the tablets’ effectiveness. one 365 mg aspirin at the first sign of chest
pain. Aspirin has an anticoagulant effect and
decreases the clotting associated with heart
attacks. The nurse must always wear gloves
when applying nitroglycerine cream or
patches to the client. Clip hair with scissors or
shave, but do not abrade area.
Tropon 1,"", CRP, LDH
The Troponin T and 1 are specific
to striated muscle and are often used to
determine the severity of the attack. Creactive
protein (CRP) levels are used
with the CK-MB to determine whether the
client has had an acute MI and the severity of
the attack. Lactic acid dehydrogenase (LDH) is
a nonspecific enzyme that is elevated with any
muscle trauma.
Ventricular tachycardia
is a rapid irregular
rhythm absence of a p-wave. Usually the rate
exceeds 140–180 bpm. The SA node continues
to discharge in-dependently of the ventricle
Ventricular tachycardia is often associated
with
valvular heart disease, heart failure,
hypomagnesium, hypotension, and ventricular
aneurysms.
Ventricular tachycardia
Ventricular tachycardia is treated
with oxygen and medication. Amiodarone
(Cordarone), procainamide (Pronestyl), or
magnesium sulfate is given to slow the rate
and stabilize the rhythm. Lidocaine has long
been established for the treatment of
ventricular tachycardia; however, it should not
be used in an acute MI client. Heparin is also
ordered to prevent further thrombus formation
but is not generally ordered with clients taking
streptokinase.
Ventricular fibrillation (V-fib)
(V-fib) is the primary
mechanism associated with sudden cardiac
arrest. This disorganized chaotic rhythm results
in a lack of pumping activity of the heart.
Without effective pumping, no oxygen is sent
to the brain and other vital organs
Ventricular fibrillation (V-fib) s/s
The client quickly becomes
faint, loses consciousness, and becomes
pulseless. Hypotension or a lack of blood
pressure and heart sounds are present
Ventricular fibrillation (V-fib) TX
Three quick, successive shocks Administration of oxygen and
antidysrhythmic medications such as
epinephrine, amiodarone, procainamide,
lidocaine, or magnesium sulfate are ordered. If
cardiac arrest occurs, the nurse should initiate
cardiopulmonary resuscitation and be ready to
administer first-line drugs such as epinephrine Cardiac catheterization is used to detect
blockages associated with myocardial
infarctions and dysthymias.
percutaneous
transluminal coronary angioplasty. Prior to and
following this the nurse should
catheterization, as with any other dye
procedure, requires a permit. This procedure
can also accompany percutaneous
transluminal coronary angioplasty. Prior to and
following this
procedure, the nurse should
• Assess for allergy to iodine or shell fish.
• Maintain the client on bed rest with the
leg straight.
• Maintain pressure on the access site for
at least 5 minutes or until no signs of
bleeding are noted.
Angio Seal is and the nursing interventions are
Angio
Seals to prevent bleeding at the insertion site.
The device creates a mechanical seal
anchoring a collagen sponge to the site. The
sponge absorbs in 60–90 days.
• Use pressure dressing and/or ice packs
to control bleeding.
• Check distal pulses because diminished
pulses can indicate a hematoma and
should be reported immediately.
• Force fluids to clear dye from the body
Coronary artery bypass graft
The family should be instructed that
the client will return to the intensive care unit
with several tubes and monitors. The client will
have chest tubes and a mediastinal tube to
drain fluid and to reinflate the lungs. If the
client is bleeding and blood is not drained from
the mediastinal area, fluid accumulates
around the heart. This is known as cardiac
tamponade.
Coronary artery bypass graft treatment afterward
A Swan-Ganz catheter for monitoring central venous
pressure, pulmonary artery wedge pressure
monitor, and radial arterial blood pressure
monitor is inserted to measure vital changes in
the client’s condition. An ECG monitor
and oxygen saturation monitor are also used.
Other tubes include a nasogastric tube to
decompress the stomach, a endotracheal
tube to assist in ventilation, and a Foley
catheter to measure hourly output. The client should be given small, frequent
meals. The diet should be low in sodium, fat,
and cholesterol. Adequate amounts of fluid
and fiber are encouraged to prevent
constipation, and stool softeners are also
ordered. Post-MI teaching should stress the
importance of a regular program of exercise,
stress reduction, and cessation of smoking
Coronary artery bypass graft teaching
The client should be given small, frequent
meals. The diet should be low in sodium, fat,
and cholesterol. Adequate amounts of fluid
and fiber are encouraged to prevent
constipation, and stool softeners are also
ordered. Post-MI teaching should stress the
importance of a regular program of exercise,
stress reduction, and cessation of smoking Because caffeine causes vasoconstriction,
caffeine intake should be limited. The client
can resume sexual activity in 6 weeks or when
he is able to climb a flight of stairs without
experiencing chest pain. Medications such as
Viagra are discouraged and should not be
taken within 24 hours of taking a nitrite. Clients
should be taught not to perform Valsalva
maneuver or bending at the waist to retrieve
items from the floor. Placing items in top
drawers helps to prevent increased
intrathoracic pressure. The client will probably
be discharged on an anticoagulant such as
enoxaparin (Lovenox) or sodium warfarin
(Coumadin).
Anticoagulants such as heparin,the therapeutic range, test and antidote
The
nurse should check the partial thromboplastin
time (PTT). The normal control level is
approximately 30–60 seconds. The therapeutic
bleeding time should be from one and a half
to two times the control. The medication
should be injected in the abdomen 2'' from the
umbilicus using a tuberculin syringe. Do not
aspirate or massage. The antidote for heparin
derivatives is protamine sulfate.
Coumadin, the therapeutic range, test and antidote
If Coumadin
(sodium warfarin) is ordered, the nurse should
check the PT or pro-time. The control level for a
pro-time is 10–12 seconds. The therapeutic
level for Coumadin should be from one and a
half to two times the control. The antidote for
Coumadin is vitamin K. The international
normalizing ratio (INR) is done for oral
anticoagulants. The therapeutic range is 2–3. If
the level exceeds 7, watch for spontaneous
bleeding
Buerger’s Disease
Buerger’s Disease
Buerger’s disease (thromboangiitis obliterans)
results when spasms of the arteries and veins
occur primarily in the lower extremities. These
spasms result in blood clot formations and
eventually destruction of the vessels.
Buerger’s Disease s/s
Symptoms
associates with Buerger’s include pallor of the
extremities progressing to cyanosis, pain, and
paresthesia. As time progresses, tophic
changes occur in the extremities
Buerger’s Disease TX
Management of the client with Buerger’s
involves the use of Buerger-Allen exercises,
vasodilators, and oxygenation. The client
should be encouraged to stop smoking.
Thrombophlebitis
occurs when an inflammation
of a vein with formation of a clot occurs. Most
thrombophlebitis occurs in the lower
extremities, with the saphenous vein being the most common vein affected
Thrombophlebitis TX s/s
Homan’s sign is
an assessment tool used for many years by
healthcare workers to detect deep vein
thrombi. It is considered positive if the client
complains of pain on dorsiflexion of the foot.
Homan’s sign should not be performed
routinely because it can cause a clot to be
dislodged and lead to pulmonary emboli. If a
diagnosis of thrombophlebitis is made, the
client should be placed on bed rest with warm,
moist compresses to the leg. An anticoagulant
is ordered, and the client is monitored for
complications such as cellulitis. If cellulitis is
present, antibiotics are ordered.
Anti-thrombolytic stockings or compression
devices are ordered
Anti-thrombolytic stockings or compression
devices are ordered to prevent venous stasis.
When anti-thrombolytic stockings are applied,
the client should be in bed for a minimum of 30
minutes prior to applying the stockings. The
circumference and length of the extremity
should be measured to prevent rolling
Raynaud’s Syndrome
Raynaud’s Syndrome occurs when there are
vascular vasospasms brought on by exposure
to cold.causing discoloration of the fingers, toes, and occasionally other areas The most commonly effected areas
are the hands, nose, and ears. Management
includes preventing exposure, stopping
smoking, and using vasodilators. The client
should be encouraged to wear mittens when
outside in cold weather.
An aneurysm
is a ballooning of an artery. The
greatest risk for these clients is rupture and
hemorrhage. Aneurysms can occur in any
artery in the body and can be due to
congenital malformations or arteriosclerosis or
be secondary to hypertension.
types of aneurysms
Fusiform—This aneurysm affects the
entire circumference of the artery.
• Saccular—This aneurysm is an
outpouching affecting only one portion
of the artery.
• Dissecting—This aneurysm results in
bleeding into the wall of the vessel.
abdominal aortic
complains of feeling her heart
beating in her abdomen or lower back pain.
Any such complaint should be further
evaluated. On auscultation of the abdomen, a bruit can be heard.
abdominal aortic DX and TX
Diagnosis can be made by
ultrasound, arteriogram, or abdominal x-rays. If
the aneurysm is found to be 6 centimeters or more, surgery should be scheduled. During
surgery the aorta is clamped above and below
and a donor
vessel is anastomosed in place. When the
client returns from surgery, pulses distal to the
site should be assessed and urinary output
should be checked. Clients who are not
candidates for surgery might elect to have
stent placement to reinforce the weakened
artery. These stents are threaded through an incision in the femoral artery, hold the artery
open, and provide support for the weakened
vessel
Congestive Heart Failure
When fluid accumulation occurs and the heart
is no longer able to pump in an efficient
manner, blood can back up. Most heart failure
occurs when the left ventricle fails. When this
occurs, the fluid backs up into the lungs,
causing pulmonary edema.
Congestive Heart Failure left side, s/s of PE
The signs of
pulmonary edema are frothy, pink tinged
sputum; shortness of breath; and orthopnea.
Distended jugular veins might
also be present. Crackles & wheezes Cough
Grunting (infants) Dyspnea
Nasal flaring Orthopnea
Head bobbing (infants) Retractions
Tachypnea
Periods of cyanosis
Congestive Heart Failure right-sided
right-sided congestive
heart failure occurs, the blood backs up into
the periphery. The nurse might also note signs
of pitting edema. Pitting can be evaluated by
pressing on the extremities and noting the
degree of pitting, how far up the extremity the
pitting occurs, and how long it takes to return
to the surface. Ascites Oliguria
Hepatosplenomegaly Weight Gain
Jugular vein distention
Peripheral edema, especially dependent &
periorbital edema
Congestive Heart Failur RX
Treatment for congestive heart
failure includes use of diuretics, Natrecor,
Primacor, and cardiotonics. Morphine might
also be ordered to manage pain Diuretics
• Cardiotonics
• Antihypertensives
• Anticoagulants
• Thrombolytics
Diagnostic Tests CHF
Arteriogram—Arteriography reveals the
presence of blockages and
abnormalities in the vascular system.
• Cardiac catheterization—A cardiac
catheterization reveals blockages,
turbulent flow, and arteriosclerotic
heart disease. CBC • Chest x-ray— ekg
Secondary hypertension Precipitating disorders or conditions
Precipitating disorders or conditions
a. Cardiovascular disorders
b. Renal disorders
c. Endocrine system disorders
d. Pregnancy
e. Medications (meds)e.g., estrogens,
glucocorticoids, mineralocorticoids
HTN Assesment
1. May be asymptomatic
2. Headache
3. Visual disturbances
4. Dizziness
5. Chest pain
6. Tinnitus
7. Flushed face
8. Epistaxis
HTN interventions 14 of them
1. Goals
a. One treatment goal is to reduce the
BP.
b. Another treatment goal is to prevent
or lessen the extent of organ damage.
2. Question the client regarding the signs &
symptoms indicative of hypertension.
3. Obtain the BP two or more times on both
arms, with the client supine & standing.
4. Compare the BP with prior
documentation.
5. Determine family history of hypertension.
6. Identify current medication therapy.
7. Obtain weight.
8. Evaluate dietary patterns & sodium
intake.
9. Assess for visual changes or retinal
damage.
10. Assess for cardiovascular changes such
as distended neck veins, increased heart
rate, & dysrhythmias.
11. Evaluate chest x-ray for heart
enlargement.
12. Assess the neurological system.
13. Evaluate renal function.
14. Evaluate results of diagnostic &
laboratory studies
Nonpharmacological TX
Nonpharmacological interventions
1. Weight reduction, if necessary, or
maintenance of ideal weight
2. Dietary sodium restriction to 2 g daily as
pre-scribed
3. Moderate intake of alcohol & caffeinecontaining
products
4. Initiation of a regular exercise program
5. Avoidance of smoking
6. Relaxation techniques & biofeedback
therapy
7. Elimination of unnecessary meds that
may contribute to the hypertension
Step approach for HTN
Step 1: A single medication is prescribed, which may be a diuretic, b-blocker, calcium
channel blocker, angiotensin-converting enzyme inhibitor, or angiotensin II receptor
blocker.
Step 2: a. Step 1 therapy is evaluated after 1 to 3 months.
b. If the response is not adequate, compliance is evaluated.
c. The medication may be increased or a new medication may be prescribed or a
second medication added the treatment plan.

Step 3: a. Compliance is evaluated.
b. Further evaluation of step 2.
c. If a therapeutic response is not adequate, a second medication is substituted or a
third medication is added to the treatment plan.
Step 4: a. Compliance is evaluated. b. Careful assessment of factors limiting the antihypertensive response is done.
c. A third or fourth medication may be added to the treatment plan.
hypertensive crisis
A hypertensive crisis is any clinical
condition requiring immediate
reduction in BP.
2. A hypertensive crisis is an acute & lifethreatening
condition.
3. The accelerated hypertension requires
emergency treatment because target
organ damage (brain, heart, kidneys,
retina of the eye) can occur quickly.
4. Death can be caused by stroke, renal
failure, or cardiac disease
Hhypertensive crisis s/s
Assessment
• An extremely high BP; usually, the diastolic
pressure is > 120 mm Hg
• Headache
• Drowsiness & confusion
• Blurred vision
• Changes in neurological status
• Tachycardia & tachypnea
• Dyspnea Cyanosis
• Seizures
hypertensive crisis intervention
Interventions
1. Maintain a patent airway.
2. Administer antihypertensive meds
intravenously as prescribed, which may
include nitroprusside (Nitropress), diazoxide
(Hyperstat), nicardipine (Cardene), or
labetalol (Trandate).
3. Monitor vital signs, assessing the BP every 5
minutes.
4. Assess for hypotension during the
administration of antihypertensives; place
the client in a supine position if
hypotension occurs.
5. Have emergency meds & resuscitation
equipment readily available.
6. Maintain bed rest, with the he Monitor IV therapy, assessing for fluid
overload.
8. Monitor intake & output
Beta blockers
Propranolol (Inderal), atenolol (Tenormin), nadolol (Corgard
Diuretics
Thiazide: Chlorothiazide (Diuril), hydrochlorothiazide (Esidrix, HydroDIURIL)
Loop diuretics: Furosemide (Lasix), ethacrynic acid (Edecrin)
Potassium sparing diuretics: Spironolactone (Aldactone), triamterene
(Dyrenium)
Calcium channel
blockers
Nifedipine (Procardia), verapamil (Calan), diltiazem hydrochloride
(Cardizem)
Angiotensin
converting
Captopril (Capoten), enalapril (Vasotec), lisinopril enzyme inhibitors (Zestril,
Prinivil)
Angiotensin receptor
Angiotensin receptor C andesartan (Atacand), losartan (Cozaar), telmisartan blockers (Micardis)
These drugs can be used alone or in conjunction with one another. Diuretics
& vasodilators are often given in combination to lower BP through diuresis &
vasodilation. Hypertensive crises exist when the diastolic BP reaches 140.
Malignant hypertension is managed with administration of IV Nitropress,
Nitroglycerine, Nipride, Lasix, & other potent vasodilators such as Procardia
HTN drugs
Diuretics, beta blockers, calcium channel blockers, angiotensin converting, angiotensin recepor
PERIPHERAL VASCULAR DISEASE (PVD) S/S
Reduced blood flow through peripheral
blood vessels characterizes all peripheral
vascular diseases. The physiologic effects of
altered blood flow depend on the extent to
which tissue demands exceed the supply of
oxygen & nutrients available. If tissue needs
are high, even modestly reduced blood flow
may be inadequate to maintain tissue
integrity. Tissues then fall prey to ischemia
(deficient blood supply), become
malnourished, & ultimately die if adequate
blood flow is not restored. Although many
types of peripheral vascular diseases exist,
most result in ischemia & produce some of
the same symptoms: pain, skin changes,
diminished pulse, & possible edema. The
type & severity of symptoms depend in part on the type, stage, & extent of the disease
process & on the speed with which the
disorder develops
ARTERIOSCLEROTIC HEART DISEASE
Arteriosclerosis ("hardening of the arteries")
The process whereby abnormal deposits of
lipids, cholesterol & plaque buildup, leading
to narrowing or blockage in arteries taking
blood to the hand, foot head or vital
organs.
Atherosclerosis
(fatty deposits
called plaque on inner lining of
vessel walls).
Calcific sclerosis (calcium
deposits on the middle layer of
the wall of the arteries
Arteriolar sclerosis
a thickening
of the arterioles caused by
hypertension)
Coronary Artery Disease
(atherosclerosis/arteriosclerosis)
A build-up
of fatty material in the wall of the coronary
artery that causes narrowing of the artery is a narrowing of
the small blood vessels that supply blood &
oxygen to the heart. CHD is also called
coronary artery disease or arteriosclerotic heart
disease.
CAUSES: of cad chd
Causes, incidence, & risk factors:
Coronary heart disease is usually caused by a
condition called atherosclerosis, which occurs
when fatty material & a substance called
plaque buildup on the walls of your arteries.
This causes them to get narrow. As the
coronary arteries narrow, blood flow to the
heart can slow down or stop. This can cause
chest pain (stable angina), shortness of breath,
heart attack, & other symptoms. CHD is the
leading cause of death in the United States for
men & women.
risk
for heart disease:
Men in their 40s have a higher risk of CHD
than women. But as women get older
(especially after they reach menopause),
their risk increases to almost equal that of a
man's risk.
• Bad genes (heredity) can increase your risk.
You are more likely to develop the
condition if someone in your family has had
a history of heart disease -- especially if
they had it before age 50. Your risk for CHD
goes up the older you get.
• Diabetes is a strong risk factor for heart
disease
High BP increases your risk of coronary
artery disease & heart failure.
• Abnormal cholesterol levels: your LDL
("bad") cholesterol should be as low as
possible, & your HDL ("good") cholesterol
should be as high as possible.
• Metabolic syndrome refers to high
triglyceride levels, high BP, excess body fat
around the waist, & increased insulin levels.
People with this group of problems have an
increased chance of getting heart disease.
• Smokers have a much higher risk of heart
disease than nonsmokers.
• Chronic kidney disease can increase risk.
• Already having atherosclerosis or
hardening of the arteries in another part of
your body (examples are stroke &
abdominal aortic aneurysm) increases your
risk of having coronary disease.
• Other risk factors including alcohol abuse,
not getting enough exercise, & excessive
amounts of stress.
• Higher-than-normal levels of inflammationrelated
substances, such as C-reactive
protein & fibrinogen are being studied as
possible indicators of an increased risk for
heart disease.
• Increased levels of a chemical called
homocysteine, an amino acid, are also
linked to an increased risk of a heart
attack
ANGINA PECTORIS
clinical syndrome usually
characterized by episodes or paroxysms of pain
or pressure in the anterior chest. The cause is
usually insufficient coronary blood flow. The
insufficient flow results in a decreased oxygen
supply to meet an increased myocardial
demand for oxygen in response to physical
exertion or emotional stress.
Stable angina
Unstable angina (also called preinfarction or
crescendo angina
Intractable or refractory angina
Variant angina (also called Prinzmetal’s
angina):
Silent ischemia:
Stable angina: predictable & consistent
pain that occurs on exertion & is relieved by
rest
• Unstable angina (also called preinfarction or
crescendo angina): symptoms occur more
frequently & last longer than stable angina.
Threshold for pain is lower, & pain may
occur at rest.
• Intractable or refractory angina: severe
incapacitating chest pain
• Variant angina (also called Prinzmetal’s
angina): pain at rest with reversible STsegment
elevation; thought to be caused
by coronary artery vasospasm
• Silent ischemia: objective evidence of
ischemia (such as electrocardiographic
changes with a stress test), but patient
reports no symptoms
RX FOR ANGINA
Medications used to treat angina include
aspirin, beta blockers, nitroglycerin, & ACE
inhibitors. Other meds that may be used to treat
angina include calcium channel blockers to
relax blood vessels, allowing greater blood flow
to the heart & a lower BP; antihypertensive &
lipid-lowering agents; & oral antiplatelets, such
as clopidogrel bisulfate (Plavix), which stop
platelets from clumping together to form clots
MANAGEMENT OF ANGINA , WHAT TO WATCH FOR WITH THE RX
A
beta blocker dose may be withheld or
decreased at the physician’s discretion if the
heart rate is below 50 or 60 or if the patient
becomes symptomatic. Both ACE inhibitors &
beta blockers can lower BP & may need to be
withheld if the systolic BP drops below 90. These
parameters are often part of standing orders in
the telemetry unit, Monitoring of vital signs is an important
component of medication management
gANGRENE, TYPES- DRY AND GAS AND WET
Wet gangrene (also called
moist gangrene)necrotizing fasciitis, or
infection of the skin & tissues directly beneath
the ski occurs when dry gangrene
becomes infected, often due to injury, & the
infection causes the tissue to die.
Gas gangrene, the most serious form of wet
gangrene, often is caused by Clostridium
bacteria, which are normal inhabitants of the
gastrointestinal, respiratory, & female genital
tracts. Areas of either dry or moist gangrene
are initially characterized by a red line on the
skin that marks the border of the affected
tissues.
Dry gangrene occurs when a portion of bodily
tissue dies because its blood supply has been
decreased or completely cut off. This type of
gangrene will not spread to other healthy
tissue, & infection is not present.
Some of
the most common causes of dry gangrene
include:
arterial obstruction, or occlusion of an
artery, caused by arteriosclerosis, diabetes
mellitus, AIDS or blood clot
• severe blunt trauma to a part of the body
causing damage & therefore obstruction
of an artery
• frostbite, which occurs when tissue
becomes so cold that it is literally deprived
of blood & therefore oxygen, & dies
• diseases that affect the blood vessels, &
especially the arteries, such as Buerger's or
Raynaud's disease
• traumatic occurrences such as crushing
injuries, fractures, burns, & even injections
given into skin or muscle
Causative organisms for wet gangrene infection
include:
• Streptococcus
• Staphylococcus
symptoms of gas
gangrene include
edema, or swelling, at the injury site that
expands quickly
• pain in the area surrounding the skin injury
• crepitus, a bubbly, crackling sound often
heard upon palpation
• pallor at the injury site, then increasingly
dusky discoloration
• low-grade to moderate temperature
elevation
Myocarditis
Myocarditis describes any
inflammation that occurs within the heart
muscle. It is induced by various infections which
will include viruses like sarcoidosis, & distinct
immune diseases. The most prevalent form of
infection is the viral kind that assaults the heart
muscle resulting in local inflammation. Once the
infection subsides the immune response will still
endure. Because of this, myocarditis will
continue to plague the heart muscle long after
the infection has ceased.
Myocarditis s/s early and late
It is not unusual for the disease to
be completely asymptomatic. Pain in the
chest is the most likely sign of myocarditis astringent instances the disease may
progress into degeneration of the heart
muscle. It is then unfortunately able to trigger
heart failure with the associated symptoms:
shortness of breath or difficulty breathing,
edema or swelling of feet & ankles, fatigue
among others.
Myocarditis DX
ECG or electrocardiogram will be used to
detect deviations within the heartbeat. MRI
or magnetic resonance imaging tests will be
applied to reveal heart muscle peculiarities.
Blood tests will be performed to search for
any likely infection & also for the possible rise
in level of heart muscle enzymes
Myocarditis Prognosis
There is much uncertainty about
the likelihood of recovery in the early phases
of the disease. A fair portion of individuals
achieve total recovery while some may
eventually be inflicted with chronic heart
failure due to extravagant damage to the
heart muscles. Infrequently a person may be
struck with fulminant heart failure which will
necessitate a heart transplant. If the
degeneration of the muscle is enormous a
defibrillator may be implanted to better the
heart’s ability to function
PERICARDITIS DEF AND RISK
Pericarditis is a disease that
causes inflammation of the pericardium. The
pericardium is the fluid sac that envelopes the
heart. It provides lubrication to the heart thus
decreasing friction during activity & also firmly
secures the heart to the surrounding walls within
the cavity.
The cause of pericarditis may possibly be
unexplained however there are some factors
that may induce the disease. These will include:
• Some tumors & cancers
• Specific metabolic disorders potentially
hypothyroidism & uremia (kidney failure)
• Infection with a virus or bacteria
• Prior impairment to the heart, for example
heart attack, trauma & heart surgery
• An underlying connective tissue disease
such as sarcoidosis & rheumatoid arthritis
• An unexpected reaction to a particular
type of medication
PERICARDITIS S/S
pain when
swallowing.a slight fever,- The most defining symptom will be
chest pain or angina pectoris that is
generally expressed as a cutting, intense
pain that migrates from the chest area to the
shoulder blades, back & neck. It is also quite
possible to experience pain near the
diaphragm that extends to the back. When
inhaling deeply the chest pain will become
significantly worse. The pain is typically
unbearable when lying flat but will be
bettered by leaning forward.
PERICARDITIS TX
The primary treatment is the
administering of anti-inflammatory meds,A narcotic pain
medication,Pericardiocentesis may be applicable as a
form of progressive treatment. It will remove
excessive fluid from the sac & or will detect
the pathogen of origin that may have
induced the condition
PERICARDITIS DX
Diagnosis will begin
with an assessment of the pain symptoms to
distinguish it from pain associated with
another condition. an ECG
electrocardiogram, chest x-ray & ultrasound
of the heart will be utilized. A blood test may
be undertaken to detect any other
underlying conditions that may have
triggered the development of pericarditis, pericardial friction rub IS SIGN OF INFLAMMATION BUT NOT PERICARDITIS FOR SURE
ENDOCARDITIS
Endocarditis is induced by an
infection of the endocardium or inner lining of
the heart resulting in pronounced inflammation.
It will present itself when pathogens from other
regions of the body infect the bloodstream &
affix to defective areas of the heart. If it is not
treated speedily it may cause partial or
complete damage to the heart valve or may
develop into a life-threatening condition. It
usually affects individuals who have an artificial
heart valve in place or have suffered
degeneration of a heart valve. Having a preexisting
heart defect also increases the odds of
developing the condition. It does not normally
affect healthy people.
ENDOCARDITISs/s risk
fairly long period of time or may manifest
quite suddenly corresponding heart defect or infection
o Unexplained & sudden weight loss
o Joint & muscular pain
o Fever & chills
o Visible purple or red spots exhibited in
the mouth on the skin or on the whites
of the eyes
o Heart murmurs (irregular sounds arising
from the heart)
o Constant coughing
o Blood in the urine
o Edema or swelling of the feet &
abdomen
o Fatigue & unusual tiredness
o Night sweats
o Tenderness below the rib cage that is
associated with the spleen
o A pale complexion
o Areas of red tender spots just below
the skin of the fingers.
o Shortness of breath or difficulty
breathing/ people at risk are people with an artificial heart valve or heart condition and Intravenous drug users are at a greater
risk of developing the condition
because of needle sharing. The
bacterium that may incite this condition
is commonly harbored in contaminated
needles
ENDOCARDITIS dx
Diagnosis
• Blood tests will be applicable. They will
discover the source of bacterial
infection.
• An echocardiogram will be employed
to properly assess the heart’s condition.
• An ECG or electrocardiogram & x-ray
will also be used to confirm diagnosis.
• MRI magnetic resonance or CT
computerized tomography imaging
scan will be used if it is believed the
infection may have traveled to other
areas of the body
ENDOCARDITIS tx
The main treatments are
antibiotics in less intense cases & possible
surgery where damage is significantly
compromising.
RHEUMATIC FEVER, HEART/ VALVE DISEASE
DX and test
1. Rheumatic fever is an inflammatory
autoimmune disease that affects the
connective tissues of the heart, joints,
subcutaneous tissues, & blood vessels of the
central nervous system.
2. The most serious complication is rheumatic
heart disease, which affects the cardiac
valves, particularly the mitral valve.
3. Rheumatic fever presents 2 to 6 weeks
following an untreated or partially treated
group A beta-hemolytic streptococcal
infection of the upper respiratory tract.
4. Jones criteria are used to determine the
diagnosis.,1. Fever: Low-grade fever that spikes in the
late afternoon
2. Elevated antistreptolysin O titer
3. Elevated sedimentation rate
4. Elevated C-reactive protein level
5. Aschoff bodies (lesions): Found in the heart,
blood vessels, brain, & serous surfaces of the
joints & pleura
Interventions
RHEUMATIC FEVER, HEART/ VALVE DISEASE
Assess vital signs.
2. Control joint pain & inflammation with
massage & alternating hot & cold
applications as prescribed.
3. Provide bed rest during acute febrile
phase.
4. Limit physical exercise in the child with
carditis.
5. Administer antibiotics (penicillin) as
prescribed.
6. Administer salicylates & anti-inflammatory
agents (prednisone [Deltasone]) as
prescribed; these meds should not be
administered before the diagnosis is
confirmed, because these meds mask the
polyarthritis).
7. Initiate seizure precautions if the child is
experiencing chorea.
8. Instruct the parents about the importance
of follow-up & the need for antibiotic
prophylaxis for dental work, infection, &
invasive procedures. 9. Advise the child to inform the parents if
anyone in school develops a streptococcal
throat infection
KAWASAKI DISEASE DX
1. Known as mucocutaneous lymph node
syndrome & is an acute systemic inflammatory
illness.
2. The cause is unknown but may be
associated with an infection from an organism
or toxin.
3. Cardiac involvement is the most serious
complication; aneurysms can develop.
Assessment
1. Acute stage
a. Fever
b. Conjunctival hyperemia
c. Red throat
d. Swollen hands, rash, & enlargement of
the cervical lymph nodes
2. Subacute stage
a. Cracking lips & fissures
b. Desquamation of the skin on the tips of
the fingers & toes
c. Joint pain
d. Cardiac manifestations
e. Thrombocytosis
3. Convalescent stage: Child appears normal
but signs of inflammation may be present
KAWASAK INTERVENTIONS
Interventions
1. Monitor temperature frequently.
2. Assess heart sounds, rate, & rhythm.
3. Assess extremities for edema, redness, &
desquamation.
4. Examine eyes for conjunctivitis.
5. Monitor mucous membranes for
inflammation.
6. Monitor strict intake & output.
7. Administer soft foods & liquids that are
neither too hot nor too cold.
8. Weigh the child daily.
9. Provide passive range-of-motion exercises
to facilitate joint movement.
10. Administer acetylsalicylic acid (aspirin) as
prescribed for its antipyretic & antiplatelet
effects.
11. Administer immune globulin intravenously
as prescribed to reduce the duration of the
fever & the incidence of coronary artery
lesions & aneurysms; IV immune globulin (IVIG)
is a blood product, so blood precautions when
administering it are warranted.
12. Parent education
CHF IN CHILDREN
2. In infants & children, inadequate cardiac
output most commonly is caused by
congenital heart defects (shunt, obstruction,
or a combination of both) that produce an
excessive volume or pressure load on the
myocardium.
3. In infants & children, a combination of leftsided
& right-sided heart failure is usually
present
CHF S/S EARLY SIGNS
Assessment of early signs
1. Tachycardia, especially during rest & slight
exertion
2. Tachypnea
3. Profuse scalp diaphoresis, especially in infants
4. Fatigue & irritability
5. Sudden weight gain
6. Respiratory distress
CHF INTERVENTIONS FOR CHILDREN
2. Monitor for respiratory distress (count
respirations for 1 minute).
3. Monitor apical pulse (count pulse for 1
minute) & monitor for dysrhythmias.
4. Monitor temperature for hyperthermia & for
other signs of infection, particularly respiratory
infection.
5. Monitor strict intake & output.
6. Weigh diapers as appropriate.
7. Monitor daily weight to assess for fluid
retention; a weight gain of 0.5 kg (1 lb) in 1
day is caused by the accumulation of fluid.
8. Monitor for facial or peripheral dependent
edema, auscultate lung sounds, & report
abnormal findings indicating excessive fluid in
the body.
9. Elevate the head of the bed in a semi-
Fowler's position.
10. Maintain a neutral thermal environment to
prevent cold stress in infants.
11. Provide rest & decrease environmental
stimuli.
12. Administer cool humidified oxygen as
prescribed, using an oxygen hood for young
infants & a nasal cannula or face mask for
older infants & children.
13. Organize nursing activities to allow for
uninterrupted sleep.
14. Maintain adequate nutritional status.
15. Feed when hungry & soon after awakening,
conserving energy & oxygen supply.
16. Provide small, frequent feedings, conserving
energy & oxygen supply.
17. Administer sedation as prescribed during the
acute stage to promote rest.
18. Administer digoxin (Lanoxin) as prescribed
a. Assess apical heart rate for 1 minute before
administration
b. Hold digoxin if pulse is < 90 beats/min in
infants & young children & < 70 beats/min in
older children, as prescribed
c. Be aware that infants rarely receive more
than 1 mL of digoxin in one dose
19. Monitor digoxin levels & for signs of digoxin
toxicity, including bradycardia, headache, &
vomiting.
a. Normal digoxin level is 0.5 to 2.0 mg/dL
b. Digoxin toxicity occurs when level is above
2.0 mg/dL
20. Administer angiotensin-converting enzyme
inhibitors (captopril [Capoten] or enalapril
[Vasotec]) as prescribed.
a. Monitor for hypotension, renal dysfunction, &
cough when angiotensin-converting enzyme
inhibitors are administered.
b. Assess the BP, serum protein, albumin, blood
urea nitrogen, & creatinine levels, white blood
cell count, urine output, urinary specific
gravity, & urinary protein level.
21. Administer diuretics (furosemide [Lasix]) as
prescribed
a. Monitor for signs & symptoms of hypokalemia
(serum potassium level < 3.5 mEq/L), including
muscle weakness & cramping, confusion,
irritability, restlessness, & inverted T wave on
the electrocardiogram (ECG).
b. If signs & symptoms of hypokalemia are
present & the child is also being administered
digoxin, then monitor closely for digoxin
toxicity because hypokalemia potentiates
digoxin toxicity.
22. Administer potassium supplements &
provide dietary sources of potassium as
prescribed.
a. Supplemental potassium should only be
given if indicated by potassium levels & i& if
adequate renal function is evident, & is
usually necessary when giving a non–
potassium-sparing diuretic such as
furosemide.
b. Encourage foods that the child will eat that
are high in potassium, as appropriate, such as
bananas, baked potato skins, & peanut
butter.
23. Monitor electrolyte levels, particularly the
potassium level (normal level is 3.5-5.1 mEq/L).
24. Restrict fluid as prescribed in the acute
stage.
25. Monitor for signs/symptoms of dehydration,
including sunken fontanel, nonelastic skin
turgor, dry mucous membranes, decreased
tear production, decreased urine output, &
concentrated urine.
26. Monitor sodium levels as prescribed.
a. Normal level is 135 -145 mEq/L.
b. Many infant formulas have slightly more
sodium than breast milk.
27. Instruct the parents regarding the
description of the diagnosis & administration
of meds.
28. Instruct the parents in CPR.
NSR RATE
60 TO 100
SINUS BRADY INTERVENTIONS
a. Attempt to determine the cause of
sinus bradycardia; if a medication is
suspected of causing the bradycardia,
hold the medication & notify the
physician.
b. Administer oxygen as prescribed.
c. Administer atropine sulfate as
prescribed to increase the heart rate to 60
beats/min.
d. Be prepared to apply a noninvasive
(transcutaneous) pacemaker initially as
prescribed if the atropine sulfate does not
increase the heart rate sufficiently.
e. Avoid additional doses of atropine
sulfate because this will induce
tachycardia
f. Monitor for hypotension & administer
fluids intravenously as prescribed.
g. Depending on the cause of the
bradycardia, the client may need a
permanent pacemaker
A FIB Description
a. Multiple rapid impulses from many foci
depolarize in the atria in a totally
disorganized manner at a rate of 350 to
600 times/min.
b. The atria quiver, which can lead to the
formation of thrombi.
c. No definitive P wave can be observed,
only fibrillatory waves before each QRS.
A-FIB
Interventions
Administer oxygen.
b. Administer anticoagulants as
prescribed because of the risk of emboli.
c. Administer cardiac meds as prescribed
to control the ventricular rhythm & assist in
the maintenance of cardiac output.
d. Prepare the client for cardioversion as
prescribed.
e. Instruct the client in the use of meds as
prescribed to control the dysrhythmia
PVC'S INTERVENTIONS
a. Notify the physician if PVCs occur.
b. Identify the cause & treat based on the
cause.
c. Evaluate oxygen saturation to assess for
hypoxemia, which can cause PVCs.
d. Administer oxygen as prescribed.
e. Evaluate electrolytes, particularly the
potassium level, because hypokalemia
can cause PVCs.
f. Lidocaine may be prescribed.
g. Notify the physician if the client
complains of chest pain or if PVCs
increase in frequency, are multifocal,
occur on the T wave (R on T), or occur in
runs of ventricular tachycardia.
VENTRICULAR TACHYCARDIA 140 TO 250
Ventricular tachycardia occurs
because of a repetitive firing of an irritable
ventricular ectopic focus at a rate of 140
to 250 beats/min or more.
TREATMENT FOR STABLE AND UNSTABLE V=TACH
Stable client with sustained VT (with pulse
& no signs or symptoms of decreased
cardiac output)
a. Administer oxygen as prescribed.
b. Administer antidysrhythmics, such as
amiodarone (Cordarone), lidocaine
(Xylocaine), or procainamide (Pronestyl)
as prescribed.
3. Unstable client with VT (with pulse & signs &
symptoms of decreased cardiac output)
a. Administer oxygen & antidysrhythmic
therapy as prescribed.
b. Prepare for synchronized cardioversion
if the client is unstable.
c. Attempt 'cough' cardiopulmonary
resuscitation (CPR) by asking the client to
cough hard every 1 to 3 seconds.
4. Pulseless client with ventricular
tachycardia:
VENTRICULAR FIBRILLATION DX AND TREATMENT
VF is fatal if not successfully terminated
within 3 to 5 minutes.
d. Client lacks a pulse, BP, respirations, &
heart sounds.
2. Interventions
a. Defibrillate the client immediately, up to
3 times consecutively at 200, 300, & 360
joules (J).
b. Initiate CPR.
c. Administer oxygen as prescribed.
d. Administer epinephrine or vasopressin &
antidysrhythmic therapy with amiodarone
or lidocaine as prescribed; other
antidysrhythmics also may be prescribed
MI RX TX
Medical management includes betaadrenergic
blockers (propranolol-Inderal,
Lopressor) * contraindicated if patient also has
CHF, hypotension or bronchospasm.
treatment: May be referred for immediate
PTCA. Same meds as Pt with unstable angina
with possible additions of thrombolytics,
analgesics, & ACE Inhibitors. Thrombolytic
therapy includes the use of Streptase, &
Eminase. These are contraindicated if the
patient has had recent surgery, or
experienced a fall or head wound concurrent
with the MI.
Mitral valve prolapse DX
is one or both valve
leaflets protruding into the left atrium. It
has an unknown etiology. ECG shows
prolapse of the mitral valve into the left
atrium
Mitral stenosis -DX
obstructs blood flow from
the left atrium to the left ventricle. Can
be caused by rheumatic fever. Diagnosiscardiac
catheterization shows diastolic
pressure gradient across the valve &
elevated left atrial & pulmonary artery
wedge pressures. Echocardiography shows thickened mitral valve leaflets.
ECG shows left atrial hypertrophy & x-ray
shows left atrial & ventricular enlargement.
Mitral Regurgitation
blood flowing back
from the left ventricle into the left atrium
during systole. Often the margins of the
mitral valve cannot close during systole.
Left atrium stretches & eventually
hypertrophies & dilates, diminishing
volume of bloods flowing into the atrium
form the lungs – lungs become congested
adding extra strain on the right ventricle.
Acute episode usually presents as severe CHF
Aortic Stenosis -
narrowing of the orifice
between the left vent. & aorta
Aortic Regurgitation – Aortic Insufficiency
results in blood flowing back into the left
ventricle during diastole (rest), creating
fluid overload in the left atrium &
pulmonary system. Causes include
endocarditis, hypertension, rheumatic
fever, & syphilis. Diagnosisechocardiography
shows left ventricular
enlargement, x-ray shows left ventricular
enlargement & pulmonary vein
congestion
CARDIOMYOPATHY CAUSES
increased muscle mass
to compensate for flabby L. ventricle, altering
cardiac function & resulting in decreased
cardiac output. Causes include alcoholism,
infection, metabolic & immunologic disorders,
pregnancy & postpartum disorders,
hypertension, myeloidosis & cancer or other
infiltrative disease.
CARDIOMYOPATHY S/S
Signs & symptoms -murmur
(S3, S4), dyspnea, cough, crackles, jugular vein
distention, dependent pitting edema, fatigue.
CARDIOMYOPATHY DX
Diagnosis- echo indicates left ventricular
hypertrophy & nonspecific changes. TX- betaadrenergic
blockers, calcium channel
blockers, diuretics, inotropic drugs (dopamine),
anticoagulants. Interventions include
monitoring for arrhythmias & ischemia, monitor
for hypokalemia (s/e of diuretics), monitor
respiratory & cardiovascular status for signs of
heart failure, & administer O2 & meds to
improve oxygenation & cardiac output.
Shock can be classified by etiology & may be
described as 4 TYPES
(1) hypovolemic shock, (2)
cardiogenic shock, or (3) circulatory or
distributive shock. Some authors identify a
fourth category, obstructive shock, that results
from disorders that cause mechanical
obstruction to blood flow through the central
circulatory system despite normal myocardial
function & intravascular volume
SHOCK RESULTS TO THE CELLS
produce energy through anaerobic
metabolism. This results in low energy yields
from nutrients & an acidotic intracellular
environment. Because of these changes,
normal cell function ceases. The cell swells &
the cell membrane becomes more
permeable, allowing electrolytes & fluids to
seep out of & into the cell. The sodiumpotassium
pump becomes impaired; cell
structures, primarily the mitochondria, are
damaged; & death of the cell results.
In the
compensatory stage of shock,
the
compensatory stage of shock, the
patient’s blood pressure remains within
normal limits. Vasoconstriction, increased
heart rate, & increased contractility of the
heart contribute to maintaining adequate
cardiac output. This results from stimulation
of the sympathetic nervous system &
subsequent release of catecholamines
(epinephrine & norepinephrine). The
patient displays the often-described “fight or flight” response. The body shunts blood
from organs such as the skin, kidneys, &
gastrointestinal tract to the brain & heart to
ensure adequate blood supply to these
vital organs. As a result, the patient’s skin is
cold & clammy, bowel sounds are
hypoactive, & urine output decreases in
response to the release of aldosterone &
ADH Normalbp
>100 bpm
>20 breaths/min
Cold, clammy
Decreased URINARY OUTPUT
Confusion
Respiratory alkalosis
In the progressive
stage of shock,
In the progressive
stage of shock, the mechanisms that
regulate blood pressure can no longer
compensate & the MAP falls below normal
limits, with an average systolic blood
pressure of less than 90 mm Hg Systolic <80–90 mm Hg
>150 bpm
Rapid, shallow
respirations; crackles
Mottled, petechiae
0.5 mL/kg/hr
Lethargy
Metabolic acidosis
The irreversible (or
refractory) stage of shock r
represents the
point along the shock continuum at which
organ damage is so severe that the
patient does not respond to treatment &
cannot survive. Despite treatment, blood
pressure remains low. Complete renal &
liver failure, compounded by the release of
necrotic tissue toxins, creates an
overwhelming metabolic acidosis.
Anaerobic metabolism contributes to a
worsening lactic acidosis. Reserves of ATP are almost totally depleted, & mechanisms
for storing new supplies of energy have
been destroyed. Multiple organ
dysfunction progressing to complete organ
failure has occurred, & death is imminent.
Multiple organ dysfunction can occur as a progression along the shock continuum or as a syndrome unto itself Requires mechanical
or pharmacologic
support
Erratic or asystole
Requires intubation
Jaundice
Anuric, requires dialysis
Unconscious
Profound acidosis
THE MOST LIFE THREATENING SHOCK
Hypovolemic shock, the most common type of
shock, is characterized by a decreased
intravascular volume. Body fluid is contained in
the intracellular & extracellular compartments.
Intracellular fluid accounts for about two thirds
of the total body water. Hypovolemic shock occurs
when there is a reduction in intravascular
volume of 15% to 25%. This would represent a
loss of 750 to 1,300 mL of blood in a 70-kg (154-
lb) person.
HYPOVOLEMIC SHOCK- S.S
acute pancreatitis,
dehydration from excessive perspiration,
intestinal obstruction, severe diarrhea,
protracted vomiting, inadequate fluid intake &
diuresis. Signs & symptoms - cold, pale, clammy
skin, decreased sensorium, hypotension with
narrowing pulse pressure, reduce urine output,
tachycardia, rapid, shallow respirations.
HYPOVOLEMIC SHOCK DX
Blood tests (elevated K, serum
lactate, BUN urine specific gravity (greater
than 1.020), ABG reveals metabolic acidosis
(decreased pH) decreased PO2 & increased
PCO2. treatment- blood & fluid replacement
control of bleeding.
CARDIOGENIC SHOCK- CAUSES AND S/S
LIFE THREATENING!
Heart fails to adequately pump, reducing
cardiac output & compromising tissue
perfusion. Decreased stroke volume increases
back volume in the left ventricle. Blood from
the left ventricle backs up into the lungs
creating pulmonary edema. Compensation
for decreased CO is increased heart rate &
contractility, increasing the need for O2. An
imbalance between supply of O2 & demand
for O2 increase myocardial ischemia further
impairing the heart’s pumping action. Causes
include MI, heart failure, Myocarditis,
cardiomyopathy & advanced heart block.
Signs & symptoms - cold, clammy skin,
hypotension with a narrow pulse pressure,
Oliguria (less than 30 ml/hr), S3 & S4 heart sounds, tachycardia, tachypnea, & weak,
thready pulse.
CARDIOGENIC SHOCK- DX AND MEDS
EKG shows enlarged
Q wave, elevated ST segment (MI). Drug
treatment includes adrenergic (epinephrine_,
digoxin, dopamine, diuretics, vasodilators
(Nitro-press) & vasopressors (norepinephrine).
Interventions include NPO status to reduce risk
of aspiration, administer meds, fluids, oxygen to
maximize cardiac, pulmonary & renal Fx. Use
of IABP (intra-aortic balloon pump) - an
inflatable balloon is inserted through the
femoral artery into the descending aorta.
Coronary artery perfusion increases when the
aortic valve closes & the balloon inflates during diastole (rest). It deflates during systole
(squeeze) to reduce cardiac workload by
reducing resistance to ejection.
CIRCULATORY SHOCK THREE TYPES, CAUSES
Circulatory or
distributive shock occurs when blood volume is
abnormally displaced in the vasculature—for
example, when blood volume pools in peripheral blood vessels. The displacement of
blood volume causes a relative hypovolemia
because not enough blood returns to the
heart, which leads to subsequent inadequate
tissue perfusion. The ability of the blood vessels
to constrict helps return the blood to the heart.
Thus, the vascular tone is determined both by
central regulatory mechanisms, as in blood
pressure regulation, & by local regulatory
mechanisms, as in tissue demands for oxygen
& nutrients. Therefore, circulatory shock can be
caused either by a loss of sympathetic tone or
by release of biochemical mediators from
cells. The varied mechanisms leading to the
initial vasodilation in circulatory shock further
subdivide this classification of shock into three
types:
(1) septic shock, (2) neurogenic shock, & (3)
anaphylactic shock.
SEPTIC SHOCK – CAUSED BY
Septic shock is the most
common type of circulatory shock & is caused
by widespread infection. Despite the
increased sophistication of antibiotic therapy,
the incidence of septic shock has continued to
rise during the past 60 years. IToxic shock syndrome is a specific form of
septic shock
Septicemia
The presence of infective agents
or their toxins in the bloodstream. Septicemia is
a serious infection & must be treated promptly;
otherwise, the infection leads to circulatory
collapse, profound shock, & death
NEUROGENIC SHOCK CAUSES S/S THAT DIFFER OF OTHER SHOCK
In neurogenic shock,
vasodilation occurs as a result of a loss of
sympathetic tone. This can be caused by
spinal cord injury, spinal anesthesia, or nervous
system damage. It can also result from the
depressant action of meds or lack of glucose
(eg, insulin reaction or shock). Neurogenic
shock may have a prolonged course (spinal
cord injury) or a short one (syncope or
fainting). It is characterized by dry, warm skin
rather than the cool, moist skin seen in
hypovolemic shock. Another characteristic is
bradycardia, rather than the tachycardia that
characterizes other forms of shock
ANAPHYLACTIC SHOCK
- ANAPHYLACTIC shock
is caused by a severe allergic reaction when a
patient who has already produced antibodies
to a foreign substance (antigen) develops a
systemic antigen–antibody reaction. This
process requires that the patient has previously
been exposed to the substance. An antigen–
antibody reaction provokes mast cells to
release potent vasoactive substances, such as
histamine or bradykinin that cause widespread vasodilation & capillary permeability.
Crystalloids
- 0.9% sodium chloride
(normal saline solution)
- Lactated Ringer’s
- Hypertonic saline (3%, 5%,
7.5%)
Widely available, inexpensive
- Lactate ion helps buffer
metabolic acidosis
- Small volume needed to restore
intravascular volume
Requires large volume of infusion; can
cause pulmonary edema
- Requires large volume of infusion; can
cause pulmonary edema
- Danger of hypernatremia
Albumin (5%, 25%)
- Dextran (40, 70)
- Hetastarch
Rapidly expands plasma volume
- Synthetic plasma expander
Synthetic; less expensive than
albumin; effect lasts up to 36 h
- Expensive; requires human donors;
limited supply; can cause heart
failure
- Interferes with platelet aggregation;
not Recommended for hemorrhagic shock
- Prolongs bleeding & clotting times
ANEMIAS:
IRON DEFICIENCY ANEMIA- s/s and TX
Signs & symptoms -
tongue that is red, smooth, & sore, pallor, &
sensitivity to cold, weakness & fatigue.
Diagnosis- decreased Hgb, HCT, & iron.
treatment- diet high in iron, fiber, & protein
with increased fluids. Avoid teas & coffee
which reduce absorption of iron. Increase
the intake of vitamin C
IRON DEFICIENCY ANEMIA interventions
include iron injection deep into the muscle
using Z-track technique to avoid subQ
irritation & discoloration from leaking drug.
IM B12. make sure infants have iron fortified
cereals.
APLASTIC ANEMIA s/s dx tx
rare decrease of blood
cells from bone marrow failure, S&S are
bleeding, bruises, fatigue, DX with bone
marrow BX & may need a transplant
MEGALOBLASTIC ANEMIAS
an anemia (of
macrocytic classification) which results from
a deficiency of vitamin B12 & folic acid; can
be result of a lack of intrinsic factor;
characterized by many large immature &
dysfunctional red blood cells (megaloblasts)
in the bone marrow; associated with
pernicious anemia.
PERNICIOUS ANEMIA-
ANEMIA-chronic, progressive,
macrocytic anemia caused by a deficiency
of intrinsic factor which prevents the
absorption of dietary vitamin B12. Without
intrinsic factor RBCs are defective as they
mature.
PERNICIOUS ANEMIA-TX, DX, S/S
Signs & symptoms - tingling &
paresthesia of hands & feet, weight loss,
anorexia, dyspepsia. Diagnosis- bone
marrow aspiration shows increased
megaloblasts, few maturing erythrocytes &
defective leukocyte maturation. Peripheral
blood smear reveals oval, macrocytic,
hyperchromic erythrocytes. treatment- diet
high in iron & protein & restricting highly
seasoned or extremely hot foods. Vitamins
especially B12 & B6, Vitamin C & folic acid.
MYELODYSPLASTIC SYNDROMES (MDS) formerly known as "preleukemia")
are a
diverse collection of hematological
conditions united by ineffective production
of blood cells & varying risks of
transformation to acute myelogenous
leukemia. Anemia requiring chronic blood
transfusion is frequently present. Although
not truly malignant, MDS is nevertheless
classified within the hematological
neoplasms.
HEMOLYTIC ANEMIAS
anemia due to
hemolysis, the abnormal breakdown of red
blood cells either in the blood vessels
(intravascular hemolysis) or elsewhere in the
body (extra vascular). It has numerous
possible causes, ranging from relatively
harmless to life-threatening. The general
classification of hemolytic anemia is either
acquired or inherited. Treatment depends
on the cause & nature of the breakdown
.SICKLE CELL ANEMIA-
The RBCs are rigid & rough,
forming an elongated sickle shape &
impairing circulation by “clumping”
together. This happens during periods of
hypoxia which can be provoked by
strenuous exercise, high altitude,
unpressurized aircraft, cold &
vasoconstrictive drugs.
SICKLE CELL ANEMIA- S/S
aching bones, jaundice, pallor,
tachycardia, family history, frequent
infections, joint swelling & leg ulcers,
especially on ankles. Sickle cell crisis is very
painful.
SICKLE CELL ANEMIA-DX
Diagnosis- decreased RBC,
elevated WBC & platelet counts, decreased
ESR. HB electrophoresis shows HbS.
SICKLE CELL ANEMIA-TX
iron & folic acid supplements
prevent dehydration & analgesics for pain.
Interventions during crisis include warm
compresses to painful areas, (cold
aggravates the condition) maintain bed
rest to reduce workload on the heart & to
reduce pain, encourages fluid intake to
prevent dehydration, which can precipitate
crisis
THALASSEMIA / THALASSEMIA MAJOR (Cooley’s
Anemia)-
an group of inherited disorders
associated with defective hemoglobinchain
syntheses; occurring worldwide,
highest prevalence in people of Mediterranean, African & Southeast Asian
ancestry.